nuraynnnn-.

Topic B: Ocular Manifestations of Systemic Diseases

2012-01-29T04:03:00.001-08:00

1. Vitamin Deficiency
*Vitamins are essential for healthy growth and development, cannot be synthesised by an organism and are obtained from an individual's diet.
*Vitamin Deficiency is caused by nutritional deficiency and/or socio-economic status.
*Vitamin Deficiency can manifest ocularly, systemically or psychologically.

2. Vitamin A Deficiency
*Vitamin A is essential to maintain mucus membranes, skin and vision.
*Vitamin A Deficiency can manifest ocularly into Xeropthalmia.
*Xeropthalmia progresses in the order of night blindness to Bitot's Spots (foamy grey, triangular spots of keratinised epithelium in the conjunctiva) to conjunctival Xerosis (abnormally dry conjunctiva) to corneal Xerosis (abnormally dry cornea) to Keratomalacia (softening and necrosis (morphological changes indicative of cell death due to the progression of enzymatic degradation) of the cornea) to blindness.

3. Cotton Wool Spots (CWS)
*CWS is the accumulation of mitochondria and ruptured cells within areas of swollen nerve fibre layers.
*CWS is caused by the vascular disease that stops or reduces axoplasmic transport.
*CWS is a sign of ischemia (insufficient supply of blood) or microinfarct(mini localised area of ischemic necrosis due to the arterial occlusion or venous drainage of that part).
*CWS reabsorbs over 6-8 weeks leaving a groove defect on the nerve fibre layers and an arcuate visual field defect.

4. Hard Exudates
*Hard Exudates are lipid and liporotein depositions between areas of functional and diseased retina.
*Hard Exudates are caused by an increase in vascular permeability.
*Hard Exudates are seen as well defined, waxy, shiny areas within the outer plexiform layer. They can be individual dots, circinate (circular or ring-like) or a macular star.

5. Retinal Oedema
*Superficial Retinal Oedema is seen as a diffuse haze in the nerve fibre layers. It is common at the posterior pole and optic nerve head. It occurs in hypertension and papilloedema.
*Deep Retinal Oedema is seen as a dense haze in the outer fibre layers. It is common at the posterior pole and macular. It occurs in post-cataract surgery and diabetes.
*Cloudy Retinal Oedema is seen as white or opaque. It is caused by arterial occlusion or ischemia.

6. Retinal Haemorrhages
*Pre-retinal Haemorrhage is posterior to the inner limiting membrane. It obscures the retinal blood vessels. It is seen as patches or D-shaped/boat-shaped. It may or may not be due to ocular disease(s).
*Flame-shaped Haemorrhage is within the nerve fibre layers. It follows the structure of the ganglion cell fibres. It is associated with the vascular disease that affects the superficial and peripapillary capillary tissue. Roth's spots is seen as a flame-shaped haemorrhage with a white or pale centre and is associated with systemic inflammation.
*Dot-blot Haemorrhage is between the inner nuclear layer and outer plexiform layer or middle retina. It is seen as round dots as it follows the divergence of axons. It takes longer to resolves in comparison to a superficial haemorrhage.
*Sub-retinal Haemorrhage is between the sensory retina and RPE. It is seen as dark coloured with retinal veins clearly visible above. It is amorphous. It is associated with retinal detachment (RD) and RPE (retinal pigmented epithelium) detachment, and resolves slowly.
*Sub-RPE Haemorrhage is between the RPE and Bruch's membrane. It has the same appearance as a sub-retinal haemorrhage but with well-defined borders. It is associated with RD and RPE detachment, and resolves slowly.

7. Microaneurysms
*Microaneurysms are the saccular balooning of weakened endothelial walls.
*Microaneurysms are caused by the cappilary occlusion or venous stasis in the inner nuclear layer.
*Microaneurysms are seen as small, round, dark red dots 1/2 the size of central retinal vein (CRV).
*Microaneurysms are very leaky and may cause oedema.

8. Neovascularisation
*Neovascularisation is a response of an ischemic retina. The starved retina releases angiogenic molecules known as vascular endothelial growth factor (VEGF) to promote the growth of new vessels.
*Areas of neovascularisation is include at the disc (NVD), at the iris (NVI) and elsewhere (NVE)
*Neovascularisation involves fibrotic proliferation and thus a risk of tractional retinal detachment.

9. Arteriosclerosis
*Arteriosclerosis is the thickening and hardening of the arterial walls. It is seen as arterial thinning, silver wiring or copper wiring. It presses down on the underlying thin-walled veins therefore partially occluding them.
*A/V nipping occurs when the vein dilates upstream of the crossing.
*A/V crossing occurs when the vein moves at a right-angle in an attempt to minimise occlusion.

10. Vein Occlusion

11. Arterial Occlusion

12. Diabetic Retinopathy
*Diabetes Mellitus is classified into 2 types: IDDM and Non-IDDM.
*Insulin Dependent Diabetes Mellitus is type 1 and is young in onset. It requires insulin due to the failed pancreas which are unable to produce insulin.
*Non-insulin Dependent Diabetes Mellitus is type 2 and is adult in onset. It requires diet control, physical exercise and oral therapy due to the failure of insulin to function although present.
*Diagnostic tests for Diabetic Mellitus include Blood Glucose Level and Glycated Haemoglobin. Diabetics will have a blood gluocose level of 4-8mmol/L and a glycated haemoglobin level of 7%. Normal individuals will have a glycated haemoglobin level os 4-6%.
*Complications of Diabetes Mellitus include kidney failure, cardiovascular disease, blindness in adults and amputation.
*Risk factors of Diabetic Retinopathy include duration of diabetes (>5years), poor glycemic control, hypertension, hyperlipidemia, pregnancy, smoking.
*Non-proliferative Diabetic Retinopathy (NPDR): Mild is seen as a microaneurysms, dot-blot haemorrhage and hard exudates away from the macula.
*Non-proliferative Diabetic Retinopathy (NPDR): Moderate is seen as microaneurysm, dot-blot haemorrhage, hard exudates away from the macula, cotton wool spots and venous beading in 1 quadrant.
*Non-proliferative Diabetic Retinopathy (NPDR): Severe is seen as dot-blot haemorrhage in all 4 quadrants, venous beading in 2 quadrants or IRMA (ischemic retinal microvascular abnormality) in 1 quadrant.
*Proliferative Diabetic Retinopathy (PDR) is seen as neovascualrisation elsewhere (NVE) and/or neovascularisation at the disc (NVD) which leads to fibrotic proliferation and thus a risk of tractional retinal detachment.
*Diabetic Maculopathy: Macula Oedema (MO) is seen as hard exudates/retinal oedema within 2 disc diameters (DD) of the macula centre.
*Diabetic Maculopathy: Clinically Significant Macula Oedema (CSMO) is seen as hard exudates/retinal oedema within 1/3 DD of the macula centre. Alternatively is may appear as more or equal to 1 DD within 1 DD of the macula centre.
*Other ocular signs of Diabetes include paralysis of 3rd/4th/6th cranial nerves, Blepharitis and Xanthelasmia, reduced tear production/TBUT, corneal oedema, decreased corneal sensitivity, delayed corneal healing, neovascularisation at the iris and AC angle, reduced physiological hippus and poor diation of pupil, snowflake cataract and fluctuation of refractive error.

13. Hypertensive Retinopathy

14. Papilloedema

15. Papillitis

16. Ischemic Optic Neuropathy (ION)
*Non-arteritic Ischemic Optic Neuropathy
*Arteritic Ischemic Optic Neuropathy
*Posterior ION

17. RAPD

18. Hyperthyroidism Graves Disease

Topic B: Ocular Manifestations of Systemic Diseases

2012-01-24T17:55:00.000-08:00

1. Vitamin Deficiency
-vitamins are essential for healthy growth and development
-vitamins cannot be synthesised from an organism
-vitamins are obtained from an individual's diet
-vitamin deficiency is due to nutritional deficiency and/or socio-economic status
-vitamin deficiency manifests into ocular, psychological or systemic disease(s)

2. Vitamin A Deficiency
-vitamin A is essential to maintain mucus membrane, skin and vision
-vitamin A deficiency manifests into an ocular disease known as Xeropthalmia
Xeropthalimia:
-night blindness
-Bitot's spots (foamy grey, triangular spots of keratinised epithelium on the conjunctiva)
-conjunctival xerosis (abnormally dry conjunctiva)
-corneal xeroxis (abnormally dry cornea)
-Keratomalacia (softenng and necrosis (morphological changes indicative of cell death due to the progression of enzymatic degradation) of the cornea)
-blindness
(ocular disease progresses in the abovementioned order)

3. Cotton Wool Spots (CWS)
-accumulation of mitochondria and ruptured cells within areas of the swollen nerve fibre layers
-caused by the vascular disease that stops/reduces the axoplasmic transport
-sign of ischemia (insufficient supply of blood) or microinfarct (mini localised area of ischemic necrosis produced by the occlusion of arterial supply or venous drainage at that part)
-reabsorbs over 6-8 weeks
-leave groove defect in the nerve fibre layers
-arcuate visual field defect

4. Hard Exudates
-lipid and lipoprotein deposition between areas of functional and diseased retina
-caused by increased vascular permeability
-seen as well-defined, waxy, shiny, areas in the outer plexiform layer
-can be in the form of individual dots, circinate (circular or ring-like) or a macular star

5. Retinal Oedema
-Superficial
-seen as a diffuse haze in the nerve fibre layer
-common at the optic nerve head and the posterior pole
-occurs in hypertension or papilloedema
-Deep
-seen as a dense haze in the nerve fibre layer
-common at the macula and the posterior pole
-occurs in post-cataract surgery or diabetes
-Cloudy
-seen as white/opaque
-due to arterial occlusion and ischemia

6. Retinal Haemorrhages
-Pre-retinal
-posterior to the inner limiting membrane
-obscures retinal blood vessels
-seen as patches or D-shaped/boat-shaped
-may or may not be due to ocular disease(s)
-Flame-shaped
-within the nerve fibre layer
-follows the structure of the ganglion cell fibres
-associated with the vascular disease that affects the superficial and peripapillary capillary bed
-Roth's spots
-flame-shaped haemorrhage with a white/pale centre
-associated with systemic inflammation
-Dot-blot
-between inner nuclear layer and outer plexiform layer
-seen as round dots as they follow the divergence of axons
-requires a longer time to resolve as compared to superficial haemorrhages
-Sub-retinal
-between sensory retina and RPE
-seen as dark coloured with retinal vessels clearly visible above
-amorphous shape
-associated with RD (retinal detachment) and RPE (retinal pigmented epithelium) detachment
-resolves slowly
-Sub-RPE
-between RPE and Bruch's membrane
-same appearance as sub-retinal haemorrhage but with well-defined borders
-associated with RD and RPE detachment
-resolves slowly
-Vitreous
-blood leaks through thte inner limiting membrane into the vitreous
-seen in trauma and RD

7. Microaneurysms
-saccular balooning of weakened endothelial walls
-caused by capillary occlusion or venous stasis in the inner nuclear layer
-seen as small, round, dark red, dots 1/2 the size of CRV (central retina vein)
-very leaky, may cause oedema

8. Neovascularisation
-caused ischemic retina
-starved retina releases angiogenic molecules vascular endothelial growth factor (VEGF) to promite the growh of new vessels
-areas of growth:
-NVE (elsewhere)
-NVD (at the disc)
-NVI (at the iris)
-fibrotic proliferarion
-risk of tractional retinal detachment

9. Arteriosclerosis
-arterial walls thicken
-arterial thinning
-copper wiring
-silver wiring
-press down on the underlying thin-walled veins
-partially occlude the veins
-A/V nipping: vein dilates upstream of crossing
-A/V crossing: vein moves at a right angle in an attempt to minimise occlusion

Topic B: Ocular Manifestations of Systemic Diseases - Retinal Response to Injury

2012-01-23T22:05:00.000-08:00

Cotton Wool Spots (CWS) is the accumulation of mitochondria and ruptured cells within areas of the nerve fibre layers. It is caused by the vascular disease that stops/reduces the axoplasmic transport. It is a sign of ischemia or microinfarct. Ischemia is an insifficient blood blood supply. Microinfarct refers to the mini localised area of ischemic necrosis produced by the occlusion of arterial supply or venous drainage at that part. CWS reabsorbs over 6-8 weeks in which it will leave a groove in the nerve fibre layers and an arcuate visual field defect.

Hard exudates is the lipid and lipoprotein deposition between areas of functional and diseased retina. It is caused by an increased vascular permeability. It is seen as a well-defined, waxy, shiny area in the outer plexiform layer. It can be in the form of individual dots, circinate (circular or ring-shaped) or a macular star.

Retinal Oedema consists of 3 types namely Superficial, Deep and Cloudy. Superficial retinal oedema is seen as a diffuse haze in the nerve fibre layers. It is common at the optic nerve head and posterior pole. It occurs in hypertension and/or papilloedema. Deep retinal oedema is seen as a dense haze in the nerve fibre layers. It is common at the macula and posterior pole. It occurs in post-cataract surgery and diabetes. Cloudy retinal oedema is seen as white/opaque. It is caused by arterial occlusion and ischemia.

Retinal Haemorrhages consists of 6 types namely Pre-retinal, Flame-shaped, Dot-blot, Sub-retinal, Sub-RPE and Vitreous. Pre-retinal haemorrhage is posterior to the inner limiting membrane. It obscures the retinal blood vessels. It is seen as patches or boat-shaped/D-shaped. It may or may not be due to ocular disease(s). Flame-shaped haemorrhage is within the nerve fibre layer. It follows the stucture of the ganglion cell fibres. It is associatied with the vascular disease affecting th esuperficial and peripapillary capillary bed. Roth's spots is a flame-shaped haemorrhage with a white/pale cente and is associated with systemic inflammation. Dot-blot haemorrhage is between the inner nuclear layer and outer plexiform layer. It is seen as round dots because they follow the divergence of axons. It takes longer to resolve as compared to superficial retinal haemorrhage. Sub-retinal haemorrhage is between the sensory retina and RPE. It is seen as sark coloured with retinal vessels clearly visible above it. It is amorphous. It is associated with retinal detachment and retinal pigmented epithelium detachment. It resolves slowly. Sub-RPE haemorrhage is between the RPE and Bruch's membrane. It has the same appearance as a sub-retinal haemorrhage but with well-defined borders. It is associated with retinal detachment and retinal pigmented epithelium detachment. It resolves slowly. Vitreous haemorrhage is caused when blood leaks through the inner limiting membrane into the vitreous. It is seen in trauma and/or retinal detachment.

Microaneurysms is the saccular balooning of weakened endothelial walls. It is caused by capillary occlusion or venous stasis in the inner nuclear layer. It is seen as small, round, dark red dots, 1/2 the size of the central retinal vein. It is very leaky and may cause oedema.

Neovascularisation is the response of an ischemic attack. It is caused by the starved retina which releases angiogenic molecules VEGF (vascular endothelial growth factor) to promote new vessel growth. Areas of growth include everywhere (NVE), at the disc (NVD) and iris (NVI). It is a fibrotic proliferation and there is a risk of a tractional retinal detachment.

Topic B: Ocular Manifestations of Systemic Diseases - Vitamin Deficiency

2012-01-23T21:55:00.000-08:00

Vitamins are essential for healthy growth and development. It canno tbe synthesised from an organism. It is obtained from one's diet. Vitamin deficiency is due to socio-economic status and/or nutritional deficiency. It can manifest psychologically, systematically or in the ocular region.

Vitamin A is required to maintain mucus membranes, skin and vision. Vitamin A deficiency results in Xeropthalmia which progresses in the order of night blindness to Bitot's spots to conjunctival Xerosis to corneal Xerosis to Keratomalacia and ends in blindness. Bitot's spots are foamy grey, triangular spots of keratinised epithelium on the conjunctiva. Conjunctival and cornea Xerosis refer to abnormally dry conjunctiva and cornea respectively. Keratomalacia is the softening and necrosis of the cornea. Necrosis refers to the morphological changes indicative of cell death due to the progression of enzymatic degradation.

Topic B: Ocular Manifestations of Systemic Diseases

2012-01-23T18:33:00.000-08:00

Sub-retinal Haemorrhages
Sub-RPE Haemorrhages
Vitrous Haemorrhages
Microaneurysms

Remaining ocular diseases to cover for today:
Neovascularisation
Arteriosclerosis
CRVO
BRVO
CRAO
BRAO

Topic B: Ocular Manifestations of Systemic Diseases - Microaneurysms

2012-01-23T18:30:00.000-08:00

Microaneurysms
-saccular balooning of weakened enodthelial walls
-due to capillary occlusion or venous stasis in the inner nuclear layer
-appears as small round dark red dots 1/2 the size of CRV (central retinal vein)
-very leaky, may cause oedema

Topic B: Ocular Manifestations of Systemic Diseases - Retinal Haemorrhages Part 2

2012-01-23T15:57:00.000-08:00

Sub-retinal Haemorrhage
-between the sensory retina and RPE (retinal pigmented epithelium)
-seen as dark-coloured with retinal vessels clearly visible above
-amorphous
-associated with RD (retinal detachment) and RPE detachment
-resolves slowly

Sub-RPE Haemorrhage
-between the RPE and Bruch's membrane
-same appearance as sub-retinal haemorrhage but with well-difined borders
-associated with RD and RPE detachment
-resolves slowly

Vitreous Haemorrhage
-blood leaks throught the inner limiting membrane into the vitreous
-seen in trauma and/or RD

Topic B: Ocular Manifestations of Systemic Disease - Day 1 Recap

2012-01-23T14:34:00.000-08:00

Vitamins
-essential for healthy growth and development
-cannot be synthesized by an organism
-obtained from diet
Vitamin Deficiency
-due to socioeconomic status and/or nutritional deficiency
-manifests into systemic, psychological or ocular disease(s)

Vitamin A
-essential to maintain mucus membranes, skin and vision
Vitamin A Deficiency
-Xeropthalmia
-night blindness
-Bitot's spots(foamy grey, traingular spots of keratinised epithelium on the conjunctiva)
-conjunctival Xerosis (abnormal dryness of the conjunctiva)
-corneal Xerosis (abnormal dryness of the cornea)
-keratomalacia (softening and necrosis (morphological changes indicative of cell death due to the progression of enzymatic degradation) of the cornea)
-blindness

Cotton Wool Spots (CWS)
-accumulation of mitochondria and ruptured cells within areas of swollen nerve fibre layers
-caused by vascular disease that stop/reduce axoplasmic transport
-sign of ischemia (insufficient blood supply) or microinfarct (mini localised area of ischemic necrosis produced by occlusion of arterial supply or venous drainage at the part)
-reabsorbs over 6-8 weeks
-leaves groove defect in nerve fibre layer
-arcuate visual fiel defect

Hard Exudates
-lipid and lipoprotein deposition between functional and diseased retina
-due to increased vascular permeability
-seen as well-defined waxy, shiny areas in outer plexiform layer
-can be little dots, circinate (circular or ring-like) or macular star

Retinal Oedema
Superficial
-seen as diffuse haze at nerve fibre layer
-common at optic nerve head and posterior pole
-occurs in hypertension and/or papilloedema
Deep
-seen as dense haze at the outer plexiform layer
-common at macular and posterior pole
-occurs in post-cataract surgery and/or diabetes
Cloudy
-seen as white/opaque
-due to arterial occlusion adn ischemia

Retinal Haemorrhages
Pre-retinal Haemorrhage
-posterior to the inner limiting membrane
-obscures the retinal blood vessels
-can be in patches or boat-shaped/D-shaped
-may or may not be due to ocular disease
Flame-shaped Haemorrhage
-within the nerve fibre layer
-follows the structure of ganglion cell fibres
-associated with vascular disease affecting sperficial and peripapillary capillary beds
-Roth's sots
-flame-shaped haemorrhages with white/pale centre
-associated with systemic inflammation
Dot-blot Haemorrhage
-between inner limiting membrane and outer plexiform layer or middle retina
-appears as round dots as it follows the divergence of axons
-takes a longer time to resolve as compared to superficial haemorrhage
Sub-retinal Haemorrhage
Sub-RPE Haemorrhage
Vitreous Haemorrhage

Topic B: Manifestations of Ocular Disease - Retinal Oedema

2012-01-23T02:19:00.000-08:00

Retinal Oedema
Superficial
-seen as diffused haze in nerve fibre layer
-common at optic nerve head and posterior pole
-occurs in hypertension and/or papilloedema
Deep
-seen as dense haze in outer plexiform layer
-common at macula and posterior pole
-occurs in post-cataract seurgery and/or diabetes
Cloudy
-seen as white/opaque
-due to arterial occlusion and ischemia

Topic B: Manifestations of Ocular Disease - Hard Exudates

2012-01-23T01:13:00.000-08:00

Hard Exudates
-lipid and lipoprotein deposition between areas of functional and diseased retina
-due to increased vascular permeability
-seen as well-defined wacy, shiny areas in Outer Plexiform Layer
-can be individual dots
-or can be circinate (circular or ring-like)
-or can be macular star

Topic B: Manifestations of Ocular Disease - Cotton Wool Spots

2012-01-23T00:17:00.000-08:00

Cotton Wool Spots (CWS)
-accumulation of mitochondria and ruptured cells within areas of swollen nerve fibre layers
-caused by vascular disease that stops/reduces axoplasmic transport
-signs of ischemia (insufficient supply of blood) or microinfarct (mini localised area of ischemic necrosis produced by occlusion of arterial supply or venous drainage of th part)
-reabsorbs within 6-8 weeks
-leaves groove defect in nerve fiber layer(s)?
-arcuate visual field defect

Topic B: Manifestations fo Ocular Disease (Vitamin A Deficiency)

2012-01-22T23:47:00.000-08:00

Vitamins
-essential for healthy growth and development
-cannot be synthesized by an organism
-obtained from diet

Vitamin Deficiency
-due to socio-economic status
-or due to nutritional deficiency
-manifests systematically
-or manifests psychologically
-or ocular manifestation

Vitamin A
-maintains mucus membranes, skin and vision

Vitamin A Deficiency
Xeropthalmia
-night blindness
-Bitot's spots (foamy grey, triangular spots on the conjunctiva)
-conjunctival Xerosis (abnormally dry conjunctiva)
-corneal xerosis (abnormally dry cornea)
-Keratomalacia (softening and necrosis (morphological changes indicative of celldeath caused by progressive enzymatic degradation) of the cornea)
-blindness

2012-01-15T00:03:00.000-08:00

My big fat void deck wedding. The title of an article in The Sunday Times.

The writer focused on the fact that Malay couples go big on wedding decorations to turn public spaces into dream wedding venues. 2 grooms interviewed shared that they spent $100,000 and $30,000 on their wedding(s) respectively.

I am not in favour of this. It depicts the nature of pembaziran. When my time comes, I pray that I will be able to plan my finances wisely. I'd like to have a decent wedding, but at the same time ensure that I don't splurge. I wouldn't want my first day of married life to be spent calculating costs etc. I'd want to enjoy my marriage, start it on a good note.

Just my 2 cents worth; in response to the article written by Kimberly Spykerman.

To each his own.

1 January 2012

2012-01-01T00:11:00.000-08:00

It's 2012 already.

I want to be a better Muslim.

And I want a GPA of 4.0 for both DOPT & PCS for the remaining semesters.

I know, I can, I will, I must.

InsyaAllah, Amin.

2011-12-06T17:29:00.000-08:00

Dystrophy.

Degeneration.

Conjunctival Degeneration:

Pingueculum

Pterygium

Concretion

Corneal Degeneration:

Arcus Senillis

Vogt Limbal Girdle

Crocrodile Shagreen

Band Keratopathy

Corneal Guttata

Corneal Dystrophy:

Epithelial Basement Membrane Dystrophy

Meesman Dystrophy

Reis-Buckler's Dystrophy

Macular Dystrophy

Lattice (Type 1) Dystrophy

Granular (Type 1) Dystrophy

Fuch's Dystrophy

2011-10-09T16:22:00.000-07:00

Salam,

My TPJC girlfriend, Afiqah Liyana tied the knot yesterday. The first (of many, I'm pretty sure) of my friends to get married (Natalie's this November). Afiqah looked so beautiful (but then again, she is already beautiful au naturale; what more with make-up). It was the first time I actually saw her husband (Hamiley) in real life. Both the bride and groom looked very nervous but exceptionally happy.

The theme centred around blue. The food was good and the company, great. It was also a mini catch-up session for us all; between Cedar girls, TPJCians and NTU/NIE students. Everyone looked good!

Focusing on the wedding reception itself, two things made me feel all tingly and dreamy inside. One, when the chorus from Maher Zain's "For The Rest Of My Life" played the moment Afiqah and Hamiley cut the cake. That moment gave so much promise of a life together for them as a unit; husband and wife. Secondly, when the 'bersalaman' with parents was held, the song "Ayah Dan Ibu" by Sudirman was played. Very good planning there, people!

So anyway, I wish Afiqah Liyana and Hamiley all the best in their future endeavours. May Allah bless them with the great things in life. InsyaAllah, Amin.

Girlfriends with whom I attended Afiqah's wedding with.
Top (from left): Ruzanna, Jassika
Bottome (from left): Myself, Liyana (Ghani), Huda

A sweet surprise having bumped into Rau and family.
"Kak, you're lucky Abang tak datang"-Rau.
(Fir and I used to quarrel all the time back in secondary school).

Best Regards,
Nur Ain

2011-09-26T20:19:00.000-07:00

I celebrated 26th September on my own. I bought myself gift(s).

It's really heart-wrenching to know of individuals who share the same birthday as myself but are remembered. As they turn a year older, others celebrate their day with them.

But for me, I'm left on the shelf. Forgotten and ignored.

So tell me, what's my worth?

Because at the end of the day, I realise that people will fail me all the time. I myself am my strongest companion. And God of course.

I'm done with blogging. Let's call it a night.

2011-09-25T21:35:00.000-07:00

I'm independant. I don't need others to remember me. I exist for my own well being. (:

2011-09-25T21:26:00.000-07:00

It's the eve of my birthday and I'm feeling lousy. I don't think I'm going online tomorrow. Because it'd hurt to find out how little people remember or actually remember your day. I'm officially depressed.

2011-09-25T06:07:00.001-07:00

I'm covered, I'm modest. But that doesn't mean I ought to be overlooked. It's a sad thing when skimpily dressed flirty girls get all the attention and are remembered whilst them other girls are just treated as a passing. Go figure.

2011-09-25T05:55:00.000-07:00

As I turn a year older, I pray for good health. I pray for His guidance in my efforts to become a better Muslimah.

Deep inside, I wish to be more beautiful on the exterior whilst I work on my interior. I want to not only feel beautiful but also be seen as beautiful. Perpetually overshadowed in terms of appearance, I sometimes do wish I'm referred to as the pretty one. But then again, I guess that will never be a reality.

Lets see the amount of people who bother to wish me for my birthday. To hope for anything more is a ridiculous thought. (:

2011-09-16T05:03:00.001-07:00

I'm human. I'm female. 2 of the traits to be blamed upon whenever I get jealous. Brains over beauty, they say. But sometimes, you want to be beautiful too.

Sometimes, all I need is "You're beautiful".

2011-09-12T21:14:00.000-07:00

Sometimes, you need to realise that people are not going to always be there for you.

I pride myself in being an independent woman. But let's face it, there are times when I just want to share certain things with a certain someone. And it really brings out all the negativity in me when the individual is just not there.

I need someone who will always be there for me. I want to be the priority, not the option.

I'm tired. I wasted close to an hour waiting for you but to no avail. I have so many things to tell you.

Single life, probably the best times of my life. Go figure.

2011-09-11T20:44:00.000-07:00

I overhead Cikgu Rani sharing with his students about how mothers who get pregnant and give birth after the age of 30 have a high risk of their child suffering from down syndrome; and that it is compulsory to check for this possible defect. That really set me thinking. In my pursuit of a stable and/or better future, I intend to push marriage to later on in my life. But now, I realise that I'd be risking it for my future children.

So tell me, what now?

Physical Properties of CL Materials

2011-08-24T03:03:00.001-07:00

Physical Properties of CL Materials

Wettability: the ability of the liquid to cover the solid; an indication of the adherence of the liquid to the solid apart from the cohesive forces holding the liquid together. The larger the contact angle, the lesser the wettability of the lens material; the smaller the contact angle, the more the wettabilityof the lens material. Wetting is dependent on (1) surface tensions of the liquid and solid respectively and (2) interfacial tension between the liquid and the solid. Wetting can be improved by (1) decreasing liquid surface tension, (2) decreasing liquid-solid interfacial tension or (3) increasing solid surface tension. In-vivo tests of wettability include (1) tears coverage: ability of tears to form a complete layer on the lenses and (2) break-up time: ability of lenses to maintain complete tear layer. In-vitro tests of wettability include (1) sesile drops (liquid-in-air method; reccomended for RGPs) in which advancing angle surpasses value of receeding angle and (2) captive bubble (air-in liquid method; reccomended for SCLs) in which receeding angle surpasses value of advancing angle.

Dimensional Stability: the ability of lens material to retain its original dimensions under conditions of use. Variations in temperature (heat resistance: ability of lens material to withstand extreme heat without reforming). Thermoplastics are non-crosslinked polymers which generally do not withstand heat; can be reheated, softened and moulded into a new shape. Thermosettings are crosslinked polymers which can generally withstand extreme heat. Variation in pH (monomer dependant; HEMA + methacrylic acid). pH<7 = no dissociation = less methacrylic ions = less repulsion = decreased water entering = lens shrinks = becomes tight. ph>7 = dissociation = more methacrylic ions = more repulsion = more water entering = lens swells = becomes loose.

Refractive Index: constant that characterises lens material; inversely proportional to water content and directly proportional to density.

Water Content (only for SCLs): ability of lens to absorp water and swell. increase warer content = increased dissolved oxygen into lens material = increased atmospheric oxygen reaching cornea. Water content = [wet (wet weight - dry weight)/wet weight] x100.

Physiological Properties of CL Materials

2011-08-24T02:41:00.000-07:00

Physiological Properties of CL Materials

Oxygen Permeability: an inherent material property; not a function of thickness, power or curvature. P=Dk. P represents oxygen permeability with units 1o^-11. D represents diffusion coefficient which is how rapid gas molecules enter the lens material; important for RGPs. k represents solubility coefficient which is the amount of gas dissolved in a unit of cube of lens material for every unit of pressure overlying the lens material; important for SCLs.

Oxygen Transmissibility: amount of oxygen that enter the lens material of given thickness. T= Dk/L. T represents oxygen transmissibility with units 10^-9. Dk represents oxygen permeability with units 10^-9. L represesents the lens material thickness; high myopes tend to have a thin centre and thus high oxygen transmissibility whilst aphakes tend to have a thick centre and thus low oxygen transmissibility. To increase oxygen transmissibility; (1) increase D value by having loose/flexible arrangement of polymer chains, (2) increase Dk value by increasing water content within polymer matrix or (3) decrease L value by fabricating lens material thickness to as thin as possible. In-vitro oxygen transmissibility values are 24 for daily wear and 87 for extended wear.

Equivalent Oxygen Performance: indirect measure of cornea's oxygen thirst. Obtained by comparing measurement of cornea's oxygen demand after 5 minutes of wearing contact lenses and calibration of cornea's oxygen deman within 5 minutes of not wearing contact lenses. In-vivo EOP values are 9.9% for daily wear and 17.9% for extended wear.

Biocompatibility: ability of lens material to be compatible to ocular tissue. (1) Lens material must be inert (ie: should not react or cause other materials to react with ocular tissue, tear or lens care products it comes into contact with). (2) Lens material must not contain leachables which can be transported from contact lenses to external eye through water movement within polymers of lens material; common leachables include unreacted monomers, cross-linking agents, unbound tinting chemicals and other chemicals used in manufacturing. (3) Lens material must not be selectively absorbing of metabolites, toxic substances, microorganisms and other substances present in the environment.

RGP Lens Design

2011-08-24T02:38:00.000-07:00

RGP Lens Design

Single Cut Lens: one curve anteriorly irregardless of the number of posterior curves

Lenticular Cut Lens: anterior optic curve and carrier curve respectively irregardless of the number of posterior curves

Monocurve Lens: one curve posteriorly

Bicurve Lens: two curves posteriorly

Multicurve Lens: mutiple curves posteriorly

Instruments and Tolerances for CL Verification

2011-08-24T02:26:00.000-07:00

Instruments and Tolerances for CL Verification

Radii of Curvature (radiuscope or modified keratometer with tolerance of +/- 0.05mm)

Edge Profile (projection magnifier or palm test)

Power (focimeter with a tolerance of +/- 0.12D within +/- 10.00D and +/- 0.25D exceeding +/- 10.00D; +/-0.25D tolerance within power (for back vertex power) added for soft lenses within)

Lens Quality (magnifying loupe (hand-held magnifier), projection magnifier, slit-lamp biomicroscope or dark-fieldmicroscope)

Lens Parameters( Diameter, Optic Quality Peripheral Curve Width, Lens Thickness)

Diameter (v-gauge with tolerance of+/- 0.10mm or magnifying loupe x10(hand-held magnifier) with tolerance of+/- 0.10mm for no blend, +/- 0.20mm for light,+/-0.30mm for medium and +/- 0.40mm for heavy)

Optical Quality (magnifying loupe x10 (hand-held magnifier) with tolerance of +/- 0.10mm for no blend, +/- 0.20mm for light, +/- 0.30mm for medium and +/- 0.40mm for heavy)

Peripheral Curve Width (magnifying loupe x10 (hand-held magnifier) with tolerance of +/- 0.10mm for no blend, +/- 0.20mm for light, +/-0.30mm for medium, +/- 0.40mm for heavy)

Lens Thickness (thickness gauge with tolerance of +/- 0.05mm or rediuscope with tolerance of +/- 0.02mm)

2011-06-26T05:44:00.001-07:00

chapter 4
• anisometrope: difference in power for both eyes/lenses >1.50
• vertical imbalance: >1 prism diptre; anisometropes will find discomfort and possibly double vision
• solutions to vertical imbalance:
i) contact lenses: lenses follow eye movements
ii) 2 pairs of spectacles: one for distant vision, one for near vision (oc lowered to near visual point)
iii) Educate patient to use central portion of lenses when reading (ie to tilt head downwards instead of gazing downwards)
iv) Fresnel prism: made of PVC; can be trimmed to sized up to 30 prism diopter; stick to back surface of lens with water; cosmetically not so nice; flexible
v) Bicentric grinding: 2 optical centres – one for distant vision, one for near vision – for lens with higher prism
vi) Bifocal lenses with dissimilar segments: round seg bifocals; flat top bifocals, a seg bifocals. segment is plus lenses in different shape
• Creating prism in spectacles
i) Prescribe prism: lab will use decentration with the formula P = cF
ii) Grind-in prism: thickness difference between apex edge and base edge

2011-06-26T04:36:00.000-07:00

Chapter 3
• refractive index: ratio of the velocity of light in air to that of in the refractive medium
• higher refractive index = thinner/flatter lens
• thinner/flatter lens are cosmetically acceptable for high refractive errors (>3.00)
• tolerable constringence value = 0.15 prism diptres
• high refractive index = high constringence
• abbe no.: >45 low dispersion, <45/>39 medium dispersion, <39 high dispersion
• high refractive index = high density = low volume (ie lighter)
• plastic vs glass
i) plastic is lighter
ii) plastic is superior for impact resistance
iii) plastic is generally more expensive but becoming cheaper
iv) plastic is more prone to scratches
v) plastic has more tinting options
vi) plastic has a wider frame selection
vii) plastic does not fog up so easily
viii) plastic offers better UV protection
ix) plastic will warp if grind too thin in the middle (minus lenses)

2011-06-26T03:03:00.001-07:00

Chapter 2
1) Aberrations
• Distortion
a) Pin cushion distortion: positive lenses, magnification increases toward the borders
b) Barrel distortion: negative lenses, minification increases toward the edges
• Oblique astigmatism
a) Controlled by aspheric lenses
b) Peripheral light rays strike the lenses obliquely → causes a break in the off-axis light rays into tangential focus and saggital focus → tangential focus and saggital focus do not coincide → causes blurry peripheral vision
• Chromatic aberrations
a) Occurs because of lens material when polychromatic light is used
b) Lens is unable to focus various colours of light onto one spot
c) Shorter wavelength = ↑ refractive index
d) cF/V
c = distance from the optical centre
F = lens power
V = abbe no. (how dispersive a material is: ↑ abbe no. = less dispersive)
e) Image with high contrast: coloured fringes around image
f) Image with low contrast: blurry image
• Coma
• Spherical aberrations
• Field of curvature
2) Prismatic effects
• Base IN + OUT = cancel out (cancelling effect)
a) In + in = add up
b) Out + out = add uo
• Base UP + DOWN = add up (compounding effect)
a) Up + up = cancel out
b) Down + down = cancel out
3) Effective power (Fe) = F / (1-dF)
F = lens power
d = vertex distance
4) Lens centration
• Vertex distance: distance between back surface of lens and front surface of eye
• Horizontal distance: distancebetween R&L lenses optical centres
• Height: vertical distance between the top & bottom of lens → must be equal for both R&L lenses
• Pantoscopic tilt: dependent on frame position on patient face → determines portion of lens used
• Wrap angle
5) Field of view
• ↓ vertex distance = ↑ field of view
• Vertex distance R+L → similar f.o.v. for both eyes

Opthalmic Optics MST - 27 June 2011

2011-06-26T02:00:00.001-07:00

Chapter 1
• Minus lenses: myopia, 2 surfaces DS
• Plus lenses: hyperopia, 2 surfaces DS
• Astigmatic lenses: astigmatism, 1 surface DS 1 surface DC
• Lens Power (F) = F1 + F2
• Lenses used for Specs: Meniscus (front surface convex, back surface concave)
• Meniscus minus lenses: thick edge, thin centre
• Meniscus plus lenses: thin edge, thick centre
• ↑ power = ↑ thickness + ↓ refractive index
• F1 = (n-1) / r1

2011-04-24T16:13:00.000-07:00

When I first entered SP last year, I was not interested in making friends or even the slightest bit concerned about widening my network. My world only revolved around DOPT. That too, was limited to peers from my batch.

But things change. People change.

Sometime in Year 1 Semester 2, I received a warning email from DSD informing me that my CCA points was dangerously low as compared to the minimum average of 15. It was made known to me, only then, that my continuous participation in the SPOT Programme is not only dependant on my academic performance but my CCA involvement as well.

So I signed up for FLC, with only the need to get CCA points in mind. Little did I realise there was more to it than just accumulating CCA points.

Through FLC, I met many amazing individuals. I made new friends and learnt more about the old. I saw the good, the bad and the ugly side of me. I learnt to appreciate my strengths and acknowledge my flaws.

Truth be told, I'm glad things turned out the way they did. I find myself to be a much happier (more complete even?) individual now as compared to previously when I was cooped up in my own little world. It feels nice to actually know others from the various courses within your school and be able to say "Hey, I know her/him!" rather than just walk past someone a total stranger to you. It creates a sense of camaraderie, really.

Year 2 Semester 1 Week 1 is over.
Hello Week 2! (:

MELLY GOESLOW & ARI LASSO - APA ARTINYA CINTA

2011-04-15T05:39:00.000-07:00

2011-03-24T04:47:00.001-07:00

Hello my dear readers,

I'm back from CLS FLP Camp 2011. I hope you missed me.

So anyway.

Day 1:
"Change is the only constant". A wake-up call for me. The last time I attended a leadership-related thing was in 2007. That was also the last year I uptook a leadership role. I found that I was out of my element. I was team leader for Blind Domino. We came in third place. Personally, I found that my team mates respectd my role as team leader and were very cooperative. They gave me a rating of 8-9 as a leader whom they woulld follow in any situation. Only Hannah rated my a 6. But I understood where she came from. I played a double role; both as Hannah's partner and team leader. In the chaoticness (is there such a word?) of it all, I left Hannah unattended, blindfolded and feeling uneasy.

Day 2:
"These problems are real, and you can't turn off real life. So I won't try. Instead, I'll give you a set of tools to help you deal with real life." Land Expedition: Johnathan stepped up and volunteered to be the team leader. Shi Yong was assistant as he was in-charge of the expedition planning the previous night. REDDY completed only 2 out of 4 stations. However, we were contented and proud of ourselves. Our aim was to connect with each other and have a fun time; which we did. I was personally impressed with Johnathan, because he put the team's needs over his wants. As a leader, he would have wanted REDDY to win the challenge. However, as a team mate and friend, he prioritised our safety and well-being. For that, he deserves recgnition. Survival Game: I was the only individual 'survivor' in REDDY. But as a team, REDDY was the only team which 'survived'. (: The way the game/challenge was conducted required our utmost focus and the ability to think on our feet. It was very stressful and the reenactment was very realistic (kudos to Tony!). I personally feel that it was a very good activity because it forces you to RESPOND under pressure. *THUMBS UP*

Day 3:
"Leadership is communicating to people their worth and potential so clearly that they come to see it in themselves." The quote I've just shared was a reflection of the previous day. Tony had a chat with the great leaders and seeked our help to boost the poor leaders. Personally, I didn't see the individuals identified as poor leaders in my Events Committee to be. To me, they're good leaders at the very least. True enough, Whai Ee and Joaquim proved their worth. Whai Ee stepped up; volunteered to lead in the activity River Crossing which led to a win-win situation whereby all 4 committees worked hand-in-hand. Joaquium, althugh afraid of heights, stepped up to lead in the final challenge: Ropes Course. Our final night turned out pretty well, I must say. I won best leader/camper for Events Committee. Chloe came in second. Am truly appreciative of my fellow team mates for recognising my efforts and seeing it as signs of great leadership. The performances were very very entertaining - Team Socket (Editor Team & Logistics) acted out a Pokemon skit and dance, Powerpuff Aiders (Security and First Aid) reenacted Powerpuff Girls, SociaR (Social) conducted a and us REDDY (Events) had our Mango Idol.

Day 4:
I cried. We cried. Everyone cried. The reflection Tony made us do really made us dig deep inside to see how it impacted us and moulded us into the leaders that we are today. We then had an appreciation session where we presented a coloured pebble to someone whom we want to acknowledge their strengths. My heart was filled with warmth by the acknowledgement received from fellow campers.

Overall, CLS FLP 2011 was an awesome experience. I shall treasure the memories and keep it in my heart. (:

Love,
Nur Ain Binte Abdul Razak

2011-03-20T11:29:00.000-07:00

A random note from me to you, in alphabetical order of initials (used to protect identity).

AR. I had a crush on you. I really did. Fortunately I got over you. Frankly, you're not a good guy. Your values and mindset are very different from mine. You smoke and are into skimpily dressed Chinese girls. Well, you're with one now. I hope you're happy. Because I for one, am glad I did not pursue my feelings and left it at that. You were afterall, just a crush.

AZ. I thought you were the one after the heartache of having my feelings toggled by someone who was into me but couldn't bear to leave his gf. For the record, I was not aware of his relationship status. You were all kinds of wonderful. On a side note, I dreamt of you a few nights back. You asked for my hand in marriage without informing me, but rather, went straight to my father who accepted. Alas, it's just a dream. She is a really lucky girl. Because you and I both know that a man like you is a dream come true. You're grounded both duniawi and ukhrawi. Someone who will be able to guide his wife and eventually family ke jalan yang diredhaiNya.

EC. We were great together, really. The random calls to my house without worrying about being questioned by my mother, the late night chats, the expensive birthday gifts, our private moments. A pity religion got in the way, I really did like you. It's been quite awhile since we contacted each other. I hope things are good on your end.

FM. Everytime I try to erase you from my mind and heart, I fail. It's been 4 years and still counting. Words alone cannot describe how I feel. It hurts. But I'm sure I'll get over you eventually with His help. Because, if you're not my jodoh then you're not my jodoh. If you think you're meant for her, treat her well okay? Don't treat me like a boyfriend would, because you're only ruining me; and cheating on her. I don't want to be the other woman. I choose to be alone rather than hurt a fellow lady's heart.

FR. Graduation Night; you asked me to be your girlfriend. But I said no. Truth be told, I did have feelings for you prior to the offer, but it faded because I simply got tired of waiting and I wasn't sure you were worth the wait. I was infatuated, not in love with you. I did ask you though, why did you ask me only on graduation. Your reply? You were afraid of being rejected. I was disappointed at the response, truly. Proved how cowardly you can be as a guy. You found me on FB recently and added me up. You're engaged now. I wish you all the best.

FS. So tell me, what are we now? Are we even friends? Or strangers? You used to tell me everything; from family to friends to work to school to affairs of the heart. Mum even thought we were together. Literally everything. And you did alot of things for me. I loved your company and presence in my life. We were the best of friends. But things have changed. Where are you? Who are you now? Do I even cross your mind? I bet the answer is no. So much for "I'll be there for you.." *rolls eyes infinitely*

HD. Big joke. You asked me if you had a chance. You asked me if I'd consider you if you tried to woo me. I said maybe, because affairs of the heart is something that is complicated and needs very careful consideration. Slowly but surely, you disappeared from my life. The next thing I knew, you had a gf. What on complete earth were you thinking? No, what on complete earth was I thinking? One word: hopeless.

MH. You're a good guy. The only reason I rejected you when you asked me to be your gf was the age barrier. I've a thing about dating younger guys. Plus, dating you would complicate matters considering our multiple connections. I'm sure you'll find someone better than me; seorang wanita yang baik untuk lelaki yang baik. I'm glad to see you doing well in life. Happier still that we're friends despite what happened.

Every single day, I pray to Him to guide me through the right path. And dipertemukan with the one for me. Every. Single. Day.

Only HE knows.

With love,
Nur Ain Binte Abdul Razak

7 Habits of Highly Effective Youth

2011-03-19T18:10:00.000-07:00

Salam dear readers,

So we had our CLS FLP Pre-Camp training yesterday (18 March 2011, 0830-1715h). Zara, our trainer, guided us through the 7 habits of highly effective youth. Thought I'd share some insights.

Habit 1: Be Proactive
See: I am responsible for my choices.
Do: I choose to act, not react.
Get: I am in control.

In future, I will stop and pause to think before I do something. I will act, and not react. InsyaAllah.

Habit 2: Begin with the End in Mind
See: I visualise results.
Do: I have a mission statement that documents my purpose in life.
Get: I live according to my mission.

Currently a relief teacher with MOE; I will attain a Diploma in Optometry by 2013, a Bachelor of Science (with Honours) in Optometry by 2015, a Post-Graduate Diploma in Education (PGDE) by 2016, complete teaching bond with MOE by 2018/19, then set up my own Optometric Practice by 2021. InsyaAllah.

Habit 3: Put First Things First
See: I focus on what's important.
Do: I plan my time according to my priorities.
Get: I achieve my goals.

I used to be a 'half-blood'; both a Yes-Man and a Prioritizer. But now, I choose to only be the Prioritizer. I will exercise regularly (sit-ups and streches everyday, run twice a week on weekends), study smart (make notes upon completion of each chapter by the lecturer once year 2 begins), have at least 6h of sleep (be in bed by 11pm latest) and go on dates with my close friend(s) once a month on a Friday/Saturday. Only then, will my life be more balanced and fulfilling with fewer cries and less stress. InsyaAllah.

Habit 4: Think Win-Win
See: I get better results by cooperating rather than competing.
Do: I persist in looking for win-win outcomes.
Get: I have more trusting relationships.

I will strive to not feel inferior to others. I am just as good if not better. As such, together with my fellow DOPT coursemates, I shall lead everyone's mindset to want to come to mutually beneficial decisions by first changing my own. I know, I can, I will. InsyaAllah.

Habit 5: Seek First to Understand, then be Understood
See: If I listen to understand, I'll be understood.
Do: I use Empathic Listening Skills.
Get: I gain stronger relationships.

I used to practice selective listening. But now I realise the impacts of my habit. As such, I pledge to listen with my eyes, heart and ears; stand in the other person's shoes and practice mirroring. I will avoid ignoring, pretend listening and selective listening. InsyaAllah.

Habit 6: Synergize
See: I value differences in others.
Do: I seek the Third Alternative.
Get: I achieve better results.

With effect from Year 2, I will work well with my project group mates; ie: I will not bear the burden of haphazard work or late submissions alone but instead share the responsibilities and voice out my concerns rather than bitch. Indeed, am looking forward to fantabulous group dynamics with Leanne Lee Hui Xin and Sennette Shek Ming Wei, since the 3 of us have agreed to bend together for projects in Year 2 Semester 1. InsyAllah.

Habit 7: Sharpen the Saw
See: I continually improve as I take time for myself.
Do: I set and acheive goals and plan time for myself.
Get: I am recharged.

For my body, I will exercise regularly and get sufficient sleep(as stated in Habit 3). For my mind, I will frequent the library for self-help books. For my heart, I will cultivate personal relationships and create an uplifting environment for those around me. For my soul, I will indulge in my religious practices by reading the Al-Quran more often and not miss my prayers or do so only at the last minite. I need to learn to sit back, relax and enjoy myself once in a while.

That's all for now. Look forward to more insight posts from me. (:

Wassalam,
Nur Ain Binte Abdul Razak

2011-03-18T20:15:00.000-07:00

HAVE A FANTABULOUS WEEKEND PEOPLE;
WHILST I HAVE A WELL-RESTED ONE. (:

2011-03-16T19:55:00.000-07:00

EYE CANDY!! :D

It has been a long while since I had one. You make me excited just looking at you (:

2011-03-05T22:42:00.000-08:00

Hello. I am a happy goober. Last night was wonderful. Really spectacular. From dinner at Popeyes to brief Coffee Bean exchange then Hotfudge Ice Cream Sundae and the journey home. Marvelous.

2011-03-04T16:44:00.000-08:00

AYN
whom have always been there
to help me out
no matter what the problem is
Especially during the aftermath
of my o levels.
She was there and an absolute
help and a shoulder I needed.
I've yet to meet you since secondary school.
The reason is because I do not want to.
I feel that I'm not ready to meet you.
I want you to see me excel
and reach my goals.
Only then I would meet you
cause you are that one person,
I wouldn't wanna let down.
You are one of the few
who really thinks highly of me
and I really am grateful for everything
you've done
and I will keep my promise that
I would meet you again
once I'm really settled and ready

its been years, and i still have this piece from you.
what's become of us? i miss you. i miss us.
life must go on.

2011-03-02T02:33:00.001-08:00

Chapter 3.1: Duplex Nature of Retina
1. Photopic Vision vs Scotopic Vision
- visual acuity: more @ 6/6 vs less @ 6/6
- mediated by: cone photoreceptors vs rod photoreceptors
- lighting: bright illumination vs dim illumination
- sensitivity to light: less sensitive vs more sensitive
- colour vision: colour vs black&white
2. Cone Photopigments vs Rod Photopigments
- bleaching: bleached when m/q absorbs light & unable to capture another quanta of light
- regeneration: 1.5mins vs 5mins
- peak sensitivity: 565nm(red)+535nm(green)+430nm(blue)=555nm(yellow) vs 507nm (green)
- name/type: erythrolabe(red-L), chlorolabe (green-M), cyanolabe (blue-S) vs rhodopsin (purple - 10^15 m/qs)
3. Photochromatic Interval (PI)
- difference in sensitivity b/w photopic & scotopic vision
- =O: long wavelngths
- >O: other wavelengths
4. Purkinje Shift
- change in peak spectral sensitivity from scotopic to photopic vision
- scotopic: green brightest @ 507nm
- photopic: yellow brightest @ 555nm
5. Cone PRs vs Rod PRs
- most densely packed @ fovea vs most densely packed @ periphery 20degrees from fovea
- 150 000 cones/mm2 vs 150 000 rods/mm2
- present in fovea & periphery vs absent in fovea

2011-03-02T02:03:00.000-08:00

Chapter 2: Psychophysical Methods
1. Visual psychophysics measures the capability of the subject's vision using non-invasive methods.
2. Threshold is the minumum quantity of stimulus that can be detected.
3. Absolute threshold is the minimum quantity of stimulus that can be detected against a totally dark background (=0cd/m2).
4. Difference threshold is the minimum quantiti of stimulus that can be detected against a background that is not dark (>0cd/m2).
5. Threshold = 1/ Sensitivity (the higher the threshold value, the lower the sensitivity; the lower the threshold value, the higher the sensitivity)
6. Factors affecting threshold value are luminance background (absolute threshold against a totally dark background - 0cd/m2; difference threshold against a background that is not dark - >0cd/m2), attention, motivation, perfect (machines respond to either just seeing or just not seeinf) vs non-perfect observer (humans response is in probabilistic terms - 50% chance) and fatigue.
7. Method of Adjustment (increment/decrement of stimulus varies): increase stimulus intensity from non-seeing to just seeing; decrease stimulus intensity from seeing to just non-seeing. +ve: quick; obtain estimate threshold. -ve: habituation (delayed response); anticipation (response prior to threshold).
8. Method of Limits (discrete uniform steps): ASCENDING....invisible stimulus->increase stimulus intensity discretely->visible stimulus(just); DESCENDING....visible stimulus->decrease stimulus intensity discretely->invisible stimulus(just). +ve: quick. -ve: habituation; anticipation (only for descending).
9. Staircase Method (mixture/reversals of method of limits-ascending+descending): invisible stimulus->increase stimulus intensity discretely->visible stimulus (just)->REVERSAL->decrease stimulus intensity discretely->invisible stimulus (just). ReversalsX3-4. -ve: habituation (delayed response); anticipation (response prior to threshold).
10. Method of Constant Stimuli: 4 stimulus above threshold + 5 stimulus below threshold + estimated threshold = 10 stimulus -> presented randomly 20 times each -> subject to respond yes-no to seeing or non-seeing of stimulus. +ve: controls anticipation. -ve: time consuming.
11. Yes-No procedure: lowest % correct = 0%. highest % correct = 100%.
12. Forced Choice Procedure (plot stimulus intensity against percentage seen): 2AFC - lowest % correct (chance performance) = (100/2)%; highest % correct (perfect performance) = 100%; threshold = (chance+perfect)/2. 4AFC - lowest % correct (chance performance) = (100/4)%; highest % correct (perfect performance) = 100%; threshold = (chance+perfect)/2. 6AFC - lowest % correct (chance performance) = (100/6)%; highest % correct (perfect performance) = 100%; threshold = (chance+perfect)/2.
13. Adaptive method: SITA programme used in Humphrey Visual Field Analyser
14. Psychophysical Procedures commonly used in eyecare are Visual Acuity Testing, Visual Field Testing, Refraction, Binocular Vision Test and Colour Vision Test.

2011-03-02T00:35:00.001-08:00

Chapter 7: Motion Perception
1. Definition
2. Studied
- First Order Stimuli (Simple Stimuli): to study apparent motion
-flashing lights
t<30ms: no movement
t=60ms: optimum movement
60ms -sine wave gratings
2 waves: exchange b/w dark & bright bars leads to motion perception
- Second Order Stimuli: to study global motion perception
-random dot kinematogram
Dmin: min dist dots move to illicit motion perception
Dmax: max dist dots move to illicit motion perception
Coherence Threshold: % coherence that results in motion perception in a defined direction
3. Pathway
- magno pathway
-where
-when
- parietal pathway
-what
magno+parietal pathway = motion perception
4. Difference in Sensitivity in Detecting Motion
- sine wave gratings stimulus
-more sensitive to motion
-less sensitive to colour
- isoluminant stimulus
-more sensitive to colour
-less sensitive to motion
-motion perception (if any) due to parvo cells
5. Motion and Visual Acuity
- smooth pursuit
-inability to accurately follow moving stimulus with eye movement
- dynamic visual acuity
ability to detect moving stimulus
6. Saccadic Eye Movement
- selective suppression of magno pathway
-blur image in b/w
-clear image @ start/end
7. Clinical Applications
- diagnosis of glaucoma because magno pathway is affected

2011-03-01T23:54:00.001-08:00

Chapter 6: Temporal Aspects of Vision
1. Definition
- analysis of changes in illumination over time
2. Characteristics of Temporal Sinusoids
- Depth of Modulation
percentage depth of modulation = (amplitude/time) x 100%
-low depth of modulation
appears steady
no perception of flicker
-large depth of modulation
do no appear steady
perception of flicker
- Temporal Frequency
-low temporal frequency
flicker @ slow rate
-high temporal frequency
flicker @ fast rate
-critical flicker frequency (C.F.F.)
high temporal frequency that can just be resolved
3. Temporal Modulation Transfer Function (TMTF) Graph
- low temporal frequency
- middle temporal frequency (10Hz)
- critical flicker frequency (60Hz)
- X-axis labelled temporal frequency (Hz)
- Y-axis labelled relative sensitivity (percentage modulation)
- temporal sensitivity = 1/percentage modulation depth threshold
- anything under the graph = temporally resolved = perceived as flickering
- anything above/outside the graph = temporally unresolved = perceived as non-flicker
4. Temporal Visual Effects
- Talbot-Plateu Law
-TF beyond CFF
-TF(fused) appear as bright as steady light of same average luminance
- Brucker-Bartley Effect
-stimuli of same frequency
-flicker; appears brighter
-non-flicker; appears dimmer
- Broca- Sulzer Effect
-stimuli between 50-100ms; appear brighter
-stimuli <50ms or >100ms appear dimmer
5. Clinical Considerations
- Diagnosis
-open angle glaucoma
- Clinical Information
-retinal pigmentation
-age-related macular degeneration
6. Effect of Stimulus Size on C.F.F.
- Granit-Harper Law: increase in log stimulus area = increase in C.F.F.
7. Effect of Background Illumination on C.F.F.
- Ferry-Porter Law: increase in log retinal illumination = increase in C.F.F. (does not affect low frequency)

2011-03-01T22:58:00.000-08:00

Chapter 5: Spatial Vision
1. Definition
- ability to detact and/or analyse changes in brightness across space
2. Acuity Tests
- Detection
-ability to see an image
-yes or no response
- Recognition
-define what is seen
- Resolution
-ability to detect gaps
- Localisation
-ability to detect difference in gap sizes
3. Characteristics of Sine Wave Gratings
- Frequency
-no. of cycles of grating per degree substended @ eye
-1cycle=1dark bar + 1bright bar
- Contrast
-difference in brightness and darknes of object and background
-Lmax-Lmin/Lmax+Lmin=change in L/Laverage
-unit: Weber
- Phase
-position of grating
- Orientation
-loaction/position of grating relative to horizontal midline
4. Fourier Analysis
- SMTF Graph of Lens
-normal
-out of focus system
-transluscent lens
-X-axis labelled spatial frequency (cycles/degree)
-Y-axis labelled image contrast/object contrast
-Human Contrast Sensitivity Funtion
-low spatial frequency
-middle spatial frequency (4 cycles/degree)
-high spatial frequency
-very high spatial frequency (30[correctedhumanvision]-60[perfectvision] cycles/degree); no longer able to detect a gap
-X-axis labelled spatial frequency (cycles/degree)
-Y-axis labelled contrast sensitivity; obtained by 1/threshold contrast (non-seeing-seeing the gap)
5. Features of Contrast Sensitivity Function
- Low Spatial Frequency
-low sensitivity due to lateral inhibitions
-bright bar on surround and centre
- Middle Spatial Frequency
-cut off @ 4 cycles/degree
-dark bark on surround
-bright bar on centre
- High Spatial Frequency
-cut off @ 30-60 cycles per degree
-dark & bright bars on surround & centre
-decreased sensitivity due to packing density of retinal photoreceptors
-decreased sensitivity due to eye aberrations
*light falls on centre = excitation
*light fall on surround = inhibition
6. Clinical Implications of Contrast Sensitivity Functions
- Ocular Disease
-refractive error
-cataract
- Relationship with VA
-30 cycles/degree; 6/6 vision(snellen fn)
-60 cycles/degree; 6/3 vision(snellen fn)
*Minimum Angle Resolution = reciprocal of Snellen Fn

2011-03-01T20:11:00.000-08:00

Chapter 4.1: Colour Vision
1. Trichromatic Theory
- normal human colour vision
- any colour can be matched using 3 primary colours
2. Monochromacy
- 1 photopigment
- distinguished via intensity
- made the same by altering intensity
3. Dichromacy
- 2 photopigments
- distinguished via wavelength
- made the same by matching 1 wavelength with a metamer (composed of 2 wavelengths)
4. Trichromacy
- 3 photopigments
- distinguished via wavelength
- made the same by matching 1 wavelength with a metamer (composed of 3 wavelengths)
*metamers are stimuli that appear identical but are physically different
5. Experiments to Determine Spectral Sensitivity of Cone Photopigments
- Psychophysical Colour Matching Experiment: using dichromats and trichromats to match colours within a bipartite field
- Retinal Densitonometry: comparison b/w incident vs reflected light (wrt retina) @ different wavelengths to determine absorption spectrum (incident-reflected=absorption spectrum)
- Microspectrophotometry: comparison b/w incident vs transmitted light (wrt retina) @ different wavelengths to determine cone absorption spectrum (incident-transmitted=cone absorption spectrum)
- Electrophysiologic Recordings: determination of spectral sensitivity of cone using energy threshold value (sensitivity=1/energy)
6. Molecular Genetics of Photopigments
- Cone: consists of chromophore (absorb light quanta for vision) & opsin (determines absorption characteristics of each photopigment molecule)
-erythrolabe (red-L): coded on X chromosome
-chlorolabe (green-M): coded on X chromosome
-cyanolabe (blue-S): coded on chromosome 7
- Rod: coded on chromosome 3
7. Grassman's Law
- Additivity Property: metamers->add same wavelength to both stimuli->remains metamers
- Scalar Property: metamers->add/subtract same wavelength to both stimuli->remains metamers
- Associative Property: metamers (1); metamers (2) -> substitute (2) into (1) -> metamer (3) obtained
8. Colour Labels
- Hue (wavelength)
- Saturation (colour purity); desaturation occurs upon addition of white
- Brightness; longer wavelength appear brighter; brightest at 555nm
9. Hue Discrimination Function
- W-shaped
- blue (6nm)
- yellow (2nm)
- red
- X-axis labelled wavelength(nm)
- Y-axis labelled change in wavelength(nm)
10. Saturation Discrimination Function
- U-shaped
- blue (7 units)
- yellow (2 units)
- red
- X-axis labelled wavelength(nm)
- Y-axis labelled saturation power
11. Munsell Colour System
- Hue (wavelength): primary hues - red, gree, blue, purple, yellow
- Value (brightness): range 0(darkest)-10(brightest)
- Chroma (colometric purity/saturation): range 1-14
12. CIE Colour Specification System
- real primaries
-falls within CIE diagram
- imaginary primaries
-falls outside CIE diagram
-replaced with X, Y, Z labelling
- chromaticity coordinates
-transform imaginary primaries to chromaticity coordinates to obtain real primaries
-X=x/x+y+z
-Y=y/x+y+z
-Z=z/x+y+z
Chapter 4.2: Abnormal Colour Vision
1. Colour Perception Theories
- Trichromatic Theory: presence of all 3 cone photopigments
-erythrolabe (red-L)
-chlorolabe (green-M)
-cyanolabe (blue-S)
- Young's Trichromatic Theory: presence of all 3 cone photopigments @ receptor stage
-erythrolabe (red-L)
-chlorolabe (green-M)
-cyanolabe (blue-S)
- Herring's Opponent Colours Theory: presence of 3 colour combinations @ neural stage
-BlueYellow: b, r+g
-RedGreen: r, g
-BlackWhite (brightness): rgb
2. Classifications of Abnormal Colour Vision
- Monochromacy: presence of only 1 photopigment
-Cone Monochromats
all 3 cone photopigments present but do not function
normal VA
no nystagmus
no photophobia
-Blue Cone Monochromats
only cyanolabe (blue-S) present
photopic spectral sensitiviy = cyanolabe spectral sensitivity
poor VA
nystagmus
-Typical Rod Monochromats
absence of cone photopigments
rare
poor VA
nystagmus
colour blind
photophobia
- Dichromacy: absence of 1 photopigment
-Protanopia
replace erythrolabe (red-L) with chlorolabe (green-M)
-Deuteranopia
replace chlorolabe (green-M) with erythrolabe (red-L)
-Tritanopia
replace cyanolabe (blue-S) with erythrolabe (red-L)
or replace cyanolabe (blue-S) with chlorolabe (green-M)
- Anomalous Trichromacy: absorption of 1 photopigment displaced to abnormal position
-Protanomaly
erythrolabe (red-L) displaced to shorter wavelength
-Deuteranomaly
chlorolabe (green-M) displaced to longer wavelength
-Tritanomaly
cyanolabe (blue-S) displaced to lower sensitivity
3. Causes of Abnormal Colour Vision
- Acquired Defects
- Kollner'S Rule
BlueYellow defect: retinal disease
RedGreen defect: optic nerve disease
exceptions:
Blue-Yellow: glaucoma or dominant optic atrophy
Red-Green: juvenille macular degeneration
- Hereditary
-normal CV
-carrier of CVD
-suffers CVD
4. Colour Vision Tests
- Pseudoisochromatic (PIC) Plate
-vanishing design: invisible to R-G defect
-hidden design: invisible to normal CV
-transformation design: normal CV observe different image compared to CVDs
-classification design: protans confuse RedGrey, deutans confuse GreyPurple, tritans confuse PurpleBrown
Types
-Ishihara
-L'Anthony Album Tritan
-City University Test
-F2
- Hue Discrimination (Arrangement Tests)
-H16
-D-15
-L'Anthony Desaturated Test
-Fransworth-Munsell 100 Hue
- Nagel Anamaloscope
- colour matching of spectrum colours
- match red (superior semicircle) and green (inferior semicircle) to obtain yellow (full circle)
- Lantern Tests
-Holmes Wright B
-Holmes Wright Lanter A
-Farnsworth Lantern
5. Basic Definitions/Referrals
- Protans
-protanopes: missing long wavelength cone photopigment
-protanomats: anomalous long wavelength
- Deutans
-deuteranopes: missing medium wavelength cone photopigment
-deuteranomats: anomalous medium waelength
- Tritans
-tritanopes: missing short wavelength cone photopigment
-tritanomats: anomalous short wavelength

2011-02-27T21:40:00.001-08:00

CORNEA
Corneal Transparency
1. Lattice arrangement of corneal stroma’s collagen fibrils
2. Absence of blood vessels
3. Absence of cells
4. Absence of pigments
5. Corneal Deturgescence
Corneal Deturgesence
1. Anatomic integrity of corneal epithelium and endothelium (barrier function)
2. Metabolic pump
• Corneal endothelium without intercellular junctions
no junctions = no barrier = no pump function
• Normal corneal endothelium (2000-3000cells/mm2)
endothelial tight junction as barrier and Na/K-ATPase as metabolic pump
pump = leak
• Stressed corneal endothelium (800-1500cells/mm2)
increase in metabolic pump sites
pump = leak
• Decompensated corneal endothelium (<500cells/mm2)
lack of lateral membranes to contain any more increase in metabolic pump sites
leak > pump
3. Changes in osmolarity
4. Intra-Ocular Pressure (IOP)
• Increased IOP to more or equal to 50mmHg → abnormal endothelial cell functions → increased stromal swelling and corneal edema
• Corneal edema is a sign of one type of glaucoma
i. Signs: what the patient complains (redness)
ii. Symptoms: what we find on examination (conjunctival congestion)
Corneal metabolism
• a series of chemical processes in which energy is obtained and utilized to provide for normal tissue functions
• derived from ATP formed from glucose, that enters the eye via aqeous humor, tear film and limbal blood vessels
• highest metabolic rates in corneal epithelium and endothelium
• essential for:
1. renewal of cells
2. wound healing
3. transport processes (eg: metabolic pump)
4. maintain temperature
• 3 pathways:
1. Anaerobic Glycolytic Pathway
• Produced lactic acid and 2mols ATP
2. Aerobic Krebs Cycle
• Produces 2mols ATP-efficient
3. Pentose Phosphate Pathway
• Mainly functions to produce NADPH for synthesis of RNA, DNA, fatty acids and proteins

AQEOUS HUMOR
Formation of Aqeous Humor
1. Aqeous humor is formed by filtration from the blood capillaries through “blood-aqeous barrier” (non-leaky endothelial cells of the iris capillaries and non-pigmented epithelium).
2. The plasma which contains 10-20% of its proteins fill up the extracellular spaces between the capillaries and the lateral cell walls of the pigmented epithelium.
3. The “blood-aqeous barrier” excludes large molecules from the aqeous humor and maintains the clarity of the aqeous humor.
4. Solutes are actively transported from the cells into the intercellular channel by a solute pump thus making the the channel-fluid hypertonic.
5. Diffusion of solutes across the cell membranes occur down a concentration gradient (osmotic gradient) until the solutes are equally distributed throughout the space in which they are contained.
6. As the solutes move toward the openings of the channel, water enters across the walls.
7. Dilution of the newly formed aqeous humor occurs in both the anterior and posterior chambers, but at different rates.
8. As such, aqeous humor formed is clear, transparent and diluted.
Mechanisms of Aqeous Humor Formation
1. Dilution
2. Ultrafiltration
3. Active Transport
Drainage of Aqeous Humor
1. Ciliary Body
2. Anterior Chamber – Anterior Chamber Angle
3. Trabecular Meshwork
4. Canal of Schlemm – Collecting Channel
5. Aqeous Vein – Episcleral Plexus
6. Anterior Ciliary Vein

INTRA-OCULAR PRESSURE (IOP)
Glaucomatous Condition
1. Abnormality in outflow (resistance to drainage) from the anterior chamber is a more common cause for an increase in IOP as compared to an increased rate of aqeous humor formation in a glaucoma case.
2. Higher diurnal variation (8-10mmHg) as compared to that of a normal individual (4-6mmHg).
3. Maximum pressure can occur at any time as compared to that of a normal individual which occurs during the day.
Resistance to Drainage
1. Ciliary muscles contract to open up the trabecular meshwork and promote the drainage of fluid.
2. Alteration of size of the inner walls of the canal of schlemm leads to either an increase or decrease in resistance.
3. Shrinkage or swelling of the cells lining the trabecular meshwork leads to an increase in resistance.
4. If episcleral venous pressure is sufficiently raised, interruption of blood through the veins may occur; changes in blood flow affects aqeous drainage.

VITREOUS
Physical Components
1. 99 % water
2. Hyaluronic Acid (HA)
3. Collagenous Fibres
4. Glycoproteins
5. Amino Acids & Proteins
6. Ascorbic Acids, Salts
Functions of Vitreous
1. Mechanical role
2. Optical role
3. Carrier of nutrients
4. Removal of waste products
Functions of Vitreous – Optical Role
Transparency is achieved by minimizing light scatter
1. Low concentration of macromolecular solutes ie majority of the material within the vitreous that are considered to be solid are shorter than the wavelength of light thus minimizing light scatter.
2. Collagen of small diameter minimizes light scatter.
3. HA may act as a physiochemical barrier to prevent the influx of cells and macromolecules into the vitreous.
4. Hyalocyte synthesizes “anti-angiogenic” factor that may to a certain extent inhibit neovascularisation.
Vitreous Attachments
1. Attached to the retina at the ora serrata (vitreous base)
2. Attached to the retina at the optic disc margin
3. Attached to the lens capsule (behind the lens) in a ring-like manner along the peripheral hyaloids fossa

IRIS & PUPIL
Types of Pupillary Reflex
1. Direct Pupillary Reflex
2. Consensual Pupillary Reflec
3. Near Pupillary Reflex
Consensual Pupillary Reflex: partial decussations at the optic chiasm causes pupil constriction in one eye when light is being placed on the retina of the fellow eye
Near Pupillary reflex
• Change of fixation (from distance to near) causes the stimulation of CN3 resulting in pupil constriction
• Independent of any changes in illumination
• Accomodation-convergence-pupillary constriction reaction
• Results from the association between ciliary muscles, medial rectus and sphincter papillae
Near Pupillary Reflex – When We Read
1. Convergence (eye-teaming)
• Contraction of medial rectus in order for image close to the eyes to fall on the fovea
2. Accomodation
• Contraction of ciliary muscles in order for image close to the eyes to focus on the fovea
3. Pupillary Constriction
• Pupillary constriction act as a further optical aid by increasing the depth of focus on the fovea
Abnormal Pupillary Reflex: Argyll-Robertson Pupil
• Rare syndrome involving the central nervous system
• Innervational defect of the sphincter
• Affected pupil is constricted
1. Pupils are irregular, unequal in size and miotic.
2. Pupils do not dilate in dim illumination.
3. Abnormal direct and consensual papillary reflexes in the presence of good vision.
4. Normal near papillary reflex (light-near dissociation).
5. Dilate poorly to all mydriatic drugs and to sensory stimuli.
6. Both pupils usually involved but the degree of involvement may be asymmetrical.
It is important to detect this condition as neurosyphillis, diabetes, brain tumor and inflammation of the brain are prominent causes.
Afferent Pathway (Light Reflex): retina photoreceptors → optic nerve → optic track → pretectal nucleus → Edinger-Westphal Nucleus (EWN)
Afferent Pathway (Near Reflex): retina photoreceptors → optic nerve → optic track → lateral geniculate → occipital cortex → pretectal nucleus → EWN
Efferent Parasympathetic Pathway: EWN → exits midbrain with CN3 → synapses in ciliary ganglion → parasympathetic fibres travel via short ciliary nerves → ciliary muscles (accommodation) + medial rectus (convergence) + iris sphincter (constriction)

RETINA
Layers of Retina
1. Retinal Pigment Epithelium (RPE); contains cell nuclei
2. Photoreceptors – receptor cells
3. External Limiting Membrane
4. Outer Nuclear Layer – receptor cells; contains cell nuclei
5. Outer Plexiform Layer – receptor cells
6. Inner Nuclear Layer – bipolar cells; contains cell nuclei
7. Inner Plexiform Layer – bipolar cells
8. Ganglion Cell Layer – ganglion cells; contains cell nuclei
9. Nerve Fibre Layer
10. Internal Limiting Membrane
Transmission of Light Signals
Light → photoreceptors (glutamate reduced) → amacrine cells (bipolar cells and ganglion cells) + bipolar cells (depolarized and hyperpolarized) + horizontal cells → ganglion cells (“on” and “off” centre) → nerve fibre layer
Transmission of Visual Signals
1. Transmission of light across the retina
• Photoreceptors (neurotransmitter – glutamate reduced)
• Bipolar Cells
Depolarized (excited)
Hyperpolarized (inhibited)
• Amacrine Cells: feedback onto other bipolar cells
Make connections with ganglion cells
• Horizontal Cells (GABA neurotransmitter)
inhibition
2. Ganglion Cells (“on” and “off” centre receptive field)
3. Nerve Fibre Layer (optic nerve)
Ganglion Cell Receptive Field
• Consists of “on” and “off” centre
• An “on” centre receptive field is stimulated when its centre is exposed to light and is inhibited when its surround is exposed to light
• An “off” centre receptive field is stimulated when its surround is exposed to light and is inhibited when its centre is exposed to light
• This allows them to transmit info: about contrast and discontinuities of light distribution on the retina; these specify the edges of objects

2011-02-27T16:54:00.001-08:00

AQEOUS HUMOR
Aqeous Humor Formation
1. Aqeous humor is formed by filtration from the blood capillaries through the "blood-aqeous barrier" (non-leaky endothelium cells of the iris capillaries and non-pigmented epithelium).
2. The plasma with about 10-20% of its plasma proteins fills the extracellular spaces between the capillaries and the lateral walls of the pigmented epithelium.
3. The "blood-aqeous barrier" excludes large molecules from the aqeous humor and maintains the clarity of the aqeous humor.
4. Solutes are actively transported from the cells into the intercellular channel by a solute pump thus making the channel-fluid hypertonic.
5. Diffusion of solutes across cell membranes occur down a concentration gradient (osmotic gradient) until the solutes are equally distributed throughout the space in which they are contained.
6. As the solutes move toward the open ends of the channl, water enters across the walls.
7. Dilution of the newly formed aqeous occurs in both the anterior and posterior chambers but at different rates.
8. As such, the aqeous humor formed is clear, transparent and diluted.
Mechanisms of Aqeous Humor Formation
1. Dilution
2. Ultrafiltration
3. Active Transport
Aqeous Humor Drainage
1. CIliary Body
2. Anterior Chamber - anterior chamber angle
3. Trabecular Meshwork
4. Canal of Sclemm
5. Aqeous Vein - episcleral plexus
6. Anterior Ciliary Vein

2011-02-27T15:41:00.001-08:00

CRYSTALLINE LENS
Aging Changes in Lens
1. small increase in size with formation of new lens fibres
2. increase in lens diameter (birth=6mm adult=9mm)
3. increase in lens thickness (birth=3.5mm 80yo=5mm)
4. older lens fibres at lens centre become dehydrated, compacted and sclerosed and less flexibles (presbyopia) ie: loss of accomodation
5. yellow-brown pigment accumulates, due to denatured crystallin proteins
6. about 80% of humans experience alterations in lens transparency after the age of 65 years
7. progression of lens changes varies between individuals
Lens Cortex
1. Lens fibres: consists of newer/younger cell fibres; has lower density therefore lower refractive index
2. Crystallin (soluble)
Lens Nucleus
1. Lens fibres: consists of older cell fibres; has higher density therefore higher refractive index, fibres becomes yellow with age
2. Protein: albuminoids (insoluble)

2011-02-27T15:24:00.002-08:00

LACRIMAL SYSTEM
1. Lipid/Oily Phase
Glands:
-Melbomian/Tarsal Glands
-Gland of Moll
-Gland of Zeiss
Functions:
-protective hydrophobic layer
-reduce evaporation of aqeous component of PCTF
-formation of tear meniscus along lid margin to prevent spillage of tears at lid margin
2. Aqeous/Watery Phase
Glands:
-Main Lacrimal Gland
-Acessory Gland of Krause
-Acessory Gland of Wolfring
Functions:
-enables gaseous exchange
-flush away noxious stimuli
-provide delivery route for immunologic cell response (white blood cells) and immunoglobulins to epithelium
-hydrating medium for epithelium cells and carries metabolites to them
-lubricate at lid-globe interface to decrease friciton when blinking
-antibacterial activity: contains lysozymes
-exit pathway for debris and desquamated epithelium cells
-PCTF slightly hypertonic to control corneal dehydration state
-delivery of Vitamin A from lacrimal gland to cornea (for growth and differentiation)
3. Mucous Phase
Glands:
-Conjunctival Goblet Cells
Functions
-decrease surface tension of tear film by forming hydrophillic coating over hydrophobic corneal epithelium so as to enhance the spread, stability and coherence of tear film
-lubricate ocular surface and decrease friction when blinking
-hydrates underlying epithelia
-provide foundation for smooth optical surface by covering irregular corneal surface
Tear Drainage:
1. Lacrimal fluid passes from lacrimal gland into conunctival fornix.
2. Tears swept across cornea with lid closure.
3. Movement of tears in lacrimal river. Tear meniscus formed.
4. Contraction of Obicularis Oculi shortens canaliculi and expands lacrimal sac.
5. Valve of Hasner closed when lids are closed.
Gravity - at lateral canthus to form inferior meniscus.
Cappilary attraction of tears into lateral puncta and vertical canaliculi.
Blinking moves the tears towards the puncta (with each blink) as a zipper-like function due to the firm attachment of Obicularis Oculi at its medial ligament.
When the Obicularis Oculi contracts, the punctum is drawn nasally, ampulla will be compressed and horizontal limbs of canaliculus will be shorterned.
When Obicularis Oculi contracts, it will also pull on the lateral wall of the lacrimal sac, aspiring tears into the sac.
When Obicularis Oculi expands, lacrimal sac colapses and tears drained into the nasolacrimal duct.

2011-02-27T15:24:00.001-08:00

EYELIDS & EYEBROWS
Function of Cilia
-screening and sensing action of cila: touching the cilium is enough to excite the nerve plexus of the follicles producing a reflex blink which protects the eye from foreign particles and against trauma
-for protection of the eyeball from trauma and foreign bodies
Function of Eyebrows
-to prevent perspiration from falling onto the globe
-traps dirt
-forms part of the human facial expression
Bell's Palsy
-weakening or paralysis of muscles that control facial expression (CN7)
-results from damage of one of a pair of nerves that run from beneath the ears to the muscles
-causes one side of the face to droop; affects self-esteem of patient; not a serious problem
-on affected side: corner of mouth droops; saliva cannot be contained; difficulty in eye closure
Bell's phenomenon
-medical sign in patients with peripheral facial paralysis
-on paralysed side: unable to close the eyes; attempt at eye closure results in upward movement of the eye

2011-02-27T15:11:00.001-08:00

VISUAL PATHWAY
1. Retina
2. Optic Nerve
3. Optic Chiasm
4. Optic Track
5. Lateral Geniculate Body
6. Optic Radiations (146 nasal 235 temporal)
7. Visual Cortex

2011-02-27T14:56:00.000-08:00

EXTRA-OCULAR MUSCLES (EOM)
Nerve Inneration
1. Herring's Law of equal innervation states that when an impulse to perform and eye movement is received by on eye, muscles of the fellow eye receive equal innervation to either contract or relax.
2. Sherrington's Law of reciprocal innvervation states that when a muscle contracts, its antagonist is inhibited.
Muscle Actions
1. Lateral Rectus (LR): abduction (pri)
2. Media Rectus (MR): adduction (pri)
3. Superior Rectus (SR): elevation (pri) incycloduction (sec) adduction (sec)
4. Inferior Rectus (IR): depression (pri) excycloduction (sec) adduction (sec)
5. Inferior Oblique (IO): excycloduction (pri) abduction (sec) elevation (sec)
6. Superior Oblique (S0): incycloduction (pri) abduction (sec) elevation (sec)
Version: both eyes move in the same direction
Vergence: both eyes move in the opposite direction
Levo: to the left
Dextro: to the right
Duction: one eye movement

2011-02-27T14:55:00.001-08:00

RETINA
Layers of the Retina
1. Retinal pigmented Epithelium (RPE); contains cell nuclei
2. Photoreceptors - receptor cells
3. External Limiting Membrane
4. Outer Nuclear Layer - receptor cells; contains cell nuclei
5. Outer Plexiform Layer - receptor cells
6. Inner Nuclear Layer - bipolar cells; contains cell nuclei
7. Inner Plexiform Layer - bipolar cells; contains cell nuclei
8. Ganglion Cell Layer - ganglion cells
9. Nerve Fibre Layer
10. Internal Limiting Membrane
Transmission of Light Signals
light -> photoreceptors (glutamate reduced): amacrine cells (bipolar cells, ganglion cells) + bipolar cells (depolarised, hyperpolarised) + horizontal cells -> ganglion cells ("on" and "off" photoreceptors) -> nerve fibre layer
Transmission of Visual Signals
1. Transmission of light across the retina
-Photoreceptors (neurotransmitter - glutamate reduced)
-Bipolar cells
.depolarised (excited)
.hyperpolarised (inhibited)
-Amacrine cells: feedback onto bipolar cells
.make connections with ganglion cells
-Horizontal cells (GABA neurotransmitter)
.inhibition
2. Ganglion cells ("on" and "off neurotransmitter)
3. Nerve fibre layar (optic nerve)
Receptive Fields of Ganglion Cells
-an area that influences ganglion cell response upon illumination
An on-centre receptive field is stimulated when its centre is exposed to light and inhibited when its surround is exposed to light.
An off-centre receptve field is stimulated when its centre is exposed to surround and inhibited when its centre is exposed to light.
This allows them to transmit information: about contrast and discontinuities of the light distribution falling on the receptive fields; these define the edges of the objects.

2011-02-27T06:49:00.000-08:00

IRIS & PUPIL
Types of Pupillary Reflexes
1. Direct Pupillary Reflex
2. Consensual Pupillary Reflex
3. Near Pupillary Reflex
Consensual Pupillary Reflex
-partial decussation at optic chiasm causes pupillary constriction of one eye when light is placed on the retina of the fellow eye
Near Pupillary Reflex
-change of fixation (from distance to near) stimulates CN3 thus causing pupillary constriction
-independant of changes in illumination
-accomodation-convergence-pupillary constriction reaction
-result of association between ciliary muscle, medial rectus and sphincter pupillae
Near Pupillary Reflex - When We Read
1. Convergence (eye-teaming)
-contraction of medial rectus causing image close to the eye to fall on the fovea
2. Accomodation
-contraction of ciliary muscles causing image close to the eye to focus on the fovea
3. Pupil Constriction
-pupils contrict to increase depth of focus (further optical aid)
Abnormal Pupillary Reflex: Argyll-Robertson Pupil
-rare syndrome involving CNS
-innervational defect in sphincter
-affected pupil is constricted
1. Pupils are irregular, unequal in size and miotic
2. Pupils do not dilate in dimm illumination
3. Abnormal Direct and Consensual Pupillary Reflexes in presence of good vision
4. Normal Near Pupillary Reflex (light-near dissociation)
5. Dilate poorly to all mydriatic drugs and to sensory stimuli
6. Both pupils are involved but the degree of involvement may be asymmetrical
Afferent Pathway (Light Reflex): retinal photreceptors -> optic nerve -> optic track -> pretectal nucleus -> Edinger-Westphal Nucleus EWN)
Afferent Pathway (Near Reflec): retinal photoreceptors -> optic nerve -> optic track -> lateral geniculate -> occipaital cortex -> pretectal nucleus -> Edinger-Westphal Nucleus (EWN)
Efferent Parasympathetic Pathway: Edinger-westphal Nucleus (EWN) -> exits midbrain with CN3 -> ssynapse in ciliary ganglion -> parasympathetic fibres travel via short ciliary nerves -> ciliary muscles (accomodation) + medial rectus (convergence) + iris sphincter (constriction)
Anisocoria
-difference in pupillary size between 2 eyes
-physiologic (congenital)
-pathologic (acquired)
-never caused by afferent pathway
Physiological Anisocoria
-equal in bright and dim illumination
-less or equal to 1mm
Pathological Anisocoria
-failure to dilate in dim illumination -> sympathetic pathway -> dilator muscle
-failure to constrict in bright illumination -> parasympathetic pathway -> sphincter muscle

2011-02-27T05:10:00.001-08:00

VITREOUS
Physical Components
1 99% water
2. Hyaluronic Acid (HA)
3. Collagenous Fibres
4. Glycoproteins
5. Amino Acids & Proteins
6. Ascorbic Acids, Salts
Functions of Vitreous
1. Mechanical role
2. Optic role
3. Carrier of nutrients
4. Removal of waste products
Functions - Optical Role
-transmission of light
-transparency is achieved by minimising light scatter:
1. Low concentration of macromolecular solutes; ie majority of the material within the vitreous considered to be solid is smaller than the wavelength of light thus minimising light scatter
2. Collagen of small diameter minimises light scatter
3. HA may act as a physiochemical barrier to prevent the influx of cells and macromolecules into the vitreous
4. Hyalocyte synthesizes "anti-angiogenic" factor which may to a certain extent inhibit neovascularisation
Vitreous Attachments
1. attached to the retina at the ora serrata (vitreous base)
2. attached to the retina at the optic disc margin
3. attached to the lens capsule (back of lens) in a ring-like manner along the periphery of hyaloid fossa; attachment weakens with age

2011-02-27T04:38:00.000-08:00

INTRA-OCULAR PRESSURE (IOP)
Glaucomatous Condition
-abnormality in aqeous humor outflow (resistance to drainage) from anterior chamber resulting in increased IOP is a more common cause of a glaucoma case as compared to an increase in aqeous humor formation resulting in increased IOP
-higher diurnal variation of 8-10mmHg as compared to that of a normal individual of 4-6mmHg
-maximum pressure may occur at any time as compared to that of a normal individual in the day
Resistance to Drainage
-contraction of ciliary muscles to open up the trabecular meshwork and promote drainage of aqeous humor
-alteration of size of inner walls of canal of schlemm leads to either an increased or a decreased resistance to drainage
-shrinkage or swelling of cell lining of trabecular meshwork leads to an increased resistance to drainage
-if episcleral venous pressure is suffuciently raised, interruption of blood through vein may occur; changes in blood flow affects aqeous drainage

2011-02-27T04:08:00.001-08:00

CORNEA
Corneal Transparency
1. Lattice (regular) arrangement of corneal stroma's collagen fibrils (collagen fibrils are equidistant, of equal diameter and in an orderly arrangement thus allowing maximum light transmission from the cornea to the retina)
2. Absence of blood vessels (thus allows maximum light transmission from the cornea to the retina)
3. Absence of cells (thus allows maximum light transmission from the cornea to the retina)
4. Absence of pigments (thus allows maximum light transmission from the cornea to the retina)
5. Corneal deturgescence (mechanism in which corneal stroma remains relatively dehydrated - 78% water)
Corneal Deturgescence
1. Anatomic integrity of corneal epithelium and endothelium (barrier function)
-Corneal epithelium functions to provide a smooth optical surface via tears and microvilli, a regular surface for light to pass through without interference via uniform cell arrangement and extreme clarity with minimum light scatter due to minimum spacing between cells due to the tight packing of cells. Removal of epithelium cells would lead to the cornea imbibing fluid from the corneal stroma within 4-6 hours and regeneration takes up to 6 weeks (mitosis to produce fresh epithelium cells by the basal cells which migrate to the wing cell layers then subsequently to the superficial cell layers)
-Corneal endothelium functions to maintain corneal transparency, metabolic pump and barrier against aqeous humor. Disruption (pleomorphism or pleomegathism) of endothelium cells would lead to aqeous humor being unopposed thus entering corneal stroma causing corneal edema (swelling).
2. Metabolic pump
-Epithelium pump: osmotic gradient formed by epithelium pump; Na+ and Cl- drawn into tears. 2 pumps (Na+-Cl- and Na+-K-) to balance Na+ and K+. increase in concentration of Cl- leads to osmolarity imbalance (osmotic gradient) being created thus Cl- flows out of cell and water diffuses out. Ends with pumping of solutes (salts) out and water follows (diffusion).
-Endothelium pump: does not plump fluid. transports ions through enzymes and ion channels (from corneal stroma into aqeous humor). generation of osmotic gradient by transporting sodium and bicarbonate ions.
-Corneal endothelium with no intercellular junctions: no junctions = no barrier = no pump function
-Normal corneal endothelum (2000-3000cells/mm2): tight junctions of endothelium cells as barrier and Na/K-ATPase as metabolic pump. pump = leak
-Stressed corneal endothelium (800-1500cells/mm2): increase in amounts of pump sites. pump = leak
-Decompensated corneal endothelium (<500cells/mm2): lateral membranes of endothelium cells unable to contain any more pump sites. leak>pump
3. Changes in osmolarity
-swimming in fresh water pool (presence of chlorine in pool affect osmolarity)
-lacrimation (tearing) water to enter the cornea and thus a decrease in osmolarity
-hypoxia (lack of oxygen) results in the build up of lactate causing a decrease in pH value thus causing osmotic imbalance which leads to corneal edema
4. Intra-ocular pressure (IOP)
-increased IOP of more or equal to 50mmHg indicates an abnormal corneal endothelium function which results in an increased stromal swelling and corneal edema
-corneal edema is a sign of 1 type of glaucoma: signs is what the patient complains (redness) and symptoms is what we optometrists find on examination (conunctival congestion)
Corneal Metabolism
-a series of chemical processes in which energy is obtained and utilised to provide for normal tissue functions
-derived from ATP formed from glucose which enters the eye via limbal vlood vessels, tear film and aqeous humor
-highest metabolic rate: corneal epithelium and endothelium
-essential for: cell renewal. wound healing. transport processes (metabolic pump). maintaining temperature.
-3 pathways: Anaerobic Glycolytic Pathway produces lactic acid and 2mols ATP. Aerobic Krebs Cycle produces 36mols ATP-efficient. Pentose Phosphate Pathway mainly functions to produce NADPH for the synthesis of fatty acids, proteins, DNA and RNA.

MicroB and all its madness :/

2011-02-21T17:22:00.001-08:00

Chapter 1: History and Scope of Microbiology
1. Leeuwenhoek made the first observations of microbial life using a single lens microscope which he constructed. Leeuwenhoek made detailed drawings of “animalcules” (bacteria and protozoa) and was the first scientist to attempt classification of microbial life logically.
2. 4 groups of microorganisms of medical interest are fungus, bacteria, parasites and viruses.
3. Aristotle came up with the theory of spontaneous generation in which he believed that microorganisms arise spontaneously on non-living matter. Redi refuted Aristotle and proved the claim that fresh air was required for spontaneous generation untrue with Redi’s experiments. Louis Pasteur, through scientific logic and experiment stated that microorganism can be found on non-living matter (solids, liquids, gasses) and can contaminate sterile solutions. This discovery led to the development of the scientific method known as pasteurization which is to heat or boil just enough to kill the bacteria. The method was used to reduce food spoilage and to kill potentially harmful bacteria. The prevention of contamination of unwanted microorganisms is known as aseptic technique. Robert Koch stated that microorganisms (bacteria) cause disease. This was proven with Koch’s postulates in which 1 specific infectious disease is related to 1 specific microbe. Joseph Lister used the germ theory in medical procedures. The method termed as antiseptic technique used phenol solution which kills bacteria to treat surgical wounds, leading to a decrease in the incidents of infections and deaths. Edward Jenner experimented for a cure for smallpox using the most unethical yet advanced microbiology. Jenner scrapped cowpox blisters from an infected individual and inoculated (scratched) a healthy 8 year old boy. The scratch turned into a bump and the boy fell mildly ill but recovered shortly, never to contract cowpox or smallpox ever again. This led to the discovery that similar viruses are immune to both viruses and thus led to the development of vaccines for immunity. Alexander Flemming discovered penicillin grown from fungus which inhibits the growth of bacteria.
4. Koch isolated microorganisms from a dead (or sick) animal, grew the microorganisms in pure culture and identified them. Koch then injected the microorganisms into a healthy animal where the disease reproduced itself. Koch again isolated microorganisms from the second animal, grew the pathogenic microorganisms in pure culture and identified identical disease.
5. Among the modern applications of microbiology are development of antimicrobial chemotherapy, microbial genetics, bioremediation and bioterrorism. Bioterrorism is the generation of killer organisms that spread very fast. Bioremediation uses microbes to clean up pollutants and toxins. Microbial genetics makes use of microorganisms which inherit traits and genetically modify them to manufacture large amounts of human hormones and other urgently needed medical substances. Development of antimicrobial chemotherapy is to hunt down and destroy pathogen without having to destroy the infected host. However, there are some problems with the application because chemotherapeutical drugs can be toxic to humans and may interfere with viral reproduction thus affecting uninfected cells. Also, it may result in the emergence and spread of new microorganisms which are resistant to antibiotics.

Chapter 2: Classification, Microscopy and Staining
1. Classification is required to determine the correct treatment strategy for a specific group.
2. Linnaeus classification is termed as taxonomy. It consisted of 3 steps – classification (grouped based on similarities), nomenclature (naming) and identification (to determine place/position within taxon).
3. Whittaker’s 5-kingdom classification consisted of fungi (fungus), protista (parasites), prokaryote (bacteria), animalia (humans) and plantae.
4. 1km=1000m, 1m=10dm, 1dm=10cm, 1cm=1mm, 1mm=1μm, 1μ=1000nm, 1nm=1000pm.
5. General principles of microscopy include wavelength, magnification, resolution and contrast. Wavelength is the length of visible light. Magnification is the ability to make things appear bigger (4x, 10x, 40x, 100x – use oil). Resolution is the ability to distinguish fine structure and detail. Contrast is the ability to distinguish colour and light between parts of an image.
6. Various types of microscopy include bright-field microscopy, dark-field microscopy, phase-contrast microscopy, fluorescent microcopy, confocal microscopy and electron microscopu. Bright-field microscopy is used to examine very small specimens and very fine detail against a white background; consists of simple and compound. Simple microscope uses single lens (Leeuwenhoek’s). Compund microscope uses multiple lens and visible light for illumination. Dark-field microscopy is used against a black background to examine living microorganisms that either are invisible in ordinary light microscopy, cannot be stained using standard methods or are so distorted by staining that its characteristics can no longer be identified. Phase-contrast microscopy is used to examine in detail internal structures of living microorganisms; not necessary to stain or fix specimen. Fluorescent microscopy is used for naturally fluorescent specimens; absorbs UV (short wavelengths) and gives off visible light (long wavelengths). Confocal microscopy is used to reconstruct 3D images; focused on 1 area at a time (area is sharp but other areas blur). Electron microscopy consists of TEM (transmission) and SEM (scanning). TEM gives a striking view of specimen. SEM gives a striking 3D view of specimen via crossing electron pathways.
7. Staining is a method in which specimens are coloured with dye to emphasize certain structures. Simple stains are carried out to determine the cellular shape and arrangement. Procedures include adding aqueous or alcohol solution of a basic dye (methylene blue, carbolfuchsin, safranin, crystal violet) to fixed smear for a certain period of time; wash off; dry; examine; adding mordant to increase affinity of stain to biological specimen or to coat a structure so as to make it thicker and easier to see after staining with dye. Differential stains consist of gram staining and acid-fast staining. Gram stains are carried out to distinguish between different bacteria. Procedures include staining with crystal violet for 1 minute; wash off; staining with iodine for 1 minute; wash off; treat with alcohol (decolourises gram negative bacteria); staining with safranin for 30 seconds. Gram positive bacteria will appear a purple rod-shaped while gram negative bacteria will appear a pink coccus-shaped. Acid-fast stains are carried out to distinguish between mycobacteria and certain nocardia. Procedures include staining with carbolfuchsin for several minutes; cool slide; wash off; treat with acid-alcohol (decolourises non acid-fast bacteria); stain with methylene blue. Acid-fast bacteria will remain red while non acid-fast bacteria will appear blue. Special stains include negative staining, endospore staining and flaggela staining. Negative stains are carried out to demonstrate the presence of capsule. Procedures include mixing in Indian ink; staining with safranin. Capsule will appear as halos. Endospore stains are carried out to demonstrate the presence of endospores. Procedures include smearing with malachite green; heating for 5 minutes; wash down for 30 seconds; staining with safranin. Endospores will appear green within pink or red cells. Flagella stains are carried out to demonstrate the presence of flagellum. Procedures include using mordant; staining with carbolfuchsin. Flagellum will appear as wavy extensions.

Chapter 3: Microbial Nutrition and Growth
1. Cytosol is present in all prokaryotes and eukaryotes. Intrusions are present in all prokaryotes and eukaryotes. Cell wall is present in most prokaryotes and eukaryotes. Flagella is present ins ome prokaryotes and eukaryotes. Endospores are present in some prokaryotes but absent in all eukaryotes. Fimbriae and pili are present in some prokaryotes but absent in all eukaryotes. Cilia is present in some prokaryotes and absent in all eukaryotes. Nucleus is absent in all prokaryotes and present in some eukaryotes. Organelles bound with phospholipid membranes are absent in all prokaryotes and present in eukaryotes. Ribosomes absent in all prokaryotes and present eukaryotes. Size is commonly 0.2-2.0μm in diameter for prokaryotes and 10-100μm in diameter for eukaryotes. Chromosomes are commonly single, circular and lack histones for prokaryotes and more than one, linear and has histones for eukaryotes. Motility is simple flagella for prokaryotes and complex flagella and cilia for eukaryotes. Cytoplasmic membrane lack carbohydrates, usually sterols for prokaryotes and lack glycolipids, glycoproteins and sterols for eukaryotes. Glycocalyx present as organized capsule or unorganized slime layer in prokaryotes and present surrounding some animal cells in eukaryotes.
2. Cytoplasm is the site for metabolism. Cytoplasmic membrane regulates entry and exit of materials. Cell wall supports and protects. Capsule sticks cells together and act as food reserve. Pili is for twitching motility, cell to cell adhesion, attachment to solid surface and apparatus used in transfer of DNA material from one cell to another. Ribosomes is for protein synthesis. Flagella provides motion toward food and away from danger. Nucleoid contains genetic information.
3. Bacteria reproduction is via binary fission – division of single cells into 2, based on logarithmic progression (2 cells to 4 cells to 8 cells and so on). Other methods of bacteria reproduction include budding, aerial spore formation and fragmentation. Generation time is the time taken for a cell to divide into 2 or a population to double. Phases of bacteria growth consist of lag phase, log phase, stationary phase and death phase. In the lag phase, there is little to no change in the number of cells but the metabolic activity is high. In the log phase, bacteria multiply at the fastest rate possible. In the stationary phase, there is an equilibrium between cell division and death. In the death phase, cell death exceeds number of cells formed.
4. Chemical requirements of microorganisms include carbon, oxygen and nitrogen. Carbon consists of autotrophs, heterotrophs, chemotrophs and phototrophs. Autotrophs generate own energy. Heterotrophs absorb energy from the environment. Chemotrophs generate energy from chemical reactions. Phototrophs photosynthesise to obtain energy. Oxygen consists of obligate aerobes, facultative anaerobes, obligate anaerobes, aerotolerant aerophiles and microaerophiles. Obligate aerobes allow only aerobic growth and requires oxygen. Growth only occurs once large amounts of oxygen have entered the medium. Presence of enzymes catalase and SOD allows for neutralization of toxic forms of oxygen. Faculatative anaerobes allow both aerobic and anaerobic growth and grows best in the presence of oxygen. Presence of enzymes catalase and SOD allows for neutralization of toxic forms of oxygen. Obligate anaerobes allow only anaerobic growth and ceases in presence of oxygen. Lack of enzymes diallows neutralization of toxic forms of oxygen. Aerotolerant aerophiles allow only anaerobic growth. Presence of oxygen has no effect of growth. Presence of 1 enzyme, SOD allows partial neutralization of toxic forms of oxygen. Microaerophiles allow only aerobic growth and requires low concentrations of oxygen. Exposure to atmospheric oxygen leads to formation of large amounts of toxic forms of oxygen. Nitrogen is required for protein synthesis. Physical requirements of microorganisms include temperature, pH and water. Psychrophiles grow best at 10-20˚C. Mesophiles grow best at body temperature. Thermophiles grow best at 60-70˚C. Hyperthermophiles grows in excess beyond boiling point. Neutrophiles grow best at pH 6.5-7.5. Acidophiles grow best below pH 6.5. Alkalinophiles grow best above pH 7.5. Halophiles (halogens) survive under salt concentrations. Barophiles survive under water pressure.
5. Broth is used for fast growth of microorganisms. Agar is used for better detection of different forms of microorganisms. Source is the origin of spread of microorganisms. Pure plate consist of streak plate and pour plate. Streak plate is used to isolate majority members of a mixed population. Pour plate is used for pure culture isolation of bacteria. Defined media: known every single component and exact amount. Complex media: not known individual component and exact amount. Enrichment media: enrich particular microorganisms without affecting the rest. Selective media: growth of selected desired microorganisms. Differential media: to distinguish between different microorganisms. Aerobic media: no oxygen. Transport media: contained to be transferred to another area. Virology contains virus. Low oxygen (or high carbon dioxide) is to add oxygen tank to enclosed incubator to increase supply of oxygen.

Chapter 4: Control of Microbes
1. Sterilisation: to entirely remove microorganisms
2. Sanitisation: to reduce amount of microorganisms to a public health standard
3. Aseptic: to prevent contamination of microorganisms
4. Antiseptic: to remove microorganisms using chemical agents
5. Disinfect: to remove microorganisms from surface
6. Degerm: to remove microorganisms from surface using mechanical agents
7. Pasteurisation: to heat or boil to kill potentially harmful bacteria while maintaining integrity of object
8. –static/stasis: inhibit but not kill
9. –cide/cidal: methods to kill

1. Moist heat: protein denaturation – for utensils and/or equipments
• Boiling
• Autoclaving
2. Pasteurisation: protein denaturation – for milk, cream and alcohol
3. Dry heat
• Hot-air sterilization: oxidation – for sterilization of medical equipment
4. Filtration: separates bacteria from suspending liquid – for treatment of liquid
5. Cold: decreases chemical reactions and possible changes in proteins – for culture, drug and food preservation
• Freezing
• Refrigeration
• Lyophylisation
6. Dessication: disruption of metabolism – for food preservation
7. Osmotic pressure: plasmolysis – for food preservation
8. Radiation
• Ionising: disrupts DNA – for partial sterilization of medical equipment
• Non-ionising: damges DNA – UV

1. Phenols and phenolics: disruption of plasma membrane and denaturation of enzymes – for surfaces and 1st line of defense
2. Halogens: iodine inhibits protein function and is an oxidizing agent; chlorine forms an oxidizing agent – for antiseptic and disinfectant
3. Alcohols: protein denaturation and lipid dissolution – for disinfectant and degerming
4. Heavy metals: denaturation of enzymes and other essential protein – for diseases
5. Surfactants: mechanical removal of microbes using scrubs – for skin
6. Chemical food preservatives
7. Aldehydes: protein denaturation - medical
8. Ethylene oxide and other gases: inhibits vital cellular functions – material damaged by heat
9. Oxidising agents: oxidation – surfaces

Chapter 5: Antimicrobial Agents and Chemotherapy
1. Inhibits cell wall synthesis
• Peptidoglycans determine final rigidity of wall imparted by cross-linking of peptide chains (gram positive bacteria cell walls are thicker than gram negative)
• B-lactams (penicillin) are effective against gram negative spirochetes and coccus
2. Inhibits protein synthesis
• Chloroamphenicol, macrolides, aminoglycosides and tetracyclines inhibit protein synthesis at 70s(50s+30s) ribosomes
3. Inhibits nucleic acid synthesis
• Quinolones and fluoroquinolones inhibit FNA gyrase for treatment of urinary tract infection
4. Inhibits metabolic pathway
• Sulfanomides and PABA attack chemical reactions within cells leading to faulty structures
5. Disrupts cytoplasmic membrane
• Ergosterol and amphotericin-B inhibits and disrupts phospholipids
6. Prevents virus attachment
• Attachment antagonists prevent viruses form attaching to specific partners

1. Spectrum of Action
• Broad spectrum: caters to a wide range of microorganisms; prescribed at first consultation
• Narrow spectrum: cater to a specific range of microorganisms; prescribed at subsequent consultations (requires 2 days to identify, prescribed after 3rd day)
2. Efficacy
• Susceptibility testing: the larger the zone of inhibition, the more effective the antibiotics
• MIC: minimum concentration of antimicrobial required to inhibit growth of microorganisms after overnight incubation
• MBC: minimum amount of bacteria required to kill microorganisms
3. Route of Administration
• Per os: orally
• IV: intravenous
• IM: intramuscular
• Distribution: throughout the body
4. Safety and Side Effects
• Toxicities: extent of damage to immune system
• Allergies: strong reactions against generally unharmful substances
5. Resistance to antibiotics
• B-lactamase: enzymes produced by microorganisms that are resistant to antibiotics
• Horizontal Gene Transfer: exchange of gene material without producing ‘offspring’

Chapter 6: Infection Epidemiology
1. Mutialism: both organisms benefit
2. Commensalism: 1 organism benefits the other neither benefits nor is harmed
3. Parasitism: 1 organism benefits the other is harmed

1. Resident microbiota: is ther to stay
2. Transient microbiota: forms; then sheds off

1. Adhesions: sticks on (eg: fimbriae)
2. Extracellular enzymes
• Hydroluronidase and collagenase: invasive bacteria reaches epithelium tissues; bacteria produced hydroluronidase and collagenase; bacteria invades deeper into tissues
• Coagulase and kinase: bacteria produces coagulase; clot forms; bacteria produces kinase; dissolves clot and release bacteria
3. Toxins
• Exotoxin: bacteria release exotoxins (cytotoxins); kills infected host cells
• Endotoxins: dead gram-negative bacteria release endotoxins that induces effects such as fever, inflammation diarrhea, shock and blood coagulation
4. Antiphagocytosis factors
• Phagocytosis blocked by capsule
• Incomplete phagocytosis

1. Portals of entry:
• Ear
• Conjunctiva
• Nose
• Mouth
• Broken skin
• Anus
• Urethra
• Insect bites
• Placenta
• Vagina (females)/penis (males)
2. Portals of exit:
• Ear (wax)
• Eyes (tears)
• Nose (mucous membranes)
• Mouth (saliva, suptum)
• Broken skin (blood)
• Anus (feces)
• Urethra (urine)
• Skin (scalp)
• Semen and lubricating secretions
• Mammary glands: milk and secretions; vagina: secretions and blood

1. Contact transmission
• Direct: kissing, handshaking, sexual intercourse
• Indirect: drinking glasses, toothbrushes
• Droplet: sneezing
2. Vehicle transmission
• Airborne: dust particles
• Waterborne: streams, swimming pools
• Foodborne: poultry, seafood, meat
3. Vector transmission
• Mechanical: found on insect bodies
• Biological: mosquitoes, mites

Chapter 7: Introductory Immunology

1. First line of defense
• Skin: structure of intact skin and waterproof protein keratin provide resistance to invasion of microbes; perspiration washes microbes off surface of skin
• Mucous membranes: traps entry of foreign elements
• Lacrimal system: tearing to prevent entry of foreign bodies
• Normal microbiota: alters environment conditions to prevent growth of pathogens
• Other chemicals/processes: urine clears the urinary tact of microorganisms; vaginal secretions rids vagina of microorganisms; saliva washes microorganisms away from gums and teeth
2. Second line of defense
• Plasma: fluid in blood
• Leukocytes: prevents infectious disease and entry of foreign elements
• Phagocytosis: removes pathogens and cell debris
• Complement system: group of serum proteins activate one another to destroy invading microorganisms
• Interferons: antiviral proteins produced in response to viral infections; host-cell specific but not viral specific

2011-02-14T17:04:00.000-08:00

Chapter 1: Atherosclerosis

Normal Arterial Structure
1. Tunica Intima - endothelium that lines thelumen of all vessels
2. Tunica Media - smooth muscles cells and elastic fibres
3. Tunica Adventitia - collagen fibres

Cells of Vascular Wall
1. Endothelial Cells
Properties & Functions:
-maintenance of permeability factor
-modulation of blood flow and vascular reactivity
-production of ECM
-regulation of inflammation, immunity and cell growth
-oxidation of low density lipoprotein
2. Smooth Muscle Cells
Properties & Functions:
-participate in normal vascular repair
-able to proliferate when appropriately stimulated
-synthesize ECM colalge, elasticin and proteoglycans
-elaboration of growth factors and cytokines
-vasoconstriction and vasodilation

What is Atherosclerosis
-degenerative disease -> any hardening and loss of elasticity in large and medium arteries
-characterised by intimal lesions -> consists of a slightly raised lesion of lipids covered by a firm, white fibrous cap

Risk Factors of Atherosclerosis
1. Age (40-60 years)
2. Gender (Male)
3. Genetics (family history of Iscahemic heart disease)
4. Diabetes Mellitus
5. Cigarette Smoking
6. Hypertension
7. Hyperlipidemis (major component : LDL)

Prevention of Atherosclerosis
1. Quit smoking
2. Healthy diet
3. Exercise

Morphology of Atherosclerosis
1. Fatty Streak
-earliest lesions in atherosclerosis
-composed of foamy lipid-filled macrophages
2. Atherosclerotic Plaque (3 principle components)
-cells (t-cells, macrophages, smooth muscle cells)
-lipids (intracellular, extracellular)
-ECM (collagen, elastic fibres, proteoglycans)

Complications of Atherosclerosis
1. narrowing of lumen size -> obstruction of blood flow -> ischaemia -> necrosis
2. rupturing of blood vessels -> neovascularisation -> haemorrhage within plaque
3. ulceration of plaque (from a contained haematoma which causes distension of plaque)
4. formation of aneurysm (atherosclerotic pressure/ischaemic atrophy of media -> weakness of vessel wall)
5. formation of thrombus (increased exposure to thrombogenic substances due to ulceration/rupture/erosion of luminal surface)
6. atheroembolism (plaque rupture can discharge debris in blood stream)

Pathogenesis of Atherosclerosis
Endothelial injury is the triggering factor of Atherosclerosis that is commonly caused by hyperlipidemia.
1. High levels of LDL/bad cholestrol, causing accumulation of lipids on the endothelium.
2. Weakening of endothelium tight junctions, causing edema to surrounding tissue.
3. Activation of macrophages. Recruitment of smooth muscle cells from the media to the intima.
4. Engulfment of lipids by the macrophages and smooth muscle cells, causing formation of fatty streaks.
5. Proliferation of smooth muscle cells give rise to synthesis of ECM leading to intimal thickening and formation of atheromatous plaque.
Protrusion of plaque into lumen causes lumen size to narrow leading to ischaemia.

Chapter 2: Thrombosis

Normal Hemostasis
1. In a normal blood vessel - process of maintaining blood in fluid clot-free state
2. In vascular injury - formation of hemostatic plug @ site of injury to prevent further bleeding

Sequence of Events (Normal Hemostasis)
1. Vasoconstriction
After vascular injury, local neurohumoral factors induce a transient vasoconstriction.

2. Primary Hemostasis
Platelets adehere to exposed ECM and are activated, undergoing change in shape and granule release.
Release of ADP and TxA2 lead to further platelet aggregation to form primary hemostatic plug.
The platelets and coagulation systems to prevent bleeding.

3. Secondary Hemostasis
Local activation of coagulation cascade (involves tissue factor which is a procoagulant synthesized by endothelium and platelet phospholipids) causing thrombin generation.
Thrombin cleaves circulating fibrinogen into insoluble fibrin creating a fibrin meshwork deposition thus "cementing" platelets into a definitive secondary hemostatic plug.

4. Antithrombotic Counter-regualtion
Counter-regulatory mechanism such as release of t-PA (fibrolytic product) and thrombomodulin (interferes with coagulation cascade) limits hemostatic process to the site of injury.

Thrombosis: pathologic form of hemostasis in which a thrombus is formed in uninjured/injured blood vessel

Thrombus
-can obstruct an artery or vein
-solid ass of blood constituents formed within vascular system

Sequence of Events (Thrombosis)
1. In its earliest phase, atheromatous plaque may consist of a slightly raised fatty streak on the intimal surface of any artery.
2. With time, the plaque nelarges and becomes sufficiently raised to protrude into the lumen, causing a certain degree of turbulence in blood flow. This turbulence eventually causes loss of intimal cells and the denuded plaque surface is presented ot the blood cells, including platelets.
3. The turbulence itself will predispose to fibrin deposition and platelet clumbing and the bare luminal surface of the vessel will have colalgen exposed and the platelets will settle on this surface.
4. Thus, precipitation of a fibrin meshwork in which red cells are trappedn and a layer of this meshwork is developed. This complex structure now protrudes further into the lumen, causing more turbulence and forms the basis for further platelet deposition.

Clinical Complications (Thormbosis)
1. Arterial Thrombosis - thrombus superimposed on atheroma
2. Venous Thrombosis - thrombus formation due to blood stasis at the valves that protrude into the lumen

Outcomes of a Thrombus
1. Propogation to heart
2. Organised and recanalised
3. Resolution
4. Embolisation to lungs
5. Organised incorporation to the walls

Chapter 3: Embolism

Embolism: consition whereby an intravascular mass is dilodged @ point of origin and carried by blood to a distant location

Types of Intravascular Mass
1. Solid
2. Liquid
3. Gaseous

Types of Embolism
1. Atheroembolism
2. Thromboembolism
3. Air or Nitrogen Gas Embolism
4. Fat Embolism
5. Amniotic Fluid Embolism
6. Tumor, Plateley, Infective and Foreign Matter Embolism

1 Atheroembolism
-casued by ulcerated atheroma that release cholestrol into the circulation
-commonly lodged @ arteries of lower limbs and ocular

2. Thromboembolism
-caused by detached fragments of thrombus into the circulation
-commonly lodged @ pulmonary circulation and veins of pelvis/calf

3.1 Gas Embolism
-caused by entry of enough air bubbles into the vascular system by surgery, trauman, childbirth, abortion, blood transfusion

3.2 Nitrogen Gas Embolism
-caused by entry of enough air bubbles into the vascular system when exposed to sudden changes in atmospheric pressure

4. Fat embolism
-caused by entry of fat globules into circulation after a large bone fracture
-commonly lodged @ pulmonary circulation

5. Amniotic Fluid Embolism
-caused by entry of amniotic fluid into maternal circulation via tear in placental membran and rupture of uterine vein during labour
-commonly lodged @ lungs

Chapter 4: Tumour

Tumour: an abnormal mass of tissue as a result of abnormal proliferation of cells that exceeds and is uncoordinated with that of a normal tissue (neoplasm)

Types of Tumour
1. Benign (non-cancerous)
2. Malignant (cancerous)

1. Benign Tumor
Characteristics:
-slow growing
-localised
-does not matastasize
-well-circumscribed
-exophytic lesion
-has close resemblance to parent cell
Clinical Complications:
-exerts pressure on adjacent cells (stress on adjacent cells)
-obstruction of fluid flow
-cosmetic concern
-patient anxiety
-progression to malignant tumor

2. Malignant Tumor
Characteristics:
-fast-growing
-invasive
-may metastasize
-not well-circumscribed
-endophytic lesion
-has variable histologic resemblance to parent cell
Clinical Complications:
-exerts pressure on adjacent tissues (invasion of adjacent tissues)
-obstruction of fluid flow
-cosmetic concern
-pain
-weight loss
-loss of function
-loss of blood from ulcerated surface
-formation of secondary tumor

Comparison between Benign vs Malignant Tumor
1. Clinical Features
-rate of growth
-presence of haemorrhage
-precense of ulceration
-presence of metastasis
2. Gross Appearance
-regularity of tumor edge
-invasion of adjacent tissues
-direction of growth
3.Microscopial features
-resemblance to tissue of origin
-regularity of cell shape and size
-normalcy of mitotic tissue
-invasion of blood vessels, lymphocytes and perineural space
-displasia into adjacent tissues

Risk Factors of Tumor
1. Age
2. Gender
3. Race
4. Geography
5. Environment (UV)
6. Chemical (cigarette smoke)
7. Food (bbq)

Metastasis
1. Detachment of tumor cells
2. Invasion of surrounding connective tissue to facilitate passage of metastasis
3. Intravasationinto lumenof blood vessel
4. Evasion of host defence mechanism
5. Adhesion to endothelium at distant location
6. Extravasation into surrounding tissue

Carcinogenesis
-transformation of normal cell into cancerous cell via genetic mutation
-site of action @ DNA
-caused by carcinogens (chemicals, viruses, ionising and non-ionising radiations, hormones, mycotoxins and parasites, miscellaneous agents)

Carcinogenesis is a multi-step process which begins when a carcinogen causes a genetic change or damages DNA of a normal cell. The cell becomes more vulnerable to other genetic changes. This stage is called "Initiation". If the process stopped here and the cancerous cells doe not grow and replicate, cancer will not form.
The next stage in carcinogenesis is "Promotion". This occurs when the initiated cell is exposed to an agent that enhances its growth into a larger mass.
When a tumor is formed, the cells have the same basic needs as a normal cell. Because it is genetically damaged, it robs the normal cells of important oxygen and nutrients. In addtion, it grows uncontrollably and may interfere with the functions of vital organs such as the liver.

2011-02-14T06:30:00.000-08:00

Carcinogenesis:
-transformation of a normal cell into a cancerous cell via genetic mutations
-site of action @ DNA
-caused by carcinogens:
viruses
ionic and non-ionic radiation
hormones, mycotoxins, parasite
chemicals
miscellaneous agents

Sequence of Events (Carcinogenesis):
-Carcinogenesis is a mulit-step process that begins when a carcinogen causes a genetic change or damages the DNA f a normal cell. This makes the cell vulnerable to other genetic changes. This stage is called "Initiation". If the process ended here, and the cancerous cell does not grow or replicate, no cancer would form.
-The next stage of carcinogenesis is called "promotion". This occurs when the initiated cell is exposed to agents that enhances its growth into a larger mass.
-When a tumor actually forms, the tumor cell has the same basic needs as a normal cell. Because the tumor cells are genetically damaged, it robs the normal cells of the important oxygen and nutrients. In addition, a malignant tumor grows uncontrollably and may interfere with the functions of vital organs, such as the liver.

2011-02-14T05:32:00.001-08:00

Metastasis:
1. Detachment of tumor cells
2. Invasion of surrounding tissue to faciliatate passage of metastasis
3. Intravasation into lumen of blood vessel
4. Evasion of defence host mechanism
5. Adhesion to endothelium at distant location
6. Extravasation into surrounding tissue

2011-02-14T04:55:00.001-08:00

Tumor

Tumor: abnormal mass of tissue as a result of abnormal proliferation of cells that exceeds and is uncoordinated to that of a normal tissue (neoplasm)

Types of Tumor:
1. Benign (non-cancerous)
2. Malignant (cancerous)

Benign Tumor:
-characteristics:
slow growing
localized
does not metastasize
well-circumsribed
exophytic lesion
has close resemblance to parent cell/tissue
-clinical complications:
exertion of pressure on adjacent tissue
obstruction of fluid flow
cosmetic concern
patient anxiety
progression to malignant tumor

Malignant Tumor:
-characteristics:
fast growing
invasive
may matastasize
not well-circumscribed
endophytic lesion
has variable histologic resemblance to parent cell/tissue
-clinical complications:
exertion of pressure on adjacent tissue
obstruction of fluid flow
cosmetic concern
weight loss
pain
loss of function
loss of blood from ulcerated surface
formation of secondary tumor

Comparisons between Benign vs Malignant Tumor:
-Clinical features:
rate of growth
presence of haemorrhage
presence of ulceration
presence of matastasis
-Gross appearance:
regularity of tumor edge
invasion of adjacent tissue
direction of growth
-Microscopial features
resemblance to tissue of origin
regularity of cell shape and size
normalcy of mitotic tissues
invasion of blood vessels, lymphatics and perineural space
displasia into adjacent tissue

2011-02-14T04:16:00.000-08:00

Embolism

Embolism: a condition in which an intravascular mass is being dislodged from the point of origin and carried away by blood to a distant site

Types of Intravascular Mass:
-Solid
-Liquid
-Gaseous

Types of Embolism:
1. Atheroembolism
2. Thromboembolism
3. Gas or Nitrogen Gas Embolism
4. Fat Embolism
5. Amniotic Fluid Embolism
6. Tumor, Platelet, Infective & Foreign Matter Embolism

1. Atheroembolism
-caused by ulcerated atheroma that release cholestrol into the circulation
-commonly lodged @ arteries of lowers limbs and ocular

2. Thromboembolism
-caused by detached fragments of thrombus into the circulation
-commonly lodged @ pulmonary circulation and veins of pelvis/calf

3.1 Gas Embolism
-caused by entry of enough air bubbles into the vascular system by surgery, trauma, childbirth, abortion, blood transfusion

3.2 Nitrogen Gas Embolism
-caused by entry of enough air bubbles into the vascular system when exposed to changes in atmospheric pressure

4. Fat Embolism
-caused by entry of fat globules into the circulation after a large bone fracture
-commonly lodged @ pulmonary circulation

5. Amniotic Fluid Embolism
-caused by entry of amniotic fluid into maternal circulation via tear in placental membrane and rupture of uterine veins during labour
-commonly lodged @ lungs

2011-02-14T03:36:00.000-08:00

Thrombosis

Thrombosis: a form of hemostasis which involves the formation of thrombus in uninjured/injured blood vessels

Thrombus:
-a solid mass of blood constituents within the vascular system
-can obstruct veins or arteries

Causes (Virchow' Triad):
-Endothelial Injury
-Hypercoagulability
-Abnormal Blood Flow

Sequence of Events:
1. In the earliest phase, atheromatous plaque may consist of a slight raised fatty streak on the luminal surface of any artery.
2. With time, the plaque enlarges and becomes sufficiently raised to protrude into the lumen and causes a certain degree of turbulence. This turbulence increases the loss of intimal cells and the denuded plaque surface is presented to the blood cells, including the platelets.
3. The turbulence itself will predispose into fibrin deposition and platelet clumping and the now bare luminal surface of the vessel will have collagen exposed and the platelets will settle on this surface.
4. Thus, precipitation of the fibrin meshwork in which red blood cells are trapped and a layer of this meshwork is developed. The complex structure now protrudes further into the lumen causing more turbulence and forming the basis for further platelet deposition.

Clinical Complications:
1. Arterial Thrombosis - thrombus superimposed on atheroma
2. Venous Thrombosis - thrombus formation due to blood stasis at the valves which protrude into the lumen

Outcome of Thrombus:
-Propogation to the heart
-Organised and recanalised
-Resolution
-Embolisation to the lungs
-Organised incorporating to the walls

2011-02-14T01:03:00.000-08:00

Hemostasis

Normal Hemostasis:
1. In the blood vessel - process of maintaining blood in a fluid, clot-free state
2. In a vascular injury - formation of hemostatic plug at site of injury to prevent further bleeding

Sequence of Events (Normal Hemostatis):
1. Vasoconstriction
After vascular injury, local neurohumoral factors induce a transient vasoconstriction

2. Primary Hemostasis
-Platelets adhere to exposed ECM and are activated, undergoing change in shape and granule release
-Released ADP and TXA2 leads to platelet aggregation forming primary hemostatic plug
-The platelet and coagulation systems to prevent bleeding

3. Secondary Hemostasis
-Local activation of coagulation cascade (involves tissue factor which is a procoagulant synthesized by endothelium and platelet phospholipids) causing thrombin generation
-Thrombin cleave circulating fibrinogen into insoluble fibrin creating a fibrin meshwork deposition "cementing" platelet into a definitive secondary hemostasis.

4. Antithrombotic Counter-Regulation
-Counter-regulatory mechanisms such as release of t-PA (a fibrolytic product) and thrombomodulin (interferes with coagulation cascade) limits hemostatic process to site of injury

2011-02-13T23:49:00.000-08:00

Atherosclerosis

Normal Arterial Structure:
1. Tunica Intima: endothelium that lines the lumen of all vessels
2. Tunica Media: smooth muscle cells and elastic fibres
3. Tunica Adventitia: collagen fibres

Muscles of Vascular Wall:
1. Endothelial Cells
Properties and Functions:
-Maintenance of permeability factor
-Modulaton of blood flow and vascular reactivity
-Production of ECM
-Regulation of inflammation, immunity and cell growth
-Oxidation of low desity lipoproteins
-Pro-thrombotic (platelet, pro-coagulant, anti-fibrinolitic effects)
-Anti-thrombotic (anti-platelet, anti-coagulant, fibrinolitic effects)
2. Smooth Muscle Cells:
Properties and Functions:
-Participate in normal vascular repair and pathological processes
-Able to proliferate when appropriately stimulated
-Synthesize ECM collagen, elasticin and proteoglycans
-Elaboration of growth factors and cytokines
-Vasoconstriction and vasodilation

What is Atherosclerosis:
1. Degenerative disease - any hardening and loss of elasticity in large and medium arteries
2. Characterised by intimal lesions (atheromas)
-protrude into the lumen
-consists of a raised lesion of lipids covered by a firm, white fibrous cap

Risk Factors of Atherosclerosis:
1. Age (40-60 years)
2. Gender (Male)
3. Genetics (Family history of Ischaemic Heart Disease)
4. Diabetes Mellitus
5. Obesity (due to sedentary lifestyle)
6. Cigarette Smoking
7. Hypertension
8. Hyperlipidemia (major component LDL - Low Density Lipoprotein)

Prevention of Atherosclerosis:
1. Quit smoking
2. Healthy diet
3. Exercise

Morphology of Atherosclerosis:
1. Fatty Streaks
-earliest lesions in Atherosclerosis
-composed of foamy lipid-filled macrophages
2. Atherosclerotic Plaque
-ECM (collagen, elastic fibres, proteoglycans)
-Cells (t-cells, macrophages, smooth muscle cells)
-Lipids (intracellular, extracellular)

Complications of Atherosclerosis:
1. Narrowing of lumen size -> obstruction of blood flow -> ischaemia -> necrosis
2. Rupturing of blood vessels -> neovascularisation -> haemorrhage within plaque
3. Ulceration of plaque (from a contained haematoma which causes distension of plaque)
4. Formation of aneurysm (atherosclerotic pressure/ishaemic atrophy of media -> weakens vessel walls)
5. Formation of thrombus (increased exposure to thrombogenic substances due to rupture/ulceration/erosion of luminal surface)
6. Atheroembolism (plaque rupture can discharge debris into blood stream)

Pathogenesis of Atherosclerosis:
Endothelium injury is the triggering factor of Atherosclerosis which is mainly caused by hyperlipidemia.

1. High levels of LDL/bad cholestrol, causing accumulation of lipids on endothelium.

2. Weakening of endothelial tight junctions, causing edema to surrounding tissue.

3. Activation of macrophages.
Recruitment of smooth muscle cells from the media to the intima.

4. Engulfment of lipids by macrophages and smooth muscles cells, causing formation of fatty streaks.

5. Proliferation of smooth muscle cells give rise to synthesis of ECM
leading to intimal thickening and formation of atherosclerotic plaque.
Protrusion of plaque into lumen causes lumen to narrow
leading to ischaemia.

Affairs of the heart; or is it?

2011-02-04T23:25:00.000-08:00

Do you have a significant other? I don't. But more often than not, I wish I do. Mungkin it may seem like a desperate call to some. But really, only if you have ever been in my shoes then you'd understand.

I want to fall in love, I really do. I want to be showered with loads of care and concern; to feel as if I'm the only one that matters. I want to be the priority and not the option.

I have the image of the ideal guy in my mind. Tall, dark and pretty decent looking (he doesn't have to be extremely good-looking or what we term nowadays as 'hot'). The typical Malay boy but with an edge. He has plans for the future, respects his parents, is a family man, faithful, can guide me etc etc.

I need to meet my 'him'. I don't want to end up alone. I really don't.

So dear God, please answer my prayers.

2011-02-03T19:08:00.000-08:00

7 Feb: Physiological and Visual Optics Test 2
7 Feb: Submission of Introductory Ocular Microbiology Lab Report
9 Feb: Ocular Physiology Test 2
11 Feb: Submission of Report Writing and Presentation Individual Written Long Report
15 Feb: Introductory Pathology Test 2
15 Feb: Submission of The World Today 1 Essay (Child Labor)
22 Feb: Introductory Ocular Microbiology Final Exam
24 Feb: Ocular Anatomy Final Exam
28 Feb: Ocular Physiology Final Exam
3 March: Physiological and Visual Optics Final Exam

12 March: MAHKP Youth Club Visit to Darul Takrim
17 March: SP CLS FLC Pre-Camp Training
18 March: SP CLS FLC Pre-Camp Training
21 March: SP CLS FLC
22 March: SP CLS FLC
23 March: SP CLS FLC
24 March: SP CLS FLC
4 April: SPOT LTC
5 April: SPOT LTC
6 April: SPOT LTC
7 April: SPOT LTC

2011-02-03T06:25:00.000-08:00

I had a weird dream.

I dreamt that I was back volunteering at Toa Payoh Senior Citizen's Healthcare Centre.
I dreamt that I met the same Malay guy whose name till now, I'm still unaware of.
I dreamt that we were both doing our own stuff, helping in whatever way we can.
I dreamt that we bumped into each other.

I dreamt that we had a short convo which went something along the lines of
"Want to hang out sometime?"
"Are you asking me out on a date?"
"Well, it is if you think it is...."
"SURE."
Afterwhich we went our separate ways.

I dreamt that we went for lunch together.
I dreamt that he followed me around after that, by my side all along.
I dreamt that we shared some intimate moments of conversation.
I dreamt he was an NUS medical student.
I dreamt he was the one.

I had a weird dream. Such a weird dream. But pleasant to a certain extent.

Back to reality. There's no such thing as perigi cari timba. At least, not in my world. So, I guess I'll just wait until Mr Right comes along and notices me. Oh yes, such is my life. (:

Someone who loves me should....

2011-02-01T20:10:00.000-08:00

Someone who loves me will....

1. Learn to like the songs I like, and even borrow my CDs, because he wants to know what I like. To him, my likes are his likes.

2. I was sick the last time we met, a few days later he sends an SMS to ask how I'm doing because he's worried.

3. If I tell him I'll be sitting for a test or an exam he will ask when it is, and at the moments before the test or exam he will send a 'good luck' SMS to motivate me.

4. He who loves me will give me something he owns which to me is just another thing, but it is actually something special to him.

5. He who loves me will behave more like a relative than a lover.

7. He who loves me will always want to be near me and spend his days with me.

8. If I move to another place, he will advice me to always be careful with the new surroundings that may bring danger to me.

9. When he misses me and does silly things that irritate me and I tell him he is affecting me he will apologise and not repeat.

10. He who loves me always does weird things like calling me a couple of times a day, or wake me up in the middle of the night with an SMS or a call simply because he misses me at that moment in time.

11. If I ask him to teach me something, he will do so with utmost patience even if I were the most stupid individual on earth!

12. When I look at his handphone, my name fills a huge portion of his 'inbox' and he keeps my messages even though they were sent months or even years ago.

13. If I reject him one day, he will realise it and run away from me and my life, even though he is very hurt at that point in time.

I have yet to meet someone who does all that. Bits and pieces, yes.

9 January 2010

2011-01-09T18:06:00.000-08:00

The 2 most common questions posed to me:

1. Bila nak jadi Optometrist?
InsyaAllah, dalam masa 2 tahun lebih. Tapi kalau boleh Ain nak sambung belajar, dapatkan honours degree sekali. Jadi mungkin dalam masa 4 tahun lebih?

2. Bila nak kahwin?
Sensitive question, never pose it to me. Or I'd loathe you. (:

8 January 2010

2011-01-08T21:36:00.000-08:00

Because I shall refrain from being the 3rd party.

I'm not the other woman.

7 January 2011

2011-01-07T21:40:00.000-08:00

Thank God It's Friday.

6 January 2011

2011-01-06T21:44:00.000-08:00

Ocular Anatomy: Dissection of Pig's Eye.

A million thank yous to Leanne (Kuku2);

for understanding my circumstance/plight

and carrying out the dissection on her own,

whilst I snapped pictures.

5 January 2011

2011-01-05T21:51:00.000-08:00

Keeler, Neitz, Heine or Welch Allyn?

4 January 2011

2011-01-04T21:55:00.000-08:00

My pathology grades are suffering.

It's time to close my eyes and open my ears.

No more staring at the hot lecturer;

but rather, start listening to him.

Oh yeah.

3 January 2011

2011-01-03T21:58:00.000-08:00

New year, old semester, new term.

Time to pull up my GPA.

InsyaAllah.

2010-12-30T17:52:00.000-08:00

No, I don't do countdowns. Firstly, I find it unethical to party my night away as a Muslimah. Secondly, I find it stupid to find myself wasted on the first day of the new year. But then again, to each his own.

2010 has been a relatively good year. I experienced working life - relief teaching for a term at Loyang Primary School, a few days at Rivervale Primary School and a week at Siglap Secondary School. I enrolled into SP Optometry; something I'd wanted to do since 2007. To set the record straight, my GCE A Level results qualified me for university but I simply wanted to diverge. I met awesome people - DOPT students and maintained contact with my friends - Madra mates, TPJC clique/classmates, PRCS Council etc. I developed crushes here and there, but have yet to fall in love.

In the coming 2011, I aspire to stay happy despite the odds that come my way. I will strive in my studies to attain my desired grades and GPA. And the most important thing; I shall take things in my stride and continue my perjuangan to become a better Muslimah, insyaAllah.

2010-12-27T18:49:00.000-08:00

have you ever felt you're ugly?
have you ever felt you're stupid?
have you ever felt you're clumsy?
have you ever felt you're unworthy of anyone?

well that's how i feel. every single day.

2010-12-24T08:09:00.000-08:00

Kamu. Yes kamu. Kamu sungguh comel. Really comel. Hati terpaut despite it being only two days, but whatever. You didn't go for solat Jumaat. So, bye-bye Mister 'Perfect'. Thank God that was the last we'll be meeting each other and I found a flaw or I'd be pining or smth, which would be stupid. Really

2010-12-16T09:24:00.000-08:00

Does anyone ever think of me,

does anyone even care?

Because I'm stupid and ugly in more ways than one.

Always one to love, never to be loved.

So I guess everyone else out there should just count their blessings.

2010-11-27T07:23:00.000-08:00

Physiological and Visual Optics. Ocular Anatomy. Ocular Physiology. Introductory Pathology. Introductory Ocular Microbiology.

So tell me, where do I start?

2010-11-24T03:02:00.001-08:00

Highlights of the Week (thus far):

Fid came by SP on Monday an brought me cookies from Famous Amos JP. ((:
TWT Presentation's finally over, no Tuesday morning tutorial next week. ((:
Wore an SP shirt for TWT Presentation (trust me, its very rare).
My eye-candy in SP has been frequently trying to chat me up, haha. ((:
OPhy tutorial for tmr cancelled, hoho.

Okay dah, time for PHYVIO.

2010-11-05T20:10:00.000-07:00

If you're alone, I'll be your shadow.
If you want to cry, I'll be your shoulder.
If you want to hug, I'll be your pilllow.
If you need to be happy, I'll be your smile.
But anytime you need a friend, I'll just be me.

2010-11-03T18:41:00.000-07:00

fin just texted to meet him for dinner. and i just got home. why must nights off be last minute? i freaking hate it luhh. am taking a raincheck, sorry fin.

long weekends ahead. reserved for dearest cousin mia afterwhich, back to ocular anatomy, ocular physiology and introductory pathology.

2010-10-24T11:07:00.000-07:00

"A woman is like a tea bag.
It's only when she's in hot water that you realise how strong she is."
-Eleanor Roosevelt

2010-10-23T13:44:00.000-07:00

Year 1 Semester 2 Week 1 down; 20 weeks to go.

Monday.
Alternate week practicals for PHYVIO - school started at 11am instead of 8am. ONAT tutorial was redundant - merely a get-to-know-you session (more for the lecturer, considering 03 & 04 are very much well-aquainted by now). Informed by Ho Chee Kong that for one of the 5 practicals, we were to dissect pig's eye. If I may quote, 'Malays are exempted, but please go home and ask your parents if you can carry out the dissection. If not, you'll have to pair up with someone who can and still sit-in for the practical as well as snap photos for your lab reports." I felt tempted to correct him - Muslims, not Malays. But ohwhattheheck. Am not going to dissect "it" eitherway. IOCMIC lecture with Ben Yang was pretty slack - talked about right brain and its usage blablabla. Pretty cool if I say so myself. Lastly, PHYVIO lecture with ZMX was irritating, confusing and an untangled mess. Her lecture left us more clueless that when we entered MLT 1.

Tuesday.
Unlike my 04 classmates, I started school at 8am - TWT1 since I'm in SPOT Programme. Cool bunch of kids, wonderful tutor. If I may quote Norman New, "It's nice to see a familiar face." For those not in the know, Norman New was previously a GP lecturer in TPJC. He recently joined SP in early Feb. ONOW with ZMX was squeezed to 1h and started at 12pm instead of the designated 11am. Laptops were required, but class rep Choo JS informed us via sms only at seven-ish in the morning when I was already in the train on my way to school. Apparently, text with given instruction was sent by ZMX to both 03 & 04 class reps the evening before, at six-ish. Clara forwarded the text to 03 a.s.a.p. whilst 04's 'competent' class rep decided to do so only >12h later. How convenient - for him. When told about my plight, I was blamed by him instead because apparently, if I may quote him "How do I know that you have an 8am class?" So he had me cursing under my breath. How irresponsible, I thought. I still stick to my stand. PHYVIO tutorial was much better as compared to Monday's. ZMX conveyed her lecture in a manner which was more simple to understand. INTPAT lecturer's hot. "OMG. I'm so going to a get a Distinction for this module.", I said to Syafiq and Leanne. Assignment for INTPAT due after MST had us grouped according Eu Jin (lecturer). Groupmates include classmates MingWei, XiaoWei, Yudah and Felicia (a forward module student).

Wednesday.
OANAT consists of lots and lots (and lots!) of drawing, as I found out during the 8-10am lecture. OPHYS was tough, but Ms Suma's really good!

Thursday.
Stay-at-home-Thursday. Alternate week practicals for IOCMIC and OANAT left 04 with only IOCMIC and OPHYS tutorials - both an hour each. IOCMIC tutorials are "tutorials" which left 04 with only and hour of OPHYS tutorial with Ms Suma. Coaxed our PT, and voila! No school on Thursday (but ONLY for Thursday Week 1).

Friday.
OPHYS practical was super duper cool. We measure things such as HVID, VVID etc. For those of you not in the know, its something along the lines of measuring patient's cornea dimensions for things such as contact lenses fitting. After practical, clique went to buy KOI. I stayed to consult Ms Suma wrt to OPHYS lecture stuff I was unsure of, afterwhich I joined Kodi/JZ/JS for consultation with OANAT tutor Ho Chee Kong. Managed to coax him to try to obtain Buffalo's eyes for Muslim students so that we weould get to experience the dissection exercise and learn from it. No promises on his end though (well,at least he said he'll TRY. so, that's good enough I guess.). ZMX was darn bitchy during PHYVIO lecture. Details shall be kept within DOPT students. RWP was okay - did a "mahjong" picking of groups. Ended up with YT/MW/TCC. Cool cool people. We were pretty much done last night despite the assignment being tasked to us only yesterday. Productive and efficient, I like(:

Weekends seem short. Its Saturday afternoon already. Oh wells.

2010-10-19T06:41:00.000-07:00

"ah tkper. not my problem."
those harsh harsh words.

Dear Allah,keep me strong.

2010-10-14T23:58:00.000-07:00

Gilmore Girls Season 7 Episode 17: Its just like riding a bike.

Besides the usual town folk adventures, the episode centred around the lives of Paris Geller and Rory Gilmore, where they decide on options upon graduation from Yale. Following her gut feel, Rory rejected a job offer at a reputable paper for a fellowship at another paper where she'd only get 6 weeks internship. She ended up getting neither. As for Paris Geller, she was accepted into numerous law and med schools and becomes a wreck not knowing which to choose. She ended up set on something at least - med over law.

The episode got me thinking. Well, more of reflecting.

Pre-prelims, I was dead set on NUS Dentistry. Well, that was the supposed track I was eyeing for ever since I chose the JC option over SP Optometry (yes, believe me, i was veering toward SP Otpmetry. the only reason i crossed it off my list was due to the absence of opto degree offered in the local unis. itd be costly to fly etc).

Pre-ALvls, I was veering toward NUS Faculty of Science to either major in Physics or Mathematics. Alternative route was to do Engine.

Post-ALvls pre-results, I was veering toward NTU-NIE having done (and loved!) permanent relief teaching for a term at LYPS. Alternative route was to do Mathematical Sciences. Another alternative was to go for an NIE Diploma.

Come A Level Results.
(1) SP Optometry (they finally have fsi wef 2009!)
(2) Diploma in General Education
(3) NTU-NIE
(4) NTU Mathematical Sciences

I knew at that point of time, that SMU was definitely out of the equation. And I didn't even want to consider NUS. My gut feeling told me that. I followed my heart.

I'm now in SP Optometry. Something I'd wanted to do from the start.
Alhamdulillah, I'm happy with the way things are.

2010-10-14T14:56:00.000-07:00

An old saying goes, "It is better to have loved and lost than to have never loved at all."

Define "to have loved and lost". Is it to have had an infatuation? Is it to have had a crush? Is it to have liked someone more than a friend? Is it to have had been in a relationship? What is it, really?

Truth is, there are many different scenarios which can be fit into this clause. It is human to err, and I'm sure everyone from the innocent passer-by to your best friends, have had their heart broken at some point; more often than not, from unrequited love.

I have had my fair share of eye candies, crushes, infatuations and the like.
I daresay I've experienced heart break in many forms.

But when I come to think of it, what I experience through my adolesence from having found out (1)my eye candy doesnt even know i exist (2)my object of infatuation envies someone else or (3)my crush views me as only a friend, only makes me stronger. Another cliche saying "What doesn't kill us only makes us stronger." True much.

Life is about making mistakes.
Life is about making amends.
Life is about moving on.

Life is about embracing the ones who love and care for you.
Life is about appreciating the differences between us humans.
Life is about acceptance.

To the ones who broke my heart, I forgive you.
To the ones whose hearts I broke, my sincere apologies.

Love all, trust few, do wrong to none.

2010-10-12T18:50:00.000-07:00

3 years - Diploma in Optometry at Singapore Polytechnic.
2 years - Bachelor of Science (with Honours) in Optometry at Singapore Polytechnic/University of Manchester.
2 years - Master in Optometry at University of Manchester.

Because studying keeps me happy. And studying secures my future.

2010-10-12T00:16:00.000-07:00

and if you ask me
the feeling that i'm feeling is ~~overjoyed~~
and it's ~~golden~~, it goes to show then
the ending of this song should be left alone
and so on `cause the way it unfolds is yet to be told

2010-10-05T01:06:00.000-07:00

Alhamdulillah, Year 1 Semester 1 results were pretty okay. Have been offered to apply for a Diploma Plus Programme by 7 October - briefing(which I skipped) was today. Doubt I'm applying though, considering the fact that the certificates available to me as an Optomery student are very very limited and out of which none appear to be very appealing to me. So, we'll just see how things go I guess.

Am looking forward to the coming semester - Year 1 Semester 2. 7 +1(TWT, since I'm in SPOT Programme) modules in which more than half include 3h practicals. Timetable's sucky - only improvement is the lack of long breaks in between; neglecting the fact that I've yet to slot in TWT. Add that to NYAA Gold and SPOT Programme. I'm jam packed. Tight schedule. Busy woman. But its good. I need to immerse myself in school to get my mind of things. So yeah (:

2010-10-03T03:39:00.000-07:00

For my 21st on 26Sept;

Gilmore Girls Season 1-7 from Ayah/Adik Hadi/Adik Kasim,

a plaque fom Ibu, a billabong waterbottle and a rose from Erdiah/Fiza O.

ThankYou.

2010-10-02T14:01:00.000-07:00

I NEVER MEANT TO START A WAR
YOU KNOW I NEVER MEANT TO HURT YOU

2010-10-01T23:16:00.000-07:00

http://www.loyangpri.moe.edu.sg/index.php?option=com_content&view=article&id=102&Itemid=181

2010-09-29T23:26:00.000-07:00

Gilmore Girls; Season 3: Those are strings, Pinocchio.

The life of fictional character Rory Gilmore is truly inspirational. I want to graduate from SP with a Gold Medal awarded Diploma in Optometry. I want to be the Valedictorian. I know, I can, I WILL.

InsyaAllah, Amin.

2010-09-26T23:58:00.000-07:00