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OP2205 > 2. Diabetes and hypertension > Flashcards

2. Diabetes and hypertension Flashcards

1
Q

What is meant by diabetes mellitus

A

Sustained hyperglycaemia secondary to lack of, or diminished efficacy of endogenous insulin.

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2
Q

Describe the 2 types of diabetes

A

Type 1: Also known as insulin dependent diabetes (IDD)- The pancreas doesn’t produce enough insulin.
Type 2: Also known as non- insulin- dependent diabetes (NIDD)- Body does not respond to the insulin available.

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3
Q

What is the treatment of type 1 IDD

A
  1. Insulin injections
  2. Diet control
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4
Q

What is the treatment of type 2 NIDD

A
  1. Diet control
  2. Oral hypoglycaemic agents
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5
Q

2 oral hypoglycaemic agents include biguanides and sulfonylureas. Give an example for each and explain its role.

A

Biguanides e.g. metformin - inhibition of liver glucose production
Sulfonylureas e.g. gliclazide - stimulate insulin production in pancreas

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6
Q

Role of insulin

A

Regulate blood sugar

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7
Q

Side effect of gliclazide

A

Patients will put on weight

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8
Q

8 ocular complications associated with diabetes

A
  1. Cataracts - snowflake cataract
  2. Diabetic Retinopathy
  3. Refractive changes -myopic shift
  4. Colour vision defect - blue yellow defect
  5. Corneal changes- reduced sensitivity, tear abnormalities
  6. Glaucoma (open angle)
  7. Recurrent infections e.g, blepharitis
  8. Cranial nerve palsies (cranial nerve 7 most likely affected)
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9
Q

Risk factors of diabetic retinopathy (DR)

A
  1. Duration of diabetes - longer the duration higher the risk
  2. Metabolic control - high blood glucose level
  3. Cataract surgery -increased risk of progression
  4. Other factors (pregnancy, hypertension, renal diseases, obesity and smoking).
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10
Q

Describe the pathogenesis of DR

A

Diabetes affects the microvasculature (small blood vessels), causing microvasculature occlusion and leakage. The small blood vessels are vulnerable to damage from high glucose levels.

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11
Q

5 biochemical pathways that affect DR

A
  1. Increased expression of growth factor VEGF.
  2. Polyol pathway- Glucose entering cells is metabolized to sorbitol that accumulates in the body. - contributes to the retinopathy
  3. Oxidative stress
  4. Inflammation
  5. Genetic factors- affect the severity
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12
Q

Clinical features of DR- STAGES OF SEVERITY

A
  1. Non-proliferative DR (NDR)- Mild, Moderate, Severe
  2. Proliferative DR (PDR)
  3. Diabetic maculopathy
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13
Q

Describe Mild NPDR- What is seen?

A

At least 1 micro aneurysm with or without the presence of retinal hemorrhages, hard exudates, cotton wool spots or venous loops.

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14
Q

What is seen in the fundus photograph of a patient with microaneurysms?

A

Dots seen at the posterior pole in the inner nuclear layer. This is created by weakness of vessel walls.

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15
Q

2 forms of intraretinal haemorrhages

A

Dot and blot haemorrhages

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16
Q

Intraretinal haemorrhages are caused due to?

A

Leakage from damaged blood vessels due to bleeding in the inner nuclear layer and plexiform layer

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17
Q

What are hard exudates made of? and found in which layer?

A

Made of lipids and found in the outer plexiform layer

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18
Q

Describe what is seen in moderate NPDR

A

Numerous micro aneurysms and retinal hemorrhages (cause: retina is oxygen deprived) are present.
Limited cotton wool spots and venous beading may also be seen.

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19
Q

Describe how cotton wool spots look and what causes them?

A

Grey- whitish patches
It is caused by the occlusion of precapillary arterioles in retinal nerve fiber layer caused by the build up of axonal debris in the nerve fiber layer.

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20
Q

Define severe NPDR using (4-2-1 rule)

A

ANY OF THE FOLLOWING:
1.Numerous hemorrhages and micro aneurysms in 4 quadrants of the retina
2. Venous beading in 2 or more quadrants
3. Intraretinal microvascular abnormalities in at least 1 quadrant

21
Q

Describe proliferative DR signs (4)

A
  1. Neovascularisation
  2. Vitreous detachment
  3. Haemorrhage - preretinal, vitreous
  4. Retinal detachment
22
Q

Describe how preretinal haemorrhage looks in proliferative DR

A

Boat shaped

23
Q

Describe Diabetic maculopathy :Why it occurs, types and what does it lead to?

A

Occurs when there is involvement of the fovea by oedema, hard exudates or ischaemia
Various types eg. focal, diffuse
Leads to central visual loss

24
Q

Diabetic maculopathy becomes clinically significant when?

A

When hard exudates and oedema are closer to the centre of the fovea

25
Q

Treatment of DR

A
  1. Laser therapy
  2. Focal/grid, panretinal photocoagulation
  3. Vitrectomy
  4. Intravitreal injections of corticosteroids (triamcinolone)
  5. Intravitreal injections of VEGF inhibitors eg Lucentis, Avastin
26
Q

Before treating DR what is required?

A

Patients have to get their systemic diabetes into control

27
Q

Elevated systolic BP and diastolic BP values

A

Systolic (when heart is contracting): Greater then 140 mmHg
Diastolic (when heart is relaxing): Greater then 90 mmHG

28
Q

Laser therapy is used to treat what 2 conditions? And what is its aim?

A

Proliferative diabetic retinopathy and diabetic macular oedema. Aim: limit vascular leakage through series of laser burns limiting visual losses.

29
Q

What is the role of VEGF Inhibitors Lucentis and Avastin

A

Block VEGF to downregulate neovascularisation

30
Q

Hypertension is a risk factor for which 3 conditions?

A
  1. Cardiovascular diseases
  2. Heart failure
  3. Stroke
31
Q

Hypertension risk factors

A
  1. High salt intake
  2. High alcohol intake
  3. Smoking
  4. Family history
  5. Age
  6. Race
  7. Stress
32
Q

Hypertension prevention

A

Lifestyle changes:
Weight loss
Reduce dietary sodium intake
Balanced diet
Exercise - regular aerobic physical activity
Limit alcohol consumption

33
Q

Hypertension treatments- 5

A

Antihypertensive drugs

  1. Beta blockers
  2. Diuretics
  3. ACE (Angiotensin-Converting Enzyme) Inhibitors
  4. Angiotensin receptor blockers
  5. Alpha-2 agonist
34
Q

Describes what happens to the ocular health of patients with hypertensive retinopathy:

A

Narrowing of the retinal arterioles
Depends on:
1. Rigidity of retinal arterioles
2. Sclerosis in older px
Additionally:
Blood-retinal barrier disrupted
Increased vascular permeability

35
Q

What are the 3 general features associated with hypertensive retinopathy

A
  1. Vasoconstriction
  2. Arteriosclerosis
  3. Leakage
36
Q

Describe vasoconstriction

A

Arteries are narrowed due to which overtime BP increases causing endothelial damage leading to arteriosclerosis.

37
Q

Describe 4 things seen due to arteriosclerosis

A
  1. Thickening of vessel walls
  2. Copper wiring
  3. Arterial tortuosity
  4. AV nipping/ crossing
38
Q

What causes AV nipping?

A

Pressure of thickened arteries pressing down on the veins

39
Q

Describe how hypertensive retinopathy causes leakage

A

Disruption of blood retinal barrier and leakage of plasma exudates into the retina causing fluids and blood to accumulate into multiple layers of the retina.

40
Q

Describe what is seen in hypertensive retinopathy causes leakage

A
  1. Cotton wool spots
  2. Abnormal vascular permeabilty leading to flame- shaped haeomorrhages and hard exudates
41
Q

What happens in malignant hypertension and what is observed

A

The optic nerve head swells (edge of the disc is indistinct) and macular star is seen (this star is hard exudates around the fovea)

42
Q

Type 1 vs Type 2 diabetes which one has a higher prevalence to cause diabetic retinopathy?

A

Type 1

43
Q

Release of VEGF promotes?

A

It promotes the release of new abnormal blood vessels that increase vascular permeability.

44
Q

2 retinal vascular disorders
Why?

A
  1. Diabetic retinopathy
  2. Hypertensive retinopathy
    Because this are disorders that affect the blood vessels.
45
Q

Aim of Antihypertensive drugs

A

Prevent complication of high BP example stroke

46
Q

How do beta blockers work?

A

Reduce heart rate and force of heart beat

47
Q

Role of diuretics’?

A

Increase salt and water passed in urine- reduces fluid in circulation reducing blood pressure.

48
Q

Role of ACE Inhibitors

A

Reduce angiotensin in the blood stream (this are chemical that constrict or narrow blood vessels) having less of this chemical reduce BP.

49
Q

Release of VEGF promotes?

A

Promotes the release of new abnormal blood vessels, increasing vascular permeability

OP2205 (8 decks)

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