PBL 5 - Diabetes Complication Flashcards

1
Q

What class of drugs are (i) enalapril and (ii) losartan?

A

Angiotensin converting enzyme (ACE) inhibitor.

(ii) Angiotensin 1 (AT1) receptor antagonist .

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2
Q

A frail 80-year-old female with a low creatinine level would be considered
normal, explain why.

A

Creatinine is the byproduct of muscle metabolism. An elderly female with low
muscle mass would have lower circulating creatinine as a result of reduced
muscle metabolism.

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3
Q

What are the four variables in the MDMR equation integrated in the calculation
of the eGFR?

A

Concentration of creatinine in blood. Age of the patient .

Sex of the patient. Ethnic origin.

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4
Q

) List the three components of the physical barrier to glomerular filtration. (ii)
The glomerular barrier selects filtrates on the basis of two basic molecular
features: what are they and how does it work?

A
  • Fenestrated capillary endothelium.
  • Glomerular basement membrane (GBM)
  • Podocytes layer of Bowman’s capsule. [1/2 mark for each]
    (ii) size (the diameter of the diaphragm slit excludes big proteins) [1/2] and charge
    (negatively charged plasma proteins are repelled by negatively charged proteins of
    the GBM AND diaphragm slit AND the endothelial glycocalyx) [1.5 mark].
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5
Q

How can a funduscopy be informative of condition of the patient’s
kidneys in this situation? (ii) Why is it advantageous to use this method?
[2 mark]

A

Both diabetic nephropathy and retinopathy are caused by Diabetes
Mellitus-related micro blood vessels damage, and the presence and severity of
one reflects that of the other. [1]
(ii) Funduscopy is a non-invasive method (compared to a kidney biopsy) [1]

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6
Q

What kind of diet would you suggest Rena follows to help manage her
diabetes? [1 mark]

A

Low GI diet

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7
Q

MDRD formula

A

Modification of Diet in Renal disease (Used to calculate the estimated GFR to check kidney function)
= Serum creatinine, age, ethnicity, gender

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8
Q

What causes podycyturia

A

Molecular insults (glomerulonephritis/metabolic disturbances) –> contract their actin fibres –> decrease in adherence –> detach after mechanical stress -> BM uncovered.

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9
Q

Layers of the glomerular filtration barrier

A

o Endothelium of the capillary - Has fenestrae
o Basement membrane – meshwork of collagen and proteoglycan fibrillae w/ gaps
o Epithelial layer (Podocytes) – long foot like processes separated by slit pores

• Endothelial cells, BM proteoglycan and podocytes – negative charges don’t allow plasma proteins through

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10
Q

What is freely filtered through the GFB and what isnt

A

• Freely filtered – Electrolytes, glucose. Albumin is not – 6nm/ whereas pores are 8 BUT has negative charge and so repulsion by negative charge by negatively charged proteoglycans on BM.

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11
Q

Why does pt have high plasma fasting glucose + glucose in urine

A

Above the threshold for glucose in the Na/glucose co-transporters that allow reabsorption

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12
Q

Why high HbA1c in plasma

A

prolonged elevation in plasma glucose (within 120 days) so glucose residues attach to proteins

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13
Q

Why high creatinine

A

o Freely filtered by the glomerulus under normal conditions
o In glomerular damage – creatinine will accumulate in the body - hypertension
 Albumin sits in the gaps so creatinine cannot pass through

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14
Q

Why low albumin in plasma and high albumin in urine

A

o Albumin is not usually filtered out of the plasma

o With glomerular damage it leaks out

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15
Q

What causes diabetic nephropathy

A

• Damage of glomerular basement membrane by glomerulo-sclerosis + thickening– glycation of BM – allows albumin to pass

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16
Q

What causes glomerular sclerosis

A

• Afferent arteriole becomes vasodilated > efferent arteriole –> Increases intraglomerular filtration pressure –> damages glomerular capillaries (increased shearing forces) –> Mesangial cell hypertrophy + matrix secretion –> Glomerular sclerosis

17
Q

What is microalbuminaemia

A

albumin excretion between 30-300mmg over 24hrs or ACR>3mg/mmol

18
Q

What is Proteinuria

A

albumin excretion >300mg/day or ACCR >30mg/mmol

19
Q

Diabetic retinopathy and nephropathy link

A

o Retinal vessels are visible and can assessable clinically –> can indicate microvascular disease
o T1D: no retinopathy = no nephropathy BUT T2D = nephropathy even w/ no retinopathy

20
Q

Why should BP in patients with nephropathy be lower

A

reduce proteinuria + intraglomerular pressure

21
Q

How does high BP cause nephropathy

A
  • High blood pressure → artery damage (kidneys have bare arteries) –> Causes nephropathy
  • Treatment of hypertension improves albuminuria and results in delated onset, 135/85 mmHg or 125/75 mmHg for those with heavy proteinuria is desired.
22
Q

MoA of ACE-I

A

Angiotensin converting enzyme inhibitor)
Inhibits conversion of angiotensin I to angiotensin II
Reduces vasoconstriction –> efferent dilation –> reduces intraglomerular pressure
Angiotensin II acts on efferent

23
Q

Egs of ACE-I

A

Enalapril

Ramipril

24
Q

MoA of ARB

A

Angiotensin II receptor blocker)
o Block the action of angiotensin II
o Blood vessels dilate and blood pressure is reduced

25
Q

Eg of ARB

A

o Losartan, Candesartan

26
Q

What is diabetic retinopathy

A

• Disease of the retina involving damage to the blood vessels in the fundus

27
Q

What is non-proliferative diabetic retinopathy

A

Dilation of the retina veins and micro aneurysms which can cause internal haemorrhaging and oedema in the retina
o Oedema in the central retina – main cause of vision loss in this case
o The blood glucose levels in these blood vessels increases and damages pericytes which control blood flow to retina

28
Q

Proliferative diabetic retinopathy

A

o Lack of oxygen causes fragile, new blood vessels to form (Bc VEGF) near the optic disk and grow on the vitreous chamber and elsewhere in the retina
o They can bleed – reduce vision – lead to separation + detachment of areas of the retina
o Cotton wool spots, copper wiring

29
Q

What increases retinopathy in diabetes

A

Hyperglycaemia increases blood viscocity

30
Q

Diagnosis of diabetic retinopathy

A

o Visual acuity test, pupil dilation, fundoscopy
o Look at the retina for signs of leaking blood vessels, retinal swelling, fatty deposits in the retina or changes in blood vessels

31
Q

Treatment of diabetic retinopathy

A

o Laser photocoagulation
o Corticosteroids
o Anti-VEGF drugs

32
Q

What is diabetic neuropathy

A

• Damage to nerve fibres and blood vessels supplying nerves due to high glucose

33
Q

Peripheral neuropathy

A

pain or loss of feeling in arms, feet and legs

34
Q

Autonomic neuropathy

A

changes in digestion, bowel and bladder control, erectile dysfunction and the nerves supplying the heart

35
Q

Proximal neuropathy

A

pain in thighs and hips and weakness in legs

36
Q

Focal neuropathy

A

can affect any nerve in the body and it causes pain or weakness
• 60-70% of people with diabetes develop some sort of nerve disease