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Urinary > 7- Nephritic, Nephrotic, Diabetes, Glomerulus Path > Flashcards

7- Nephritic, Nephrotic, Diabetes, Glomerulus Path Flashcards

1
Q

What is glomerulonephritis

A

Inflammation of glomeruli

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2
Q

What structures of glomerulus can be damaged (4)

A

Capillary endothelium
Glomerular basement membrane
Mesangial cells
Podocytes

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3
Q

What is normally involved with glomerulonephritis

A

Over response from immune system

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4
Q

Characteristics of Nephrotic

A

Podocyte damage leading to glomerular charge barrier disruption so doesn’t repel proteins
Proteinuria
Oedema

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5
Q

Why oedema in nephrotic injury

A

Low albumin in plasma so less oncotic pull so fluid pools in tissue

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6
Q

Characteristics of Nephritic injury

A

Inflammation disrupting glomerular basement membrane
Haematuria
Coca cola urine

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7
Q

What is the triad of Nephrotic syndrome

A

Proteinuria >350mg/mmol
Hypoalbuminaemia
Oedema

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8
Q

What usually accompanies Nephrotic syndrome

A

High cholesterol as liver tries to compensate and make more albumin and a byproduct is cholesterol.

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9
Q

Other features of Nephrotic syndrome

A

Normal BP

Creatinine may be normal

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10
Q

Primary causes of Nephrotic

A

Minimal change disease- podocyte damage
Membranous glomerulonephritis
Focal segmental glomerulosclerosis

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11
Q

Secondary causes of Nephrotic

A

Diabetes
SLE
Amyloid

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12
Q

Management of Nephrotic syndrome

A

Diuretics- oedema
ACE-I- anti-proteinuric
Statins- Hypercholesterolaemia
Treat underlying steroid- MCD

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13
Q

Triad of Nephritic disease

A

Haematuria
Reduced GFR
Hypertension

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14
Q

Other features of Nephritic disease

A

Some proteinuria
Disruption of endothelium = inflammatory response and damage to glomerulus
Acute or rapid onset
Rapid progressive

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15
Q

Common causes of Nephritic

A

Goodpastures (Anti GMB)
Rapidly progressive GN
IgA Nephropathy (Bergers))
Post Streptococcal GN

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16
Q

Management

A

BP control - ACE-I, salt restriction
Diuretics for oedema- if adequate renal function
Immunosuppressants - disease specific- 90% remission. 1-2 weeks from start of treatment
Stop smoking- manage CV risk
Dialysis- if acute onset- short term

17
Q

Commonest cause of end stage renal disease

A

Diabetic nephropathy

18
Q

Is it a glomerulopathy or glomerulonephritis

A

Glomerulopathy- physical changes not due to inflammation

19
Q

Pathological changes in diabetic nephropathy

A 
Hyperfiltration
Capillary hypertension
Glomerular basement membrane thickening
Mesangial expansion
Podocyte injury
Glomerular sclerosis/atherosclerosis
20
Q

Why does hyperfiltration and hypertrophy occur with diabetes

A

Hyperglycemia causes high blood sugar which causes increase in GFR

21
Q

How is glucose taken up in Kidneys

A

SGLT2 (Na and Glucose) Powered by Na/K ATPase

coupled with Na

22
Q

Whats the max glucose that the kidneys can reuptake

A

10mmol then glucose in urine

23
Q

What leads to RAAS activation

A

Low delivery of NaCl to macula densa
Lots more Na absorbed so macula densa sense low Na and activate RAAS. Vasodilation of afferent and vasoconstriction efferent = hyperfiltration

24
Q

Stages

A

Hyperfiltration and hypertrophy- GFR increased

Latent stage- Normal albumin, GBM thickening

Microalbuminuria- Mesangial expansion, GBM thickening, podocyte change, GFR normal

Overt proteinuria- diffuse histo changes, systemic HTN, decreased GFR

ESRD

25
Q

What is microalbuminuria

A

First clinical sign
GBM thickening and mesangial expansion
Potentially reversible
Dipstick test

26
Q

Over proteinuria

A

GFR normal initially
Mesangial expansion and sclerosis- reduced SA for filtration
Proteinuria >300mg/day- oedema
Worsening systemic hypertension
Microvascular changes- hyalinosis of arterioles = tissue ischemia
Not reversible

27
Q

What is the average decline in GFR for those with overt proteinuria

A

12mls/min/year

ESRD- 3-7 years

28
Q

Diabetic nephropathy risk factors

A

Genetics, race, hypertension, hyperglycemia, age, duration of diabetes, smoking

29
Q

Prevention of diabetic nephropathy

A

Tight glucose control- can reduce microalbuminuria

Tight blood pressure control

30
Q

How would SGLT 2 inhibitors help

A

Prevent glucose reabsorbed and also Na = RAAS not activated = no hyperfiltration

31
Q

Management of microalbuminuria and proteinuria

A

Inhibition of RAAS, tight BP control, CV risk management (exercise, smoking, diet), moderate protein intake

32
Q

How does RAAS blockade help

A

Reduce glomerular hyperfiltration
Efferent more than afferent
Antiproteinuric effect more than BP reduction as it decreases the pressure forcing proteins through.

Limited by hyperkalemia in CKD as kidney no longer functioning well = reduced filtration

Urinary (11 decks)

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