Clinical Disorders Flashcards

1
Q

What are the features of glomerulonephritis?

A

Haematuria
Proteinuria
Hypertension
Renal insufficiency

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2
Q

Differential diagnosis for nephrotic syndrome?

A

Congestive heart failure

Hepatic disease

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3
Q

Two classifications of glomerulonephritis?

A

Proliferative

Non-proliferative

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4
Q

Diffuse?
Focal?
Global?
Segmental?

A

Diffuse >50% of glomeruli
Focal <50% of glomeruli
Global: all the glomerulus
Segmental: part of the glomerulus

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5
Q

Types of proliferative glomerulonephritis?

A

Post infective
IgA nephropathy
Focal necrotising and crescentic
Anti-GBM disease

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6
Q

Types of non-proliferative glomerulonephritis?

A

Minimal change disease
Focal and segmental
Membranous nephropathy

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7
Q

How might proliferative glomerulonephritis present?

A

With nephritic syndrome
Blood on STIX
Variable proteinuria
Can cause rapid decline

Early diagnosis and treatment key

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8
Q

How might non-proliferative glomerulonephritis present?

A

Present with nephrotic syndrome
Renal biopsy is key investigation
Identify cause if possible

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9
Q

Post-infective glomerulonephritis treatment?

A

Antibiotics for infection
Loop diuretics for oedema (frusemide)
Vasodilators for hypertension (amlodipine)

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10
Q

What is the commonest cause of glomerulonephritis?

A

IgA nephropathy

IgA deposition in mesangium

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11
Q

Anti-GBM disease management?

A

Aggressive immunosuppression:
Steroids
Plasma exchange
Cyclophosphamide (cytotoxic)

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12
Q

Crescentic glomerulonephritis management?

A
Immunosuppression:
Corticosteroids
Plasma exchange
Cyclophosphamide
B-cell therapy
Complement inhibitors
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13
Q

Nephrotic syndrome management?

A

General measures:
Treat oedema, hypertension
Reduce risk of thrombosis, infection
Treat dyslipidemia (statins)

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14
Q

Minimal change disease management?

A

Prednisolone, taper once remission achieved
Initial relapse treated with further steroids
Subsequent relapses cyclophosphamide, cyclosporin, tacrolimus

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15
Q

Focal and segmental glomerulosclerosis management?

A

General measures
Trial of steroids
Alternatives: cyclosporin, cyclophosphamide, rituximab

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16
Q

Membranous nephropathy management?

A

General measures for 6 months
Immunosuppression if symptomatic nephrotic syndrome
Cyclophosphamide and steroids alternate for 6 months
Cyclosporine, rituximab

17
Q

What crosses the glomerular basement membrane (GBM)?

A

Water
Electrolytes
Urea
Creatinine

18
Q

What crosses the GBM but is reabsorbed in the proximal tubule?

A

Glucose

Low molecular weight proteins (α₂ microglobulin)

19
Q

What does not cross the GBM?

A

Cells (RBC, WBC)

High molecular weight proteins (albumin, globulins)

20
Q

CKD definition?

A

Either:
eGFR<60 ml/min/1.73m²
or
The presence of kidney damage that is present for >3 months

21
Q

What is the clinical approach to CKD?

A

Detection of underlying aetiology
Slowing rate of renal decline
Assessment of complications related to reduced eGFR
Preparation for renal replacement therapy

22
Q

Investigations in CKD?

A

Bloods: EUC, FBC, COAG, LFT, CK, IGS, SEP, BIC
Urine: STIX, PCR, ACR, 24hr
Histology: Biopsy
Radiology: Ultrasound

23
Q

Slowing the rate of renal decline?

A

BP control
Control proteinuria
Treat underlying cause

24
Q

Complications related to reduced eGFR? and treatment?

A

Acidosis - bicarb
Anaemia - EPO and iron
Bone disease - diet and phosphate binders
CV risk - BP, aspirin, etc
Death and dialysis - counsel
Electrolytes - diet, drugs?
Fluid overload - salt, fluid restrictions, diuretics
Gout - optimise meds
Hypertension - weight, diet, fluid balance, drugs
Iatrogenic issues - be aware

25
Q

Preparation for end stage renal disease and replacement therapy?

A

Education

Selection of modality e.g. HD/PD/transplant/conservative

26
Q

AKI definition?

A

Increase in serum Creatinine by >26.5 within 48hrs or to >1.5x baseline within the last 7 days
or
Urine volume <0.5 ml/kg/h for 6 hours

27
Q

Dangerous consequences of AKI?

A
AEIOU
Acidosis
Electrolyte imbalance
Intoxication
Overload
Uraemic complications
28
Q

Three types of AKI?

A

Pre-renal
Intrinsic
Post-renal

29
Q

Causes of pre-renal AKI?

A
Volume depletion
Hypotension/shock
Congestive cardiac failure
Arterial occlusion
NSAIDs/ACE inhibitors
30
Q

Causes of renal (intrinsic) AKI?

A
Acute tubular necrosis
Toxin-related
Acute interstitial nephritis
Acute glomerulonephritis
Myeloma
Intra renal vascular obstruction
31
Q

Causes of post-renal AKI?

A

Obstruction

intraluminal, intramural, extramural

32
Q

What is radiocontrast nephropathy (RCN)?

A

AKI following administration of iodinated contrast agent
Usually transient, resolving in 72hrs
Can lead to permanent loss of function

33
Q

Risk factors for RCN?

A
Diabetes mellitus
Renovascular disease
Impaired renal function
Paraprotein
High volume of radiocontrast
34
Q

Patients at risk of AKI?

A
STOP
Sepsis
Toxins
Optimise BP and volume
Prevent harm
35
Q

5 R’s for IV prescribing?

A
Resuscitation
Routine maintenance
Replacement
Redistribution
Reassessment
36
Q

What is Goodpasture’s syndrome?

A

Nephritis with lung haemorrhage