Clinical Disorders Flashcards

(36 cards)

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
Preparation for end stage renal disease and replacement therapy?
Education | Selection of modality e.g. HD/PD/transplant/conservative
26
AKI definition?
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
Dangerous consequences of AKI?
``` AEIOU Acidosis Electrolyte imbalance Intoxication Overload Uraemic complications ```
28
Three types of AKI?
Pre-renal Intrinsic Post-renal
29
Causes of pre-renal AKI?
``` Volume depletion Hypotension/shock Congestive cardiac failure Arterial occlusion NSAIDs/ACE inhibitors ```
30
Causes of renal (intrinsic) AKI?
``` Acute tubular necrosis Toxin-related Acute interstitial nephritis Acute glomerulonephritis Myeloma Intra renal vascular obstruction ```
31
Causes of post-renal AKI?
Obstruction | intraluminal, intramural, extramural
32
What is radiocontrast nephropathy (RCN)?
AKI following administration of iodinated contrast agent Usually transient, resolving in 72hrs Can lead to permanent loss of function
33
Risk factors for RCN?
``` Diabetes mellitus Renovascular disease Impaired renal function Paraprotein High volume of radiocontrast ```
34
Patients at risk of AKI?
``` STOP Sepsis Toxins Optimise BP and volume Prevent harm ```
35
5 R's for IV prescribing?
``` Resuscitation Routine maintenance Replacement Redistribution Reassessment ```
36
What is Goodpasture's syndrome?
Nephritis with lung haemorrhage