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MRCP > Nephrology > Flashcards

Nephrology Flashcards

1
Q

goserelin - action & other name?

A

GnRH agonist
zoladex
locally advanced prostate cancer

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2
Q

spike and dome appearance on EM - what dx?

A

membranous GN

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3
Q

anti-phospholipase a2 antibodies what dx?

A

membranous GN

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4
Q

why is nephrotic syndrome hypercoagulable

A

loss of antithrombin 3 from kidneys

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5
Q

why does ckd cause anaemia

A

due to reduced levels of EP

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6
Q

whats most common cause of peritonitis 2o to peritoneal dialysis

A

coag negative staph eg epidermis, capitis

2nd most common: staph aureus (coag +ve)

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7
Q

sterile pyuria and white cell casts with rash + fever

A

Acute interstitial nephritis
- Commonly due to abx

Features

- Fever, rash, arthralgia
- Eosinophilia
- Mild renal impairment
- HTN

Histo: marked interstitial oedema + interstitial infiltrate in connective tissue between renal tubules

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8
Q

+ve congo-red stain - when polarised light shone, it appears apple green

A

amyloidosis

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9
Q

tx for AD PKD?

A

tolvaptan = vasopressin rec 2 antag

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10
Q

GNs that present with nephritic syn

A

Rapidly progressive GN
- goodpasture’s, anca positive vasculitis/wegener’s

IgA nephropathy/berger’s/mesangioproliferative GN

Alport syndrome

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11
Q

what presents with a mixed nephritic/nephrotic pic

A

Diffuse proliferative GN

- Post-strep GN in child
- Nephritic syn/AKI
- Most common form of renal disease in SLE

Membranoproliferative GN (mesangiocapillary)
- Type 1: cryoglobinaemia, hep C
Type 2: partial lipodystrophy

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12
Q

what presents w nephrotic syndrome

A

Minimal change disease

- Child w nephrotic syn
- Causes: hodgkin's, NSAIDs
- Good response to steroids

Membranous GN

- Proteinuria/nephrotic syn/CKD
- Causes infections, rheumatoid drugs, cancer
- 1/3 resolve, 1/3 respond to cytotoxics, 1/3 ckd

FSGS
- idiopathic, or due to HIV/heroin
Proteinuria/nephrotic syn/ckd

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13
Q

young women who dev AKI after starting ACEi

A

Fibromuscular dysplasia: consider in young women who dev AKI after starting ACEi
Renal artery stenosis: old = atherosclerosis. Young F = FMD

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14
Q

upper resp tract signs (recurrent sinusitis), nosebleeds, saddle-shaped nose, vasculitic rash

A

granulomatosis w polyangiitis

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15
Q

haemoptysis

A

Goodpasture’s: haemoptysis

Crescentic GN

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16
Q

lower resp symptoms EG recent dx asthma, eosinophilia on bloods

A

Eosinophilic granulomatosis w polyangiitis

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17
Q

young pt w macroscpoic haematuria just after an acute upper rest infection

A

IgA nephropathy

18
Q

enlarged and hypercellular glomeruli w starry sky (granular)

A

Post-strep GN:

19
Q

Microscopic haematuria, bilateral SN deafness, progressive renal failure, longitudinal splitting of lamina densa of GBM on EM (basket weave appearance)

A

Alport’s:
• X-linked dominant
• Defect in gene for type IV collagen > abnormal GBM
• Failing renal transplant – anti-GBM Abs&raquo_space; goodpasture’s picture
• Microscopic haematuria, bilateral SN deafness, progressive renal failure, longitudinal splitting of lamina densa of GBM on EM (basket weave appearance)
• More severe in M (women rarely get renal failure)

20
Q

stag horn calculi - made of?

A

Stag horn calculi: struvite
(ammonium, magnesium, phosphate; triple phosphate)
form in alkaline urine
- so ammonia producing bacteria eg ureaplasma and proteus predispose to it

21
Q

tx of BPH?

A
  1. if mod-severe voiding symptoms = alpha-1 antags (tamsulosin, alfuzosin)
    • SE: dizzy, postural hypotension, dry mouth, depressed
    • If persistent can add in tolterodine, darifenacin (anticholingeric/antimuscarinic)
  2. if sig enlarged prostate and at high risk of progression: finasteride (5 alpha reductase inhibitor) - takes 6 months to work but slows disease progression
    - SE: erectile dysfunction, reduced libido, ejaculation problems, gynaecomastia

If both – use both together
Or: TURP

22
Q

how does chemotx cause kidney disease

A

hyperuricaemia

23
Q

what effect does alcohol binge drinking have on the kidneys

A

Alcohol binge drinking can > ADH suppression in posterior pit gland > polyuria
• Hypernatraemia, raised serum osm, low urine osm

24
Q

Bicalutamide

A

Bicalutamide: androgen receptor blocker. Used in prostate cancer

25
Q

bladder problems in M

  • mainly voiding syms:
  • mixed voiding and storage?
  • mainly overactive bladder?
A

Mainly voiding syms in M: conservative. If mod: a-blocker. If big prostate/high risk: 5-a reductase inhibitor. If both: have both drugs
• If mixed voiding and storage not responding to a-blocker, add antimuscarinic

Mainly overactive bladder in M: conservative. If persist: antimusc (oxybutynin, tolterodine, darifenacin) if fail: mirabegron

26
Q

GN & low complement (4)

A
  • Post strep GN
    • Subacute bacterial endocarditis
    • SLE
      mesangiocapillary GN
27
Q

most common histo pattern in lupus nephritis

A

diffuse proliferative GN

28
Q

causes of cranial DI

& tx

A

Cranial: desmopressin

Causes of cranial DI
	• idiopathic
	• post head injury
	• pituitary surgery
	• craniopharyngiomas
	• histiocytosis X
	• DIDMOAD/wolfram's syndrome 
- Haemochromatosis
29
Q

nephrogenic DI
causes
tx

A

Causes of nephrogenic DI
• genetic: ADH rec (more common),aquaporin 2 channel
• electrolytes: high calcium, low K
• lithium
• demeclocycline
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis

nephrogenic: thiazides, low salt/protein diet

30
Q 
alport's syndrome
- inheritence
gene defect
features
renal biopsy ft
A
30
Q 
alport's syndrome
- inheritence
gene defect
features
renal biopsy ft
A

ost: x-linked dominant
· defect in the gene which codes for type IV collagen&raquo_space; abnormal GDM
· More severe in M (females rarely get renal failure)

NB renal transplants often fail: due to anti-GBM Abs > goodpasture’s like pic

Usually presents in children
	• microscopic haematuria
	• progressive renal failure
	• bilateral SN deadness
	• lenticonus: protrusion of the lens surface into the anterior chamber
	• retinitis pigmentosa

EM: basket-weave (longitudinal splitting of lamina densa of GBM)

DETAILS
Diagnosis
• molecular genetic testing
• renal biopsy

NB 10-15% autosomal recessive

31
Q

HOW TO TELL ATN FROM AIN ON URINE DIP

A

Urine dip can differentiate ATN from acute interstitial nephritis:

- AIN: inflam process = more white cells in urine (can be caused by penicillin abx)
- ATN: not inflam - no white cells 
- If protein is present = rules out pre or post renal cause
32
Q

stages of diabetic nephropathy

A

Stage 1
• hyperfiltration: increase in GFR
• may be reversible

Stage 2 (silent or latent phase)
	• most patients do not develop microalbuminuria for 10 years
	• GFR remains elevated
Stage 3 (incipient nephropathy)
	• microalbuminuria (albumin excretion of 30 - 300 mg/day, dipstick negative)

Stage 4 (overt nephropathy)
• persistent proteinuria (albumin excretion > 300 mg/day, dipstick positive)
• hypertension is present in most patients
• histology shows diffuse glomerulosclerosis and focal glomerulosclerosis (Kimmelstiel-Wilson nodules)

Stage 5
• end-stage renal disease, GFR typically < 10ml/min
• renal replacement therapy needed

The timeline given here is for type 1 diabetics.
T2DM progress through similar stages but in a different timescale - some T2DM patients may progress quickly to the later stages

33
Q

how does alcohol cause polyuria

A

Alcohol binge > ADH suppression in posterior pituitary gland > polyuria

34
Q

renal stones
- radiolucent (2)
- semi opaque (1)
opaque (4)

A

radiolucent: urate, xanthine stones
semi opaque: cystine
opaque: calcium oxalate, calcium phosphate, triple phosphate/struvite, mixed ca oxalate/phosphate stones

35
Q

membranoproliferative GN

  • mx?
  • types and their causes/fts
A

· may present as nephrotic syndrome, haematuria or proteinuria
· poor prognosis

Management: steroids may be effective

Type 1 (90%)
	· cause: cryoglobulinaemia, hep C
	· EM: subendothelial + mesangium immune deposits of electron-dense material = 'tram-track' appearance

Type 2 - ‘dense deposit disease’
· causes: partial lipodystrophy (loss of SC tissue from face), factor H deficiency
· caused by persistent activation of alternative complement pathway
· low circulating levels of C3
· C3b nephritic factor in 70%
○ an antibody to alternative-pathway C3 convertase (C3bBb)
○ stabilizes C3 convertase
· renal biopsy
○ EM: intramembranous immune complex deposits with ‘dense deposits’

Type 3 causes: hepatitis B and C

36
Q

metabolic acidosis

  • anion gap eqn
  • normal range for anion gap
  • normal anion gap MA causes (5)
  • raised causes (4)
A

Classified according to the anion gap

- calculated by: (Na+ + K+) - (Cl- + HCO-3)
- If a question supplies the chloride level then this is often a clue that the anion gap should be calculated
- normal range = 10-18 mmol/L

Normal anion gap ( = hyperchloraemic metabolic acidosis)
• GI bicarb loss: diarrhoea, ureterosigmoidostomy, fistula
• renal tubular acidosis
• drugs: e.g. acetazolamide
• ammonium chloride injection
• Addison’s disease

Raised anion gap
	• lactate: shock, sepsis, hypoxia
	• ketones: diabetic ketoacidosis, alcohol
	• urate: renal failure
	• acid poisoning: salicylates, methanol

Metabolic acidosis secondary to high lactate levels may be subdivided into two types:
• lactic acidosis type A: sepsis, shock, hypoxia, burns
• lactic acidosis type B: metformin

37
Q

ATN v prerenal uraemia

A

Prerenal uraemia - kidneys hold on to sodium to preserve volume
- Fractional sodium excretion <1%, urine sodium <20

38
Q

High calcium in urine & kidney stones

A

thiazide diuretics

39
Q

plasma exchange
indications (7)
comps (5)

A

Indications for plasma exchange (also known as plasmapheresis)
• GBS
• myasthenia gravis
• Goodpasture’s
• ANCA positive vasculitis if rapidly progressive renal failure or pulmonary haemorrhage
• TTP/HUS
• cryoglobulinaemia
• hyperviscosity syndrome e.g. secondary to myeloma

Complications of plasma exchange
	• Low calcium
	• metabolic alkalosis
	• removal of systemic medications
	• coagulation factor depletion
immunoglobulin depletion

MRCP (16 decks)

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