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AMK > Renal > Flashcards

Renal Flashcards

1
Q

Nephrotic syndrome

A

Proteinuria, hypoalbuminaemia, oedema

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2
Q

Nephritic syndrome sx

A

Haematuria
Hypertension
RBC casts

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3
Q

Function of juxtaglomerular cells

A

Detects changes in pressure

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4
Q

Function of macula densa

A

Detects changes in concentration

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5
Q

Cause of nephrotic syndrome

A

Podocyte damage and glomerulonephritis

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6
Q

Tx nephrotic syndrome

A

Furosemide and monitor salt/fluid intake

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7
Q

What is rhabdomyolysis?

A

Breaking down muscle tissue

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8
Q

Cause of rhabdomyolysis

A

Trauma

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9
Q

Sx rhabdomyolysis

A

Hyperkalaemia and red/brown urine

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10
Q

Treatment for rhabdomyolysis

A

Treat hyperkalaemia (insulin)
IV calcium gluconate

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11
Q

Osmotic diuretics
E.g.
Location
MOA

A

Mannitol
Glomerulus
Decrease H2O reabsorption

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12
Q

CA inhibitor diuretics
E.g.
Location
MOa

A

Acetazolamide
PCT
No breakdown of carbonic acid means no H+ to be exchanged for Na+ so no H2O reabsorbed

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13
Q

Loop diuretics
E.g.
Location
MOA

A

Furosemide
LOH
Inhibits Na+/K+/Cl- transporter

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14
Q

Thiazide diuretics
E.g.
Location
MOA

A

Hydrochlorothiazide
DCT
Block Na+/Cl- co-transporter

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15
Q

K+ sparing diuretics
E.g.
Location
MOA

A

Triamterene
CD
Aldosterone antagonist

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16
Q

Calcium gluconate MOA

A

Stabilises myocardium

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17
Q

How does insulin act on potassium?

A

Shifts from ECF to ICF

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18
Q

How does calcium resonium act on potassium

A

Removes potassium from body

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19
Q

At which level do the kidneys lie?

A

T12 to l3 (right is lower due to liver)

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20
Q

Are kidneys retroperitoneal or intraperitoneal

A

Retroperitoneal

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21
Q

Kidney layers deep to superficial

A

Renal capsule
Perirenal fat
Renal fascia
Pararenal fat

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22
Q

Posterior relations to kidneys (3 muscle)

A

Psoas major, quadrates lumborum and transverus abdominis

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23
Q

Blood supply to kidneys

A

Renal arteries (from abdominal aorta)

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24
Q

How does the renal artery divide once it reaches the kidney?

A

Renal artery - segmental artery - interlobular artery - arcuate arteries - afferent arterioles

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25
Q

Where do kidneys drain?

A

para-aortic

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26
Q

Pelvic kidney

A

In utero, kidneys ascend from pelvis - this may not happen and one may remain at the level of the common iliac artery

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27
Q

Horseshoe kidney

A

Two developing kidneys fuse together and become stuck under the inferior mesenteric artery

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28
Q

Which rib is the upper pole of both kidneys?

A

11th rib

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29
Q

Hilum of left kidney

A

L1

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30
Q

Hilum of right kidney

A

L1-2

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31
Q

Lower border of kidneys

A

L3

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32
Q

Level of adrenals

A

t12

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33
Q

What is an ectopic kidney?

A

Located below, above or on the opposite side of normal

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34
Q

E.g. osmotic diuretics

A

Mannitol

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35
Q

How do osmotic diuretics work?

A

They are not reabsorbed along the nephron - less water is reabsorbed and more is excreted

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36
Q

S/e osmotic diuretics

A

hyponatraemia and hypokalaemia

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37
Q

How do potassium sparing diuretics work?

A

Inhibit sodium reabsorption from DCT by antagonising aldosterone

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38
Q

e.g. potassium sparing diuretic

A

spironolactone

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39
Q

diuretic for heart failure

A

spironolactone

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40
Q

e.g. thiazide diuretics

A

hydrochlorothiazide

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41
Q

thiazide diuretics moa

A

act on DCT and CD and inhibit sodium/chloride co-transporter

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42
Q

loop diuretics e.g.

A

furosemide

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43
Q

loop diuretics moa

A

act on sodium/potassium/chloride channel on ascending LOH so no chloride reabsorbed

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44
Q

Most common type of renal stone

A

Calcium oxalate

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45
Q

Cystine renal stones

A

Inherited recessive disorder = abnormal reabsorption of cystine from intestine and renal tubes

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46
Q

Where is majority of glucose reabsorbed in nephron

A

PCT

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47
Q

What is Goodpasture’s disease?

A

Vasculitis associated with glomerulonephritis

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48
Q

Antibodies present in good pasture’s syndrome

A

Anti-GBM

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49
Q

HLA association good pasture’s

A

HLA DR2

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50
Q

Sx Goodpasture’s syndrome

A

Progressive glomerulonephritis - AKI
Nephritis ->proteinuria and haematuria

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51
Q

Type fo hypersensitivity goodpastures

A

II

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52
Q

Where does left testicular/gonadal vein drain?

A

Left renal vein

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53
Q

Where does right testicular/gonadal vein drain to

A

IVC

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54
Q

Most common cause of acute prostatitis

A

e coli

55
Q

Sx prostatitis

A

Referred pain, fever, tender, enlarged prostate

56
Q

Tx prostatitis

A

quinolone

57
Q

What is rhabdomyolysis?

A

Breakdown of muscle

58
Q

Causes of rhabdomyolysis

A

Trauma, EBV, alcohol, drugs

59
Q

How to treat rhabdomyolysis

A

Fluids

60
Q

Sx rhabdomyolysis

A

Red-brown urine, hyperkalaemia, renal failure

61
Q

What is IgA nephropathy?

A

IgA immune complexes deposited in mesangium causes glomerular injury

62
Q

Is IgA neuropathy nephritic or nephrotic

A

Nephritic

63
Q

What kind of hypersensitivity is IgA nephropathy

A

3

64
Q

Pathophys IgA nephropathy

A

Abnormal glycosylation of IgA means the compound is galactose deficient
Therefore not identified and broken down by body
Abnormal IgA accumulates
Body releases IgG to target
Immune complex forms in mesangium
Glomerular injury

65
Q

sx iga nephropathy

A

Haematuria shortly after URTI in young male

66
Q

Sx post-streptococcal glomerulonephritis

A

headache
haematuria and proteinuria
hypertension

67
Q

What is post-streptococcal glomerulonephritis

A

1-2 weeks after strep progenies infection, infection spreads to glomerulus where it is deposited

68
Q

Tx post-streptococcal glomerulonephritis

A

Self-limiting

69
Q

Describe post-streptococcal gloemrulonephritis immunofluorescence appearance

A

Granular/starry sky

70
Q

Which chemicals are deposited in the glomerulus in post-streptococcal glomerulonephritis?

A

IgM, IgG and C3

71
Q

What is Henoch-Schonlein purport?

A

Small cell IgA mediated vasculitis

72
Q

Tx Henoch-Schonlein purpura

A

Self limiting

73
Q

Sx hence-schonlein purpura

A

Purpuric rash + oedema
Rash on buttocks and extensor surfaces
Abdo pain

74
Q

Inheritance of Alport’s

A

X-linked dominant

75
Q

What is Alpert’s syndrome

A

Defect in type 4 collagen forms abnormal GBM -> Goodpasture’s

76
Q

Mx Alport’s

A

ACEi/ARB

77
Q

Dx Alport’s

A

Splitting of lamina densa = basket weave appearance

78
Q

Why do renal transplants fail?

A

Anti-GBM antibodies -> Goodpasture’s

79
Q

Sx Alport’s syndrome

A

Haematuria
Renal failure
Sensorineural deafness

80
Q

What is Goodpasture’ syndrome

A

Anti-GBM ABs against type 4 collagen
IgG in basement membrane

81
Q

Hypersensitivity type Goodpasture’s

A

2
HLA-DR2 association

82
Q

Tx Goodpasture’s

A

Steroids and cyclophosphamide

83
Q

Sx Goodpasture’s syndrome

A

Glomerulonephritis and pulmonary haemorrhage

84
Q

Where does adrenal artery come from

A

aorta

85
Q

Contents of hilum from anterior to posterior

A

Renal vein
Renal artery
Ureter

86
Q

When demyelinated, which nerves cause urinary retention?

A

Pelvic splanchnic

87
Q

Parasympathetic innervation to bladder

A

pelvic splanchnic

88
Q

risk factors for bladder cancer

A

smoking and 2-naphthylamine

89
Q

most common type of bladder cancer

A

transitional cell carcinoma

90
Q

sx bladder cancer

A

painless macroscopic haematuria

91
Q

staging and diagnosing bladder cancer

A

TURBT and pelvic MRI

92
Q

How does alcohol act as a diuretic?

A

Suppreses ADH from post pituitary

93
Q

Sx hypocalcaemia

A

tetany (muscle spasm), paraesthesia, long QT, cataracts
trousseau’s sign: wrist flexion
Chvostek’s sign: tapping parotid makes face twitch

94
Q

Hyperkalaemia causes

A

metabolic acidosis, AKI, K+ sparing diuretics, ACEi, heparin, Addison’s, rhabdomyolysis

95
Q

causes of hypocalcaemia

A

vit D deficiency, CKD, hypoparathyroidism, rhabdomyolysis

96
Q

management of hypocalcaemia

A

calcium gluconate

97
Q

Mx hypocalcaemia

A

calcium gluconate

98
Q

Eosinophilis granulomatosis with polyangiitis

A

Churg-Strauss
pANCA +ve
Severe asthma, eosinophilia
Tx = steroids

99
Q

Granulomatosis with polyangiitis

A

Wegener’s disease
cANCA +ve
Saddle nose deformity
Tx = steroids

100
Q

first line treatment for CKD

A

ACEi/ARB

101
Q

Acute tubular necrosis

A

Necrosis of epithelial cells in tubules caused by toxins (ahminoglycosides, methotrexate etc)
Necrotic cells obstruct lumen
MUDDY BROWN CASTS

102
Q

mussy brown casts

A

acute tubular necrosis

103
Q

acute interstitial nephritis

A

inflammation of extra-glomerular tissue

104
Q

causes of intra-renal AKI

A

acute tubular necrosis and acute interstitial nephritis

105
Q

What is minimal change disease?

A

Most common cause of nephrotic syndrome in children, normally idiopathic

106
Q

Pathophysiology minimal change disease

A

Podocytes lose negative charge
- Unable to repel ions
- Ions cross into urine = proteinuria

107
Q

Sx minimal change disease

A
  • Nephrotic syndrome
  • Normotension
  • Proteinuria
  • Hypoalbuminaemia
  • Oedema
108
Q

Diagnosis minimal change

A

electron microscopy

109
Q

Tx minimal change

A

oral corticosteroids

110
Q

What is rapidly progressive glomerulonephritis/

A

destruction of glomeruli due to nephritis

111
Q

tx rapidly progressive GN

A

steroids and cyclophosphamide

112
Q

what is CKD?

A

kidney dysfunction >3 months characterised by abnormal creatinine and electrolyte levels

113
Q

CKD stages

A
  • CKD 1: eGFR >90
  • CKD 2: eGFR 60-89
  • CKD 3a: eGFR 45-59
  • CKD 3b: eGFR 30-44
  • CKD 4: eGFR 15-29
  • CKD 5: eGFR <15 (kidney failure)
114
Q

sx CKD

A

Normally asymptomatic - characterised by abnormal creatinine and electrolytes
Can have pruritus, lethargy, insomnia, HTN

115
Q

what is hepatorenal syndrome?

A

AKI + liver failure

116
Q

cardiorenal syndrome

A

congestive HF + renal failure

117
Q

acute interstitial nephritis

A

‘allergic reaction’ - inflammation of extra-glomerular tissue
caused by ABx, NSAIDs, diuretics, PPIs, or infections

118
Q

symptoms acute interstitial nephritis

A

pyuria (oesinophils), crystals

119
Q

tx acute interstitial nephritis

A

discontinue drugs, add fluids

120
Q

muddy brown casts

A

acute tubular necrosis

121
Q

what is acute tubular necrosis

A

necrosis of epithelial cells in tubules

122
Q

causes of acute tubular necrosis

A

ischaemia, toxins, haemoglobin, proteins (rhabdomyolysis)

123
Q

tx acute tubular necrosis

A

no treatment - terminal

124
Q

Nephritis 1-2d post URTI

A

IgA nephropathy

125
Q

nephritis 1-2w post URTI

A

post-strep GN

126
Q

why do you give steroids in IgA nephropathy?

A

if renal function starts declining, due to immune reaction - steroids will counteract this

127
Q

cANCA +ve with saddle-nose deformity

A

Wegener’s

128
Q

pANCA +ve granulomatosis

A

Churg-Strauss (eosinoPhilic)

129
Q

Severe asthma + severe renal failure + high eosinophil count

A

churg - strauss (eosinophilic granulomatosis with polyangiitis)

130
Q

antibodies against t4 collagen, destroys GBM

A

Goodpasture’s syndrome

131
Q

mutated gene for t4 collagen

A

alport

132
Q

most common cause of nephrotic syndrome in adults

A

membranous nephropathy

133
Q

mx membranous nephropathy

A

ACEi/ARBs

134
Q

most common cause of SIADH

A

small cell lung cancer

AMK (33 decks)

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