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MD Y1S1 > Renal review > Flashcards

Renal review Flashcards

1
Q

What innervates the detrusor muscle?

A

Pelvic nerve (parasympathetic, S2-4 –> Ach on muscarinic receptors causes contraction)

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2
Q

What innervates the internal sphincter?

A

Hypogastric nerve (sympathetic, T10-L2) –> acts on alpha receptor

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3
Q

Effects of hypogastric nerve?

A

Contraction of internal sphincter (a receptors)

Relaxation of bladder wall (b2 receptors)

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4
Q

Potential effect of a-inhibitors (eg. prazosin)

A

Incontinence

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5
Q

What innervates the external urethral sphincter?

A

Pudendal nerve (somatic, S2-4)

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6
Q

Voiding physiology

A
  1. Relaxation of internal sphincter with increased volume and reduced SNS input
  2. Voluntary relaxation of external sphincter
  3. Suprapontine and pontine centres withdraw inhibition to detrusor muscle
  4. Detrusor contracts
  5. Voluntary contraction of abdominal muscles
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7
Q

PNS involvement in micturition

A

Bladder contraction

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8
Q

SNS involvement in micturition

A

Internal sphincter contraction at low volumes
Maintains tone during filling
Innervates blood vessels

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9
Q

Micturition reflex

A

Bladder fills –> stimulates stretch receptors –> excites PNS in bladder and inhibits motor neuron to external sphincter (overridden by voluntary control) –> bladder contraction and relaxation of external sphincter –> urination

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10
Q

Common types of kidney stones

A

Calcium oxalate 75-80%
Uric acid 15%
Cystine <5%

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11
Q

Which types of kidney stones are radiopaque/can be seen on X-ray?

A

Calcium oxalate

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12
Q

Conservative Mx of kidney stones

A

Analgesia (NSAIDs –> diclofenac or indomethacin per rectum)

Wait for stone to pass (if pain controlled and no sepsis)

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13
Q

Stone prevention

A

Diet - normal calcium, high fibre, low salt, low protein

Increased fluid intake

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14
Q

OAB conservative Mx

A 
Fluid intake, caffeine, alcohol
Weight loss
Stop smoking
Pelvic floor (30/day for 3 months)
Bladder retraining
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15
Q

OAB drugs

A

Antimuscarinics –> side effects include dry mouth, dry eyes, constipation
B3-adrenergic agonist –> can increase BP

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16
Q

SUI conservative Mx

A

Weight loss
Stop smoking
Pelvic floor (30/day for 3 months)

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17
Q

Acute urinary retention Mx

A 
Catheterization
A blockers (Tamsulosin) for males
Treatment of cause --> UTI, constipation, BPH, neurological cause, medication related
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18
Q

BPH conservative Mx

A 
Fluid intake
Stop smoking
Limit caffeine, alcohol
Timing of diuretics
Restriction of fluids at night
Bladder retraining
Reassurance
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19
Q

BPH medical Rx

A

Alpha blockers (tamsulosin)
5-alpha reductase inhibitors
Combination of both

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20
Q

Alpha blockers mechanism

A

Smooth muscle relaxation in bladder neck and prostate therefore improved flow of urine

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21
Q

5-alpha reductase inhibitor mechanism

A

Blocks testosterone –> DHT

Prostate no longer grows and may shrink

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22
Q

BPH surgical gold standard

A

TURP

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23
Q

What type of genetic abnormality is congenital cystinosis?

A

Autosomal recessive defect

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24
Q

Immunosuppressants post transplant

A

Tacrolimus (monitor levels)
Presnisone
Mycophenolate
Cyclosporin

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25
Q

Nephrotoxins

A

Aminoglycosides (gentamicin)
ACEi/NSAIDs/diuretic
Contrast dyes
Myoglobin (rhabdomyolysis, statins)

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26
Q

Indications for dialysis

A 
Acidosis <7.1
Electrolyte (>6 K+, elevated T wave ECG)
Ingestion
Overload
Uremic
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27
Q

cANCA

A

Wegener granulomatosis

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28
Q

pANCA

A

Not Wegeners (Microscopic polyangitis, Churg Strauss syndrome)

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29
Q

anti-GBM

A

Goodpastures

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30
Q

ANA

A

Negative excludes SLE

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31
Q

Infection risks post transplant

A

CMV
Urosepsis
Influenza
EBV negative recipient with EBV donor

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32
Q

UTI rx for non-pregnant women

A

Trimethoprim

Nitrofurantoin

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33
Q

UTI rx for pregnant women

A

Cefalexin

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34
Q

Hyperacute transplant rejection

A

Minutes to hours
Mediated by pre-existing antibodies to ABO and MHC antigens
Unresponsive to immunosuppressive treatment

35
Q

Acute transplant rejection

A

1-3 weeks post-transplant
Caused by T cells
Immunosuppressive therapy may help

36
Q

Chronic rejection

A

Months or years post-transplant
Hard to detect
Cell-mediated and Ab-mediated
Immunosuppressive therapy often fails

37
Q

Side effect of statins

A

Myalgia –> look at LFTs on r/v

38
Q

Are creatinine levels a reliable indicator of AKI?

A

No - they only increase 48hrs post injury

39
Q

What results from prolonged pre-renal AKI?

A

Acute tubular necrosis

40
Q

What 4 structures can be damaged in intra-renal AKI?

A

Tubules
Glomerulus
Vascular structures
Interstitial tissue

41
Q

Causes of ATN

A

Hypoperfusion

Nephrotoxins

42
Q

Pre-renal AKI Rx

A

Fluid resus
Blood transfusion
Stop ACE-i/NSAIDs

43
Q

Intra-renal AKI Rx

A

Dialysis
Nutrition
Avoid further nephrotoxins
Review

44
Q

Post-renal AKI Rx

A

Bladder catheter
Ureteric stents
Percutaneous nephrostomy

45
Q

RTA type I

A

Distal tubules
Can’t secrete H+
Stones

46
Q

RTA type II

A

Proximal tubules
Can’t absorb HCO3
Bone problems

47
Q

RTA type IV

A

Low aldosterone
Increased K+
Decreased Na+

48
Q

Normal anion gap

A

Base loss: diarrhoea, RTA, CA inhibitor

49
Q

Increased anion gap

A

Acid load: renal failure, toxins, DKA, shock

50
Q

RCC risk factors

A

Men 50-70yo
Smoking
Obesity

51
Q

TCC risk factors

A

Phenacetin
Smoking
Aniline dyes
Cyclophosphamide

52
Q

CKD risk factors

A 
Diabetes
Hypertension
Established CVD
Family hx of kidney failure
Obesity
Smoker
Aboriginal or Torres Strait Islander >30 years
Hx of AKI
53
Q

CKD Screen

A

Blood test - eGFR
Urine test - albumin/creatinine ratio
BP check

54
Q

Albuminuria BP goal

A

<130/80

55
Q

CKD BP goal

A

<140/90

56
Q

BP Mx in CKD

A

Lifestyle modifications

ACE-i or ARB

57
Q

Albuminuria mx in CKD

A

ACE-i or ARB

58
Q

CKD hyperparathyroidism pathway

A

CKD –> PO4 retention –> increased FGF23 –> decreased calcitriol –> decreased serum Ca, increased serum PO4 –> 2˚ hyperparathyroidism

59
Q

Polycystic KD I

A

younger presentation, faster progression

60
Q

Polycystic KD II

A

older presentation, slower progression

61
Q

PKD renal manifestations

A 
Impaired urinary concentration
Hypertension (precedes GFR decline)
Proteinuria
Cyst haemorrhage
UTI
Nephrolithiasis
62
Q

PKD extra-renal manifestations

A

Liver cysts
Intracranial aneurysms
Mitral valve prolapse
Seminal vesical cysts

63
Q

PKD Mx

A

Manage HTN and proteinuria

ACE-i

64
Q

Alport syndrome

A

X-linked basement membrane disorder arising from mutations in genes coding for type IV collagen proteins

65
Q

AD Tubulointerstitial disease

A

Suspect in teenage pt with progressive kidney disease with bland urinary sediment in the setting of strong family history

66
Q

Arthralgia / fever / weight loss with loss of kidney function?

A

SLE, ANCA-associated vasculitis

67
Q

Nosebleeds / hearing loss with loss of kidney function?

A

ANCA-associated vasculitis

68
Q

Petechial rash with loss of kidney function?

A

ANCA-associated vasculitis, IgA vasculitis (Henoch-Schönlein purpura), cryoglobulinaemia

69
Q

Haemoptysis with loss of kidney function?

A

Anti-GBM disease (Goodpastures), ANCA-associated vasculitis

70
Q 
Which GN?
Peak incidence is young men
Haemoptysis
Active urine sediment
Usually abrupt presentation
A

Anti-GBM disease (Goodpastures disease)

71
Q

Which GN?
Haematuria, proteinuria, renal impairment
Fever, malaise, anorexia, weight loss, myalgias, arthralgias
Purpura most common on legs and occurs in ‘crops

A

ANCA-associated vasculitis

72
Q

Which GN?
Peak incidence in 20-40’s
Male predominance 2:1
Most common cause of GN in Australia

A

IgA nephropathy

73
Q 
Which GN?
Nephrotic
30% adults with NS
80-90% >30yrs
may have microscopic but not
macroscopic haematuria
HTN, CKD
A

Membranous GN

74
Q 
Which GN?
35% of nephrotic syndrome in adults
more likely to have mild haematuria,
hypertension and impaired renal function
afroamericans with HIV
A

FSGS

75
Q

Which GN?
usually sudden onset
usually normal kidney function
commonest cause NS children (80%)

A

Minimal change disease

76
Q

How to control proteinuria?

A

ACE-i
Non-dihydropyridine CCBs
Reduce salt intake
Reduce protein intake

77
Q

MCD Rx

A

Steroids

78
Q

Primary FSGS Rx

A

Corticosteroids

Immunosuppressives

79
Q

Secondary FSGS Rx

A

Manage BP

ACE-is and ATRA

80
Q

Membranous nephropathy Rx

A

Immunosuppression

81
Q

IgA nephropathy Rx

A

Controversial - ACEis, corticosteroids, fish oil

82
Q

ANCA - associated disease Rx

A

Immunosuppression

83
Q

Goodpastures Rx

A

Plasma exchange
Immunosuppression
Corticosteroids and cyclophosphamide

84
Q

Alpha blockers side effects

A

postural hypotension and retrograde ejaculation

MD Y1S1 (8 decks)

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