renal Flashcards

1
Q

Which medications should be stopped in AKI as they may worsen renal function

A

NSAIDs
Aminoglycosides
ACEi
ARB
Diuretics

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2
Q

what is the key diagnostic sign of rhabdomyolysis

A

elevated CK levels

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3
Q

what are the features of rhabdomyolysis ?

A

AKI
Raised CK
myoglobinuria : reddish / dark brown urine
elevated phosphate
metabolic acidosis
hypocalcaemia
hyperkalaemia

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4
Q

what is the management of rhabdomyolysis

A

IV fluids

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5
Q

what causes rhabdomyolysis

A

seizure
collapse/com
crush injury
ecstasy
statins ( esp. with clarithromycin)

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6
Q

how to distinguish between IgA nephropathy and post streptococcal glomerulonephritis ?

A

IgA nephropathy : macroscopic haematuria within a day or two of developing an URTI in young males
Post streptococcal glomerulonephritis : onset of nephritis is generally 1-3 weeks after initial infection - also presents with proteinuria

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7
Q

how do you screen a patient for diabetic nephropathy ?

A

albumin : creatine ratio in early morning specimen

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8
Q

what is the screening test for adult polycystic kidney disease

A

renal ultrasound scan

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9
Q

what features are seen in Alport’s syndrome

A

Microscopic haematuria
Renal failure
bilateral sensorineural deafness
ocular abnormalities

All ports affected

eyes
ears
urine

or
cant see
cant pee
cant hear a buzzing bee

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10
Q

what cancer are patients who have had an organ transplantation most at risk of ?

A

skin cancer = squamous cell carcinoma

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11
Q

most common cause of glomerulonephritis

A

IgA nephropathy

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12
Q

how do you distinguish between HSP and ITP

A

polyarthralgia : presents in HSP
absent in ITP

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13
Q

what is the common pattern of presentation of HSP ?

A

It usually present in children following an infection.

Features : IgA mediated

palpable purpuric rash with oedema on buttocks and extensor surfaces of arms and legs
abdominal pain
polyarthritis
( haematuria, renal failure)

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14
Q

what type of hyperparathyroidism does CKD cause ? how does it present ?

A

secondary hyperparathyroidism
low calcium
high phosphate
low vitamin D

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15
Q

Most common cause of AKI

A

Acute tubular necrosis

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16
Q

what is acute interstitial nephritis ? what are its triggers ? how does it present ?

A

Acute inflammation of renal tubulo-interstitium, usually due to medications.

Triggered by :
PRIDE
Penicillin
Ramipril
Ibuprofen and other NSAID’s
Diuretics
Extras : SLE, Sarcoidosis, Sjogren’s

Presentation

fever, rash, arthralgia
eosinophilia
mild renal impairment

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17
Q

how does IgA nephropathy present on biopsy ?

A

Mesangial hyper cellularity
Positive immunofluorescence for IgA and C3

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18
Q

What are the features of Goodpasture’s disease?

A

-pulmonary haemorrhage
-rapidly progressive glomerulonephritis leading to rapid onset SKI
nephritis –> proteinuria + haematuria

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19
Q

what type of deposits are seen in Goodpasture’s syndrome

A

IgG deposits

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20
Q

how would you distinguish IgA nephropathy and Minimal change disease ?

A

Minimal change disease : most common cause of nephrotic syndrome presenting with proteinuria and NO HAEMATURIA
whereas IgA nephropathy presents with HAEMATURIA

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21
Q

raised ureA : creatinine ratio represents what cause for AKI

A

prerenal such as dehydration

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22
Q

what causes anaemia in CKD patients

A

reduced erythropoietin levels

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23
Q

how do you manage anaemia in CKD

A

ferrous sulphate
erythropoiesis stimulating agents

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24
Q

____________are the preferred method of access for haemodialysis

A

Arteriovenous fistulas

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25
Q

what conditions caused a raised anion gap ?

A

lactate : shock, sepsis, hypoxia
Ketones : DKA, alcohol

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26
Q

what is the screening test for ADPKD ?

A

abdominal ultrasound

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27
Q

what medication can be used to slow down the progression of cyst development in ADPKD?

A

Tolvaptan

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28
Q

In the management of hyperkalaemia give drugs used for the following :

  1. stabilisation of cardiac membrane
    2.short term shift in potassium from extracellular to intracellular
  2. removal of potassium from the body
A
  1. Calcium gluconate
  2. insulin / dextrose, nebulised salbutamol
  3. calcium resonium
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29
Q

how should HSP be monitored ?

A

Blood pressure and urine analysis

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30
Q

what is the management of minimal change disease ?

A

oral corticosteroids
cyclophosphamide

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31
Q

what conditions constitute nephrotic syndrome ?

A

Minimal change disease
Membranous GN
Focal segmental glomerulosclerosis
Amyloidosis
diabetic nephropathy

proteinuria, oedema

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32
Q

what conditions constitute nephritic syndrome?

A

rapidly progressive GN
IgA nephropathy
Alport syndrome
GOODPASTURES
haematuria , hypertension

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33
Q

what is the clinical triad of nephrotic syndrome?

A

Proteinuria ( > 3 g / 24h)
Hypoalbuminaemia
Oedema

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34
Q

name 3 main complications of nephrotic syndrome

A

HIT

Hyperlipidaemia ( DVT, PE, renal vein thrombosis)
Infection
Thromboembolism

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35
Q

what is the cellular pathology behind rhabdomyolysis ?

A

Tubular cell necrosis

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36
Q

what is the best way to distinguish between AKI and CKD?

A

Bilateral small kidneys

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37
Q

what medications are used in the management of CKD and when are they introduced ?

A

ACEi = used in the management of proteinuria in CKD and are introduced if the albumin creatinine ratio is > 30 mg / mmol

SGLT2 inhibitors = proteinuric CKD

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38
Q

what are the complications of CKD ?

A

Anaemia : reduced erythropoietin levels
Renal bone disease : secondary hyperparathyroidism
CVD
Peripheral neuropathy

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39
Q

triad of symptoms seen in HUS

A

thrombocytopenia
AKI
haemolytic anaemia

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40
Q

what causes HUS

A

shiga toxin producing E.Coli

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41
Q

according to guidelines how do you describe an AKI

A

rise in serum creatinine of 26 mmol/l or greater within 48 h
50% / greater rise in serum creatinine within past 7 days
fall in urine output to less than 0.5 ml/kg/h for > 6h in adults

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42
Q

Nephrotic syndrome is associated with a hypercoagulable state due to loss of _______________________ via the kidneys

A

Antithrombin III

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43
Q

what is the management of nephrogenic diabetes insipidus

A

Thiazides
low salt / protein

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44
Q

what are the most common extra renal manifestations of ADPKD

A

liver cysts

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45
Q

what are the indications for acute dialysis ?

A

AEIOU

Acidosis
Electrolytes
Intoxication ( overdose)
Oedema
Uraemia symptoms- nausea, seizure, pericarditis, encephalopathy, high uric acid

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46
Q

what stage requires long term DIALYSIS

A

end stage kidney disease ( CKD-5)

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47
Q

what is the catheter in peritoneal dialysis known as

A

Tennckhoff

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48
Q

what are the options available for haemodialysis

A

tunnelled cuffed catheter
AV fistula

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49
Q

what are the types of AV fistula available??

A

Radiocephalic
brachiocephalic
brachiobasilic

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50
Q

what are the complications of haemodialysis

A

aneurysm
infection
thrombosis
stenosis
high output hf

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51
Q

which cancers are caused by immunosuppression

A

skin - SCC
Non Hodgkin’s lymphoma

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52
Q

which condition is associated with IgA deposits

A

IgA nephropathy

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53
Q

which condition is associated with IgG and complement deposits on the basement membrane

A

membranous glomerulonephritis

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54
Q

what condition is associated with tonsillitis

A

post-streptococcal glomeronephritis

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55
Q

which condition is associated with pulmonary haemorrhage

A

goodpasture;s

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56
Q

what is the management of minimal change disease ?

A

first line : oral corticosteroids
steroid resistant : cyclophosphamide

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57
Q

what does minimal change disease show on renal biopsy?

A

normal glomeruli on light microscopy
electron microscopy = fusion of podocytes and effacement of foot processes

58
Q

what is the prognosis of minimal change disease

A

1/3rd - 1 episode
1/3rd - infrequent relapses
1/3rd - frequent relapses before adulthood

59
Q

what are the non idiopathic causes of minimal change disease?

A

drugs - NSAID’s rifampicin
Hodgkin’s lymphoma, thymoma
Infectious Mononucleosis

60
Q

when is a renal biopsy indicated in minimal change disease

A

poor response to steroids

61
Q

what is the time period after which a PSA level can be done in the following activities

1) ejaculation or vigorous activity
2) DRE
3) UTI
4)prostate biopsy

A

1) 48h
2) 1 week
3) 4 weeks
4) 6 weeks

62
Q

what is the initial management of renal colic ?

A

NSAIDs such as parenteral diclofenac
IV paracetamol if NSAID’s are c/i

alpha blockers may be considered if the stones are < 10 mm in size

63
Q

what imaging is performed to diagnose renal colic ?

A

non contrast CT-KUB - within 24h of admission
ultrasound for pregnant women and children

64
Q

what is the management of renal colic ?

A

if stones are < 5 mm and asymptomatic
watchful waiting

5-10 mm - shockwave lithotripsy
10-20 mm- shockwave lithotripsy / ureteroscopy
> 20 mm Percutaneous nephrolithotomy

65
Q

what is the management of uretic stones

A

shockwave lithioscopy +/- alpha blockers >

66
Q

what is the management of renal stones with signs of infection

A

Urgent renal decompression and IV Antibiotics ( nephrostomy)

67
Q

when do you need to need to classify CKD stage 1/ 2?

A

sign of kidney damage

68
Q

when is renal replacement therapy recommended in the management of an AKI?

A

when a patient is not responding to medical treatment of complications - hyperkalaemia, pulmonary oedema, acidosis, uraemia

69
Q

what are the various types of incontinence ?

A

overactive bladder/ urge incontinence : detrusor overactivity
stress : leaking when coughing or laughing
mixed : both stress and urge
overflow : due to bladder outlet obstruction
functional

70
Q

what initial investigations are performed in suspected urinary incontinence?

A

bladder diaries - 3 days
vaginal exam
urine dip and culture
urodynamic studies

71
Q

what is the stepwise management of urge incontinence

A

bladder retraining - 6 weeks
bladder stabilizing drugs - antimuscarinics ( oxybutynin, unless frail in which case use mirabegron)

72
Q

what is the stepwise management of stress incontinence ?

A

pelvic floor muscle training
duloxetine
retropubic mid urethral tape procedures

73
Q

why does gynaecomastia occur with testicular tumours

A

increased oestrogen : androgen ratio

74
Q

which drugs should be stopped in AKI

A

DIANA

Diuretics
Iodinated contrast
ACEi/ ARB
NSAIDs
Aminoglycosides

75
Q

which medications may have to stopped during an AKI

A

metformin
lithium
digoxin

76
Q

what is the risk of using large volumes for fluid therapy

A

hyperchloraemic metabolic acidosis

77
Q

what medications are used in the management of CKD related bone disease ? what side effects can it present with

A

reduced dietary intake of phosphate
phosphate binders ( calcium based binders such as calcium acetate)
side effects are hypercalcaemia and vascular calcification

78
Q

what class of medication is finasteride ? how long does one need to take it before results are seen?

A

5 alpha reductase inhibitor
6 months

79
Q

how is anaemia due to CKD investigated and managed

A

iron studies before ESA
oral iron - if patient not on haemodialysis
switch to IV iron if target Hb not met

80
Q

when are 5 alpha reductase inhibitors recommended in the management of BPH

A

significantly enlarged prostate and considered to be at high risk of progression

81
Q

what are the side effects of 5 alpha reductase inhibitors

A

erectile dysfunction
reduced libido
ejaculation problems
gynaecomastia

82
Q

when is a combination of Tamsulosin and finasteride recommended

A

if a man has bothersome moderate to severe voiding symptoms and prostatic enlargement

83
Q

what is a sign of acute interstitial nephritis on microscopic examination of the urine ?

A

eosinophilic casts

84
Q

when should ACEi be used in CKD

A

co-existent HTN and CKD if the ACR is > 30 mg/mmol
ACR > 70 mg/ mmol regardless of BP

85
Q

which actions reduce renal stones

A

fluid
lemon juice
limit salt
thiazide diuretics
potassium citrate

86
Q

what medications reduce oxalate stones

A

cholestyramine
pyridoxine

87
Q

which medications reduce uric acid stones

A

allopurinol
urinary alkalisation

88
Q

what condition does a bladder still palpable after urination point to

A

retention with urinary overflow

89
Q

what is the stepwise management of CKD mineral bone disease

A

reduced dietary intake of phosphate
phosphate binders
vit d
parathyroidectomy

90
Q

what type of an AKI is a disproportionately high urea associated with

A

prerenal like dehydration

91
Q

what is the key investigation in diagnosing early CKD

A

Albumin: creatinine ratio

92
Q

how is an ACR collected

A

1st pass morning urine

3-70 - repeat
>70 - no repeat

93
Q

what is the mechanism of action of tamsulosin

A

alpha 1 antagonist

94
Q

what is TURP syndrome and how does it present ?

A

rare and life-threatening complication of trans-urethral resection of prostate

caused due to irrigation with large volumes of glycine which is hypo-osmolar.

this causes hyponatraemia, CNS, resp and systemic symptoms

95
Q

which bacteria is the most common cause of epididymis-orchitis

A

chlamydia trachomatis - sexual history
E.Coli- no sexual history

96
Q

how does epididimorchitis present and what is an important differential?

A

unilateral testicular pain and swelling
urethral discharge

important differential is testicular torsion

97
Q

which organism is likely to cause staghorn calculi

A

Proteus mirabilis

98
Q

what medications are used to treat hyperphosphatemia ? give an example

A
  • non calcium based phosphate binder like sevelamer
99
Q

what is the most common type of kidney stone

A

calcium oxalate

100
Q

what is the cause of a staghorn calculus

A

struvite

101
Q

what lifestyle factors can inapropriately decrease e gffr

A

pregnancy
muscle mass
red meat 12h prior

102
Q

what are the two main causes of acute tubular necrosis

A

ischaemia : shock and sepsis
nephrotoxins : aminoglycosides, myoglobin, lead, radiocontrast agents

103
Q

what is the management of hydronephrosis ?

A

immediate renal decompression via a nephrostomy tube to reduce the risk of permanent renal damage.

104
Q

how would you distinguish between acute interstitial nephritis and acute tubular necrosis

A

acute interstitial nephritis : higher white cell count

105
Q

what acid-base abnormality is renal tubular acidosis associated with ?

A

Hyperchloremic metabolic acidosis ( normal anion gap)

106
Q

Type 1 RTA

A

no H+ secretion in urine
hypokalaemia
autoimmune stuff causes it

107
Q

type 2 RTA

A

decreased bicarb reabsorption
hypokalaemia

108
Q

type 4 RTA

A

reduction in aldosterone secretion
hyperkalaemia

109
Q

most common cause of peritonitis secondary to peritoneal dialysis

A

staph. epidermis

110
Q

which valvular disorder is ADPKD associated with

A

mitral prolapse

111
Q

which drug can cause hyaline casts in urine

A

furosemide

112
Q

When prescribing fluids, the potassium requirement per day is

A

1 mmol/kg/day

113
Q

which test can be used to test post-streptococcal glomerulonephritis

A

Anti-streptolysin O titre

114
Q

how to distinguish primary and secondary aldosteronism

A

high renin = secondary causes like renal artery stenosis
low renin =primary

115
Q

most common cause of death in patients on haemodialysis

A

IHD

116
Q

management of acute clot retention causing aki

A

irrigation of bladder followed by flexible cystoscopy

117
Q

most patients with CKD have bilateral small kidneys. Exceptions to this rule include:

A

autosomal dominant polycystic kidney disease
diabetic nephropathy (early stages)
amyloidosis
HIV-associated nephropathy

118
Q

which nephritis is most common with malignancy

A

membranous nephropathy

119
Q

Gold standard for bladder cancer diagnosis is

A

cystoscopy

120
Q

first line treatment for a patient not on haemodialysis requiring iron replacement

A

oral ferrous gluconate

121
Q

side effects of erythropoietin

A

HTN
Bone ache
flu
rash and urticaria
red cell aplasia - risk reduced with darbepoetin

122
Q

hyper acute rejection of renal transplant

A

minutes –> hours
due to pre-existing antibodies against ABO/HLA
type II hypersensitivity
no treatment, remove graft

123
Q

acute graft failure

A

due to mismatched HLA
asymptomatic, decreasing kidney function
CMV
manage with steroids and immunosuppressants

124
Q

chronic graft failure

A

antibody and cell mediated
fibrosis

125
Q

action of calcium resonium

A

removal of potassium from the body

126
Q

management of diabetic nephropathy

A

start ACEi or ARB if urinary 3 mg/mmol or more
statins
dietary protein restriction
tight glycaemic control

127
Q

what is the preferred method for access for haemodialysis ? How long do they take to be functional

A

AV fistulas
6 to 8 weeks

128
Q

fibromuscular dysplasia

A

can lead to renal artery stenosis in young females
HTN
CKD
flash pulmonary oedema

129
Q

when to refer CKD to nephrologist

A

ACR > 70
urinary ACR of 30 mg/ mmol or more with persistent haematuria and no UTI
ACR < 30 but declining

130
Q

renal cell carcinoma

A

haematuria, loin pain and abdominal mass
left varicocele

131
Q

Causes of transient or spurious non-visible haematuria

A

urinary tract infection
menstruation
vigorous exercise (this normally settles after around 3 days)
sexual intercourse

132
Q

what happens to the sodium in prerenal and renal AKI

A

Pre-renal : urine osmolality high, urine sodium low
Renal : urine osmolality low, urine sodium high

133
Q

There are several types of renal replacement therapy available to patients:

A

haemodialysis
peritoneal dialysis
renal transplant

134
Q

haemodialysis

A

most common form of renal replacement therapy through dialysis machine in hospital
patients need AV fistula

135
Q

peritoneal dialysis

A

filtration within the abdomen
CAPD
APD

136
Q

side effects of haemodialysis

A

site infection, endocarditis, stenosis, hypotension, diseequilibration syndrome

137
Q

rare but serious complication of haemodialysis

A

dialysis disequilibrium syndrome

138
Q

which conditions are associated with cystine stones

A

inherited metabolic disorder

139
Q

radiolucent stones

A

uric acid

140
Q
A