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Revision Flashcards

1
Q

what is the classical presentation of bladder cancer

A

painless frank haematuria, may be intermittent as bladder contracts and voids

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2
Q

what cancer will an ultrasound miss

A

transitional cell carcinoma of the collecting system of the ureter

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3
Q

what usually causes painful frank haematuria

A

infection or renal stone

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4
Q

what investigations for frank haematuria

A

always requires a cystoscopy and at least one mode of upper urinary tract imaging (IVU or renal ultrasound)

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5
Q

does renal and bladder cancer cause intermittent or constant haematuria

A

intermittent

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6
Q

what are the defences against getting an STI

A

Immune system, acid in periurethral tissues (post-menopausal women have a change in these pH), length of the urethra (4cm) makes it more vulnerable than men to infections, urothelium (if this is damaged more vulnerable to infection)

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7
Q

what might recurrent UTIs in childhood suggest

A

anatomical abnormality

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8
Q

who is at risk of UTIs

A

Elderly (in BPH there is a post void residue where bacteria can replicate), catheterised, diabetics, immunocompromised, abnormal urinary tract anatomy, renal calculi, stents

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9
Q

what can help prevent UTIs

A

Drinking lots, avoid perfumed products, voiding after intercourse

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10
Q

what can you give for frequent UTIs

A

prophylactic antibiotics for a few months, bladder instillations

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11
Q

why are you more susceptible to UTIs when you are pregnant

A

get mild hydronephrosis and dilation of upper urinary tract, may get gestational diabetes

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12
Q

what are the symptoms of polynephritis

A

constant ache in relation to fever

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13
Q

what antibiotic for complicated UTI in men and women

A

men- trimethoprin (dont give in renal impairment)

women- nitroflutonin

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14
Q

how do stones affect youre chance of getting an infection

A

increase likely hood of it

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15
Q

what organisms are associated with kidney stones

A

proteus organisms

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16
Q

how does incomplete voiding affect chances of UTI

A

increases them

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17
Q

what is nocturnal polyuria

A

Producing more urine that normal during the night (affects men and women) e.g. cardiac failure (diagnose with urine diary)

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18
Q

what is enuresis

A

wetting the bed

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19
Q

what are the voiding symptoms

A

hesitancy, poor flow, incomplete voiding

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20
Q

what are the storing symptoms

A

frequency and urgency

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21
Q

what does a palpable bladder suggest

A

urinary retention

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22
Q

what is PSA a marker for

A

(prostate specific antigen)
raised in prostate cancer
can be normal in prostate cancer
also raised in BPH, stones, catherterisation (+ anything that causes prostate inflammation)

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23
Q

what is the treatment for BPH

A

Alpha blockers, anti cholinergics (if they have urgency), 5- alpha reductase inhibitors, then surgery

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24
Q

what are the three types of AKI

A

pre renal
renal
post renal

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25
Q

what causes a pre renal AKI

A

hypovolaemia (haemorrhage, burn, D&V, diuresis)

oedema (CHF, cirrhosis, nephrotic syndrome)

hypotension

cardiac problems (failure, arrhythmias)

renalhypoperfusion (NSAIDS, ACEi, ARBs, AAA, renal artery stenosis/ occlusion, hepatorenal syndrome, sepsis)

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26
Q

what can cause renal AKI

A

glomerular disease (GN, thrombosis, HUS)

tubular injury (acute tubular necrosis following prolonged ischaemia, nephrotoxins- aminoglycosides (gentamicin), contrast, myoglobin, cisplatin, metals, light chains in the kidney)

acute interstitial nephritis due to drugs (NSAIDs), infection or autoimmune diseases

vascular disease (vasculitis, renal artery/vein stenosis, malignant hypertension)

eclampsia

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27
Q

what can cause a post renal AKI

A

calculus, blood clot, papillary necrosis, urethral stricture, prostatic hypertrophy/ malignancy, bladder tumour, radiation fibrosis, pelvic malignancy

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28
Q

what are the clinical markers of an AKI

A

decreased urine output (less than 0.5 mL/kg/hr for more than 6 hours)
and a rise in serum creatinine (26 micromol/L within 48 hrs/ 50% increase within 7 days)

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29
Q

what are the symptoms of an AKI

A 
urine output: abrupt anuria= acute obstruction, acute and severe GN, acute renal artery occulsion. gradual decrease= urethral stricture, bladder outlet obstruction. 
nausea, vomiting, diarrhoea
confusion 
hypertension 
dehydration 
palpable bladder 
fluid overload, oedema 
pericardial rub (pericarditis due to uraemia)
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30
Q

what investigation for post renal AKI

A

USS to see size, obstruction, hydronephrosis

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31
Q

what is the treatment for hydronephrosis

A

put in catheter to relieve pressure then nephrostomy or stent to treat obstruction

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32
Q

if you have an AKI with blood and protein in your urine what is the most likely type of AKI

A

renal

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33
Q

is furosemide nephrotoxic

A

no but can injury kidneys if given when patient already dehydrated

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34
Q

what can increase urea in a GI bleed

A

digestion of blood

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35
Q

what treatment for a peptic ulcer bleed

A

IV PPI infusion
use blecthford score to see what treatment needed
inject adrenaline to vasoconstrict during endoscopy

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36
Q

how does ibruprofen affect the kidneys

A

inhibit prostaglandins causing vasoconstriction, decreasing blood supply to kidney,= acute ischaemic necrosis

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37
Q

what is the normal potassium range

A

3.5-5.3

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38
Q

what is the treatment for hyperkalaemia

A

Give 10ml calcium gluconate 10% intravenously. This doesn’t lower
serum potassium, but protects the heart against arrhythmias.
Give 10 units Actrapid insulin with 50ml glucose 50% intravenously.
Insulin causes potassium to move into cells. Glucose must be given
with insulin to prevent hypoglycaemia, and blood glucose level
monitored.
Give 2.5mg salbutamol by nebuliser. β-agonists also cause potassium
to enter cells.

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39
Q

what ECG for hyperkalaemia

A

tall tented t waves (look sore to sit on) and broadened QRS

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40
Q

what are the indications for dialysis

A

hyperkalaemia refractory to Tx
acidosis
pulmonary oedema which is refractory to diuretics
uraemia

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41
Q

what are the possible complications of ureamia

A

uraemic pericarditis

uraemic encephalopathy

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42
Q

what vasculitis: pulmonary renal syndrome with signs of a pulmonary haemorrhage

A

good pastures

pulmonary renal syndrome= bleeding in lungs and glomerulonephritis

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43
Q

when would you give plasma exchange in vasculitis

A

if they have pulmonary haemorrhage and vasculitis

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44
Q

what is the treatment for goodpastures

A

cyclophosphamide initially then azathiprine/ MMF as maintenance

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45
Q

what makes up the myeloma screen

A

immunoglobulin levels, serum protein electropharesis, complement, bence jones protein

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46
Q

what is first line therapy for patients with hypertension and CKD

A

ACEi

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47
Q

what warning should be given with ace inhibitors

A

they are teratrogenic

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48
Q

can you give an ice inhibitor in bilateral renal artery stenosis

A

no will cause further vasoconstriction and hypoperfusion

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49
Q

what medication for urge incontinence

A

oxybutin- (antimuscarinic)

50
Q

what drug for stress incontinence

A

duloxetine if pelvic floor exercises not working

51
Q

what is the usual presentation of adult polycystic kidney disease

A

usually in middle age, sometimes in young adults

may present with features of chronic renal failure, an abdominal mass or a subarachnoid haemorrhage

52
Q

where does the haemorrhage usually occur in PKD

A

rupture of a berry aneurysm in the circle of willis

53
Q

why do you get LVH in PKD

A

systemic hypertension as a result of chronic renal failure

54
Q

where else can you get cysts in PKD

A

pancreas, liver, lung (doesnt usually affect function)

55
Q

what inheritance is PKD

A

AD- short arm of chromosome 16 (tubuloscelrosis)t

56
Q

is PKD in children AD or AR

A

AR (much more severe)

57
Q

how can glomerular disease present

A

haematuria (macro or micro)
proteinuria
acute nephritic syndrome (= oliguria, haematuria, dusky coloured urine, mild facial oedema)
nephrotic syndrome (= hypoalbuminaemia, pitting oedema, hypercholesterolaemia)
renal failure (acute/ chronic- chronic may present as hypertension)

58
Q

what is epithelial cresent formation

A

manifestation of severe glomerular damage

proliferation of the epithelial cells in bowans capsule causes compression and distortion of the glomerular tuft

59
Q

what is glomerular scelrosis

A

complete and irreversible

end stage process in severe glomerular disease

60
Q

what is the other name for acute diffuse proliferative GN

A

post infectious

61
Q

what is the difference between membranous GN and membranoproliferative

A

membranous= nephrotic, non proliferative, complement deposition in the basement membrane causing it to thicken with spikes

membranoproliferative- nephritic. nephrotic, proliferative, tram track membranes (big lobulated hypercellular glomeruli with thick memebranes)

62
Q

what is the difference between post infectious and IgA GN

A

IgA- IgA deposits on mesangium, macroscopic haematuria few days after infection (URTI)

post infectious- nephritic, several weeks after infection

63
Q

what GN is associated with cresents

A

rapidly progressing GN (caused by vasculitis)

64
Q

what is the buzzword for histological sign for diabetic nephropathy

A

kimmel stiel wilson nodule

65
Q

what are the renal manifestations of myeloma

A

glomerular- AL amyloidosis, immunoglobulin (heavy/light chain) deposition
tubular - light chain cast nephropathy

66
Q

congo red stain, apple green birefringence=

A

amyloid

67
Q

what can cause amyloid deposition

A

myeloma, RA, chronic inflammatory conditions

68
Q

is a seminoma radio or chemo sensitive

A

radio sensitive

69
Q

what is PLAP

A

placental alk phos- tumour marker for seminoma

70
Q

is AFP used as a seminoma tumour marker

A

no produced by yolk sac non seminoma

71
Q

what is different about mets of prostatic carcinoma

A

they are sclerotic lesions (most mets to bone are lytic)

72
Q

what is malignant hypertension

A

a hypertensive emergency where a recent increase in BP causes organ damage (encephalopathy, cardiovascular or renal)
in malignant hypertension there is papiloedema

73
Q

what causes a hypertensive emergency (accelerated/ malignant hypertension)

A 
renal artery stenosis 
renin secreting tumour
kidney trauma
renal vasculitis 
phaeochromocytoma 
cocaine 
pre eclampsia
hyper/hypo thyroidism
74
Q

what is the presentation of a hypertensive emergency (accelerated/ malignant)

A 
headache 
fits 
n&v
chest pain 
visual disturbance 
cardiac failure 
haematuria 
papilloedema and retinal haemorrhages
75
Q

what are causes of secondary hypertension

A

Renal artery stenosis (can cause flash pulmonary oedema), Diabetic nephropathy, glomerular disease, PKD, renovascular disease. Any thing that causes kidney damage can cause hypertension

76
Q

what is pevicalyceal dilation

A

hydonephrosis

77
Q

what are the complications of renal calculi

A

Loin to groin pain, haematuria, dysuria, UTI, urinary obstruction, AKI

78
Q

how do you quantify proteinuria

A

protein: creatinine ratio / measure protein in a 24 hr urine collection

79
Q

what are the features of nephrotic syndrome

A

proteinuria, hypo-albuminaemia, oedema, hyperlipidaemia

80
Q

what usually presents with nephrotic syndrome, normal renal function and BP

A

minimal change GN, membranous GN

81
Q

what is primary GN

A

GN with no underlying disorder

82
Q

what drugs can cause GN

A

gold, penicillamine

83
Q

what tests need to be done before a biopsy is done

A

blood count and coagulation screen

renal USS to check that two kidneys are present and the size and position of the kidneys

84
Q

what are the contraindications to a renal biopsy

A

clotting abnormalities
small kidneys (increased risk of bleeding, scarred biopsy is uninformative)
uncontrolled hypertension (bleed)
untreated urine infection (2nd haemorrhage 10 days after biopsy)
presence of a single kidney (not absolute contraindication)

85
Q

what treatment for minimal change GN

A

prednisolone strarting at 40-60 mg daily

PPI to protect against peptic ulceration

86
Q

what is the prognosis of minimal change nephropathy

A

good
renal function shouldn’t deteriorate
responds well to steroids
if relapse then may need further steroids/ immunosuppressive drugs

87
Q

why do you get low potassium in nephrotic syndrome

A

losing protein in urine
water follows protein
aldosterone and ADH stimulated to retain water
cause hypernatraemia and hypokalaemia

88
Q

how can you confirm IgA nephropathy diagnosis

A

renal biopsy

89
Q

what is seen in urinalysis in IgA GN

A

haematuria and proteinuria

90
Q

what 2 things do ACE inhibitors help with

A

reducing hypertension

reduce proteinuria

91
Q

what is the prognosis of IgA GN

A

Many patients with IgA nephropathy maintain good renal function indefinitely, but in about 25%, renal function progressively declines, and eventually dialysis or transplantation is required.
v important to control BP and proteinuria (via ACi)

92
Q

what are poor IgA prognostic markers

A

heavy proteinuria

sclerosis and interstitial scarring

93
Q

where is the most likely source of isolated haematuria (no proteinuria) in young and old patients

A 
young= kidneys 
old= bladder
94
Q

what happens when there is prolonges renal hypoperfusion

A

acute tubular necrosis

95
Q

why does rhabdomyolysis and haemolysis cause acute renal fialure

A

(large destruction of skeletal muscle)

haemoglobin and some products of muscle breakdown are toxic to renal tubules

96
Q

what are the complications of ARF

A

hyperkalaemia, metabolic acidosis, fluid overload

97
Q

what will most kidneys in CKD be like of USS

A

small

98
Q

what are the stages of CKD

A 
1- normal/ increased GFR (>90) with evidence of kidney damage 
2- 60-90 with kidney damage 
3- 30-60
4- 15-30
5- GFR< 15/ on renal replacement therapy
99
Q

what is evidence of kidney damage

A

proteinuria, abnormalities on scanning

100
Q

what risk increases as GFR decreases

A

cardiovascular risk

101
Q

when do you start to get symptoms of reduced GFR

A

when under 20

102
Q

what groups are more likely to get CKD

A

diabetes, hypertension, heart failure

103
Q

how do you screen high risk patients for CKD

A

urinalysis; proteinuria increases the risk of progression of CKD;
haematuria may indicate renal disease or a lesion of the lower urinary tract.
If proteinuria is present, quantify by sending a urine sample for
measurement of protein:creatinine ratio (PCR). A ratio of 100mg/mmol is
approximately equivalent to 1G per day protein excretion.
Decide whether referral to Renal Clinic is necessary
treat CV risk factors

104
Q

what are the indications for referral to renal unit

A 
nephrotic syndrome 
Stage 3 CKD with urine PCR >100mg/mmol
Stage 3 CKD with progression (GFR falling by >20% over 6
months)
Stage 3 CKD in younger people (age <60)
Stage 4 CKD
Haematuria (after exclusion of ‘urological’ causes in older
patients)
105
Q

what can you hear over femoral arteries in peripheral vascular disease

A

bruits

106
Q

in someone with peripheral artery disease and reduced kidney function what should you worry about

A

renal artery stenosis

107
Q

what will USS show in renal artery stenosis

A

small irregular kidneys (damaged by the ischaemia)

108
Q

should you do CT/MR angiogram in renal stenosis

A

no as can tubuar toxicity of scan can cause intra arterial contrast induced nephropathy

109
Q

what treatment for hypertension retinopathy with suspected renal artery stenosis

A

CCB and alpha blocker (doxazozin)

dont use ACEi in renal artery stenosis as cause cause AKI in renovascular disease

110
Q

do you give ACEi/ ARB in renovascular disease

A

no will cause AKI

111
Q

when is the peak incidence for contrast induced nephropathy

A

48-72 hrs after the procedure

112
Q

how can the risks contrast induce nephropathy be reduced

A

give fluids before and after procedure

113
Q

what is the treatment for hyperkalaemia

A

IV calcium gluconate 10 mls 10% over 2-3 mins, 10 units of insulin dextrose 50% in 50 mls, nebulised salbutamol

114
Q

what causes kidney damage in diabetes

A

retention of fluid due to high glucose cause increase in circulating volume= increase in kidney perfusion
= a hyperfiltration injury - high flow through the kidneys injures the glomerulus
(a microvascular complication)

115
Q

when might a renal biopsy be indicated

A

when there is blood in urine, abnormal antibody tests

116
Q

how do you evaluate anaemia

A

iron, folate, B12, blood film for erythropoietin levels, measure thyroid levels, FBC

117
Q

what is the treatment for anaemia in CKD

A

erythroietin injections, iron supplements

118
Q

what can happen to phosphate and PTH in CKD

A

get high phosphate as not clearing it effectively which causes a rise in PTH

119
Q

how do you treat high phosphate and PTH in CKD

A

reduce phosphate will a low phosphate diet or phosphate binders
if phosphate lowered nut PTH still high can give activated for of vit D = alfocalcidol

120
Q

what can you give if bicarb low

A

sodium bicarbonate

Renal (27 decks)

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