CSIM renal medicine Flashcards

1
Q

what role do the kidneys have in metabolism?

A

excrete metabolites in urine

metabolise vit. D and some proteins

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2
Q

what is nephrotic syndrome and what are the clinical signs

A

loss of protein through the kidenys

protein urea >3.5g / day
oedem
hypoalbuminaemia
hyperlipidaemia

the 3.5 is arbitrary - it just needs to be enough to make you hypoalbuminaemic

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3
Q

what is nephritic syndrome?

A

inflammation of the kidneys leading to:

haematurea
protein urea
hypertension
oligourea

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4
Q

what will the creatinine be like in nephrotic syndrome?

A

normal

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5
Q

what will the urine look like in nephrotic syndrome?

A

frothy due to the protein

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6
Q

in suspected renal disease how should the BP be assessed?

A

lying and standing

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7
Q

causes of AKI

A

PRE: Secondary to sepsis, low BP, nephrotoxins etc
INTRINSIC: nephritis ( inflammation)
POST- obstruction

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8
Q

what are the symptoms of advanced kidney disease

A
Tiredness (anaemic) 
swollen ankles, feet or hands (due to water retention)
shortness of breath
nausea
blood in the urine
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9
Q

symptoms of acute glomerular nephritis

A
AKI ->
Oedema, hypertension
Smoky or coca- cola coloured urine
Hypertension, reduced urine volumes 
Systemic symptoms- rash,  haemoptysis 

could be asymptomatic

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10
Q

where does the creatinine in the urine come from?

A

mostly freely filtered through glomerular

some secreted in proximal tubules

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11
Q

what information is used to get eGFR?

A

creatinine
sex
ethnicity (black or other)
age

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12
Q

why dont we measure the actual GFR anymore?

A

requires 24hr urine collection

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13
Q

what kind of kidney injury does proteinurea indicate?

A

Marker of intrinsic renal disease

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14
Q

2 ways of quantifying proteinurea and whats the difference?

A

albumin : creatinine for small protein urea

protein : creatinine for large protein urea

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15
Q

what is a hyaline cast? and what is it dependent on

A

glycoprotein formed in the renal tubules

seen in small quantities in normal adults

dependent on urine flow and pH

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16
Q

what can light microscopy of a MSU tell you

A

red cell casts : diagnostic of glomerular disease
white cell casts : inflammation or infection
organisms and white cells during a urinary infection
tubular debris : in acute tubular necrosis

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17
Q

which scan will most kidney patients get?

A

USS

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18
Q

what does a chronically damaged kidney look like on USS?

A

shrunken

less well demarcated regions

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19
Q

what do the inflammatory cells in the kidney look like?

A

crescent moons

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20
Q

in monitoring urine output, when should you catheterise?

A

only if they cant collect urine themsleves

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21
Q

how small does a molecule have to be to filter through the glomerulus?

A

<30A

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22
Q

why kidney damage in trauma ?

A

large release of protein is neprotoxic

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23
Q

how many red cells is normal in the urine?

A

1-2 per micro litre

conveniently this is also the cut off for what dipstix can detect

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24
Q

causes of haematuria that aren’t related to glomerular disease?

A

renal malignancy
renal stone disease
bladder tumours

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25
Q

which protein does the kidney produce and why?

A

Tamm-Horsfall

thought to protect against infection

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26
Q

what is normal protein in urine?

A

<150mg / day

this is NOT detectable on dipstix

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27
Q

what does the amount of protein urea tell you about where the pathology is?

A

> 1 g / day = glomerular disease

<1 g / day = somewhere after the glomerular e.g. tubules, upper/ lower UTI, stones

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28
Q

benign causes of proteinurea

A

exercise

orthostatic

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29
Q

two non-renal conditions that cause protein urea?

A

fever

HF

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30
Q

effect of low albumin on lipoprotein level?

A

increases

liver is trying to make more proteins which includes cholesterol etc

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31
Q

effect of nephrotic syndrome on clotting?

A

pro-thrombotic due to loss of anti-thrombin protein

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32
Q

why at risk of infection in nephrotic syndrome?

A

loose immunoglobulins

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33
Q

why do you need to include creatinine when measuring urine protein?

A

to account for hydration status

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34
Q

5 things that effect serum creatinine?

A

production:
liver function
muscle mass
muscle metabolism

diet (if very malnurished)

RENAL DISEASE

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35
Q

the better you filter, the ____ your serum creatinine will be

A

LOWER

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36
Q

two people with the same serum creatinine, one with large muscle mass the other with small muscle mass. which has the lower GFR?

A

small muscle mass

the large guy/girl has more creatinine due to large amount of muscle

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37
Q

3 main causes of nephrotic syndrome?

A

glomerulonephritis
DM
amyloidosis

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38
Q

3 main primary disease of nephrotic syndrome

A

minimal change
membranous
focal segmental glomerulosclerosis

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39
Q

what kind of glomerulonephritis is associated with malignancy?

A

membranous

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40
Q

how to manage persistent low levels of proteinurea?

A

if all else normal monitor but no need to intervene

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41
Q

how can AKI be distinguished from CKD?

A

previous bloods
repeate creatinine 6 hrs later
USS
Hx

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42
Q

how is post-renal AKI diagnosed?

A

USS: gross dilation downstream of kidneys due to obstruction

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43
Q

main causes of post renal AKI?

A

stones

older patients:
prostate
cancer

44
Q

define azotaemia

A

appropriate response to reduced renal perfusion:

increased nitrogen

45
Q

causes of pre renal azotaemia?

A
decreased cardiac output
decreased effective circulating volume:
   hypovolaemia (reduced fluid intake etc)
   volume redistribution
   bleeding
renal vascular disease
drugs
46
Q

definition of AKI we were told to use?

A

increase in serum creatinine of >0.3mg/dl in 48hrs

47
Q

which drugs can cause pre renal azotaemia?

A

NSAIDS
ACE i
cyclosporin (immunosuppressant)

48
Q

two types of tubulo-interstital disease?

A

acute tubular necrosis

acute allergic interstitial necrosis

49
Q

what two things can cause ATN?

A

toxins e.g. aminoglycosides, radio contrast

ischaemia due to hypo perfusion

50
Q

which drugs commonly cause an acute allergic interstitial necrosis?

A
NSAIDS
bendrofluazide
frusomide
PPIs
penicillin
51
Q

what Ix distinguishes between glomerular disease and tubulo-intertial disease?

A

urinalysis

52
Q

what are the features of rapidly progressive GN?

A

haematuria
proteinurea
oedema
hypertension

53
Q

examples of RPGN

A
goodpastures syndrome
lupus
post infective
Wegeners
microscopic polyangitis
54
Q

all causes of haematurea

A
Urinary tract infection
Catheter trauma
Infarction
Stone
Tumour 
Glomerulonephritis
55
Q

finding of blood and protein in urine should prompt what?

A

microscopy and culture

56
Q

how does urine microscopy differentiate between Glomerular versus Tubulo-interstitial causes of AKI?

A

GN: red cell casts and inflammatory cresents

57
Q

what are the three types of RPGN?

A

type I - Anti-glomerular basement membrane antibody disease (Goodpastures syndrome)

type II - immune complex
lupus nephritis
post-infectious

type III - pauci immune (pauci as in latin for few)
Wegener’s granulomatosis
Microscopic polyangiitis

58
Q

what is the triad for Goodpastures syndrome?

A

anti- GBM antibodies
pulmonary haemorrhage
RPGN

59
Q

what organism is responsible for post infectious RPGN?

A

group A, ß-haemolytic streptococcus

60
Q

what does a low compliment tell you about the cause of RPGN?

A

likely to be post infectious

61
Q

diagnosis of lupus nephritis?

A

ANA
renal biopsy
immunoflourescence shows ‘full house’ immune deposits

62
Q

what type of RPGN is SLE?

A

type II - immune complex

63
Q

what type of RPGN will give systemic symptoms of night sweats, weight loss, fever, lethargy?

A

type III - pauci immune

64
Q

pANCA is associated with what type of RPGN?

A

type III - pauci immune - microscopic polyangitis

65
Q

what is Wegeners granulomatosis and what auto-antibody is associated with it?

A

RPGN

cANCA

66
Q

what auto-antibody is associated with microscopic polyangitis?

A

pANCA

67
Q

when would you NOT renal biopsy RPGN?

A

in type II - immune complex if there is sufficient clinical evidence that it is post-infectious (culture, reduced compliment and clinical picture)

68
Q

what % of hypertension is secondary?

A

10%

69
Q

causes of secondary ht?

A
CRAP
C onns
C ushings
C oarctation of the aorta
R enal
A cromegaly
P haechromocytoma
P arathyroidism (HYPER)
P ills
70
Q

renal causes of hypertension?

A

GN
renal artery stenosis
autosomal dom. polycystic KD
pyelonephritis

71
Q

what is the problem is Conns?

A

too much aldosterone (produced in the adrenals)

72
Q

what is the problem in Cushings?

A

too much cortisol

73
Q

what is the problem in phaeochromocytoma?

A

too much catecholamines

74
Q

below what age do you start thinking ht is secondary?

A

40

75
Q

what is first line imaging if suspecting Conns?

A

CT adrenals

76
Q

what is the Ix for phaeochromocytoma?

A

serum catecholamines and serum metanephrines

77
Q

where is renin made?

A

kidney- juxtaglomerular apparatus

78
Q

what does an ACE i do to the kidneys?

A

stops all the things angiotensin II would do therefore:
vasodilation
reduced aldosterone production (reduced Na retention)

79
Q

what clinical signs make you think ht is due to coarc1tation of the aorta?

A

scapular vessels
absent pulses
machinery mummer
radio-radial delay

80
Q

food that can raise BP? other than salt obvs

A

liquorice

81
Q

what sign of chronic ht is seen in the eyes?

A

papiloedema

82
Q

what effect on the heart does chronic ht have?

A

LV hypertrophy

83
Q

how does increased filtration of proteins cause CKD?

A

nephrotoxc inflammatory process

84
Q

on USS kindey, what would one normal and one small kidney suggest?

A

renal artery stenosis

85
Q

1st line drug for CKD? why?

A

ACE-i to reduce proteinuria

86
Q

If you want to increase your dietary protein for gains, what should you do?

A

Drink the piss of a patient with nephrotic syndrome

87
Q

which of the following are complications of CKD?

Uraemia
Hypokalaemia
Acidaemia
Mineral bone disorder
Dehydration
Anaemia
A
Uraemia - YES
Hypokalaemia - NO (HYPERKALAEMIA)
Acidaemia - YES
Mineral bone disorder - YES
Dehydration - NO (FLUID OVERLOAD)
Anaemia - YES
88
Q

why anaemia in CKD?

A

kidneys produce erythropoiten

89
Q

why hyperkalaemia in CKD?

A

unable to actively remove K

90
Q

effect on pH of CKD?

A

acidaemia - role in acid base regulation

91
Q

what is the clinical manifestation of high phosphate?

A

pruitis

92
Q

what is the tx for low erythropoeitin?

A

EPO and iron

93
Q

what is better transplant or dialysis?

A

transplant

cheaper
restores all function
knock on effect for the rest of the family

94
Q

what is the hall mark of interstitial nephritis?

A

white cell cast

need a biopsy to SHOW it’s that but you can infer it from the lack of another cause

95
Q

another name for Good pastures syndrome?

A

anti glomerular basement membrane disease

96
Q

what do crescent cells tell you?

A
indicate severe aggressive immune damage
guide prognosis (10% good 100% BAD)
97
Q

what first Ix in a women with recurrent UTIs?

A

US renal tract

98
Q

Mx of recurrent UTIs?

A

low does prophylactic abx

one off abx after intercourse

99
Q

4 indications for urgent dialysis?

A

uraemia
severe acidosis
high potassium
refractory pulmonary oedema

100
Q

when do you get re cell casts?

A

when there is significant haematuria i.e. when there is inflammation in the kidney…

not when there is just a bit of nephropathy

101
Q

effect of CKD on iron metabolism?

A

inefficient metabolism: iron is less readily available for haemoglobin synthesis

102
Q

calcium in CKD? why?

A

low

functional vit. D deficiency

103
Q

PTH in CKD? why

A

high due to low calcium

104
Q

what is the target BP in CKD?

A

130/80

105
Q

why give drugs to bind phosphate in CKD?

A

prevent absorption- it will be high :(