Renal 2 Flashcards

1
Q

damage to the podocytes

A

non prolif

proteinuria

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2
Q

damage to the endothelial cells or meningeal cells

A

prolif

haematuria

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3
Q

franc haematuria 1-2 days after URTI

A

Ig A neph

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4
Q

nephrotic syndrome occurring 1-3w after a strep infection

A

post infective GN

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5
Q

haemoptysis with rapidly porgressing GN

A

good pastures

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6
Q

obesity linked to which nephropathy

A

FS

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7
Q

nephrotic syndrome

A

proteinuria, hypoalbuminuria, oedema, increased cholesterol

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8
Q

nephritic syndrome

A

AKI, oliguria, hypertenion, urine has RBCs and RBC and casts

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9
Q
minimal change neuropathy commones cause for what 
ix
cx
causes
treatment
A

commonest cause ofr nephrotic syndrome in children
children with atopy. follows URTI

EM - podocyte foot fusion

doesn’t cause progressive RF

idiopathic, IL-13, NSAIDs

steroids. relapse cyclophosphamde

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10
Q
focal segmental commonest cause of what 
causes
ix
cx
rx
A

nephrotic syndrome in adults

idiopathic. HIV

50% go onto end stage renal failure over 10y

steroids, relapse - cyclophosphamide

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11
Q
membranous nephropathy commonest cause for what
causes
ix
rf
rx
A

second commonest cause of nephrotic syndrome in adults (esp elderly)

thickened BM on silver stain

30% progress tp ESRF in 10y

steroids/alkylating agents/B monoclonal ABs

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12
Q
IgA nephropathy commonest wha 
symp
causes
ix
cx
rx
A

commonest GN in the world

young men frank haematuria 1-2 days after URTI

idiopathic. HSP

meningeal cells prolif. IGA deposits in mesangium

25% progress to ESRF in 10-30y

BP control ACEI/ARBs

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13
Q

Rapidly progressing GN causes

A

crescents on biopsy

ANCA pos - wegners, microscopic polyangitis
ANCA neg - SLE, HSP, good pastures

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14
Q

TBW male and female

A

male 60% of body weight

females 50%

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15
Q

TBW = what

A

ICF (67%) and ECF (33%)

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16
Q

ECF

A

20% plasma
80% interstitial fluid
lymph and transcellular fluid

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17
Q

ADH and vasopressin type 2 receptor causes what

A

ATP -> cAMP
which increases H2O permeability
which leads to a concentrated urine output

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18
Q

aldosterone

A

sodium reabsorption and potassium secretion

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19
Q

ANP is stored in what
how is it released
what does it lead to

A

atrial cells
cells stretching due to increased plasma volume causes it to be released

leads to increased BP
leads to increased excretion of sodium and diuresis leading to a decrease in plasma volume

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20
Q

renal transplantation HLAs

A

HLA A
HLA B
HLA DR

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21
Q

rejections hyper acute
acute
chronic

A

hyper acute - within mins
acute <6m - B/T cell mediated. treat with immunosuppression
chronic >6m - immunological and vascular - deterioration of transplant

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22
Q

anti rejection therapy cyclosporin and tacrolimus

A

renal dysfunction
tremor
hypertension
DM

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23
Q

anti rejection therapy azathioprine and myelophenate

A

leucopenia, anaemia, GI S/E

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24
Q

anti rejection therapy steroids

A

osteoporosis, weight gain, infection, DM

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25
ADPKD chromosomes signs and symp cx
type 1 chromosome 16 - develop ESRF faster type 2 - chromosome 4 hypertension. big kidneys with cysts intracranial aneurysms
26
ARPKD chromosome | who
6 | young children
27
Alports genetics | symp/signs
X linked recessive sensineural hearing loss - bilateral proteinuria, haematuria
28
anderson fabric disease is what genetics ix rx
inborn error of glycosphingolipid metabolism. lysosomal storage disease plasma/leucoyte alpha GAL activity on renal/skin biopsy fabryz - enzyme replacement
29
medullary CK what happens age
medulla and cortex shrink | age 28
30
medullary cystic kidneys
looks like a sponge
31
myeloma ix | rx
roulex BJP lytic lesions hypercalcaemia, avoid contrast agents, plasma exchange to remove light chains, chemo, dialysis
32
GPA
saddle nose rhinorrhea sinusitis otitis media
33
EGPA (charge strauss)
eosinophilia | asthma - late onset
34
microscopic polyangitis
segmental necrotising GN with crescents
35
DM is the leading cause of what ix symp
chronic renal failure kimmelsteil Wilson lesions NO HEAMTURIA
36
fibromuscular dysplasia
renal htn | familial 10% (both kidneys)
37
atherosclerotic renovascular disease
Aki after treatment of htn (usually using a ARB/ACEI) | flash pulmonary oedema
38
organisms of UTI commonest other gram neg other
E coli klebsiella, enterobacter, proteus SA
39
proteus and UTIs
associated with stones foul smelling produces urease which with urea becomes ammonia which decreases the pH leading to stones
40
organisms of UTI and enterococcus
feaclis | feacum - harder to treat
41
staphylococcus sap sophoycis UTI organism
coag neg staph | women of child bearing age
42
pseudomonas aeruginosa
gram neg bacilli catheter/instrument only ciprofloxacin works
43
treatment of UTI in female lower uncx male uncathterised cx UTI/poly in GP cx UTI/Poly in hopistal
trim or netro PO (3d) T or N (7d) co amoxiclav or co tramoxazole for 14d amox (co tram) and gent IV for 3d
44
BPH cause | treatment
hormonal imablance between androgen and oestrogen | alpha blockers. 5 alpha reducatse
45
prostate cancer
multifocal adeno | 70% in peripheral zone
46
what increases PSA
``` cancer BPH prostitis UTI retention catheter ```
47
testicular tumours symp
painless testicular enlargement | gynamacamastia
48
seminoma
rare before puberty | potato
49
teratoma
can be in childhood | trophoblastic
50
AFP HCG LDH PLAP
yolk sac components, never increased in seminoma trophoblastic composants tumour burden seminoma
51
nephroblastic (WILMS tumour)
children malignant abd mass arises from residual primitive renal tissue
52
renal carcinoma where what kind what can it secrete
``` porximal tubules clear cell or papillary erythropoietin - polycythaemia rennin - htn PTH - hypercalcaemia ```
53
von hippel lindau
ADom | tumours in kidneys, eyes, CNS, gonads, adrenal and pancreas
54
TCC/uroepithelial | types
90% transition 9% squamous transition - most papillary (striped) non papillary - all malig
55
TCC who gets it | where
bilateral and multi centric rubber, dye, smoker, analgesia 75% occur in the trigone area - obstruction
56
dialysis HD complications
fluid overloads, blood leaks, loss of vascular access hypokalaemia and cardiac arrest intradialytic hypotension need arteriovenous fistula
57
peritoneal dialysis
continous 4 bags a day | automated - 1 bag in all day - overnight machine
58
PD cx
infections either contaminates - staph, strep, diphtheroids or from gut - EColi, klebsiella intraperitoneal ABs, bag removed membrane failure - fluid overload - switch to HD hernias due to increased pressure - treat hernia and small volumes
59
chronic kidney disease stages
``` >90 and kidney disease 60-90 and KD 3A 45-60 3B 30-54 15-30 <15 or on RRT ```
60
what causes faster progression in CKD
more proteinuria
61
causes of CKD
DM htn vascular
62
stop CKD progressing
decrease proteinuria and BP: ACEI/ARBs, stop smoking , control BG decrease CVD risks - statins, BP, stop smoking
63
complications of CKD
anaemia due to decreased erythropoietin - IV iron, then EPO by injection target Hb 10.5-12.5 secondary hyperparathyroid.
64
AKI is what
abrupt (48h) reduction in kidney function
65
pre renal causes | treatment
hypovalaemic shock - haemorrhage, volume depletion hypotension - shock renal hypo perfusion - NSAIDs, ACEI/ARB fluid rechallange 0.9 NaCL in hypovalaemic shock
66
renal AKI causes | treatment
vasculitis. contrast. TB. sarcoid. gentamicin. contrast ABs if septic. stop nephrotoxins. dialysis if remains anuric and anaemic
67
post renal AKI
stones, cancer, strictures, extrinsic pressure relieve obstruction - catheter
68
complications of AKI
severe acidosis <7.15 uraemia pericardial effusion/rub urea >40 fluid overload hyperkalaemia
69
hyperkalaemia level | treatment
>5.5. bad >6.5 life threatening 10% 10ml over 10 mins calcium gluconate prevent arryhtmias in myocardium Actrapid 10 units with 50mls 50% dextrose (30mins) nebulaised salbutamol over 90 mins both push K back into cells calcium resonium in none acute
70
urgent indications for HD
acidosis <7.15 hyperkalaemia >7 or >6.5 and not responding to medical therapy fluid overload urea >40, uraemia pericardial rub/effusion