Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y3 Clinical Case Revision > Renal Medicine > Flashcards

Renal Medicine Flashcards

1
Q

AKI pre renal causes

A

hypovolaemia
decreased effective circulating volume
decreased CO
impaired renal auto-regulation - NSAIDS, cyclosporine, ACEis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

AKI intrinsic causes

A

glomerular: acute glomerular nephritis
vascular: vasculitis, malignant hypertension
tubular: sepsis, ischemia, nephrotoxins (aminoglycosides, cisplatin, contrast, rhabdomyolysis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

AKI post renal causes

A

bladder outlet obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

if + blood and protein on urine dip, what tests next?

A 
c-ANCA (PR3)
p-ANCA (MPO)
? vasculitis, anti-GBM
ANA C3 / C4
? SLE
serum immunoglobulins
electrophoresis
? myeloma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Test for ? post-streptococcal GN

A

anti-streptolysin O titres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

indications for renal replacement therapy

A

refractory to medical management - hyperkalaemia, metabolic acidosis, anuria (diuretics > fluid overload)
uraemic pericardiditis
uraemic encephalopathy
intoxications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

S/Sx of uraemic encephalopathy

A

vomiting
confusion
drowsiness
altered consciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

nephrotic syndrome features

A

oedema
albumin < 30
urine PCR > 350
- hypercholesterolaemia

(foamy urine, weight gain / fluid retention, fatigue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

nephrotic syndrome causes

A 
Minimal change 
FSGN
Amyloidosis / DM / myeloma 
membranous nephropathy 
membranoproliferative GN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

nephrotic syndrome complications

A 
infection 
VTE 
worsening CKD
HTN
Hyperlipidaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

nephritic syndrome presentation

A 
AKI
\+/- blood and protein on urine dip 
mild oedema
visible haematuria
HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

post infectious GN features

A

Post group A Beta-haemolytic strep infection
(1-2 weeks post tonsillitis / pharyngitis OR 3-4 weeks post impetigo / cellulitis)
typically in children 3-12 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

post infectious GN investigations

A

+ anti-streoptolysin O titres

immune complex deposition (IgG, IgM, C3) in sub epithelium on biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

post infectious GN treatment

A

supportive = ACEi / ARB, v Na diet

RRT (if ESRF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

IgA nephropathy features

A

post URTI / GITI / strenuous exercise
> gross haematuria
M > F
20-30% progresses to ESRF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

IgA nephropathy investigations

A

asymptomatic haematuriaa / microhaemiaturia
^ serum IgA
mesangial immune complex deposits on glomerular biopsy

17
Q

IgA nephropathy treatment

A

supportive = ACEi / ARB + v Na diet

18
Q

small vessel GN features

A

pulmonary / nasopharyngeal involvement eg. ulcers / polyps / asthma / allergic rhinitis

19
Q

small vessel GN investigations

A

c-ANCA (PR3)
p-ANCA (MRO)
segmental necrotising GN

20
Q

small vessel GN treatment

A

immunosuppression

21
Q

Anti-GBM disease alternative name

A

Goodpasture’s disease

22
Q

Anti-GBM disease features

A

Ab against type IV collagen => pulmonary haemorrhage+ haemoptysis
> RPGN

23
Q

Anti-GMN disease investigations

A

Anti-GBM Abs
pulmonary infiltrates
IgG deposits on BM

24
Q

Anti-GBM treatment

A

plasma exchange

immunosuppression

25
Q

Thin BM disease features

A

hereditary

Type IV collagen abnormalities

26
Q

Thin BM disease investigations

A 
microscopic haematuria (persistent)
diffuse BM thinning on biopsy
27
Q

thin BM disease treatment

A

monitor renal function

supportive = ACEi / ARB + v Na diet

28
Q

Alport syndrome features

A

X linked
Type V collagen gene mutation
> hearing loss + eye abnormalities
> ESRF

29
Q

Alport syndrome investigations

A

microcytic haematuria / visible haematuria
SN hearing loss
GBM splitting / thinning + thickening
Fx of disease

30
Q

Alport Syndrome treatment

A

supportive
RRT
renal transplant (alport can > anti-GBM)

31
Q

LN features

A

compilation of SLE

nephritic / nephrotic

32
Q

LN investigations

A

ANA +
ds-DNA +
biopsy

33
Q

LN treatment

A

supportive

immunosuppressive therapy

34
Q

management of GN

A 
supportive = ACEi/ARB (proteinuria), salt / fluid restrictive + diuretics (fluid overload), control BP, statins (hypercholesterolaemia), LMWH (hypoalbuminaemia - VTE risk)
immunosuppressive = oral corticosteroids, IV methylprednisolone, rituximab, azathioprine etc. 
invasive = RRT / haemodialysis (sev AKI / ESRF), plasma exchange (Anti-GBM)
35
Q

nephrotoxic drugs

A

aminoglycosides
NSAIDs
ACEi/ARB
diuretics

36
Q

renally excreted drugs

A

metformin
opioids
lithium
digoxin

37
Q

RBC change associated with CKD

A

anaemia of chronic disease

Burr cells

38
Q

What is the most common cause of idiopathic nephrotic syndrome in adults?

A

1 - FSGS

2 - membranous glomerular disease

39
Q

what is the long term management for CKD

A

underlying cause: DM, HTN
CVD risk: weight loss, exercise, statin, smoking cessation
Complications of CKD: EPO, vit B12, iron, folate / diuretics (furosemide) / phosphate binders, v phosphate diet / v potassium diet
Definitive: RRT

Y3 Clinical Case Revision (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions