Renal teaching with Jess Flashcards

1
Q

What is creatine broken down from?

A

Creatine phosphate from muscle - broken down into creatinine, excreted unchanged in the kidney

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

What affects the rate at which urea is reabsorbed?

A

More reabsorbed if flow is slow

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

What goes up in dehydration? Why?

A

Urea high in dehydration -> low volume so slower flow, so more reabsorbed

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

Creatinine clearance equation

A

Cockcroft-Gault equation

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

Why else might urea be elevated?

A

High protein meal
GI bleed
Drugs - steroids, tetracyclines, sodium valproate
Dehydration

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

What is AKI

A

Acute decline in renal function defined by increases in creatinine and urea

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

What is oliguria

A

Less tahn 400ml / day

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

What is oliguria

A

Peeing less than 400ml / day

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

What is anuria

A

Peeing less than 50ml/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Causes of AKI

A

Prerenal (2/3) - anything that reduces renal perfusion pressures
Post renal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Causes of prerenal AKI

A

Loss of blood e.g. haemorrhage, dehydration, burns, severe gut loss (D&V)

Third spacing - peritonitis, pancreatitis (may look overloaded but intravascularly deplete)

Cardiogenic shock - MI, acute valve lesion (chorda tympani lesion), cardiac tamponade, acute HF

Loss of systemic vascular resistance (causing vasodilation) - anaphylaxis, sepsis, anti-HTN drugs

Hepatorenal syndrome - AKI in context of fulminant liver failure

Renal vasoconstriction - renal artery stenosis, ACEi, ARBs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the intrinsic renal causes of AKI?

A

only 1/5 are true intrinsic in origin, most are from

Prerenal acute tubular necrosis

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

?

A

ACEi/ARB

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

Drugs causing AKI to tubular

A

?

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

Drugs causing AKI to institiium?

A

?

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

Drugs that are not nephrotoxic but excreted renally must be stopped. Give some examples

A

Metformin
if GFR less than 30

Lithium
Digoxin

17
Q

Post renal causes of AKI

A

Obstructive nephropathy,

Bilateral obstruction:

ie..e 
stones
schistosomiasis induced strictures
SCA
Clots
renal TB
Bilateral paillary necrosis
External urethral compresssion 
pelvic malignancy 
BPH 
Retroperitoneal fibroids
posterior uretral valve (congenital valve in boys - blocks outflow at level of bladder) 
Constipation
18
Q

When do you get uremic symptoms?

A

If eGFR lower than 15

19
Q

Uremic symptoms

A
Anorexia
NV
Pruritis
Cofusion
Drowsiness
Uremic uncephalopathy
Uremic serositis - pericarditis, pleural effusion, ascites 
metalic taste
platelet dysfunction & coagulation (platelet disrupted by urea)
20
Q

What do you do to examine a patient with AKI?

A
Reduced skin turgor
reduced mucous membranes
Reduced cap refill 
High HR 
BP 
JVP
21
Q

Signs of SIRS

A

Systemic immune response syndrome (SIRS)

22
Q

Signs of reduced ECF

A

?

23
Q

Signs of expanded intravasculaly circulating volume

A

?

24
Q

Signs of expanded interstitial compartment

A

?

25
Q

Signs of systemic disease

A

?

26
Q

Signs of obstruction

A

Bladder distention (if the extra fluid is
Suprapubic discomfort
DRE - abnormal prostate

27
Q

?

A

Normally you give IV

28
Q

Investigations

A

Basic obs
ECG - hyperkalemia (tall tented q waves, short pr interval)
Urine dip - blood might point towards intrinsic cause

Bloods:
VBG for potassium levels and acidosis (and to work out whether it’s AKI or on background of CKD), lactate, FBC, U and E, LFT, high phosphate in CKD hence do bone profile

Renal ultrasound within 24hrs to check for pathology/obstruction

Avoid contrast - CT KUB can be used as doesn’t have contrast

Renal biopsy if pre and post renal causes excluded

29
Q

Management

A

ABCDE and treat adverse features like high news, pulmonary oedema, high potassium over 6 with ECG changes

??????????

30
Q

When to initiate renal replacement therapy

A

?

31
Q

AKI vs CKD

A

CKD - elevation in urea/creatinine from

32
Q

?

A

?

33
Q

Nephrotic vs nephritic syndromes

A

Glomerulonephritis can present with a spectrum of signs ranging from proteinuriea (nephrosis) to haematuria (nephritic)

34
Q

Nephritic syndrome triad

A

Haematuria
HTN
Moderate to severe renal impairment

Red cells on dip

35
Q

Causes of nephritic syndrome

A
IgA nephropathy - sore throat
POst streptococcal 
HSP (igA with systemic component e.g. GI bleeds)
Anti- good pastures 
Rapidly progressive GN
Alport's syndrome - congential
36
Q

Nephrotic syndrome

A

Leakage of proteins through glomerular membrane, as opposed to blodo leakage

37
Q

Triad for nephrotic syndrome

A

Hypoalbuminemia
Proteinuria
Oedema - periorbital, sacral, ankle, genital, ascites

38
Q

?

A

Total higher than 3.5g/24hrs

39
Q

Causes of nephrotic syndrome

A

Minimal change disease - only seen on electron microscopy

Membranous nephropathy, due to infections, rheum/

Focal segmental glomeruloscleorosis

Mesagniocapillary