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Y6 Senior Med > Renal > Flashcards

Renal Flashcards

1
Q

What are causes of AKI

A

Pre-Renal (most likely approx 70%): hypoperfusion

  • hypovolaemia (bleeding, shock, dehydration)
  • Oedema (cardiac /liver failure, nephrotic syndrome
  • Renal hypoperfusion (renal artery stenosis, vasculitis, drugs)

Renal: intrinsic kidney damage, classified on location (vasculitis, glomerulonephritis, tubular, interstitial)

Post-Renal: obstruction to urinary flow (calculi, tumours, strictures, BPH)

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2
Q

what are A>E findings for AKI

A 
A.	Vomiting
B.	Tachypnoea, cough (pulmonary oedema), bibasal crackles
C.	Tachycardia, fluid overload
D.	Confusion (uraemia), oliguria
E.	Abdominal pain (retention)
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3
Q

what is workup for AKI

A 
•	Bedside: ECG (hyperkalaemia), urine dipstick, urine sample (MC&S, ACR), ABG (acidosis, hyperk)
•	Bloods: U&E, calcium, phosphate, FBC, CRP/ESR, LFTs, CK (for rhabdo), renal screen
•	Imaging: bladder scan, renal uss
Renal biopsy (if unsure of cause - rarely done)
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4
Q

What is management for AKI

A

• Treat HYPERKALAEMIA
o 10-30mL Calcium Gluconate IV over 2-10 mins (can repeat every 15 mins up to 5 doses until K+ corrected) (N.B. IV calcium gluconate must be administered by a dr due to risk of arrhythmia)
o 10 U Actrapid with 100mL 20% glucose IV over 10 mins
o Consider 5 mg Salbutamol nebuliser
o Monitor ECG and ensure quick access to defibrillator
o Repeat U&E
o ABG to check for acidosis

Review drugs - stop drugs that reduce renal perfusion (NSAIDS) are nephrotoxic (aminoglycosides) are renally escreted (metforming) can cause hyperk (ACEi/ARB)

  1. Fluid resus
  2. Catheterise, monitor UO
  3. Treat the CAUSE
    o Hypovolaemia > IV fluids
    o Retention > catheterise
    o Pulmonary oedema > cautious use of furosemide
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5
Q

What are indications for dialysis

A

Acidosis (refractory to treatment / severe <7.2)
Electrolyte imbalance (refractory hyperkalaemia)
Intoxication (CKD stage 5; GFR <15)
Oedema pulmonary /overload of fluid
Uraemia complications (encepalopathy, nausea, pruritus, pericarditis)

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6
Q

How can you define AKI

A

KDIGO guidelines:

  • increase serum creat >26 within 48hours
  • increase serum creat >1.5x baseline within past 7 days
  • urine vol <0.5ml/kg/h for 6 hours
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7
Q

How can you classify AKI

A

Based on creatinine compared to baseline or based on URINE OUTPUT

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8
Q

What is presentation of AKI

A 
oliguria / anuria
dehyrdation, thirst, dry mouth 
confusion 
uraemia: malaise, nausea, vomiting, pruritus, drowsiness 
hypotension, hypovolaemia (if prerenal) 
palpable bladder (if postrenal) 
renal bruits (if renovasc disease)
dehydration
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9
Q

What are two blood markers of renal function

A

Urea

Creatitinine

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10
Q

What is creatinine

A

breakdown of protein metabolism within muscles

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11
Q

How does creatinine travel through kidneys

A

creatinine enters the blood

is freely filtered through kidneys

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12
Q

what pathology can alter creatinine amount in the blood

and why

A

Creatinine is produced and excreted through kidneys at constant rate

So if RENAL FUNCTION DECREASES

You reduce creatinine excretion > increased in creatinine in blood

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13
Q

what is eGFR

A

Serum creatinine + age + sex + ethnicity

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14
Q

What is creatinine clearance

A

eGFR + height + weight

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15
Q

why is creatinine clearance importannt

A

because the amount of creatinine produceed is dependent on our muscle mass

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16
Q

What is urea

A

a nitrogenous waste product

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17
Q

what conditions can cause urea to be elevated in the blood

A

DEHYDRATION - as urea is reabsorbed by kidneys when dehydrated

UGI BLEED - as RBC breakdown cause increased urea

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18
Q

What is classification of AKI

A

KDIGO stages 1-3
Stage1: serum creatinine 1.5 to 1.9x reference; bodyweight in urine mLs every 2 hours for <12 hours
Stage 2: serum creatinine 2.0 to 2.9x reference; bodyweight in urine mLs every 2 hours for over 12 hours
Stage 3: serum creat >3; anuric >12h

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19
Q

Drugs that need to be stopped in AKI

A

DAMN

Diuretics
ACEi, ARB
Metformin
NSAID

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20
Q

What are three forms of renal replacement therapy

A

Haemodialysis
Peritoneal dialysis
Renal transplant

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21
Q

How does peritoneal dialysis work

A

Peritoneum is used as semipermeable membrane. Dialisate is instilled in peritneum

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22
Q

What is advantage and disadvantage of peritoneal dialysis

A

Advantage: can be done at home
Disadvantage: risk of infection

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23
Q

Explain how haemodialysis works

A

Access via AV fistula / tesio
Takes blood out, passes it through dialysate. It is separated from dialysate via a semipermeable membrane
Electrolyte imbalances are corrected via diffusion; fluid overload is corrected via negative pressure in the dialysate (draws out water from blood=)

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24
Q

What are problems that occur with renal failure (link back to the specific renal function)?

A

Fluid balance&raquo_space; FLuid overload
Electrolyte homeostasis&raquo_space; hyperkalaemia, acidosis
Waste excretion&raquo_space; uraemia
Hormone production&raquo_space; anaemia, hypercalcaemia (hyperphosphataemia)

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25
Q

Ix for CKD

A 
UE 
blood glucose 
K+ 
FBC 
Antibodies, USS, biopsy
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26
Q

stages of CKD

A

1: eGFR >90
2: eGFR >60
3: eGFR >30
4. eGFR >15
5. eGFR <15

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27
Q

How do you manage CKD

A
  1. modify RF => antihypertensives, good dlycaemic control)
  2. fluid balance => restrict fluid + salt
  3. Anaemia => EPOstimulating agents
  4. hypocalcaemia => phosphate binders, vit D supplements
  5. consider renal replacement therapy
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28
Q

Nephritic syndrome triad

A

BPH
Blood (Haematuria)
proteinuria
Hypertension

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29
Q

What are causes of nephritic syndrome

A

Immune-mediated

  • IgA nephropathy
  • Post strep glomerulonephriitis
  • Henoch Schonein , HUS, SLE, Goodpastures

CAUSE INFLAMMATION OF GLOMEROLUS AND NEPHRON > CAPILLARY BECOMES LEAKY

30
Q

Describe what occurs in IgA nephropathy

A

Following resp/GI infection
Abnormal IgA is produced
Immune system makes antibodies against it
Sticky immune complexes are produced

31
Q

Explain how IgA nephropathy presents

A

5-7 days post infection

Abdo pain, rash, arthritis

32
Q

Explain how Post-Strep Glomerulonephritis presents

A

4-6 weeks post infection

33
Q

What must you manage in Post-Strep Glomerulonephritis

A

HTN

34
Q

what is triad of nephrotic syndrome

A

PHO
Proteinuria
Hypoalbuminaemia
Oedema

+ Thrombosis (due to loss of antithrombin III thhrough kidneys)

35
Q

Causes of nephrotic syndrome

A

Minimal change diisease
FOcal segmenral glomerulonephritis (MOST COMON)
Membranous glomerulonephritis

36
Q

what are causes of CKD

A 
long term renal injury 
usually linked to: 
- DM
-HTN 
- chronic inflammation (glomeerulonephritis, vasculitis, myeloma, amyloidosis)
37
Q

what is mode of inheritance for PKD

A

Autoomal dominant

38
Q

what occurs in PKD

A

multiple renal cysts develop and cause damage to adjacent nephrons

39
Q

how and when does PKD present

A

in > 30 years old

liver cysts: flank pain, haematuria, HTN
berry aneurysm: SAH
Mitral valve prolapse

40
Q

HOw can you manage PKD

A

give TOLVAPTAN to slow down progression

41
Q

what is the usual cause of RAS

A

atherosclerosis

42
Q

what occurs to renal enzymes in RAS

A

Renal hypoperfusion> increased angiotensin 2, increased aldosterone > increased BP

43
Q

whhat drug is AWFUL if you have RAS and wy

A

ACEi

because in RAS renal perfusion is actually maintained by constriction of the efferent arteriole

ACEi remove that constriction > glomerular filtration pressure drops > little blood flows to kidey > severe AKI

44
Q

Gold standard Ix for RAS

A

Digital subtraction angiography

45
Q

WHAT IS fibromuscular dysplasia

A

Proliferation of cells in the walls of the arteries causing the vessels to bulge or narrow.

This most commonly affects YOUNG WOMEN

Susceptible to AKI after the initiation of an ACE inhibitor.

On MR angio: ‘string of beads’ appearance.

46
Q

What are stimuli for renin secretion

A

low Na
low perfusion
sympathetic stimulation (beta adrenergic receptors)

47
Q

how does renin act on the RAS

A

Renin releasedd from JGA

Renin converts angiotensinogen to Angiotensin 1

48
Q

What occurs to angiotenssin 1

A

Angiotensin 1 is cleaved in lung by ACE to At2

49
Q

What is function of At2

A

Stimulates adrenal production of aldosterone

also constricts arterioles

50
Q

how do you distinguish glomerulonephritis from AIN on urine dip

A

glomerulonephritis = NEPHRITIC syndrome = blood and protein in urine

AIN = NePHROTIC syndrome = protein and WCC

51
Q

what do you do if a patient has CKD but needs a scan with contrast?

A

give IV saline before and after - this reduces the risk of precipitating an AKi

52
Q

what CK levels are you expecting for rhabdomyolysis

A

CK >10 000

otherwise (if lower than that) it could just be a soft tissue injury

53
Q

what histopathological findings do you expect with a carcinoma

A

nuclear enlargement
hyperchromasia
pleomorphism

54
Q

difference between IgA and post infection nephropathy in terms of timing

A

IgAA is FEW DAYS

post-infectious is FEW WEEKS

55
Q

How does urinary sodium differ between prerenal and renal AKI, and why?

A

prerenal: LOW urinary sodium
because the kidney works fine and is desperately trying to hold on to sodium to raise BP

renal: HIGH urinary sodium
because the kidney is damaged so loses lots of sodium

56
Q

classify and name causes or intrinsic renal AKI

A

VASCULITIS - affects the blood vessels

  • small vessels (microangiopathic): HUS, TTP, DIC, GPA
  • large vessel (obstructive): renal artery / vein thrombosis or embolus

GLOMERULONEPHRITIS - affects the glomerolus

  • minimal change disease (in children)
  • membranous glomerulonephritis (in adults)

ATN - affects tubules
- rhabdomyolisis, post-hypovolaemia

AIN - affects intersttium
- NSAIDS, PENICILLIN, SULFA-DRUGS, PPI, CIPROFLOX, ALLOPURINOL, FUROSEMIEDE

57
Q

most common extarenal presentation of PKD

A

cystic liver > hepatomegaly

58
Q

what is a dangerous unique complication of haemodysalisis

A

Dialysis disequilibrium syndrome

causes cerebral oedema (headache, drowsiness)

59
Q

why do you need to STOP LITHIUM in AKI?

A

because may cause toxic accumulation of lithium (although lithium itself does not actually cause AKI)

60
Q

what dose of aspirin can you continue for AKI

A

low dose (75 mg)

61
Q

how do you treat cranial DI

A

DESMOPRESSIN

62
Q

how do you treat nephrogenic DI

A

thiazide

63
Q

when does a GP need to refer to nephrology someone with CKD

A

if;

  • eGFR below 30
  • eGFR falls progressively by > 15 in a year
64
Q

what else other than GFR do you need to diagnose CKD stages 1 and 2

A

you need supportive evidence (e.g. from urine dip, USS, symptoms)

otherwise likely not CKD, as GFR is simply variable in peoopke

65
Q

what dose of potassium is safe to give IV per hour WITHOUT CARDIAC MONITORING

A

10mmol / h

66
Q

what must a patient be on if receiving 20mmol KCl /h

A

requires cardiac monitoring

via central line preferred

67
Q

what is the pathophysiology of goodpasture

A

anti-GBM antibodies against T4 collagen

68
Q

what are symptoms of goodpasture

A

pulmonary haemorrhage > haemoptisis

glomerulonephritis > NEPHRITIC syndrome (proteinuria + haemoaturia)

69
Q

how much does creatininee need to increase by to recognise an AKI

A

> 26 micromol / L

70
Q

what are the three ways of removing potassium from the body (rather than merely shifting it into cells) in hyperkalaemia

A

calcium resonium (enema > oral)
loop diuretics
dialysis

71
Q

what electrolyte imbalance can large volumes of NaCL cause

A

hyperchloraemic metabolic acidosis

72
Q

which vit D supplement is good for end stage kidney disease a

A

alpha calcidiol

Y6 Senior Med (29 decks)

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