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Phase 3b > RENAL > Flashcards

RENAL Flashcards

1
Q

Describe how the kidneys respond to an acidosis

A
  1. Secretes H+ and resorbs all the plasma bicarb
  2. Secretes more H+ and adds new bicarb to blood via bicarb generated by phosphate buffer
  3. Upragulates ammonia buffer - which metabolises glutamine in cells to produce ammonia (excreted) and bicarb moved into blood
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2
Q

Describe how the kidneys respond to an alkalosis

A
  1. Rate of H+ secretion from tubular cells not enough to match bicarb so excess bicarb excreted
  2. Down regulation of phosphate buffer
  3. Down regulation of ammonia buffer
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3
Q

What is normal urine output

A

around 1 ml/minute (this equates for 1.4 litres a day)
normal range is 800ml - 2L a day
AKI when less than half of BW per hour

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4
Q

What happens to creatinine during pregnancy

A

Falls because plasma clearance increases (the volume of blood that the kidney filters)
GFR increases by 50%

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5
Q

What 3 things grade/ affect AKI

A

rise in creatinine
fall in urine output
duration of fall in urine output

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6
Q

What 3 things grade/ affect AKI

A

rise in creatinine
fall in urine output
duration of fall in urine output
No urine output

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7
Q

What factors can cause a raised / low creatinine

A 
Muscle mass
Diet - High protein diet 
Surgery - ischemia
Dilution - low (i think)
Pregnancy - low
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8
Q

What amount of kidney injury produces a rise in urea and cr

A

50-60%

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9
Q

Why is creatinine used over egfr for AKI

A

Creatine more dynamic physiology, eg will increase in response to sudden injury. More of a moment to moment picture.
GFR better indicator for overall kidney function. Can have a low GFR and normal creatine (as the kidney has a lot of reserve to compensate for a low gfr)

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10
Q

What are the stages of AKI

A
  1. 1.5-1.9 x BL cr; <0.5 ml/kg/hr for 6-12 hrs
  2. 2.0-2.9 x BL cr; <0.5 ml/kg/hr for >12 hrs
  3. > 3.0 x BL cr; <0.3 ml/kg/hr for >24 hrs OR anuria for 12 hours
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11
Q

What clinical picture is typical of acute tubular necrosis

A

Raised Cr following hypovolaemia or nephrotoxic drug
Raised Urine
Raised K
Metabolic acidosis

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12
Q

What value indicates a moderate, significant, and severe hyperkalaemia

A

5-6
>6
>6.5

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13
Q

Is hyperkalaemia symptomatic

A

Usually not
But common manifestations can be muscle weakness and ECG changes, with the latter having the potential to progress to a life-threatening arrhythmia

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14
Q

What is the management of hyperkalaemia

A
  1. Cardio protection - calcium gluconate IV
  2. Move K+ into cells - insulin + glucose (to avoid hypo)
  3. Salbutamol neb
  4. If can’t control need renal replacement (haemodialysis or haemofiltration)
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15
Q

What drug groups are renotoxic and should be stopped in AKI

A

ACE - inhibitors
ARB (think antihypertensives)
NSAIDs
Aminoglycosides - gentamicin, neomycin, streptomycin

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16
Q

What antibiotic can cause a temporary rise in creatinine

A

Trimethoprim

17
Q

When should you suspect acute tubular necrosis

A

Anybody with a severe and prolonged pre renal cause of AKI
Anybody with AKI that has started a new nephrotoxic drug
With a bad AKI - eg met acidosis and high potassium
Muddy brown casts

18
Q

What are the risk factors for ATN

A

Poor renal function
Severe and prolonged hypovolaemia / under perfusion to kidneys
New nephrotoxic drug
Underlying renal disease

19
Q

what is azotaemia

A

High levels of nitrogen compounds/ products in blood, eg urea, cr, other body waste products with N in

20
Q

What chronic condition causes small kidneys, what are the exceptions to this rule

A

CKD

Exceptions - diabetes, HIV

21
Q

What causes enlarged kidneys

A

Hydronephrosis

Pyenephrosis

22
Q

How can USS be used to elicit causes of AKI

A 
mainly to rule out/ in obstructive cause that would cause large kidneys
asymmetry - eg renal artery cause
small - CKD
large - infection, obstruction
normal - ATN, intrinsic renal causes
23
Q

What investigations should be done to confirm acute tubular necrosis

A

Urea-creatinine ratio (10-1 in ATN because issue is in tubule not glomerulus, unless overlap with pre-renal)
Urinary sediment analysis - muddy brown casts
Urinary sodium - high because na-k pump stops working
Urine osmolality - high because tubules dont resorb

24
Q

What are the life threatening complications of AKI

A

Pulmonary oedema
Metabolic acidosis
Hyperkalaemia

25
Q

How should you assess a patient with AKI

A

A-E
Plus:
VBG
Bloods- FBC, U&E, LFT (hepato-renal syndrome), CRP, cultures, group & save, clotting
Bladder scan (obstructive cause)
Urinalysis, dip, catheter, monitor fluid
Ultrasound (within 24hrs if not resolving)
ECG

26
Q

How should you manage a patient with AKI

A

Identify and treat cause
Treat volume - fluid replacement
Protect the kidney’s - stop nephrotoxics, stop drugs that could worsen complications (eg diuretics)

27
Q

What drugs should be stopped in a patient with AKI because they can cause / contribute towards a metabolic acidosis

A

Metabolic aciDosis
M = metformin
D = diuretics

28
Q

list some common nephrotoxic drugs

A 
aminoglycosides 
amphotericin 
cytotoxic chemo 
immunosupressants 
diuretics (via volume depletion)
nsaids 
metformin 
lithium 
contrast media
29
Q

describe nephrotoxic pathological states

A

Hypoperfusion: reduces oxygen and nutrient supply to the kidney.

Sepsis: endotoxins and inflammatory mediators from infection can damage the renal vascular endothelium resulting in thrombosis.

Rhabdomyolysis: myoglobin released from damaged muscles precipitates in renal tubules and also reduces blood flow in the outer medulla.

Hepatorenal syndrome: patients with end-stage liver disease often have renal vasoconstriction.

30
Q

when should crcl be used over egfr

A

estimating renal function in patients with renal disease
older adults
patients at extremes of age
patient on medicine with low therapeutic index

31
Q

when should you not use egfr to estimate renal function

A

weight, children, pregnancy, or catabolic states

32
Q

what should you check before making dose adjustments in renal function

A

renal function - but need to make sure you have the right measure, eg egfr or crcl

33
Q

what is the difference between lowering a dose and extending between doses

A

lowering = reduced peak concentration

extending gap between doses = maintain a peak or trough

34
Q

what percentage sodium bicarb can you prescribe in aki and when

A

Sodium bicarbonate 1.26%

if bicarb is <20 mmols

35
Q

what antibiotics cant you prescribe when someone has an aki and infection

A

aminoglycosides eg gentamicin

can prescribe cephalosporins and carbapenams

Phase 3b (13 decks)

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