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Medicine & Surgery (overlap) > AKI > Flashcards

AKI Flashcards

1
Q

criteria for an AKI?

KDIGO guidelines

A

1 of:
• ↑ creatinine >26 in 48 hours
• ↑ creatinine x 1.5 baseline in 1 week
• ↓ urine output <0.5 ml/kg/hr for 6 hours (8 in kids)
• (in kids: ↓ GFR 25 percent over 7 days)

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2
Q

aldosterone:
• where secreted and in response to what?
• where does it act?
• what does it do to Na+ and K+ levels?

A
  • secreted in the adrenal cortex in response to low blood P.
  • acts on the distal CT and collecting duct
  • reabsorbs Na+ (and therefore H2O, ↑ BP), and exchanged for K+ (therefore ↓ K+ in blood)
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3
Q

ADH (vasopressin):
• where secreted?
• where does it act?

A
  • posterior pituitary

* collecting duct to ↑ aquaporins, and ↑ H2O retention

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4
Q

renin
• where’s it from and what is it?
• how is it released? (3)
• how does it ↑BP

A

• juxtaglomerular cells (JGC) in kidneys, enzyme
• 1) baroreceptor mechanism when ↓ P. in afferent arteriole
2) SYMP nerve mechanism
3) macula densa mechanism which detects ↓ NaCl in distal CT and tells JGC to get a move on
• meets angiotensinogen (from liver), becomes angiotensin 1, meets ACE enzyme (from lungs), becomes angiotensin 2

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5
Q

ΔΔ causes pre-renal AKI?

A
  • D + V, burns, pancreatitis
  • shock, haemorrhage, sepsis, major surgery, MI
  • ↓ CO (HF)
  • hepatorenal syndrome
  • DHx: NSAIDs, ACEi/ARBs, diuretics
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6
Q

what do NSAIDs do in AKI?

A

exacerbate by constricting afferent arterioles

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7
Q

what do ACEi and ARBs do in AKI?

A

dilate Efferent arterioles

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8
Q

what do diuretics do in AKI?

A

hypovolaemia

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9
Q

is there renal cell injury in pre-renal AKI?

A

no, reperfusion restores function

unless acute tubular necrosis from prolonged hypoperfusion

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10
Q

ΔΔ causes intrinsic AKI? (3)

A

1) glomerular:
• acute tubular necrosis (ischaemia)
• GN
2) interstitial:
• acute interstitial nephritis (allergy, infection, sarcoid)
3) vessels:
• vascilitis - afferent constriction (RAS, malignant HT, HUS, TTP, DIC, PET)

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11
Q

ΔΔ causes postrenal AKI?

A
  • kidney stones
  • catheter
  • urethral strictures, CA
  • BPH
  • UTI
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12
Q

Hx: patient hasn’t passed much urine in last few days (<0.5/kg/hr), has developed SOB waking up in the night?

Ex: lung crackles and swollen ankles?

A

general Sx of AKI

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13
Q

Hx: patient not passing much urine, and is fatigued, with N, V, confusion?

A

uraemic Sx of AKI

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14
Q

Hx: patient has had 3 days of D+V, not passed much urine, is feeling dizzy upon standing?

Ex: marked diff in BP between sitting and standing, and tachycardic?

A

prerenal AKI

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15
Q

Hx: pregnant woman with headaches and changes in vision hasn’t passed much urine?

Ex: HIGH BP?

A

intrinsic AKI secondary to PET (microangiopathy, like HUS, TTP, etc)

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16
Q

Hx: patient with loin to groin pain, can’t sit still, and hasn’t passed urine in 24 hours?

A

postrenal AKI (kidney stones)

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17
Q

what is the polyuric phase?

A
  • as the kidney heals from an AKI, the tubules regenerate but water concentration is the last function to return
  • toxins accumulate in the kidney which increases the osmotic load
  • = massive polyuria
  • make sure enough IVT to replace!!!
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18
Q

nephrotoxic drugs? “FANG”

A
  • Furosemide
  • ACEi/ARBs
  • NSAIDs
  • Gentamicin
19
Q

Ix AKI?

A 
BEDSIDE:
• ECG (K+)
URINALYSIS
• dipstick: blood + protein (GN, stones, UTI, Ca, trauma), microscopic blood (interstitial nephritis), wbcs (UTI, interstitial)
• microscopy: red cell casts (rapid GN), eosinophils (interstitial), granular/tubular epithelial cell casts (acute tubular necrosis)
• low Na+ (pre-renal)
• myoglobinuria (rhabdomyolysis)
• culture (infection)
• immunoelectrophoresis (myeloma)

BLOODS:
• FBC: low Hb (CKD), wbcs (infection), eosinphilia (interstitial), low plts (HUS, TTP)
• U+E: high urea, creatinine, K+, check bicarb and Ca++
• LFTs (hepatorenal syndrome)
• coag: DIC (sepsis), weird clotting (CKD)
• CK (rhabdo)
• CRP (infection)
• ABG (metabolic acidosis)
+/-
• immune: ANCA, anti-GBM, ANA, anti-dsDNA, RF, etc
• electrophoresis (myeloma)
• culture (sepsis)

IMAGING:
• US: hydronephrosis (postrenal obstruction), small (CKD)
• +/- AXR, abdo CT
• CXR (pulmonary oedema)

20
Q

Ix if suspicion of rapidly progressive GN or prolonged acute tubular necrosis?

A

biopsy

21
Q

how to distinguish AKI from CKD?

A
  • look at previous bloods
  • see if GFR risen over 48 hours
  • US shows small kidney in CKD
  • nocturia in CKD
  • shorter Sx, Hb and Ca++ normal, in AKI
  • can be acute on chronic failure!
22
Q

approach to managing AKI?

A

Ex for life-threatening complication:
• HR, BP, JVP, CRT
• VBG (K+)
• ECG (K+)

Fluids + monitoring
• 250-500ml bolus (<2 litres)
• fluid balance + catheter
• monitor K+, lactate, creatinine

Ix
• dipstick (pre-catheter)
• USS w/n 24 hours
• LFTs (hepatorenal)
• platelets +/- film for haemolysis (HUS, TTP)
• autoAb if indicated (IgG/A, ANA, ANCA, anti-GBM)

Tx:
• sepsis 6
• stop DHx

23
Q

complications of AKI?

A
  • metabolic acidosis
  • high K+
  • pulmonary oedema
24
Q

when to give RRT (dialysis) in AKI?

“Ahhh FUK”

A
  • Acidosis pH <7.1
  • Fluid overload/pulmonary oedema
  • Uraemia (Sx - pericarditis, encephalopathy)
  • K+ >6.5 and refractory, ECG Sx
25
Q

types of RRT (dialysis)?

A

• intermittent haemodialysis (i.e. in those in the community)
• continuous RRT:
- haemofiltration (PRESSURE gradient across membrane, best used in haemodynamic instability)
- haemodialysis (CONCENTRATION gradient)
- or combined haemodiafiltration

26
Q

causes of acute tubular necrosis?

“MIRACLE”

A
  • Myoglobin (rhabdo)
  • Ischaemia
  • Radiocontrast
  • Aminoglycosides (gentamicin)
  • Cisplatin
  • Li+
  • Excess urate (gout)
27
Q

Ix urine dipstick in acute tubular necrosis?

A

often normal

28
Q
  • what causes acute interstitial nephritis?
  • Sx? (in 30 percent)
  • Ix on dipstick?
  • Ix on microscopy?
A
  • 90 percent are hypersensitivity reactions to drugs (NSAIDs, B-lactams), or infection (GAS, legionella)
  • Sx: rash, fever, arthralgia, eosinophilia
  • dipstick: leukocytes +/- mild protein and blood
  • microscopy: eosinophils and eosinophil casts
29
Q

Ix: dipstick shows blood + protein?

A

GN, stones, UTI, Ca, trauma

30
Q

Ix: dipstick shows microscopic blood?

A

acute interstitial nephritis

31
Q

Ix: dipstick shows wbcs?

A

UTI

acute interstitial nephritis

32
Q

Ix: urine microscopy: red cell casts?

A

rapid progressive GN

33
Q

Ix: urine microscopy shows: eosinophils?

A

acute interstitial nephritis

34
Q

Ix: microscopy shows granular/tubular epithelial cell casts?

A

acute tubular necrosis

35
Q

Ix: urinalysis shows myoglobinuria?

A

rhabdomyolysis

36
Q

Ix: myeloma?

A

immunoelectrophoresis

37
Q

what is rapidly progressive GN?
Sx?
Tx?

A
  • rapid decline in kidney function - GFR halves in 3 months to end-stage kidney disease (eg, crescenteric GN)
  • oliguria, haematuria, proteinuria, oedema, V, fatigue, fever
  • methylpred IV + cyclophosphamide IV
38
Q

causes of rapidly progressive GN?

“PIG”

A
  • Pauci-immune vasculitis (c-ANCA, p-ANCA)
  • Immune complex disease (SLE, post-infectious, IgA nephropathy)
  • anti-Glomerular BM disease (Goodpasture’s syndrome if + pulmonary haemorrhage, IgG deposition)
39
Q

basic Tx for each type of AKI?

A
  • prerenal = fluids +/- Abx
  • intrinsic = stop DHx, immunosuppress if GN
  • postrenal = catheter
  • ALL = fluid balance
  • referral (intrinsic - nephrology) (postrenal - urology)
40
Q

when to refer an AKI to renal team?

A
  • unresponsive to Tx
  • complications (↑K+, acidosis, fluid overload)
  • stage 3 AKI (<0.3ml, or >3 x baseline, or RRT)
  • low A-, HF, pregnant
  • intrinsic cause possible
  • HT
41
Q

Ex ↓volaemia?

A

•↓BP, ↓urine vol, non-visible JVP, poor tissue turgor, ↑HR, daily weight loss

42
Q

Ex ↑ fluid overload?

A

↑BP, ↑JVP, lung crepitations, peripheral oedema, gallop rhythm

43
Q

Tx fluid overload? (eg in oliguria, excessive fluid resuscitation, sepsis when capillary permeability affected)

A
  • (O2)
  • fluid restriction
  • if oliguria AND fluid overload (not just oliguria alone) - diuretics
  • RRT

Medicine & Surgery (overlap) (13 decks)

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