227 - Acute Renal Failure Flashcards

1
Q

what are the functions of the kidney?

A

homeostasis of:

  • water
  • solutes - NA, CL, K, Ca, PO4, H+
  • disposal of waste products
  • hormone secretion (endocrine function)
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2
Q

describe the renal arterial system

A

renal artery enters at hilum, splits into interlobar arteries to carry blood through medulla into cortex, split into interlobular arteries which radiate out to surface of cortex, give off side branches afferent arterioles which carry blood to glomeruli

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3
Q

what are the two types of nephrons?

A
  • cortical nephrons - 7/8th of nephrons have short loops of henle which only reach outer medulla
  • juxtaglomerular nephrons - have long loops of henle which penetrate into medulla
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4
Q

what makes up a nephron?

A
  • renal corpuscle - containing glomerulus, bowman’s capsule (podocytes and simple squamous epithelium)
  • Renal tubule - deep cortex, reabsorption (water, ions, glucose) and secretion of penicillin and furosemide), has convoluted and straight parts
  • loop of henle - deep cortex entering medulla, formation of conc. urine, descending and ascending and thick ascending limbs
  • distal convoluted tubule - superficial cortex, water homepstasis, contains macula densa when tubule in contact with JGA
  • collecting tubule - mid cortex, water homeostasis, drains into collecting duct
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5
Q

what does the glomerulus ultrafiltrate?

A
  • allows free passage of water & small solutes (Na, K, Ca, PO4, HCO3, H+), glucose, CK
  • prevents passage of large plasma proteins, cells
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6
Q

what is the average GFR for a 70kg adult male?

A

125ml/min - 180L of filtrate produced each day

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7
Q

How can GFR be calculated?

A
  • Inulin clearance

* creatine clearance

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8
Q

what do the different parts of the loop of henle do?

A
  • reabsorp 1/5th of water, Na and CL, produce high Na in medulla
  • descending limb - permeable to water and solute
  • ascending limb - permeable to solute but not water
  • thick ascending limb - actively pumps Na into medulla but impermeable to water
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9
Q

what does the macula densa do?

A
  • senses Na in distal convoluted tubule
  • if Na is high - high filtration rates - secrete adenosine and inhibit NO >constriction of afferent arteriole
  • if Na is low - reduced filtration rates - secrete prostaglandins> granular cells secrete renin >afferent arteriole dilatation
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10
Q

what are the 3 major mechanisms for autoregulation of GFR?

A
  • Myogenic response - ↑BP causes ↑stetch on afferent arteriole walls > depolarisation and contraction of smooth muscle cells > vasoconstriction > ↓GFR
  • Adenosine from macular densa in response to ↑Na > vasoconstriction and ↓GFR but NO produced by vascular epithelium> vasodilation >↑GFR
  • Renin Angiotensin system - Renin secreted by granular cells due to ↓ aff. art. P, ↓Na, B1 adrenergic stimulation, cleaves circulating angiotensinogen to angiotensin I, converted to II by ACE from lungs >constricts aff & eff art., more eff so ↑GFR, ↑syno activity, ↑ tubular Na reabsorption and K excretion, ↑Aldosterone, ↑ ADH, ↑PGE release
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11
Q

what are the effects of unilateral and bilateral renal artery stenosis?

A
  • uni - ↑renin secretion, ↑ angiotensin/aldosterone >refactory HTN - but mild renal impairment
  • bi - refactory HTN > pulm oedema - significant renal impairment
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12
Q

what drugs affect the renin angiotensin system?

A

*Aliskiren - binds to renin
*ACE inhibitors
*angiotensin Receptor blockers eg Losartan
»> reduces systemic BP, ↓ intraglomerular P (reduces angiotensin II mediated efferent arteriolar vasoconstriction
*spironolactone - aldosterone antagonist diuretic
*NSAIDs - inhibit COX enzymes that produce prostaglandins > reduce dilatation
*Ca channel blockers - inhibit vasoconstriction - more pronounced on eff.

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13
Q

what is azotemia?

A

incr. BUN (Blood Urea Nitrogen) concentration

* incr BUN to Cr ie 20:1 sugests pre-renal failure

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14
Q

what are the causes of Pre-renal Acute kidney injury?

A

VOLUME DEPLETION

  • hypovolaemia
  • cadiogenic shock
  • sepsis
  • Drugs affecting aff./eff. art. tone - NSAIDs constict aff, ACE inhib & ARBs dilate eff.
  • hepatorenal syndrome - vasodilation of coeliac/mesenteric art.
  • 3rd space sequestration - loss of intravascular fluid to interstitial fluid> ↑abdo P>ascites, bowel obst peritonitis, pancreatitis
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15
Q

how might pre-renal failure present?

A
  • ↓GFR and hypovolaemia
  • thirst, ↓urine output, diziness and orthostatic hypotension
  • Hx of vol loss - vomiting diarhorrea, haemorrhage
  • Hx of cardiac failure
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16
Q

what are the causes of intrinsic acute kidney failure?

A

DAMAGE OF GLOMERULUS OR TUBULE

  • Acute Tubular necrosis - nephrotoxic drugs (ABX (Aminoglycosides), antifungals (Amphotericin)), contrast media, rhabdomyolysis, haemolysis
  • Glomerulonephritis
  • vaculitis
  • interstitial nephritis - due to ABXs (Penicillin, cephalosporins, sulphonamides, rifampicin), furosemide, NSAIDs
  • infection
17
Q

how might intrinsic renal failure present?

A
  • gomerular - haematuria, oedema, HTN
  • acute tubular necrosis - hypotension following ischaemic event, drugs or radiological contrast, rhabomyolysis
  • interstitial nephritis - fevers, rash, arthralgia after drugs
18
Q

what are the causes of post-renal acute kidney failure?

A

*obstruction causing ↑ tubular P and reduced GFR. Eff art try to ↑igP by constricting leading to hypoperfusion of peri-tubular capillaries. caused by
Bence-Jones protein, myoglobin, renal stones, UT obstruction by tumour/mass/fribrotic process/clots»> leads to loss of conc capicity and loss of acidification capacity.

19
Q

how might post-renal failure present?

A
  • only if both kidneys obstructed
  • prostatic - urgency, frequency and hesitancy
  • renal calculi - flank pain, haematuria, urinary WCC
  • surgery
20
Q

what is rhabdomyolysis?

A

muscle necrosis leading to the release of intracellular constituents into circulation> electrolyte imbalance and obstruction with haem pigment casts and tubular injury by haem iron

  • red brown urine, ↑serum enzyme levels of CK, LDH, electolyte abnormalities ↑K↑Po4↑Ur decr Ca
  • caused by trauma or martahon running, hot weather, hypokalaemia, hypophosphotaemia, convulsions, alcohol, opiates, statins
  • hypokalaemia with disease and hyperkalaemia in recovery + hypercalcaemia
21
Q

what is the RIFLE criteria?

A
Risk - Cr ↑1.5 GFR decr >25%
Injury - Cr ↑2.0 GFR decr 50%
Failure Cr ↑3.0 GFR decr 75%
Loss failure persisting for  >4weeks
End stage kidney disease >3months
22
Q

what would different urine Na and urine osmolality values indicate?

A

decr urine Na value 40 ATN
incr osm >500 mOsmols/L - pre renal
decr osm

23
Q

how would you treat renal failure?

A
  • correct hypovolaemia with fluids
  • treat sepsis
  • USS for obstruction
  • stop nephrotoxic drigs
  • check for vasculitis
  • hyperkalaemia (ECG changes tented twaves) - IV calcium, insulin and glucose, salbutamol
  • pulm oedema - high flow o2, vasodilators, furosemide
  • bleeding due to urea in blood - fresh frozen plasma and platelets, blood transfusion, desmopresin
  • Rhabdomyolysis - fluid repletion, forced alkaline duiresis with sodium bicarbonate, mannitol forced diuresis with osmostic diueretic
24
Q

what are the 3 methods of drug excretion in the kidneys?

A
  • glomerular filtration
  • active secretion in the tubules
  • passive reabsorption in the tubules
25
Q

what drugs can cause pre-renal failure?

A
  • NSAIDs and COX2 inhibs - reduce prostaglandin production > failure of aff. arteriolar dilatation
  • Radiocontrast media and cyclosporine > causes aff art vasoconstriction
  • ACE inhibs and Angiotensin receptor blockers > failure of eff. art constriction
  • loop diueretics and laxatives - vol depletion
26
Q

what drugs can cause intrinsic renal failure?

A
  • Direct nephrotoxicity - Abx (aminoglycosides, cephalosporins), antifugals (amphotericin), paracetamol and aspirin
  • allergic or immunological damage - ABX (gentamicin, cephalosporins, penicillins, erythromicin, rifampicin), allopurinol, NSAIDs, furosemide and thiazides
27
Q

what drugs can cause post renal failure?

A
  • retroperitoneal fibrosis - B blockers, dopamine agonists
  • crystalluria (obstruction) - aciclovir, ganciclovir, methotrexate.cisplatin
  • tubular blockage by proteinuria - radiological contrast
  • tubular blockage by myoglobin - statins