Case study - renal papillary necrosis

DEHYDRATION = HIGH HR, low cap refill time, dark pink mucous membranes (seen in infection - systemic inflammation)

blood - most sig = low total protein

proteins could be lost through gut/protein = not enough coming in/ too much excreted = PLE/PLN

thickened colonic wall - intestinal tract issue

peritoneal fluid - measure lactate conc = released if tissue is infarcted/necrotic - no evidence of twist/ischaemic area

elevated urea, not creatinine = expect both to be elevated in renal failure

can be seen in high protein meal/bleeding into gut = only urea elevation

RDC - gets ulcerated easily - due to length of vessels in wall. Whole tissue is susceptible to ischaemic injury

GI ulcers -> protein and water leaking out into lumen -> sepsis

blood cloting - thrombus formation, blood vessel damage = segment becomes necrotic, ischaemic -> infarct

dose was not tapered - prostaglandin house keeping functions in gut wall prohibited

if process was left to develop - heal by scarring - loss of nephrons

papillary necrosis- prostaglandins and dehydration. Kidneys slow GFR to conserve fluid.

RAA system activated - angiotensin constricts afferent/efferent arterioles

decrease GFR

cortex = well perfused

goes to medulla - O2 taken out

most at risk of hypoxia - juxtamedullary nephrons in medulla

continual vasoconstriction = hypoxia

loss of PGE release to counteract

ultimately -> leads to renal papillary necrosis

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