RENAL- acute renal disease

Question 1

define acute kidney injury

Answer 1

abrupt decline in renal function

Question 2

how is an AKI clinically manifested

Answer 2

reversible acute increase in nitrogen waste products measured by blood urea nitrogen (BUN) and serum creatinine levels - over the course of hours to weeks

Question 3

why is an AKI an important problem

Answer 3

mortality is between 25-40 % 
accounts for 20% of hospital admissions
20-30% of cases are preventable 
AKI is more deadly than MRSA
long term sequalae - CKD, ESKD (end stage), death

Question 4

list the factors involved in producing glomerular filtrate

Answer 4

high renal perfusion and adequate renal blood flow
glomerular capillary pressure and glomerular filtration
signs of increased sympathetic tone
GFR

Question 5

how does high renal perfusion and adequate renal blood flow relate to glomerular filtrate

Answer 5

required to allow glomerular filtration thereby producing urine
K+ and H+ secreted in DCT
hypovolaemia= increase reabsorption of wate and sodium = less volume to DCT = less K+ and H+ secreted

Question 6

how does glomerular capillary pressure and glomerular filtration relate to glomerular filtrate

Answer 6

colloid osmotic pressure = 30mmHg
hydrostatic pressure in bowman’s capsule 15mmHg
normal glomerular capillary pressure = 55mmHg

Question 7

what are signs of increased sympathetic tone

Answer 7

cold limbs, poor palpable peripheral pulses, tachycardia, sweaty, dilated pupils

Question 8

why is the GFR being too high an issue

Answer 8

substance that are needed cannot be reabsorbed back into the body quickly enough and are lost in the urine

Question 9

why is the GFR being too low an issue

Answer 9

everything is reabsorbed - including waste

Question 10

what is the effect of angiotensin converting enzyme inhibitors and angiotensin II receptor blockers on glomerular filtration

Answer 10

decrease arteriolar resistance
decrease arteriolar vasoconstriction
decrease cardiac output
reduce potassium excretion in the kidneys
inhibit angiotensin converting enzyme to reduce levels of angiotensin II

Question 11

outline the excretion pathway for angiotensin II

Answer 11

decrease in blood pressure = angiotensinogen is secreted by liver and rennin is secreted by kidneys = combine to form angiotensin I = angiotensin converting enzyme converts to angiotensin II

Question 12

what effects does angiotensin II have

Answer 12

decrease in blood pressure = angiotensinogen is secreted by liver and rennin is secreted by kidneys = combine to form angiotensin I = angiotensin converting enzyme converts to angiotensin II

angiotensin II:

adrenal cortex - aldosterone = retains Na and water

proximal tubule - resorbs more Na = increased thirst, = increased blood pressure

efferent arterioles - constriction = increase in GFR

Question 13

what are four indications for initiating renal replacement therapy

Answer 13

hyperkalaemia
pulmonary oedema
acidaemia
uraemia (encephalopathy)

Question 14

outline why polyuria can be associated with AKI

Answer 14

onset - kidney injury
oliguric phase - urine output decreased from renal tubular damage - kidney is unable to excrete water

polyureic phase - increase in GFR as the kidneys try to heal - urine output increases but there is tubular scarring and damage - this results in solute diuresis and therefore increase water movement leaving the kidney

recovery - tubular oedema resolves, renal function improves