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APP Level 4 Renal Review ORIGKEY
APP Level 4 Renal Review ORIGKEY
APP Level 4 Renal Review ORIGKEY
(4 marks)
• Important for homeostasis of fluids – maintain fluids to keep blood flowing around the
body and help in maintaining osmolality.
• This helps to control blood pressure via the renin-angiotensin system
• Produce erythropoietin, Regulate acid base balance.
• Excretion of waste products, drugs and any metabolites.
7) What causes fluids and small molecules out of the capillary in the glomerulus into the tubular
lumen of the nephron
The relative vasoconstriction or vasodilation of the afferent and efferent arterioles
determines the pressure in each glomerulus and that pressure pushes it into the tubular
lumen
9) The renin-angiotensin system is activated by [decreased blood flow to the kidney, the result is
a rise in Angiotensin 2 which [constricts the efferent arteriole and raises the glomerular
capillary pressure and [maintains the glomerular filtration rate.
renin-angiotensin system blockers such as ACE inhibitors and angiotensin receptor blockers
[block this action and lower Glomerular capillary pressure, this action may be [protective in
chronic kidney disease especially diabetes.
However in states of volume loss and decreased kidney perfusion such as congestive heart
failure, trauma, cirrhosis, acute volume depletion, acute gastroenteritis, the use of these drugs
may [decrease Glomerular capillary pressure and GFR.
In these same states of iron depletion, prostaglandins may preserve kidney perfusion and gfr
by [dilating the afferent arteriole however NSAIDS block this protective action of
prostaglandins and may also decrease glomerular pressure and GFR.
Together the use of NSAIDS and renin-angiotensin blockers results in both afferent
[vasoconstriction and efferent [vasodilation and leads to a dramatic decrease in glomerular
pressure and GFR causing [acute kidney injury.
Put the flow chart in the correct order
10) l 8 a) renin release release (from juxtaglomerular
11) k 1 cells of nephrons)
12) b 2a b) renal hypoperfusion
13) d 2b c) This then binds angiotensin receptors (site of
14) i 2a i action of ARBs) to cause Vasoconstriction,
increased sympathetic NS activity,
15) h 2a ii
aldosterone release (from adrenal cortex),
16) j 2b i increased Na absorption (in proximal tubule),
17) a 3 endothelial dysfunction, promthrombotic
18) e 4 effects (increases PAI-1)
19) f 5 d) activation of aortic/ carotid baroreceptors
20) c 6 e) angiotensin (produced in the liver) is
21) g 7 converted by renin to angiotensin I
.
23) Acute kidney injury is not a disease, it just tells you how unwell a patient is
a) True
b) False
.
24) In which of the following can acute kidney injury (AKI) be acquired?
a) hospital
b) community
c) both
.
36) What is the following caused by acute tubular necrosis (ATN), interstitial nephritis
Acute tubular necrosis (ATN)
• Hypovolaemia and hypotension
• Drugs
Interstitial nephritis
• Drugs
• Infection
37) Which of the following is true for Acute tubular necrosis (ATN)
a) its a kidney disorder involving damage to the tubule cells of the kidneys, which can
lead to acute kidney failure
b) Can be caused by hypotension or drugs or poisons or just by hypoperfusion.
c) Caused by an enlarged prostate
d) Radiocontrast media can cause vasoconstriction and reduce blood flow.
e) Muscle injury releases myoglobin which can cause ATN via nephrotoxicity.
f) Can be caused by Drugs such as aminoglycosides, ciclosporin, NSAIDS, and
cisplatin.
.