APP Level 4 Renal Review ORIGKEY

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1) What is the function of the kidney?

(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.

2) Kidneys receive approximately A% of blood flow. They are B organs.


a) A=10-20, B= tiny
b) A=30-40, B=large
c) A= 20-25, B= tiny
d) A=15-25, large
.

3) Renal cells are not easily damaged


a) True
b) False
.

4) Which of the following is not found in the nephron


a) glomerular capillaries
b) jejunum
c) peritubular capillary
d) afferent arteriole
.

5) What are the three major renal processes


1) Glomerular filtration filtrate leaves blood and enters the glomerular capsule of renal
tubule
2) tubular resorption of what body wants to keep
3) tubular secretion of what body still wants to excrete

6) Which part of kidney does filtering take place?


a) Glomerulus
b) Nephron
c) afferent arteriole
d) jejunum
.

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

Word Bank acute kidney injury block


blood constrict constricts
decrease decreased dilating
greater maintains prostaglandins
Prostaglandins protective Renin-Angiotensin- Aldosterone
System (RAAS)
two vasoconstriction vasodilation
8) How do we maintain good kidney function?
We need to ensure that the kidneys have a good [blood supply – they are [two of your vital
organs.
• Blood flow is regulated through [Renin-Angiotensin- Aldosterone System (RAAS) and
[prostaglandins.
• [Prostaglandins help to open the afferent arteriole. They increase renal blood flow and
glomerular filtration rate under conditions associated with decreased actual or effective
circulating volume, resulting in [greater tubular flow and secretion of potassium.
• Angiotensin II helps to [constrict the efferent arteriole to reduce the glomerular filtration
coefficient

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
.

f) Angiotensin I converted by ACE on vascular


endothelium (site of action of ACE inhibitors)
into Angiotensin II
g) increased blood volume and increased blood
pressure
h) decreased NaCl delivery to macula densa
i) low afferent arteriole pressure
j) increased sympathetic tone
k) Hypotension or hypovolemia
l) hypotension or hypovolemia
.

22) What can go wrong with hypotension and the kidneys?


• Reduced blood flow to the kidneys
• Damage to the renal tissue
• Blocked ureters and urine and waste cannot leave the body

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
.

25) with acute kidney injury


The rapid deterioration in renal function -could take [days or even hours. Tend to have
[reduced urine output and/or [increased creatinine.

26) List 3 risk factors of acute kidney injury


increased age, congestive heart failure, previous kidney disease or injury, diabetes,
hepatic disease.
27) Which of the following is not a sign and symptom in Acute kidney injury?
a) Reduced urine output but not always the case
b) Nausea and vomiting
c) Confusion (can be accumulation of toxins)
d) Jaundice
e) Drowsiness
f) Abdominal pain
g) Oedema
h) Shortness of breath
.

28) Which of the following is false regarding prerenal renal failure?


a) occurs from anything that reduces the blood flowing into the kidney like poor perfusion of
nephrons
b) Accounts for about 80% of the acute renal injury along with acute tubular necrosis.
c) caused by Hypovolaemia or decreased intravascular pressure
d) occurs when an obstruction in the urinary tract below the kidneys causes waste to
build up in the kidneys
.

29) Define Hypovolemia


refers to a state of low extracellular fluid volume, generally secondary to combined
sodium and water loss. It is a condition that occurs when your body loses fluid, like
blood or water. Fluids are essential to keep your organs functioning. Symptoms of
hypovolemia include weakness, fatigue and dizziness. Treatment with IV fluids
rehydrates and replenishes the fluid your body lost.

30) The narrowing and dilation of what is seen in hypovolaemia


Narrowing of the afferent arteriole
• Dilation of the efferent arteriole

31) Give a differential diagnosis for hypovolaemia


• Kidneys can also be damaged by a reduced cardiac output/hypotension, i.e. after a
heart attack, congestive cardiac failure.
• Infections can cause a profound drop in blood pressure, i.e. sepsis, which also makes
the vessels a bit rubbish and wobbly.
32) a Glomerulonephritis a) inflammation of the glomeruli, can be acute or
33) c Nephrotic syndromes chronic, can be caused by infections, immune
34) d Interstitial nephritis diseases and things that scar the glomeruli
like high blood pressure or diabetic
35) b Radiocontrast media
.
nephropathy
b) the agents used to increase the contrast of an
image, to enhance the visibility of internal
structures in imaging technology.
c) excrete too much protein caused by damage
to tiny blood vessels in the kidney, presents
with oedema, causes include heart failure,
blood clots and other more unusual things!
d) inflammation of tissues around the renal
tubules
.

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.
.

38) what xan impair kidney function


• Blood clots in the kidneys.
• Blockages caused by cholesterol deposits.
• Many other things: thrombotic thrombocytopenic purpura (TTP), scleroderma, toxins
such as cocaine

39) what can cause interstitial nephrititis


• Hypersensitivity reaction, usually drug-mediated or infection-related.
• Drug-mediated: antibiotics like penicillin's and quinolones, NSAIDs, PPIs, azathioprine,
captopril, thiazides, vancomycin, isoniazid, erythromycin and allopurinol, etc.
40) What is post renal caused by
• Can be caused by:
• Blood clots in urinary tract
• Bladder/cervical/colon cancer
• Enlarged prostate
• Urethral stricture
• If urine cannot be excreted, then it can back up.

41) what can be done to protect renal function?


Try to avoid nephrotoxic drugs (remember the CANDA acronym!).
• If we do need to use these sorts of drugs, monitor renal function and electrolytes -
remember to compare against the patients own levels also not just reference ranges.
• Consider temporarily withdrawing drugs (remember the CANDA acronym!) if the
patient becomes unwell.

42) What does the CANDA acronym stand for


Contrast media, ACE inhibitors, NSAIDs, Diuretics and Angiotensin receptor blockers.

43) What should you do if AKI develops (6 marks)


• Review drugs for nephrotoxic agents.
• Remember to review doses and drugs that are renally excreted.
• Treat underlying cause – i.e. infection, myocardial infarction.
• Try to optimise renal blood flow with fluids but avoid fluid overload.
• Monitor closely fluid input and output.
• Some patients may need renal replacement therapy.

44) AKI is managed with drugs


a) True
b) False
.

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