Renal Flashcards

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1
Q

What type of diuretic is Acetazolamide? On what part of the nephron does it elicit its effect? How does it work? What common side effect results?

A

It is a carbonic anhydrase inhibitor

It works on the proximal convoluted tubule

It inhibits carbonic anhydrase which is responsible for reabsorption of Na for excretion of H ions. The result is that Na stays in filtrate (water follows Na) and H ions are not excreted into filtrate (metabolic acidosis)

Common side effect is metabolic acidosis

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2
Q

What is the main side effect of loop diuretics? Where on the loop of henle do they commonly act? Which drug allergy is also associated with potential allergy to loop diuretics? Which transporters in the loop of henle do loop diuretics work on and how?

A

Hypokalemia

The thick ascending loop

Sulfanomides

Na/K/Cl pumps, blocking them as to not allow Na or K to be reabsorbed —> this leads to water loss via Na loss and K loss.

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3
Q

Why should loop diuretics be avoided in patients with renal insufficiency and not used to promote diuresis and kidney activity?

A

Can promote renal ischemia due to hypovolemia and promote the build of toxins in renal tubules leading to tubal ischemia and renal damage

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4
Q

Where does mannitol mainly elicit its effect on the nephron? how does it work?

A

Said to work on the descending loop of henle, it is a molecule that is completely filtered at the glomerulus and reduces reabsorption of water in filtrate.

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5
Q

Why is mannitol used to reduce ICP (what is the mechanism)? Does it still work if the BBB is not in tact?

A

Mannitol pulls water from intracellular space to extracellular and intravascular space thus reducing ICP by reducing cerebral edema.

If the BBB is not intact, mannitol will spill into the brain and possibly worsen ICP by increasing cerebral edema

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6
Q

What type of diuretic is spironolactone? Where does it work on the nephron and how?

A

It is a potassium sparing diuretic that works on the collecting ducts. It prevents activation of a pump that reabsorbs Na and excretes K; thus promoting Na loss and diuresis, as well as preserving K.

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7
Q

What type of diuretic are the following and where is there primary site of action in the nephron…acetazolamide, furosemide, spironolactone, hydrochlorothiazide, mannitol

A

Acetazolamide: a carbonic anhydrase inhibitor workin on the proximal tubule

Furosemide: a loop diuretic working mainly on the thick ascending loop of henle

Spironolactone: a potassium sparing diuretic exerting its main effects on the collecting duct

Hydrochlorothiazide: a Thiazide diruetic working on the distal tubule of the nephron and the thick ascending loop of henle

Mannitol: an osmotic diuretic eliciting its main effect at the descending loop of henle by preventing water reabsorption and promoting water to remain in filtrate

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8
Q

What is the difference between aldosterone and spironolactone?

A

Aldosterone promotes Na reabsorption and K loss at the collecting duct of the nephron while spironolactone work on the same channels, but reduce Na reabsorption and prevent K excretion.

Aldosterone: Na reabsorption and water retention, K excretion
Spironolactone: Na reabsorption is blocked and diuresis is result. K is retained.

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9
Q

What is a normal GFR? What percent of GFR is typically reabsorbed? Where is the majority of Na reabsorbed in the nephron? What % of Na is typically excreted in the urine? What is excessive excretion of Na in the urine indicative of?

A

125 ml/min

99%

The proximal tubule

1-2%

High levels of Na in urine indicate a lack of reabsorption in the nephron tubules and tubular damage

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10
Q

Which part of the kidney is the cortex and which is the medulla? What structures of the nephron lie in each?

A

The cortex is the outer portion and the medulla is the inner portion. The proximal tubule and the distal tubule as well as bowmans capsule lie in the cortex while the loop of henle and the collecting duct lie in the medulla

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11
Q

What pressure is needed in the kidney to maintain the autoregulatory mechanisms of the organ? What happens if pressures fall outside this range?

A

The autoregulation of the kidney takes place between 60-160 mm Hg. If pressures fall outside of this value, perfusion of the kidney is compromised.

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12
Q

What is the role of the juxtaglomerular apparatus? Where is the macula densa in the kidneys? Where is this structure located? How does it influence the kidney?

A

It’s role is to help regulate perfusion of the kidney. It is located at the distal tubule. It influences the afferent and efferent arterioles to vasoconstrict or dilate to increase or decrease perfusion at bowmans capsule.

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13
Q

What stimulates the release of renin? How does renin affect the rest of the body (discuss its influence on the RAAS system)?

A

Renin is release by the kidney in response to decreased pressure or blood flow. Renin converts angiotensin to angiotensin I (from the liver), which is then converted to angiotensin II via angiotensin converting enzyme. Angiotensin II has a variety of effects including thirst, vasoconstriction, ADH release, aldosterone stimulation for salt and water reabsorption at the collecting duct.

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14
Q

Does keeping a patient normotensive during a procedure guarantee adequate perfusion of the kidneys and explain? What are risk factors for AKI during general anesthesia? Do anesthetic agents directly compromise kidney function?

A

No, the sympathetic nervous system can shunt blood away from the kidneys despite adequate blood pressure.

Increased age / CHF / Diabetes / Hypertension / Intraperitoneal Surgery

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15
Q

What is ANP? Where is it synthesized? What circumstances promotes its release? How (and where) does it effect the kidneys? What other effects does it have on the body?

A

ANP is atrial natriuretic peptide, it is synthesized in the atria of the heart and is stimulated with increased blood return (pressure) in the atria. ANP acts on the collecting ducts of the nephron and inhibit sodium reabsorption. ANP also has vasodilatory effects on the systemic circulatory system. In a few words, the role of ANP is to decrease preload to the heart.

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16
Q

How might positive pressure ventilation interfere with urine output in regards to its effects on the atria of the heart?

A

PPV reduces atrial distention and can reduce ANP release contributing to Na and sodium retention (reduction in urine output)

17
Q

How does Vasopressin influence Na? How does it effect H2O

How does aldosterone influence Na? How does it effect H2O? How does it effect K+

A

Vasopressin causes the insertion of aquaporins in the collecting ducts; it promotes reabsorption of water only and does not influence Na

Aldosterone promotes the reabsorption of Na at the distal tubules and the collecting duct, water will follow Na thus it promotes reabsorption of Na and H2O. Aldosterone will result in the excretion of K+

18
Q

What is the normal amount of Serum Crt? What might elevated levels of serum crt indicate and why?

A

Normal serum Crt is 0.7-1.5 mg/dL

Elevated levels of serum crt can be an indication of nephron damage and a lack of filtration at kidneys. Serum crt is filtered and NOT reabsorbed at the nephron

19
Q

What is a normal blood urea nitrogen (BUN)? How is urea produced in the body? What problems might kidney failure and elevated BUN lead to? What BUN value is a strong indicator of GFR dysfunction?

A

A normal BUN is 10-20 mg/dL. Urea is produced by the liver due to amino acid breakdown in the body. Urea is excited in urine and if kidney failure exists then this toxic by product can build up in the body.

Urea can lead to: platelet dysfunction, uremic cardiomyopathy, etc.

BUN > 50 mg/dL is a strong indicator of decreased GFR. If values are elevated otherwise it can be due to dehydration, high protein metabolism, etc.

20
Q

What is normal urine specific gravity?

A

1.003 - 1.030

21
Q

Describe the RIFLE criteria for acute kidney damage and what indicators mark each stage. What does RIFLE stand for? What is a normal serum crt? What is normal GFR?

A

RIFLE is an indicator of severity of renal impairment, it is marked most notably by serum crt and/or GFR. Normal serum crt is 0.7-1.5 mg/dL and normal GFR is 125 ml/min

R: serum crt increased by 50% or GFR reduced by 25%
I: serum crt increased by 100% or GFR reduced by 50%
F: serum crt increased by 200% or GFR reduced by 75%
L: loss of function for >1 month requiring replacement therapy
E: loss of function for >3 months requiring replacement therapy

RIFLE = Risk, Injury, Failure, Loss of Function, and ESRD

22
Q

What urine output values defines clinical oliguria? What should the response to oliguria be? What about the administration of diuretics?

A

< 0.5 ml/kg/hr. A fluid challenge should be administered provided it is clinically appropriate; 500 ml bolus should produce results if related to volume. Diuretics do not help prevent AKI in cases of oliguria.