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Medicine related kidney questions

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Kidney 2

Question 1 of 19

1

Sodium enters passively down the membrane down its concentration gradient. It is actively extruded across the basolateral membrane by the Na/K/ATPase pump. Na+ reabsorption is in the PCT, followed by the LOH, DCT and CD.
In the PCT- exchanger at the apical membrane, at the basolateral membrane NA/K/ATPase and Na/HCO3 transporter.
In the thick limb of the LOH - cotransporter (NKCC2)...which can be inhibited by , leading to increased sodium in the DCT and therefore less water loss.
Na transport in the DCT is via transcellular reabsorption (Na/Cl transporter NCC)--thiazide diuretics can inhibit this.
In the cortical collecting duct, Na transport is mediated primarily by the principle cells. It crosses through ENAC's and can be inhibited by amiloride. reabsorption in the proximal tubule is linked to Na+ reabsorption.

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    apical
    largest
    least
    Na/H
    Na/Cl-
    Na/K
    Na/K/Cl
    Na/HCO3
    Na/Glucose
    frusemide
    thiazide
    aldosterone
    Water
    chloride
    glucose

Explanation

Question 2 of 19

1

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( Angiotensin 2, Angiontensin 1 ) binds to AT1 receptors of the proximal tubule. They also stimulate Na-H exchange in the TAL and ENAC's in the initial collecting tubules. All promote ( sodium, calcium, potassium ) reabsorption.
Aldosterone stimulates sodium reabsorption by the initial tubule and CCT. It upregulates apical ENAC's and therefore Na+ permeability.
ADH- overall effect is to produce urine which a ( high, low ) osmolality. In the TAL, ADH stimulates NKCC2 receptors and K+ channels. In the principle cells of the initial collecting tubule and CCT, ADH stimulates Na+ transport by increasing the number of open Na+ channels.

Explanation

Question 3 of 19

1

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Most of the K is absorbed in the as well. The cell is the Major Regulator of Potassium with % of potassium being managed here.
The Epithelial Na Channels gets us to dump all the potassium by an gradient
The sodium delivered the more potassium dumped. In the proximal tubule K+ reabsorption occurs passively and is via solvent drag. In the TAL K+ is reabsorbed paracellularly and through the - contransporter. In the cortical collecting duct- K+ reabsorption by intercalated discs occurs through the apical K+ uptake mediated by the Pump, followed by passively efflux across the basolateral membrane. In the cortical collecting ducts (principle cells), the K+ occurs by active uptake across basolateral membrane, followed by passive diffusion through apical K+ channels.

Explanation

Question 4 of 19

1

Stimulators of K+ excretion include?

Select one or more of the following:

  • Increased K+ intake

  • Increased pH

  • Aldosterone

  • ADH

  • Increased sodium delivery

  • Ameloride

  • Thiazides

Explanation

Question 5 of 19

1

Chloride is reabsorbed via the pathway early in the PCT via solvent drag,
Later in the PCT at the apical memrane via Cl-base exchanger (Cl- out of lumen, Base in), following + out of lumen. At the basolateral membrane via Cl- channels and K/Cl- cotransporter.
In the thick ascending limb via - cotransporter.
In the ducts via paracellular reabsorption, apically via Cl-HCO3- exchanger and Cl- channels basolateral membrane.

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    paracellular
    transcellular
    Na
    Ca
    K
    Na/K/2Cl
    Cl/HCO3-
    collecting
    distal

Explanation

Question 6 of 19

1

What are the two most important regulators of calcium?

Select one of the following:

  • Na and PTH

  • PTH and Vitamin D

  • TSH and Vitamin D

  • PTH and K

Explanation

Question 7 of 19

1

Most (80%) of the phosphate is reabsorbed at the PCT.
Which factors increase phosphate reabsorption?

Select one or more of the following:

  • high plasma calcium

  • PTH

  • low plasma calcium

  • ADH

Explanation

Question 8 of 19

1

The pre-renal causes of AKI include?

Select one or more of the following:

  • Volume expansion

  • Volume depletion

  • GI losses

  • Glomerulonephritis

  • NSAID's

  • Cutaneous losses

  • Bladder Disease

Explanation

Question 9 of 19

1

Renal causes of AKI include?

Select one or more of the following:

  • Inflammatory glomerulonephritis

  • Acute tubular necrosis

  • Rhabdomyolysis

  • Extra-tubular obstruction

  • Acute Interstitial Nephritis

  • Nephrotoxicity

Explanation

Question 10 of 19

1

A serum creatinine level of 2-3 x the normal amount would place the person in which stage of kidney disease?

Select one of the following:

  • 1

  • 2

  • 3

Explanation

Question 11 of 19

1

Which of these is not a novel biomarker for acute kidney injury?

Select one of the following:

  • Urinary Neutrophil Gelatinase- Associated Lipocalin

  • Urinary IL-22

  • Urinary IL-18

  • Urinary Kidney-Injury molecule 1

  • Cystatin C

Explanation

Question 12 of 19

1

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In the RIFLE classification of AKI. Describe the following components.
R- (Risk) = 1.5 x increase in serum creatinine, GFR less 25% or urine output <( 0.5mL, 1mL )/kg per hour for 6 hours
I- (( Injury, Ischaemia )) = 2 x serum creatinine, GFR 50%, or urine output <0.5mL/kg for 12 hours
F- (Failure) = 3 x SC, GFR 75% drop, urine output <0.5mL/kg 24 hours or ( anuria, proteinuria ) 12 hours
L- (Loss) = complete loss of kidney function > ( 4 weeks, 8 weeks, 12 weeks )
E- (ESRD) = > 3 months

Explanation

Question 13 of 19

1

Acute Tubular Necrosis is due to tubular injury and prolonged disturbances in blood flow. Which of these is not a common histological feature?

Select one of the following:

  • Loss of brush border

  • Cell detachment

  • Distal tubule casts

  • Areas of cellular regeneration

  • Low tubule calcium

Explanation

Question 14 of 19

1

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The classic triad of Acute Interstitial Nephritis is: , Eosinophilia and .
It is most commonly caused by drugs such as , and NSAID's.
It often after halting these.

Explanation

Question 15 of 19

1

Hyperkalemia is a common problem of AKI. The mainstay of treatments are
- to drive K+ intracellularly
-Resonium which exchanges K+ and Na+ in the large intestine reducing intake
-Insulin and Glucose which drives K+ intracellularly
- to correct myocardium potential

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    B2 agonist
    Isotonic Saline
    Digoxin
    Lasix
    Calcium gluconate
    Sodium Hydrate
    Calcium Phosphate

Explanation

Question 16 of 19

1

Which of these is not a role of the mesangium (the space between the capillaries of glomerulus)?

Select one of the following:

  • Provide structural support to glomerulus

  • Contractile components

  • Phagocytic function

  • Sequester iron

  • Proliferation and laying down of collagen

Explanation

Question 17 of 19

1

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A thin layer of endothelial cells with tight junctions surround the capillary lumen

Explanation

Question 18 of 19

1

Nephrotic Syndrome is characterised by:

Select one or more of the following:

  • Large amount of Red Blood Cells

  • Heavy protein > 3.5g/ day

  • Oedema

  • Hyperalbuminaemia

  • Hypoalbuminaemia

  • Lipids

Explanation

Question 19 of 19

1

NSAID's, ACE-Inhibitors and Diuretics can impair kidney function by?

Select one or more of the following:

  • Dilation of afferent arteriole

  • Constriction of afferent arteriole

  • Dilation of efferent arteriole

  • Constriction of efferent arteriole

  • Promoting increased perfusion via volume expansion

  • Promoting decreased perfusion via volume contraction

Explanation

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