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Medicine related kidney questions

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Kidney 2

Pregunta 1 de 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.

Arrastra y suelta para completar el texto.

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

Explicación

Pregunta 2 de 19

1

Selecciona la opción correcta de los menús desplegables para completar el texto.

( 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.

Explicación

Pregunta 3 de 19

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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.

Explicación

Pregunta 4 de 19

1

Stimulators of K+ excretion include?

Selecciona una o más de las siguientes respuestas posibles:

  • Increased K+ intake

  • Increased pH

  • Aldosterone

  • ADH

  • Increased sodium delivery

  • Ameloride

  • Thiazides

Explicación

Pregunta 5 de 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.

Arrastra y suelta para completar el texto.

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

Explicación

Pregunta 6 de 19

1

What are the two most important regulators of calcium?

Selecciona una de las siguientes respuestas posibles:

  • Na and PTH

  • PTH and Vitamin D

  • TSH and Vitamin D

  • PTH and K

Explicación

Pregunta 7 de 19

1

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

Selecciona una o más de las siguientes respuestas posibles:

  • high plasma calcium

  • PTH

  • low plasma calcium

  • ADH

Explicación

Pregunta 8 de 19

1

The pre-renal causes of AKI include?

Selecciona una o más de las siguientes respuestas posibles:

  • Volume expansion

  • Volume depletion

  • GI losses

  • Glomerulonephritis

  • NSAID's

  • Cutaneous losses

  • Bladder Disease

Explicación

Pregunta 9 de 19

1

Renal causes of AKI include?

Selecciona una o más de las siguientes respuestas posibles:

  • Inflammatory glomerulonephritis

  • Acute tubular necrosis

  • Rhabdomyolysis

  • Extra-tubular obstruction

  • Acute Interstitial Nephritis

  • Nephrotoxicity

Explicación

Pregunta 10 de 19

1

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

Selecciona una de las siguientes respuestas posibles:

  • 1

  • 2

  • 3

Explicación

Pregunta 11 de 19

1

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

Selecciona una de las siguientes respuestas posibles:

  • Urinary Neutrophil Gelatinase- Associated Lipocalin

  • Urinary IL-22

  • Urinary IL-18

  • Urinary Kidney-Injury molecule 1

  • Cystatin C

Explicación

Pregunta 12 de 19

1

Selecciona la opción correcta de los menús desplegables para completar el texto.

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

Explicación

Pregunta 13 de 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?

Selecciona una de las siguientes respuestas posibles:

  • Loss of brush border

  • Cell detachment

  • Distal tubule casts

  • Areas of cellular regeneration

  • Low tubule calcium

Explicación

Pregunta 14 de 19

1

Rellena los espacios en blanco para completar el texto.

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.

Explicación

Pregunta 15 de 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

Arrastra y suelta para completar el texto.

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

Explicación

Pregunta 16 de 19

1

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

Selecciona una de las siguientes respuestas posibles:

  • Provide structural support to glomerulus

  • Contractile components

  • Phagocytic function

  • Sequester iron

  • Proliferation and laying down of collagen

Explicación

Pregunta 17 de 19

1

Rellena el espacio en blanco para completar el texto.

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

Explicación

Pregunta 18 de 19

1

Nephrotic Syndrome is characterised by:

Selecciona una o más de las siguientes respuestas posibles:

  • Large amount of Red Blood Cells

  • Heavy protein > 3.5g/ day

  • Oedema

  • Hyperalbuminaemia

  • Hypoalbuminaemia

  • Lipids

Explicación

Pregunta 19 de 19

1

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

Selecciona una o más de las siguientes respuestas posibles:

  • 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

Explicación

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