Nephro/uro Flashcards

(31 cards)

1
Q

Where do loop diuretics act and on what transporter?

A

Thick ascending loop of Henle
Block NCCK transporter -> Na/K/Cl not reabsorbed = less medullary hypertonicity = less concentrated urine

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2
Q

Where do potassium sparing diuretics act and what receptor?

A

Act on the last part of the distal convoluted tubule and collecting duct - block aldosterone receptors therefore block its action = Na excreted and K+ kept

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3
Q

What are the transporters involved in the principal cell in the distal part of DCT and collecting duct? What hormone acts here? What is the overall result of this hormone?

A

Transporters: Na/K pump on basolateral membrane maintains low intracellular conc of sodium so sodium diffuses out of tubular lumen into cell -> pumped into interstitial fluid then into capillary
Potassium channels on luminal side so potassium excreted
Aldosterone acts here
Results in sodium conservation and potassium loss

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4
Q

What is the role of intercalated A cells in the distal convoluted tubule/cortical collecting duct?

A

Involved when body in ACIDOSIS.
CO2 from blood diffuses into cell - combines with water using carbonic anhydrase to make carbonic acid (H2CO3). Immediately splits to make H+ and HCO3-.
H+ excreted from cell into tubular lumen via H+/K+ transporter and H+ transporter (both need ATP).
HCO3- moves out of cell and into blood - BUFFER. Moves via HCO3-/Cl- transporter (counter transporter). Cl- then diffuses across cell into tubular lumen.

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5
Q

What is the role of intercalated type B cells in distal part of DCT/cortical collecting duct?

A

BASIC - in alkaline conditions
CO2 diffuses into blood, binds with H20 and carbonic anhydrase catalyses reaction to make H2CO3 (carbonic acid). Splits into H+ and HCO3-.
HCO3- out of cell into tubular lumen via Cl-/HCO3- cotransporter called PENDRIN.
H+ into interstitial fluid via H+/K+ pump and H+ pump (both need ATP). K+ diffuses over cell into tubular fluid.

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6
Q

What are the 3 layers of the basement membrane of the glomerulus?

A

Fenestrated endothelium - contains many fenestrae which allow solutes and water to pass through
Basement membrane: mesh of collagen and proteoglycans allow stuff to pass, has a negative charge so does not allow proteins
Podocytes (epithelial cells): have projections called pedicels which form slit pores, have negative charge so don’t allow proteins etc through

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7
Q

What factors determine GFR?

A
  1. Pressures across glomerular capillary (starling’s forces - hydrostatic pressure in arteriole, hydrostatic pressure in bowman’s capsule, oncotic pressure in arteriole, oncotic pressure in bowman’s capsule (nb this is nearly always 0)).
    NET FILTRATION PRESSURE
  2. Glomerular kF (filtration coefficient). Takes into account conductivity and surface area.

GFR = Kf x net filtration pressure

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8
Q

What is the mechanism for bradykinin formation?
What is the effect of bradykinin on vessels?

A

Bradykinin formed from alpha-globulins in circulation.
Alpha globulins cleaved to kallidin then to bradykinin.

Globulin-> kallidin mediated by kalleikrin enzyme. Inactived kalleikrin normally in tissues, activated in tissue damage

Bradykinin causes increased capillary permeability

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9
Q

What is tubuloglomerular feedback?

A

Macula dense cells in first part of distal convoluted tubule detect changes in NaCl.
Decreased NaCl delivery to macula densa:
1. Stimulates renin release from juxtaglomerular apparatus (constriction of efferent arteriole) which increases glomerular hydrostatic pressure and therefore increases GFR
2. Decreases afferent arteriole resistance -> increases glomerular bloodflow -> increased hydrostatic pressure -> increased GFR

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10
Q

Where is ADH produced and secreted from?

A

ADH produced in magnocellular nerves (supraoptic nuclei predominantly, some paraventricular N) in hypothalamus. Stored in vesicles which move down axon and live in nerve ending -> nerve ending in posterior pituitary gland

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11
Q

What stimulates ADH secretion?

A
  1. Increased plasma osmolarity -> detected by osmoreceptors in anterior hypothalamus
  2. Baroreceptor and cardiopulmonary reflex to lesser extent
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12
Q

What is the vasa recta and what is its role?

A

Capillary network that goes from efferent arteriole in glomerulus down loop of Henle.
Helps produce countercurrent mechanism by preventing washout of solutes -> maintains these from being dissipated

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13
Q

What generates medullary hypertonicity?

A
  1. Na+ from NCCK pump in ascending loop of Henle -> pumped into medulla
  2. Ca2+ from ascending loop goes into medulla as some back flow of K+ from NCCK so causes +ve charge inside tubule -> Ca repelled
  3. Urea from collecting duct - collecting duct permeable to urea here, diffuses into medullary interstitium. Then diffuses back into loop of Henle -> urea recycling
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14
Q

What does ADH increase expression of?

A

Aquaporin 2 in collecting duct to increase water resorption

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15
Q

What is reabsorbed in proximal convoluted tubule?

A

65% filtered Na+
65% filtered H2O
100% of glucose (if filtered amount below renal threshold)
Cl-
Amino acids
Bicarb
K+

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16
Q

What is actively secreted in the proximal convoluted tubule?

A

H+ via Na+/H+ transporter
Organic acids
Bases
Drugs

17
Q

What is reabsorbed in the descending thin loop of Henle?

A

Just water - nothing else
Reabsorbed due to countercurrent - medullary hypertonicity
Via aquaporins

18
Q

What is reabsorbed in the ascending thick loop of Henle?

A

Whole of ascending loop impermeable to water
Na+/K+/2Cl via NCCK transporter
Also some Ca and Mg due to +ve charge after K+ back flow -> repelled
Also some HCo3

19
Q

What is reabsorbed in the distal convoluted tubule?

A

NaCl (5%) via NaCl cotransporter

20
Q

What is the mechanism and site of action of thiazide diuretics?

A

Block action of Na/Cl cotransporter in distal tubule

21
Q

What transporters are involved in reuptake of glucose in the PCT? What do they cotransport with?

A

SGLT2 in first part of PCT - approx 90% of glucose reabsorbed here.

SGLT1 in last part of PCT - approx 10% of glucose reabsorbed here.

Cotransport with sodium

22
Q

How is sodium reabsorbed from PCT?

A

Diffuses down a concentration gradient into tubular epithelial cell due to Na/K pump on basolateral side

Preferentially cotransport with glucose/amino acids in first part of PCT
Then with Cl- and Na/H+ pump

23
Q

What channels does potassium move through in the distal convoluted tubule and collecting duct?

A

ROMK (renal outer medullary potassium channels)
BK (big potassium channels)

24
Q

How does high tubular flow rate result in increased potassium secretion?

A

Increased tubular flow rate decreases concentration of K+ in tubule = greater osmotic gradient
Increased tubular flow rate also increases expression of BK channels

25
How does acute acidosis lead to decreased potassium secretion?
Primarily via inhibiting sodium/potassium pump - H+ ions inhibit pump = less K+ into cell to be excreted
26
What percentage of calcium is reabsorbed in the proximal tubule and how? Is this PTH dependent?
65% (similar to sodium) NOT mediated by PTH 80% moves paracellularly 20% due to Na/Ca counter transporter on basolateral membrane (3Na in, Ca out) and Ca-ATP pump.
27
Where does PTH act on the kidney?
Thick ascending limb of loop of Henle Distal tubule
28
How does PTH cause calcium reabsorption in the ascending loop of Henle/distal tubule?
Calcium binds to receptor on basolateral membrane - causes expression of PKA which phosphorylates calcium channels on luminal membrane = more reabsorption.
29
Where is ANP released from and in response to what?
From cardiac atrial muscle fibres Released in response to STRETCH eg increased volume
30
What are the actions of ANP?
ANP acts on kidneys to suppress renin secretion, reduce sodium reabsorption in collecting ducts, slightly increases GFR Overall action = increased sodium and water excretion
31