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Anatomical Sciences > Kidney > Flashcards

Kidney Flashcards

1
Q

roughly how many nephrons do humans have

A

1 million

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2
Q

which is most outermost; the medulla or the cortex?

A

cortex

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3
Q

average osmolarity in the PCT

A

300-400mOsm

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4
Q

average osmolarity at the bottom of the loop of henle

A

1000-1200mOsm

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5
Q

average osmolarity of the thick ascending loop of henle

A

100-200mOsm

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6
Q

how many litres of water are filtered a day

A

180 litres

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7
Q

how many litres of water are excreted a day

A

1.5 litres

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8
Q

name the three layers in the filtration membrane of the bowmans capsule

A

endothelial with fenestrations
gel-like basement membrane
slit diaphragms with filtration slits between the podocytes

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9
Q

symptoms of nephrOtic syndrome

A

high prOtein
Oedema
lOw albumin
hyperlipidemia (increased triglycerides and chOlesterOl)

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10
Q

symptoms of nephrItic syndrome

A

mild levels of protein in urine
hematuria
hypertension
blurred vision

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11
Q

post streptococcal glomerulonephritis is caused by?

A

autoimmune reaction 10-14 days after infection caused by streptococcus
immune complexes deposit at glomerular membrane leading to damaged filtration barrier –> loss of protein/albumin in urine

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12
Q

symptoms of post streptococcal glomerulonephritis

A 
hematuria
loss of protein in urine
decreased blood-albumin
oedema 
(pretty similar to nephrOtic syndrome)
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13
Q

how to diagnose streptococcal glomerulonephritis?

A

biopsy –> nothing is linear

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14
Q

how to treat strep glomerulonephritis?

A

no specific treatment - just relieving symptoms
antibiotics used to kill strep
blood pressure meds and diuretics to control swelling and high blood pressure
corticosteroids NOT effective
limit salt diet

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15
Q

what percent of plasma is filtered into the bowman space and PCT

A

20%

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16
Q

what are diuretics

A

drugs that increase urine output

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17
Q

what are diuretics used to treat

A

oedema
congestive heart failure
hypertension

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18
Q

how does mannitol work

A

increases plasma osmolarity
increases osmotic pressure in glomerular filtrate
decreases h20 reabsorption from nephron
draws fluids from tissues - not brain or eye

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19
Q

what conditions would mannitol be used to treat

A

forced diuresis - poisonings
glaucoma
cerebral oedema
must be slow filtration to avoid dehydration

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20
Q

what percent of sodium is reabsorbed in the PCT

A

65-70%

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21
Q

how does sodium leave the nephron tubular lumen into the proximal tubule epithelial cell

A

co-transport with glucose/amino acids

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22
Q

how does sodium leave the proximal tubule epithelial cell to the blood capillary

A

3Na+ - 2K+ antiport

sodium out and potassium in

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23
Q

what is SGLT2

A

sodium/glucose cotransporter

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24
Q

which is more common, SGLT1 or 2

A

SGLT2 (>90%)

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25
Q

how does SGLT2 work

A

it pumps both sodium and glucose out of the nephron tubular lumen and into the proximal tubule epithelial cell

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26
Q

how does glucose leave the proximal tubule epithelial cell into the blood capillary

A

via facilitated diffusion

27
Q

what do SGLT2 inhibitors treat and how do they work

A

treat diabetes

by preventing glucose reuptake

28
Q

what does acetazolamide do? (Carbonic anhydrase diuretic)

A

suppresses H+ production so reduces Na+ - H+ exchange so less Na+ reabsorption
causes mildly alkaline urine and metabolic acidosis
effect is self limiting

29
Q

loop of henle TAL - impermeable or permeable to water?

A

impermeable

30
Q

what percent of sodium from original filtrate is reabsorbed in the TAL

A

25%

31
Q

is the TAL thick or thin?

A

thick

32
Q

describe the countercurrent multiplication in the loop of henle

A
  • NaCl actively pumped out of TAL until the ascending limb is 200mOsm
  • descending limb is permeable to salt and water so both move back into the loop of henle
  • salt and water move up the TAL and salts are pumped out again
  • this continues making the salt trapped in the lower medullary interstitum and loop of henle
33
Q

where do loop diuretics operate

A

in the ascending limb of the loop of henle

34
Q

what do loop diuretics target

A

Na+/2Cl-/K+ co transporter

35
Q

loop diuretics cause what percent of sodium to be excreted

A

15-25%

36
Q

what percent of sodium is reabsorbed in the DCT

A

5%

37
Q

how do thiazides work

A

block Na+/Cl- co transporter resulting in high osmolarity of urine and decreased water reabsorption
effect is self limiting

38
Q

where do thiazides work

A

DCT

39
Q

how are thiazides self limiting

A

lower blood volume –> renin secretion –> angiotensin formation and aldosterone secretion –> limitation of the effect of thiazides

40
Q

what percent of sodium is reabsorbed in the collecting duct

A

1-2%

41
Q

control of water excretion in the collecting duct is regulated by……?

A

ADH

42
Q

what happens to the walls of the distal nephron in the absence of ADH

A

they are impermeable to water

43
Q

what is the effect of ADH

A

increases water permeability of the cortical and medullary collecting ducts

44
Q

where is ADH produced

A

hypothalamus

45
Q

where is ADH stored

A

posterior pituitary

46
Q

what receptors does ADH bind to

A

V2 receptors on the apical cell membranes of the principal cells

47
Q

what does ADH stimulate the insertion of

A

aquaporins

48
Q

what triggers the release of ADH

A

increase in osmolarity is detected by osmoreceptors which shrink leading to increased frequency of nerve impulses to the posterior pituitary gland leading to the secretion of ADH from nerve terminals

49
Q

what condition does reduced effectiveness of ADH cause

A

diabetes insipidus

50
Q

Symptoms of diabetes insipidus

A

excretion of large volumes of dilute urine

thirst

51
Q

what is pituitary (central) diabetes insipidus

A

head

  • no/reduced release of ADH from pituitary gland
  • can be successfully treated by self-administered nasal spray providing ADH replacement therapy
52
Q

what is nephrogenic (peripheral) diabetes insipidus

A

kidney

  • unresponsive to circulatory ADH (lack of V2 receptors in collecting duct)
  • genetic - disrupts ability to synthesise aquaporins
53
Q

what is the mode of action of ENaC blockers

A

K+ sparing diuretics
directly block epithelial Na+ channel (eNaC) in DCT, collecting tubules and ducts
used in conjunction with loop and thaizide duiretics to maintain K+ balance

54
Q

what is the mode of action of spironolactone

A

aldosterone antagonist

55
Q

action of aldosterone on Na+ reabsorption

A

early phase: increases opening of ENaC

late phase: promotes DNA transcription, increases synthesis of ENaC and Na+,K+-ATPase

56
Q

where in the kidney is renin secreted from

A

juxtaglomerular cells in afferent/efferent arterioles

57
Q

sympathetic nervous system stimulation increases because of falling blood pressure due to……..

A

baroreceptors in periphery

intrarenal baroreceptors innervating the juxtamedullary nephron

58
Q

renin inhibitor inhibits what converting to what

A

angiotensinogen to angiotensin 1

59
Q

ACE inhibitor inhibits what converting to what

A

angiotensin 1 to 2

60
Q

kidney helps the formation of the active form of which vitamin

A

vitamin D

61
Q

what does vitamin D deficiency result in

A

weak bones in children and adults

62
Q

what does EPO do in the blood stream

A

binds with receptors in the bone marrow stimulating red blood cell production

63
Q

how is EPO synthesised

A
  • reduced oxygen delivery to renal cortex (due to anaemia, altitude, CO poisoning, respiratory disease)
  • HIF
  • EPO release stimulates bone marrow progenitor cells –> erythrocytes
64
Q

the kidney accounts for ____% of EPO production in adults

A

80%

Anatomical Sciences (6 decks)

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