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renal > physiology and Ix > Flashcards

physiology and Ix Flashcards

1
Q

JG cells - where and what signals do they receive?

A

around afferent arteriole
1. mechanoreceptors -> stimulated when low BP
2. chemoreceptor: have SNS innervation from aortic arch > stimulated adrenergically with low BP
3. PGE2 from macula densa

–> to secrete renin

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2
Q

macula densa cells - where and what do they do?

A

part of DCT wall
if GFR low > low SODIUM (i.e. a chemoreceptor) > send signal to JG cells via PGE2

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3
Q

describe RAAS pathway

A

renin cleaves angiotensinogen to leave ACEI
Angiotensin I converted to angiotensin II by ACE (found on endothelial cells, esp in lungs)
ang II binds to its receptors in smooth muscle cells, inc at kidneys
— efferent more responsive than afferent

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4
Q

paradox of low ang II vs high ang II action on GFR

A

low ang II - only efferent arteriole constricts –> inc GFR
high ang II - both afferent and efferent constrict –> low renal blood flow, therefore, low GFR

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5
Q

actions of Ang II

A

PCT: inc Na absorption > inc H2O
hypothal: inc ADH > inc H2O
glom: constricts eff > aff arterioles
increased thirst
adrenals: zona glomerulosa > aldosterone (MC) > inc Na/K ATPase expression

other arterioles: inc TPR

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6
Q

how can inc RAAS activity cause hypokalaemia?

A

aldosterone > inc Na/K ATPase > inc Na absorption, inc K excretion

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7
Q

how many nephrons per kidney at birth?

A

1mil per kidney

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8
Q

what is the rate limiting step of the RAAS?

A

the JG production of renin

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9
Q

ACEI vs ARB

A

ACEI = ‘prils’ = inc BK > cough, angioedema risk
ARB = ‘sartan’ = no dry cough

both - need low K diet, not in pregnancy

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10
Q

actions of aldosterone

A

Stimulates Na/K/ATPase pump on basolateral side of cortical collecting tubule AND increases sodium permeability on luminal side of the membrane (activates ENAC)

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11
Q

ANP - what triggers its release, and what does it do?

A

from atria in response to atrial stretch > main job: lower BP

Acts to:
i.Dilates afferent + constricts efferents = ↑ GFR > diuresis
ii. Inhibits aldosterone + renin secretion
iii. Inhibits Na Cl reabsorption in CD
iv. Inhibits ADH action on kidney

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12
Q

what does PGE2 do for renal blood flow?

A

released to dilate afferent arteriole and inc BF

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13
Q

how do NSAIDs affect the kidney?

A

inhibit PG production > less dilation of afferent arteriole > reduced GFR

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14
Q

what happens in renal artery stenosis?

A

renal artery stenosed > reduced afferent arteriolar flow
so kidney increases BP > systemic HTN and renal atrophy from low flow

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15
Q

how do caffeine and alcohol act to increases diuresis?

A

caffeine - dilates afferent arteriole > plasma too quick
alcohol - inhibits ADH

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16
Q

when does renal growth and GFR cease?

A

GFR increases until renal growth ceases (18-20 years)

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17
Q

When does GFR reach adult values?

A

GFR >100 by 12/24mo

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18
Q

filtration through BM depends on what 3 factors?

A
  • charge (neg will bounce)
  • size <3mm
  • binding to proteins - e.g. Ca and FFA bound to plasma proteins
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19
Q

what is the triple whammy and how does it affect the kidney?

A

ACE-I = Dilates the efferent arteriole reducing the GFR
NSAID = Prevents PG mediated vasodilation of the afferent arteriole to maintain GFR; thereby further reducing GFR
Diuretics = reduce plasma volume and GFR

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20
Q

How do the following move through the PCT?
Na
HCO3
urea
water
glucose

A

Sodium:
1) cotransporters e.g. Na-glucose on apical
2) Na/K ATPase on basolateral keeps gradient
3) Na /H exchanger
4) paracellular route via leaky tight junctions

HCO3:
H and HCO3 = H2CO3 with CA => CO2+H2O => both diffuse into the cell, then another type of CA puts them back together = H2CO3 => H and HCO3 again

urea and water = diffusion

glucose:
Na-glu cotransporter on apical > GLUT1/2 on basolateral

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21
Q

What happens at the loop of Henle?

A

countercurrent multiplication:

Thin descending limb
- inc concentration from passive absorption of water (via aquaporins) up to 1200osm in medulla at the end

Thin ascending limb
- no aquaporins, water doesn’t move
- has Na and Cl channels -> start moving out

Thick ascending limb (cuboidal epithelium)
- Active reabsorption of 15-25% of filtered Na+/K+/Cl- via the cotransporter!
- Secondary resorption of Ca2+ and Mg2+
- impermeable to water as well - no aquaporins

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22
Q

what gets excreted in the PCT?

A

ammonia
organic acids e.g. penicillins

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23
Q

what is 100% absorbed in the PCT?

A

glucose and amino acids

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24
Q

How and where do these diuretics act:
- carbonic anhydrase inhibitors
- loop diuretics

A
  • loop diuretics in thick ascending limb on Cl portion of Na/K/Cl transporter&raquo_space; more Na and therefore H2O excreted
25
Q

what is absorbed in the DCT?

A

early DCT:
- active Na and Cl absorption 5% via co-transporter- Na is LOAD dependent absorption
- Ca2+ reabsorption under PTH control

late DCT:
ENAC at principal cells, Na in and K out
alpha intercalated cells - H ATPases to pump H into wee

and ADH -> aquaporins!

26
Q

how does PTH work at the DCT?

A

inc Ca channel on apical side, and Na/Cl transporter on basolateral side

27
Q

how does aldosterone act to increase Na reabsorption?

A

at DCT. increases ENAC, and Na/K ATPase on basolateral

28
Q

where is most Mg absorbed?

A

loop of Henle - 70-80%

29
Q

what do the beta-intercalated cells do cf the alpha cells, in the collecting duct?

A

beta = secrete bicarb, resorb H+ i.e. help in alkalosis
alpha = secrete H, resorb bicarb i.e. help in acidosis

30
Q

how does H+ excretion differ in the CD vs PCT?

A

CD have H/K ATPase so can pump it out againt large concentration gradient

31
Q

angiotensin vs aldosterone - where do they act to cause Na reabsorption?

A

angiotensin = PCT
aldosterone = DCT

32
Q

name some factors that cause K shift into a cell

A

insulin, aldosterone, beta adrenergic stimulation, alkalosis

33
Q

where is most Ca reabsorbed in the nephron, and how?

A

PCT, via paracellular

34
Q

what is the only electrolyte that is not mostly absorbed at the MCT?

A

Mg - mostly at loop of henle via paracelular action

35
Q

what is used as a buffer for H+ for excretion?

A
  1. ammonia
  2. PO4
36
Q

why is alkalosis associated with hyperkalaemia?

A

H/K transporter in DCT - they compete.

37
Q

quick summary of urea resorption

A

50% in PCT
other 30% via medullary CD - via urea transporters -> can be resorbed in thin descending loop

urea can circulate several times before excretion

38
Q

osmolality of ECF vs ICF determine by what?

A

Osmolality of ECF = Na
Osmolality of ICF = K

39
Q

aetiology of hyponatraemia

A
  1. hypovolaemia: GI losses, meds e.g. diuretics, cerebral salt wasting/renal wasting
  2. euvolaemia but ADH inappropriate:
    - dilute urine: adrenal insufficiency / drinking too much
    - concentrated urine: SIADH
  3. hypervolaemia: oedema > lower circulating volume > inc ADH: CCF, nephrotic syndrome, cirrhosis
40
Q

pseudohyponatraemia caused by?

A

inc lipids/protein causes lab instruments to report it incorrectly - normal Na and TBW

41
Q

how are serum osm, urine Na and urine osm helpful in hyponatraemia?

A

serum osm = if low, then its true hypoNa not pseudo
urine Na: high urine Na = renal /cerebral wasting/SIADH, low urine Na = hypovolaemia
urine osm: dilute or concentrated urine (>100mOsm/kg = SIADH)

42
Q

target rate of Na correction for hypoNa

A

8mmol/L in 24 hours OR

if seizures: no more than 2mmol/L per hour in first 3-4 hours (because risk of morbidity from delayed treatment is greater than the risk of osmotic demyelination from overly rapid correction)

43
Q

aetiology of hypernatraemia

A
  1. hypovolaemia
    - GI losses
    - skin losses
    - renal losses
    - diabetes insipidus
  2. sodium excess
    - hyperaldosteronism (primary vs secondary e.g. CCF/nephrotic syndrome, steroids)
    - iatrogenic - TPN, hypertonic saline
44
Q

signs of severe (>160) hypernatraemia

A

Altered mental status
Lethargy
Seizures
Hyperreflexia
Coma

45
Q

how does urine/serum osm help in hypernatraemia?

A

Urine osmolality < serum osmolality
Indicates urinary concentrating defect
central DI, nephrogenic DI, renal disease, osmotic diuresis

Urine osmolality > serum osmolality
Indicates intact urinary concentration
Causes: gastrointestinal losses, increased insensible losses eg burns, excess sodium intake

46
Q

target rate of Na change in hyperNa

A

rate of sodium correction should be slow, no more than 0.5 mmol/L/hour

47
Q

5 types of diuretics, order of potency

A

LOTCK:
Loop
Osmotic
Thiazide / thiazide like
CA inhibitors
Potassium sparing

48
Q

loop diuretics:
- examples
- site of action
- receptor of action
- main indications
- side effects

A
  • e.g. frusemide
  • thick ascending limb
  • Na/K/2Cl- transporter - on the Cl part
  • oedematous states
  • hypoCa / Mg / K, hypoK metabolic alkalosis, ototoxicity, (less gout than thiazides)
49
Q

thiazide/thiazide-like:
- examples
- site of action
- receptor of action
- main indications
- side effects

A
  • HCT or thiazide like (sulfonamide derivatives - indapamide, metolazone)
  • DCT
  • Na/Cl co-transporter
  • oedematous states
  • hypERcalcaemia, gout+++, hypoK metabolic alkalosis
50
Q

why do loop and thiazide diuretics cause hypokalaemia and metabolic alkalosis?

A

they increase sodium delivery to the distal segment of the distal tubule
this increases potassium loss (potentially causing hypokalemia) because the increase in distal tubular sodium concentration stimulates the aldosterone-sensitive sodium pump to increase sodium reabsorption in exchange for potassium and hydrogen ion, which are lost to the urine. The increased hydrogen ion loss can lead to metabolic alkalosis

51
Q

loop vs thiazide effects on Ca, and why

A

thiazides = hyperCa: reduced Na in cell causes Na/Ca exchanger on the other side to pump Na into cell and Ca into blood

loop: movement of K through the cell causes electrochemical gradient for Ca (and Mg absorption) -> so less K = less Ca

52
Q

K sparing diuretics:
- examples
- site of action
- receptor of action
- main indications
- side effects

A
  • collecting duct
  • Aldosterone antagonist = spiro = MC receptor
  • Na+ Channel Antagonist = Amiloride = ENAC
  • gynaecomastia, hyperK
53
Q

how does spiro cause hyperkal?

A

aldosterone usually acts to inc Na/K ATPase on basolateral and ENAC on apical
so less ENAC action means less Na driven Na/K action, so less K goes out&raquo_space; hyperkalaemia

54
Q

example of osmotic diuretic

A

mannitol

55
Q

CA inhibitors:
- examples
- site of action
- receptor of action
- main indications
- side effects

A

acetazolamide
PCT
CA enzyme: less action means less H produced to spit out on apical side, so less Na
paraesthesia, drowsiness

56
Q

Why does Cr overestimate GFR?

A

because a small amount is secreted - so will overestimate esp in renal disease

57
Q

what is the gold standard susbtance to measure GFR? the most accurate in a clinical setting?

A

inulin is gold standard, but research only
51Cr-EDTA/DTPA is most accurate in clinical setting

58
Q

ddx for bright, echogenic kidneys on neonatal USS - some examples

A

• Renal dysplasia
• ARPKD, ADPKD
• Glomerulocystic disease (HNF1b deletions)
• Beckwith-Wiedemann syndrome
• Congenital nephrotic syndrome
• Congenital infection

renal (6 decks)

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