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Renal > Manipulating Renal Physiology > Flashcards

Manipulating Renal Physiology Flashcards

1
Q

What haem problem may occour 2ndry to kidney damage?

A

Anaemia d/t lack of EPO

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2
Q

Functional unit of the kidney?

A

Nephron

  • glomerulus, bow mans
  • PCT
  • loop of henle (descending , ascending thin AND thick ascending) and vasa recta
  • distal tubule
  • connecting tubule, collecting tubule (cortical and medullary portions) collecting duct
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3
Q

Outline set up of the glomerulus

A
  • 2 set sof capillaries in series (afferent and eggerent arteriole either side of 1st capillary bed)
  • high pressure glomerular capillaries
  • glomerular basement membrane
  • podocytes of visceral epithelium (slit pores)
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4
Q

functions of the PCT

A
  • returns 70% filtered load to plasma
  • non-selective reabsorption
  • SODIUM cotransport (glucose, aas, hydrogen ions (bicarb reabsorption) phosphate (PTH and FGF regulated) chloride flux, water follows passive)
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5
Q

How does the Loop of Henley function? What is its purpose and what is the fluid leaving the loop like?

A
  • counter current (salt and creatinine)
  • descending loop impermeable to SALT, ascending loop impermeable to WATER
  • thick ascending limb active transport Na, K, Cl out of tubule (no water)
  • vasa recta (glomerular tubular feedback)
  • HYPOtonic fluid leaves loop of henle, enters distal tubule
  • animals with more concentrated urine have longer loops
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6
Q

Where is the Macula densa situated and what is its function|?

A
  • in distal convoluted tubule
  • passes right next to afferent arteriolar, senses chloride passing per unit time to signal glomerulus and regulate GFR
  • glomerular tubular feedback
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7
Q

Blood supply throug kidney

A

Afferent Arteriole, glomerulus, efferent Arteriole, tubular

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8
Q

Renin secreted by what?

A

Modified smooth muscle, afferent Arteriole

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9
Q

What stimulates renin secretion?

A
  • reduced stretch
  • signals from macula densa (if ^ flow, v renin, ^ adenosine to constrict arterioles)
  • sympathetic nerves
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10
Q

Actions of renin ?

A

Cleaves ATsinogen -> AT1, cleaved by ACE -> AT2

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11
Q

Effects of AT2?

A

^ BP

  • constricts efferent aa
  • enhances Na and water absorption (PCT)
  • stimulates aldosterone secretion (encourages salt conservation)
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12
Q

What effects will ACE inhibitors (benazepril) or Ang2 R blockers (telmisartan) have in the kidney?

A
  • Inhibits RAAS but only if this system has been activated anyway
  • ie. could v GFR -> ^ creatinine if dehydrated or over-diuresed
  • if normal healthy little effect on kidney
  • useful in CKD to v hyperfiltration (stop lossof important things through kidney) -> expect creatinine to rise slightly but not excessively (shouldn’t make animal ill)
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13
Q

Where is the site of action of aldosterone?

A

Distal tubule (regulation of sodium resorption and therefore potassium excretion)

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14
Q

What does aldosterone stimulate?

A
  • more Na channels inserted and sodium pumps
  • more K channels inserted
  • Distal tubule site of fine control of acid base balance (regenerating bicarbonate used as buffer, carbonic anhydrase needed)
  • H+ ions secreted by protion pump and buffered in urine by phosphate (net bicarb reclaimed)
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15
Q

What effect may inhibiting the aldosterone system have?

A
  • ^ blood potassium
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16
Q

Where does PTH act? What does it do?

A

Regulates resorption of Ca in distal tubule ensuring right amount excreted
PTHs actions on phosphate reabsorption occour in proximal tubule

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17
Q

Effects of ADH? Where does it act?

A

Inserts more Water channels and ^ urea permeability

  • acts on connecting tubule, collecting tubule and collecting duct
  • as duct passes through concentrated medulla, water reabsorbed if ADH present and urine concentrated
  • urea recycled to be used as concentration gradient
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18
Q

Why may Urea and creatinine levels change independently?

A

(Urea will be maintained to help concentrate urine so will rise disproportionate to creatinine which is excreted proportionally to GFR)

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19
Q

What effects creatinine and urea level

A

Urea meat consumed

Creatinine muscle mass

20
Q

Connecting tubule, collecting tubule and duct

A
  • sensitive to ADH (covered on another slide)
21
Q

Principles of mechanism of diuretic function

A
  • most direct action on nephron (later sections not really bowmans)
  • inhibit sodium chloride reabsorption to increase salt and water excretion
  • counter act salt and water retention in heart failure
  • activate renin secretion
22
Q

Functions of the kidney

A
  • excretion nitrogenous waste
  • regulation water, electrolyte, minerals and acid base
  • production activation hormone s (calcitriol, active vit D3, epo) q
23
Q

What site of action would you give ACE inhibitors as diuretics?

A

PCT

24
Q

Where do loop diuretics act?

A

on ascending LOH from tubule side

25
Q

What type of drugs are loop diuretics and how do they reach their site of action?

A
  • highly plasma protein bound so must reach site of action by active secretion in PCT
26
Q

Which are the most efficacious diuretic class?

A

Loop diuretics (25% filtered load can be lost)

27
Q

What other actions do loop diuretics have?

A
  • pulmonary venodilator action if given IV (so good if animal drowning in pulmonary oedema)
  • ^ renal flow rate (hence GFR) ^ Ca loss so used for hypercalceamia
28
Q

Most commonly used loop diuretic?

A

Furosemide

29
Q

How long does furosemide take for onset, when is peak action and duration?

A
  • IV: 5 min, peak effect 30mins, duration 2hrs

- oral: 1 hr, peak effect 2 hrs, duration 6hrs

30
Q

Where do thiazide diuretics act? How do they work?

A
  • early DCT

- bind Cl- bit of NaCl transporter

31
Q

How efficacious are thiazides?

A
  • PROMOTE 10% LOSS of filtered load (less efficacious than loop diuretcis)
32
Q

What side effects may thiazides have?

A

Promote calcium retention in humans (don’t know wh)

- anti-hypertensive effects including vascular action

33
Q

Egs of thiazides used in dogs?

A
  • chlorothiazide

- hydrochlorothiazide

34
Q

What is the bioavailability of thiazides? Time of onset, peak activity and duration of action?

A
  • orally active
  • onset within 1hr
  • peak @ 4hrs
  • duration 6-12hrs
35
Q

How do potassium sparing diuretics work? Are they powerful diuretics?

A
  • act on collecting tubule, inhibit action of aldosterone

- weak on their own, work syndergistically with other diuretcis, used mainly to prevent K loss

36
Q

Egs of potassium sparing diuretics? How do these work?

A
  • Spironolactone competitive antagonist of aldosterone

- Triamterene and amiloride non-competitive inhibitors (block Na channels)

37
Q

Potential adverse effects of K+ sparing diuretics? Which type of diuretic is most likely to cause this?

A

> Hyperkalaemia

  • esp. non-competitive inhibitors
  • competitive (ie spironolactone) will eventually be overcome by ^ levels aldosterone if K+ needs to be excreted, but non-compeotive wont
38
Q

What other effects does spironolactone have?

A
  • death from progressive HF and sudden cardiac causes decreased (not sure of this mechanism??)
  • minimal side effects
39
Q

Explain beneficial effects of aldosterone R antagonists to the heart failure patient FURTHER READING

A

-

40
Q

General adverse effects of diuretics

A
  • volume v and circulatory impairment

- synergistic with vasodilators that reduce pre-load

41
Q

How can adverse effects of diuretics be overcome?

A
  • ID cases that are PRELOAD depenedant
  • monitor HR, BP, muscle strength
  • reduce dose when congestion resolved
  • Hypokalaemia (furosemide)
  • Hypomagnesaemia (Thiazides)
  • Hyperkalaemia (K sparing diuretics)
  • HYPONATRAEMIA - very poor prognosis if seen, can occour with all diuretics, indicates refractory HF d/t inappropriate ADH secretion
  • hypochloraemic metabolic alkalosis (furosemide and thiazide)
42
Q

What causes hypokalaemia and hypomagnesaemia and why are these important for HF patients?

A
  • caused by hyperaldosteronism

- exacerbate ventricular arryhythmias and digoxin toxicity

43
Q

How do NSAIDs affect renal activity?

A
  • Renal PGs are natriuretic (salt losing)
  • NSAIDs -> exacerbated salt and water retention in HF (reduces diuretic efficacy)
  • COX1 and COX2 equally
44
Q

How may the pharmacokinetics of diuretics be affected?

A
  • onset of action faster with IV
  • duration of action shorter with IV
  • bioavailability poorer with RSHF
45
Q

Which combinations of diuretics are synergistic?

A
  • Loop + thiazide
  • Loop/thiazide + K sparing
  • Vasodilator + diuretic
46
Q

What do effective diuretics promote ?

A

K+ and Mg2+ loss by activating RAAS

47
Q

What is torasemide?

A

More potent form of furosemide

Renal (23 decks)

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