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My Renal > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What do diuretics do?

A

increase urine flow by inhibiting reabsorption of electrolytes and enchanting excretion of salt and water

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2
Q

What are some causes of oedema?

A

nephrotic syndrome
congestive heart failure
hepatic cirrhosis with ascites

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3
Q

What is the pathway for the formation of oedema?

A
  • low capillary oncotic pressure
  • high formation of interstitial fluid
  • low blood vol and low CO
  • activation of RAAS
  • Na and H2O retention
  • high hydrostatic pressure and low oncotic pressure
  • oedema
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4
Q

What is the mechanism for congestive HF causing oedema?

A
  • low CO and renal hypoperfusion
  • RAAS activated
  • increased venous and capillary pressure and low oncotic pressure
  • pulmonary and peripheral oedema
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5
Q

How does hepatic cirrhosis with ascites cause oedema?

A
  • high pressure in hepatic portal vein
  • lower production of albumin so loss of fluid into peritoneal cavity and oedema
  • activation fo RAAS due to low circulating volume
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6
Q

What diuretics work in the PCT?

A

carbonic anhydrase inhibitors

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7
Q

What drug work in the thick ascending loop of Henle?

A

loop diuretics

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8
Q

What drugs work in the early DCT?

A

carbonic anhydrase inhibitors and thiazide diuretics

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9
Q

What drugs work in the collecting tubule and duct?

A

potassium-sparing diuretics

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10
Q

How do the diuretics enter filtrate?

A

most work at apical membrane so must enter the filtrate by glomerular filtration or secretion via OATs (acidic drugs eg thiazides and loop) and OCTs (basic drugs) in PCT

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11
Q

How do loop diuretics work?

A
  • inhibit Na+/K+/2Cl- transporter by binding to the Cl- site and v potently cause Na to not be reabsorbed as well
  • also causes Ca2+Mg2+ excretion
  • venodilator
  • eg furosemide
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12
Q

What are loop diuretics used for?

A
  • acute pulmonary oedema
  • chronic HF
  • chronic KF
  • hepatic cirrhosis with ascites
  • nephrotic syndrome
  • HTN
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13
Q

What are the adverse effects of loop diuretics?

A

low electrolyes
low blood volume
low blood pressure

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14
Q

How do thiazide diuretics work?

A
  • inhibit Na+Cl- carrier by binding to Cl- site so increased load of Na+ delivered to collecting tubule so it is less diluted
  • increases reabsorption of Ca2+
  • not as potent
  • vasodilators
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15
Q

What are thiazide diuretics used for?

A 
mild HF
hypertension
severe oedema
renal stones
nephrogenic DI
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16
Q

What do loop and thiazide diuretics both cause?

A

potassium loss (complicated mechanism)

17
Q

What do potassium sparing diuretics do?

A
  • block apical sodium channel and decrease Na+ reabsorption eg amiloride
  • compete with aldosterone eg spironolactone
18
Q

What action does spironolactone have?

A

increases Na+ excretion and decreases K+ excretion

19
Q

Why are potassium sparing diuretics used with loop/thiazide?

A

they increase the power of them but alone cause hyperkalaemia

20
Q

What are potassium sparing diuretics used for?

A

HF
Conn’s
resistant essential HTN
secondary hyperaldosteronism

21
Q

What are the features of osmotic diuretics?

A
  • IV and in filtrate to increase osmolarity so less water reabsorbed
  • work at PCT and decrease Na+ reabsorption
22
Q

What are osmotic diuretics used for?

A

to prevent acute hypovolaemic renal failure to maintain urine flow and urgently treat increased ICP and IOP

23
Q

What do carbonic anhydrase inhibitors do?

A

increase excretion fo HCO3- with Na, K and H2O

used in glaucoma, altitude sickness prophylaxis and infantile epilepsy

24
Q

What does aldosterone from renal cortex do?

A

enhanced tubular Na+ reabsorption and salt retention

25
Q

What does vasopressin from the posterior pituitary do?

A

enhanced H2O reabsorption

26
Q

What is nephrogenic DI?

A

inability of the nephron to respond to vasopressin

27
Q

What are aquaretics/vaptans?

A
  • competitive antagonists of ADH receptors to excrete water without Na+ so increased Na conc in plasma
  • used in siADH
28
Q

What are prostaglandins?

A
  • vasodilators of afferent arteriole

- made in response to ischaemia, mechanical trauma, angiotensin 2, ADH and bradykinin

29
Q

What do prostaglandins do?

A

vasodilator afferent arteriole, release renin so increased levels of angiotensin 2 which vasoconstricts efferent arteriole to filtration pressure increases

30
Q

What are uricosuric agents?

A

treat gout by blocking reabsorption of urate in PCT

31
Q

When are adverse drug reactions common?

A

elderly who take many drugs

drugs with narrow therapeutic index eg digoxin, vanc, gent and warfarin

32
Q

What is Type A ADR?

A

augmented pharmacological effect

  • dose dependent and predictable
  • mechanisms can be renal, pre renal or post renal
33
Q

What is Type B ADR?

A

bizarre effects

  • dose independent and predictable
  • high mortality eg hepatic necrosis or drug rashes
34
Q

What is Type C ADR?

A

chronic

- prolonged therapy eg steroids NSAIDs or BB

35
Q

What is Type D ADR?

A

delayed

- years after medications eg teratogenic or carcinogenic

36
Q

What is Type E ADR?

A

end of treatment

- abrupt withdrawal or rebound eg steroids or BB

37
Q

What is Type F ADR?

A

failure of therapy

My Renal (8 decks)

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