pharmacology Flashcards

1
Q

how do diuretics increase urine outflow

A

by inhibiting the resorption of electrolytes at various sites in the nephron

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2
Q

when do diuretics enhance secretion of salt and water

A

in an increase of interstitial fluid causing tissue swelling

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3
Q

what conditions causes oedema

A
  • nephrotic syndrome
  • congestive heart failure
  • hepatic cirrhosis with ascites
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4
Q

how do diuretics enter the filtrate

A

by either:

  • glomerular filtration
  • secretion via transport process in the proximal tubule
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5
Q

what are the two transport systems

A
  • the organic anion transporters

- the organic cation transporters

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6
Q

what do organic anion transporters transport

A

acidic drugs

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7
Q

what do organic cation transporters transport

A

basic drugs

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8
Q

where do organic anions enter the cell

A

the basolateral membrane

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9
Q

where do organic anions enter the lumen

A

apical membrane

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10
Q

where do organic cations enter the cell

A

basolateral membrane

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11
Q

where do organic cations enter the lumen

A

at the apical membrane

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12
Q

what do loop diuretics do

A

inhibit the Na/K/2Cl transporter by binding to the Cl site

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13
Q

where are loop diuretics absorbed

A

in the GI tract

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14
Q

clinical indications of loop diuretics

A

to reduce salt and water overload associated with:

  • chronic heart failure
  • chronic kidney failure
  • hepatic cirrhosis with ascites
  • nephrotic syndrome

to increase urine volume in acute kidney failure
to treat hypertension
to reduce acute hypercalcaemia

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15
Q

contraindications of loop diuretics

A
  • severe hypovolaemia or dehydration
  • severe hypokalaemia and/or hyponatraemia
  • hepatic encephalopathy
  • gout
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16
Q

side effects of loop diuretics

A
  • causing low electrolyte states
  • hypovolaemia and hypotension
  • hyperuricaemia
  • dose-related loss of hearing
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17
Q

what do thiazide diuretics do

A

inhibit the Na/Cl carrier by binding to the Cl site

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18
Q

which mechanism do thiazide diuretics enter the nephron by

A

the OAT mechanism

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19
Q

clinical indications for thiazide diuretics

A
  • mild heart failure
  • hypertension
  • severe resistent oedema
  • renal stones
  • nephrogenic diabetes insipidus
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20
Q

contraindications for thiazide diuretics

A
  • hypokalaemia
  • hyponatraemia
  • gout
21
Q

adverse effects of thiazide diuretics

A
  • hypokalaemia
  • metabolic acidosis
  • hypovolaemia and hypotension
  • hypomagneasmia
  • hyperuricaemia
  • erectile dysfunction
  • impaired glucose tolerance
22
Q

what type of drugs are amiloride, triamterene, spironolactone and eplerenone

A

potassium sparing diuretics

23
Q

what do amiloride and triamterene do

A

block the apical sodium channel and decrease sodium reabsorption

24
Q

what do spironolactone and eplerenone do

A

compete with aldosterone for binding to intracellular receptors

25
what happens if potassium sparing diuretics are given alone
they cause hyperkalaemia
26
what are aldosterone antagonists used for (spironolactone)
- heart failure - primary hyperaldosteronism - resistant essential hypertension - secondary hyperaldosteronism
27
contraindications of potassium sparing diuretics
- severe renal impairment - hyperkalaemia - addisons disease
28
what do osmotic diuretics do
increase the osmolality of the filtrate, opposing the absorption of water in parts of the nephron that are freely permeable to water
29
where is the major site of action of osmotic diuretics
the proximal tubule
30
clinical uses of osmotic diuretics
- prevention of acute hypovolaemia renal failure to maintain urine flow - urgent treatment of acutely raised intracranial and intraocular pressure
31
adverse effects of osmotic diuretics
transient expansion of blood volume and hyponatraemia
32
what do carbonic anhydrase inhibitors do
increase excretion of HCO3 with Na, K and H2O, alkalinising the urine
33
what are carbonic anhydrase inhibitors used for
- glaucoma and following eye surgery - prophylaxis of altitude sickness - infantile epilepsy
34
what can alkalinising the urine be useful in
- relief of dysuria - prevention of crystallization of weak acids - enhancing the excretion of weak acids
35
what happens at the kidneys when aldosterone is secreted from the adrenal cortex
enhanced tubular sodium reabsorption and salt retention
36
what happens at the kidneys when vasopressin is secreted from the posterior pituitary
enhanced water reabsorption
37
what causes neurogenic diabetes insipidus
lack of vasopressin secretion from the posterior pituitary
38
what causes nephrogenic diabetes insipidus
inability of the nephron to respond to vasopressin
39
what can the act of vasopressin on the kidney be inhibited by
- lithium - demeclocycline - vaptans
40
what is Tolvaptan used in
SIADH to correct hyponatraemia
41
where is SGLT1 found
kidneys and intestine
42
where is SGLT2 found
proximal tubule of the kidneys
43
what does inhibition of SGLT2 result in
glucosuria
44
what do SGLT2 inhibitors cause
- excretion of glucose - decreases in HbA1c - weight loss
45
what prostaglandins are synthesised by the kidneys
PGE2 | PGI2
46
how do prostaglandins affect GFR
- a direct vasodilator effect upon the afferent arteriole - releasing renin leading to increased levels of angiotensin II that vasoconstricts the efferent arteriole - filtration pressure increases
47
what is the 'triple whammy' (three drugs that combined could have detrimental effects)
ACEI (or ARB), diuretic and NSAID
48
what do uricosuric agents do
used in treatment of gout by blocking reabsorption of urate in the proximal tubule
49
side effect of diuretics
gout