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RB Y2 Renal > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

diuretic action of potassium sparing diuretics

A

These are weak diuretics on their own (the site on which they act accounts for 2% of total sodium reabsorption), they are used as compound preparations with thiazide or loop diuretics, which activate the RAAS system in response to natriuresis and hypovolaemia

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2
Q

clinical indications for potassium sparing diuretics

A
  • They potentiate the actions of thiazide and loop diuretics by blocking the effects of aldosterone
  • Used to treat primary/secondary hyperaldosteronism, which can cause refractory oedema
  • Used to counter K+ loss due to more potent diuretics
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3
Q

mechanism of action of spironolactone and eplerenone

A

compete with aldosterone to bind to its receptors

  • Decrease gene expression and reduced synthesis of a protein mediator that activates Na+ channels in the apical membrane
  • Decreased numbers of the Na/K/ATPase pumps in the basolateral membrane
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4
Q

mechanism of action of amiloride and triamterene

A

block the apical Sodium channel in the distal tubule that are controlled by aldosterone’s protein mediator and decrease Na reabsorption

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5
Q

is amiloride or triamterene more potent

A

amiloride - 10x

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6
Q

what is spironolactone metabolised inthe liver to

A

canrenone

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7
Q

adverse effects of spironolactone

A

hormonal disturbances: there is some blocking on androgen and progesterone receptors

  • gynaecomastia
  • impotence
  • menstrual irregularities

note eplerenone doesnt cause these

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8
Q

what must potassium sparing diuretics not be adminstered with

A

potassium supplements and ACEi/ARB - risk of hyperkalaemia

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9
Q

clinical used of K sparing diuretic

A
  • Heart failure – moderate to severe CHF
  • Secondary hyperaldosteronism, due to hepatic cirrhosis with ascites or nephrotic oedema
  • Primary hyperaldosteronism (Conn’s syndrome)
  • Resistant essential hypertension
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10
Q

where is the CA enzyme present

A

renal tubules, gastric mucosa, pancreas, eye brain and RBC

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11
Q

systemic CA inhibitor

A

acetazolamide

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12
Q

describe the action of CA inhibitors in the proximal tubule

A
  • increase the excretion of bicarbonate with Na, K and water by blocking CA
  • results in an alkaline diuresis, hypokalaemia and metabolci acidosis
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13
Q

what is the use of CA inhibitors in acute mountain sickness

A
  • prophylaxis and treatment
  • Prevents the respiratory alkalosis caused by inhibiting the formation of CO2
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14
Q

why would one want to alkalinze the urine

A

to excrete acidic drugs eg salicylates (poisoning) and barbituates

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15
Q

what drugs can be use to alklinize the urine

A

CA inhibitors

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16
Q

what are the adverse effetcs of using CA inhibitors to alkalinize the urine

A

can cause dysuria or UTI

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17
Q

how is mannitol given

A

10-20% solution IV - there is no oral form

18
Q

action of mannitol

A

Pharmacologically inert substances, that are filtered in the glomerulus but not reabsorbed by the nephron. To cause a diuresis they must constitute an appreciable fraction of the osmolality of the tubular fluid.

Within the nephron, their main effort is exerted on the parts of the nephron that are permeable to water: the proximal tubule, the descending limb of loop of Henle, and (in the presence of ADH) the collecting ducts. Passive water reabsorption is reduced by the presence of non-reabsorbable solute within the tubule – consequently a larger volume of fluid remains in the proximal tubule. This has the secondary effect of reducing Na+ reabsorption.

19
Q

what is the use of mannitol in raised ICP/IOP eg acute angle closure glaucoma

A
  • increased plasma osmolality by the addition of a solite that doesnt enter these compartments, water effluxes out down its concentration gradient
20
Q

what is the action of V2 receptor in the kidney

A
21
Q

what receptors does ADH bind to

A

V 1 2 and 3

22
Q

V1 receptor action

A
  • vasoconstriction of smooth muscles, particularly cardiac muscles
  • very high concentrations of ADH are needed for this to happen eg in severe hypovolemic states
23
Q

desmopressin

A
  • ADH analogue
  • longer durationof action and more potent
  • several routes available, including nasal spray
24
Q

second line ADH analogue

A

terlipressin

25
Q

clinical uses of ADH analogues

A
  • Neurogenic diabetes insipidus
    • Desmopressin
  • Nocturnal enuresis in children (>10 years)
    • Oral/intranasal desmopressin
  • Control variceal bleeding in portal hypertension – vasoconstrictory activity
    • Vasopressin infusion/Terlipressin
26
Q

vaptans

A

competitive antagonists of ADH receptors

27
Q

action of vaptans

A
  • Electrolyte free aquaresis
  • Reducing urine osmolality
  • Raise serum Sodium
28
Q

clinical indications for vaptans

A

conditions of excess ADH to correct hyponatraemia

  • SIADH
  • CHF
  • cirrhosis
29
Q

conivaptan

A

non selective V1/V2 antagonists

IV only

30
Q

what receptor is Tovlaptan selective to

A

V2

oral

31
Q

what effect do vaptans have on thirst

A

increase it

32
Q

formation of PG

A
  • PGs are formed from the fatty acid arachidonic acid (in membrane phospholipids) by COX 1 and 2
  • The PGs that are important in the kidneys are PGE1 ad PGI2.
33
Q

action of PG in the renal system

A
  • In the renal system, cause vasodilation and natriuresis. Are necessary to increase renal blood flow and GFR (in angiotensin induced vasoconstriction in volume depleted states).
  • PG synthesis is low under basal conditions, however when vasoconstrictors (e.g. angiotensin II and noradrenaline) are release, they cause compensatory vasodilation in the kidney.
  • Exert a diuretic effect – increased water, Sodium and potassium excretion
    • Increase potassium secretion mainly by stimulating secretion of renin and activating RAAS
    • Also acts as a counter-regulatory factor and decreases Sodium reabsorption via inhibition of triple co transporter in the thick ascending Loop of Henle
34
Q

triple whammy combination

A

do not give ACEi/ARB + diuretic + NSAID – detrimental to renal function, leading to sodium retention, oedema, blunted diuretic and antihypertensive effects of drug

35
Q

action of NSAIDs in heart failure etc

A
  • NSAIDs increase blood pressure in patients treated for hypertension by impairing PG mediated vasodilatation and salt excretion
  • They exacerbate salt and water retention in patients with heart failure
36
Q

digoxin mechanism

A
  • increases intracellular Ca stores: inhibiting NaK ATPase - increases intracellular Na and activates Na Ca exchanger. this increases the force of myocardial contraction
  • stimulates vagal nerve (acts via ACh) - acts on SA and AVN to slow heart rate and slow AVN conduction
37
Q

signs of digoxin toxicity

A

nausea, yellow vision, bradycardia, lethargic and tired, hypotension, vomiting, arrhythmia

38
Q

digoxin toxicity

A
  • has a very narrow therapeutic window
  • at toxic concentrations, causes ectopic beats which can lead to arrhythmias
  • bradycardia etc due to excessive CNX stimulation
39
Q

what effect does renal failure have on the excretion of drugs

A

those that are excreted renally will have a longer half life

40
Q

renal failure and digoxin toxicity

A
  • longer half life due to renal excretion
  • if patient is on diuretics these cause hypokalaemia, meaning that digoxin doesnt have to compete with K for binding at NaK ATPase so it is upregulated
  • increased risk of toxicity

RB Y2 Renal (26 decks)

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