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Renal > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Loop diuretics work at the ___________ and interfere with the operation of ____________

A

thick ascending limb of the loop of henle

Na/K/Cl co-transporter

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2
Q

Describe what the Na/K/Cl co-transporter usually does? What is the effect of loop diuretics blocking this?

A

Usually drives ions out of the lumen to make the medulla salty which allows reabsorption of water in the descending limb (ascending limb is impermeable to water). The pump also drives the movement of Ca2+ and Mg2+ into the interstitium.

Blockage means less water can be reabsorbed and Na+ and water are lost in the urine.

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3
Q

Loop diuretics are more or less powerful than thiazides?

A

More

They produce rapid and profound diuresis

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4
Q

Loop and thiazide diuretics as well as diuresis cause?

A

Venal dilation (mechanism not fully understood) and this occurs even before the onset of diuresis.

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5
Q

Examples of loop diuretics?

A

Furosemide and bumetanide

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6
Q

Clinical indications for loop diuretics?

A

Acute PO, CKD when acutely unwell, hepatic cirrhosis with ascites, CHF, nephrotic syndrome, add on therapy in hypertension , to reduce acute hypercalcaemia

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7
Q

5 side effects of loop diuretics?

A 
Hypokalaemia
Metabolic Alkalosis 
Hypovolaemia and hypotension
Hypocalcaemia and hypomagnaesia
Hyperuricaemia and predisposition to gout
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8
Q

How is hypokalaemia corrected in those on loop or thiazide diuretics?

A

Potassium supplements or concomitant use of potassium sparing diuretics

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9
Q

Why do you get metabolic alkalosis with use of thiazide and loop diuretics?

A

H+ follows excretion of potassium

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10
Q

Why do loop and thiazide diuretics predispose to gout?

A

Competition between uric acid and diuretic agent for transporter meaning less uric acid is secreted so higher levels in the blood, hyperuricaemia predisposes to gout.

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11
Q

Thiazide diuretics work in the _____ and block the __________ therefore ______________

A

distal tubule
NaCl transporter
preventing water reabsorption as Na is followed by water

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12
Q

Examples of thiazide diuretics?

A

Bendroflumethiazide/ bendrofluazide

Hydrochlorothiazide

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13
Q

Indications for thiazide diuretics?

A

Widely used in: Mild HF and hypertension

Also have some uses in severe resistant oedema (usually combined with a loop), renal stone disease and nephrogenic DI.

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14
Q

7 side effects of thiazide diuretics?

A 
Hypokalaemia
Metabolic Alkalosis
Hypovolaemia and Hypotension
Depletion of Magnesium (BUT NOT CALCIUM)
Hyperuricaemia
Male sexual dysfunction (in high doses)
Impaired glucose tolerance (not fully understood but should be given in caution in diabetics)
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15
Q

Loop or thiazides cause hypocalcaemia?

A

Loops cause hypocalcaemia

Thiazides actually increase reabsorption of calcium

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16
Q

Potassium sparing diuretics work in the ______ by blocking ________

A

collecting duct tubule

ENAC sodium channel

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17
Q

Potassium sparing diuretics work _______ and are mainly used to _________

A

poorly as diuretics

prevent potassium loss

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18
Q

Examples of potassium sparing diuretics?

A

Amiloride and Triamterene

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19
Q

Major clinical indication for potassium sparing diuretics?

A

In conjunction with thiazides or loops to correct hypokalaemia

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20
Q

Side effects of potassium sparing diuretics?

A

On their own they cause hyperkalaemia

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21
Q

Examples of aldosterone antagonists?

A

Spironolacton and eplerone

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22
Q

Why can spironolactone help with action of thiazides and loops?

A

Thiazides and loops activate RAAS which increases BP and fluid retention but blocking aldosterone with spironolactone would reduce this

23
Q

Major indications for aldosterone antagonists?

A

HF, primary and secondary hyperaldosteronism, resistant essential hypertension

24
Q

Explain contraindications of aldosterone antagonists?

A

On their own these drugs cause hyperkalaemia so are contraindicated in Addisons, severe renal impairment and hyperkalaemia

25
Q

Mechanism of osmotic diuretics?

A

Increase osmolarity of the filtrate opposing the absorption of water in parts of the nephron that are freely permeable (make filtrate hypertonic)
Reduce water reabsorption and sodium in the tubule decreasing gradient for sodium reabsorption collaterally so there is excretion of sodium.

26
Q

Example of osmotic diuretic?

A

Mannitol

27
Q

Clinical indications for an osmotic diuretic?

A

Acute hypovolaemic failure to maintain renal urine flow e.g. in massive haemorrhage. Also in acutely raised ICP or IOP as the solute doesn’t enter the eye or the brain but increased plasma osmolarity extracts water from these compartments.

28
Q

Mechanism of carbonic anhydrase inhibitors?

A

Increase excretion of HCO3 with Na, K and H2O causing an alkaline diuresis

29
Q

Carbonic anhydrase inhibitor example?

A

Acetazolamide

30
Q

Clinical uses of carbonic anhydrase inhibitors?

A

No longer have a role as diuretics as very weak but used in:
Glaucoma and following eye surgery as production of aqueous humour is dependent on availability of HCO3
Prophylaxis of altitude sickness as sickness thought to mediated by carbonic anhydrase causing changes in CSF
Some forms of infant epilepsy
Alkanising the urine in relief of dysuria, enhancing excretion of weak acids e.g. stone forming issue or aspirin overdose

31
Q

Explain when vasopressin agonists are used? What is the drug called?

A

Synthetic ADH desmopressin is used in treatment of Neurogenic Diabetes Insipidus when the problem is that the pituitary is not producing enough ADH and kidneys are responsive.

32
Q

Mechanism of action of the Vaptans/ Aquaretics?

A

Vasopressin antagonists block V2 receptors and cause water loss but NO sodium loss so plasma osmolarity increases.

33
Q

3 uses of the vaptans/ aquaretics?

A

Used in HF- still being debated
SIADH to correct hyponaetremia
Autosomal dominant polycystic kidney disease as inhibits cAMP thought to drive cyst growth (cAMP increases when ADH binds to GCPR which triggers AQP2 recruitment)

34
Q

___________ reabsorb 100% of glucose in the proximal tubule. Reabsorption is by ___________

A

SGLT1 and 2

Secondary active transport and facilitated diffusion

35
Q

Why its SGLT2 a more attractive target than SGLT1?

A

SGLT2 is largely confined to the kidney whereas SGLT1 is also in the gut

36
Q

SGLT2 inhibitor mechanism?

A

Selectively and competitively block SGLT2 meaning glucose is lost in urine as SGLT1 cannot take all the glucose. Cause excretion of glucose, decrease in HBA1c, weight loss all independent of insulin

37
Q

Examples of SGLT2 inhibitors?

A

Empagliflozin, dapagliflozin and canagliflozin

38
Q

Side effect of SGLT2i?

A

increased infections and thrush due to glucose rich urine

39
Q

Prostaglandins are part of prostanoid family and formed from the _______1_____________

Major kidney prostaglandins are _______2__________

Both act as ____3______, are ____4______, and are synthesised in response to _________5___________

A

1) fatty acid arachidonic acid by COX1 and 2 enzymes
2) PGE2 from medulla and PGI2 (AKA prostacyclin) from glomeruli
3) vasodilators
4) natriuretic (promote sodium loss)
5) ischaemia, mechanical trauma, Angiotensin 2, ADH and bradykinin.

40
Q

Under normal conditions prostaglandins have __________

A

little effect on renal blood flow or GFR

41
Q

How can prostaglandins help maintain GFR even if hypovolaemic?

A

Prostaglandins effect GFR by vasodilation of afferent arteriole and then cause release of renin leading to increased levels of angiotensin 2 that vasoconstricts the efferent arteriole so filtration pressure increases.

42
Q

Why may NSAIDS precipitate acute renal failure?

A

NSAIDs inhibit COX and may precipitate acute renal failure in conditions where renal blood flow is dependent upon vasodilator prostaglandins (renal artery stenosis, hypovolaemia, cirrhosis, HF or nephrotic syndrome)

43
Q

Explain why combination of ACEi/ARB, Diuretic and NSAID is bad?

A

ACEi blocks efferent arteriole vasoconstriction, NSAIDs block production of prostaglandins so no vasodilation in afferent arteriole, Diuretics decrease plasma volume decreased volume means decreased pressure, greatly reduced GFR

44
Q

Describe the difference between a side effect and an adverse drug reaction?

A

Adverse drug reaction is an undesirable reaction which can include more than just side effects
Side effects are a type of adverse drug reaction

45
Q

Type A reaction?

A

Augmented pharmacologic effects- dose dependent and predictable
Mechanism to it that can look back and understand

46
Q

3 types of type A interaction?

A

Drug drug interactions
drug disease interactions
drug food interaction

47
Q

Type B reaction?

A

Bizarre effects (or idiosyncratic) dose independent and unpredictable. Often life threatening don’t fit with mechanism of drug

48
Q

Examples of type B reactions?

A

Drug rashes are most common
Bone marrow aplasia with chloramphenicol
Hepatic necrosis with halothane

49
Q

Type C reaction?

A

Chronic effects of a drug

50
Q

2 examples of type c reactions?

A

Cushings disease in prolonged steroids

Diabetes in prolonged beta blockers (this is why they were removed first line for straightforward hypertension)

51
Q

Type D reactions?

A

Delayed effects
Remote from treatment often many years after stopping therapy and difficult to relate back. Teratogenic and carcinogenic effects. Less frequent now due to rigorous testing

52
Q

Type E reactions?

A

End of treatment effect

Due to abrupt withdrawal and rebound effects

53
Q

3 examples of type E reactions?

A

E.g. addisonian crisis in patient suddenly taken off steroids

E.g. beta blocker withdrawal as get rebound tachycardia

E.g. anticonvulsant withdrawal/ changes and epilepsy frequency

54
Q

Type F reactions?

A

Failure of therapy

Renal (19 decks)

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