Pharmacology 3: Other Renal Drugs Flashcards

1
Q

how do osmotic diuretics enter the nephron

A

given IV - by glomerular filtration and are not reabsorbed

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2
Q

how do osmotic diuretics work (2)

A

1) increase osmolarity of filtrate which attracts water and sodium across 2) opposes water reabsorption in some parts of the nephron

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3
Q

where do osmotic diuretics act in the nephron

A

proximal tubule

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4
Q

what are clinical indications for osmotic diuretics (2)

A

1) prevents acute hypovolaemic renal failure by maintaining flow 2) urgent treatment of raised ICP or raised intraoccular pressure (increases plasma osmolarity)

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5
Q

what are adverse effects of osmotic diuretics (2)

A

transient expansion of blood volume, hyponatramia

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6
Q

how can hyperglycaemia cause osmotic diuresis

A

reabsorptive capacity in proximal tubule by SGLT1/2 is exceeded - glucose stays in filtrate and causes water to be excreted with it

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7
Q

how can iodine radiocontrast dyes cause osmotic diuresis

A

dye is filtered but not reabsorbed which increases osmolarity of the filtrate and causes fluid to be excreted

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8
Q

name an osmotic diuretic

A

IV mannitol

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9
Q

how do carbonic anhydrase inhibitors work

A

carbonic anhydrase supplies H for Na/H exchange so this is inhibited - also excreted HCO3 with some Na, K and H20

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10
Q

what can carbonic anhydrase inhibitors cause

A

metabolic acidosis and alkaline diuresis

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11
Q

when are carbonic anhydrase inhibitors used

A

glaucoma after surgery, prophylaxis of altitude sickness, infant epilepsy

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12
Q

what other agents can alkalise urine and why is this useful

A

citrate salts - relieves dysuria, prevents weak acid crystals, enhances excretion of weak acids

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13
Q

where is aldosterone released from and what does it eventually cause

A

adrenal cortex –> enhanced tubular Na reabsorption and retention

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14
Q

how does aldosterone effect Na/KATPase and ENaC to increase Na reabsorption

A

increases synthesis of Na/KATPase pump (K excretion) /// increases activity of ENaC which is a Na channel

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15
Q

where is vasopressin released from and what does it eventually cause

A

enhanced H2O reabsorption by increases number of aquaporin channels in apical membrane

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16
Q

what is neurogenic diabetes insipidus

A

lack of ADH (vasopressin) released from post pit which causes increases water excretion

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17
Q

how is neurogenic diabetes insipidus treated

A

desmopressin

18
Q

what effects do nicotine and ethanol have on ADH

A

ethanol inhibits ADH secretion and nicotine enhances ADH secretion (raised BP)

19
Q

what is nephrogenic diabetes insipidus and what usually causes it.

A

nephron does not respond to vasopressin - usually caused by X-linked recessive gene on V2 receptor

20
Q

how do you treat nephrogenic diabetes insipidus

A

no current treatment

21
Q

what drugs can cause vasopressin inhibition in the kidneys (3)

A

lithium, demeclyocyline (AB), vaptans

22
Q

when is vasopressin used in children

A

bedwetting (nocturnal enuresis) >10

23
Q

how do vaptans/ aquaretics work

A

competitive antagonist of vasopressin receptor (v1 and 2) - stops aquaporins being activated and causes water excretion with no Na loss

24
Q

what can vaptans cause

A

hypernaetraemia

25
Q

what are clinical indications for vaptans

A

HF, hypervolaemic hyponatremia, SIADH

26
Q

what is the vaptan used in SIADH

A

tolvaptan

27
Q

how is glucose reabsorped in the nephron and where

A

in the proximal tubule by SGLT1/2 (some secondary active transport and facillitated diffusion)

28
Q

where is SGLT1 also located

A

intestines

29
Q

what is the renal threshold for glucose and what can happen when this is exceeded

A

11mmol - glucosuria

30
Q

what effect on glucose do SGLT2 inhibitors cause

A

excretion of glucose, decreased HbA1c, weight loss (through calorie loss)

31
Q

name 3 SLGT2i

A

canagliflozin, dapagliflozin, empagliflozin

32
Q

how are prostaglandins formed

A

formed from fatty acid and arachidonic acid by COX 1 and 2

33
Q

what are the 2 main prostaglandins produced by the kidneys

A

PGE2 (formed by medulla), PGI2 (formed by glomeruli)

34
Q

what are the actions of the kidney prostoglands and what causes them to be formed

A

synthesised in response to: ischaemia, trauma, angiotensin II, ADH and bradykinin (low BP and vasoconstriction) // cause vasodilation and sodium excretion

35
Q

what effect on GFR can prostaglandins have

A

increase GFR by vasodilation of afferent arterioles and release of renin from granular cells (RAAS)

36
Q

how do you inhibit the formation of prostaglandins and which drugs can do this

A

inhibit COX enzyme - NSAIDs

37
Q

what 3 drugs are said to cause the ‘triple whammy’ effect on the kidneys

A

ACEi/ diuretics and NSAIDs

38
Q

how is uric acid formed

A

catabolism of purines

39
Q

what foods are purines typically found in

A

red meat

40
Q

how does elevated urate predispose gout

A

crystals are deposited in joints and soft tissue

41
Q

name 2 drugs uses to treat gout and how they work

A

uricosuric agents (probenecid and sulfinpyrazone) - block reabsorption of urate in proximal tubule

42
Q

name a drug that inhibits urate synthesis and it’s drug class

A

allopurinol - xanthase oxidase inhibitor