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
what are clinical indications for vaptans
HF, hypervolaemic hyponatremia, SIADH
26
what is the vaptan used in SIADH
tolvaptan
27
how is glucose reabsorped in the nephron and where
in the proximal tubule by SGLT1/2 (some secondary active transport and facillitated diffusion)
28
where is SGLT1 also located
intestines
29
what is the renal threshold for glucose and what can happen when this is exceeded
11mmol - glucosuria
30
what effect on glucose do SGLT2 inhibitors cause
excretion of glucose, decreased HbA1c, weight loss (through calorie loss)
31
name 3 SLGT2i
canagliflozin, dapagliflozin, empagliflozin
32
how are prostaglandins formed
formed from fatty acid and arachidonic acid by COX 1 and 2
33
what are the 2 main prostaglandins produced by the kidneys
PGE2 (formed by medulla), PGI2 (formed by glomeruli)
34
what are the actions of the kidney prostoglands and what causes them to be formed
synthesised in response to: ischaemia, trauma, angiotensin II, ADH and bradykinin (low BP and vasoconstriction) // cause vasodilation and sodium excretion
35
what effect on GFR can prostaglandins have
increase GFR by vasodilation of afferent arterioles and release of renin from granular cells (RAAS)
36
how do you inhibit the formation of prostaglandins and which drugs can do this
inhibit COX enzyme - NSAIDs
37
what 3 drugs are said to cause the 'triple whammy' effect on the kidneys
ACEi/ diuretics and NSAIDs
38
how is uric acid formed
catabolism of purines
39
what foods are purines typically found in
red meat
40
how does elevated urate predispose gout
crystals are deposited in joints and soft tissue
41
name 2 drugs uses to treat gout and how they work
uricosuric agents (probenecid and sulfinpyrazone) - block reabsorption of urate in proximal tubule
42
name a drug that inhibits urate synthesis and it's drug class
allopurinol - xanthase oxidase inhibitor