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Pharmacology Flashcards

1
Q

what force drives water out of capillaries

A

hydrostatic pressure in the capillary (Pc)

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2
Q

what drives water into the capillary

A

oncotic pressure of plasma (derived from plasma proteins)

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3
Q

examples of diseases that increase Pc and decrease oncotic pressure of plasma

A

nephrotic syndrome
CHF
hepatic cirrhosis with ascites

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4
Q

what causes nephrotic syndrome

A

there is a disruption to filtration barrier causing proteins to leave circulation and enter the filtrate

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5
Q

classic urine presentation of proteinuria

A

frothy urine

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6
Q

how does CHF cause oedema?

A

there is reduced CO and renal hypoperfusion activating RAAS causing retention of Na+ and H2O

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7
Q

how does cirrhosis with ascites cause oedema

A

increased pressure in hepatic portal veins and decreased production of albumin (liver disease) causes loss of fluid into peritoneal cavity which activates RAAS due to reduced circulating volume-thrombosis danger

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8
Q

where is the triple co-transporter Na+/K+/2Cl- found?

A

thick ascending loop of Henle

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9
Q

which diuretic blocks the triple co-transporter?

A

loop diuretics

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10
Q

which (now obsolete) diuretic blocks Na+/H+ exchange?

A

carbonic anhydrase inhibitors (found in PCT and early DCT)

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11
Q

where is the Na+/Cl- co-transporter found?

A

early DCT

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12
Q

which diuretic blocks Na+/Cl- co-transport?

A

thiazide diuretics

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13
Q

where is Na+/K+ exchanger found?

A

collecting duct

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14
Q

what blocks the Na+/K+ exchanger?

A

potassium-sparing diuretics

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15
Q

to act diuretics must enter the filtrate by?

A
  • glomerular filtration (when not bound to large plasma proteins)
  • secretion by PCT
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16
Q

two transport processes in PCT that secrete diuretics into the filtrate?

A
  • organic anion transporters (OATs)

- organic cation transporters (OCTs)

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17
Q

what does OATs transport?

A

acidic/negatively charged molecules e.g. PAH, thiazides and loop

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18
Q

what do OCTs transport?

A

basic/ positively charged e.g. triamterene and amiloride

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19
Q

describe OA secretion

A
  • OA- enters the tubular cell from the blood in exchange for alpha-KG via OAT1,2,3
  • alpha-KG re-enters via NaDC3
  • OA- crosses to the filtrate via MRP2/4 and BCRP
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20
Q

describe OC secretion

A
  • OC+ enters the tubular cell via OCT2

- OC+ enters the lumen and filtrate via MATE or MDDR1

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21
Q

examples of loop diuretics

A

furosemide

bumetanide

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22
Q

what do loop diuretics bind to?

A

bind to Cl- on the triple co-transporter in PCT

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23
Q

action of loop diuretics

A

increased Na+ load is delivered to distal region of the nephron causing increased K+ loss with excretion of Ca2+ and Mg2+

also have a venodilator action

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24
Q

how do loop diuretics enter the filtrate?

A

strongly bind to plasma protein so enter via OAT

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25
what are loop diuretics used in?
``` acute pulmonary oedema CHF CKF (increase UO in AKF) ascites nephrotic syndrome hypertension acute hypercalcaemia ```
26
contra-indications of loop diuretics
severe hypovolaemia | dehydration
27
cautions with loop diuretics
hypokalaemia hyponatraemia hepatic encephalopathy gout
28
adverse effects of loop diuretics
- hypokalaemia (correct with potassium-sparing diuretics or supplements) - metabolic alkalosis (Na+/H+) - hypocalcaemia - hypomagnesemia - hypovolaemia - hyperuricaemia (competition between uric acid and loop) - dose related loss of hearing
29
which drugs does hypokalaemia increase toxicity of?
``` digoxin class III AADs ```
30
example of a thiazide diuretic
bendroflumethiazide
31
what do thiazides bind to?
Cl- binding site on Na+/Cl- in early DCT
32
action of thiazides
increase Na+ in collecting duct causing K+ loss and increased reabsorption of Ca2+ which causes diuresis also vasodilation action
33
how do thiazides enter the filtrate?
OATs
34
clinical indications for thiazides
- hypertension (mild HF) - severe resistant oedema - renal stone disease (reduces Ca2+) - nephrogenic DI
35
contra-indications and cautions of thiazides
hypokalaemia hyponatremia gout
36
adverse effects of thiazides
``` hypokalaemia metabolic alkalosis hypovolvaemia hypomagnesemia hyperuricaemia ED impaired glucose tolerance in diabetes ```
37
on what receptors does aldosterone act?
via cytoplasmic receptors
38
action of aldosterone
increase synthesis of protein that activates ENaC and increases Na+/K+ ATPase
39
why do spironolactone and eplerenone have limited diuretic action?
modulated by aldosterone
40
action of spironolactone and eplerenone
antagonists of aldosterone receptor so increase excretion of Na+ while decreasing excretion of K+
41
action of amiloride and triamterene
block luminal Na+ channels in collecting duct
42
how do potassium sparing diuretics enter the nephron
OCT in PCT
43
clinical indications of potassium-sparing diuretics
- in conjunction with diuretics that cause potassium loss (alone cause hyperkalaemia) - heart failure - primary aldosteronism (Conn's) and secondary (cirrhosis and ascites) - resistant hypertension
44
contra-indications of potassium-sparing diuretics
severe renal impairment hyperkalaemia Addisons
45
example of osmotic diuretic
mannitol
46
where does mannitol act
PCT
47
how does mannitol enter the filtrate?
glomerular filtration
48
clinical indications of mannitol
- prevent acute hypovolaemia renal failure to maintain UO | - acutely raised ICP and IOP
49
adverse of mannitol
transient expansion of blood volume and hyponatraemia
50
causes of osmotic diuresis
mannitol hyperglycaemia iodine radiocontrast dyes
51
examples of carbonic anhydrase inhibitors
azetazolamide
52
clinical uses of carbonic anhydrase inhibitors
``` no longer used as diuretics glaucoma following eye surgery (reduce IOP) prophylaxis of altitude sickness infantile epilepsy ```
53
when is alkalising the urine useful?
dysuria prevention of uric stones excretes weak acids
54
how to alkalinise the urine
- citrate salts (generate HCO3- in Krebs) | - carbonic anhydrase inhibitors
55
substances that inhibit ADH
lithium demeclocycline vaptans
56
example of vaptan
tolvaptan
57
action of tolvaptan
competitive antagonist of ADH receptors which causes excretion of water (but not Na+)
58
what is tolvaptan used in?
SIADH
59
when can glucose appear in the urine
diabetes when glucose concentration exceeds renal threshold (11mmol)
60
example of SGLT2i
empagliflozin
61
action of SGLT2i
excretes glucose decreases HbA1c weight loss
62
adverse of SGLT2i
genital bacterial and fungal infections
63
where is SGLT2 found?
PCT | responsible for reabsorption of glucose (against gradient with Na+ symport)
64
examples of prostaglandins synthesised by the kidney
PGE2 (medulla) | PGI2 (glomeruli)
65
action of prostaglandins
vasodilation | loss of Na+
66
when is synthesis of prostaglandins enhanced?
``` ischaemia trauma angiotensin II ADH bradykinin ```
67
when do prostaglandins have the largest effect
when there is vasoconstriction or hypovolaemia as vasodilates afferent arteriole and releases renin (angiotensin II vasoconstricts efferent) allowing kidneys to maintain UO
68
examples of NSAIDs
aspirin naproxen diclofenac
69
action of NSAIDs
inhibit COX and precipitate ARF in patients with low GFR e.g. bilateral RAS or hypovolaemia
70
describe the triple whammy effect
combination of ACEI/ARB, diuretic and NSAID
71
how is uric acid formed?
catabolism of purines
72
what does high urate in the serum predispose to?
gout
73
what blocks reabsorption of urate in PCT?
probenecid | sulfinpyrazole
74
action of allopurinol
stops urate synthesis

Renal (54 decks)

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