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342 > renal pharmacology 2 > Flashcards

renal pharmacology 2 Flashcards

1
Q

4 relevant types of drugs

A

altering urine pH drugs

altering excretion of organic molecule drugs

drugs for treating urinary tract disorders

drugs for treating renal failure

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2
Q

healthy urine pH

A

6

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3
Q

the urine’s pH is slightly acidic due to the metabolites - 3

A

urea
ureic acid
createnine

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4
Q

pH altering drugs can change the pH of urine to

A

5-8.5

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5
Q

what causes acidification of urine - 4

A

meat heavy diet

sodium heavy diet

metabolic acidosis - excessive bicarbonate loss

thiazide diuretics

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6
Q

what causes alkination of urine - 3

A

citrus fruit -heavy diet

respiratory alkalosis

urinary tract infection as bacteria converts urea to ammonia

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7
Q

patients with ___ urine may be more susceptible to UTIs

A

alkali

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8
Q

clinical benefits of alkaline urine - 5

A

antibacterial

improves dysuria (difficult urination)

inhibits urinary stone formation

solubilisation of weak acid drugs

enables excretion of toxic substances

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9
Q

example where drug excretion is effected by urine pH

A

methamphetamine - acidic urine = more excretion in less time

less in alkaline urine

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10
Q

carbonic anhydrase inhibitors

A

convert carbon dioxide and water intocarbonic acid, protons, bicarbonate ions - so may be used as diuretic

stop bicarbonate reabsorption in nephron

inc bicarbonate excretion so inc urine pH

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11
Q

sodium bicarbonate can be used to treat __ overdose

A

salicylate

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12
Q

carbonic anhydrase inhibitor example

A

acetazolamide

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13
Q

carbonic anhydrase inhibitor - when does tolerance develop

A

after 3 days

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14
Q

citrate admin

A

oral as Na and K salts

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15
Q

calcium citrate treats

A

calcium deficiency

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16
Q

potassium citrate treats

A

renal tubular acidosis (kidney stone formation)

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17
Q

citrate metabolism is via

A

citric acid/ Krebs cycle

excretes bicarbonate resulting in alkaline urine

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18
Q

at what point in the krebs cycle does citrate feed in

A

when citrate converted to isocitrate via aconitase

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19
Q

drugs that alter the excretion of organic molecules are particularly relevant in treatment of

A

gout

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20
Q

what is gout

A

form of acute arthritis
causes uric acid crystal formal in joints due to accumulation

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21
Q

what is gout caused by

A

hyperuricaemia - serum uric acid level of larger than 404micromol per L

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22
Q

what is gout exacerbated by - 3

A

alcohol consumption

meat consumption

diuretic ise

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23
Q

what is hyperuricaemia

A

serum uric acid level of larger than 404micromol per L

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24
Q

gout is more common in which sex

A

men

as inc consumption of meat, alcohol vs women

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25
Q

kidneys are an important __ of uric acid secretion

A

regulator

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26
Q

approx __% of uric acid is secreted by kidneys

A

65%

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27
Q

approx __% of uric acid is secreted by intestine

A

35%

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28
Q

how is uric acid formed

A

through the catabolism of purines

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29
Q

uric acid excretion via kidneys pathway

A

uric acid passes into glomerular filtrate

then most reabsorbed in proximal tubule

small amount excreted into tubule via an anionic secreting mechanism

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30
Q

small amount excreted into tubule via an anionic secreting mechanism. how much?

A

8-12% filtered urate is excreted

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31
Q

treatment focus to treat gout

A

inc elimination of urate

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32
Q

types of drugs used to treat gout by inc elimination of urate - 2

A

uricosuric agents

inhibition of urate synthesis

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33
Q

examples of uricosuric agents used to treat gout by inc elimination of urate - 2

A

probenecid

sulfinpyrazone

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34
Q

examples of drugs used to treat gout by inc elimination of urate that inhibit urate synthesis

A

allopurinol

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35
Q

probenecid inhibits

A

penicillin excretion

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36
Q

when using uricosuric agents, uric acid excretion

A

decreases before it begins to increase - nike tick shape on graph hehe

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37
Q

probenecid mechanism of action

A

inhibits URAT1 and OAT4 transporters in human proximal tubule

cannot facilitate uric acid reabsorption

so excreted

38
Q

where are URAT1 and OAT4 transporters located

A

in human proximal tubule

39
Q

xanthine oxidase

A

enzyme

oxidises xanthine to convert it to uric acid

40
Q

s-allyl cystine and allopurinol

A

inhibits xanthine oxidase

41
Q

what is renal failure

A

waste product accumulation

decline in kidney functions

potentially fatal

42
Q

renal failure causes - 2

A

congenital disease

acquired disease

43
Q

renal congenital disease example

A

polycystic kidney disease - formation of cysts on kidney
inherited autosomal dominant
1 PKD1 or PKD2 mutated copy per cell

44
Q

renal acquired diease example

A

hypertension (cause and symptom of renal failure)

45
Q

types of renal failure - 2

A

acute aka acute kidney injury

chronic aka end stage renal disease ESRD

46
Q

acute kidney injury causes - 5

A

not enough blood reaching kidneys

kidney damage

blocked ureter

drug abuse

heart attack

47
Q

chronic kidney disease causes - 5

A

diabetes

autoimmune disease e.g. lupus

genetic disease e.g. PKD

nephrotic syndrome

urinary tract problems

48
Q

three main approaches to treating renal failure

A

artificial dialysis/ filtration

renal transplantation

pharmaceuticals

49
Q

three types of drugs that treat consequences of renal failure (renal failure itself is not always reversible)

A

antihypertensive drugs

ACE (angiotensin converting enzyme) inhibitors

Angiotensin II antagonists

50
Q

angiotensin

A

blood pressure increasing-hormone

51
Q

healthy kidneys produce a hormone called

A

erythropoetin or EPO

52
Q

erythropoetin or EPO

A

stimulates RBC formation

unhealthy kidneys produce less EPO causing anemia

53
Q

vitamin D preparations examples - 2

A

calcitriol

alphacalcidol

54
Q

use of vitamin D preparations

A

treat osteodystrophy / defective bone development

55
Q

canaglifozin

A

new

reduce risk of chronic kidney disease/ cardiovascular events in diabetic patients

56
Q

canaglifozin mechanism of action

A

binds and inhibits sodium glucose cotransporter 2

SGLT2 is found in proximal tubule of nephron and reabsorbs glucose

inhibition leads to inc glucose excretion

57
Q

renal failure leads to plasma imbalances. what are two examples of these

A

hyperphosphataemia
hyperkalaemia

these can be treated with pharmaceuticals

58
Q

what is hyperphosphataemia

A

phosphate levels in plasma above 1.45 mmol/L

59
Q

hyperphosphataemia clinical consequences - 3

A

vascular smooth muscle cells differentiate into osteoblast like cells - can lead to cardiac disease

calcium phosphate deposits in joints, dec mobility

conjuctivitis in eye

60
Q

drugs used to treat hyperphosphataemia - 3

A

aluminum hydroxide or antacid

calcium carbonate

sevelamer hydrochloride

61
Q

aluminum hydroxide or antacid mechanism of action

A

binds phosphate in GI tract to prevent absorption

62
Q

calcium carbonate side effect

A

predispose to tissue calcification due to calcification of arteries

63
Q

aluminum hydroxide or antacid side effect

A

long term use can cause loss of bone density

64
Q

sevalmer hydrochloride mechanism of action

A

lowers plasma phosphate conc

lower risk of arterial calcification than caclium carbonate

lowers LDL cholesterol

65
Q

sevalmer hydrochloride side effects - 2

A

GI disturbance

contraindicated in bowel obstruction

66
Q

what is hyperkalaemia

A

elevated potassium ion conc in plasna abive 6.5mmol/L

67
Q

hyperkalaemia causes - 5

A

renal failure

metabolic acidosis (as inc protons inc K+ expelled)

potassium sparing diuretics

drugs that interfere with renin secretion

angiotensin II formation/ action (ACE inhibitors)

68
Q

hyperkalaemia treatments IV - 4

A

calcium gluconate
glucose + insulin
salbutamol
sodium bicarbonate

counteracts cardiac toxicity
admin IV

69
Q

hyperkalaemia treatments IV mechanism of reaction

A

shift K+ into intracellular compartment, out of circulation

70
Q

cation exchange resins - hyperkalaemia treatment

A

new

e.g. Na polystyrene sulfonate orally or as enema

removes K+ from system

dialysis often needed

71
Q

patiromer - hyperkalaemia

A

new drug

potassium binder

promoted faecal potassium ion excretion

72
Q

renal vulnerability to drug toxicity may be

A

patient specific
kidney specific
drug related - e.g. crystal formation, interactions with pH

can vary based on age, sex, pharmacogenomics, metabolic enzyme expression

73
Q

urinary tract disorders include - 3

A

enuresis - bed wetting

urinary incontinence

urinary tract infections/ UTIs

74
Q

noctural enuresis causes - 3

A

uti

constipation

anxiety

75
Q

noctural enuresis treatments - 2

A

desmopressin

amitriptyline

also use alarm and restrict fluid intake

76
Q

desmopressin

A

antidiuretic hormone analog - red in water vol excreted by kidneys

77
Q

amitriptyline

A

tricycline antidepressant

78
Q

amitriptyline admin length

A

up to 3 months

79
Q

amitriptyline side effect

A

behaviour disturbance as is psychoactive

80
Q

urinary incontinence causes - 2

A

structural problems (e.g. prostatic hypertrophy, unterine prolapse)

neurogenic detrusor muscle instability - becomes more active

81
Q

urinary incontinence structural problems treatment

A

surgery

82
Q

urinary incontinence neurogenic detrusor muscle instability treatments - 2

A

pelvic floor exercises

AND

muscarinic receptor antagonists

83
Q

muscarinic receptor antagonist example

A

oxybutinin

84
Q

uti infections are more common in women than men because

A

they have a shorter urethra, so bacteria can enter bladder more easily

85
Q

example of uti

A

cystitis

86
Q

cystitis cause

A

e. coli

87
Q

uti treatment

A

antibiotics like

ciprofloxacin (broad spec quinolone)

88
Q

congenital disease leading to kidney failure

A

mutations/ abnormal development of kidneys during fetal life e.g. polycystic kidney disease PKD

89
Q

acquired disease leading to kidney failure

A

after birth develop due to external factors, more common in adults e.g. acute kidney injury

90
Q

NSAID induced acute kidney injury example case study

A

elderly osteoarthritis patient used high dose ibuprofen for pain management, developed acute kidney injury indicated by elevated serum creatinine levels

treated via discontinuation of ibuprofen and inc supportive care

importance of preventative measures - dose adjustment and personalisation od NSAIDs to reduce nephrotoxicity risk, hydration preventing crystal formation, alt to nephrotoxic meds

342 (21 decks)

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