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Renal > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what do uricosuric drugs do

A

promote excretion of uric acid into the urine

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2
Q

what is the role of diuretic

A

increase urine flow (usually by inhibiting the reabsorption of electrolytes at various sites of the nephron)
to enhance secretion of salt and water in conditions with tissue swelling due to increase ECF (oedema)

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3
Q

what ions are mostly excreted by duiretics

A

sodium and chloride

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4
Q

what diseases increase plasma hydrostatic pressure causing oedema

A

nephrotic syndrome
CHF
hepatic cirrhosis with ascites

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5
Q

what is nephrotic syndrome

A

a disorder of glomerular filtration which allows large protein (mainly albumin) to appear in the urine (protein uria)

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6
Q

how does nephrotic syndrome cause oedema

A

as protein lost from plasma into urine
decreased capillary oncotic pressure (water not sucked into capillaries as much as a result)
increased interstitial fluid (=oedema)
ALSO increased ECF= decreased blood volume and CO
= activation of RAAS
= Na+ and H20 retention
= increased plasma hydrostatic pressure and decreased oncotic pressure
= makes oedema worse

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7
Q

can you have protein in filtrate normally

A

can be filtered after exercise but always reabsorbed within proximal

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8
Q

what causes oedema in congestive heart failure

A

reduced cardiac output = renal hypoperfusion = activates RAAS = increased blood volume= increased venous and capillary pressures + reduced plasma oncotic pressure = pulmonary and peripheral oedema

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9
Q

how does hepatic cirrhosis cause ascites

A

increased pressure within the hepatic portal vein + decreased production of albumin = loss of fluid into the into the peritoneal cavity = ascites

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10
Q

what causes activation of RAAS

A

decreased circulating volume

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11
Q

what do loop duiretics target

A

Na+/K+/2Cl- co transporter in the thick ascending limb of the loop of henle, bind to Cl- site

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12
Q

what do thiazide like diuretics target

A

Na+/Cl- co transporter in the early distal convoluted tubule

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13
Q

what do carbonic anhydrase inhibitors target

A

Na/H+ exchange in the proximal convoluted tubule

used for reducing intra-ocular pressure and altitude sickness prophylaxix

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14
Q

what do potassium sparing diuretics target

A

Na/K+ exchanger in the collecting tubule and duct

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15
Q

why is potassium lost in the use of non potassium sparing diuretics

A

Na+/K+ exchanger in the collecting tubule and duct

anything that increases the amount of sodium that gets into the late/ distal tubule will also cause potassium loss

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16
Q

how do duiretics reduce oedema

A

cause the excretion of salt and water- concentrating the albumin in plasma- increasing plasma oncotic pressure
water drawn in from from the interstitial fluid
helped by the reduced hydrostatic pressure of the vessels aswell

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17
Q

where do most duiretic work (cellular level)

A

on the apical membrane of tubular cells (why they need to enter the filtrate to work if hydrophilic)

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18
Q

how do duiretics enter the filtrate

A 
glomerular filtration (for drug not bound to large plasma proteins)
secretion via organic anion transporters (acidic drugs) or organic cation transporters (basic drugs)
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19
Q

what drugs enter tubular epithelium cells via organic anion trasnporters at the apical membrane

A

duiretics (furosemide, hydrocholorothiazide)

simvastatin, penicillins, NSAIDs, endogenous urate

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20
Q

why does furosemide precipitate gout

A

as competes at organic anion transporters to get into lumen epithelium and be excreted

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21
Q

what drugs enter tubular epithelium via organic cation transporters

A

duiretics (amoliride), atorpine, metformin, morphine, procainamide, endogenous catecholamines

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22
Q

what drives the reabsorption of calcium and magnesium in the thick ascending limb (paracellular route)

A

potassium recycling

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23
Q

how are calcium and magnesium reabsorbed in the thick ascending limb

A

via paraceelular route, driven by electrogradient created by potassium recycling, in thick ascending limb

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24
Q

what are the two main loop duiretics

A

furosemide and bumetanide

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25
Q

what are the actions of loop duiretics

A

decrease tonicity of interstitium of the medulla (by decreases reabsorption)
prevent dilution of the filtrate in the ascending limb (as AL water impermeable)
increase load of Na+ delivered to distal nephron (causes K+ loss)
increase excretion of Ca and Mg+

has a venodilator effect before diuresis

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26
Q

how much water loss do loop diuretics cause

A

‘torrential’

15-25% of filtered load of Na+

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27
Q

why are loop duiretics good in pulmonary oedema cause by heart failure

A

as have a venodilator effect before duiresis effect

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28
Q

where are loop duiretics absorbed

A

from GI tract (can vary in CHF due to oedema of the intestines, esp furosemide)

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29
Q

what do loop duiretics bind to in blood

A

plasma proteins

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30
Q

how do loop duiretics enter the nephron

A

via OAT

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31
Q

what are the clinical indications for loop duiretics

A

to reduce salt and water overload associated with:

  • acute pulmonary oedema
  • chronic kidney/ heart failure
  • hepatic cirrhosis with ascites
  • nephrotic syndrome

to increase urine volume in AK failure

HPTX (thiazides preferred- used if resistant/ cormorbid renal insufficiency)

acute hypercalcamia

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32
Q

what do nitrates do

A

vasodilate - good for pulmonary oedema

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33
Q

what are the contraindications for loop duiretics

A

severe hypovolaemia/ dehydration

cautioned in severe hypokalaemia and /or hyponatraemia, hepatic encephalopathy, gout

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34
Q

what are the adverse affects of loop duiretics

A

hypokalaemia (co prescribe potassium sparing duiretic. potassium supplements)
metabolic alkalosis (increased H+ secretion)
hypocalcaemia and hypomangesaemia
hyperuricaemia - can precipitate gout
loss of hearing

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35
Q

how do thiazide duiretics work

A

block the Na+/Cl- co transporter in the distal convoluted

tubule by binding to Cl- site

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36
Q

what do thiazide like duiretics do

A

prevent dilution of filtrate in early distal tubule
increase the load of Na+ delivered to the collecting tubule (causing K+ loss)
increase reabsorption of Ca2+

cause vasodilation- helpful in treating hypertension

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37
Q

what are the main thiazide duiretics

A

bendroflumethiazide (thiazide)
chlortalidone
indapamide and
metolazone (thiazide-like)

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38
Q

how much duiresis do thiazides cause

A

5% of Na+ to be excreted- moderate

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39
Q

where are thiazides absorbed

A

GI tract

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40
Q

how do thiazides enter the nephron

A

via OAT

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41
Q

what is the clinical indication for a thiazide

A

mild heart failure
hypertension

severe resistant oedema
renal stone disease (reduced calcium excretion in urine stops stone formation)
nephrogenic diabetes insipidus

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42
Q

what causes nephrogenic diabetes insipidus

A

diminished vasopressin responsiveness of the collecting ducts

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43
Q

what are the contraindications for thiazides

A

hypokalaemia

cautioned in:
hyponatraemia, gout (block urate transport system in proximal tubule)

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44
Q

what are the adverse effects of thiazides

A 
hypokalaemia 
metabolic alkalosis
hypovolaemia 
hypotension 
hypomagnaesmia (NOT hypocalcaemia)
hyperuricaemia 
erectile dysfunction 
impaired glucose tolerance in diabetes
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45
Q

why is there an advantage of using thiazides instead of loops in the elderly

A

if patients have osteoporosis then thiazides wont cause hypocalcaemia

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46
Q

what does aldosterone do

A

increases synthesis of a protein that activates the epithelial Na+ channel (ENaC)
=increases intracellular sodium, decreases potassium

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47
Q

what do ROMK and BK channels do

A

secrete K+ into the urine in the collecting channel

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48
Q

what does Na+ reabsorption cause

A

potassium secretion

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49
Q

explain how potassium is lost when there is high Na+ in the distal tubule/ collecting duct

A

more excretion further up causes more excretion further down
this creates negative charge in lumen
increases driving force on K+ across the lumenal membrane = enhanced secretion
potassium washed away by increased urine flow

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50
Q

how do potassium sparing duiretics work

A

amiloride + triametrene= block the apical sodium channel to decrease Na+ reabsoprtion in the late and distal collecting tubule

spironolactone + eplerenone = compete with aldosterone for binding to intracellular (cytoplasmic) receptors prevent the actions of aldosterone (increases Na, decreases K)

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51
Q

where are sprionolcatine, eplerenone and triamterene absorbed

A

GI tract

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52
Q

how do potassium sparing duiretics enter the luminal epitheliem

A

amiloride and triamterene= OCT in proximal tubule

sprinolonatone and eplerenone= basolateral membrane

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53
Q

what are the clinical indications for potassium sparing duiretics

A

used in conjunction with other agents that cause potassium loss (cant give alone)

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54
Q

what do potassium sparing duiretics cause when given alone

A

hyperkalaemia

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55
Q

what do thiazide and loop duiretics activate

A

RAAS

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56
Q

what can be given to potentiate the actions of thiazides and loop agents

A

aldosterone receptor antagonists (block action of aldosterone- increasing Na and decreasing K+)

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57
Q

what are aldosterone antagonists used in

A

heart failure
conns (primary hyperaldosteronism)
resistant essential hypertension
secondary hyperaldosteronism (hepatic cirrhosis with ascites)

58
Q

what are the contraindications for a potassium sparing duiretic

A

severe renal impairment, hyperkalaemia, addisions

59
Q

how do osmotic diuretics enter the nephron

A

glomerular filtration

60
Q

name an osmotic duiretic

A

mannitol

61
Q

how do osmotic diuretics work

A

increase the osmolarity of the glomerular filtrate, opposing the reabsorption of water in nephron

62
Q

what are the major sites of action of osmotic diuretics

A

proximal tubule (where most iso-osmotic reabsorption of water re-occurs)

63
Q

how do osmotic diuretics affect sodium

A

cause decrease of reabsorption in proximal tubule (more water decreases sodium conc and electrochemical gradient for reabsorption)

64
Q

when are osmotic diuretics used

A

in the prevention of acute hypovolaemic renal failure to maintain urine flow

in urgent treatment for acutely raised intraocular and intracranial pressure

65
Q

how do osmotic diuretics lower intra-ocular/ intra-cranial pressure

A

solute cannot pass blood brain barrier (cant enter brain/ eye) - increased plasma osmolarity extracts water from these compartments (ICF)

66
Q

what are the adverse effects of osmotic diuretics

A

transient expansion of blood volume

hyponatraemia

67
Q

when can osmotic diuresis also occur

A

in hyperglycaemia (glucose remaining in filtrate retains fluid)

as a consequence of contrast dye in imaging (filtered but not reabsorbed creating an osmotic load)

68
Q

name a carbonic anhydrase inhibitor

A

acetazolamide

69
Q

what do carbonic anyhydrae inhibitors do

A

increase excretion of HCO3- with Na+, K+, and H20

= alkaline diuresis and metabolic acidosis

70
Q

what are carbonic anhydrase inhibitors used for

A

glaucoma and following eye surgery to reduce IOP (suppress the formation of aqueous humour from ciliary body)
prophylaxis of altitude sickness
infantile epilepsy

71
Q

how does aldosterone affect the kidney

A

causes enhanced tubular Na+ reabsorption and salt retention
(increases activity of sodium channel ENaC and increases synthesis of Na/K ATPase channels. binds to cystoplasmic mineralocorticoid receptor to alter gene expression)
(in collecting tubule)

72
Q

hoe does vasopressin affect the kidney (ADH)

A

enhanced H20 reabsorption

bins to V2 GPCR to increase cAMP, increases number of aquaporins in the collecing tubule

73
Q

cause causes neurogenic DI

A

lack of vasopressin secretion from the posterior pituitary

74
Q

what is the treatment for neurogenic DI

A

desmopressin (synthetic analogue of vasopressin)

75
Q

what causes nephrogenic DI

A

inability of the nephron to respond to vasopressin (usually caused by AR/ X linked mutations)

76
Q

what are aquaretics/ vaptans

A

competitive antagnoists of vasopressin receptors

77
Q

what do vasopressin receptors do

A

V1A mediates vasoconstriction

V2 mediates H20 reabsorption (directs AQP2)

78
Q

what does the blackage of vasopressin receptors (by aquaretics/ vaptans do)

A

causes excretion of eater without accompanying Na+= raises plasma Na+ conc

79
Q

when is tolvaptan used

A

SIADH

80
Q

where does reabsorption of glucose occur

A

proximal tubule of

81
Q

what mediates glucose reabsorption

A

SGLT 1 and 2 (should be 100% efficient)

82
Q

when would glucose appear in the urine

A

if filtrate concentration of glucose exceeds the renal threshold (11 mmol)

83
Q

where are SGLT 1 and 2 expressed

A

SGLT 1 in intestine and kidney
SGLT 2 in the kidney (proximal tubule of nephrone)
SGLT 2 absorbs 90% and SGLT 1 absorbs 10% (2 before 1)

84
Q

what type of movement is glucose reaborsption

A 
secondary active transport (apical membrane) 
facilitated diffusion (basolateral membrane)

SGLT both transport glucose against concentration gradient by coupling with Na+ influx glucose

85
Q

what does inhibition of SGLT 2 cause

A

glycosuria - excretion of glucose
decrease in HbA1c
weight loss (calorific loss and mild osmotic diuresis)

86
Q

what are the adverse effects of SGLT inhibitors

A

increased genital bacterial/ fungal infections

87
Q

name some SGLT 2 inhibitors

A

canagliflozin
dapagliflozin
empagliflozin

88
Q

what are the major prostaglandins made by the liver

A

PGE2 - medulla

PGI2- glomeruli

89
Q

what do prostaglandins do

A 
vasodilate 
natruietic 
synthesised in response to ischaemia 
mechanical trauma 
angiotensin II 
ADH 
bradykinin
90
Q

when are prostaglandins useful

A

when there in vasoconstriction/ decreased effective arterial blood volume = they cause compensatory vasodilation

91
Q

how do prostaglandins affect GFR

A

cause vasodilation of the afferent arteriole
= releases renin
= increases angiotensin II
=vasoconstriction of the efferent arteriol
= filtration pressure increases

92
Q

how can NSAIDs cause renal failure

A 
inhibit COX (enzyme that forms prostaglandins) 
which causes greatly decreases GFR and can precipitate acute renal failure in conditions where renal blood flow is dependent upon vasodilator prostaglandins (cirrhosis, heart failure, nephrotic syndrome)
93
Q

what is the triple whammy effect

A

combo of ACEi/ ARB, duiretic and NSAIDs = decreased GFR = acute renal failure

94
Q

what forms uric acid

A

the catabolism of purines

95
Q

what are the treatments for gout

A

NSAIDS and colchine
(probenecid and sulfinpyrazole can block reabsorption of urate in the proximal tubule)

allupurinol inhibits urate synthesis, used as prophylaxis not in acute flares

96
Q

what is pharmacokinetics

A

behaviour of a drug with regard to absorption, distribution, metabolism and elimination

97
Q

where are most drugs excreted

A

by kidneys

98
Q

name a drug that is directly nephrotoxic to the kidneys

A

gentamicin

99
Q

give an example of how a drug can be indirectly nephrotoxic

A

taking a diuretic when already dehydrated

100
Q

what drugs cause renal vasoconstrictions

A

NSAIDs
ACEi/ARB
radiocontrast

101
Q

what drugs cause rapidly progressing GN

A

penicillamine
hydralazine
propythiourcil

102
Q

what drugs can cause acute tubular necrosis

A

radiocontrast
heavy metals
cisplatin
aminoglycosides (gentamicin)

103
Q

what drugs can cause acute interstitial nephritis

A 
antibiotics (penicillins, cephalosporins, rifampicin, cirpofloxacin)
NSAIDs
loop and thiazide diuretics 
allopurinol 
mesalazine
104
Q

what drugs can cause intratubular obstruction and crustal formation

A

acyclovir
methotrexate
sulphonamide

105
Q

what drugs can cause post renal obstruction

A

papillary necrosis- NSAIDs, compound analgesics

urinary retention- anticholinergics, tricyclic antidepressants

106
Q

what drugs can cause pre renal azotemia (hypernataemia)

A

antihypertensive agents

duiretics

107
Q

what enzyme do statins inhibit

A

HmgCoA reductase

108
Q

what are the types of calcium channel blockers

A

dihydrapyridine (-ipines used for hypertension)

and non dihydrapyridine (Verapamil, Diltiazem which also slow HR)

109
Q

when can you not use a beta blocker

A

asthma, COPD and peripheral vascular disease (causes peripheral vasoconstriction)

110
Q

why can you go into heart failure in AF

A

as LA contributes 20% of cardiac output

111
Q

what are the signs of heart failure of CXR

A 
cardiomegaly 
pulmonary oedema 
blunting of costophrenic angle 
upper lobe diversion of fluid (blood cant get oxygenated in lower lobes)
periphilar oedema 
curly B lines (lymphatic engorgement)
112
Q

how can NSAIDs cause HF

A

as cause Na and fluid retention

113
Q

would you stop bendroflumethiazide in gout

A

yes as increased uric acid

114
Q

what will taking an ACEi or diuretic when dehydrated do

A

cause AKI/ decrease renal function

115
Q

what do you get high levels of circulating in HF

A

ADH as RAAS system activated

116
Q

why would you give diuretics IV in HF

A

as wont absorb as well orally due to GI oedema

117
Q

what should you do to the dosage of drugs in renal dysfunction

A

reduce them

with digoxin half or quarter the load dose

118
Q

what are the features of digoxin toxicity

A

heart block, brady cardia, yellow vision, vomiting, abnormal renal function

119
Q

what is the treatment for HF

A

diuretics
CCBs
amiodarone
anticoagulants

120
Q

do you give ACEi in an AKI

A

NO (can introduce them if needed once kidney function has stabilised)

121
Q

what drugs to you need to monitor when a patient with an AKI taking them

A

diuretics, ACEi/ ARBs, digoxin,

122
Q

what happens to half life of digoxin in CKD

A

it doubles

123
Q

what are the signs of hyperkalaemia on ECG

A

broadened QRS
tall tented T waves
flattening of P waves
sine waves

124
Q

what is the management for hyperkalaemia

A

IV calcium gluconate 10mls 10% (to stabilise the cardiac membrane)
IV insulin and dextrose (moves potassium into the cells
Salbutamol (forces potassium into the cells)
fluids (saline) if hypovolaemic (or IV sodium bicarbonate if metabolic acidosis present)

125
Q

what is a CVP

A

central line (tells you filling pressure of heart so you dont overload the patients with fluid)

126
Q

what is ACEi good for

A

improve survival in HF
reduces pressure in kidney
reduces endothelial dysfunction
reduces RAAS system (upregulated in HF)

127
Q

what do penicillamine do

A

given in wilsons (collates copper)

immunosuppressant, reduces RF (given in RA)

128
Q

what is diclofenac

A

an NSAID (v toxic, long term CV risk) useful in gout

129
Q

why is diclofenac given with misoprostol

A

misoprostol is a prostaglandin analogue so given with diclofenac which is a very potent COX2 inhibitor

130
Q

what can you get as a result of NSAIDs

A

hypertension (cause Na retention)

131
Q

what happens to kidneys in hypertension

A

get glomerular sclerosis

132
Q

what is a potential side effect of penicilliamine

A

bone marrow aplasia (if see platelets falling stop drug, restart when platelets recover)

133
Q

what deposits can you get in RA

A

amyloid

134
Q

what do you need to monitor in RA

A

BP as increased risk of CVD and hypertension

135
Q

is a thiazide or a loop more potent

A

loop on its own more potent but when given together thiazide is v potent

136
Q

how do you assess fluid status

A

Mucous membranes, skin turgor, E+S BP, JVP, (creps in chest)

Bloods: urea, haematocrit, osmolarity + urine osmolarity

137
Q

can you be dehydrated and have peripheral oedema

A

yes just means fluid is in the wrong place

138
Q

what drugs improve survival in HF

A

ACEi/ARB (with monitoring), beta blocker

139
Q

what is sprionolactone

A

a potassium sparing diuretic

is an aldosterone antagonist- reduces BP by dampening RAAS and prevents myocardial fibrosis (caused by aldosterone)

140
Q

what are side effects of allopurinol

A

steven johnson syndrome

bone marroe suppression

141
Q

what is solpadol

A

soluble mix of paracetamol and codeine- has v high salt content

Renal (27 decks)

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