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CPT - Summary > S4 Diuretics and Renal pharmacology > Flashcards

S4 Diuretics and Renal pharmacology Flashcards

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1
Q

what are the functions of the kidneys ?

A

regulation
excretion
endocrine - renin, erythropoietin, prostaglandins
Metabolism - active form of Vit D, catabolism of insulin, PTH calcitonin
control ; volume, PH

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2
Q

in which section of the nephron do different diuretics work ?

A

PT - carbonic anhydrase inhibitors ( e.g acetozoloamide) and osmotic diuretics (e.g mannitol) but not really used any more
LoH - loop diuretics (inhibit NaK2Cl symport furosemide, bumetanide)
DCT - thiazide diuretics (inhibit NaCL symport e.g metolazone)
CD- K+ sparing diuretics (EnaC blockers e.g amiloride), aldosterone antagonists - also spare K+ (e.g spironolactone), ADH antagonist (lithium)

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3
Q

what is the effect of aldosterone on channels ?

A

increase expression of NaK ATPase and ENaC and K+ channels
alcohol inhibits ADH release, caffeine increases GFR and decreases Na reabsorption and both have diuretic actions
ADH antagonists - lithium, tolvaptan

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4
Q

what are the ADRS for diuretics

A

generic : anaphylaxis, hypotension (which activates RAAS), electrolyte disturbance
Thiazide : gout, hyperglycaemia
Spironolactone : Hyperkalaemia, impotence
Frusemide : ototoxicity, alkalosis
Bumetanide : myalgia

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5
Q

what are uses of diuretics ?

A

hypertensions : TD, spironolactone
Heart failure : LD
decompensated liver disease : spironolactone, LD
Nephrotic syndrome : LD, add TD if high K+
Chronic kidney disease : LD

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6
Q

describe what is meant by diuretic resistance ?

A

during delivery to the renal tubule, diuretics are absorbed through the gut, so gut cant be oedematous. Diuretic enters bloodstream so cant have HF, furosemide is albumin bound so cant have albumin deficiency. Fursoemide secreted into PT via OATs, then LoH so PTand LoH must be functioning

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7
Q

describe all the diuretics in summary with usage and main side effect

A

drug - usage - main side effect
carbonic anhydrase inhibitor - glaucoma, altitude sickness - acidosis, renal stones
osmotic diuretics - reduce high intracerebral pressure - allergic reactions
Loop diuretic - oedema ( may be hypertension in CKD)- alkalosis, metabolic effects (increase urate, lipids)
thiazides - hypertension - electrolyte disturbance, metabolic effects (increased urate, glucose , lipids, impotence)
potassium- sparing diuretics (amiloride )- low potassium where diuretic required - hyperkalaemia
aldosterone antagonist - heart failure, ascites, hypertension, hyperadrenalism - hyperkalaemia, gynaecomastia (spironolactone)
ADH antagonist - hyponatremia - hypernatraemia, deranged liver function

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8
Q

why can drugs cause pre-renal AKI ?

A

NSAIDS : inhibit prostaglandins, which normally dilate the afferent arteriole
ACEi/ARB : reduce ANG II so less vasoconstriction of efferent
both drop the perfusion pressure so GFR falls much faster than normal

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9
Q

what precautions should be taken in patients with CKD

A

avoid nephrotoxins
dose carefully with vancomyocin
side effects of drugs are more common in renal disease

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10
Q

what are causes of hyperkalaemia?

A 
excessive intake
movement out of cells e.g acidosis
reduced urine loss
diabetic ketoacidosis
Drugs - ACEi, NSAIDS
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11
Q

what is seen in the ECG in hyperkalaemia?

A

life threatening arrhythmias, tall T small P waves , sine waves

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12
Q

how is hyperkalaemia managed

A

reduced effect on heart with IV Ca2+ gluconate, remove excess K+ by dialysis or calcium resonium, reduce intake

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13
Q

how is blood pressure controlled ?

A

controlled by ANS and RAAS

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14
Q

what is hypertension ?

A

defined as 140/90 mmhg

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15
Q

what are the causes of hypertension

A

primary hyp : no known cause, affects 90% of hyp people. Causative agents include oral contraceptive pill, corticosteroids or high alcohol intake
Secondary Hyp : has a discrete, identifiable underlying cause

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16
Q

what is the treatment of hypertension

A

identify and treat underlying cause if present
lifestyle advice/non-pharmacological therapy
Pharmacological therapy (bp > 160/100)

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17
Q

what are examples of lifestyle therapy

A

patient education, reduce salt, exercise and reduce alcohol

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18
Q

what are Ace Inhibitors

A

usually given in under 55s E.g Lisinopril or Ramipril
Stop Ang1 —> Ang2 causing less vasoconstriction, Na retention and aldosterone release
also increases bradykinin (vasodilator) and has some venodilation
side effects cough other adverse side effects : angio-oedema , renal failure and hyperkalaemia

19
Q

what angiotensin receptor blockers

A

e.g losartan, candersartan
Bind to Ang1 receptor preventing Ang2 formation so no vasoconstriction or aldosterone release
side effects : renal failure, Hyperkalaemia

20
Q

what are some calcium channel blockers

A

usually in over 55’s
bind to specific alpha subunit of L - tyoe calcium chanel reducing cellular calcium entry
vasodilates peripheral, coronary and pulmonary arteries

21
Q

what are the three groups of CCBS ?

A

Dihydropyridines (Nifedipine, Amlodipine) - have good oral absorption and are metabolised by the liver - adverse effects - sympa NS activation
Phenylalkylamines (verapamil) - acts on the myocardial and smooth muscle membrane reducing Ca transport- causes vasodilation and reduces myocardial contractility adverse effects - constipation and bradycardia ( so cant be given beta blockers)
Benzothiazepines (Diltiazem) - acts on the myocardial and smooth muscle membrane reducing Ca transport
Causes - vasodilation and reduces myocardial contractility
Adverse effects - bradycardia and slight negative inotropy

22
Q

how are thiazide diuretics used to control BP ?

A

e.g indapamide , Bendroflumethiazide
reduce distal tubular sodium reabsorption by blocking NaCl symporter
reduces bp by reducing blood volume and then TPR
Adverse effects : hypokalaemia , increased urea and impaired glucose tolerance and increased cholestrol

23
Q

what are some other anti - hypertensive drugs

A

other diuretics - spironolactone (ARB) amiloride (k+ sparing)

24
Q

how do alpha blockers treat hypertension

A

e.g doxazosin
act via selective antagonism at post-synaptic a1 adrenoreceptors and antagonise the contractile effects of noradrenaline on vascular smooth muscle so reducing TPR
adverse effects - postural hypotension and oedema

25
Q

how do beta - blockers treat hypertension

A

e.g atenolol , bisoprolol, nebivolol
antagonise the action of B1 - adrenoreceptors on the ventricular myocardium reducing HR and CO. inhibit renin release
adverse effects : lethargy, bradycardia and raynauds

26
Q

what is aliskiren ?

A

direct renin inhibitor

binds to renin preventing cleavage of Ang1 –> Ang2

27
Q

what are centrally acting agents

A

these include methylodopa (potent a2 - adrenoreceptor agonist), clonidine (pre-synaptic a2 - adrenoreceptor agonist) or moxonidine (some a2 - adrenoreceptor agonism) all reduce sympathetic outflow to reduce bp
adverse effects : lethargy , depression

28
Q

how is combination therapy used to treat hypertension

A

thiazide diuretics lower Bp but can raise glucose or lower K+
amiloride lowers bp but has no effect on glucose
combination of two shall lower Bp and have no effect on glucose or K+

29
Q

describe heart failures aetiology and management

A

ischaemic heart disease, hypertension, cardiomyopathies (e.g alcohol)
management : correct underlying cause
pharmacological therapy diuretics ACEi, B blocker , Ivabradine and sacubtril ( increase natriuretic peptides), hydralazine, digoxin, inotropes and phosphodiesterase inhibitors
lifestyle ; reduce salt and alcohol and increase exercise
beta blockers reduce HR and Bp so reduces the heart workload. they also reduce mobilisation of glycogen

30
Q

how is mean arterial BP measured ?

A

Mean arterial BP = CO (SV X HR) X TPR

31
Q

describe short term regulation of BP

A

baroreceptor reflex. BP control for acute changes and can’t sustain as the threshold for baroreceptor firing resets (accommodation)
nerve endings in carotid sinus + aortic arch sensitive to stretch, increased arterial pressure increases stretch, increased firing of AP detected in medulla. Decreases sympathetic outflow so reduces HR, CO and TPR (bradycardia and vasodilatation). Vice versa for low BP

32
Q

describe long term regulation of BP

A

interaction of neuronal and hormonal responses which control Na + balance and therefore ECV : RAAS, sympathetic NS, ADH and natriuretic peptides
hormonal response to low renal perfusion and to increase bp : RAAS, sympa NS, prostaglandins, ADH

33
Q

where is renin released from

A

granular cells of juxtaglomerular apparatus (JGA) of the afferent arteriole of the kidneys

34
Q

what are the factors that stimulate renin release

A

reduced NaCl delivery to distal tubule
reduced perfusion pressure (blood volume) in the kidney, detected by baroreceptors in the afferent arteriole
sympathetic stimulation
decreased circulating volume stimulates renin release

35
Q

describe how renin stimulates Na+ reabsorption

A

Renin converts angiotensinogen to angiotensin 1
ACE converts angiotensin 1 to angiotensin 2
angiotensin 2 acts both directly on blood vessels causing vasoconstriction and also directly on kidneys to stimulate sodium reabsorption increasing blood volume and hence CO and Bp. Increases thirst in hypothalamus via ADH release from the pituitary
Angiotensin 2 interacts with adrenal cortex to release aldosterone
aldosterone increases Na reabsorption

36
Q

describe the nature of aldosterone receptors

A

two types of Ang II receptors - AT1 and AT2
main actions via AT1 receptor ; g protein coupled receptor
there is vasoconstriction of efferent > afferent arteriole so enhanced Na+ reabsorption at the PCT

37
Q

what is the action of aldosterone on the kidney

A

acts in principal cells of collecting duct
stimulates Na + and therefore water reabsorption via apical eNaC and ROMK
also increases basolateral Na + excretion via Na/K/ATPase so bigger gradient for sodium to move in

38
Q

how does the sympathetic NS regulate BP

A

HIGH SNS activity decreases renal blood flow by vasoconstricting arterioles and decreasing GFR, so sodium excretion is decreased so blood pressure increases. stimulates renin release so increases Ang II, aldosterone and increases Na+ reabsorption. water follows so BP increases

39
Q

how does the introduction of prostaglandins regulate BP

A

causing vasodilation of the afferent arteriole so GFR increases. Produced by RAAS and SNS, decrease Na + reabsorption, important when Ang II is high

40
Q

describe how ADH can increase BP

A

ADH forms concentrate urine by retaining water to control plasma osmolarity - it increases water reabsorption through AQP2 and stimulates sodium reabsorption by acting on NAK2CL in thick ascending limb. released from posterior pituitary when there is high plasma osmolarity or severe hypovolaemia. causes vasoconstriction

41
Q

how does ANP reduce BP

A

acts via vasodilation of AA ( increases blood flow and thus GFR) and inhibits sodium reabsorption which causes natriuresis - sodium excretion in urine so would also lower BP

42
Q

what is hypertension defined as

A

a sustained increase in blood pressure which diastolic > 90 mmhg or systolic > 140 mmhg. often asymptomatic byt damages heart and vasculature so can lead to MI, stroke, HF
primary - cause not definable may be genetic or environmental
secondary - identifiable cause which needs treating

43
Q

what are examples of secondary hypertension

A

renal vascular disease : RA stenosis , fall in kidney perfusion, increased renin, RAAS activation, vasoconstriction and sodium retention, water follows and BP increases
Renal parenchymal disease - early loss of vasodilation , later sodium and water retention due to inadequate glomerular filtration
coarctation of the aorta
adrenal causes : conns syndrome - aldosterone - secreting adenoma causing hypertension and hypokalaemia
cushings syndrome - increased cortisol, acts on aldosterone receptors, sodium and water retention
chronic kidney disease - inability to excrete excess salt and water due to reduced kidney function (reduced GFR), causing hypertension and oedema
Nephrotic syndrome - massive proteinuria, hypoalbuminemia, oedema. often due to podocyte injury

CPT - Summary (8 decks)

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