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Pharmacology > Antihypertensives > Flashcards

Antihypertensives Flashcards

1
Q

Define hypertension and state the two main determinants of hypertension and define them

A

HPT is a persistently high arterial blood pressure that is above “normal B.P“
•i.e. Systolic - >140 mmHg and/or Diastolic - >90 mm Hg

The two main determinants of B.P. are
•cardiac output (CO) -measure of blood volume ejected from the heart over a given time.it maintains blood flow throughout the body
and
•total peripheral resistance (TPR).
•Total peripheral resistance refers to the amount of force affecting resistance to blood flow throughout the circulatory system.

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2
Q

What is the calculation for bp and CO

A

CO-stroke volume x heart rate

Bp-CO x TPR

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3
Q

Define stroke volume

A

Amount of blood ejected from the ventricles during one heartbeat

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4
Q

HPT is usually asymptomatic but progressive

  • If not effectively managed or controlled
  • hypertension could lead to complications such as heart failure, myocardial ischaemia, stroke, kidney failure

•The higher the B.P., the greater the risk of cardiovascular and other complications

True or false

A

True

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5
Q

What are the types of hypertension and causes of hypertension

A

Primary Hyperension:
•In about 90% of the hypertensive cases, no specific underlying cause can be identified
•Incresing age, family history, excess body weight, lack of physical activity and excessive alcohol intake may be predisposing factors.

2. Seconday Hypertension:
In about 10% of cases, the cause of HPT may be secondary to some definite abnormality such as
•Kidney related
•Chronic kidney disease,
•Polycystic kidney disease
•Endocrine
•Phaechromocytoma
•hyperaldosteronism (Conn’s disease)
•Hypercortism (Cushing’s disease)
•hyperthyroidism
•Acromegaly
•Vascular
•Renal artery stenosis
•Coarction of the artery

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6
Q

What are the treatment objectives in managing hypertension

A

To reduce blood pressure to recommended targets
•<140/90 mmHg for age below 60 yrs, diabetes and CKD patients
•<150/90 mmHg for age above 60 yrs
•To manage co-morbid conditions such as obesity, diabetes etc
•To prevent cardiovascular, cerebrovascular and renal complications
•To promote therapeutic lifestyle changes
•To identify and manage secondary hypertension appropriately

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7
Q

What are the classes of drugs used in the management of hpt

A

Any the first five classes can be used is 1st Line
•Diuretics (mainly thiazide diuretics)
•Calcium channel blockers
•Angiotensin Converting Enzyme inhibitors (ACEIs)
•Angiotensin II receptor Blockers (ARBs)
•β- blockers

  • Others
  • - receptor antagonists
  • Centrally acting agents
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8
Q

Name the three main classes of diuretics used in the management of hypertension

A

The three main classes of diuretics include
•Thiazides & Thiazide-like Diuretics
•Loop diuretics
•Potassium(K+) Sparing Diuretics

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9
Q

Give some examples of thiazides and thiazide like drugs

A 
Common examples of drugs in this class are
•Thiazides: Bendrofluazide, hydrochlorthiazides, cyclopenthiazide, chlothiazide etc
•Thiazide-like Drugs:- Chlorthalidone, indapamide, xipamide etc
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10
Q

What is the mechanism of action of thiazides

A

They lower blood pressure initially, by increasing sodium and water excretion.
•This causes a decrease in extracellular volume, resulting in a decrease in cardiac output and renal blood flow.
•With long-term treatment, plasma volume approaches a normal value, but a hypotensive effect persists that is related to a decrease in peripheral resistance by reducing vasoconstriction. If used for long they act like calcium channel blockers cuz calcium causes contractions or constrictions
•They possibly cause a fall in smooth muscle Na+ which causes a secondary reduction in intracellular Ca 2+ so that the muscle becomes less responsive to endogenous vasoconstrictors

If there’s a lot of water t increases blood volume thereby affecting the stroke volume but diuretics reduce or prevent water reabsorption by causing sodium retention thereby reducing blood volume and reducing stroke volume

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11
Q

The antihypertensive effect of the thiazides occur at relatively low doses.
•No additional B.P reduction benefit is achieved with high dose of thiazides but more side effects
•This may cause electrolyte disturbances

True or false

A

True

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12
Q

The antihypertensive effect of thiazides last for how long, and must be administered how many times,

A

The antihypertensive effect is long-lasting and may persist for 24 hours.
•Drugs must be administered once daily in the management of hypertension

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13
Q

When hpt is complicated by renal failure and other complications what is used instead of thiazides

A

Where the hypertension is complicated by renal failure,
•it may be necessary to use a more potent diuretic like loop diuretic or metolazone (thiazide-like diuretic)

Loops diuretics make the patient pass out more urine but thiazide works better for the anti hypertensive effect. It loops will be used in people with no hypertension but have edema or used in treatment of hypertension when complications such as ccf arise

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14
Q

Potassium is important for cardiac rhythm . How do you avoid cardiac rhythm disturbances with diuretics induced hypokalemia

A

To avoid cardiac rhythm disturbances with diuretic-induced hypokalaemia,
•It may be necessary to add a K+ sparing diuretic such as amiloride or triamterene or a potassium supplement to thiazides or loop diuretics

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15
Q

The most important toxic effect associated w thiazide diuretics is
And what is the most unwanted effect of thiazides

A

Hypokalemia

Other dose related problems are

The most important toxic effect associated with this class of diuretics is hypokalemia

  • Other dose-related problems include hyperuricaemia precipitating gout and hyperglycaemia
  • The commonest unwanted effect not obviously related to the main renal actions of the thiazides is erectile dysfunction
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16
Q

Thiazides should be used cautiously in the presence of severe renal and hepatic disease, since azotemia (high level of urea or nitrogen containing compounds)and coma may result
•Hyponatraemia is potentially serious, especially in the elderly

True or false

A

True

Cuz thiazides being out water and water loss causes thick blood volume causing decreased blood flow to the kidneys causing increased nitrogen compounds
So anything that will cause decreased blood flow to the kidneys will cause azotemia

As people age their sodium levels reduce
If care is not taken the diuretic will cause further sodium loss leading to confusion and severe ones lead to coma

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17
Q

Give some examples of loop diuretics and the mechanism of action

A

Examples include:
•Frusemide, Torasemide(book of Torah) Piretanide (pirate) bumetanide, ethacrynic acid

Mechanism of Action
•They act by blocking sodium and chloride reabsorption in the kidneys, even in patients with poor renal function or those who have not responded to thiazide diuretics.

  • They are more potent than thiazide diuretics & increase both K+ & Ca2+ loss
  • When used for HPT, the potent diuretic effect of the loops may provoke reflex stimulation of the R-A-A-S. that may counter any fall in Blood pressure.
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18
Q

Why are loop diuretics not potent in their anti hypertensive effect

A

When used for HPT, the potent diuretic effect of the loops may provoke reflex stimulation of the R-A-A-S. that may counter any fall in Blood pressure.

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19
Q

Name some clinical uses of loops

A

Clinically the loop & other potent diuretics are used in patients with conditions leading to salt and water overload such as:
•Pulmonary oedema
•Congestive heart failure
•Nephrotic syndrome
•Renal failure
•Hepatic cirrhosis complicated by ascites
•In hypertensive patients with renal or heart failure the loop diuretics may be preferred over thiazides

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20
Q

Mechanism of action of potassium sparing diuretics ,give examples of them a negative state which are aldosterone antagonists and sodium channel blockers as well as uses of them

A

These are weak diuretics
Mechanism of Action
•They are inhibitors of epithelial sodium transport at the late distal and collecting ducts.

  • Amiloride & Triamterene are sodium channel blockers, controlled by aldosterone’s protein mediator
  • Spironolactone and eplerenone are aldosterone antagonist
  • All of these agents reduce potassium loss in the urine.
  • They are sometimes used in combination with loop diuretics and thiazides to reduce the amount of potassium loss induced by these diuretics.
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21
Q

Which other conditions can spironolactone be used and what’s re the side effects

A

Other conditions in which spironolactone may be used include:
•Resistant oedema associated with excess aldosterone including nephritic syndrome, cirrhosis and heart failure.

  • Side effects include:
  • Nausea
  • Gynaecomastia in men
  • Menstrual irregularities in women.
22
Q

What is the mechanism of action of calcium channel blockers,examples,adverse reactions

A

Mechanism of Action:
•They bind to the L-type channels and, by blocking the entry of Ca 2+ into the cell, cause relaxation of the arteriolar smooth muscle.
•This reduces the peripheral resistance and results in a fall in blood pressure.

Examples of drugs in this class include Verapamil, Diltiazem (Dildo) & the Dihydropyridines
DVD,
Arterial dilation: headache, flushing and dizziness, ankle edema (resistant to diuretics)
•Bradycardia (verapamil(has the most negative chronotropic and inotropic effects on the heart) and diltiazem), constipation (verapamil)
•Verapamil has potentially hazardous additive effects with beta-blockers, reducing the force of myocardial contraction and slowing the heart rate.
•Tachycardia (nifedipine, nisoldipine).
•Gingival hyperplasia

23
Q

Why are dihydropyridines more effect calcium channel blockers and give examples of them

A

All the different groups of the CCB’s may be used as antihypertensive agents but the dihydropyridines are the most effective because of their peripheral vasodilating properties.
•The longer acting dihydropyridines such as amlodipine and felodipine are also preferred over nifedipine since they are suitable for once daily administration.

24
Q

Which dihydropyridine is selective for cerebral vessels and may be used clinically to prevent cerebral vasospasm following subarachnoid haemorrhage
And which calcium channel blocker is needed for managing hypertension with angina

A

Nimodipine

Verapamil or diltiazem

25
Q

How does the RAAS system regulate Bp

A

Inadequate blood flow to the kidneys leads to the release of renin via sympathetic activity
•Renin acts on angiotensinogen, converts it to angiotensen I, which is then converted to Angiotensen II by Angiotensen Converting Enzymes (A.C.E).
•Angiotensen II is a potent vasoconstrictor which causes an increase in B.P by increasing TPR.
•It also raises the levels of aldosterone and stimulates thirst.
•The net effect is an increase in fluid and salt retention, leading to a rise in the B.P

26
Q

What is the function of aldosterone

A

Conserves water by reabsorption of water and salt

Regulates volume of blood by conserving water and causing thirst when water level is low

27
Q

Dihydropyridines act more on where in the heart and how many times in the day are they administered and at what rate? Which calcium channel blockers act more on the calcium channels of the heart and does their adverse effect cause reflex tachycardia?

A

Acts more on blood vessels

Once daily administration (are released slowly)

Nifedipine
Nisoldipine

28
Q

How does activation of the sympa during decreased bp cause increased bp

A
  1. When the baroreceptors sense a decrease in bp the increase the sympa which activates the Beta 1 receptors on the heart thereby increasing rate and force at which the heart bears thereby increasing CO
  2. when the sympa is increased it activates alpha 1 receptors on smooth muscle or blood vessels causing vasoconstriction thereby increasing venous return and increased TPR(total peripheral resistance)
  3. Increased sympa causes activation of Beta 1 receptors on kidney causing increase of renin. Angiotensin 2 increases TPR by vasoconstriction and also increases release of aldosterone thereby causing sodium and water retention,increased blood volume and increased stroke volume
29
Q

How does the body respond to a decreased bp other than activating sympa (mention the two ways)

A

It reduces blood flow to the kidney causing reduced glomerular filtration rate
Increased water and sodium retention increased blood volume increasing stroke volume and increasing cardiac output

Or
Reduced blood flow to kidney causes increased renin causing increased angiotensin 2 causing either increased peripheral resistance,increased venous return,increased cardiac output or it causes an increased aldosterone leading to increased sodium and water retention causing increased blood volume causing increased stroke volume and increasing cardiac output

30
Q

Renin is produced from kidney and angiotensinogen is produced from where

A

Liver

31
Q

In anti hypertensive drugs you change the drugs not the doses due to the plateau effect cuz it gets to a point where when you increase the the dose it’ll have no effect on the patient. True or false

A

True

The dose-response relationship for B.P. reduction is linear initially but a plateau could be reached within the therapeutic dosage range,
•where further increases in doses do not increase the antihypertensive effect.

32
Q

Explain how bradykinin comes about and how it’s degraded and what will happen if it’s accumulated , what does bradykinin increase the production of?

A

Kininogen is inactive and is activated by Kallikrein to bradykinin.

it’s degraded by ANgiotensinogen 1 converting Enzyme (kinase II) to degraded products

Accumulation of bradykinin causes vasodilation by reducing TPR and dry cough by acting like prostaglandin

Nitric oxide and prostacyclin which are both potent and vasodilators

33
Q

How do ACE inhibitors work

A

Angiotensen II stimulates the release of aldosterone which causes Na+ and H2O retention as well as K+ loss from the kidney
•BV and BP would increase as a result of the salt & water retention plus the vasoconstriction caused by AGII
•Reducing the circulating levels of Angiotensen II in the body also
•reduces increased sympathetic outflow facilitated by Angiotensen II both centrally and peripherally.

Vasodilation of both arterioles and veins occurs as a result of
•decreased vasoconstriction (from diminished levels of angiotensin II) and
•enhanced vasodilation (from increased bradykinin)

34
Q

ACEIs aren’t safe in people w ischemic heart events true or false

A

False

Unlike other vasodilators, ACEIs do not provoke reflex tachycardia & are thus safe in patients with ischemic heart events

35
Q

What are 3 contraindications of ACEIs

A

ACEIs combine well with thiazides or Ca2+ channel blockers for management of hypertension.

ACEIs
•K+ supplements and K+ sparing diuretics should be used with caution with A.C.E. Inhibitors because of the risk of hyperkalaemia, especially in patients with pre-existing renal impairment.

• The use of NSAIDS could compromise the antihypertensive effect of ACEI cuz NSAIDs induce an increase in blood pressure they also inhibit vasodilation effects and causes increased sodium and water retention

  • ACEIs are contra-indicated absolutely in 2nd and 3rd trimester of pregnancy due to
  • Fetal hypotension
  • Fetal renal failure
  • Fetal malformation/death
36
Q

Which populations have high renin activity and which have low renin activity and give four examples of ACEIs

A

Caucasian populations have HIGH renin activity and thus respond well to beta blocker and A.C.E.I

•Black populations usually have LOW renin activity and thus respond poorly to beta blockers and the angiotensin blockers

Common examples include
•Captopril, Enalapril, Lisinopril, Fosinopril, Quinapril and Ramipril.

37
Q

What are the side effects of ACEIs

A

ACEIs cause profound hypotension, which is much higher in patients with Na+ or water depletion.
•There is the need for dosage adjustment when used together with diuretics.

  • Others side effects include:
  • Skin rashes (hypersentivity reaction)
  • Neutropenia .
  • Reversible renal failure precipitated in patients with renovascular disease.
  • Dry non-productive & irritant cough (mediated by the build up of bradykinins)
  • Angioedema
38
Q

Mechanism of action of angiotensin 2 receptor blockers(ARB),contraindications and examples of it

A

They block AG II receptors and thus all the effects associated with raised plasma levels of AgII in the body
•It has no effect on bradykinin metabolism
•Like ACEI, the ARBs are also contraindicated in pregnancy.
•Common examples include: Losartan, Valsartan and Candesartan, Irbesartan

39
Q

Differences between ARBs and ACe inhibitors

A

AT1-antagonists (ARBs) differ from ACE inhibitors in the following ways

• They do not interfere with degradation of kinins
(so no rise in level or potentiation of bradykinin).

•They block completely AT1-receptors and therefore
alternative pathways of AT generation do not have
any importance

40
Q

If a patient comes w cough as a side effect of taking ACe inhibitors what do you give instead and why

A

ARBs (angiotensin II receptor blockers( formally angiotensin II receptor type 1 (AT1) antagonists)) work in place of ACe inhibitors to stopbradykinin from staying for long cuz normally it doesn’t stay for long and it’s degraded. This is done only for people who present w the dry cough

41
Q

How do beta adrenoreceptors work

A

β-adrenergic stimulation in the heart, the kidneys and the nervous system could lead to
•Increase in CO via β1 stimulation of heart.
•Increase aldosterone mediated Na+ and water retention (RAAS) via stimulation β1 adrenoceptors on the kidneys.
•All of the above effects could be antagonized with the use of β-blockers to cause a reduction in B.P.

•Block of β1-receptors in renal juxtaglomerular granule cells that secrete renin may be involved and such a mechanism could explain why β-blockers are less effective in older patients who may have low renin levels.

42
Q

What are the variations among beta blockers

A

β-blockers vary in the way in which they are eliminated from the body.
•Lipid soluble β blockers such as propranolol depend on liver metabolism and clearance from the body
•Water soluble derivatives like atenolol and bisoprolol are eliminated through the kidneys.

43
Q

Which has a longer or shorter action? Propanolol or atenolol

A

Propranolol has a short t1/2 & is extensively metabolized in the liver
•Atenolol has a longer t1/2 and may be administered once daily.

44
Q

Which beta blockers have intrinsic sympathomimetic or partial agonist activities
And which beta blockers have both α1 & β adrenergic blocking properties

A

Pindolol and sotalol have intrinsic sympathomimetic or partial agonist activities
• Some beta blockers have both α1 & β adrenergic blocking properties e.g. Labetalol & Carvedilol

45
Q

Name the uses of Beta blockers and indications and contraindications of beta blockers

A

For the management of hypertension and other cardiovascular diseases,
•the selective β1 blockers (E.g. Atenolol, Bisoprolol) may be preferred as they are administered once daily & also have less central adverse effects .
•Β-blockers with additional α1 adrenoceptor blocking effects such as labetalol and carvedilol may also preferred over non-selective β blockers for HPT .

Indications and contra-indications

The primary therapeutic benefits of β-blockers are seen in hypertensive patients with concomitant heart disease, such as
•supraventricular tachyarrhythmia (for example, atrial fibrillation),
•previous myocardial infarction, stable ischemic heart disease, and
•chronic heart failure.

•Conditions that discourage the use of β-blockers include reversible bronchospastic disease such as asthma, second- and third-degree heart block, and severe peripheral vascular disease

46
Q

What are the side effects of beta blockers

A

The β-blockers may decrease libido and cause erectile dysfunction, which can severely reduce patient compliance.

  • Antagonism of β-adrenergic effects in the CNS is associated with
  • reduced sympathetic outflow which may cause a sense of malaise, vivid dreams, nightmares, hallucinations & sedation.
  • These central side effects are common with the lipid soluble β-blockers such as propranolol.
  • Bradycardia

Bronchospasm (β2-mediated), not recommended for asthmatics
•Tiredness and fatigue.
•NB: β2-stimulation of skeletal muscle is associated with increased muscle activity so blockade will lead to tiredness and fatigue especially during exercise
•β-blockers could mask the signs of hypoglycaemia and must be used with caution in diabetics
•Non-cardioselective β-blockers may disturb lipid metabolism, decreasing high-density lipoprotein cholesterol and increasing triglycerides.
•Beta blockers could cause AV Block & complicate peripheral Vascular Diseases

47
Q

What is the mechanism of alpha 1 adrenoreceptors and examples of em and uses of em

A

These have dilatation effects on vascular smooth muscles.
•Common examples include: Prazocin, Indoramin, Terazocin, doxazocin and tamsulosin.
•Terazocin and Doxazosin are longer acting and well tolerated.
•They are used once daily for hypertension.
•They are used with other antihypertensives in cases of resistant hypertension.
Mechanism:
•They cause vasodilatation by selectively blocking vascular α1-adrenoceptors.
•Unlike non-selective α-blockers, these drugs are not likely to cause tachycardia, but the may cause postural hypotension.

48
Q

Centrally acting anti hypertensives mechanism of action and examples

A

Drugs acting on presynaptic α2 receptors in the brain stem reduces sympathetic out flow and eventually, reduces B.P.

These drugs are associated with central side effects. Examples are Clonidine and Methydopa,nitroprusside,reserpine

49
Q

Mechanism of action clonidine ,adverse effects and clinical uses

A

acts centrally as an α2 agonist to produce inhibition of sympathetic vasomotor centers,
•decreasing sympathetic outflow to the periphery.
• This leads to reduced total peripheral resistance and decreased blood pressure.
•It is used primarily for the treatment of hypertension that has not responded adequately to treatment with two or more drugs.
•Its adverse effects sedation, drowsiness, dry mouth and interference with sexual performance in men.
•Abrupt cessation with the use of clonidine will lead rise to a rebound hypertensive effect.

50
Q

Mechanism of action methyldopa(alpha -methyldopa) ,adverse effects and clinical uses

A

α-Methyldopa
•It is an α2 agonist that is converted to methylnorepinephrine centrally to diminish adrenergic outflow from the CNS.
•Its side effect of sedation and drowsiness coupled with multiple administration, limit their use as antihypertensive agents in recent times.
•However, methyldopa is very safe in the management of hypertension in pregnancy.
•Apart from the side effects listed for clonidine, methyldopa is associated with immunological effects leading to hepatitis and pyrexia.
•M-dopa could also cause haemolytic anaemia

51
Q

Mechanism of action nitroprusside ,adverse effects and clinical uses and route of administration and name two other vasodilators

A

is an inorganic nitro-vasodilator which acts by releasing nitric oxide, an unstable compound which causes vasodilation.
It is reserved for hypertensive emergencies.
It dilates arterioles and veins, reducing both peripheral resistance and venous return.
It is given by i.v. infusion and has a duration of effect of less than 5 min.

ADRs: Confusion, psychosis, metabolic acidosis.
Other vasodilators include hydralazine and minoxidil
Reserpine

52
Q

What is reserpine,Mechanism of action of reserpine ,adverse effects,contraindications and clinical uses and route of administration

A

Reserpine is an alkaloid obtained from Rawoulfia spps.
•It was originally used in psychiatry
•Reserpine acts by inhibiting the transport of dopamine and noradrenaline into the storage granule/vessicles
•Thus reserpine causes the depletion of neuronal stores of the catecholamines both centrally and peripherally.
•The major central side effect is depression/impotence
•Currently reserpine is not indicated for use antihypertensive in Ghana

Pharmacology (11 decks)

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