Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Drugs > Hypertension 2 > Flashcards

Hypertension 2 Flashcards

1
Q

Calcium channel blockers

A

target L type calcium channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

People over 55 and African

A

calcium channel blockers are first line treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

2 types of calcium channel blockers

A

1) cardio selective

2) vaso selective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cardio selective

A

selective for heart

verapamile and diltiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Vaso selective (dihydropyridines)

A

act principally on peripheral blood vessels

get name from being derivatives of 1,4 dihydropyridine

in clinical use since 1980s

highly effective for mild to moderate hypertension

names end in dipine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What calcium blockers are mostly used?

A

Vaso selective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What determine selectivity?

A

1) different subunit combinations in L type calcium channel from smooth muscle compared to heart?

2) different states of the channel predominate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Vascular channel selectivity

A

more time in inactivated state (smooth muscle more depolarized, depolarization favors inactivation, higher affinity to inactivated state)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Mechanism of vaso selective calcium channel blocker

A
  • diameter of resistance arterioles is one of the main determinants of blood pressure (small vessels connect arteries to capillaries)
  • resistance arterioles have a layer of smooth muscle thats innervated by the SNS
  • when SNS is activated the smooth muscle contracts reducing diameter of arteriole and increasing blood pressure
  • even at rest there is small underlying level of sympathetic activation known as sympathetic tone which means vessel will be partially constricted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cardio selective drugs selectivity

A

bind tighter to open state of calcium channel and with frequent depolarization of cardiac muscle, channel spend more time in this state so open state favored

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Signalling in vascular smooth muscle

A

smooth muscle contains 1 alpha adrenoceptor which are activated by noradrenaline released by SNS and by adrenaline from circulation via a Gq coupled signaling cascade

results in smooth muscle depolarizing and activation of L type calcium channels

calcium’s entry to these channels leads to smooth muscle contraction and narrowing of the resistance arteriole

blocking calcium channels means smooth muscles unable to contract and diameter of resistance arteriole will increase

this is how calcium blockers decrease blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Side effects of calcium channel blockers

A

CCBs are normally well-tolerated by patients and are considered safe drugs.

The most common side effects are headache (caused by dilation of blood vessels in the brain), flushing, dizziness and swollen ankles.

They can also sometimes cause gastrointestinal problems such as nausea and abdominal pain, palpitations (where you are conscious of your heartbeat) and reflex tachycardia (when the body tries to compensate for lowered blood pressure by speeding up the heart).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Drugs that act on RAAS (4)

A
  • renin inhibitors
  • aldosterone antagonists
  • ACE inhibitors
  • ARBs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

ACE inhibitor examples (3)

A
  • captopril (prescribed less commonly)
  • lisinopril
  • ramipil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

ACE inhibitor use

A
  • first line treatments for people under 55 (most common)
  • second- line treatment for older patients in combination with CCBs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Actions of ACE inhibitors

A
  • they block angiotensin converting enzymes and prevent conversion of inactive angiotensin to active angiotensin 2 and 3
  • this prevents activation of angiotensin II type 1 receptors decreasing blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Side effects of ACE inhibitors

A
  • ACE inhibitors are usually safe drugs but many people taking them experience a persistent, dry cough (common)
  • angiotensin converting enzyme, in addition to its role producing angtotensin II, is responsible for the breakdown of a peptide called bradykinin. Bradykinin plays a role in pain signalling, inflammation and also has vasodilatory effects. It is the accumulation of bradykinin that leads to the cough.
  • bradykinin can cause blood vessels to become more permeable and lead to angioedema (rare), where the tissues become swollen. This is a potentially life-threatening condition. It is more common in African people which is why angiotensin receptor blockers are preferred over ACE inhibitors for these patients.
  • produce postural hypotension, which can make you feel dizzy when changing position suddenly. They can also cause gastrointestinal problems and headaches.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Angiotensin Receptor Blockers

A
  • alternative to ACE
  • have become cheaper so used more
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Actions of angiotensin receptor blockers

A
  • end in artan (angiotensin, receptor, antagonist)
  • act on opposite end of renin angiotensin aldosterone system cascade, competitively antagonizing the angiotensin II type 1 receptor AT1R
  • this causes less vasoconstriction and lower levels of aldosterone release reducing blood pressure
16
Q

Examples of angiotensin receptor blockers

A
  • losartan
  • candesartan
17
Q

Side effects of angiotensin receptor blockers

A
  • ARBs are generally well-tolerated by patients
  • they don’t block ACE, there is no build up of bradykinin and so there is a much lower risk of a cough
  • they avoid the more dangerous bradykinin-mediated side effect of angioedema. This makes them safer to use with Black African over ACE inhibitors for people in these groups.
  • they do, however, share with the ACE inhibitors the tendency to produce gastrointestinal problems, headache and postural hypotension
18
Q

Basic mechanism of thiazide diuretics

A
  • get rid of water in urine
  • lower blood volume
  • decrease blood pressure
19
Q

Mechanism of thiazides

A
  • sodium and chloride reabsorption in the distal convoluted tubule occurs via a sodium-chloride cotransporter (NCC).
  • this is the target of the thiazide diuretics such as bendroflumethiazide and thiazide-like diuretics such as chlortalidone
  • if reabsorption of sodium chloride is blocked, the osmotic pressure of the urine will increase because it will contain more NaCl.
  • this means that less water can be reabsorbed in more distal parts of the tubule and urine volume will increase.
  • this will lead to an immediate decrease in blood pressure
  • however, longer term the thiazides decrease blood pressure via vasodilation.
19
Q

Use of thiazides

A
  • 30% of patients with hypertension receiving a thiazide in North America and Western Europe
  • they are first-line options for some patients in the US and are second line treatments in the UK.
  • although their use has declined in recent years due to changes in the NICE guidelines, around 10-20% of people with hypertension in the UK are currently prescribed a thiazide
19
Side effect of thiazides
- increase urine production. Can increase urine production by 1-2 litres per day (50-100% increase) during the early stages of treatment, although this will decrease once the patient is stabilized on the drug. - excess sodium, potassium and magnesium to be lost in the urine, leading to electrolyte imbalance. This can be countered acted by dietary supplements. - increase in the risk of developing type 2 diabetes - GI tract problems, headache and postural hypotension (especially during the early phase of treatment).
20
Autonomic control of blood pressure
autonomic nervous system provides rapid control over blood pressure sympathetic nervous system acts on the vasculature and the heart to increase blood pressure blocking these effects can decrease blood pressure parasympathetic also modulates blood pressure via effects on heart it has minor effects on vasculature- no drug to target this
21
What effects will reduce blood pressure? (Beta 1 receptor)
- antagonize beta 1 receptors we will reduce heart rate and force of contraction - reduce activation of renin angiotensin aldosterone system by reducing renin release by juxtaglomerular apparatus
21
What effects will reduce blood pressure? (antagonists alpha 1 adrenoceptors)
- reduce vasoconstriction produced by activation of these receptors
22
What kind of drugs needed?
we need drugs that are selective for the specific type of receptor that we are targeting as other receptors could cause side effects
22
Beta blockers
- fourth-line treatments for hypertension usually in combination with other drugs - beta blockers more commonly used for hypertension include atenolol and bisoprolol. - more frequently used in angina and cardiac dysrhythmias. They are also used to treat the sympathetic nervous system symptoms of acute anxiety. - beta blockers have antihypertensive actions by reducing cardiac output and also by decreasing renin secretion. - lipid soluble beta blockers, which are able to penetrate the CNS may also exert small effects on blood pressure by acting on beta 1 adrenoceptors in the vasomotor control centre and reducing sympathetic tone. Longer term, the combination of these effects can lead to reductions in vascular resistance.
23
Propranolol
seldom used for hypertension these days because it has poor selectivity for beta 1 vs beta 2 adrenoceptors, which gives it a poor side effect profile.
24
Side effects of the beta blockers 2 categories
1) those due to actions on beta 1 adrenoceptors in tissues other than the heart 2) those caused by actions on beta 2 adrenoceptors
24
How to mediate side effects?
having drugs that are more beta 1 adrenoceptors selective e.g. atenolol and bisoprolol. However, the beta 1-mediated effects are an inevitable liability of the drug class
25
Beta 1 mediated side effects
- heart failure: beta 1 adrenoceptors control cardiac output beta blockers are capable of precipitating heart failure and so need to be used with caution in vulnerable patients. - postural hypotension - lipid soluble beta blockers like propranolol can cause CNS side effects. Propranolol, for instance, is renowned for producing vivid dreams. Atenolol and bisoprolol are much less lipid soluble so do not produce this effect.
26
Beta 2 mediated side effects (3)
Selectivity therefore only reduces the risk of beta 2 mediated side effects rather than eliminating them. bronchodilation- agonists at beta 2 receptors are important drugs for treating asthma. Blocking these receptors can have serious consequences – it can trigger an asthma attack- beta blockers are used with caution in people with asthma. peripheral vasoconstriction and in people with peripheral artery disease- claudication. Vasoconstriction can also occur in other tissues. This can result in a condition called Raynaud’s phenomenon, which occurs most commonly in the fingers (and toes).
27
Beta blockers and diabetes
beta blockers increase the likelihood of developing type II diabetes by several different mechanisms
27
What effects do beta 2 receptors have?
reduction in insulin release and reduced insulin sensitivity
28
Percentage of diabetes increase due to beta 2 receptor effects
effects can increase the risk of diabetes by around 30%
29
Beta 2 receptors for people that already have diabetes
For people with established diabetes, beta blockers also pose a risk. First, activation of the sympathetic nervous system by low blood sugar levels (hypoglycaemia) produces effects such as sweating, anxiety, trembling and palpitations. Ignoring symptoms can lead to confusion, dizziness, seizures, loss of consciousness and ultimately coma and death. warning signs rely on activation of beta adrenoceptors and so blocking them will mask the signs of sympathetic activation.
30
Beta 2 receptors and hypoglycaemia
beta 2 adrenoceptors increase glycogen breakdown by the liver which is one of the mechanisms the body uses to counteract hypoglycaemia. Non-selective beta blockers will also block this compensatory mechanism.
31
How do beta 2 receptors increase risk of type 2 diabetes?
reduced insulin secretion--> reduced insulin sensitivity-->increase likelihood of type 2 diabetes
32
How do beta 2 receptors increase risk of hypoglycaemia?
reduced warning of hypoglcaemia--> reduced glycogen breakdown--> increase likelihood of hypoglycaemia
33
Alpha adrenoceptor blockers
fourth line treatments for hypertension
34
How do alpha adrenoceptor blockers end?
zosin eg: prazosin and doxazosin
35
How do alpha adrenoreceptors treat hypertension?
Alpha 1 adrenoceptor antagonists treat hypertension by dilating resistance arterioles. They act at the start of the signalling pathway that the vasoselective calcium channel blockers act on. Despite acting on the same general pathway, they aren’t as effective as the CCBs in treating hypertension and are currently used mainly as add-on drugs in patients who are proving difficult to treat.
36
Side effects of the alpha blockers
generally well-tolerated and aren’t associated with common dangerous side effects in the same way as the beta blockers. postural hypotension and can cause GI tract upsets

Drugs (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions