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MCQ exam > cardiovascular system > Flashcards

cardiovascular system Flashcards

1
Q

what happens when you activate the ALPHA-1 receptors

A
  • increase in calcium causes vasoconstriction which increases peripheral resistance. This increases blood pressure
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2
Q

Name some visceral smooth muscle tissue that can contract due to activation of ALPHA-1 receptors

A
  • bladder sphinctor
  • uterus
  • iris radial muscle
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3
Q

what happens when you activate ALPHA-2 receptors

A
  • inhibits adenylyl cylcase (cAMP)a and protein kinase A (PKA)
  • This decreases neurotransmitter release (noradrenalien/acteylcholine)
  • Also decreases insulin release
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4
Q

what happens when you activate BETA-1 receptors

A
  • increase in adenylyl cylcase (cAMP) and protein kinase A (PKA)
  • Beta-1 receptors in the SA node are activated and this increases heart rate
  • beta-1 receptors in the cardiac myocytes are activated and this increases force of attraction.
  • Beta-1 receptors in the kidneys are activated and renin is secreted which increases blood pressure

(all of the above increase blood pressure)

  • activation of Beta-1 receptors in the adipocytes causes lipolysis so increase in fats available for working muscle
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5
Q

which 2 types of receptors can be activated to increase blood pressue

A
  • ALPHA-1 receptors

- BETA-1 receptors

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6
Q

what happens when you activate BETA-2 receptors

A
  • increase in cAMP and PKA causes bronchodilation and vasodilation (of only the blood vessels in the skeletal muscle)
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7
Q

why does activation of BETA-2 receptors have no effect on the overall blood pressue

A

because activation of beta-2 receptors only causes vasodilation in the blood vessels of the skeletal muscles. It doesn’t affect all the other blood vessels so the vasodilation of skeletal muscle has no effect on the overall/net blood pressue

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8
Q

what happens to some visceral smooth muscles when BETA-2 receptors are activated? Name some examples of these smooth muscles

A

The visceral smooth muscles relax. eg:

  • bladder
  • uterus
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9
Q

what can happen as a side effect when BETA-2 receptors are activated

A

muscle tremor

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10
Q

which receptors does adrenaline activate

A

adrenaline activates all receptors (alpha 1, alpha 2, beta 1 , beta 2)

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11
Q

what is the difference between which receptors noradrenaline and adrenaline activate

A
  • adrenaline activates all receptors (alpha 1, alpha 2, beta 1, beta 2)
  • Noradrenaline acitvates all the same as adrenaline except it doesn’t activate beta 2 receptors
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12
Q

name an example of a BETA-2 agonist

A

salbutamol

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13
Q

name an example of an ALPHA-1 agonist

A

phenylephrine

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14
Q

name an example of a BETA-1 receptor agonist

A

dobutamine

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15
Q

what receptors do bronchodilators activate

A

BETA-2 receptors

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16
Q

what are the unwanted side effects of bronchodilators (beta-2 agonists)

A
  • tremor (caused by activation of muscle spindle)
  • tachycardia (caused by activation of beta-2
    receptors in the heart)
  • nervous tension (due to effect on CNS)
  • hypokalaemia (stimulation of sodium/potassium ATPase in skeletal muscle)
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17
Q

how do you limit the unwanted side effects caused by bronchodilators

A

by using inhalation administration instead of oral

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18
Q

what drug class of propranolol

A

beta-antagonist

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19
Q

which 2 types of receptors does propranolol inactivate

A

beta-1 receptors AND beta-2 receptors

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20
Q

what drug class is atenolol

A

beta-1 antagonist

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21
Q

what receptor does atenolol inactivate

A

beta-1 receptor

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22
Q

what are beta-blockers

A

beta-1 anatagonists

23
Q

what are the unwanted effects of beta-blockers (beta-1 anatagonists)

A
  • Bronchoconstriction (do not use in asthma, bronchitis, or emphysema)
  • Worsening of cardiac failure/ heart block (do not use in patients with heart failure unless taken with oxprenolol too)
  • Hypoglycaemia (dangerous in diabetics because beta-blockers mask symptoms of hypoglycaemia)
  • Cold extremities (Raynaud’s disease)
  • Vivid dreams (caused by propranolol but not atenolol)
24
Q

why should you never use a beta-blocker in people with asthma/bronchitis/emphysema

A

because beta-blockers cause bronchoconstriction

25
Q

why should you never use beta-blockers in patients with heart failure

A

because beta-blockers can cause worsening of cardiac failure/heart block

26
Q

why are beta-blockers dangerous in diabetics

A

because beta-blockers cause hypoglycaemia so taking beta-blockers can mask the symptoms of hypoglycaemia in diabetic patients

27
Q

which beta-blocker causes vivid dreams as a side effect

A

propranolol

28
Q

what is atrial fibrillation/flutter

A

an irregular and rapid heart beat

29
Q

what is paroxysmal supraventricular tachycardia

A

a rapid but REGULAR heart beat. it happens from time to time (paroxysmal)

30
Q

what is an ectopic heartbeat

A

both an irregular heart rate and irregular heart rhythm

- extra/ skipped heartbeats

31
Q

what is multifocal atrial tachycardia

A

electrical impluses coming from multiple locations in the atria

32
Q

what is ventricular fibrillation/tachycardia

A

a rapid heartbeat that is initiation in the ventricles

- it is life threatening when rapid and sustained or pulseless

33
Q

what is heart block

A

fibrosis or ischaemic damage to the AV node. The atria and ventricles beat independentally

34
Q

what is asystolic arrest

A

when the electrical activity in the heart completely stops

35
Q

what are the 5 main mechanisms that lead to dysrhythmia

A
  • ectopic pacemakers (cardiac tissue other than sa node initiates heart beat)
  • delayed after-depolarization (build of calcium in cells leads to chain of action potentials)
  • re-entry circuits (tissue damage causes action potential to travel in circles)
  • congenital abnormalities (new conducting pathways formed between atria and ventricles)
  • heart block (damage to av node causes atria and ventricles to beat independentally)
36
Q

what is wolf-parkinson-white syndrome

A

an inherited abnormality where new conducting pathways between atria and ventricles are formed known as kent bundles. These kent bundles can cause atrial flutter which causes sudden death. They can also form a re-entry circuit

37
Q

why are dysrhythmias dangerous

A
  • because the heart needs to co-ordinate properly to pump blood around the body. If it doesn’t this can lead to poor blood supply to the rest of the body.
  • also turbulent blood flow in the heart may lead to thrombosis/ embolism
38
Q

when are sodium channel blockers used? name an example of a sodium channel blockers

A

an example is lidocaine
- it is used IV for ventricular dysrhythmia to suppress rapid action potentials. It works by blocking open or inactivated sodium channels

39
Q

name two clinical uses for beta-blockers (propranolol and atenolol)

A
  • Hypertension
  • Angina
  • used in supraventricular and ventricular dysrhythmias
40
Q

What is the clinical use for potassium channel blockers?

name an example

A

an example is amiodarone

clinical uses:

  • supraventricular and ventricular dysrhythmias
  • treat wolff-parkinson-white syndrome
41
Q

how do potassium channel blockers work to slow down the heart rate

A

blocking the K+ channels prolongs the action potential and refractory period which slows down the heart rate as less action potentials occur

42
Q

how does amiodarone (a potassium channel blocker) cause grey-skin discolouration as side effect

A

Because the amiodarone builds up in the skin and eyes. it is photo-reactive which causes the grey-skin discolouration

43
Q

describe vaughan-williams classification of antidysrhythmic drugs

A
  • class 1: sodium channel blockers
  • class 2: beta-1 blockers
  • class 3: potassium channel blockers
  • class 4: calcium channel blockers
    class 5: various
44
Q

what is the first line treatment for hypertension in under 55s

A

ace inhibitor or angiotension inhibitor

45
Q

what is the first line treatment for hypertension in over 55s or black african/carribeans

A

calcium channel blocker

46
Q

what is high blood pressure

A

a blood pressure of 140/90mmhg or more

47
Q

Name 3 things that high blood pressure leads to if left untreated

A
  • stroke
  • ischaemic heart disease
  • peripheral vascular disease
48
Q

How is the angiotensin-converting enzyme involved in blood pressure control

A

When blood pressure is low, renin is released by the kidneys which produces angiotensin. Angiotensin is converted to angiotensin 2 by the angiotensin-converting enzyme (ACE) which causes vasoconstriction and increases blood pressure

49
Q

How to (angiotensin-converting enzyme) ACE inhibitors work?

Name some examples of ACE inhibitors

A

They prevent angiotensin being converted to angiotensin 2. This dilates the blood vessels and decreases cardiac workload so reduced blood pressure.

examples: Ramipril, lisinopril, enalapril

50
Q

Name a few side effects angiotensin converting enzyme (ACE) inhibitors

A
  • persistent dry cough
  • rash
  • hypotension
51
Q

can ACE inhibitors be used in pregnacy

A

NO. They should not be used in pregnancy as it can increase risk of congenital abnormalities

52
Q

how do angiotensin receptor blockers (ARB) (also known as angiotensin 2 antagonists) work?

name an example of these drugs

A

They block angiotension receptors so less/no angiotensin 2 formed. So decrease in vasoconstriction (vasodilation occurs)

examples: Losartan, Candesartan, Valsartan

53
Q

how do calcium channel blockers work?

Name some examples of calcium channel blockers

A

They inhibit the opening of L-type calcium channels. The reduces the contraction of cardiac myocytes and reduced AV node conduction which decreases heart rate

examples: amlodipine, verapamil, nifedipine, diltiazem

54
Q

which class of drugs interacts with grapefruit juice

A

calcium channel blockers

MCQ exam (6 decks)

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