Elm 8/9/10 Hypertension Flashcards

1
Q

Q: What are some types of cardiovascular disorders?

A

A: Hypertension, hyperlipidaemia, atherosclerosis, coronary artery disease, thrombosis, angina, dysrhythmias, stroke, heart failure, heart attack.

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2
Q

Q: What can cause cardiovascular disorders?

A

A: Cardiovascular disorders can be caused by both lifestyle factors and genetics.

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3
Q

Q: How is blood pressure measured and what do the numbers represent?

A

A: Blood pressure is measured as systolic/diastolic (e.g., 120/80). Systolic pressure is the pressure while the heart is contracting (maximum pressure), and diastolic pressure is the pressure while the heart is filling (minimum pressure). Pulse pressure is the difference between the two.

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4
Q

Q: What are the key features of hypertension?

A

A: Increased systolic pressure, increased diastolic pressure, increased pulse pressure.

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5
Q

Flashcard 39:
Q: How is hypertension quantified?

A

A: - Severe: Diastolic BP >120 mm Hg

Moderate: Diastolic BP 105-120 mm Hg
Mild: Diastolic BP 90-105 mm Hg

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6
Q

Q: What is hypotension?

A

A: Hypotension is decreased blood pressure.

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7
Q

Q: What are the two classifications of hypertension and their causes?

A

A: - Primary (essential or idiopathic) hypertension: cause unknown.

Secondary hypertension: identified cause (e.g., polycystic renal disease, renal artery stenosis, phaeochromocytoma).

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8
Q

Q: What are some lifestyle factors that increase the risk of primary hypertension?

A

A: Obesity, insulin resistance, high alcohol intake, high sodium/low potassium intake, age.

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9
Q

Q: What genetic factors are associated with primary hypertension?

A

A: Up to 65% (found from twin studies), around 10 genes identified that alter salt/water balance, other genes may affect obesity and alcohol consumption, epigenetics (such as maternal diet).

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10
Q

Q: What are the consequences of prolonged hypertension?

A

A: Coronary artery disease (myocardial infarction), stroke (cerebral haemorrhage, thrombosis, thromboembolism), heart failure.

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11
Q

Q: What lifestyle modifications can help treat hypertension?

A

A: Lose weight, limit alcohol intake, increase aerobic activity, reduce sodium intake, maintain potassium intake, maintain calcium and magnesium intake, stop smoking, reduce dietary fat and cholesterol.

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12
Q

Q: What types of antihypertensive drugs are used to treat hypertension?

A

A: ACE inhibitors, ATII antagonists, calcium channel blockers, beta blockers, diuretics.

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13
Q

Q: What is the basic principle behind antihypertensive medication?

A

A: The basic principle is to interfere with control mechanisms, aiming to reduce blood pressure by affecting cardiac output and peripheral resistance.

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14
Q

Q: Why are several studies conducted on the best medications for hypertension?

A

A: Most people with hypertension are taking multiple drugs, so studies are conducted to determine the most effective medications.

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15
Q

Q: What was compared in the ASCOT Trial (Anglo-Scandinavian Cardiac Outcomes Trial)?

A

A: The ASCOT Trial compared Amlodipine (+ perindopril) with Atenolol (+ bendroflumethiazide-diuretic).

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16
Q

Q: What were the results of the ASCOT Trial regarding blood pressure and incidence of CV disease?

A

A: Blood pressure was reduced in both groups, but the reduced incidence of associated cardiovascular disease was significantly greater in the amlodipine group.

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17
Q

Q: What medications were compared in the ALLHAT Trial (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial)?

A

A: The ALLHAT Trial compared chlortalidone (thiazide-like diuretic) with amlodipine or lisinopril.

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18
Q

Q: What were the findings of the ALLHAT Trial regarding blood pressure and heart attack risk?

A

A: Blood pressure was reduced in all three groups, but chlortalidone was superior. The risk of heart attack was similar in all three, but the risk of some associated cardiovascular diseases was lower with chlortalidone.

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19
Q

Q: What conclusion did the ALLHAT Trial reach about thiazide diuretics compared to other medications?

A

A: The ALLHAT Trial concluded that thiazide diuretics were superior to calcium channel blockers or ACE inhibitors.

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20
Q

Q: What should be the primary course of treatment for hypertension based on these studies?

A

A: A calcium channel blocker, ACE inhibitor, ATII antagonist, or thiazide-like diuretic should be the primary course of treatment.

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21
Q

Q: How are calcium channels classified?

A

A: Calcium channels are usually classified according to a system based on their location or functional characteristics.

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22
Q

Q: Where are L-type calcium channels found, and why are they ideal targets for blood pressure modulation?

A

A: L-type calcium channels are found in both cardiac and vascular smooth muscle, making them ideal targets for blood pressure modulation.

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23
Q

Q: What is the role of noradrenaline in determining the diameter of an arteriole?

A

A: Noradrenaline acts on the alpha 1-adrenoreceptor, activating phospholipase C, which triggers a cascade leading to intracellular calcium release and smooth muscle contraction.

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24
Q

Q: What are the steps in the process controlled by noradrenaline that leads to smooth muscle contraction?

A
  1. Noradrenaline activates the alpha 1-adrenoreceptor.

This activates phospholipase C.
Phospholipase C triggers inositol trisphosphate (InsP3) release.
InsP3 releases calcium from intracellular stores.
This activates calcium-sensitive chloride channels, causing depolarization.
Depolarization opens L-type calcium channels.
Increased intracellular calcium leads to smooth muscle contraction.

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25
Q

Q: At which step do calcium channel blocker (CCB) drugs act?

A

A: CCB drugs act at step 6 by blocking the opening of L-type calcium channels.

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26
Q

Q: What are the three types of calcium channel blockers?

A

A: Diltiazem (a benzothiazepine), Amlodipine (a dihydropyridine), Verapamil (a phenylalkylamine).

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27
Q

Q: Which calcium channel blockers mainly act on cardiac muscles, and which mainly act on vasculature?

A

A: Diltiazem and Verapamil mainly act on cardiac muscles, while Amlodipine mainly acts on vasculature.

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28
Q

Q: What is the summary of the effects of calcium channel blockers?

A

A: - Reduce the opening of L-type calcium channels.

Target organs: vasculature and heart.
Vessels: inhibit calcium entry.
Heart: reduced contractility and A-V conduction.
Side effects: headache and constipation.

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29
Q

Q: How can you recognize the names of ACE inhibitors, AII antagonists, calcium blockers, beta-blockers, and alpha-blockers?

A

A: - ACE inhibitors end in –pril.

AII antagonists end in –artan.
Calcium blockers end in –dipine.
Beta-blockers end in –olol.
Alpha-blockers end in –zosin.

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30
Q

Q: What is the purpose of the Renin-Angiotensin-Aldosterone System (RAAS)?

A

A: RAAS is used for slow compensatory control of blood pressure.

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31
Q

Q: How is the RAAS controlled and what does it respond to?

A

A: The RAAS is controlled by the sympathetic nervous system and responds to decreased blood flow to the kidney.

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32
Q

Q: What happens when the RAAS is stimulated?

A

A: When stimulated, there is a decrease in the production of renin.

33
Q

Q: What is the role of renin in the RAAS?

A

A: Renin catalyzes the production of angiotensin hormones, which increase aldosterone production (increasing salt and water retention) and cause vasoconstriction.

34
Q

Q: How does reducing renin affect blood pressure?

A

A: Reducing renin reduces the effects of the following hormones, thereby reducing blood pressure.

35
Q

Q: Describe the generation process of angiotensin hormones.

A

A: - Angiotensinogen (inactive) is produced by the liver.

Renin cleaves angiotensinogen to produce angiotensin I (inactive).
Angiotensin I is cleaved by ACE to produce angiotensin II (active).
Angiotensin II can be further cleaved to form angiotensin III and IV (partially active).

36
Q

Q: What are the effects of angiotensin II and occasionally angiotensin III?

A

A: They bind to the angiotensin I receptor, causing aldosterone secretion and vasoconstriction.

37
Q

Q: What stimulates the production of renin?

A

A: Adrenaline, prostacyclins, decreased Na in the distal tube, decreased blood pressure in the kidney, and actions of other hormones.

38
Q

Q: Where is renin released from and where is ACE found?

A

A: Renin is released from the juxtaglomerular apparatus into circulation. ACE is found in many tissues, allowing for local production of angiotensins.

39
Q

Q: What does Aliskiren do, and what are its side effects?

A

A: Aliskiren inhibits renin. Side effects include kidney problems, stroke, and hypotension.

40
Q

Q: Why are ACE inhibitors recommended and what are some examples?

A

A: ACE inhibitors prevent the production of active angiotensin II, reducing blood pressure. Examples include captopril and lisinopril.

41
Q

Q: What are the side effects of ACE inhibitors?

A

A: Initial hypotension and a cough.

42
Q

Q: What type of receptors are angiotensin receptors and which receptor is of interest?

A

A: All angiotensin receptors are G protein-coupled receptors. The angiotensin II type 1 receptor (AT1) is of interest because it modulates vascular effects and aldosterone release.

43
Q

Q: What do Angiotensin II Antagonists (ARBs) do, and what are some examples?

A

A: ARBs block the angiotensin receptor, preventing its function. Examples include losartan and candesartan.

44
Q

Q: What are the side effects of Angiotensin II Antagonists (ARBs)?

A

A: Hypotension, but no cough.

45
Q

Q: What is a diuretic?

A

A: A diuretic is any drug that produces diuresis (increased urine output).

46
Q

Q: What is the general effect of diuretics on electrolyte excretion?

A

A: Diuretics generally increase the excretion of Na, Cl, and water.

47
Q

Q: How do the effects of diuretics vary?

A

A: The pattern of electrolyte excretion and the maximum response vary with the class of diuretic.

48
Q

Q: Name the three main classes of diuretics.

A

A: Loop diuretics, thiazide diuretics, and potassium-sparing diuretics.

49
Q

Q: How do loop diuretics work and where do they act?

A

A: Loop diuretics work by stopping water absorption in the descending limb of the loop of Henle by blocking NaCl release. Examples: Furosemide, bumetanide.

50
Q

Q: Where do thiazide diuretics act and how do they work?

A

A: Thiazide diuretics work in the distal convoluted tubule (DCT) by blocking NaCl release, passing increased NaCl to other segments. Examples: Bendroflumethiazide, chlortalidone.

51
Q

Q: What are potassium-sparing diuretics used for, and name two examples.

A

A: They are used alongside other diuretics to prevent hypokalemia. Examples: Spironolactone, amiloride.

52
Q

Q: What is a major problem with loop diuretics and thiazides?

A

A: Hypokalemia (low potassium levels).

53
Q

Q: How do potassium-sparing diuretics help overcome hypokalemia?

A

A: They decrease trans-principal cell Na movement and the negative lumen potential.

54
Q

Q: What system do adrenoceptor antagonists target?

A

A: The sympathetic nervous system.

55
Q

Q: What effects do alpha 1 and beta 1 adrenoceptors have?

A

A: Alpha 1 adrenoceptors cause vasoconstriction, and beta 1 adrenoceptors increase heart rate and force of contraction.

56
Q

Q: What does doxazosin do and when is it used?

A

A: Doxazosin dilates arterioles and veins by blocking alpha 1 adrenoceptors. It is used when other therapy has proved ineffective or unacceptable.

57
Q

Q: Name the side effects of doxazosin.

A

A: Postural hypotension, urinary incontinence, retrograde ejaculation.

58
Q

Q: What type of drug is propranolol and what are its characteristics?

A

A: Propranolol is a competitive, non-selective beta-adrenoceptor antagonist that is very lipid-soluble.

59
Q

Q: Compare atenolol and bisoprolol in terms of beta 1 selectivity and water solubility.

A

A: Both atenolol and bisoprolol are beta 1 selective antagonists. Bisoprolol is more selective and moderately penetrates the blood-brain barrier, while atenolol has poor penetration and is more water-soluble than propranolol.

60
Q

Q: How do beta-blockers affect the heart, kidneys, and vasomotor center?

A

A: Beta-blockers reduce cardiac output (heart), decrease renin release (kidneys), and reduce sympathetic tone (vasomotor center).

61
Q

Q: What are some side effects of beta-blockers?

A

A: Bronchoconstriction, Raynaud’s syndrome, claudication, cardiac failure/heart block, glucose control issues, and vivid dreams.

62
Q

Q: Why should caution be used when prescribing beta-blockers to diabetic patients?

A

A: Beta-blockers can reduce insulin sensitivity and mask the warning signs of hypoglycemia.

63
Q

Q: What is the British National Formulary (BNF)?

A

A: A little book doctors use to choose a person’s prescription medicine.

64
Q

Q: What is the common suffix for beta blockers?

A

A: Beta blockers always end in –olol.

65
Q

Q: List some conditions beta blockers are used to treat.

A

A: Hypertension, angina, heart failure, dysrhythmias, and the physical symptoms of anxiety.

66
Q

Q: Through which receptors do beta blockers mainly exert their therapeutic effect?

A

A: Beta-1 adrenoceptors found in the heart.

67
Q

Q: What are cardioselective beta-blockers?

A

A: Drugs with high potency at beta-1 adrenoceptors and low potency at beta-2 adrenoceptors.

68
Q

Q: What are non-selective beta blockers?

A

A: Drugs that do not distinguish between beta-1 and beta-2 adrenoceptors.

69
Q

Q: Define the term “Indications” in the context of the BNF.

A

A: Conditions or factors that suggest a drug should be used.

70
Q

Q: Define the term “Cautions” in the context of the BNF.

A

A: Conditions or factors that increase the risk associated with the drug.

71
Q

Q: Define the term “Contra-indications” in the context of the BNF.

A

A: Conditions or factors that suggest a drug should not be prescribed.

72
Q

Q: Define the term “Side effects” in the context of the BNF.

A

A: Unwanted effects of a drug.

73
Q

Q: What happens during a bronchospasm?

A

A: Contraction of smooth muscle surrounding the airway, caused by an asthma attack or anaphylactic reaction.

74
Q

Q: How do bronchodilator drugs like salbutamol work?

A

A: They reverse the contraction of smooth muscle by relaxing it.

75
Q

Q: How can bronchospasms be reversed?

A

A: Using beta-2 adrenoceptor AGONISTS like salbutamol.

76
Q

Q: What is the role of noradrenergic tone in non-constricted bronchiole smooth muscle?

A

A: It helps to keep the smooth muscle relaxed.

77
Q

Q: What type of drug is Nadolol?

A

A: A beta-blocker.

78
Q

Q: What is a potential issue with some beta-blockers regarding asthma?

A

A: Some beta-blockers are non-selective between beta-1 and beta-2 adrenoceptors, which can affect bronchospasm management.