Hypertension Flashcards

(42 cards)

1
Q

What is the normal pathway which involves angiotensin converting enzyme?

A

When BP drops, renin is released by the kidneys which acts acts on angiotensinogen released by liver to form angiotensin I. ACE is then released from the lungs to convert Angiotensin I to Angiotensin II.

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2
Q

What is the function of angiotensin II?

A

Acts on the adrenal gland to stimulate the release of aldosterone which acts on the kidneys to stimulate reabsorption of salt. It also acts on blood vessels stimulating vasoconstriction.

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3
Q

What is the function of ACE inhibitors?

A

Inhibits the conversion of angiotensin I to angiotensin II, lowering total resistance in the blood vessels and reducing release of aldosterone (thereby reducing salt retention).

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4
Q

What are some common ACE inhibitors?

A

Ramipril, Enalapril, Lisinopril, Perindopril
commonly ending in ‘pril’

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5
Q

What are some common side effects of ACE inhibitors?

A

Cough (excess bradykinin), diziness, orthostatic hypotension, acute kidney injury, Hyperkalaemia (excess potassium)

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6
Q

What is a rare side effect of ACE inhibitors?

A

Angioedema (swelling of the mouth). African descent and smokers most at risk

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7
Q

How do Angiotensin II receptor blockers (ARB) work?

A

Work by blocking the action of angiotensin II by binding to AT1 (receptor) and preventing angiotensin II from binding.

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8
Q

What are the downstream effects of ARBs?

A

Increase vasodilation and reduce aldosterone secretion, lowering salt retention.

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9
Q

What are some common ARBs?

A

Candesartan, Irbesartan, Losartan
commonly ending in ‘sartan’

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10
Q

What do calcium channel blockers do?

A

Prevent calcium from entering the cells. They cause peripheral vasodilation, coronary vasodilation and reduce the rate & force of contractions.

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11
Q

What are the two different types of calcium channel blockers?

A

Dihydropyridines and non-dihydropyridines

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12
Q

How do dihydropyridines work (CCB)?

A

Cause vasodilation of blood vessels, helping to lower hypertension

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13
Q

How do non-dihydropyridines work (CCB)?

A

Slow the heart rate affecting myocardial tissue.

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14
Q

What are some common dihydropyridines (CCB)?

A

nifedipine, amlodipine, felodipine
commonly ending in ‘dipine’

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15
Q

What are some common side effects of calcium channel blockers?

A

Edema (from peripheral vasodilation, especially common in the ankles), flushing, dizziness, reflex tachycardia, headache

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16
Q

How do thiazide-like diuretics work?

A

They inhibit sodium and water resorption in the kidneys. More sodium is excreted in urine and therefore more water. Reduced blood flow overtime decreases BP

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17
Q

What are the names of some common thiazide like diuretics?

A

Bendroflumethiazide, indapamide

18
Q

What are some side effects of thiazide-like diuretics?

A

Dizziness, electrolyte imbalance, GI disturbance, gout (low doses achieve full effect with fewer side-effects)

19
Q

Why are beta blockers not an overall first line treatment?

A

Effective at reducing BP but not as effective as other drugs in reducing overall risk of stroke and cardiovascular disease

20
Q

When are beta blockers a first line treatment?

A

If younger women of child bearing age, evidence of increased sympathetic drive, intolerance/contraindications to ACE/ARBs

21
Q

What are the names of some common beta blockers?

A

Atenolol, carvedilol, metoprolol

22
Q

What are some common side effects of beta blockers?

A
  • Bronchospasms in susceptible individuals (avoid in asthma)
  • fatigue
  • cold extremities
  • nightmares
  • adversely affect carb metabolism and increased risk of T2 diabetes
23
Q

What is the mechanism of alpha blockers?

A

Binds to alpha I receptors. Prevents norepinephrine from tightening the muscles in the walls of the smaller vessels allowing them to stay open, improving BP and blood flow

24
Q

What are the names of some common alpha blockers?

A

Doxazosin, prazosin

25
What are some common side effects of alpha blockers?
dizziness, drowsiness, headache, low BP (postural hypotension), nasal congestion
26
What are some key factors that contribute to BP regulation?
Circulatory volume, force of ventricular contractions, elasticity of arteries, peripheral resistence
27
What kinds of things affect peripheral resistance?
Viscosity: sticky blood harder to pump Length: longer vessels=more surface area=more friction Radius: much greater significance on BP than length or viscosity
28
What is the role of arterial baroreceptors and where are they located?
Pressure receptors located in carotid sinus and aortic arch conduct signal to medulla which then signals back though the vagus nerve to either vasodilatoe/vasoconstrict or increase/decrease HR.
29
Describe the role played by atrial stretch receptors?
Atrial myocytes detect changes in blood volume (esp. in venous return) and release atrial naturietic peptide (ANP) which promotes secretion of sodium in urine and inhibits the secretion of ADH
30
How do stroke volume, heart rate and peripheral resistance affect BP?
Heart rate (HR): Increases cardiac output by pumping more times per minute → raises blood pressure. Stroke volume (SV): More blood ejected per beat increases cardiac output → raises blood pressure. Peripheral resistance (PR): The amount of force exerted on circulating blood by the vasculature. Narrower or constricted blood vessels increase resistance to blood flow → raises blood pressure.
31
In what circumstances can hypotension and hypertension arise?
Hypotension: blood loss, dehydration, sepsis, heart failure, endocrine disorders (e.g., Addison’s disease-autoimmune). Hypertension: essential (genetic, lifestyle), kidney disease, endocrine disorders (e.g., Conn’s disease (tumor of adrenal cortex), RAAS overactivity, medications.
32
How is ADH involved in the long-term regulation of blood pressure?
Increases permeability of the kidney’s collecting ducts to water, promoting reabsorption back into the bloodstream, increasing blood volume and pressure. At higher concentrations, it causes blood vessels to constrict, increasing peripheral resistance and raising blood pressure.
33
Summarize the pathophysiology of hypertension
Hypertension results from increased cardiac output and/or peripheral resistance due to: -Overactive sympathetic nervous system causing vasoconstriction -Excess fluid retention via RAAS activation -Impaired kidney sodium excretion -Vascular remodeling increasing resistance -Genetic and lifestyle factors also contribute, leading to sustained high blood pressure.
34
What are some consequences of untreated hypertension?
Heart attack, stroke, narrowing of blood vessels in kidneys, atherosclerosis (narrowing of blood vessels due to plaque build-up)
35
What is stage 1 hypertension?
Clinic blood pressure ranging from 140/90 to 159/99 mmHg.
36
What is stage 2 hypertension?
Clinic blood pressure ranging from 160/100 to 179/119 mmHg.
37
What is stage 3 hypertension?
Clinic systolic BP is ≥180 mmHg or clinic diastolic blood pressure ≥120 mmHg.
38
What tests would you run to detect end organ damage or other complications of hypertension?
Urinalysis (albumin/creatinine ratio), ECG, U+E, lipid profile, BM/HbA1C, Fundoscopy, check for neurological symptoms and heart sounds
39
How can hypertension be managed by lifestyle changes?
Weight management (1kg=1mmHg), lower alcohol intake, aerobic exercise (helps with artery elasticity), reduce salt and fat intake.
40
What is cardiac output?
Volume of blood each ventricle pumps (L/minute)
41
What is pulse pressure?
The difference between systolic and diastolic blood pressure
42
How do beta-blockers work?
Act on the heart to reduce cardiac output and on the kidneys to inhibit renin secretion.