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BMS3052 > WEEK 3 SYSTEMIC AND PULMONARY HYPERTENSION > Flashcards

WEEK 3 SYSTEMIC AND PULMONARY HYPERTENSION Flashcards

1
Q

What are risk factors for hypertension?

A
  • genetics, smoking, stress, environment, diet
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2
Q

Are there generally symptoms for hypertension?

A
  • NO ‘silent killer’

-

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3
Q

What is hypertension a risk factor for? (3 main things)

A
  • Stroke
  • Heart failure
  • Coronary Artery disease
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4
Q

What is secondary hypertension?

A
  • It is when hypertension is secondary to other conditions
  • So other conditions CAUSE hypertension
  • e.g, drugs, renal and vascular disease, conns disease, cushings disease, tumours on adrenals, VEGF inhibitors in cancer treatment
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5
Q

What is the average normal systemic BP?

A
  • 120/80
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6
Q

What is the normal pulmonary blood pressure?

A
  • 25/8
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7
Q

What is a main factor that drives increases in blood pressure in terms of physiological measurements?

A
  • TPR (total peripheral resistance)

- TPR= MAP/CO

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8
Q

What do most drugs that lower BP dreduce?

A
  • They resduce TPR (afterload) - good vasodilators

- They do this by either directly or indirectly affecting the arteriole tone

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9
Q

What is the main reason as to whyhigh blood pressure occurs in the elderly or those resistant to medications?

A
  • The TPR increase
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10
Q

What is the BP for hypertension related target organ damage (TOD)?

A
  • more than 140/90
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11
Q

What are the effects of TOD?

A
  • Long term will cause target organ damage, exacerbates tissue inflammation, oxidative stress, hormones e.g. Ang II
  • affects the pulmonary blood vessels
  • Also affects the organs e.g. heart, kidney, eyes etc.
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12
Q

In terms of TOD, what does decreasing BP prevent?

A
  • Prevents target organ damage thus reducing morbidity and mortality rates of stroke, HF, CHD
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13
Q

What is the broad classification of drugs that are used to treat hypertension and HF?

A

ABCD

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14
Q

Which of the ABCD drugs is the first line of treatment for hypertension?

A
  • Usually ACE inhibitors or Angiotensin converting enzyhme blockerand ANgiotensin receptor blockers
  • Also Calcium channel blockers
  • If these don’t work, then they are given in combination, and if not, then diuretics are added, and if not then possibly adding a beta blocker if there are no contraindications
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15
Q

Why are beta blockers NOT the first line of treatment for hypertension?

A
  • Because patients may have other comorbidities that will be affected with the use of beta blockers
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16
Q

What are the central effects of angiotensin II?

A
  • Increase in blood pressure
  • Vasopressin release
  • Drinking response
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17
Q

What is important for long term blood pressure control that the body makes?

A
  • Angiotensin II
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18
Q

What are the peripheral effects of angiotensin II?

A
  • Vasoconstriction
  • Aldosterone release (sodium reabsorption,kidney)
  • Increase in NA release (sympathetic response)
  • Fibrosis
  • Hypertrophy
  • Oxidative stress
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19
Q

What is the rate limiting step in the formation of Ang II?

A
  • Renin release from kidneys
  • this leads to angiotensinogen release from the liver and the formation of angiotensin I which renin catalyses
  • then leads to Ang II from ACE enzyme catalysis
  • It is here where ACE inhibitors act
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20
Q

Which type of receptors does Ang II act on?

A
  • AT1 type receptors

- These are located in the target organs

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21
Q

After Ang II binds to the ATI receptors in the target organs, what are 3 main downstream events that occur?

A
  1. Vascular growth (hyperplasia and hypertrophy)
  2. Vasoconstriction (Can be direct or via increased NA release from symp nerves)
  3. Salt retention (via the secretion of Aldosterone from cortex of adrenals, and tubular Na+ reabsorption occurs)
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22
Q

What do the ACE inhibitor medications for hypertension releif end in?

A

‘Pril’

- e.g. Captopril, enalapril, perindopril

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23
Q

What is the action of ACE inhibitors?

A
  • Prevent angiotensin II formation and ninhibit bradykinin breakdown (Decrease ang II and increase BK)
  • this leads to a decrease in TPR (vasodilator)
  • Also leads to an increase in sodium and water excretion
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24
Q

What are the indications for ASCE inhibitors?

A
  • For hypertension and heart failure

- Preserve renal function in diabetes (diabetic nephropathy)

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25
Q

What are the adverse effects of ACE inhibitors?

A
  • Cough (due to increase in BK), headache
  • Hypotension (thus start with low dose)
  • Hyperkalaemia (too much K+. can cause arthymia)
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26
Q

What are the contraindications for ACE inhbitiors?

A
  • Renal failure if you have bilateral artery stenosis

- Avoid in pregnancy

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27
Q

What are the angiotensin receptor blockers known as ? -

A
  • ARBs; sartans

- ‘sartan’ is the name at the end of the differenet variants of drugs. e.g. Iosartan, Irbesartan, candesartan

28
Q

How do the ARBs/Sartans work?

A
  • They are AT1R antagonists
  • So they Inhibit the angiotensin induced vasoconstriction and aldosterone output
  • Decrease in the TPR (vasodilator)
  • Increase sodium and water excretion
29
Q

Is there a decrease in Ang II, and BK in ARBas/sartans?-

A
  • there is technically an increase in Ang II but it can’t bind to the receptor so it won’t be able to act
  • There is NO change in BK so if you are experiencing a cough, then you can switch to this one instead of the ACE inhibitors.
30
Q

What are the indications for ARBs/sartans?

A
  • Hypertension, HF, diabetic nephropathy

- For patients intolerant to ACE inhibitors (e.g. cough)

31
Q

What are the adverse effects of ARBs/sartans?

A
  • Same as the ACE inhibitors, e.g. hypotension (but less than ACEi) and hyperkalaemia (too much K+)
32
Q

What is involved in the protective arm of the RAS and what does this arm act to do in general?

A
  • ACE2! This then results in formation of Ang1-7
  • Acts to reduce inflammation, hypertropy and proliferation via the Mas receptor
  • Vasodilation, natriuretic
33
Q

Is ACE2 blocked by ACE inhibitors?

A
  • NO
34
Q

Is Ang (1-7) (formed by ACE2) thought to have cardioprotective effects?

A
  • YES
  • This is thought to occur via the MAS receptor
  • In corona virus, this is involved. The virus binds to the ACE2 receptor and results in a downregulation of the Ang (1-7) which leads to a build up of Ang II and thus activation of the RAS system (via AT1R) which could be involved in the lung/heart injury and thus increased stroke incidence post infection
35
Q

Which types of receptors does NA act on in the smooth muscle vaculature?

A
  • a1 receptors (alpha-1)
36
Q

Which types of receptors does NA act on in the heart?

A
  • B1 adrenoceptors (beta-1)
37
Q

By blocking the B1 receptor (heart), what does this result in?

A
  • Decrease in the sympathetic drive to the heart
  • Decrease in CO, HR, TPR
  • Inhibit renin release (thus decrease in Ang II)
  • not B1 receptors not only in the heart; also in kidney hence the decrease of renin release
38
Q

What is the general name given at the end of the beta blocker drug names?

A
  • ‘olol’

- e.g. propanolol, atenolol, metropolol

39
Q

Out of the beta blockers propranolol, atenolol and metroprolol, which one is non-selective for B1 and B2 adrenoceptors?

A
  • Propranolol is NON SELECTIVE
  • It is a B1 and B2 blocker
  • B2 receptors are found in the lungs so you do not want to be blocking these as they, when stimulated, cause relaxation of the blood vessels.
40
Q

What are 5 conditions that Beta blockers can be used for?

A
  1. Hypertension (but NOT the first line)
  2. Angina
  3. Post MI (by reducing the activity of NA on B1 receptors in heart)
  4. Arrythmias
  5. Clinically stable heart failure*
41
Q

It seems unusual, so why can Beta antagonists be used for the treatment/management of chronic stable HF?

A
  • They decrease the symp drive to the heart so this will remove the body trying to compensate by increasing the sympathetic drive to heart
  • Patients have too much release of NA and by reducing B1 stimulation, you can reduce the toxic effect in the heart and thus reduce arrythmia and ischaemia
42
Q

What are two types of beta blockers that are used for the treatment of heart failure?

A
  • Carvedilil and nebivolol
  • these are antiarryhmic
  • antiischameic
  • reduce the catecholamine toxcicity
43
Q

Should beta blockers for heart failure be given at ful dose straight away?

A
  • NOO
  • Because there is risk of hypotension and worsening renal function and also worsening heart failure thus should slowly increase dose and only when the patient is stalbe
44
Q

What are the adverse effects of beta blockers?

A
  • if non selective could lead to bronchoconstriction (due to B2 blockade)
  • Decreased heart contractility, bradycardia, AV block, exercise intolerance, claudication, impotence
  • Can exacerbate and mask hypoglycemia in those with diabetes
45
Q

What is the brief mechanism of action of Ca2+ channel blockers?

A
  • They block the L-type Ca2+ channel
  • This reduces the Ca2+ entry into the vascular (via a reflex) /cardiac cells but NOT skeletal muscle cells
  • So reduction in intracellular Ca2+
46
Q

Which two Ca2+ blocker drugs have more effects in the vasculature rather than directly on the cardiac cells?

A
  • Nifedipine and Amlodipine
  • These have more effects on SMCs
  • Lead to a decrease in BP and then an increase in HR due to the Baro reflex, and then a decrease in overal TPR
47
Q

Which two Ca2+ blocker drugs act directly on the cardiac cells to induce effects?

A
  • Verapamil and Diltiazem
48
Q

Order the 3 Ca2+ blocker drugs from most to least potent in the heart:

A

Verapamil> dilitazem>nifedipine

49
Q

What conditions are Ca2+ blockers used for?

A
  • Hypertension, angina, tachyarrythmias (supraventricular)
50
Q

What are the contraindiciations with Ca2+ blockers?

A
  • DO NOT USE if someone has HF

- Do not use verapamil or dilitiazem when combined with a beta blocker

51
Q

Why shouldn’t you use Ca2+ blockers if someone has HF?

A
  • Because if the heart is not working well, (low ejection fraction), then you don’t want to block that more
52
Q

Why shouldn’t you use verapamil or diltiazem when combined with a beta blocker (so Ca2+ + Beta blockers) ?

A
  • because these are working via different mechanisms and can lead to collapse
53
Q

In general, what do diuretics lead to?

A
  • Na+ excretion which leads to H2O excretion which leads to:
  • Decrease in blood volume, venous pressure and venous return (reduced capillary hydrostatic pressure promotes fluid reabsoption and thus less oedema)
54
Q

In general terms, what do diuretics initially lead to?

A
  • A decrease in CO
55
Q

In general terms, what do diuretics lead to in the longer term?

A
  • A decrease in normal CO and decrease in TPR (possibly y direct vasodilation)
56
Q

What are the three major classes of diuretics?

A
  1. Loop diuretics
  2. Thiazide diuretics
  3. Aldosterone receptor antagonists
57
Q

Where do loop diuretics act and what is their mechanism of action (also what is the name of one) ?

A
  • At the THICK ascending limb of Loop of Henley to block Na+/K+2Cl- symporter (type of cotransporter)
  • blocks 15-25% of filtered Na+
  • E.g. Furosemide
58
Q

Which diuretic class has the greatest diuretic efficacy?

A
  • The Loop diuretics e.g. Furosemide
59
Q

Where do the thiazide diuretics act and what is an example of one?

A
  • Act on the distal convoluted tubules to block the Na+/Cl- symporter
  • There is a modest increase in sodium excretion (5-10%)
  • so less sodium excreted but good at causing water and sodium loss
    e. g. Hydroclorothiazide
60
Q

What are the uses of diuretics (which conditions)?

A
  • mild-moderate hypertension e.g. thiazide (cheap and good)
  • Oedema due to:
  • Congestive HF (with or without hypertension)
  • pulmonary congestion
  • Renal/ lvier disease e.g. Furosemide
61
Q

Where does hydrochlorothiazide act?

A
  • In the distal convoluted tubules
62
Q

What are the adverse effects of loop/thiazides (diuretics, 2/3 classes)?

A
  • Electrolyte imbalance (hypokalemia- not enough K+)
  • Gout
  • High choleterol
  • High blood sugar
63
Q

Where do the aldosterone recpetor antagonists act (diuretics), what is their mechanism of action, and what is an example of one?

A
  • In the distal tubule/ collecting duct
  • They are known as K+ sparing diuretics
  • e.g. Spironolactone (Aldactone)–> blockcs Aldosterone
  • Inhibits mineralcorticoid (aldosterone) receptor (kidney) and in the heart it inhibits aldosterone induced fibrosis, so improves HF
64
Q

What are the clinical uses of spironolactone?

A
  • Combination use with thiazide or loop diuretics to produce weak diuresis without hypokalemia
  • Conditions with hyperaldosteronism
  • Interest with chronic HF
  • BUT adverse effect is hyperkalemia
65
Q

Does inhibiting RAS lead to hyperkalemia?

A
  • YES

- Due to ddecreased Na+ reabsoption

BMS3052 (14 decks)

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