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Cardiorespiratory > Drug Treatments for CVD > Flashcards

Drug Treatments for CVD Flashcards

1
Q

what are the 4 main types of CVD?

A
  1. coronary heart disease
  2. stroke and tias (transient ischaemic attack (TIA) or “mini stroke”)
  3. peripheral arterial disease (e.g. atherosclerosis in the legs)
  4. aortic disease
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2
Q

how many adults, worldwide, have hypertension? what is hypertension a risk factor for?

A

worldwide: 1/3 adults have hypertension
significant risk factor for CVD

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3
Q

what are optimal, normal, high normal, grade 1, 2 & 3 systolic and diastolic BP?

A
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4
Q

what are modifiable factors that can manage hypertension?

who gets drugs for hypertension management?

A
  • environment / lifestyle
  • salt & smoking: salt minisation
  • *all people with hypertension should** **be given lifestyle advise
  • Grade 1 hypertension with high risk for CVD immediately get drugs. but if low / moderate risk without CVD or renal disease,**after 3-6 months of lifestyle intervention & BP still not controlled = drugs
  • Grade 2: drugs
  • Grade 3: drugs
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5
Q

which patients respond to different hypertension drugs?

A
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6
Q

which pathway do angiotensin converting enzymes (ACE) inhibitors target?

A

Renin-angiotension-aldoesterone system (RAAS)

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7
Q

what activates the RAAS system? (3)

A
  1. sympathetic nerve activation (via B-adrenoreceptors)
  2. renal artery hypotension
  3. decreased sodium delivery to the distal tubules of the kidney
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8
Q

explain how RAAS mechansim works

A
  1. activation of juxtaglomerular (JG) cells cause prorenin –> renin
  2. renin converts angiotensinogen into angtiotension I
  3. Angiotension converting enzyme (ACE), converts **angiotension I -> angiotension II
  4. Angiotension II binds to eitherAngiotension type I or II receptors** and has differing effects, depening on where it binds:
    i) proximal tubule: Increases Na+ reabsorbtion, which increases blood flow, which increases BP
    ii) adrenal cortex: increases aldosterone, which causes increase Na+ reabsorbtion in distal tubule, increase bloodflow and BP
    iii) systemic arterioles: binds to GPCR = artriolar vasoconstriction = increases BP
    iv) brain: stimules release of ADH = increase Na reabsorbtion
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9
Q

what are major classes of antihypertensive agents? (5)

A
  1. angiotension converting enzyme inhibitors (ACE inhbitors): block conversion of angiotension I to II

2. angiotension II receptor blockers

3. dihydropyridine calcium channel blockers:

4. thiazide diuretics: inhibit Na-Cl contransporter in DCT = natriuresis

  1. loop diuretics: Inhibit Na-K-Cl cotransporter in loop of Henle = natriuresis
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10
Q

for awareness xoxo

A
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11
Q

what is mechanism of action of ACE-I?

A
  1. inhibit ACE
  2. decreases production of angiotension II
  3. causes vasodilation of small resistance arteries
  4. decreases systemic vascular resistance
  5. decreaeas BP.
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12
Q

how do loop diuretics work? / mechanism of action?

what does this mean regarding K scerection in urine?

good for long term or acute response?

e.g.?

A
  • inhibit the luminal Na-K-2Cl contransporter in thick ascending limb of LoH
  • get increased delivery of Na to distal tubule, enhances K secretion into urine

good for acute response, more research needed for long term reduciton in hypertension

e,g, Furosemide

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13
Q

how do thiazide diuretics work?

A
  • *inhibits Na-Cl transporter in DCT:**
  • blocks the secretion of Na (natriuresis)
  • loss of water
  • have less extracellular volume
  • have less venous return and cardiac output
  • decrease in BP

unaware of how they work long term to decrease HT.

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14
Q

how do calcium channel blockers work?

what are the two major types? & mech of action for each

A

- block Ca entry to vascualr smooth muscle and myocardial cells: interrupt excitation-contraction coupling

types:

  1. dihydropyridine CCBs: vasodilate dominately. reduced systemic vascular resistance
  2. non dihydropyridine CCBs: reduce HR, contractility, conduction. may worsen heart failure tho
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15
Q

what is angina?

A

restricted blood supply to the heart

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16
Q

what types / clases of drugs are used to treat angina?

A
17
Q

how does nitroglycerin (and glyceryl trinitrate) work to treat angina?

A

MOA:

  • nitroglycerin given - a source of nitrates
  • converted to NO by **aldehyde dehydrogenase-2 enzyme
  • NO binds toguanylyl cyclase**
  • guanylyl cylase causes GTP –> cGMP
  • cGMP activates myosin-LC-PO4 –> myosin-LC
  • causes relaxtion of muscle cell
  • vasodilation
18
Q

what is effect of nitroglycerin (and glyceryl trinitrate) in low doses and high doses?

A
19
Q

what is MOA for beta blockers for treating angina?

A

Beta Blockers

  • B1 receptor antagonist:
  • causes reduced HR (@ SA node)
  • decrease in o2 demand at SA node
  • negative inotropic effect
  • decrease BP
  • decreased myocardial oxygen demand
20
Q

what are the two MOA for calcium channgel blockers?

A
  • intracellular Ca2+ influx stopped

i) Left ventricle and HR decrease: less o2 consumption in myocardium

ii) vascular smooth muscle contraction inhibition: coronary artery dilation = coronorary BF increaeed, o2 supply in myocardium increased

decreases angina

21
Q

what is heart failure

a) symptoms?
b) signs?
c) normally caused by?

A

symptoms: breathlessness, ankle swelling, fatigue

signs: elevated JVP, pulmonary crackles, peripheral oedema

normally caused by: structural and / functional cardiac abnormality = decreased cardiac output

22
Q

what is ejection fraction?

what is normal, borderline and reduced ejection fraction?

A

ejection fraction: the percentage of blood leaving your heart each time it contracts

normal ejection fraction: 50-70% (50/70% of blood is pumped out every cardiac cycle)

borderline ejection fraction: 41-49%

reduced ejection fraction: <40%

23
Q

what are three types of drugs used for drugs in heart failure?

A
  • positive inotropic drugs
  • vasodilators
  • misceallaneous drugs for chronic failure
24
Q

what is recommended for patients with HF & preserved / mid range ejection fraction?

what is recommended for patients with HF & stable ejection fraction?

A

HF & preserved / mid range ejection fraction: diuretics

HF & reduced ejection fraction: ACE & BB

HF & stable ejection fraction: BB

Cardiorespiratory (41 decks)

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