Drug Treatments for CVD Flashcards
what are the 4 main types of CVD?
- coronary heart disease
- stroke and tias (transient ischaemic attack (TIA) or “mini stroke”)
- peripheral arterial disease (e.g. atherosclerosis in the legs)
- aortic disease
how many adults, worldwide, have hypertension? what is hypertension a risk factor for?
worldwide: 1/3 adults have hypertension
significant risk factor for CVD
what are optimal, normal, high normal, grade 1, 2 & 3 systolic and diastolic BP?
what are modifiable factors that can manage hypertension?
who gets drugs for hypertension management?
- 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
which patients respond to different hypertension drugs?
which pathway do angiotensin converting enzymes (ACE) inhibitors target?
Renin-angiotension-aldoesterone system (RAAS)
what activates the RAAS system? (3)
- sympathetic nerve activation (via B-adrenoreceptors)
- renal artery hypotension
- decreased sodium delivery to the distal tubules of the kidney
explain how RAAS mechansim works
- activation of juxtaglomerular (JG) cells cause prorenin –> renin
- renin converts angiotensinogen into angtiotension I
- Angiotension converting enzyme (ACE), converts **angiotension I -> angiotension II
-
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
what are major classes of antihypertensive agents? (5)
- 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
- loop diuretics: Inhibit Na-K-Cl cotransporter in loop of Henle = natriuresis
for awareness xoxo
what is mechanism of action of ACE-I?
- inhibit ACE
- decreases production of angiotension II
- causes vasodilation of small resistance arteries
- decreases systemic vascular resistance
- decreaeas BP.
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.?
- 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
how do thiazide diuretics work?
- *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.
how do calcium channel blockers work?
what are the two major types? & mech of action for each
- block Ca entry to vascualr smooth muscle and myocardial cells: interrupt excitation-contraction coupling
types:
- dihydropyridine CCBs: vasodilate dominately. reduced systemic vascular resistance
- non dihydropyridine CCBs: reduce HR, contractility, conduction. may worsen heart failure tho
what is angina?
restricted blood supply to the heart
what types / clases of drugs are used to treat angina?
how does nitroglycerin (and glyceryl trinitrate) work to treat angina?
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
what is effect of nitroglycerin (and glyceryl trinitrate) in low doses and high doses?
what is MOA for beta blockers for treating angina?
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
what are the two MOA for calcium channgel blockers?
- 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
what is heart failure
a) symptoms?
b) signs?
c) normally caused by?
symptoms: breathlessness, ankle swelling, fatigue
signs: elevated JVP, pulmonary crackles, peripheral oedema
normally caused by: structural and / functional cardiac abnormality = decreased cardiac output
what is ejection fraction?
what is normal, borderline and reduced ejection fraction?
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%
what are three types of drugs used for drugs in heart failure?
- positive inotropic drugs
- vasodilators
- misceallaneous drugs for chronic failure
what is recommended for patients with HF & preserved / mid range ejection fraction?
what is recommended for patients with HF & stable ejection fraction?
HF & preserved / mid range ejection fraction: diuretics
HF & reduced ejection fraction: ACE & BB
HF & stable ejection fraction: BB
