SEM 2__BM322 Pharmacology__BLOCK A Cardiovascular Flashcards
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Basics of pulmonary and systemic circulation
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Both Pulmonary and systemic have arteries with arterties carrying blood away from the heart and veins carrying blood from organs/ tissues back to the heart.
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Structure of Arteries and veins
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Arteries have thin lumen and thick wall <br></br>Veins have thick lumen and think wall
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Vascular structure consists of
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endothelial cells, smooth muscle cells, fibroblasts and PVAT
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blood pressure is created from
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force of blood being pushed against the walls of blood vessels (arteries) as it is pumped by the heart
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9
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Agonists of adenoceptors
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Noradrenaline/adrenaline<br></br>Isoprenaline <br></br>Phenylephrine
10
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Antagonists of adrenoceptors
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Propranolol - non selective beta blocker<br></br>Atenolol - Selective B1 blocker<br></br>Phentolamine - Non selective a-blockers <br></br>Prazosin - Selective a1 blocker<br></br>PAPP
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RAAS stands for
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Renin-angiotensin-aldosterone system
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15
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EDRFs
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Endotherial deirverd relaxing factors
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EDCFs
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endothelium derived contraction factors
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examples of EDRFs
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Nitric oxide (NO) <br></br>Prostacyclin (PGI2) <br></br>Hyperpolarizing factor (EDHF)
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Examples of EDCFs
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endothelin (ET-1) <br></br>Thromboxane A2 (TxA2)
19
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Systolic pressure
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the maximum arterial pressure reached druing peak ventricular ejection
20
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Diastolic pressure
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the minimum arterial pressure just before ventricular injection begins
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Pulse pressure (PP)
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the difference between SP and DP
22
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mean arterial pressure (MAP)
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the average pressure in the cardiac cycle
23
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systemic hypertension usally
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asymptomatic and often diagnosed when patient presents with another condition
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Pulmonary hypertension
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commonly found in COPD patients where the pulmonary vasculature has been afffected leading to increase in vasucalr resistance
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symptoms of pulmonary hypertension
- shortness of breath and sometimes chest pain
- sustained increase in pulmonary vasuclar resistance leads to progressive right HF (Heart failure)
- sustained increase in pulmonary vasuclar resistance leads to progressive right HF (Heart failure)
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Primary risk factors of hypertension
High salt consumption, excessive use of alcohol, age/sex, lipid disorders
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secondary hypertension risk factors
are initated by other dieases
- Thyroid disease
- Eclampsia
- cancer treatment
- Renal disease
- Thyroid disease
- Eclampsia
- cancer treatment
- Renal disease
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effects of hypertension
## Footnote
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Types of Antihypertensive drugs
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Sites of action for antihypertensice drugs
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4 types of Antihypertensice drugs
Vasodilators, sympathetic inhibitors, RAAS inhbitors, diuretics
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Sites of action for antihypertensive drugs
CNS, Kidney, Heart and blood vessels
CNS: B blockers & a2 blockers
Kidney : Diuretics, B blockers and ACE inhbitors
Heart: B blockers
Blood vessels : a1 blockers, ca2 channel blockers, vasodilators, AT1 receptor antagonists and ACE inhibitors.
CNS: B blockers & a2 blockers
Kidney : Diuretics, B blockers and ACE inhbitors
Heart: B blockers
Blood vessels : a1 blockers, ca2 channel blockers, vasodilators, AT1 receptor antagonists and ACE inhibitors.
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Antihypertenisve drugs that act on the SNS
B blockers : Atenolol and propranolol
a blockers : proazosin
a blockers : proazosin
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Atenolol & Propranolol MOA
Decrease CO
Reduce renin production (reduce Ang II)
can indirectly cause vasodilation of peripheral arteries
Reduce renin production (reduce Ang II)
can indirectly cause vasodilation of peripheral arteries
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prazosin
block post-synaptic a1 adrenoceptors leading to dilation of arterioar resistance vessels and lower peripheral resistance
Dilate venous capacitacne vessels, redcuing venous return and CO
Dilate venous capacitacne vessels, redcuing venous return and CO
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Drugs that act on RAAS
ACE inhbitors: Captopril
Ang II receptor antagonists (ARBs): Losartan, Valsartan
Diuretics: Thiazide
Ang II receptor antagonists (ARBs): Losartan, Valsartan
Diuretics: Thiazide
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captopril MOA
ACE inhbitor
reduces Ang II levels
reduces Ang II levels
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Losartan and valsartan MOA
selectively block AT1 receptors which mediate the vasoconstrictive, cariac/vasucular hypertrophy effects of Ang II
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Thiazide MOA
Diuretic
mainly acts on the early distal convoulted tuble
Act at varying site in the kidney to increase Na and water depletion leading to hypotensive effect
mainly acts on the early distal convoulted tuble
Act at varying site in the kidney to increase Na and water depletion leading to hypotensive effect
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Diltiazem, verapamil and amlodipine MOA
calcium channel blockers
block Ca2 entry into VSMCs and or cardiac muscle cells promoting relaxation of the muscle and vasodilation
block Ca2 entry into VSMCs and or cardiac muscle cells promoting relaxation of the muscle and vasodilation
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Hydralazine, Minoxidil, Nitrates, Nitroprusside, CCbs, AT1R antagonists
Vasodilators used in hypertenisve emergency
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Grade 1 hypertension
BP 140-159/90-99 mmHg
immediate drug treatment in high risk patients with CVD, CKD, DM or HMOD
immediate drug treatment in high risk patients with CVD, CKD, DM or HMOD
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Grade 2 hypertension
BP >160/100 mmHg
Immediate drug treatment in all patients
Immediate drug treatment in all patients
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RAAS regulates
BP and fluid balance/blood volume
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increase in renal sympathetic nerve activity
increase glomerular filtration
increase BP
leads to RAAS causing
increase glomerular filtration
increase BP
leads to RAAS causing
secretion of renin and ultimately production prodcution of Angiotensin 2
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Angiotensin II is a
potent vasconstrictor
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Production of Angiotensin II leads to
increase in blood pressure
increase in Aldosterone secretion
increase in Aldosterone secretion
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High activity of RAAS leads to
high BP
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RAAS involves renin beign secreted by the
kidneys.
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the release of renin is controlled by
BP, Na and sympatheitc nerves
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two types of renin
tissue and circulating
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Components of RAAS
found in heart, blood vessesl, kidneys and lungs
prodcued locally or captured from circulation
prodcued locally or captured from circulation
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Actions of angiotensin II ( Requires writing out )
Vascoconstriciton
stiumalation of aldosterone secretion
Direct effect on kidney to cause Na+ and H20 rentention
- this leads to raised Blood volume and BP
the increase BP and BV leads to
-feedback inhbition of renin seretion
increase in sympathetic nerve activity
which stimulates secretion of ADH/vasopressin whcih will also lead to increase BP
stiumalation of aldosterone secretion
Direct effect on kidney to cause Na+ and H20 rentention
- this leads to raised Blood volume and BP
the increase BP and BV leads to
-feedback inhbition of renin seretion
increase in sympathetic nerve activity
which stimulates secretion of ADH/vasopressin whcih will also lead to increase BP
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Angitontensin II has
two receptor types
AT1 and AT2
AT1 and AT2
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Action of AT1
receptor is acitvated during vasoconstriction and cardiac hypertrophy
its a GPCR that couples with Phosphilipase C
its a GPCR that couples with Phosphilipase C
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The coupling of AT1 to Phospholipase C leads
increase IP3 formation and increase smooth muscle cell contration with sutained activity leadding to vasucalr remodelling
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Actions of AT2
stimulation evokes effects oppoiste to those produced by AT1
leads to vasodilation
antiproliferative effects
antithrombotic effects (Reduces blood clots)
antiinflammatory
anti-fibrosis
leads to vasodilation
antiproliferative effects
antithrombotic effects (Reduces blood clots)
antiinflammatory
anti-fibrosis
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ACE inhibitors MOA
inhbit ACE which converts Angiotensin I into Angiotnsin II.
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ACE inhibitors in CV disease is used for treating
hypertension releated symptoms
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ACE inhibitiors in CV disease leads to
decrease BP by reducing PVR
Increase formation of Angi 1-7 which opposes actions of Angi 2
Increase formation of Angi 1-7 which opposes actions of Angi 2
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Adverse effects of ACE inhibitors
hypotension, renal failure in certain patients, adverse effects on foetus
causes cough in 35% patients
Angi-oedema - swelling of dermis/sub-cutaneous tissue
causes cough in 35% patients
Angi-oedema - swelling of dermis/sub-cutaneous tissue
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ACE stands for
Angiotensin converting enzyme
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losartan, valsartan, candesartan, Irbesartan are ARBs that selectively block
AT1 recepotors
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ARBs are similar to ACEi but do not lead to
decreease in Angi II and do not cause Cough associated with ACEi
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what is the only renin inhibitor on the market
Aliskiren
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1st generation Renin Inhibitors
Enakiren and remkiren
poor bioavailability due to peptide structure
poor bioavailability due to peptide structure
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2nd generation renin inhibitors
FK906, Zamkiren, Aliskiren
are non-peptides
are non-peptides
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Inhbition of renin prevents the conversion of
angiotensinogen into angiotensin 1
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Effects of renin inhibitiors
effective in lowering BP
decrease in Ang 1 levels
should not cause cough
decrease in Ang 1 levels
should not cause cough
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risk of renin inhibitors
combination of Aliskiren and ACEi /ARBs in patiens with kidney impairment or diabetes
still to be established if they are effective as ACEi
still to be established if they are effective as ACEi
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MRA drugs com..........
competively bind to Minrealocoticoid receptors (MR)
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examples of MRA
spironolactone, eplerenone
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Function of the kidneys
regulation of H20 and inorganic ion balance
removal of metabolic waste products from blood and excretion in unrine
removal of metabolic waste products from blood and excretion in unrine
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Classification of Diuretics and site of action
Loop diuretics, Thiazides and potassium sparing diuretics
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loop diurteics example
Flurosemide which is supplemented with spironolacotne or amiloride
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Thiazides example
Bendroflumethiazide
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Potassium sparing diuretics example
Eplerenone and spirolactone
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loop diuretics act on
ascdening lumb of henie's loop
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Thiazides act on
the early distal convoulted tuble
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Potassium sparing diuretics act on
late distal convoulted tubule and collecting duct (distal nephron)
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MOA of loop diuretics
act mainly by inhibitng the na/k/2cl co transporter
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Thiazide inhibits
inhibit the na/2cl co-transporter in the distal tubule
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aldosterone stimulates
increases
BP
Na reabsorption and K excretion by renal tuble
BP
Na reabsorption and K excretion by renal tuble
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Potasium sparing diuretics are a
distal tubule Na channle inhibitor
aldosterone receptor antagonosists
- does this by promote na and H20 excretion in the collecting tubule and duct
aldosterone receptor antagonosists
- does this by promote na and H20 excretion in the collecting tubule and duct
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Atherosclerosis
arteries become narrowed
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4 main classes of lipoproteeins
Chylomicrons, VLD, LDL, HDL
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Hyperlipoproteinaemia
poor diet and genetic factors disrupt lipid metabolism, leading to elevatedlevels of LDL and VLDL
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High LDL and VLDL levels are strongly linked to
atherosclerosis development
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higher plasma cholesterol is associated with an increased risk of
atheroscleorisis and cardiovasicalr disease
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Lipid-lowring drugs for CVD prevention
statins, Ezetemibe, Bempedoic acid, PCSK9 inhbitors ( Alirocumba, evolocumab), Bile acid sequestrants and Fibrates
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Risk factors of atherosclerosis
BAD HEART
BMI, age, diabetes, hypetension, excess fat (obesity), alcohol, relatives with CVD and tobacco
BMI, age, diabetes, hypetension, excess fat (obesity), alcohol, relatives with CVD and tobacco
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effects of atheroscletosis
reduced blood vessel lumen diamter
lower blood flow at rest
reduced oxygen supply
vasucalr cell dysfucntion
impaired vasodilation
faulty blood flow control
increased risk of blood clots
lower blood flow at rest
reduced oxygen supply
vasucalr cell dysfucntion
impaired vasodilation
faulty blood flow control
increased risk of blood clots
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Angina pectoris is reffered to as a
strangling feeling in the chest
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Angina pectoris occurs due to
ischaemia refeffeing to a restritction in blood supply
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Different types of angina
stable, unstable and variant
## Footnote
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progressive narrowing or blockage of blood vessels causes increase
serveirty of cornary heart diesease and ischaemia
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Myocardial infarction is also known as a
heart attack
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infarct is
ischaemic necrosis of a tissue
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types of Infarct
Subendocardial infarct
innermost layer is injured first (most distal meaning most center)
Transmural infarct
cell death extends throughout the whole thickness of the heart muscle
innermost layer is injured first (most distal meaning most center)
Transmural infarct
cell death extends throughout the whole thickness of the heart muscle
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Transmural infarct
cell death extends throughout the whole thickness of the heart muscle
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Cell death is irreversible and can result in 3 things on the heart
arrhythmia, heart failure and cardiogenic shock
arrhythmia being irregular heart beat
arrhythmia being irregular heart beat
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Ischaemic attack is a
brief blockage of blood flow
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treatment for stable angina attacks
Nitrates (nitroglycerine, AKA glyceryl trinitrate)
increased blood flow by icreasing the diamter of blood vessels (promoting vasodilation)
increased blood flow by icreasing the diamter of blood vessels (promoting vasodilation)
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Atherosclerosis interventions
lifestyle changes
medication for stabilszarttion and regression
medication to prevent attacks
surgical intervention
medication for stabilszarttion and regression
medication to prevent attacks
surgical intervention
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Atherosclerosis: medications for stabilzation and regression
Lipid lowering drugs - lower plasma cholesterol and transport
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Atherosclerosis: Medication to prevent attack (taken every day)
Anti-hypertensive drugs - decrease heart rate/force arteries to increase blood flow
B blocker like Atenolol - Decrease CO, reduce renin prodution, indirectly cause vasodilation to peripheral arteries
Anti-clotting drugs - prevent thrombosis
Asprin
B blocker like Atenolol - Decrease CO, reduce renin prodution, indirectly cause vasodilation to peripheral arteries
Anti-clotting drugs - prevent thrombosis
Asprin
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Anti-clotting drugs
COX-1 inhibitors and ADP receptor inhibitors
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Surgical interventions to control angina
Cornoanry angiplasty & stenting
Cornoary artery bypass graft (CABG)
Cornoary artery bypass graft (CABG)
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