angina

Question 1

angina

Answer 1

ischemic pain in heart due to coronary artery blockage
block in coronary artery –> decreased oxygen to the heart –> heart supplied by T1-T5 sympathetic nerves –> from the same part of the brain, sensory nerves arise which supply the hand, back, and middle of the chest –> referred pain in the centre of the chest referring to arms and back –> and associated with sympathetic symptoms such as sweating, anxiety and breathlessness

Question 2

types of angina

Answer 2

1. stable angina / classical angina/ exercise induced angina
2. unstable angina / part of acute coronary syndrome
3. vasospastic angina/ variant angina/ prinzmetal angina

Question 3

stable angina

Answer 3

most common variety
endothelial cells inside coronary artery –> atherosclerosis –> blood is going through but less blood –> sufficient at rest –> exercise –> increase in oxygen demand –> causes pain

Question 4

unstable angina

Answer 4

endothelial cells damage and rupture (plaque rupture) due to passage of blood through very narrow lumen which creates sharp flow –> platelets cells accumulate and form thrombus –> complete blockage –> slowly, there is damage of heart muscles –> can lead to MI

Question 5

vasospastic angina

Answer 5

blood vessel is normal bvut there is endothelial cell dysfunction –> vasospasm –> pain at rest

Question 6

anti anginal drugs for which types of angina

Answer 6

for stable angina and vasospastic angina
unstable angina treated like MI (anti platelet drugs & angioplasty)

Question 7

acute attack of angina (stable and vasospastic)

Answer 7

DOC SL nitrates

Question 8

DOC for chronic stable angina

Answer 8

DOC beta blocker ( decreases heart rate and decreases oxygen demand)
Add nitrates (oral, transdermal)
Add 2nd line drugs

Question 9

DOC for chronic vasospastic angina

Answer 9

DOC CCB (vasodilator)
Add nitrates (oral, transdermal)
Add 2nd line drugs

Question 10

1st line anti anginal drugs

Answer 10

Beta blocker
CCB
Nitrates

Question 11

2nd line nati anginal drugs

Answer 11

No DRIFT

Nicorandil
Dipyridamole
Ranolazine
Ivabradine
Fasudil
Trimetazidine

Question 12

Drug for both acute and chronic angina

Answer 12

Nitrates
acute - SL
chronic - oral/ transdermal;l

Question 13

2nd line anti anginal which is no longer used

Answer 13

Dipyridamole (causes coronary steal syndrome)

Question 14

which 2nd line anti anginal has become 1st line

Answer 14

Ranolazine (1st line for chronic stable angina)

Question 15

beta blockers

Answer 15

blocks beta 1 receptor on SAN of heart –> decreases heart rate –> decrease oxygen demand –> Doc for chronic stable angina
thus, we prefer cardioselective beta blocker like Atenolol, Metoprolol, Bisoprolol, Nebivolol

SE- blocks beta 2 receptors on coronary BV –> increased risk of vasospasm –> CI in vasospastic angina
non selective beta blockers are CI like Propranolol

Question 16

calcium channel blockers

Answer 16

DHP type (dipines) - coronary artery dilator - DOC for chronic vasospastic angina - Amlodipine, Nitrendipine, Benidipine

SE - reflex tachycardia which paradoxically increases the risk of stable angina
hence, divines are combined with beta blockers in angina

non DHP types - Diltiazem > Verapamil
on heart, they decrease heart rate and decrease oxygen demand
they also act as coronary artery dilators

they can be given for both chronic stable angina and chronic vasospastic angina

they should never be combined with beta blockers as they will lead to marked decrease in HR and bradycardia

Question 17

nitrates (organic nitrates)

Answer 17

venodilators –> reduce preload - main MoA - reduce preload - reduce EDV - reduce systole duration (has to contract less) - increase diastolic duration - reduce coronary crunch (because coronary artery supplies heart during diastole so now it gets more time) - improves blood supply

dilate coronary artery by producing NO (main MoA in vasospastic angina)–> which leads to redistribution of coronary blood flow from non ischemic are to ischemic area (Robin Hood phenomenon)

Question 18

Robin Hood phenomenon

Answer 18

nitrates
beta blockers

Question 19

nitrate drugs

Answer 19

GTN/TGN - glyceryl trinitrate / nitroglycerine) - oral, s/l, buccal, rectal, nasal spray, transdermal, iv
not im, sc - poor bioavailability - as they are lipid soluble and get deposited here
sl - 0.5mg - acute angina

ISDN - iso sorbed di nitrate - oral, sl
sl - 5mg - acute angina

ISDN - iso sorbed mono nitrate - oral

PETN - penta eryrithol tetra nitrate - oral

Question 20

chemical nature of nitrates

Answer 20

organic
highly lipid soluble (non ionic)

Question 21

FPM of nitrates in liver

Answer 21

All high FPM in liver when orally taken except ISMN which is not metabolised by liver and thus has 100% bioavailability

Question 22

nitrate which is a prodrug

Answer 22

ISDN — > active form ISMN

Question 23

shortest nitrate

Answer 23

Amyl nitrite ( inhaled - earlier it was an explosive form and used for angina) > GTN

Question 24

longest nitrate

Answer 24

PETN

Question 25

use of nitrates

Answer 25

1. angina - acute(s/l) & chronic (transdermal, oral) stable & vasospastic angina 2. acute coronary syndrome (unstable anginal and MI) - s/l nitrates 2. acute pulmonary edema / LVF - reduces preload (ventilators) 4. biliary colic, oesophageal colic, abdominal colic ---> nitrate is converted to NO which relaxes GIT muscle ( not effective in renal colic as MAD enzyme for converting nitrates into NO is not present)

Question 26

drugs for acute pulmonary edema/ LVF

Answer 26

LMNOP loop diuretics morphine NTG O2 prop up(sitting)

Question 27

adverse effects & CI of nitrates

Answer 27

1. flushing, throbbing headache 2. hypotension - CI SBP < 90mm Hg 3. reflex tachycardia - CI HR>100bpm 4. bradycardia (behold zarisch reflex) - CI HR<60bpm 5. reduces preload - CI RVF (treatment is to increase preload by giving fluids) 6. increases IOP and ICP ( as it causes vasodilation leading to increased filtration of blood which produces increased aqueous humour and CSF) - CI in glaucoma and cerebral edema

Question 28

nitrate tolerance

Answer 28

tolerance is loss of effect by MAD enzymes, nitrates release NO, which causes vasodilation nitrate tolerance results from continuous nitrate administration resulting is down regulation of MAD enzyme max tolerance - transdermal patch mi9n tolerance - s/l management - give nitrate free interval of 8 hrs (remove patch) - mostly before sleep as metabolic demand is less - this regenerates MAD nitrate

Question 29

new drug/ nitrate for angina

Answer 29

Molsidomine nitrate without tolerance direct NO donor which does not depend on MAD enzyme

Question 30

Monday's disease

Answer 30

industrial worker in nitrate or dynamite factory inhales nitrate on 1st day (Monday) side effects of inhaling nitrate like headache, flushing, hypotension are most evidence then throughout the week, tolerance builds, and symptoms improve after Sunday which is a holiday, on Monday gains, symptoms are more evident

Question 31

Nicorandil

Answer 31

KIN K+ channel opener ischemic preconditioning - makes myocardium resistant to ischema (increased activity of mitochondria - more O2 production) NO donor (direct)

Question 32

Dipyridamole

Answer 32

adenosine efflux (coronary dilator) + PDE 3 inhibitor (increase cAMP and hips in coronary dilation) - also antiplatelet drug and used in treatment of stroke however, it dilates coronary artery in non ischemic area and causes redistribution of blood from ischemic to non ischemic area - called coronary steal syndrome or reverse Robinghood phenomenon thus, CI in angina and MI

Question 33

coronary steal syndrome

Answer 33

above the myocardium there is epicardial artery and below the myocardium, there is subendocardial artery nitrates dilate the epicardial coronary artery and cause the Ropbinhood phenomenon however HIND drugs (hydralazine, isoflurane, nitroprusside, dipyridamole) cause coronary steal syndrome in which there is dilation of subendocardial artery in non ischemic areas leading to diversion of blood flow to non ischemic areas

Question 34

Ranolazine

Answer 34

blocks late sodium channels on myocardium (main MoA) ---> reduces cardiac workload and reduces oxygen demand minor action - pFOX inhibitor used as a 1st line drug for chronic stable angina advantage - it improves blood glucose/lipids - good for DM/ dyslipidemia (blocks K+ channels on pancreas-and increases insulin release) SE- it blocks K+ channels on heart - increased QT proton nation

Question 35

Ivabradine

Answer 35

I VA BRADI inhibits If current - funny channels on SAN (pacemaker potential) SE- visual abnormality as retina also has funny channels - light appears very bright (luminous phenomenon) causes bradycardias as it inhibits SAN --> decreased HR leading to decreased oxygen demand used in 1. chronic stable angina 2. chronic heart failure (cardioprotective) 3. treatment of sinus tachycardia

Question 36

Fasudil

Answer 36

rho kinase inhibitor(ROCK inhibitor) - direct coronary artery dilator use - chronic vasospastic angina and other pads like Raynaud's

Question 37

Trimetazidine

Answer 37

MoA - pFOX inhibitor ( partial fatty acid oxidation inhibitor) -- inhibits oxidation of fatty acids by inhibiting thiolase enzyme fatty acids (heart) + oxygen (more) --> ATP glucose + oxygen (less) --> ATP when Trimetazidine is used, oxidation of FA is inhibited and heart shifts to glucose for production of ATP --> so now less o2 is required used in chronic stable angina another use - Menderes disease (endolymph pressure increases leading to vertigo) - reduce endolymph pressure SE - Parkinsons disease (degrades dopamine)