Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

67 Cards in this Set

  • Front
  • Back

what causes angina?

mismatch between coronary perfusion, oxygen supply and cardiac work, oxygen demand

Therapy of stable angina?


- Beta blockers

- vasodilators

What is the cause of unstable angina?

unstable atheromatous narrowing, plaque rupture and thrombosis and vasoconstriction

what is the treatment of unstable angina?

vasodilators, B-AR blockers, aspirin and herarin

main treatment for prinzmetal's angina

calcium entry blockers

Uses of B1- antagonists in angina

-reduce heart rate and force

- increase time in diastole

Uses of calcium entry blockers in angina?

-vasodilation hence reduce TPR/ afterload

- prevent coronary vasospasm

What are the uses of organic nitrates in angina?

-Venodilation / reduce preload

- improve perfusion of ischemic zones

- prevent vasospasm

- prevent platelet aggregation

What is abnormal automaticity?

- SAN overridden by pacemaker in the the myocardium

- ischaemia

- hypokalaemia

- catecholamine activity

What is triggered automaticity?

- extra depolarisation events during myocyte action potential

- End of phase 2/ start 3 =EAD

- Phase 4 =DAD

what causes triggered automaticity?

excessive calcium entry or accumulation

what are the degrees of heart block?

1- slow impulse

2- fraction of the impuse

3- no impulse

What phase do class 1 affect?

- Depress phase 0

- can interupt re-entry circuits and reduce both abnormal and triggered automaticity

- What phase doe class II agents affect?

- depress slope in phase 4 of nodal

- Extend phase 2 of non-nodal

- prevent sinus tachycardia + both automaticity

What phase doe class III agents affect?

- delay phase 3

- extend phase 2

- might reduce re-entry circuits

what phase do class IV agents affect?

- Depress phase 0 of nodal

- Shorten phase 2 in non-nodal

- reduces triggered automaticity

what is heart failure?

Inadequate cardiac output for tissue perfusion

What are the four types of heart failure?

- systolic dysfunction

- diastolic dysfunction

- excessive haemodynamic burden

- inrealistic peripheral demands for tissue perfusion

What is systolic dysfunction?and what causes it?

- failure of contractility

- cardiomyopathy (diabetes, infection, MI)

- drug toxicity

- arrthymias

What is diastolic dysfunction? and what causes it?

- failure to fill ventricles

- caused by stiffness (senile fibrosis, cardiac hypertrophy)

what is excessive haemodynamic burden? and what causes it?

relative failure of contractillity

- valvular disease

- cogenital heart defects

- ^ TPR (left heart failure)

- ^ pulmonary resistance (cor pulmonale) RHF

What causes unrealistic peripheral demand for cardiac output? and what is it

- Relative failure of contractillity

- decrease O2 capacity, severe anaemia

- excessive metabolic demand, thyrotoxicosis

- maintenace of blood pressure in sepsis, shock

What is the aim of Heart failure therapeutics?

- support cardiac output

- remove compensation

- reduce workload

- reduce oxygen demand

- +ve iontropy

what are the compensatory mechanisms in CHF?

- Venocontriction (raise preload)

- Vasoconstriction (raise afterload)

- increase heart rate and force of contraction

What is the sypathetic nervous system role is compensation of CHF?

- Vasoconstriction + venoconstriction (a AR)

- tachycardia and +ve inotropy (b AR)

What is the role of RAAS in CHF compensation?

- Vaso and Venoconstriction (AT1 and V1)

- salt and fluid retention (V2 and MC Type 1 receptors)

How is compensation removed in heart failure?

- RAAS inhibitors

- Diuretics

- Vasodilators

how is +ve ionotropy produced in heart failure?

- cardiac glycosides

- B1-AR agonists

- PDE III inhibitors

What is primary hypertension? and what causes it?

Chronic, progressive elevation in arterial pressure

- Neurogenic (sympathetic stimulation)

- renal salt balance (too much intake)

what can cause sustained ^ TPR?

- vasoconstriction (loss of NO, PGI2)

- arteriosclerosis (hypertrophy)

- rarefaction (loss of vessels)

What are the peripheral theraputics for hypertension?

- RAAS inhibitors

- Thiazide diuretics

- B1 AR antagonists

- calcium entry blockers

- vasodilators

- a1 AR antagonists

What are the centrally acting theraputics for hypertension?

- a2 AR agonists

- imidazoline

what is the use of calcium channel blockers in hypertension?

- reduce TPR

- amlodipine

what is the use of RAAS inhibition in hypertension?

Reduce cardiac output and total peripheral resistance

name a fatty acid?

steric acid

- palmitic acid

- oleic

- arachodonic

what is a wax?

esters of fatty acids with long chain moonohydric alcohols

name some uses for lipids?

-plasma membrane

- lipoproteins for cholesterol transport

- thromboplastin

- myelin sheath

- cholesterol

what are the roles og cholesterol?

- membrane stability

- synthesis of bile acids and salts

- synthesis of steroid hormones

- synthesis of vitamin D

What hormones influence lipolysis?


- NA

- glucocorticoids

where is hormone sensitive lipase found? what does it do and what hormones activate it?

adipose tissue,

- controls release of fatty acids into the blood

- adrenaline and glucagon

what is the function of all of the lipoproteins?

- Chylomicrons (dietary)

- VLDL's (endogenous store)

- LDL's (deliver to cells throughout the body)

- HDL's (remove excess cholesterol)

what is the percentage of protein by;

- C








What apo protein solubolises highly hydrophobic lipids?

Apo B

what are the roles of apolipoproteins ?

- regulate lipid metabolising enzymes

- facilitate lipid transfer between lipoproteins and cells

- permit receptor mediated endocytosis

How is density related to TG content?


what is special about apolipoprotein B

it is integral where as others are peripheral

whare is ApoB100 found?


Name the origins of the following lipoproteins?

- chylomicrons





- Gut

- Liver

- liver

- liver

- tissues

what are the roles of the following;

- chylomicrons





- Transport dietary TG to tissue

- Transport endougenous TG

- Transport cholesterol

- Transport cholesterol

- Reverse cholesterol transport

What breaks down TG? and converts VLDL into IDL?

Lipoprotein lipase

what are the components and diameter of LDL?

- 1500 cholesteryl ester

- 800 phospholipid

- 500 unesterified cholesterol

- 1 apoB-100

- 22nm

how is LDL uptaken?

-ApoB-100 binds

- endocytosis

- lysosome digestion by cell

- LDL receptor reused

what does the endocytosis in eukaryotic cell require to take place?

Caveolin and GTPase

what makes the cholesteryl ester store?

ACAT (acyl-CoA cholesterol acyl transferase)

what occurs when there is too much cholesterol?

- Activation of ACAT

- Suppression of HMGCoA reductase expression

- Down regulation LDL receptor

what effect dose insulin and glucagon have on HMG-CoA reductase?

I- positive

G- negative

intracellular cholesterol block more extracellular cholesterol and also HMG-CoA

What are the roles of HDL?

- reverse transport

- LCAT converts free C to CE

what can be the causes of hyperlipidaemia?


- excess alcohol

- DM

- nephrotic syndrome

- renal failure

- cholestasis

how does hyperlipidaemia cause plaques?

- accumalation ion the arty wall

- oxidation

- macrophage entry

- Foam cells

- plaque grows

- rupture

what are the symptoms of hyperlipidaemia?


- stroke

- nodules of cholesterol

high levels of what other than LDL can cause CHD?

Lipoprotein A

name the drugs that mostly reduce LDL and total cholesterol?


- cholesterol absorption inhibitors

- bile acid binding resisns

name drugs that reduce LDL and TG?


name drugs that mainly reduce TG?


- omega 3 fatty acids

what drug is most effective at lowering LDL

and what drug is most effective at raising HDL?

- statins

- niacin

mechanism of statins?

HMG-CoA reductase inhibitors

- increase LDL-R expression

- pleiotropic (inprove endothelial function, reduce inflammation)

side effects of statins?


- myositis

- Rhabdomyolysis