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
Reading...
Front

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

image

Play button

image

Play button

image

Progress

1/67

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?

GTN


- 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?

-adrenalin


- 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


-V


-L


H

-2%


-10%


-25%


-40%

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?

Proportional

what is special about apolipoprotein B

it is integral where as others are peripheral

whare is ApoB100 found?

LDL

Name the origins of the following lipoproteins?


- chylomicrons


- VLDL


- IDL


- LDL


-HDL

- Gut


- Liver


- liver


- liver


- tissues

what are the roles of the following;


- chylomicrons


- VLDL


-IDL


- LDL


-HDL

- 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?

obesity


- 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?

- CHD


- 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?

statins


- cholesterol absorption inhibitors


- bile acid binding resisns

name drugs that reduce LDL and TG?

Niacin

name drugs that mainly reduce TG?

Fibrates


- 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?

-myopathy


- myositis


- Rhabdomyolysis