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IPAP Biochem Thompson > Cardio > Flashcards

Cardio Flashcards

1
Q

Cardiac muscle energy requirements?

A
  • high # of mitochondria.
  • Aerobic
  • 60% lipids (Fatty Acids/triglycerrides)
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2
Q

Sa node?

A

Inititate action potential.

Spreads through R/L Atria vis intercalated disks.

60-100min

Sympathetic increase SA+force of contraction

Parasympathetic decreases SA+force of contraction (vagal nerves)

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3
Q

AV node?

A

Delays signal.

-Independently generate action potentials at 40-60min

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4
Q

Atrial depolarization?

A

P wave

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5
Q

VEntricular depolarization?

A

QRS-complex

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6
Q

Ventricular repolarization

A

T-wave

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7
Q

Cardiac Muscle contraction relies on?

A

Voltage-dependent Calcium channels. VDCCs.

The predominant cardiac VDCC=L-type channel= pore-forming alpha1 subunit w/ 6 trans-membrane alpha-helices that opens/closes upon voltage change.

They open by depolarization of the cell membrane.

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8
Q

What kind of receptors does the heart have?

A

Beta 1 receptors.

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9
Q

Alpha 1 adrenergic?

A

Gq protein.

-Stimulates phospholipase C pathway.

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10
Q

Alpha 2 adrenergic receptor?

A

Gi protein

-Inhibits adenylyl cyclase/cAMP pathway.

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11
Q

Beta 1 and 2 adrenergic receptors?

A

Gs protein

-Stimulates adenyly cyclase/cAMP pathway.

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12
Q

Which tissue does Beta 1 receptors work on?

A

Heart + Lungs

  • Increase rate+force
  • Increase Renin

By blocking this you have decreased rate and force of contraction and deccreased renin.

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13
Q

Where do Beta 2 receptors work?

A

Main location of Lungs, GI, liver, uterus, vascular+skeletal SM.

-Smooth fuscle relaxing uterus,gi tract,bronchi, and dilation of vessesl to support sympathetic response. Increases the breakdown of glyocogen.

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14
Q

Beta 3 receptor main location?

A

Fat cells

-Increase lipolysis.

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15
Q

At low doses what is action of dopamine?

2-5ug/kg/min

A

-Binds to D1,D5 receptors found on blood vessels(Kidneys) activating Gs and INCREASE URINE PRODUCTION

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16
Q

Intermediate dose of dopamine?

5-10 ug/kg/min

A

Binds to B1 adrenergic receptors in cardiac muscle-> INCREASED contraction rate and force for treatment of shock/heart failure patients.

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17
Q

High dose of dopamine ?

10-20 ug/kg/min

A

Alpha-1 adrenergic receptors.

Contaction of blood vessels and INCREASED RESISTANCE/Blood pressure.

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18
Q

Calcium channel blockers?

A

-Affect L-type (longlasting) calcium channels.

CCBs decrease total calcium released.

Lowers heart rate and force of contraction and reduces oxygen demand.

CCB decrease CICR induced contraction-dilation of blood vessels.

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19
Q

Dihydropyridines?

A

CCB that has greater affinity for smooth muscle calcium channels.

Dilates blood vessels.

Predominately used for BP control/hypertension.

Less favored for ANGINA bc of reflex tachycardia.

NIFEDIPINE

20
Q

Phenylalkylamine/non-dihydropyridines?

A
  • Cardiac selective, less likely to cause reflex tachycardia.
  • decreased rate and force of cardiac contraction.

ANGINA.

21
Q

Benzothiazipines?

A

Intermediate CCB effects.

-Decreased rate and force of cardiac contraction+dilation of blood vessels.

COntrol BP in patients w or w/o angina.

NOT TO BE CONFUSED WITH BENZODIAZEPINES.

22
Q

Beta blockers?

A

-blocks stimulatory effect of epinephrine on cardiac b1 receptors -> REDUCES OXYGEN DEMANDS.
Helps heart heal.

-blocks stimulatory effect of epinephrine of smooth muscle B2 receptors-> CONSTRICTION IN BRONCHI

23
Q

Epinephrine works mainly via activation of ??

A

Alpha1 adrenergic receptors but can also cause vasodilation and/or vasocontriction via alpha2 and beta2 receptors.

24
Q

Steps in smooth muscle vasoconstriction?

A

CA2+ -> activated by calmodulin->activates myosin light chain kinase MLCK-> Phosphorylates regulatory myosin light chains -> vasoconstriction.

25
Q

How does NO cause vasodilation?

A

(Arginine-eNOS-NO)

  • NO activates guanylyl cyclase.
  • cGMP->activates protein kinase G-> inactivation of MLCK -> dephosphorylation of myosin light chains.
26
Q

Endogenous pathway?

Metabolism and transport of cholesterol and lipoproteins occur in 2 general ways

A

Processing of cholesterol and triacylglycerols synthesized by the liver beginning with secretion of nascent VLDL and HDL.

27
Q

Exogenous pathway?

A

Processing of ingested cholesterol and triacylglycerols beginning with secretion of chylomicrons after eating by intestinal epithelial cells initially into the lymphatic system (from the diet)

28
Q

Nascent chylomicron needs what to become chylomicron?

A

APO C2 and APO E.

29
Q

Chlyomicron needs what to become a HDL?

A

ApoA and ApoC

30
Q

vLDL?

A
  • 1st lipoprotein of the endogenous pathway made in the liver.
  • Largest, rich in TGs.

Assembled from -TG, CMRs/diet, phospholipids, Cholesterol/cholesteryl esters.

Apo B-100, apoC-I, and low amount of apoE..

31
Q

Where is Nascent VLDL assembled?

A
  • Made in liver from TG, cholesterol, ApoB, Ci and E.
  • ADDING ApoC and ApoE from HDL exchange forms mature VLDL.

ApoC-II ACTIVATES lipoprotein lipase LPL to hydrolyze TGs to adipose (re-esterified for storage) and muscle (for use)

32
Q

IDL and LDL ?

A

VLDL-TGs=smaller more dense IDL/VLDL remnants

IDL-TGs=smaller more dense LDL

33
Q

Most LDL (50-70%) binds via…

A

LDL receptors via Apo B-100 on liver hepatocytes and remainder binds LDL receptors on peripheral cells.

of LDL receptors expressed represent cholesterol need of the liver or peripheral tissue cells.

34
Q

HDL that is synthesized in liver and secreted into plasma serve as…

A

Cholesterol scavenger and facilitates its transport from periphery to the liver.

OR

Repository of apo A1, C-II, and apo E

  • Nascent HDL contain lecithin.
  • Mature HDL recieve phospholipid from tissues.
35
Q

FAmilial hypercholesterolemia?

A

-Hyperlipoproteinemia type 2a, a genetic disorder caused by defective LDL receptors or apo B.

Decreased ability to remove LDL.
Increase levels of plasma LDL.

36
Q

Atherosclerosis?

A

-Formation of plaques/blockages in blood vessels and is the most common cause of heart attacks and strokes.

Inflammation of blood vessel walls, particularly arteries, due to fatty deposits that include lipoproteins and cholesterol, and macrophages.

37
Q

LDL oxidation for Atherosclerosis?

A

LDL taken up by macrophages -> invade arterial endothelial cells (foam cells)

38
Q

STeps in Artherosclerosis?

A

Normal wall -> elevated plasma cholesterol -> lipid deposits -> atherosclerotic plaque -> narrowing of arterial lumen which can cause angina -> rupture of plaque -> thrombosis -> tissue ischemia -> infarction.

39
Q

Treatment for Atherosclerosis?

A
  • Use aspirin to inhibit platelet aggregation

- Omega-3 fatty acids are believed to act via the production of anti-inflammatory eicosanoid synthesis.

40
Q

Cardiovascular disease and cholesterol lowering drugs?

A
  • Niacin helps reduce LDL and VLDL levels by blocking the catabolism of fats in adipose tissue.
  • Exetimibe (Zetia) - reduces GI cholesterol absorption.
41
Q

When you have ischemia what happens to cells?

A
  • worsens to anoxia, an infarct, with irreversible death within 30 mins.
  • As cells die membranes lose bilayer integrity w/ mitochondria and peroxisomes dumping toxic compounds into cytosol and extracellular and intracellular compartments.
  • Contents of membrane breakdowns are the cardiac markers used to detect an MI.
42
Q

Treatment of MI?

A
  • Lower O2 demand and increase O2 delivery.
  • CCBs, B-blockers, and ASPIRIN IRREVERSIBLY INHIBITS CYCLOOXYGENASE production of thromboxanes which inhibits platelet aggregation and further blocking of blood vessels.

CCBs directly affect heart but cause vasolidation and inhibition of angiotensin vasoconstriction.

43
Q

Reperfusion injury?

A

When MI blockage is relieved and renew blood flow happens and bad stuff begins floating around.

44
Q

Prinzmetal’s angina?

A

-Spasm of coronary arteries that reduce blood flow rather than blockage.

Failure to produce or diffuse NO.

Vasoconstriction of vascular smooth muscle.

45
Q

Thrombolytics?

A
  • Streptokinase, urokinase, t-PA, tissue plasminogen activator.
  • Breakdown of a thrombus or embolus.
  • Treatment relies on plasminogen activators that initiate the cascade of the body.

MAKES PLASMINOGEN TO PLASMIN.

46
Q

Measurement of BNP is useful to both assess and follow ?

A

PATIENTS WITH CONGESTIVE HEART failure.

IPAP Biochem Thompson (4 decks)

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