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Pharmacology > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Cardiac cycle

A

Venous to right atrium
Right atrium to right ventricle
Right ventricle to pulmonary artery
Pulmonary artery to left atrium
Left atrium to left ventricle
Left ventricle to arteries

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2
Q

Diastole

A

Semilunar valves closed
Atrioventricular open

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3
Q

Systole

A

Semilunar valves open
Atrioventricular valves closed

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4
Q

Heart filling with blood

A

AV valves open and semilunar valves close

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5
Q

Blood leaving heart

A

Semilunar valves open and AV valves close

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6
Q

Cardiac Conduction system SNS

A

SNS will increase HR and contractibility
Resting SA 60-100 bpm

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7
Q

Automaticity

A

Generation of spontaneous depolarizations

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8
Q

Rhythmicity

A

Regular generation of action potentials

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9
Q

Cardiac output

A

Heart rate X stroke volume

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10
Q

CO=HR X SV

A

CO 5L/min
Increase in HR or SV= increased CO
Decrease in HR or SV= decreased CO
Factors
HR, Preload, After load, Myocardial contractibility

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11
Q

Ejection fraction EE

A

Refers to the amount ejected Per Beat
Normal range 55-75%

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12
Q

HR autonomic control

A

Increased - sympathetic beta 1 adrenergic receptors in sa node
Decreased- parasympathetic muscarinic receptors in the sa node- vagus nerve

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13
Q

Sv = blood ejected in 1 good pump/ determined

A

Myocardial contractility- SNS stimulation
Cardiac preload
Cardiac afterload

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14
Q

Preload/ stretch

A

Volume of blood in ventricles at and of diastole
Determined by force of venous return
Ventricular- end diastolic volume EDV

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15
Q

afterload

A

Pressure muscle must overcome to contract= resistance
Left ventricle must overcome to eject blood
SVR- blood leaves Lv and opens aortic value

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16
Q

Pulmonary vascular resistance

A

Pressure required to open pulmonic Valve

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17
Q

Starlings law

A

Length- tension relationship of preload to myocardial contractibility
As fiber length increases - increase in contractile force
Mine blood enters heart- more blood pumped out
Venous return increases - co increases

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18
Q

Elastic arteries

A

Aorta large branches- absorb large amounts of pressure

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19
Q

Muscular arteries

A

Medium and small arteries; farther from heart-more muscle less fiber
Smooth muscle can contract and relax - regulating blood to where it needs to go

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20
Q

Arterioles

A

Less than •5mm diameter - smooth muscle - determinant of resistance blood encounters

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21
Q

Metarterioles

A

Connective Channels

22
Q

Endothelium

A

Lining of blood vessels
Sometimes separate endocrine organ
Substance transport
Coagulation
Immune system function
Tissue and vessel growth and wound healing
Contraction and relaxation of vascular smooth muscle

23
Q

Veins - properties

A

Thin Walls
More connective tissue
Larger dramatic diameter
More than arteries
Valves for one way blood flow

24
Q

Artery and vein layers

A

Tunica externa
Tunica media
Tunica intima

25
Q

Influences of blood flow

A

Pressure gradient
Resistance
Large and small vessels
Blood viscosity

26
Q

Arterial pressure

A

Bp =co x SVR
Regulated by barorecepter reflex
RAAS
Kidneys
Natriuretic peptides

27
Q

ANS

A

Baroreceptor- pressure sensor
aims to restore bp

28
Q

RAAS_ renin angiotensin aldosterone resistance

A

Constriction of arterioles and vein - angiotensin 2
Retention of water by kidneys - aldosterone
Fluid is retained- pressure rises - venous return increases-co increases- ap increases

29
Q

Natriuretic peptides

A

ANP - Atrial natriuretic peptide
BNP - b type natriuretic peptide
CNP- C-natriuretic peptide
Counteracts volume overload - retention of Na and water
Dilation of arterioles and veins

30
Q

Orthostatic hypotension

A

Reduction of bp when moving from supine to upright position

31
Q

Right atrium pressure

A

0 mmhg sucks blood towards heart

32
Q

Factors affecting blood pressure

A

Increase blood volume
skeletal muscle pump
Respiratory pump
Venoconstriction

33
Q

Atherosclerosis

A

Thickening and hardening of vessel walls
Caused by accumulation of lipid laded macrophages within the arterial wall leading to formation of a lesion called a plaque
Not a disease but pathologic process

34
Q

Atherosclerosis step 1

A

Injury to endothelial cells
Smoking
HTN
Diabetes
Inc LDL Dec HDL

35
Q

Atherosclerosis step 2

A

Injured epithelial cells become inflamed
Inflamed epithelial cells cannot make normal amounts of atithrombotic
And vasodilating cytokines

36
Q

Atherosclerosis step 3

A

Inflamed epithelial cells express adhesion molecules that bind macrophages and other immune and inflammatory cells
Activated macrophages damage endothelium
Free radicals generate
Oxidized LDL - adhesion molecule expression

37
Q

Athenosclenosis step 4

A

Macrophages penetrate into the intima - engulf oxidized LDL
Lipid laden macrophages - foam cells
A-Lot lead to fatty streak

38
Q

Atherosclerosis step 5

A

Macrophages release growth factors that stimulate smooth muscle cell proliferation
Cells produce collagen which migrate over fatty streak - form a fibrous plaque
Plaque may calcify - protrude blood vessel and obstruct blood flow

39
Q

Atheroschenosis step 6

A

Plaque ruptures turns into complicated plaque
Rupture exposes underlying in platelet adhesion, initiation of clotting cascade, rapid thrombus formation
Thrombus may suddenly occlude vessel resulting in ischemia and infraction

40
Q

Hyperlipidemia

A

High levels of lipid level within person

41
Q

Cholesterol

A

Component of cell membrane required for hormone and bile salt synthesis
Exogenous-dietary intake saturated fats
Endogenous-made by cells, liver HMG-CoA reductase

42
Q

Treatments for LDL

A

Diet,exercise,smoking cessation
Lifelong therapy, statins

43
Q

HMG-CoA reductase inhibitors(statins)

A

Atorvastatin(Lipitor), rosuvastatin(crestor), simvastatin(zocor)
Reduces LDL increases HDL
Give at bedtime-cholesterol made during sleep
CI-pregnancy and muscle injury

44
Q

Non lipid benefits of statin therapy

A

Promote plaque stability
Reduce inflammation at plaque site
Enhance ability of blood vessels to dilate
Reduce risk of thrombosis, inhibit platelet deposition, suppresses production of thrombin

45
Q

How Statins work

A

Increase LDL receptors to increase removal of LDL
Inhibit HMG-CoA reductase-decrease cholesterol production-hepatocytes synthesize more HMG-CoA to inhibit cholesterol synthesis
Hepatocytes synthesize more LDL receptors

46
Q

Adverse effects of statins

A

Well tolerated
Avoid in pregnancy
Some will experience headache, rash, GI disturbances
Serious but rare SE-hepatotoxicity
Myopathy/rhabdomyolysis-breakdown of muscle cells-can cause renal failure
Coca-Cola urine

47
Q

Niacin

A

Nicotinic acid
Reduces LDL and TG levels
Increases HDL
AE-intense flushing, GI upset,
Liver injury

48
Q

Bile acid sequestrants

A

Cholestyramine
Reduces LDL cholesterol by binding to cholesterol in GI tract, prevents absorption and promotes excretion
Only SE are GI upset
Some drugs can bind causing decreased absorption of drugs -reduce risk by giving one hour before or four hours after meds are given
Used with statins

49
Q

Fibrates

A

Most effective at lowering TGs
Little to no effect on LDL
AE-increase Risks of bleeding in those taking warfarin
Increased risk of rhabdomyolysis(damaged ,uncle tissue releases its proteins into blood) if patient also takes statins

50
Q

Ezetimibe(zetia)

A

Inhibits dietary absorption of cholesterol, inhibits reads option of cholesterol in bile
Can be used alone or combined with statin
Generally well tolerated

51
Q

Metabolic syndrome

A

Cluster of conditions that increase the risk of heart disease, stroke, DM
Criteria needs 3
Low HDL, high TGs, hyperglycemia, HTN

Pharmacology (4 decks)

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