Cv 1 And 2

Front 1

Components of Blood

Back 1

Plasma=55%
Blood cells=45%

Front 2

Blood Cells

Back 2

Erythrocytes, Leukocytes, Platelets

Front 3

Plasma

Back 3

Water, Electrolytes, Salts, Plasma Protein

Front 4

Erythrocytes

Back 4

RBCs that filled with hemoglobin, transport CO2

Front 5

Leukocytes

Back 5

Defense and immunity

Front 6

Platelets

Back 6

Initiate blood clotting

Front 7

Hemostasis

Back 7

Stops bleading, limits hemmorage: vascular spasm, platelet plug formation, clot formation

Front 8

Platelet Plug Formation

Back 8

Vessels are damaged and Platelet adhesion, platelet activation/release, aggregation: leads to stickiness/clot formation

Front 9

How does PPF work

Back 9

Prothrombinase, Thrombine, Fibrinogen, insoluable threads that form the clot

Front 10

Fibronalysis

Back 10

Disolving of unwanted clots once the vessel is repaired

Front 11

Pathways of blood circulation

Back 11

Systemic; Pulmonary; Corinary

Front 12

Systemic Circulation

Back 12

Carries Oxygen and nutrients to body tissues and removes wastes

Front 13

Pulmonary

Back 13

Carries deox blood to lungs, excretion of CO2, returns oxygenated blood to heart

Front 14

Corinary

Back 14

Sub-pathway of systemic; removes wastes

Front 15

Chambers (four hollow) continuously filled with blood

Back 15

R/L Atria: upper (recepticles for blood coming into heart from body)
R/L Ventricle: lower (push blood back into body)

Front 16

Which system supplies blood directly to the heart?

Back 16

Coronary circulation

Front 17

Walls of blood vessels

Back 17

Tunica externa
Tunica media
Tunica interna/intima

Front 18

Tunica externa

Back 18

Fibrous connective tissue

Front 19

Tunica media

Back 19

Smooth muscle and elastic tissue

Front 20

Tunica interna/intima

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Endothelial Tissue

Front 21

Arteries

Back 21

Carry blood away from the heart; two types: muscular and elastic (expand, receive blood during systole, recoil during diastole)

Front 22

Arterioles

Back 22

Smallest type of arteries; branch into capillaries (thin walls/single cell layer!); allows O2, nutrients from blood to cells

Front 23

Valves of the heart

Back 23

Prevent backflow of blood
AV Valves
Semilunar valves
Open and close according to pressure changes in chambers

Front 24

Atrioventricular Valves

Back 24

Separate atria and ventricles: tricuspid and mitral (R&L)

Front 25

Semilunar Valves

Back 25

Regulate outflow of ventricles

Front 26

Cardiac cycle

Back 26

Systole (contracts)
Diastole (relaxes)

Front 27

Layers of the Heart

Back 27

Three layers: epicardium (outer, epithelial), myocardium (middle, striated muscle), endocardium (inner, smooth)

Front 28

Main vessels of the heart

Back 28

Aorta and coronary arteries
Superior/Inferior vena cava
R&L pulmonary veins
R&L pulmonary arteries

Front 29

Aorta and coronary arteries

Back 29

Supply body and heart with oxygenated blood

Front 30

Superior/inferior vena cava

Back 30

Return deox blood to heart

Front 31

Cycle of systemic circulation

Back 31

Ox blood from lungs--> Pulmonary veins-->
Left Atrium--> Left Ventricle--> Aorta-->
Arterial system-->
Body's Tissues and organs

Front 32

Cycle of pulmonary circulation

Back 32

Deoxygenated blood from vena cava-->right atrium--> right ventricle-->pulmonary arteries-->lungs-->blood unloads CO2, picks up O2--> Left atrium-->systemic circulation

Front 33

Cycle of coronary circulation

Back 33

O2 blood carried thru coronary arteries-->capillaries in heart tissue -->deox blood --> cardiac veins-->coronary sinus-- right atrium

Front 34

Cardiac Cycle

Back 34

Normally: 60-80 BPM
Ventricular systole: contraction
Ventricular diasole: relaxation

Front 35

Cardiac Output

Back 35

CO=HRxSV
Amount of blood ejected from the L or R ventricle each minute (mL/minute)

Front 36

Nervous System Control of BP

Back 36

Parasympathetic Stim (decreases HR & impulses)
Sympathetic Stimulation (increases HR & impulses

Front 37

Cardia Muscle Cell Contraction

Back 37

- Deplorization/ Repolarization triggers change in e` potential of cell membrane
-This releases a Ca Ion, which shortens cadiac cells
-Muscle contracts

Front 38

Blood Flow Variables

Back 38

Blood Pressure: Force exerted by flood on vessel walls
BP = CO x TPR

Front 39

TPR

Back 39

Total Peripheral Resistance: Sum of all opposition to blood flow from force of friction between blood and vessel walls

Front 40

Hormonal Control of BP

Back 40

Kidneys: nephrons filter blood and reabsorb H20
Renin-Angiotensin-aldosterone system (RAAS) regulates BP

Front 41

Malfunctions of RAAS

Back 41

Affect both cardiac output and peripheral resistance

Front 42

RAAS Flow...

Back 42

Decreased arterial pressure-->Renin (kidney)-->Angiotensin I-->Angiotensin II-->Leads to: Increase in Na/H20 Retention; in vasoconstriction; in system arterial pressure

Front 43

Other hormones involved in PB control

Back 43

ADH and ANP:
Antidiuretic hormone and Atrial Natriuretic Peptide

Front 44

Aldosterone

Back 44

Homrone that causes vasoconstriction and causes body to retain sodium and water, which means increased BP

Front 45

HYPERTENSION

Back 45

Inappropriately sustained elevation in BP

Front 46

Optimal BP for adult is:

Back 46

<120/80 mm Hg

Front 47

JNC 7 Classification

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Hypertension=BP>140/90
Prehypertension=BP between 120/80 and 139/89
Goal: to decrease elevated BP<140/90

Front 48

Primary Hypertension

Back 48

Over 95% of cases
Cause unknown

Front 49

Secondary Hypertension

Back 49

Causes: Renal, Adrenal, Other (oral contraceptives, narrowing of the aorta, hyperthyroidism)

Front 50

Possible causes of Primary Hypertension

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Genetics; fetal environment; increased activity of vasoconstrictor systems; renal Na retention; Vascular Hypertrophy; decreased activity of vasodilating systems; insulin resistance

Front 51

Other factors possibly causing Primary Hypertension

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Obesity; alcohol intake; physical activity; smoking

Front 52

True or False: prevalence of hypertension increases with age

Back 52

TRUE
More common in Men up to age 50; equal in gender between 50 & 74; after 74 more common in women (estrogen protective effect)

Front 53

Hypertension is under___, under___, and poorly con___.

Back 53

Underdiagnosed, undertreated, and poorly controlled.

Front 54

NHANES Data Stats

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Not aware: 31.1%
Not treated: 41.6%
Not controlled: 46.9% (among treated patients)

Front 55

Hypertension Diagnosis:

Back 55

-No symptoms until it's progressed to the point of damaging organs
-BP eval; Clinical eval; Lab evals

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BP Evaluations

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-Baseline calculated by averaging cuff readins at 2 or more visits
-JNC7 recs f/u if initial pressure reading is found

Front 57

Ambulatory (out of office) readings (BP evals)

Back 57

Verify white coat hypertensio; access antihypertensive treatments; improve compliance; reduce physician visits

Front 58

Clinical Evaluations

Back 58

-Medical History; Previous records; family; CV risk factors; signs/symptoms, concomitant medications
-Phyiscal exam: funduscopic; cardiac; arteries; phyiscal appearance

Front 59

Laboratory Evaluations

Back 59

Urinalysis (renal status); Blood chem eval (blood cell count, K, creatinine, LDL, glucose, BUN)
Electrocardiogram (cardiac status LVH; provide baseline pre therapy)

Front 60

Consequences of Hypertension

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1. Endothelial Damage
2. Organ Damage
3. Atherosclerotic Plaques

Front 61

Endothelial Damage

Back 61

Hypertension damages endothelium of blood vessels: lining thickens; vessel narrows; flow impeded

Front 62

Organ Damage

Back 62

Eyes: hemorrhages, blurred, blindness
Heart: ventricular hypertrophy, atherosclerosis
Kidneys: decreased blood supply, renal disease
Brain: stroke, aneurysm rupture, TIA, embolus

Front 63

Stroke

Back 63

Injury or death of brain tissue that causes loss of speech, vision, sensation, or ability to move a limb

Front 64

TIA

Back 64

Transient Ischemic Attack: a mini-stroke.
Brief cerebral vascular ischemia causing focal neurological signs/symptoms lasting less than 24 hours; precursor to stroke

Front 65

Atherosclerotic Plaques (clinical consequences of hypertension)

Back 65

Atherosclerotic plaques develop in people with high lipid levels: changes in plaque occur and blood flow obstructed

Front 66

Walls of arterials

Back 66

Tunica intima, media, externa

Front 67

Dyslipidemia (defined)

Back 67

1. Pressence of abnormal levels of lipids, lipoproteins in blood
2. Elevated levels of VLDL, LDL, IDL, TGs
3. Low levels of HDL

Front 68

Chylomicrons

Back 68

Chylomicrons: transport dietary TGs and C from small intestine to body tissues post meal

Front 69

Blood Pressure equation

Back 69

BP=COxPR
(Cardiac Output x Peripheral resistance)

Front 70

Medical definition for hypertension

Back 70

High blood pressure

Front 71

Types of Lipoproteins

Back 71

Chylomicrons; VLDLs; LDLs; HDLs

Front 72

VLDLs

Back 72

VLDLs: tranport lipids from liver to fat tissue; converted to LDLs

Front 73

LDLs

Back 73

LDLs: Tranport Cholesterol from liver to body tissue; increase risk for atherosclerosis

Front 74

HDLs

Back 74

Tranport excess Cholesterol from body tissue to liver; reduce risk for atherosclerosis

Front 75

Friedewald Formula

Back 75

Formual used to calculate LDL-C when TG are <400mg/dL:
LDL=TC - HDL - (TG/5)

Front 76

Lipid Synthesis

Back 76

Exogenous vs. Endogenous

Front 77

Exogenous

Back 77

Exogenous pathway: lipids obtained from diet

Front 78

Endogenous

Back 78

Endogenous pathway: lipids made by liver

Front 79

Lipid sythesis (cont.)

Back 79

Decrease: LDO receptors and uptake of LDL
Increase LDL in blood and risk of atherosclerosis

Front 80

Types of Lipid Disorders

Back 80

Hyperlipidemia
Dyslipidemia
(Dys/Hyperlipidemia and hypercholesterolemia used interchangably by Drs)

Front 81

Hyperlipidemia

Back 81

Elevated levels of lipids, usually VLDL, LDL, IDL & TGs

Front 82

Dyslipidemia

Back 82

Elevated levels of bad lipids and low levels of HDL

Front 83

Classifications of Dyslipidemia

Back 83

Primary vs. secondary: based on cause of dyslipidemia
Fredrickson classification: based on patterns of lipid elevations
Genotypic classifciation: based on genetic causes of primary dyslipidemias
Clincial classification: based on which lipids are elevated/reduced

Front 84

Hypertrophy

Back 84

Increased size of a part caused by an increase in the size of its cells

Front 85

Primary dyslipidemia

Back 85

Genetic/no ID'd cause
60-70% of LDL level is genetics
Due to complex interaction of gens: age, gender, saturated fat diet, physical activity

Front 86

Secondary dyslipidemia

Back 86

Known causes: Lifestyle; metabolid disorders; kidney; liver; hormonal; medications; pregnancy

Front 87

Fredrickson classifcaiton

Back 87

*Patients classified according to which lipids/lipoproteins are elevated
*I, IIa, IIb, III, IV, V
*Treatment often based on lipid phenotype
*Not based on HDL levels

Front 88

Genotypic Classification

Back 88

*Classifies lipid disorders according to known genetic cause (primary only)
*Homozygous familial hypercholesterolemia (FH): 2 mutated LDL receptor alleles
Heterozygous FH: having 1 mutated LDL receptor allele

Front 89

Clinical Classification

Back 89

Relies on results of blood tests for lipids
Four main catagories: 1. elevated cholesterol/ hypercholesterolemia
2. elevated TGs/hypertriglyceridemia
3. elevated cholesterol and TGs /mixed dyslipidemia
4. Low HDL

Front 90

NCEP ATP III

Back 90

*2001 published guidelines for classification of cho levels
*2004 addendum made to NCEP ATP III for those at very high risk

Front 91

NCEP ATP III Classificatoin of Lipid Levels

Back 91

Optional LDL: <70 mg/dL
Optimal LDL: <100
Desirable TOTAL C: <200
Low HDL: <40
High HDL: >60
Normal TGs <150

Front 92

Epidemiology of Dyslipidemia

Back 92

105 million Americans have borderline high to high range of total cholesterol

Front 93

Clinical consequences

Back 93

Can lead to atherosclerosis, which lead to: Angina, MI, Stroke

Front 94

Lipid Hypothesis

Back 94

Evolved in last 50 years
Based on study data
Central to CHD, lowering lipeds lowers risk of CHD

Front 95

Framingham Heart Study

Back 95

*1948 in Framingham, MA
*5127 people 30-62 years old w/o diseases
*Study to show CHD are related to high lipids/lipoproteins
*CHD risk increases with increased total-C

Front 96

MRFIT

Back 96

Multiple Risk Factor Intervention Trial
*Random, multicenter, 7-yr study
*12,866 mid-age men w/ no CHD but w/ mutliple risk factors
*1% reduction in total-C-->2% reduction in CHD risk

Front 97

Atherosclerosis

Back 97

Buildup of fatty substances (plaque) on walls of arteries/reduces blood flow
May take decades for symptoms to show up

Front 98

Protective Factors

Back 98

HDL-C: removes C from arterial walls, tranports to liver for exretion
Exercise: weight control, incrase levels of HDL, lower BP, reduce risk of heart attack
Alcohol: moderate intake may protect against CHD & Athscl

Front 99

Initiation of Atherosclerosis

Back 99

1. Chronic endothelial injury (from atherscl risk factors)
2. Accumulation of lipids at the site of the injury (prolif of muscle cells)
3. Oxidation/modification of LDL-C (inflammation response)
4. Formation and death of foam cells (fatty streaks)

Front 100

Progression of Atherosclerosis

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*Fatty streaks progress to atheromas: lesion-->lumen; soft lipid core, hard fibrous cap
*Growth of plaque is outward/positive remodeling
*Fibrous plaque grows/stable

Front 101

Stable Plaques

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*Thick fibrous cap, low inflammation, low lipid content
*Outcome: stenosis-->occlusion
*Symptoms: angina, claudication

Front 102

Unstable plaques

Back 102

Thin fibrous cap; high inflammation; high lipid content; may lead to thrombosis

Front 103

Complications of Atherosclerosis

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1. Clots/Thrombi form around fissures in vessel walls
2. Fibrous cap can rupture; lipid core spilled into blood

Front 104

Types of Thrombosis

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1. Mural: clot spreads along artery wall; doesn't occlude lumen
2. Occlusive: Clot fills lumen, obstructs blood flow; may cause MI

Front 105

Clinical Consequences

Back 105

Heart: Ischemic heart disease: angina, acute MI, arrhythmias, CHF
Peripheral tissues/organs: PVD: claudication, gangrene, renal stenosis, ED
Brain: ____ disease: stroke TIA

Front 106

Stroke

Back 106

CVA: cerebrovascular accident
Occurs when O2 and nutrient flow to brain is interrupted b/c a blood vessel is blocked or burst
Two types: Ischemic (blocked blood vessel) and Hemorrhagic (burst blood vessel)

Front 107

Stroke Epidemiology

Back 107

*500,000/year in US experience 1st stroke
*200,000+/year exp 2nd stroke
*3rd leading cause of deathin in US and devel countries
*Leading cause of long-term disability
*Risk factors include those for atherosclerosis