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

1/107

Click to flip

107 Cards in this Set

  • Front
  • Back
Components of Blood
Plasma=55%
Blood cells=45%
Blood Cells
Erythrocytes, Leukocytes, Platelets
Plasma
Water, Electrolytes, Salts, Plasma Protein
Erythrocytes
RBCs that filled with hemoglobin, transport CO2
Leukocytes
Defense and immunity
Platelets
Initiate blood clotting
Hemostasis
Stops bleading, limits hemmorage: vascular spasm, platelet plug formation, clot formation
Platelet Plug Formation
Vessels are damaged and Platelet adhesion, platelet activation/release, aggregation: leads to stickiness/clot formation
How does PPF work
Prothrombinase, Thrombine, Fibrinogen, insoluable threads that form the clot
Fibronalysis
Disolving of unwanted clots once the vessel is repaired
Pathways of blood circulation
Systemic; Pulmonary; Corinary
Systemic Circulation
Carries Oxygen and nutrients to body tissues and removes wastes
Pulmonary
Carries deox blood to lungs, excretion of CO2, returns oxygenated blood to heart
Corinary
Sub-pathway of systemic; removes wastes
Chambers (four hollow) continuously filled with blood
R/L Atria: upper (recepticles for blood coming into heart from body)
R/L Ventricle: lower (push blood back into body)
Which system supplies blood directly to the heart?
Coronary circulation
Walls of blood vessels
Tunica externa
Tunica media
Tunica interna/intima
Tunica externa
Fibrous connective tissue
Tunica media
Smooth muscle and elastic tissue
Tunica interna/intima
Endothelial Tissue
Arteries
Carry blood away from the heart; two types: muscular and elastic (expand, receive blood during systole, recoil during diastole)
Arterioles
Smallest type of arteries; branch into capillaries (thin walls/single cell layer!); allows O2, nutrients from blood to cells
Valves of the heart
Prevent backflow of blood
AV Valves
Semilunar valves
Open and close according to pressure changes in chambers
Atrioventricular Valves
Separate atria and ventricles: tricuspid and mitral (R&L)
Semilunar Valves
Regulate outflow of ventricles
Cardiac cycle
Systole (contracts)
Diastole (relaxes)
Layers of the Heart
Three layers: epicardium (outer, epithelial), myocardium (middle, striated muscle), endocardium (inner, smooth)
Main vessels of the heart
Aorta and coronary arteries
Superior/Inferior vena cava
R&L pulmonary veins
R&L pulmonary arteries
Aorta and coronary arteries
Supply body and heart with oxygenated blood
Superior/inferior vena cava
Return deox blood to heart
Cycle of systemic circulation
Ox blood from lungs--> Pulmonary veins-->
Left Atrium--> Left Ventricle--> Aorta-->
Arterial system-->
Body's Tissues and organs
Cycle of pulmonary circulation
Deoxygenated blood from vena cava-->right atrium--> right ventricle-->pulmonary arteries-->lungs-->blood unloads CO2, picks up O2--> Left atrium-->systemic circulation
Cycle of coronary circulation
O2 blood carried thru coronary arteries-->capillaries in heart tissue -->deox blood --> cardiac veins-->coronary sinus-- right atrium
Cardiac Cycle
Normally: 60-80 BPM
Ventricular systole: contraction
Ventricular diasole: relaxation
Cardiac Output
CO=HRxSV
Amount of blood ejected from the L or R ventricle each minute (mL/minute)
Nervous System Control of BP
Parasympathetic Stim (decreases HR & impulses)
Sympathetic Stimulation (increases HR & impulses
Cardia Muscle Cell Contraction
- Deplorization/ Repolarization triggers change in e` potential of cell membrane
-This releases a Ca Ion, which shortens cadiac cells
-Muscle contracts
Blood Flow Variables
Blood Pressure: Force exerted by flood on vessel walls
BP = CO x TPR
TPR
Total Peripheral Resistance: Sum of all opposition to blood flow from force of friction between blood and vessel walls
Hormonal Control of BP
Kidneys: nephrons filter blood and reabsorb H20
Renin-Angiotensin-aldosterone system (RAAS) regulates BP
Malfunctions of RAAS
Affect both cardiac output and peripheral resistance
RAAS Flow...
Decreased arterial pressure-->Renin (kidney)-->Angiotensin I-->Angiotensin II-->Leads to: Increase in Na/H20 Retention; in vasoconstriction; in system arterial pressure
Other hormones involved in PB control
ADH and ANP:
Antidiuretic hormone and Atrial Natriuretic Peptide
Aldosterone
Homrone that causes vasoconstriction and causes body to retain sodium and water, which means increased BP
HYPERTENSION
Inappropriately sustained elevation in BP
Optimal BP for adult is:
<120/80 mm Hg
JNC 7 Classification
Hypertension=BP>140/90
Prehypertension=BP between 120/80 and 139/89
Goal: to decrease elevated BP<140/90
Primary Hypertension
Over 95% of cases
Cause unknown
Secondary Hypertension
Causes: Renal, Adrenal, Other (oral contraceptives, narrowing of the aorta, hyperthyroidism)
Possible causes of Primary Hypertension
Genetics; fetal environment; increased activity of vasoconstrictor systems; renal Na retention; Vascular Hypertrophy; decreased activity of vasodilating systems; insulin resistance
Other factors possibly causing Primary Hypertension
Obesity; alcohol intake; physical activity; smoking
True or False: prevalence of hypertension increases with age
TRUE
More common in Men up to age 50; equal in gender between 50 & 74; after 74 more common in women (estrogen protective effect)
Hypertension is under___, under___, and poorly con___.
Underdiagnosed, undertreated, and poorly controlled.
NHANES Data Stats
Not aware: 31.1%
Not treated: 41.6%
Not controlled: 46.9% (among treated patients)
Hypertension Diagnosis:
-No symptoms until it's progressed to the point of damaging organs
-BP eval; Clinical eval; Lab evals
BP Evaluations
-Baseline calculated by averaging cuff readins at 2 or more visits
-JNC7 recs f/u if initial pressure reading is found
Ambulatory (out of office) readings (BP evals)
Verify white coat hypertensio; access antihypertensive treatments; improve compliance; reduce physician visits
Clinical Evaluations
-Medical History; Previous records; family; CV risk factors; signs/symptoms, concomitant medications
-Phyiscal exam: funduscopic; cardiac; arteries; phyiscal appearance
Laboratory Evaluations
Urinalysis (renal status); Blood chem eval (blood cell count, K, creatinine, LDL, glucose, BUN)
Electrocardiogram (cardiac status LVH; provide baseline pre therapy)
Consequences of Hypertension
1. Endothelial Damage
2. Organ Damage
3. Atherosclerotic Plaques
Endothelial Damage
Hypertension damages endothelium of blood vessels: lining thickens; vessel narrows; flow impeded
Organ Damage
Eyes: hemorrhages, blurred, blindness
Heart: ventricular hypertrophy, atherosclerosis
Kidneys: decreased blood supply, renal disease
Brain: stroke, aneurysm rupture, TIA, embolus
Stroke
Injury or death of brain tissue that causes loss of speech, vision, sensation, or ability to move a limb
TIA
Transient Ischemic Attack: a mini-stroke.
Brief cerebral vascular ischemia causing focal neurological signs/symptoms lasting less than 24 hours; precursor to stroke
Atherosclerotic Plaques (clinical consequences of hypertension)
Atherosclerotic plaques develop in people with high lipid levels: changes in plaque occur and blood flow obstructed
Walls of arterials
Tunica intima, media, externa
Dyslipidemia (defined)
1. Pressence of abnormal levels of lipids, lipoproteins in blood
2. Elevated levels of VLDL, LDL, IDL, TGs
3. Low levels of HDL
Chylomicrons
Chylomicrons: transport dietary TGs and C from small intestine to body tissues post meal
Blood Pressure equation
BP=COxPR
(Cardiac Output x Peripheral resistance)
Medical definition for hypertension
High blood pressure
Types of Lipoproteins
Chylomicrons; VLDLs; LDLs; HDLs
VLDLs
VLDLs: tranport lipids from liver to fat tissue; converted to LDLs
LDLs
LDLs: Tranport Cholesterol from liver to body tissue; increase risk for atherosclerosis
HDLs
Tranport excess Cholesterol from body tissue to liver; reduce risk for atherosclerosis
Friedewald Formula
Formual used to calculate LDL-C when TG are <400mg/dL:
LDL=TC - HDL - (TG/5)
Lipid Synthesis
Exogenous vs. Endogenous
Exogenous
Exogenous pathway: lipids obtained from diet
Endogenous
Endogenous pathway: lipids made by liver
Lipid sythesis (cont.)
Decrease: LDO receptors and uptake of LDL
Increase LDL in blood and risk of atherosclerosis
Types of Lipid Disorders
Hyperlipidemia
Dyslipidemia
(Dys/Hyperlipidemia and hypercholesterolemia used interchangably by Drs)
Hyperlipidemia
Elevated levels of lipids, usually VLDL, LDL, IDL & TGs
Dyslipidemia
Elevated levels of bad lipids and low levels of HDL
Classifications of Dyslipidemia
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
Hypertrophy
Increased size of a part caused by an increase in the size of its cells
Primary dyslipidemia
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
Secondary dyslipidemia
Known causes: Lifestyle; metabolid disorders; kidney; liver; hormonal; medications; pregnancy
Fredrickson classifcaiton
*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
Genotypic Classification
*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
Clinical Classification
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
NCEP ATP III
*2001 published guidelines for classification of cho levels
*2004 addendum made to NCEP ATP III for those at very high risk
NCEP ATP III Classificatoin of Lipid Levels
Optional LDL: <70 mg/dL
Optimal LDL: <100
Desirable TOTAL C: <200
Low HDL: <40
High HDL: >60
Normal TGs <150
Epidemiology of Dyslipidemia
105 million Americans have borderline high to high range of total cholesterol
Clinical consequences
Can lead to atherosclerosis, which lead to: Angina, MI, Stroke
Lipid Hypothesis
Evolved in last 50 years
Based on study data
Central to CHD, lowering lipeds lowers risk of CHD
Framingham Heart Study
*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
MRFIT
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
Atherosclerosis
Buildup of fatty substances (plaque) on walls of arteries/reduces blood flow
May take decades for symptoms to show up
Protective Factors
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
Initiation of Atherosclerosis
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)
Progression of Atherosclerosis
*Fatty streaks progress to atheromas: lesion-->lumen; soft lipid core, hard fibrous cap
*Growth of plaque is outward/positive remodeling
*Fibrous plaque grows/stable
Stable Plaques
*Thick fibrous cap, low inflammation, low lipid content
*Outcome: stenosis-->occlusion
*Symptoms: angina, claudication
Unstable plaques
Thin fibrous cap; high inflammation; high lipid content; may lead to thrombosis
Complications of Atherosclerosis
1. Clots/Thrombi form around fissures in vessel walls
2. Fibrous cap can rupture; lipid core spilled into blood
Types of Thrombosis
1. Mural: clot spreads along artery wall; doesn't occlude lumen
2. Occlusive: Clot fills lumen, obstructs blood flow; may cause MI
Clinical Consequences
Heart: Ischemic heart disease: angina, acute MI, arrhythmias, CHF
Peripheral tissues/organs: PVD: claudication, gangrene, renal stenosis, ED
Brain: ____ disease: stroke TIA
Stroke
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)
Stroke Epidemiology
*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