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Patho Cardiovascular
  • Two Clean Queens

  • 問題数 100 • 10/11/2023

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    問題一覧

  • 1

    Strong predictor of cardiac events

    Very-low-density lipoproteins (triglycerides)

  • 2

    Direct vasodilator lowering BP

    Mag

  • 3

    Times of decreaed O2 demand:

    Coronary spasm, hypotension, dysrhythmia, anemia, hypoxia

  • 4

    Comparing Catecholamines

    Norepinephrine has less receptor action on cardiac output and heart rate than Epinephrine but the same effect on coronary blood flow

  • 5

    Amount of blood pumped into the aorta each minute

    Cardiac output

  • 6

    Three subunits of Troponin

    Troponin I, T, and C

  • 7

    Extensive lattice of vessels that supply blood to the cells/areas of substrate exchange (thin walled with pores for permeability)

    Capillaries

  • 8

    Percent of blood in chamber that is ejected with each systole

    Ejection fraction

  • 9

    Comparing Catecholamines

    Epinephrine has more Alpha1, Beta2, and Beta3 receptor action than Norepinephrine

  • 10

    Infant = 10-15 woods/m2. 1-2 yrs old = 15-20 woods/m2. Child-Adult = 15-30 woods/m2.

    SVR

  • 11

    Chronic inflammation resulting in damage to arterial walls and plaque formation

    Atherosclerosis

  • 12

    Two polypeptide chains wrapped in spiral forming a double helix

    Myosin Tail

  • 13

    Spread of depolarization through atria, followed by atrial contraction

    P wave

  • 14

    Flexible Hinge and Arm Connected to Myosin Heads

    Myosin Cross-Bridge

  • 15

    Affinity for Calcium

    Troponin C

  • 16

    Responds to Catecholamines (epinephrine and norepinephrine), stimulates renin-angiotensin system (RASS)

    Sympathetic Nervous System

  • 17

    Dietary fat packaged in small intestine—> chylomicrons —> liver —> processed into:

    Very-low-density lipoproteins (triglycerides), Low-density lipoproteins (LDL), High-density lipoproteins (HDL)

  • 18

    Helix backbone, F-actin and G-actin

    Actin

  • 19

    Step 1 of Atherosclerosis

    Injury to endothelium—>inflammatory response—>monocytes and platelets move to site of injury

  • 20

    Transient inability of coronary arteries to deliver enough oxygen to myocardial cells (supply-demand mismatch). Begins after 10 secs (cells can survive 20 mins)

    Myocardial Ischemia

  • 21

    Indicator of cardiac risk but in context of other factors (age, diabetes, CKD)

    Low-density lipoproteins (LDL)

  • 22

    Unstable plaques prone to rupture

    Complicated lesions

  • 23

    Globular polypeptide with associated light chains

    Myosin Head

  • 24

    Supports Sodium Excretion

    K, Mag, Ca

  • 25

    Site of automaticity due to slow leak of NA ions (the most Na leak channels) that slowly increase intracellular charge until action potential is fired releasing Ca from the muscle fibers to cause myosin/actin contraction

    SA Node

  • 26

    Diffusion of Potassium

    Diffuses out of the cell causing negative intracellular charge

  • 27

    <8 weeks of age = 8-10 woods/m2. >8 weeks of age = 1-3 woods/m2.

    Pulmonary Vascular Resistance (PVR)

  • 28

    Time cardiac muscle is refractory to additional stimulation

    Refractory Period

  • 29

    Phases of Action Potential

    0: Depolarization; 1: Early Repolarization; 2: Plateau (Repolarization)-Na and Ca slowly enter cell; 3. Potassium moves out of cell; 4: Return to resting potential.

  • 30

    Contributes to blood pressure regulation, promotes cardiac contactility, controls arteriolar vasoconstriction (peripheral vascular resistance)

    Sympathetic Nervous System

  • 31

    Potassium rapidly diffuses out of the cell and the intracellular negativity increases to resting state.

    Repolarization

  • 32

    The active site for cross-bridges with myosin

    G-actin

  • 33

    HR x Stroke Volume

    Cardiac output

  • 34

    Pain without ambulation found in PAD

    Intermittent claudication

  • 35

    Thick protein filament, dark bands or A Bands (anisotropic), small projections from sides that form cross-bridges

    Myosin

  • 36

    Contraction units of Cardiac Muscle

    Myofibrils

  • 37

    Individual Myosin Molecules Bundled Together to Form the Body Where Cross-Bridge Hangs

    Myosin Filaments

  • 38

    Protein wrapped around F-actin, blocks active site

    Tropomyosin

  • 39

    Step 2 of Atherosclerosis

    LDL enters the intimas layer of the vessel—>inflammation + oxidative stress + macrophage activation—> engulf LDL = foam cells —> foam cell accumulation = fatty streak

  • 40

    Lesion in arteries filled with lipids and marcophages (stable or unstable)

    Plaque (atheroma)

  • 41

    Circumflex Artery supplies blood to?

    LA and Left lateral wall of LV

  • 42

    Step 3 of Atherosclerosis

    Further inflammation process in response to fatty streak—> smooth muscle cells produce collagen —> form over fatty streak making a plaque (May calcify = Monckeberg atherosclerosis)

  • 43

    Associated with pregnancy, cocaine and meth use, adrenal tumors, ETOH withdrawal

    HTN Crisis

  • 44

    Deposited in tunica media and assists with vasoconstriction and increasing BP

    Ca

  • 45

    Amount of blood ejected with each contraction of the heart

    Stoke volume

  • 46

    Concentration of Sodium in the Cell

    Low inside the cell membrane, High outside the cell membrane

  • 47

    Caused by underlying disease process (renal, pheochromocytoma, pregnancy) increasing PVR and CO

    Secodary HTN

  • 48

    Associated with things that remodel the atria: (HF, ischemic CV disease, HTN, Obesity, OSA, rheumatic heart disease)

    A-Fib

  • 49

    Local, temporary oxygen depravation. Cells live but cannot function normally.

    MI

  • 50

    Volume of blood returning to the heart from systemic circulation = RA pressure or CVP

    Preload

  • 51

    Deopolarization of the ventricle, followed by ventricular contraction

    QRS complex

  • 52

    Constriction and Relaxation of Smooth Muscle of Arteries and Arterioles controlled by:

    Sympathetic Nervous System, Local Tissue Metabolism, Hormone Response, Changes in Chemical Environment

  • 53

    Primary causes of dyslipidemia

    Genetics from abnormal lipid metabolism and cellular receptors

  • 54

    Persistent ischemia or complete occlusion of coronary artery. Commonly myocardial infarction.

    Acute Coronary Syndromes

  • 55

    Anount of blood in venous system

    64%

  • 56

    Myofilament and Actin Interaction

    At rest, active sites on actin are blocked troponin and Tropomyosin complexes. During action potential, troponin C binds with calcium and moves the complexes off of the actin active site. Actin and myosin interact causing muscle contraction.

  • 57

    Portion of myofibrils between two Z-Discs

    Sarcomere

  • 58

    Repolarization of the ventricles, happens just before the end of ventricular contraction

    T wave

  • 59

    Thin protein filament, light band or I band (isotopic)

    Actin

  • 60

    Vascular remodeling—> fibrosis of vessels—> organ injury (cardiac muscle, retina, kidneys, brain). LV Hypertrophy-> HF.

    Complications of HTN

  • 61

    Protective against atherosclerosis- want high level to remove access cholesterol from arterial walls

    HDL

  • 62

    Affinity for Tropomyosin

    Troponin T

  • 63

    Enzyme in Head for Energy Production

    ATPase

  • 64

    Times of increased O2 demand:

    Exercise, tachycardia, HTN, valve disease

  • 65

    Systemtic pressure = pressure the heart must pump against to circulate blood = MAP

    Afterload

  • 66

    Left Anterior Descending Artery provides blood to?

    LV and RV, Intraventricular septum

  • 67

    Affinity for actin

    Troponin I

  • 68

    Transport blood from the Venules back to the heart. Act as a reservior (low pressure system, thin walls)

    Veins

  • 69

    Site of connecting myofibrils

    Z-Discs

  • 70

    Amount of blood in a heart chamber after filling, before systole

    End-diastolic volume

  • 71

    Rapid increase in SBP> 140mmHg—> cerebral arterioles cannot regulate blood flow to cerebral capillaries—> cerebral edema—> encephalopathy

    HTN Crisis

  • 72

    LCA branches into?

    Left anterior descending artery and Circumflex artery

  • 73

    Transport blood under high pressure from the heart to the capillary bed of tissues (high pressure/thick muscular walls)

    Arteries

  • 74

    Contraction of the Heart

    Systole

  • 75

    Hypertension

    Sustained BP 130/80

  • 76

    Amount of blood that remains in the heart chamber after systole

    End-systolic volume

  • 77

    Right Coronary Artery supplies blood to?

    RV, Intraventricular sulcus, and small vessels of RV and LV

  • 78

    Diffusion of Sodium in the Cell

    Sodium diffuses into the cell causing a positive intracellular charge

  • 79

    Leak of sodium into the cell, decreases the intracellular negativity. Opens voltage gated ion channel to generate more positive ion (Na and Ca) entry. Cell becomes more positive. Action potential is generated.

    Depolarization

  • 80

    Pause in Conduction at AV Node

    PR Interval

  • 81

    Potassium concentrations in cell

    High inside cell membrane, low outside cell membrane

  • 82

    Measurement of Vascular Resistance

    Woods Units

  • 83

    Early beats without p waves. Effects: decreased CO from loss of atrial contribution to ventricular preload resulting in heart fluttering, pounding, and palpitations. Associatied with abnormal potassium, hypercalcemia, hypoxia, aging, anesthesia, caffeine, tobacco, illicit drugs, exercise

    PVCs

  • 84

    Role of Lipoproteins

    Manufacturing and repair of plasma membranes and cholesterol for bile salts and steroid hormones

  • 85

    Collect blood from the capillaries and coalesce to form veins

    Venules

  • 86

    Relaxation and Filling of the Heart

    Diastole

  • 87

    P rate > 300, no PR interval, QRS variable, irregular rhythm. Decreased filling time causing fatigue? dizziness, dyspnea, irregular pulse

    A-Fib

  • 88

    How easy it is for blood to travel through arteries

    Compliance

  • 89

    95% of HTN caused my genetics and environment

    Primary HTN

  • 90

    Walk-Along Theory

    Head myosin cross-bridge attached to the actin filaments at the active site. Intra-molecular forces cause the myosin head to tilt forward on a flexible hinge and drag the actin filament with it (power stroke). Myosin head breaks away and interacts with the next actin site. Z-disc pulls filament together at the sarcomere —> muscle contraction. ATP is cleaved to fuel process.

  • 91

    Small branches of arteries that act as conduits between arteries and the capillary beds of tissues (muscular walls and sphincters)

    Arterioles

  • 92

    Atherosclerosis of coronary arteries. Diminished blood supply.

    CAD

  • 93

    Atherosclerotic disease of the arteries

    Peripheral artery disease

  • 94

    Flow of blood to lungs: Flow of blood to body

    QP:QS

  • 95

    Secondary causes of Dyslipidemia

    Lifestyle, HTN, DMII, Hypothyroidism, Pancreatitis, Renal Nephrosis, Chronic Inflammation, Diuretics, beta-blockers, steroids, antiretrovirals, air pollution, radiation, microbiome

  • 96

    Age, male and post-menopausal women, family history

    Non-modifiable CAD risk factors

  • 97

    Flow (Q) through a blood vessel determined by?

    Pressure difference between two ends of a vessel, Resistance (diameter), Viscosity, and Length of vessel

  • 98

    At rest cell has?

    Negative charge

  • 99

    Dyslipidemia, HTN, Smoking, DMII, Insulin Resistance, Obesity, Diet, Lifestyle

    Major modifiable risk factors for CAD

  • 100

    Comparing Catecholamines

    Epinephrine and Norepinephrine have the same effect on Systolic BP but Norepinephrine has more effect on Diastolic BP