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Adv Pathophysiology > Chapter 26 & 27: Cardiovascular System > Flashcards

Chapter 26 & 27: Cardiovascular System Flashcards

1
Q

Causes of Secondary Hyperlipidemia (4)

A

Results from systemic disturbance

1) Obesity with high-caloric intake
2) DM
3) Hypothyroidism
4) Liver disease

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2
Q

Thromboangiitis Obliterans is the inflammation of _______ arteries that can extend to involved adjacent veins and nerves.

A

medium-sized

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3
Q

Risk Factors for Atherosclerosis

A 
Hypercholesterolemia
Hyperlipidemia
HTN
Smoking 
DM
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4
Q

______ has to occur for atherosclerosis to begin

A

Endothelial damage

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5
Q

Most common cause of Thromboangiitis Obliterans (Buerger’s Disease)

A

Most common in young men who smoke heavily (tobacco allergy)

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6
Q

Buerger’s Diseases affect ______ extremities

A

Lower extremities

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7
Q

Clinical Manifestations of Thromboangiitis Obliterans

A 
#1 = PAIN 
color/temperature changes
paresthesia
weak pulses in feet
loss of hair/thin, shiny skin
edema in legs
can lead to GANGRENE
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8
Q

Raynaud’s Syndrome

A

SMALL arteries and arterioles spasm and constrict in response to stimuli such as cold, exercise, and emotional stress

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9
Q

Part of the body most commonly affected by Raynaud’s

A

fingers more often than toes

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10
Q

Clinical Manifestations of Raynaud’s

A

COLOR CHANGES (W - B - R)
throbbing pain
paresthesia
fingertips thickened and nails become brittle

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11
Q

Main Cause of Chronic Arterial Disease

A

atherosclerosis

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12
Q

Main Cause of Chronic Venous Insufficiency

A

increased venous hydrostatic pressure

prolonged standing, obstruction, incompetent valves, sedentary lifestyle

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13
Q

Risk Factors for CAD

A

same as atherosclerosis

HTN, DM, smoking, hypercholesterolemia

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14
Q

Risk Factors For CVI

A 
prolonged standing
obstruction
sedentary lifestyle
DM
obesity
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15
Q

Varicose Veins

A

dilated torturous veins of the lower extremities

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16
Q

Etiology of Varicose Veins

A

Incompetent valves
Increased venous pressure
Increased intra-abdominal pressure (obesity, pregnancy, heavy lifting)

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17
Q

Pathogenesis of Varicose Veins

A

walls of the vessel stretch = incompetent valves = venous congestion = vein walls bulge out

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18
Q

Risk Factors for DVT

VIRCHOW’S TRIAD

A

Venous Stasis
Hypercoagulability
injury to Venous Wall

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19
Q

Most Common Clinical Manifestation of DVT

A

Edema in affected leg
pain
possible redness or warmth

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20
Q

Causes of Primary Hypertension

Essential/Idiopathic

A 
May not have known causes
Lifestyle factors
Family history
Age
Race (black)
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21
Q

Risk Factors of Primary HTN

A 
age, gender, race, family hx
DM
dyslipidemia
high sodium
sedentary lifestyle
abdominal obesity
excess alcohol
smoking
OSA
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22
Q

Causes of Secondary Hypertension

A

Renal disease
Adrena Cortex D/O (excess aldosterone, cortisol)
Pheochromocytoma
Oral contraceptives

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23
Q

Pheochromocytoma

A

tumor of tissue in the adrenal medulla

controls release of norepinephrine/epi

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24
Q

Target Organ Damage of HTN (5)

A 
Heart
Peripheral Arteries
Kidneys
Brain
Retina
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25
Q

Changes in Retina r/t HTN

A 
Drusen
Cotton-wool spots
Microaneurysms
A-V nicking 
Superficial retinal hemorrhages
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26
Q

Most Common Viral Causes of Acute Pericarditis (4)

A

1) Influenza
2) Epstein-Barr
3) Varicella
4) Coxsackie

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27
Q

Triad of Manifestations for Acute Pericarditis

A 
Chest pain (worse w/ deep breathing, coughing - relieved sitting up/leaning forward)
Pericardial Friction Rub
ECG changes
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28
Q

Cardiac Tamponade

A

Compression of the heart due to accumulation of fluid, pus, or blood in the pericardial sac

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29
Q

Clinical Manifestations of Cardiac Tamponade

BECK’S TRIAD

A

Hypotension
Jugular vein distention (JVD)
Muffled heart sounds

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30
Q

Key Diagnostic Finding for Cardiac Tamponade

A

Pulsus Paradoxus

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31
Q

Pulsus Paradoxus

A

Pulse is diminished or absent during inspiration and stronger in expiration

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32
Q

Myocardial oxygen supply is determined by:

A

capillary flow along with the ability of hemoglobin to deliver O2 to muscle

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33
Q

Factors that decrease coronary blood flow:

A

vasospasm
stenosis
thromobosis

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34
Q

Factors that increase myocardial oxygen demand

A

increased HR
increased LV contractility
SBP or myocardial wall stress

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35
Q

Angina

A

chest pain caused by myocardial ischemia

occurs when there is decreased blood flow to myocardium and/or increased demand for oxygen that cannot be met

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36
Q

Stable Angina

A

CP associated with stable atherosclerotic pain = occurs with exertion, emotional stress, or exposure to cold

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37
Q

Characteristics of Stable Angina

A

Precordial or substernal pain
constricting, squeezing, suffocating
Should resolve with rest/NTG

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38
Q

Treatment for Stable Angina

A

Beta-blockers

Nitroglycerin

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39
Q

Variant (Prinzmetal) Angina

A

Pain caused by coronary spasm - usually occurs during rest (nocturnal)
can cause arrhythmias

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40
Q

___________ is the initial manifestation of ischemic heart disease

A

Stable angina

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41
Q

Potential Causes of Variant Angina

A

Hyperactive SNS response
Imbalance of endothelium-derived factors
Defects in Ca handling from VSM
Alteratio in NO production

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42
Q

Treatment for Variant Angina

A

Calcium-channel blockers

Nitrates

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43
Q

Dilated Cardiomyopathy

Genetic and Nongenetic

A

SYSTOLIC dysfunction
ventricular enlargement = impaired contractility
blood builds up after systole

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44
Q

______ cardiomyopathy is one of the most common causes of heart failure.

A

Dilated cardiomyopathy

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45
Q

Hypertrophic Cardiomyopathy

Genetic

A

DIASTOLIC dysfunction
Left ventricular hypertrophy = decreased ventricle size
ventricular filling is inadequate
atrial kick is needed = LA hypertrophy

46
Q

_________ cardiomyopathy is the most common cause of sudden death in young athletes.

A

Hypertrophic

47
Q

Restrictive Cardiomyopathy

Genetic and Nongenetic

A

DIASTOLIC dysfunction

decreased ventricular compliance/filliing due to stiff, rigid ventricular walls

48
Q

Restrictive cardiomyopathy can be caused by ______ or _________

A

sarcoidosis or cancer

49
Q

Most common cause of Infective Endocarditis

A

Staphylococcus aureus

50
Q

Pathogenesis of Infective Endocarditis

A

Vegetations attach loosely to heart valves
Can break off, travel, and become emboli
Bacteremia initiates immune response
Growth causes valve destruction

51
Q

Clinical Manifestations of Infective Endocarditis (FROM-JANE)

A 
Fever
Roth Spots
Osler nodes
Murmur
Janeway lesions
Anemia
Nailbed hemorrhages (splinter)
Emboli
52
Q

Valvular Heart Disease

STENOSIS

A

Inability of leaflets to open and close properly

blood flow is impeded

53
Q

Stenosis results in decreased ____, ____, ____ and impaired ____________.

A

decreased CO
decreased EF and SV
impaired ventricular filling

54
Q

Valvular Heart Disease

REGURGITATION

A

Backflow of blood through a valve that cannot close properly due to damage or disease

55
Q

Etiologies of Mitral Stenosis

A

Acute rheumatic fever

Bacterial endocarditis

56
Q

You would hear a low-pitch diastolic murmur and an opening snap in:

A

MITRAL STENOSIS

57
Q

Mitral Stenosis results in:

A

Pulmonary HTH and R heart failure

58
Q

Mitral Regurgiation leads to

A

dilation of both chambers
pulmonary congestion
RV failure

59
Q

Etiologies of Mitral Regurgitation

A 
Endocarditis
Rheumatic fever
MVP or mitral stenosis
Papillary muscle rupture
Chordae tendinae rupture
60
Q

You would hear a pansystolic murmur in:

A

MITRAL REGURGITATION

61
Q

In mitral regurgitation, the PMI is:

A

displaced left and downward

with a palpable thrill

62
Q

Risk Factors for Aortic Stenosis

A

Congenital bicuspid aortic valve
Calcification/Hypercholesterolemia
Hx of rheumatic valve disease

63
Q

Triad of Symptoms of Aortic Stenosis

A

Angina
Dyspnea
Syncope

64
Q

You would feel a thrill in the aortic area (2nd ICS RSB) and hear a loud systolic ejection murmur in:

A

AORTIC STENOSIS

65
Q

Aortic Regurgitation leads to:

A

LV dilation and hypertrophy
Pressure and volume overlaod
Pulmonary edema

66
Q

Early changes in Aortic Stenosis leads to:

A

diastolic dysfunction

decreased compliance and unchanged contractility

67
Q

Late changes in Aortic Stenosis lead to:

A

systolic dysfunction
myocardial ischemia
abnormal wall motion
decreased contractility = decreased SV

68
Q

Risk Factors for Aortic Regurgitation

A

Rheumatic heart disease
Infective endocarditis
Marfan’s Syndrome
Hypertension

69
Q

You would see a Water-Hammer (Corrigan’s) pulse in:

A

AORTIC REGURGITATION

this is prominent carotid pulsations - head bobbing with each heartbeat

70
Q

You would hear a decrescendo diastolic murmur at Erb’s point (LSB) in:

A

AORTIC REGURGITATION

71
Q

Cardiac Reserve

A

ability of the heart to increase its CO during increased activity

72
Q

Heart failure occurs when any type of cardiac dysfunction causes:

A

Failure to empty
Reduction of cardiac output
Decrease in cardiac reserve

73
Q

HIGH OUTPUT Heart Failure

A

heart cannot pump sufficient amounts of blood to meet the increased circulatory needs of tissues
heart weakens = LV fails

74
Q

LOW OUTPUT Heart Failure

A

LV is unable to fill with adequate blood to pump out to the tissues
Occurs with impaired venous return
Inadequate O2 is delivered

75
Q

SYSTOLIC FAILURE Heart Failure

A

Reduced EF failure (<40%)
Decreased contractility
Preload increases and afterload decreases
Leads to pulmonary and peripheral edema

76
Q

DIASTOLIC FAILURE Heart Failure

A

Preserved EF failure
Relaxation of the ventricle in impaired and cannot fill properly
Common in adults with HTN
Ventricle cannot stretch but CAN contract

77
Q

Left-Sided Heart Failure leads to

A

Pulmonary fluid overload

78
Q

Main Complication of Left-Sided Heart Failure

A

Pulmonary Edema

79
Q

Clinical Manifestations of L-sided Heart Failure

A 
DOE
PND
Orthopnea
S3 or S4 gallop
Tachypnea and tachycardia
Fine crackles
Cough - may produce pink, frothy sputum
80
Q

Right-Sided Heart Failure leads to:

A

systemic fluid overload

81
Q

Signs of Systemic Fluid Overload

R-sided HF

A 
Peripheral edema
Weight gain
JVD
Hepatomegaly and ascites
Kidney enlargement
82
Q

Clinical Manifestations of R-Sided Heart Failure

A 
Dependent edema (early sign)
RUQ discomfort
Weight gain
Decreased UO or nocturia
JVD, hepatomegaly, ascites
83
Q

Compensatory Mechanisms in Heart Failure

A 
attempt to maintain CO and cardiac reserve
Frank-Starling Mechanisms
SNS Activity
RAAS
Natriuretic Peptides
84
Q

Frank-Starling Mechanisms

A

SV increased through increase in EDV
increased filling = increased stretching = increased contractile force
stretch is limited and this mechanism fails over time

85
Q

SNS Activity

compensatory activity in HF

A

helps maintain perfusion to heart and brain
stimulates HR and contractility
vasoconstricion = increased afterload
heart has to work harder but cannot do so

86
Q

RAAS

compensatory action in HF

A

activated d/t decrease in renal blood flow secondary to low CO
increases preload and afterload

87
Q

Natriuretic Peptides (ANP and BNP)

A

promote rapid natriuresis and diuresis
decrease preload and afterload
can inhibit the SNS, RAAS, and ADH

88
Q

Atrial Natriuretic Peptide (ANP)

A

released by the atria d/t increased atrial stretch/pressure
produces rapid, temporary loss of Na, water, and potassium
acts as an antagonist to renin and aldosterone

89
Q

Brain Natriuretic Peptide (BNP)

A

released by the ventricles due to ventricular volume expansion and pressure overload
acts as a vasodilator and diuretic

90
Q

3 Specific Mechanisms in Treating HF

A

Slowing HF
Increasing contractility
Reducing cardiac workload (reduce preload and/or afterload)

91
Q

Shock is defined as:

A

the acute failure of the circulatory system to maintain adequate blood flow (and therefore oxygen delivery) to body tissues and vital organs

92
Q

Compensatory Mechanisms in Shock (that eventually fail and become detrimental)

A

SNS activation
Alpha1 and Beta1 = increased HR and contractility
Beta2 = bronchodilation

93
Q

Hypovolemic Shock

A

Most common type of shock
Caused by a large reduction in circulating blood volume = unavailable for the transport of oxygen and nutrients to tissues

94
Q

Causes of Hypovolemic Shock

A

Hemorrhage
Burns
Dehydration
Third-spacing

95
Q

Treatment of Hypovolemic Shock

A

Fluid volume replacement first = crystalloids, colloids, blood prodcuts
Vasoconstricting drugs
Supplemental O2

96
Q

Cardiogenic Shock

A

Decreased CO as a result of decreased myocardial contractility, increased afterload, and excess preload

97
Q

Preload and afterload is increased in _____ shock

A

CARDIOGENIC

98
Q

Causes of Cardiogenic Shock

A

MI = most common cause

Mechanical obstructions

99
Q

Obstructive Causes of Cardiogenic Shock

A

Cardiac tamponade
Tension pneumothorax
Large pulmonary embolism

100
Q

Treatment of Cardiogenic Shock

A

Vasoactive medications first
nitroglycerin and nitroprusside
Positive inotropics = dobutamine

101
Q

Distributive Shock

A

Normovolemic shock caused by MASSIVE VASODILATION

Includes: neurogenic, anaphylactic, and septic shock

102
Q

Neurogenic Shock

A

occurs when there is a disturbance in the nervous system that interrupts sympathetic outflow = vasodilation

103
Q

Causes of Neurogenic Shock

A 
Upper spinal cord injury/disease
Spinal anesthesia
TBI
Extreme emotional distress/fear/anxiety
Hypoxia
Hypoglycemia
104
Q

Pathogenesis of Anaphylactic Shock

A

IgE attaches to mast cells
Mast cells release histamine and prostaglandins
Causes vasodilation, laryngeal edema, bronchial constriction, cardiovascular collapse, respiratory failure

105
Q

Clinical Manifestations of Anaphylactic Shock

A 
Hypotension
Urticaria and hives
Angioedema = hoarseness/stridor
Chest tightness
Abdominal cramps 
Decreased CO, SVR, PA readings
106
Q

Septic Shock

A

Most common type of distributive shock
Due to massive infectious process - bacteria multiple faster than body can kill them and release endotoxins and exotoxins

107
Q

________ is the key mediator of septic shock

A

Nitric oxide (released by activated endothelial cells)

108
Q

Causes of Septic Shock

A

Nosocomial infections

Gram negative bacteria: E. coli, Klebsiella, Pseudomonas

109
Q

Early Stages of Septic Shock

A 
Bounding pulses
Hypotension
Tachypnea
Increasd UO
Hyperthermia 
Increased CO
110
Q

Late Stages of Septic Shock

A 
Weak, rapid pulse
Hypotension
Bradypnea
Oliguria
Hypothermia
AMS
Decreased CO

Adv Pathophysiology (22 decks)

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