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Patho Exam 3 > CV > Flashcards

CV Flashcards

1
Q

Neural control centers for the heart are located here:

A

Medulla oblongata

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2
Q

What type of innervation stimulates the heart?

A

Sympathetic

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3
Q

What receptors respond to norepinephrine?

A

Beta1-adrenergic

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4
Q

What innervation generally inhibits the heart?

A

Parasympathetic

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5
Q

What receptors respond to acetylcholine?

A

Muscarinic

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6
Q

What is the pattern of electrical transmission?

A

SA node > preferred pathways > AV node > bundle of His> R/L bundle branches > purkinje fibers

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7
Q

Systole is further divided into:

A

Isovolumetric ventricular contraction and ventricular ejection

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8
Q

Diastole is further divided into:

A

Isovolumetric ventricular relaxation and ventricular filling

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9
Q

Stroke volume equals:

A

EDV -ESV

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10
Q

Cardiac output equals:

A

HR x SV

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11
Q

Ejection fraction

A

SV/ EDV

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12
Q

The most important variable of resistance is

A

The radius of the blood vessel

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13
Q

Structure of the blood vessel walls includes these 3 structures:

A
  1. Tunica intima- endothelium
  2. Tunica media- smooth muscle
  3. Tunica externa- connective tissue
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14
Q

These are low-resistance vessels that serve as conduits for blood flow.

A

Arteries

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15
Q

Arteries function as pressure reservoirs that maintain blood flow during

A

Diastole

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16
Q

Elastic arteries are closer to this and easily distend.

A

Heart

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17
Q

Muscular arteries are closer to these and have more smooth muscle.

A

Arterioles

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18
Q

These regulate blood flow and distribution by changing the radius from signals that may be extrinsic/systemic or intrinsic/local.

A

Arterioles

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19
Q

Mechanisms of intrinsic control of arterioles are:

A
  1. Active hyperemia
  2. Flow autoregulation
  3. Reactive hyperemia
  4. Response to injury
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20
Q

Mechanisms of extrinsic control include these:

A
  1. ANS

2. Hormones

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21
Q

The most important control signals for the arterioles include:

A
  1. SNS
  2. Epi
  3. Angiotensin II/ ADH
  4. ANP
  5. Prostacyclin
  6. EDRF
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22
Q

What does epi do?

A

It vasodilator skeletal muscle vessels and vasoconstricts peripheral blood vessels.

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23
Q

What does angiotensin II/ ADH do?

A

Vasodilator

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24
Q

What does prostacyclin do?

A

Vasodilator

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25
Q

What does EDRF do?

A

Nitric oxide- vasodilation

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26
Q

These are leaky thin-walled vessels with a large cross-sectional area allowing slow passage of blood that facilitates transport and exchange.

A

Capillaries

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27
Q

Difference between hydrostatic and interstitial fluid pressure favors this:

A

Filtration

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28
Q

Difference between osmotic pressures in plasma and interstitial fluid favors this:

A

Absorption

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29
Q

This is the accumulation of excess fluid in the interstitial space:

A

Edema

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30
Q

Increased hydrostatic pressure causes:

A

Increased arterial or venous pressure or arterial dilation

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31
Q

Major function of this is to maintain blood volume but also important in defense and fat absorption.

A

Lymphatic

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32
Q

Excessive accumulation of lymph due to damaged or obstructed lymph.

A

Lymphedema

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33
Q

Acute inflammation of lymph vessels

A

Acute lymphangitis

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34
Q

These return blood to heart through low-resistance blood conduits.

A

Veins

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35
Q

Sympathetic stimulation of veins causes:

A

the Smooth muscle to contract which raises venous pressure

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36
Q

This drug inhibits Na-K- ATPase which results in an increased Na to exchange with Ca. This results in an increase in Ca intracellularly which enhances cardiac contractility.

A

Digitalis

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37
Q

What cardiac drugs are vasodilators?

A

Nitroglycerin and calcium channel blockers

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38
Q

What cardiac drugs reduce contractility and heart rate which reduces myocardial demand. Increases cardiac output by increasing ventricular filling by relaxing the obstructing muscle.

A

Beta-adrenergic antagonists

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39
Q

These cardiac drugs reduce afterload through vasodilation.

A

Ace inhibitors

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40
Q

When lipids, such as cholesterol and triglycerides, collect in the blood. Normally transported in the blood by proteins, which form lipoproteins.

A

Hyperlipidemia

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41
Q

This may have a genetic basis and is a defective synthesis of apoproteins, lacks appropriate or defective receptors, and there is a defect in how the cell handles cholesterol.

A

Primary hyperlipidemia

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42
Q

Secondary causes of hyperlipidemia include:

A

High caloric intake, obesity, sedentary lifestyle, diabetes mellitus and is more common.

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43
Q

These are mostly triglycerides, very little protein

A

Chylomicrons

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44
Q

These are triglycerides, cholesterol, and protein.

A

Very-low density lipoproteins

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45
Q

These are bad cholesterol and is the main carrier of cholesterol: triglycerides, half cholesterol, one quarter protein

A

Low-density lipoproteins LDL

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46
Q

This is good cholesterol: 20% cholesterol, half protein

A

High-density lipoprotein HDL

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47
Q

Chlylomicrons are synthesized here as a part of fat reabsorption.

A

Small intestine

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48
Q

LDL and HDL are synthesized and released by this.

A

Liver

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49
Q

This is the main carrier of cholesterol:

A

LDL

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50
Q

This is a more reverse carrier, brings cholesterol from tissues to liver, allows body to recycle cholesterol.

A

HDL

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51
Q

Increase of cholesterol on the blood, characterized by LDL 70-130 mg/dL.

A

Hypercholesteremia

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52
Q

Where do we want LDL, HDL, total cholesterol, and triglyceride levels?

A

LDL <100
HDL 40-60
Total <200
Triglycerides 10-150

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53
Q

When managing hypercholesteremia what primary target?

A

To lower LDLs.

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54
Q

Type of lipid lower med that prevents the liver from manufacturing cholesterol.

A

Statins

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55
Q

Type of lipid lowering med that prevents body from absorbing cholesterol.

A

Bile acid sequestrants

56
Q

Type of lipid-lowering med that limits body’s absorption of cholesterol.

A

Cholesterol-absorption inhibitors

57
Q

Type of lipid-lowering med that decreases synthesis of VLDL by liver, stimulates clearance of triglycerides from circulation.

A

Fibrates

58
Q

Type of lipid-lowering med that blocks synthesis and release of VLDL from liver, reduces IDL and LDL level and increases HDL concentrations.

A

Nictonic acid

59
Q

A condition in which an artery wall thickens as a result of the accumulation of fatty materials.

A

Atherosclerosis

60
Q

This correlated with lipid changes in the tunica intima, endothelial layer of artery, and increased collagen in tunica media, middle layer of the vessels.

A

Atherosclerosis

61
Q

Biggest risk factor for atherosclerosis is:

A

Hypercholesteremia

62
Q

Risk factors for atherosclerosis:

A

Hypertension, smoking, elevated cholesterol, obesity, diabetes.

63
Q

These are changes in dilation of blood vessel wall, which can lead to rupture and bleeding.

A

Aneurysms

64
Q

Where do aneurysms typically form?

A

Aorta but can form in other arteries and veins

65
Q

This is bounded by complete vessel wall and all blood remains in that vascular compartment.

A

True aneurysm

66
Q

This is a localized dissection or tear in the wall of the vessel that forms a hematoma outside the vessel, enlarging it. It may be hounded only by outer layer of the vessel wall and supporting tissue.

A

False aneurysm

67
Q

Type of aneurysm that is small, spherical dilation of vessel at a bifurcation point. Seen in structures like the circle of Willis in brain, where bifurcated vessels are common.

A

Berry aneurysm

68
Q

Type of aneurysm that involves entire circumference of vessel, characterized by a gradual, progressive dilation.

A

Fusiform

69
Q

Type of aneurysm that extends over part of circumference of a vessel and appears like a sac.

A

Saccular

70
Q

A false aneurysm resulting from a tear in the tunica intima; allows blood to enter vessel wall and creates a pocket filled with blood.

A

Dissecting aneurysm

71
Q

This is a group of diseases that cause inflammatory injury and possible necrosis of blood vessel walls.

A

Vasculitides

72
Q

Involves endothelial lining and smooth muscle cells of vessel wall. Includes arteries, veins, and capillaries. Typically results from direct injury, infectious agent immune processes.

A

Vasculitis

73
Q

Obstruction of large arteries that supply the body’s peripheral structures.

A

Peripheral artery disease

74
Q

Risk factors for peripheral artery disease and typically seen in:

A

Smoking, diabetes and men 60-70s

75
Q

Vasculitis that affects medium-sized arteries. Usually found in plantar or digital vessels. Primarily arterial but can involve veins and nerves.

A

Thromboangitis obliterans

76
Q

An intensive vasospasm of arteries and arterioles, typically in fingers, less often in toes. No clear cause, but generally in young women exposed to cold or strong emotions.

A

Raynaud’s phenomenon

77
Q

Raynaud’s phenomenon occurs in nearly all individuals with this:

A

Scleroderma

78
Q

MAP is a regulated variable governed by:

A

Feedback inhibition

79
Q

Baroreceptors for pressure are found :

A

In carotid sinus and aortic arch

80
Q

Afferent pathways for Blood pressure regulation are in:

A

The carotid sinus nerve and aortic depressor nerve.

81
Q

These pathways feed information to integrating center (medullary cv center) in the brainstem.

A

Afferent pathway

82
Q

Efferent pathways for blood pressure control are:

A

In the vagus nerve (to heart) and sympathetic nerves (to heart, arterioles, and veins)

83
Q

This pathway includes variables that change heart rate and contractility, as well as vessel radius

A

Efferent pathways

84
Q

MAP equals:

A

CO x TPR

85
Q

Short term regulators of MAP:

A

Baroreceptor reflex and feedback inhibition

86
Q

Long term regulator of MAP:

A

Blood volume

87
Q

Increased tension on blood vessel walls leads to:

A

An increase in blood pressure

88
Q

Chronic elevation of blood pressure without evidence of other disease:

A

Primary or essential hypertension

89
Q

Clear other cause of hypertension such as diabetes that increases CO or TPR, and indirectly affects MAP.

A

Secondary hypertension

90
Q

A severe increase in arterial blood pressure. If untreated may result in severe damage to renal, cardiac, or cerebral function.

A

Hypertensive crisis

91
Q

Enlarges tortuous veins that may lead to edema and stasis ulcers as a result of chronic venous insufficiency.

A

Varicose veins

92
Q

These originate in the superficial sap genius veins caused by prolonged standing and increased intraabdominal pressure.

A

Primary varicose veins

93
Q

Result from impaired blood flow in the deep venous channels.

A

Secondary varicose veins

94
Q

Chronic venous disease of the lower extremities is characterized by:

A

Venous HTN
Varicose veins
Venous ulcers due to insufficiency

95
Q

Stasis of blood, increased blood coagulability and vessel wall injury are components of:

A

Virchows triad

96
Q

Acute inflammatory response that results in exudate accumulation around the heart.

A

Acute pericarditis

97
Q

Formation of scar tissue between pericardial layers.

A

Restrictive or constrictive pericarditis

98
Q

Fluid accumulation in pericardial sac.

A

Pericardial effusion

99
Q

Accumulation of exudates such as blood in pericardial sac, under pressure.

A

Cardiac tamponade

100
Q

Rapid, unchecked increase in pressure in pericardial sac that impairs diastolic filling, reduces CO, and compromises perfusion in the body.

A

Cardiac tamponade

101
Q

A lack of blood flow to tissue.

A

Ischemia

102
Q

Ischemia that can compromise or lead to cell injury.

A

Injury

103
Q

Death of myocardial cells

A

Infarct

104
Q

Results from narrowing of coronary arteries due atherosclerotic processes, reduced blood flow to heart.

A

Coronary artery disease

105
Q

Represents a disease of the heart muscle fibers that usually affects cardiac performance.

A

Cardiomyopathy

106
Q

3 main forms of CM:

A

Dilated
Restrictive
Hypertrophic

107
Q

Involves dilation of the heart chambers impairing the function of the heart as a pump.

A

Dilated cardiomyopathy

108
Q

DCM is heterogeneous and commonly shows:

A

Autosomal dominant pattern

X-linked recessive pattern

109
Q

Characterized by hypertrophy of muscle mass that can lead to obstruction of blood filling.

A

Hypertrophic cardiomyopathy

110
Q

Familial HCM is inherited as an

A

Autosomal dominant trait

111
Q

These have in the gene encoding myosin have been associated with HCM.

A

De nova mutations

112
Q

Involves rigid ventricular walls that restrict blood filling but spare contractile properties of the muscle.

A

Restrictive cardiomyopathy

113
Q

Primary causes of RCM include:

A

Endocarditis

114
Q

Secondary causes of RCM include:

A

Amyloidosis
Hemachromatosis
Sarcoidosis

115
Q

Infection of the endocardium, heart valves, or cardiac prosthesis resulting from bacterial or fungal infection.

A

Endocarditis

116
Q

Most patients with endocarditis are:

A

IV drug users
Have prosthetic valves
Have rheumatic heart disease

117
Q

Narrowing of the valve opening leads to greater resistance to blood flow through the valve.

A

Stenosis

118
Q

Failure of valve to close completely results in backflow of blood

A

Insufficiency

119
Q

Inflammatory destruction of valve in response to b-hemolytic streptococcus is a common cause

A

Rheumatic fever

120
Q

Occurs when heart cannot pump sufficient blood to meet the metabolic demands.

A

Heart failure

121
Q

Heart failure is often characterized by:

A

Intravascular and interstitial volume overload

Poor tissue perfusion

122
Q

Most common cause of heart failure is:

A 
Coronary artery disease 
Also typical:
HTN
DCM
Valvular heart disease
123
Q

Systolic dysfunction results from conditions reducing contractility such as:

A

Ischemic heart disease

Cardiomyopathy

124
Q

Most common causes of left ventricular dysfunction include:

A

HTN
Acute myocardial infarction
Valvular defects including stenosis or regurg from aortic or mitral valve

125
Q

Right sided heart failure results in:

A

Fluid backup into the systemic and hepatic systems

Peripheral edema and ascites, external jugular veins

126
Q

When right sided heart failure occurs in response to chronic pulmonary disease it’s referred to as:

A

Cor pulmonale

127
Q

Reduced tissue and organ perfusion and eventually organ dysfunction and failure.

A

Shock

128
Q

Acute life threatening condition where body tissues are inadequately perfumes or unable to use oxygen.

A

Shock

129
Q

Shock leads to:

A

Cell death, lactic acidosis, and reperfusion injury

130
Q

Type of shock where heart fails as a pump and can’t maintain CO.

A

Cardiogenic

131
Q

Type of shock where intravascular volume is inappropriately distributed, vasodilation causes hypovolemia

A

Distributive

132
Q

Examples of distributive shock:

A

Septic
Neurogenic
Anaphylactic

133
Q

Type of shock with inadequate blood volume. Venous return is reduced as fluid is lost from intravascular space that results in decreased ventricular filling and a drop in SV.

A

Hypovolemic

134
Q

Type of shock where blood flow is impeded by physical or mechanical obstruction.

A

Obstructive

135
Q

Complications of shock:

A 
Acute respiratory distress syndrome 
Acute renal failure
GI ulceration
DIC
Multiple organ dysfunction syndrome

Patho Exam 3 (3 decks)

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