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Pathophysiology > Chapter 24 - Alteration In CV Function > Flashcards

Chapter 24 - Alteration In CV Function Flashcards

1
Q

Varicose veins

A

Veins where blood has pooled producing distended and palpable vessels

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2
Q

Cause of Varicose veins

A

Trauma that damages valves or gradual distension caused by action of gravity

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3
Q

Valve damage due to

A

Increase pressure and volume of blood under pressure of gravity

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4
Q

Varicose veins typically involve what veins of the leg

A

Saphenous veins of legs

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5
Q

Pathophysiology of varicose veins

A

Enzymes remodel vessel wall, and veins swells with increased pressure and pressure pushes plasma through vessel wall

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6
Q

Risk factors for varicose veins

A

-standing for long periods which diminishes action of muscle pump
-age, obesity, genetics, pregnancy, previous leg injury

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7
Q

Varicose vein TX

A

-elevated legs, compression stockings

Invasive TX: surgical ligation -> tying up blood vessel

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8
Q

Chronic venous insufficiency

A

Inadequate venous return over ext3ended period

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9
Q

Symptoms of Chronic venous insufficiency

A

-edema of lower extremities
-hyperpigmentation of ankle and feet skin
-circulation sluggish, reduced oxygen to cells causing necrosis
-surgery

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10
Q

Venous statis ulcers

A

Infection occurs because of poor circulation in veins and impairs delivery of oxygen causing necrosis

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11
Q

Thrombus

A

Blood clot that remains attached to vessel wall

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12
Q

Thromboembolism

A

A detachedthrombus

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13
Q

Venous thrombi are more common than

A

Arterial thrombi as flow and pressure are lower in veins
-also occurs more often in lower extremity

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14
Q

The virchow triad

A

Three factors that promote deep venous thrombosis
1. Venous stasis (immboity, age, heart failure)
2. Venous endothelial damage
3. Hypercoagulable states (inc tendency of blood to thromboses)

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15
Q

Hypercoagulable states are caused by

A

Pregnancy, oral contraceptives, heredity

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16
Q

Pathophysiology of thrombus formation in veins

A

-Accumulation of clotting factors and platelets near a venous valve cause venous obstruction
-inflammation promote further planet aggregation causing pain and redness

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17
Q

Thrombus obstruction creates extremity edema causing

A

Ulceration of limb (break on surface)

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18
Q

TX for thrombus formation in veins

A

Most thrombus dissolve without treatment
-anticoagulants (aspirin, warfarin)

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19
Q

Diagnosis for thrombus formation in veins

A

Doppler ultrasonography

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20
Q

Doppler ultrasonography

A

Non invasive test that can be used to estimate blood flow through blood vessels by bouncing high frequency sound waves

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21
Q

Superior vena cava syndrome

A

Progressive occlusion of Superior vena cava leading to venous distension to upper extremities and head

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22
Q

Causes for Superior vena cava syndrome

A

Bronchogenic cancer
-75% of cases
-ontological emergency

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23
Q

Pathophysiology of Superior vena cava syndrome

A

Lung bronchi abuts Superior vena cava syndrome = bronchi cancer puts pressure on SRV

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24
Q

Result of Superior vena cava syndrome

A

Edema and venous distension in upper extremities and face

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25
Q

Effect of Superior vena cava syndrome

A

Tightness of shirt collars, necklaces, headache, visual disturbances

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26
Q

Diagnosis of Superior vena cava syndrome

A

Chest, X-ray, CT, MRI

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27
Q

Hypertension

A

Consistent elevation of systemic arterial blood pressure

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28
Q

Risk of hypertension

A

Increases with age, higher in diabetes

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29
Q

Maintenance of proper BP

A

Exercise and proper nutrition

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30
Q

Percentage of primary hypertension vs secondary hypertension

A

95% of cases and 5% of cases

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31
Q

Malignant hypertension

A

Rapidly progressive hypertension
S: >180, D: >120
-system and organ complications, can be considered a medical emergency

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32
Q

Normal BP

A

Less than 120/less than 80

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33
Q

Elevated BP

A

120-129/less than 80

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34
Q

High blood pressure (stage 1)

A

130-139/80-89

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35
Q

High blood pressure stage 2

A

140+/90+

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36
Q

Hypertensive crisis

A

180+/120+

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37
Q

Factors associated with primary hypertension

A

No specific cause
-genetic and environmental factors
-epigenetic changes

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38
Q

Epigentic

A

How behaviours and environment affect gene function

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39
Q

Hypertension results form

A

Sustained inc in peripheral resistance, inc in blood volume

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40
Q

Two primary factors of primary hypertension

A
  1. Sympathetic ns
  2. RAAS
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41
Q

SNS and primary hypertension

A

Inc SNS will cause INC HR, cardiac contractility, systemic vasoconstriction = rise in BP

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42
Q

RAAS

A

Renin angiotesin, angiotesnin II, aldosterone pathways

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43
Q

RAAS increases in (aldosterone vs angiotensin II)

A
  1. Aldosterone = inc Na reabsorption from kidney, inc blood volume, inc BP
  2. Angiotensin II = inc vasopressin which inc vasoconstriction and inc BP
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44
Q

Arteriosclerosis

A

A: Genetic term for vascular disease in which causes thickening an inelasticity of arteries

S: hardening of body tissue

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45
Q

Atherosclerosis

A

Dominant pattern of arteriosclerosis
-formation of fatty plague with core rich in lipids

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46
Q

Athero

A

From Greek word athera meaning porridge

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47
Q

TX for hypertension

A

Begin with lifestyle modifications: diet, exercise, stopping, smoking, loosing weight

Advanced: diuretics, angiotensin II blockers

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48
Q

What is orthostatic hypotension

A

Decrease in systolic BP of 20 mmHg or a decrease in diastolic BP of 10 mmHg within three minutes of standing
-mechanical dysfunction

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49
Q

Normally what happens during standing

A

Baroreceptors, vasoconstriction and heart rate adjusts to maintain normal BP

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50
Q

Signs and symptoms of orthostatic hypotension

A

Dizziness, loss of vision, reduced brain blood flow

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51
Q

Treatment for othrostatic hypotension

A

No curative treatment
-inc fluid and salt intake, wearing thigh high stockings

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52
Q

Aneurysm

A

Localized dilation of vessel wall

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53
Q

What layers of the arterial wall does an Aneurysm involve

A

All three layers, causing weakening

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54
Q

What is the most common site of an Aneurysm

A

Aorta
-constant high pressure stress

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55
Q

Risk factors of Aneurysm

A

Smoking, genetics, diet

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56
Q

What are the three CV vessel layers

A

Tunica adventitia, tunica media, tunica intima

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57
Q

Embolism

A

Vessel obstruction by an embolus (bolus of matter circulating in blood stream)

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58
Q

An embolism consists of

A

A dislodged thrombus, aggregating of fat or cancer cells, and foreign substances

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59
Q

Embolus travels in blood stream until it reaches

A

A vessel through which it can’t pass

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60
Q

Embolism causes

A

Ischemia (restricted blood supply)
-continual obstruction can cause infarction (ischmeia resulting in necrosis)

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61
Q

Thromboangiitis obliterans (buergers disease)

A

Inflammation of peripheral artery
-strongly associated with smoking
-autoimmune disease

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62
Q

How is Thromboangiitis obliterans (buergers disease), an autoimmune disease

A

Thrombus is filled with immune cells, causing an occlusion of smaller arteries

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63
Q

S/s of Thromboangiitis obliterans (buergers disease)

A

Symptoms: pain and tenderness in affected area

Signs: reddish skin, thickened and malformed nails

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64
Q

TX for Thromboangiitis obliterans (buergers disease)

A

Stopping smoking
-if you don’t stop amputation is likely required

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65
Q

Atherosclerosis

A

Formation of fatty plague with a core rich in lipid

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66
Q

What is the leading cause of CAD

A

Atherosclerosis

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67
Q

Atherosclerosis is caused by

A

Smoking, hypertension, diabetes, inc LDL, dec HDL, autoimmune

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68
Q

Pathophysiology of Atherosclerosis

A

Begins with injury to epithelial cells lining artery wall
-injured cells become inflamed
-inflamed cells express adhesions molecules that bind macrophages
-bound macrophages releases cytokines damaging vessel wall
-cause free radicals to oxidize LDL
-macrophages engulf oxidized LDL
-macrophages are now considered foam cell
-foam cells accumulatte and form fatty streak
-fatty streak results in recruitment of T cells
-macrophages release growth factors producing collagen
-collagen accumulates over fatty streak forming a fibrous plague
-fibrous plague protrudes into lumen and obstructs blood flow
-this fibrous plague may rupture (complicated plagues)
-producing rapid thrombus formation
-ishcemia or infarction

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69
Q

How does Atherosclerosis being?

A

Injury to epithelial cell lining artery wall

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70
Q

Inflammation caused free radicals to do what?

A

Oxidize LDL

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71
Q

Foam cell

A

Macrophages that have engulfed oxidized LDL
-form fatty streak

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72
Q

Fatty streak results in

A

Recruitment of T cells
-more damaged to vessel wall

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73
Q

Fibrous plague

A

Collagen accumulation from growth factors
-obstructs and occludes blood flow

74
Q

Complicated plagues

A

Fibrous plagues that have ruptures
-rapid thrombus formation

75
Q

Coronary heart disease is usually caused by

A

Atherosclerosis
-plague build up diminishing blood supply to cardiac muscle cells

76
Q

Results of Coronary heart disease

A

Myocardial ischemia and infarction deprives heart muscle of blood borne oxygen and nutrients
-impairs heart pumping ability

77
Q

Myocardial cells remain ___ but are not

A

Alive, not functioning properly

78
Q

Persistent ischemia caused

A

Acute coronary syndromes
-including myocardial infarction

79
Q

Infarction potentially triggers a

A

Heart attack

80
Q

Cardiac infarction

A

Obstruction of blood supply causing irreversible myocardial damage

81
Q

Dyslipidemia has a link between

A

Abnormal lipoprotein levels and CAD

82
Q

Lipoproteins

A

High density lipoproteins (HDL) and low density lipoproteins (LDL)

83
Q

What is responsible for delivery of cholesterol to tissues?

84
Q

What is responsible for delivery of excess cholesterol back to liver?

85
Q

LDL

A

High intake of cholesterol and saturated fats will elevate levels
-can cause LDL migration into vessel walls = atherosclerosis

86
Q

HDL

A

Plays a role in endothelial repair and decreases thrombosis
-elevated levels of HDL has not proven to prevent CV disease

87
Q

What is responsible for 2-3 fold inc in CAD risk

A

Hypertension

88
Q

Hypertension causes

A

Endothelial injury, myocardial hypertrophy which inc heart oxygen demand

89
Q

Why is cigarette smoking a risk for CAD

A

-free radical generation
-nicotine simulates catecholamines and inc HR, BP and vasoconstriction
-inc LDL, Dec HDL

90
Q

Why is obesity a risk for CAD

A

Abdominal obesity
-inflammation and Dec HDL
-strongest risk of CAD

91
Q

Why is sedentary lifestyle a risk for CAD

A

Not only inc risk of obesity but on its own inc risk of CAD

92
Q

Why is a Atherogenic diet a risk for CAD

A

Western style diet
-promotes fatty plagues in arteries

93
Q

Diet most recommended for health

A

Mediterranean diet

94
Q

Hs-CRP test

A

High sensitivity C reactive protein test
-can detect very low levels of C reactive protein
-measures general levels of inflammation in body

95
Q

Elevated serum hs-CRP is correlated to

A

Increased CAD risk

96
Q

CRP

A

Protein synthesized in liver in response to inc in inflammation in body

97
Q

Hs-CRP test is used to determine

A

Heart disease risk and stroke in people without known heart disease

98
Q

Hs-CRP value: <1 mg/L

99
Q

Hs-CRP value: 1-3mg/L

A

Average risk

100
Q

Hs-CRP value: >3 mg/L

101
Q

Adipokines

A

Hormones released from adipose cells, two of which are lepton and adiponectin

102
Q

Obesity =

A

-inc inflammation
-inc leptin
-Dec adiponectin

103
Q

Adiponectin

A

Protects vascular endothelium and is ant-inflammatory

104
Q

Myocardial ischemia develops when

A

Blood borne oxygen is insufficient to meet myocardial metabolic demands

105
Q

Common cause of myocardial ischemia

A

Atherosclerosis in coronary circulation, causing plague rupture = thrombus formation, occlusion and myocardial ischemia

106
Q

Myocardial cells become ischemia within ___ seconds of occlusion

107
Q

Shifts toward anaerobic causes

A

Lactic acid accumulation, decreased rate of ATP re-phosphorylation

108
Q

After several minutes

A

Heart loses ability to contract

109
Q

If perfusion is not restored…

A

Myocardial infarction occurs within 20 minutes

110
Q

Angina

A

Chest pain caused by myocardial ischemia

111
Q

Stable angina pectoris

A

Gradual narrowing and hardening of arterial walls associated with inflammation and decreased endothelial vasodilators

112
Q

Stable angina pectoris: affected vessels

A

Cannot respond to inc myocardial demand during exercise or emotional stress
-causing angina

113
Q

Stable angina pectoris: angina decreases with

A

Rest and nitrates

114
Q

Prinzmetals angina

A

Transient angina that occurs unpredictably and often at rest/sleep

115
Q

Cause of Prinzmetals angina

A

Vasospasm risk of cardiac event

116
Q

Silent ischemia

A

Occurs alone or with angina
-inc risk of cardiac event

117
Q

Abnormal symptoms of Silent ischemia

A

Fatigue, dyspnea (bad breathing)

118
Q

Evaluation for myocardial ischemia

A

Physical examination displays rapid pulse and extra heart sounds

119
Q

Pulmonary congestion indicates impaired

A

Left ventricle function

120
Q

Single photon emission computed tomography (SPECT) is the most

A

Effective tool

121
Q

TX for myocardial ischemia

A

Diet and exercise
-surgery in coronary vessels dilated and placement of coronary stent

122
Q

harbinger

A

Impending infarction
-Announces the coming of something

123
Q

Unstable angina: acute attack signals

A

Atherosclerotic plague has become unstable, and infarction may soon follow

124
Q

Unstable angina: superficial erosion of plague leads to

A

Transient episodes of thrombotic occlusion and vasoconstriction
-occlusions lasts no more than 10-20 minutes

125
Q

Unstable angina: distinct symptom

A

Prinzmetal angina increasing in severity

126
Q

Diagnosis of Unstable angina

A

-ECG during attack = ST depression, T wave inversion, ST segment elevation
-hs-cTnt = high sensitivity cardiac troponin T can identify tiny amounts of enzymes released from damaged myocytes

127
Q

TX for Unstable angina

A

Immediate hospitalization

128
Q

Clinically, MI is categorized as

A

Non-stemi or stemi

129
Q

Unstable angina

A

Coronary thrombosis leads to myocardial ischemia

130
Q

NON STEMI

A

Persistent occlusion leads to infarction of myocardium closest to endocardium

131
Q

STEMI

A

Continued occlusion leads to infarction from endocardium to pericardium

132
Q

Oxygen depletion in 10 seconds then…

A

After 10 seconds affected myocardium becomes cyanotic and cooler

133
Q

Aerobic metabolism stops and

A

ATP generation stops due to anaerobic metabolism
-causes H+ and lactic acid to accumulate
-reduced ATP

134
Q

Electrolyte disturbances

A

Loss of K and calcium from cells
-myocardial cells lose contractiability
-diminished ability of heart to contact

135
Q

Infiltration of immune cells causes

A

Further tissue damage

136
Q

Cardiac cells can withstand ischemia conditions for

A

20 minutes before irreversible damage `

137
Q

Manifestations of myocardial infarction

A

Acute, severe chest pain

138
Q

Diagnosis of myocardial infarction

139
Q

Photo on slide 20

140
Q

Heart failure

A

Inadequate perfusion of tissues or inc diastolic filing pressure of left ventricle
-or both in which pulmonary capillary pressures are increased

141
Q

Special thing to remember about heart failure

A

Left ventricle dysfunction will play back to pulmonary problems

142
Q

Heart failure affects ___ of individuals older than 65 yoa

143
Q

Most common reason for hospital admission in >65 YOA

A

Heart failure

144
Q

Most HF causes are due to

A

Dysfunction of left ventricle

145
Q

Left ventricular failure with reduced ejection factor

A

Left ventricle election fraction less than 40% normal which results in inability of heart to perfuse tissue

146
Q

CO =

147
Q

Determinants of SV

A

Contractility, preload, afterload

148
Q

Ventricular remodeling

A

Disruption of normal myocardial function

149
Q

Ventricular remodeling results in

A

Dilation of left ventricle

150
Q

Cause of ventricular remodeling

A

Progressive myocyte contractile dysfunction

151
Q

Result of myocyte contractile dysfunction

A

Reduced stroke volume
-left ventricle end diastolic volume increases

152
Q

Main causes of myocardial dysfunction

A
  1. Myocardial infarction
  2. Ischemic heart diseases
  3. Hypertension
153
Q

Decreased cardiac output and decreased systemic blood pressure =

A

Reduced perfusion of tissues

154
Q

Results of reduced perfusion of tissues

A

Increased sympathetic activit
Causing:
-inc secretion of catecholamines
-inc vasoconstriction

155
Q

Decreased perfusion of kidneys results in

A

RAAS activation and increased vasoconstriction and blood volume

156
Q

Overall result of Left ventricular failure with reduced ejection factor

A

-inc cardiac afterload
-inc bp
-inc hr
-ventricular remodeling

157
Q

Ventricular remodeling causes

A

Progressive myocyte remodeling over time
-dysfunction

158
Q

Decreased myocyte function =

A

Decreased contractility which results in increased preload

159
Q

Effects of increased preload

A

-stretching of myocardium and sarcomere dysfunction
-further dysfunction in myocardial function

160
Q

Effects of increased afterload

A

results of systemic hypertension
-vasoconstriction and inc blood volume

161
Q

___% of HF cases have previous hypertension

162
Q

Increased afterload =

A

Myocardial hypertrophy
-myocardial remodeling

163
Q

Hypertrophy =

A

Inc myocardial oxygen demand

164
Q

Changes are referred to as

A

Hypertensive hypertrophic cardiomyopathy

165
Q

Hypertrophic/hypertrophy

A

Increase in size of cells

166
Q

As CO decreases

A

Renal perfusion is reduced

167
Q

Results of renal perfusion

A

Further activation of RAAS pathway = continual increases in vasoconstriction and blood volume

168
Q

Baroreceptors continue to detect

A

Decreased blood pressure which results in increased catecholamines release and inc vasoconstriction

169
Q

Both activation of RAAS and Baroreceptors result in

A

Continued inc in both preload and afterload

170
Q

Pharmacology

A

Inhibition of various aspects of RAAS and SNS

171
Q

Left ventricular failure with preserved ejection factor

A

Defunded as pulmonary congestion despite normal stroke volume and cardiac output

172
Q

Left ventricular failure with preserved ejection factor prevalence in population between

173
Q

Cause of Left ventricular failure with preserved ejection factor

A

Abnormal diastolic relaxation such that a normal left ventricle volume results in an inc left ventricle end diastolic pressure

174
Q

Normal amount of blood returning to the heart results in

A

An increased ventricle pressure

175
Q

This pressure is reflected back into pulmonary circulation and results in

A

Pulmonary edema and right ventricular hypertrophy

176
Q

Diagnosis of Left ventricular failure with preserved ejection factor

A

-dyspnea on exertion
-fatigue
-evidence of pulmonary edema

177
Q

Right ventricular failure

A

Inability of right ventricle to provide adequate blood flow into pulmonary circulation at a normal venous pressure

178
Q

Cause of Right ventricular failure

A

Left ventricle failure = pressure reflected back into pulmonary system = pressure further reflected back into right ventricle

179
Q

Right ventricle is poorly prepared for inc afterload and will

A

Dilate and fail

180
Q

Result of Right ventricular failure

A

Systemic hypertension = peripheral edema

181
Q

Right ventricular failure is referred to as

A

Cor pulmonale

182
Q

Vide on slide 35

Pathophysiology (20 decks)

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