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Patho > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

what is the goal of the circulatory system

A

-transport oxygen and nutrients

-removal of metabolic waste products within the body

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2
Q

right ventricle pumps blood to the

A

lungs

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3
Q

O2 intake and release of CO2 occurs in the

A

pulmonary vasculature

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4
Q

left ventricle pumps oxygenated blood

A

systemically

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5
Q

nutrients are absorbed into the blood as it moves through the

A

GI tract

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6
Q

wastes are carried to the kindeys/lungs/liver for

A

elimination

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7
Q

systemic circuit

A

-right ventricle from heart to lungs

-through pulmonic circulation

-now oxygenated from lungs to heart through left atrium

-through left ventricle

-from heart to body tissues and systemic circulation

-from body tissues to heart through right atrium

-and in the right ventricle again

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8
Q

aorta, arteries and arterioles principle tissue is

A

smooth muscle

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9
Q

capillaries are made of

A

single layer of endothelial cells

-exchange fluid to interstitial space

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10
Q

role of the lymphatic system

A

reabsorbs fluid that leaks out of vascular network and returns to general circulation

-vessels are deep in connective tissue

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11
Q

arteries three layer structure

A

-tunica intima

-tunica media

-tunica adventitia (externa)

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12
Q

tunica intima layer of artery function and structure

A

-endothelial cells (living and active)

-direct contact with blood

-smooth, no blockages

-helps with clotting and collateral circulation

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13
Q

tunica media layer of artery structure and function

A

-smooth muscle and elastin

-constricts and dilates

-sensitive stimulation from ANS

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14
Q

tunica adventitia (externa) layer of artery structure and function

A

-supportive connective tissue

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15
Q

calcium channel blockers (CCB) block

A

vasoconstriction and treat hypertension

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16
Q

endothelium

A

innermost lining of blood vessels and arteries

-inside tunica intima

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17
Q

people with dysfunctional endothelium have what 4 diseases and what activity that can lead to dysfunctional endothelium

A

-coronary artery disease

-diabetes

-hypertension

-hypercholesterolemia

-smokers

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18
Q

lipid effect of blood composition on arteries and endothelium

A

-cholesterol (lipid not dissolved) and triglycerides (excess calories) carried by lipoproteins

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19
Q

low density (LDL) effect on arteries

A

bad!

-deposited on artery walls

-areas of endothelial injury

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20
Q

high density (HDL) effects on arteries

A

good!

-gathers excess LDL and takes to liver to get rid

-excreted from the body

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21
Q

glucose effect of blood composition on arteries and endothelium and what can these effects lead to

A

-harms endothelial lining leading to plaque formation (atherosclerosis)

-vasoconstricts (MI and strokes)

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22
Q

nicotine effect of blood composition on arteries and endothelium

A

-vasoconstrictor

-sympathetic nervous system

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23
Q

hyperlipidemia etiology and what can it lead to

A

elevated levels of lipids: cholesterol (LDL and HDL) and triglycerides

-leads to atherosclerosis!

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24
Q

what are some saturated fats that negatively contribute to hyperlipidemia

A

solid forms of animal fat: meat, eggs, cheese, butter, dairy products

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25
Q

name some unsaturated fats that can help with hyperlipidemia

A

liquid forms of fat: olive oil, peanut oil, canola oil, sesame and corn safflower oils, fish oil, margarine

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26
Q

List 7 hyperlipidemia risk factors

A

-family history

-smoking increases LDL and decreases HDL

-diabetes

-hypothyroidism

-dietary excess of calories, saturated fats, trans fats and cholesterol

-low physical activity

-obesity

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27
Q

list 6 effects of smoking on the body

A

-injures endothelium

-increased risk for thrombus formation

-vasospasm

-increased platelet aggregation (clots)

-increases HR, BP, O2 demand

-increased risk for coronary heart disease

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28
Q

why can hyperlipidemia be hard to catch and list 3 clinical manifestations

A

-silent disorder

-Xanthoma and Xanthelasma (big dots on eyes, slide 16)

-arcus senilis (yellow circle in eyes)

-metabolic syndrome

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29
Q

how do we diagnose hyperlipidemia

A

-history

-physical examination

-blood samples of lipoproteins, cholesterol, triglycerides

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30
Q

total cholesterol normal value

A

less than 200 mg/dL!

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31
Q

LDL cholesterol normal value

A

less than 100 mg/dL!

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32
Q

HDL cholesterol normal value

A

above 60 mg/dL is cardioprotective!

-less than 40 is major risk for heart disease !

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33
Q

triglycerides normal value

A

less than 150 mg/dL!

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34
Q

list 6 treatments for hyperlipidemia

A

-lifestyle changes

-drugs reducing triglycerides and cholesterol (fish oils, fibrates, statins)

-balloon or laser angioplasty

-stent

-CABG: coronary artery bypass graft

-peripheral arterial bypass

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35
Q

arterial blood pressure is produced by the force of

A

left ventricular contraction overcoming the resistance of the aorta to open the aortic valve

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36
Q

stroke volume

A

volume of blood leaving the heart with each contraction

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37
Q

peripheral vascular resistance (PVR)

A

-resistance to ejection

-degree of vessel compliance

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38
Q

vasoconstriction does what to peripheral vascular resistance

A

increases PVR

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39
Q

too much peripheral vascular resistance causes

A

pathological cardiac hypertrophy which is not good

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40
Q

what is the formula for cardiac output (CO)

A

stroke volume (volume of blood leaving heart with each contraction) x heart rate

-blood flow in arterial system

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41
Q

normal cardiac output

A

5 L/min

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42
Q

stroke volume and heart rate have an opposing relationship in the context of homeostasis meaning

A

-decreased stroke volume, increased heart rate

-increased stroke volume, decreased heart rate

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43
Q

formula for blood pressure

A

cardiac output x peripheral vascular resistance

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44
Q

how to determine MAP for blood pressures

A

systolic blood pressure + (2x diastolic blood pressure) divided by 3

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45
Q

What does systolic blood pressure represent and what is the normal value

A

cardiac contraction

-blood ejected from chamber

-lower than 120 mmHg

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46
Q

What does the diastolic blood pressure represent

A

cardiac relaxation

-end of contraction- filling

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47
Q

What is a normal left ventricle stroke volume

A

70 mL

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48
Q

difference between systolic and diastolic BP is called

A

pulse pressure

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49
Q

what is orthostatic hypotension and how do we quantify it

A

decreased BP when position is changed quickly to upright

-drop in SBP greater than or equal to 20

-drop in DBP greater than or equal to 10

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50
Q

List 6 causes of orthostatic hypotension

A

-reduced blood volume

-vasovagal response

-drug induced

-aging

-prolonged bed rest

-ANS disorders

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51
Q

List 4 clinical manifestations of orthostatic hypotension

A

-dizziness

-blurred vision

-fainting (syncope)

-injury from falls

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52
Q

orthostatic hypotension treatment

A

-move slowly

-avoid excessive vasodilation

-TED hose

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53
Q

renin angiotensin aldosterone system (RAAS) with BP regulation

A

-made and controlled in kidneys

-release stimulated by decrease in BP or volume

-end result of system is increased BP!

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54
Q

renin forms

A

angiotensin I

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55
Q

angiotensin converting enzyme (ACE) causes

A

angiotensin I conversion to angiotensin II in the lungs

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56
Q

angiotensin II is

A

potent vasoconstrictor and stimulated release of aldosterone

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57
Q

aldosterone increases

A

Na reabsorption in the kidneys and increased H2O

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58
Q

release of renin occurs when theres

A

excess sympathetic stimulation, decreased BP, decreased extracellular volume

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59
Q

ACE inhibitor

A

-pril

stop angiotensin I from turning into angiotensin II

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60
Q

how does antidiuretic hormone (ADH) relate to BP regulation

A

acts on nephron to increase water reabsorption

-increasing blood volume and BP

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61
Q

fluid volume with BP regulation

A

-increased ECF increases CO

-increased CO and increased volume increased PVR

-increased PVR increases BP

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62
Q

normal blood pressure for adults

A

-less than 120 mm Hg systolic

-less than 80 mmHg diastolic

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63
Q

hypertension diagnosis

A

-systolic BP > 130

-diastolic BP > 80

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64
Q

primary hypertension

A

-risk factors

-no known cause

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65
Q

secondary hypertension

A

clearly a side effect of another systemic disorder (a disease)

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66
Q

compare non modifiable to modifiable risk factors for primary hypertension

A

-non modifiable: increasing age, family history, african american, diabetes

-modifiable: obesity, dietary factors, tobacco, alchohol

67
Q

List 6 causes of secondary hypertension

A

-pregnancy

-renal causes

-cardiovascular

-endocrine

-drugs

-neurologic

68
Q

hypertension pathophysiology

A

high resistance against left ventricle

-damages endothelial artery lining

-susceptible to ischemia, infarction and HF

69
Q

hypertension clinical manifestations

A

-“silent”

-displaced apical pulse

-aortic bruits

-lower extremity pulses, color, temp and sensation

70
Q

hypertension measurement

A

-direct: arterial line

-indirect: mercury sphygmomanometer!

71
Q

primary hypertension treatment

A

angiotensin converting enzyme inhibitor (ACEI)

-angiotensin receptor blocker (ARB)

-calcium channel blockers

-diuretics

72
Q

primary hypertension lifestyle alterations

A

DASH diet

-low sodium and low fat food

73
Q

primary hypertension stress reduction and physical activity

A

-yoga

-exercise 30 mins a day

74
Q

primary hypertension smoking cessation

A

-nicotine raises BP

-increases resistance to flow

-free radicals

75
Q

secondary hypertension damage to heart and arteries

A

-coarctation of arteries

-vasculitis

76
Q

secondary hypertension damage to kidneys

A

-chronic kidney disease

-urinary tract obstruction

77
Q

secondary hypertension damage to brain

A

-brain tumor

-intracranial hypertension

78
Q

secondary hypertension damage to eyes

A

hypertensive retinopathy

79
Q

hypertensive emergency

A

-diastolic greater than 120

-hospitalization

-sustained organ damage

80
Q

hypertensive urgency

A

-diastolic greater than 120

-treated slower with oral medications

81
Q

atherosclerosis non modifiable risk factors

A

-more males than females

-more african americans than caucasian americans

82
Q

list 5 atherosclerosis modifiable risk factors

A

-excess saturated fat, cholesterol and salt

-obesity

-tobacco, alcohol and high stress

-hypertension

-diabetes mellitus

83
Q

atherosclerosis etiology

A

-injury to endothelial lining

-hyperlipidemia is condition that causes atherosclerosis

84
Q

atherosclerosis pathophysiology

A

-damage to endothelium with inflammation and increase vessel permeability

-thickening and luminal narrowing

-plaques develop and can rupture

85
Q

atherosclerosis clinical manifestations

A

-gradual process with no symptoms till organ dysfunction

-on exam hear bruits

86
Q

what 4 ways can we get an atherosclerosis diagnosis

A

-lipid profile

-inflammation causes elevated C-reactive protein

-cardiac cath

-CT scan

87
Q

atherosclerosis treatment

A

-lifestyle changes (same as hyperlipidemia)

-drugs reducing triglycerides and cholesterol (same as hyperlipidemia)

-surgical options

-angioplasty

88
Q

peripheral arterial disease (PAD) etiology

A

atherosclerosis involving peripheral vascular system

-disease of superficial vessels, usually legs-femoral artery

89
Q

peripheral arterial disease (PAD) pathophysiology

A

-reduced arterial flow

-develops gradual over time

-leads to ischemia

90
Q

List 7 peripheral arterial disease (PAD) clinical manifestations

A

-dependent rubor!

-elevated pallor!

-cool

-dry, thin, glossy legs

-diminished or absent pulses

-arterial ulcer

-intermittent claudication!

91
Q

peripheral arterial disease (PAD) diagnosis

A

ankle brachial index less than 1

92
Q

what is a peripheral arterial disease (PAD) ulcer

A

-painful

-pale, grey

-well defined edges

93
Q

peripheral arterial disease (PAD) treatment

A

-prevention: exercise, weight control, control blood sugar

-thrombolytic agents

-bypass grafts and stents in legs

94
Q

aneurysm etiology/pathophysiology

A

atherosclerosis/hypertension damages arterial lining

-arterial wall deteriorates till it bulges out and wall weakens collecting blood

95
Q

aneurysm risk factors

A

atherosclerosis, hypertension, smoking

96
Q

aneurysm clinical manifestations

A

-abdominal: flank or back pain, N&V, dont palpate pulsations

-cerebral: silent, “worst headache of my life”

-may hear bruit

97
Q

aneurysm diagnosis

A

-usually silent till rupture

-ultrasound

-contrast CT

-MRI

98
Q

aneurysm treatment

A

-AAA: assess progression and potential for rupture

-surgery if >4.5cm

-endovascular repair surgery

99
Q

what is an aortic dissection and what causes it

A

arterial layer tear in lining between tunica media and intima

-caused by genetics, hypertension, atherosclerosis

100
Q

list 4 aortic dissection clinical manifestations

A

-sudden

-pain in chest or back

-ripping or tearing sound

-hypertension difference between arms maybe

101
Q

raynauds disease etiology

A

vasospasm from vasoconstriction of the arterioles in the digits

102
Q

raynauds disease risk factors

A

-most common in women

-precipitated by cold or emotional stress!

103
Q

list 4 raynauds disease clinical manifestations

A

-pain

-color change pattern: white to blue to red!

-throbbing

-paresthesia

104
Q

what are 3 treatments for raynaud’s disease

A

-calcium channel blockers vasodilate

-protect from cold

-decrease stress and no smoking

105
Q

Buerger disease pathophysiology

A

rare inflammatory condition causing thrombus formation affecting small and medium sized arteries and veins

106
Q

Buerger disease risk factor

A

smoking!

107
Q

what is the function of the heard in the cardiovascular system

A

produces driving force propelling blood through vessels of circulatory system

108
Q

heart circulation

A

health assessment quizlet!

109
Q

acute coronary syndrome

A

-myocardial infarction

-unstable angina

110
Q

myocardial infarction

A

-plaque rupture and thrombus formation

-complete occlusion! resulting in necrosis

-with or without ST segment elevation

111
Q

what is unstable angina

A

-plaque rupture and thrombus formation

-partial occlusion or clot resolution!

-no ST segment elevation

112
Q

what is stable angina and what causes it

A

predictable and consistent pain that occurs on exertion and is relieved by rest and/or nitroglycerin

-from narrowing and stiffening of coronary vessels!

113
Q

cause for alarm with stable angina

A

patient takes 3 nitroglycerin tablets within a 10 min period without chest pain relief: assume MI!

114
Q

what is prinxmetals (variant) angina and what does it respond to

A

coronary vasospasms

-unrelated to increased O2 demand

-unpredictable and responds to calcium channel blockers

115
Q

unstable angina (acute coronary syndrome) etiology

A

emergency

-myocardial ischemia!

-heart muscle needs more circulation to supply cells with oxygen

116
Q

unstable angina (acute coronary syndrome) pathophysiology

A

-atherosclerosis

-thrombus

-50-70% blockage

-anemia

117
Q

unstable angina (acute coronary syndrome) clinical presentation

A

-sudden pain!

-pressure, choking, squeezing

-pain may radiate to epigastric region, jaw, neck, arm

118
Q

unstable angina (acute coronary syndrome) diagnosis

A

-BP

-lipid profile

-thallium stress test specific for angina

-similar findings to pt with artherosclerosis

119
Q

unstable angina (acute coronary syndrome) treatment

A

-prevent MI!

-oxygen

-nitrates (vasodilator), be careful with viagra because also a vasodilator

120
Q

acute myocardial infarction (MI) etiology

A

prolonged or total disruption of blood flow to myocardium

-important factors: location occlusion, length of time, collateral circulation

-ATP depletion

121
Q

what changes after MI

A

-area becomes pale

-necrotic tissue leaves weak area susceptible to rupture!

122
Q

myocardial infarction clinical manifestations

A

-severe crushing, excruciating chest pain

-may radiate to jaw, shoulder or back

-lasts more than 25 mins

-not relieved by NTG or rest

-some may be silent MIs

123
Q

big 3 diagnostic tools for MI:

A
  1. signs and symptoms
  2. electrocardiographic changes
  3. serum biomarkers
124
Q

electrocardiographic changes in diagnosing MI

A

-ST elevation indicated ongoing hypoxia, cellular injury, ischemia (STEMI)

-no ST elevation, may have depressed ST or T wave changes (NSTEMI) better outcomes

125
Q

serum biomarkers in diagnosing MI

A

-marker of choice to detect MI: elevated cardiac troponin 1 (cTnI)!

-elevated CPK-MB

126
Q

myocardial infarction treatment

A

-reestablish blood flow and minimize damage

-reduce O2 demand and increase O2 supply

-MONA

-cardiac rehab

127
Q

list 4 myocardial infarction complications

A

-dysrhythmias

-HF

-cardiogenic shock

-death, most occur before individual reaches hospital

128
Q

acute coronary syndrome workup for STEMI

A

-ST elevation

-abnormal labs with biomarkers

129
Q

acute coronary syndrome workup for NSTEMI

A

-no St elevation

-abnormal labs with biomarkers

130
Q

acute coronary syndrome workup for unstable angina

A

-no ST elevation

-normal labs with biomarkers

131
Q

what is endocardium

A

layer of endothelial cells that lines chambers of heart

132
Q

infective endocarditis etiology

A

infection of endocardial structures by microorganisms which causes inflammation

-vegetations: large, bulky bacteria deposits on heart valves interfering function!

133
Q

infective endocarditis clinical presentation

A

-non specific: low grade fever

-specific: petechiae!, splinter hemorrhages!, oslers nodes!, janeway lesions!, roth spots! (pictures on slide 99)

134
Q

infective endocarditis diagnosis

A

-positive blood cultures

-echocardiogram

-murmur

-predisposing condition

135
Q

infective endocarditis treatment

A

-6 weeks or more IV antibiotics

-surgery

-prophylactic antibiotics to prevent recurrence

136
Q

myocarditis etiology

A

-inflammation and necrosis of cardiac muscle cells

-viral infections most common cause

137
Q

myocarditis pathophysiology

A

-immune attack of the myocardium esp. the left ventricular wall

-muscles become flabby with necrotic tissue

-dilation of all 4 heart chambers

138
Q

dilated cardiomyopathy

A

-enlargement of one or both ventricular chambers

-reduces contractility/EF

139
Q

hypertrophic cardiomyopathy

A

-affects LV and septum

-exercise may cause obstruction of ventricular outflow and decreased CO

-risk of sudden cardiac death

140
Q

restrictive cardiomyopathy

A

-stiff, fibrotic LV that resists filling

-decreased CO

-left side heart failure

141
Q

pericarditis etiology

A

inflammation of pericardium resulting in fluid accumulation in pericardial sac

-thought to be viral cause

142
Q

pericarditis clinical presentation

A

-systemic inflammatory response: fever, leukocytosis, tachycardia

-pericardial effusion

-friction rub: sticking/rubbing pain radiating back and forth like sandpaper!

143
Q

compare normal pericardial space to cardiac tamponade in pericardial effusion

A

-normal pericardial space: 30-50mL

-cardiac tamponade: death 200mL or greater

144
Q

Pericarditis treatment

A

-antibiotics

-aspirin

-NSAIDS

-steroids

145
Q

Beck’s triad with cardiac tamponade

A

from shock, need to get fluid off

-hypotension

-distended neck veins

-muffled heart sounds

-pulsus paradoxus: BP changes with RR

146
Q

compare veins to arteries

A

carry blood to the heart

-have valves

-3 layers same as arteries

147
Q

deep vein thrombus (DVT) etiology

A

virchows triad: venous stasis, vascular damage, hypercoagulability

148
Q

deep vein thrombus (DVT) pathophysiology

A

-thrombus

-inflammation

-thrombus moves to lungs and causes pulmonary embolism

149
Q

deep vein thrombus (DVT) clinical presentation

A

-condition causing problem

-redness

-ropiness

-tenderness

-warmth over vein

-Homans sign

150
Q

deep vein thrombus (DVT) diagnosis

A

-clinical exam

-d dimer test: blood draw shows if clots are being broken down

151
Q

deep vein thrombus (DVT) treatment

A

-prevention :antiembolism stockings, elevate, ambulation

-heparin, warfarin, factor Xa inhibitors

-greenfield filter

152
Q

what are 5 indications of an arterial thrombus

A

-intermittent claudication

-cool to touch

-cyanotic

-arterial ulcer

-weak pulses

153
Q

venous thrombus

A

-calf or groin tenderness

-swelling

-increased skin temp

154
Q

chronic venous insufficiency etiology

A

valvular incompetence allowing back flow involving deep veins

-trauma, central obesity, pregnancy, prolonged standing

-pooling and stasis

155
Q

chronic venous insufficiency clinical presentation

A

-venous stasis ulcers when superficial veins rupture: wet, irregular border!

-thin shiny skin

-dusky discoloration

-stasis dermatitis: blood cells leak out and cause discoloration!

-reduced or absent hair

156
Q

chronic venous insufficiency diagnosis

A

doppler ultrasound, venography

157
Q

chronic venous insufficiency treatment

A

-graduated compression!

-pneumatic compression

-anticoagulants

-thrombolytic agents

-venoablation

158
Q

venous stasis ulcer from chronic venous insufficiency

A

from sluggish circulation and poor tissue oxygenation

-dark red, uneven margin, drainage

-treatment: exercise, compression stockings, topical medications

159
Q

varicose veins etiology

A

high pressure

-prolonged standing

-sitting

-more women

-smoking

160
Q

varicose veins pathophysiology

A

-valvular incompetence

-pressure on valves over time

-gravitational pull

-dont prevent backflow like they should

161
Q

varicose veins clinical presentation

A

-aching, heavy discomfort

-bulging veins

162
Q

varicose veins treatment

A

-elastic stockings

-elevate

-dont cross legs

-exercise

-sclerotherapy, vein stripping, vein ligation

163
Q
A

Patho (10 decks)

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