Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophysiology > Cardiology (Exam 2) > Flashcards

Cardiology (Exam 2) Flashcards

1
Q

Functions of CV System

A

Delivery and removal of substances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Right Heart

A

Pulmonary circulation
Pumps blood through lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Left Heart

A

Systemic circulation
Pumps blood through body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Flow of blood

A

Artery –> arteriole –> capillary –> venule –> vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Major difference between veins and arteries

A

Arteries have much thicker tunica media to tolerate higher forces of pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Hypertension

A

Damages blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hypertension is usually…?

A

Asymptomatic until organ damage occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Systole

A

Heart contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Diastole

A

Heart relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Normal Blood Pressure

A

<120/<80

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Blood pressure

A

Cardiac output x peripheral resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cardiac output

A

Amount of blood the heart pumps per minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Alpha1 Receptors

A

Vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Beta1 Receptors

A

Vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Vasodilator Hormones (3)

A

Prostacylin
Natriuretic peptides
Nitric oxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Vasoconstrictor Hormones (2)

A

Angiotensin II
Vasopressin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Blood Viscosity

A

Increase in RBCs increases viscosity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Blood Volume

A

RAAS activation increases blood volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

ACE

A

Converts angiotensin I to angiotensin II
found in lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ADH

A

Antidiuretic Hormone
Vasopressin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Renin

A

Converts angiotensinogen to angiotensin I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Release of ADH

A

Leads to water reabsorption and increase in blood volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Release of aldosterone

A

Reabsorption of NaCl and water, excretion of K+ –> increased blood volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Renin release is increased by (2)

A

Activation of renal beta1 receptors
Decrease in renal perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Primary Hypertension

A

no single identifiable cause
Genetic or environmental factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Secondary Hypertension

A

Specific medical condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

arteries have

A

low volume and high pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

veins have

A

high volume and low pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

purpose of muscle pumps and valves in veins

A

to keep blood flow in the correct direction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

the most common cardiovascular disease

A

hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

renin release is increased by

A

activation of beta 1 receptors
decrease in renal perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

hypertension is associated with

A

an increased peripheral resistance of the arterial system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

4 factors that may contribute to hypertension

A

over activation of RAAS
over activation of the sympathetic nervous system
vascular endothelial dysfunction
sodium retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

overactivation of the sympathetic nervous system

A

E/NE released from sympathetic neurons and adrenal medulla will activate beta 1 receptors in the heart, kidneys or alpha 1 in the arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

vascular endothelial dysfunction

A

damage to blood vessels and impaired vascular relaxation
biggest factor for HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

sodium retention leads to

A

increased blood volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

organs most effected from hypertension

A

eyes
heart
kidneys
brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

damage of HTN on the brain

A

ischemic or hemorrhagic stoke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

damage of HTN on the kidneys

A

chronic kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

damage of HTN on the heart

A

heart failure, arrhythmia, myocardial infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

damage of HTN on the eyes

A

retinopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

dyslipidemia

A

abnormal blood lipid levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

hyperlipidemia

A

increased blood lipid levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

patients with dyslipidemia are initially

A

asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

dyslipidemia can lead to

A

atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

atherosclerosis

A

disease of arterial system characterized by fatty plaques within vasculature
plaques lead to stenosis then ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is a major contributor to atherosclerosis

A

elevated LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

atherosclerotic cardiovascular disease (ASCVD) includes

A

cerebrovascular disease
peripheral artery disease
coronary artery disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

cerebrovascular disease

A

plaques in cerebral vasculature
can lead to ischemic stroke or transient ischemic attack

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

peripheral artery disease

A

plaques in peripheral arteries (lower limbs) reducing blood flow and oxygen supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

coronary artery disease (ischemic heart disease)

A

plaques in coronary arteries
can lead to myocardial infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

familial hypercholesterolemia

A

most common genetic disorder leading to dyslipidemia
autosomal dominant disorder, mutations of uptake of LDL by the liver, leading to more in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

which form of familial hypercholesterolemia is more severe?

A

homozygous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

lipoproteins

A

lipid protein complexes
made up of triglycerides, cholesterol, phospholipids and proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

lipoproteins are classified by

A

what protein they contain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Apo-B containing lipoprotein

A

chylomicrons
VLDL, IDL, and LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Apo-A1 containing lipoprotein

A

HDL (tissues to liver)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

chylomicrons

A

transports dietary TH and cholesterol from intestines to tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

three cholesterol pathways

A

exogenous
endogenous
reverse

60
Q

exogenous cholesterol pathway

A

cholesterol from the diet is digested and absorbed in GI tract

61
Q

endogenous cholesterol pathway

A

cholesterol synthesized in the liver
LDL transports cholesterol to tissues and excess LDL is taken up by vasculature or returned to liver for reuptake

62
Q

reverse cholesterol pathway

A

removal by HDL and degradation of cholesterol by bile

63
Q

pathophysiology of atherosclerosis

A

in liver cells
cholesterol and triglycerides packaged into VLDL particles –> exported to blood –> converted to IDL–> LDL

64
Q

hypertriglyceridemia

A

dyslipidemia that is caused by a number of drugs or conditions
elevated TG associated with increased CV risk

65
Q

extreme elevations of hypertriglycedemia can lead to

A

acute pancreatitis

66
Q

patho of acute pancreatitis

A

excessive breakdown of TG into free fatty acids –> toxicity and inflammatory response

67
Q

symptoms of acute pancreatitis

A

persistent severe epigastric abdominal pain, nausea, and vomiting

68
Q

symptoms of peripheral artery disease

A

skin loses integrity, pain in the affected area
may be asymptomatic

69
Q

intermittent claudication (PAD)

A

pain caused by ischemia to the limbs
usually during exercise, resolved at rest
pain at rest = severe PAD

70
Q

main symtptom of ischemic heart disease

A

angina (chest pain due to inadequate supply of oxygen)

71
Q

stable ischemic heart disease

A

stable angina
occurs in a predictable manner and lasts a short time
gradual stenosis over time

72
Q

acute coronary syndrome

A

acte obstruction in blood flow to the heart
due to plaque rupture followed by thrombus formation
can lead to heart attack

73
Q

types of acute coronary syndrome

A

unstable angina
non-ST elevation myocardial infarction
ST elevation myocardial infarction

74
Q

infarction

A

death of tissue

75
Q

unstable angina

A

markers not present
ST segment not elevated

76
Q

NSTEMI

A

markers present
ST segment not elevated

77
Q

STEMI

A

markers present
ST segment elevated

78
Q

mos severe acute coronary syndrome

A

STEMI = complete blockage

79
Q

after MI, what forms and what is different about it?

A

scar tissue
can’t contract and relax like healthy tissue

80
Q

2 cardiac markers

A

creatine phosphokinase MB
Troponins (cardiac troponin 1)

81
Q

heart failure

A

cardiomyopathy
heart is unable to pump enough blood to meet the metabolic demands of the body

82
Q

heart failure =

A

a reduction in cardiac output

83
Q

heart failure typically refers to

A

left side heart failure

84
Q

systolic heart failure

A

heart failure with reduced ejection fraction

85
Q

diastolic heart failure

A

heart failure with preserved ejection fraction

86
Q

CV symptoms of heart failure

A

tachycardia
peripheral edema and ascites (swelling in abdomen)

87
Q

pulmonary symptoms of heart failure

A

pulmonary edema (fluid in lungs)
dyspnea (difficulty breathing)
cough

88
Q

other symptoms of heart failure

A

sudden weight gain
fatigue

89
Q

preload

A

pressure within the ventricle or stretching of the myocytes at the end of diastole

90
Q

afterload

A

resistance to ejection of blood from the ventricle

91
Q

contractility

A

force of contraction

92
Q

cardiac output =

A

stroke volume x heart rate

93
Q

heart rate is primarily dependent on the

A

autonomic nervous system

94
Q

preload is dependent on

A

venous return

95
Q

venous return is dependent on

A

fluid volume and venous tone

96
Q

after load is dependent on

A

arterial tone (BV diameter)

97
Q

contractility is dependent on

A

ANS, Ca2+ and preload

98
Q

HFpEF (diastolic HF)

A

heart is unable to fill normally
associated with stiffening myocardium

99
Q

HFrEF (systolic HF)

A

heart is unable to contract normally
associated with dilation of heart chambers (ventricles)

100
Q

what helps us classify heart failure?

A

ejection faction (EF) = stoke volume/ end diastolic volume

101
Q

Hypertension pathophysiology

A

increase in after load –> stress on myocardium -> ventricle walls thicken/dilate –> inefficient pumping

102
Q

ischemic heart diseases pathophysiology

A

reduced blood flow to myocardium over time –> ischemia/angina and weakening of myocardium (thin walls)

103
Q

most common cause of heart failure

A

myocardial infarction

104
Q

conditions that can lead to HF

A

abnormal heart valves or congenital heart defects
cardiotoxic medications (ex: chemotherapies)
other conditions (ex: diabetes)

105
Q

compensatory mechanisms activated to increase cardiac output

A

activation of RAAS
activation of SNS
activation of RAAS and SNS –> cardiac remodeling

106
Q

activation of RAAS

A

increases blood volume –> increases preload –> increases stroke volume

107
Q

problem of activation of RAAS

A

causes edema and increases afterload

108
Q

activation of SNS

A

activation of beta1 on the heart –> increases HR and contractility

109
Q

problem with activation of SNS

A

increases after load and workload of the heart

110
Q

activation of RAAS and SNS –> cardiac remodeling

A

cardiac hypertrophy to increase contractility

111
Q

problem of activation of RAAS and SNS –> cardiac remodeling

A

scarring and tissue damage which impairs cardiac function

112
Q

compensatory mechanisms can help maintain cardiac output initially but

A

overtime lead to worsening of heart failure

113
Q

acute decompensated HF

A

sudden worsening of HF, leads to need for hospitalization

114
Q

ADHF occurs due to

A
  1. excessive fluid overload –> severe dyspnea
  2. excessive reduction in cardiac output –> hypotension
115
Q

patients with ADHF are categorized by

A

tissue perfusion and fluid status

116
Q

tissue perfusion

A

warm = stable
cold = hypoperfusion

117
Q

fluid volume

A

dry = stable
wet = fluid overload

118
Q

fluid status is measured by

A

pulmonary capillary wedge pressure

119
Q

perfusion Status is measured by

A

cardiac index

120
Q

cardiac index

A

cardiac output/ body surface area

121
Q

arrythmia

A

disturbance of electrical signals in the heart leadings to an irregular rate or rhythm

122
Q

arrhythmia can occur due to

A

damage/structural change, electrolyte alteration or drugs that alter cardiac function

123
Q

symptoms of arrhythmia

A

palpitations, lightheadedness, syncope, fatigue, cardiac arrest

124
Q

arrhythmias range from

A

asymptomatic to life-threatening

125
Q

arrhythmias can be classified by

A

where they originate, how they affect heart rate and type of impulse abnormaility

126
Q

cardiac conduction system

A

pacemaker cells generate action potential without input from the nervous system

127
Q

sinoatrial node

A

primary pacemaker of the heart

128
Q

atrioventricular node

A

spontaneously generates 40-60 action potentials per minute

129
Q

If SA node fails,

A

AV node can take over

130
Q

heart block

A

failure in the normal propagation of action potentials from atrium to ventricle

131
Q

heart block results in

A

bradycardia or skipped beats

132
Q

reentry (accessory pathway)

A

impulse reenters and excites areas of the heart more than once due to dysfunction of the refractory period

133
Q

atrial fibrillation

A

most common type of arrhythmia
unpredictable

134
Q

complications of chronic A-fib

A

stoke and heart failure

135
Q

ventricular fibrillation

A

electrical signals fire from multiple locations in the ventricular leading to inability of the ventricles to pump properly

136
Q

ventricular fibrillation is

A

life threatening and a form of cardiac arrest

137
Q

shock

A

CV system fails to refuse the tissues adequately resulting in widespread impairment of cellular metabolism

138
Q

shock leads to

A

organ failure and death

139
Q

types of shock

A

hypovolemic shock
cariogenic shock
distributive shock

140
Q

hypovolemic shock

A

low fluid volume

141
Q

cardiogenic shock

A

damage or dysfunction of the heart
unable to pump blood forward

142
Q

distributive shock

A

leaky blood vessels and excessive vasodilation

143
Q

examples of distributive shock

A

septic shock, anaphylactic shock and neurogenic shock

144
Q

pathophysiology of arryhthmias

A

due to damage or structural change in cardiac tissue, electrolyte alteration or drugs that alter cardiac function

145
Q

most arrhythmias are

A

tachyarrythmias

146
Q

if another tissue spontaneously depolarizes more frequently than the SA node,

A

it controls heart rate and rhythm

147
Q

atypical automaticity (ectopic pacemaker)

A

group of cardiac cells that gain automaticity and begin spontaneously depolarizing

Pathophysiology (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions