Brainscape's Knowledge GenomeTM

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


See full index

Bio 252 > cardiovascular disorders > Flashcards

cardiovascular disorders Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

hyperlipidemia

A

elevated lipid content in the blood

cholesterol, triglycerides, phospholipids

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

what is a apoprotein

A

a protein that transports lipids

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

what is a lipoprotein

A

a apoprotein + a lipid

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

lipoproteins are named based on

A

density

low density lipid, high density lipid

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

what is a chylomicron

A

lipoproteins that transfer lipids from the digestive tract into circulation

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

where does atherosclerosis usually occur

highest frequency sites

A

in the larger arteries

  • abdominal aorta
  • coronary arteries + carotid arteries
  • thoracic aorta, femoral + popliteal arteries
  • vertebral, basilar, cerebral arteries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is an atheroma

A

a lesion in the intima of the vessel made of lipids and fibrous tissue

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

what happens as an atheroma forms

A

the atheroma bulges into the lumen (area of least resistance because it is fluid filled)
obstructs the lumen

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

what is the progression of an atheroma lesion

A
  1. fatty streak
  2. fibrous atheromatous plaque
  3. complicated lesion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is a fatty streak made of

A

cells

macrophages, foam cells, smooth muscle cells

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

what is fibrous atheromatous plaque

A

a lesion made of swelling comprised of fibers

accumulation of lipids, scar tissue, calcification

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

what is a complicated lesion

A

hemorrhaging into the plaque

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

pathogenesis of atherosclerosis stages

A
  • endothelial cell injury (subtle changes - inflm)
  • migration of monocytes (monocytes bind/migrate into intima - become macrophages)
  • lipid accumulation + s.m. cell proliferation (clot + bulge forms in lumen)
  • plaque (atheroma forms = atherosclerotic plaque)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

an elevated CRP without underlying inflm indicates

A

atherosclerosis

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

4 control mechanisms of BP

A
  • baroreceptors (detect pressure change)
  • volume regulation (via kidneys)
  • vascular autoregulation (vasoconstriction/dilation)
  • RAAS (ADH, aldosterone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

HTN follows what cycle

A

circadian rhythm

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

when is BP lowest and highest

A 
lowest = 2-5am
highest = first thing in the morning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

primary HTN

A
  • 90% cases
  • idiopathic - can’t eradicate, just manage
  • multifactorial (problem w/ several regulatory mechanisms)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

systolic HTN

A
  • systolic > 140, diastolic < 90
  • mostly after age 50
  • poor vessel compliance - decreased elasticity - increased systolic pressure
  • could be d/t atherosclerosis
  • heart will compensate (harder+faster) - causes increased CO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

secondary HTN

A
  • 5-10%
  • renovascular = arteries supplying kidneys occluded
  • poor renal perfusion activates RAAS, increases BP systemically
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

malignant HTN

A
  • diastolic > 120

- emergency situation

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

manifestations of HTN

A
  • BP may be high unknowingly
  • AM headaches
  • palpitations
  • dizziness, fatigue, blurred vision
  • organ failure (kidney, heart, brain)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

treatment of HTN

A
  1. Lifestyle modification
    - DASH diet
    - smoking and alcohol cessation
    - exercise
  2. 1st line drug = diuretic
  3. 2nd line drug = add 1/more
    - Ca channel blocker (decrease s.m. contraction)
    - angiotensin II receptor blocker
    - ACE inhibitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the types of peripheral vascular disease

A
  • acute arterial occlusion

- atherosclerotic occlusive disease

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

what is an acute arterial occlusion caused by

A

an embolus or thrombus that disrupts perfusion

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

what is an embolus

A

something that lodges in a vessel (air, clot, malignant cells)

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

what is a thrombus

A

a stationary blood clot

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

manifestations of acute arterial occlusion

A
  • pain
  • pallor
  • pistol
  • pulselessness
  • polar
  • paresthesia
  • paralysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

diagnosis of acute arterial occlusion

A
  • blood flow assessment

- physical exam

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

treatment of acute arterial occlusion

A
  • surgery (remove clot)
  • thrombolytics (dissolve clot)
  • anticoagulants (prevention)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

atherosclerotic occlusive disease

A
  • same process as atherosclerosis but occurs mostly in peripheral vessels (femoral + popliteal arteries)
  • common in diabetics and elderly
  • perfusion is impaired d/t occlusion
  • causes inadequate venous return… complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

why does diabetes cause atherosclerotic occlusive disease

A

diabetes causes vascular damage - causes atherosclerosis

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

how does the body compensate for atherosclerotic occlusive disease

A
  • vasodilation
  • anaerobic metabolism (d/t hypoxic tissue)
  • collateralization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

manifestations of atherosclerotic occlusive disease

A
  • intermittent claudication

- complications (ulcers, loss of fx)

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

diagnosis of atherosclerotic occlusive disease

A
  • blood flow assessment

- physical exam

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

treatment of atherosclerotic occlusive disease

A
  • no clot present - must address manifestations

know complications, prevent, treat

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

what is an aneurysm

A

a localized bulge in an artery d/t degenerative change in the vessel wall
(permanent change)

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

most common arteries for aneurysms

A

femoral, iliac, popliteal arteries

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

highest pressure vessels, likely for aneurysms

A

thoracic, abdominal aorta

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

risks for aneurysm

A
  • atherosclerosis
  • uncontrolled HTN
  • congenital defects (weakened vessel walls)
  • aging
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is a true aneurysm

A

vessel wall is intact

50% increase in vessel diameter

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

what is a false aneurysm

A

vessel wall is compromised

supported by external structures

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

what are the types of aneurysms

A

true

false

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

what are the forms of aneurysms

A

fusiform (bilateral)
saccular (unilateral)
dissecting (in vessel walls)

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

a berry aneurysm is what form of aneurysm

A

saccular

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

complications of aneurysms

A
  • rupture (brain=stroke, aorta=death)
  • pressure on adjacent structures
  • distal embolization (pooling=thrombus -> dislodges)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

treatment of aneurysms

A
  • surgery to prevent complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what is coronary artery disease

A

one or more branches of the coronary circuit has advanced atherosclerosis

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

atherosclerosis in the coronary circuit leads to what

A

ischemia = MI

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

what are the types of coronary artery disease

A
  • acute coronary syndromes

- chronic ischemic heart disease

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

characteristics of arteries where aneurysms occur

A

arteries that:

  • bifurcate
  • bend
  • is not supported externally
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

acute coronary syndromes result in

A
  • unstable angina

- MI

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

chronic ischemic heart disease results in

A
  • stable angina
  • variant angina
  • microvascular angina
  • silent myocardial ischemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what is microvascular angina

A

occlusion in smaller branches of the coronary circuit = less pressing
called cardiac syndrome X

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

what is silent myocardial ischemia

A

myocardial ischemia with no manifestations

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

what is angina pectoris

A

chest pain d/t myocardial ischemia

is a manifestation of CAD

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

what is angina pectoris caused by

A
  • atherosclerosis
  • vasospasm
  • thrombus
  • hemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

how does angina pectoris occur

A

inadequate perfusion d/t atherosclerosis = ischemia = chest pain

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

why can’t atherosclerotic vessels dilate

A

b/c they are already compensating by vasodilating and are at max. dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

manifestations of angina pectoris

A

chest pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

types of angina

A
  • stable angina
  • unstable angina
  • variant/vasospastic/prinzmetals angina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what is stable angina

A
  • fixed plaque w/in the wall of the vessel protrudes into the lumen = partial occlusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

when does pain from stable angina occur

A

during exertion

= transient pain

64
Q

what is transient pain

A

eliminating the trigger makes the pain subside

65
Q

triggers for stable angina

A
  • physical exertion
  • emotional stress
  • cold
66
Q

what is variant angina

A

spasm of an artery in the coronary circuit

67
Q

when does pain from variant angina occur

A

any time; at rest, nocturnal

68
Q

what causes variant angina

A
  • endothelial dysfunction
  • inadequate handling of Ca ions by s.m. cells (intake/output is irregular = spasms)
  • hyperactive SNS (stimulation of vessel walls)
  • nitric oxide (low concentration = vasoconstriction)
69
Q

management of variant angina

A

is difficult because it cannot be triggered

70
Q

challenges of diagnosing variant angina

A

ECG must be done during episode (which can’t be triggered)

71
Q

what is unstable angina

A
  • unstable plaque/atheroma ruptures a vessel wall into the lumen causing bleeding into the wall
  • atheroma leaks fibrin, cellular debris = attracts platelets
  • thrombus forms in the lumen => occlusion
  • platelets release prostaglandins = constriction
    ===> occlusion + constriction
72
Q

when does pain from unstable angina occur

A

any time; is prolonged, severe, can’t withdraw trigger

73
Q

manifestations of unstable angina

A
  • transient and mild-severe chest pain
  • squeezing/burning pain
  • pain may radiate to left shoulder/arm, neck, jaw
74
Q

treatment of unstable angina

A
  • rest, cease activity
  • nitroglycerine (nitric oxide = vasodilator)
  • prevention (avoid triggers that will lead to MI)
  • cease smoking
75
Q

what is myocardial infarction

A

an end point/result of CAD

76
Q

% of MI: STEMI vs NSTEMI

A

70% STEMI

30% NSTEMI

77
Q

what is a STEMI

A

complete occlusion of a larger vessel

78
Q

what is a NSTEMI

A

partial occlusion of a distal vessel

79
Q

primary vessels affected by MI

A
  • R coronary artery
  • L coronary descending artery
  • L circumflex artery
80
Q

where does the R coronary artery feed

A

R atrium + R ventricle

81
Q

where does the L coronary descending artery feed

A

R ventricle + L ventricle + interventricular septum

82
Q

where does the L circumflex artery feed

A

L atrium + L ventricle

83
Q

causes of MI

A
  • atherosclerosis
  • coronary artery spasms
  • hemorrhage
84
Q

patho of MI

A
  • atherosclerosis = ischemia = hypoxia = anaerobic metablism = metabolic acidosis = arrhythmias = infarction
85
Q

why does metabolic acidosis cause arrhythmias

A

decreased oxygen affects conduction

86
Q

how does arrhythmia affect cardiac output

A

makes filling/emptying of atria/ventricles off balance

87
Q

what affects the extent of infarction

A
  • affected vessel (proximal vs distal)
  • degree of occlusion (partial vs complete)
  • duration of ischemia
  • cardiac status (rest/exercise)
  • HR, BP, rhythm
  • collateral vessels
88
Q

types of infarcts

A
  • transmural

- subendocardial

89
Q

what is a transmural infarct

A
  • result of proximal occlusion of an artery
  • the entire ventricle wall is affected
  • STEMI
90
Q

what is a subendocardial infarct

A
  • result of distal occlusion
  • partial ventricle wall affected (inner 1/2 - 2/3)
  • NSTEMI
91
Q

a STEMI will result in what on an ECG

A

ST elevation

92
Q

a NSTEMI will result in what on an ECG

A

ST depression

93
Q

manifestations of MI

A
  • crushing chest pain (acute, severe, radiating)
  • tachycardia (d/t hypoxia)
  • n+v
  • anxiety/stress
  • dyspnea, dizziness, diaphoresis, palpitations
94
Q

diagnosis of MI

A
  • ECG
  • angiogram
  • serum markers (troponin I&T, myoglobin, CKmb)
95
Q

no R wave indicates what

A

ventricles are not contracting

96
Q

treatment of MI

A 
stabilization:
- thrombolytics
- anticoagulants
- anti-arrhythmics
- morphine
- oxygen
post stabilization:
- IV diuretic (dec. workload)
- vasodilator
- inotrope
- revascularization surgery (angioplasty, bypass)
97
Q

what is cardiomyopathy

A

defective cardiac muscle

98
Q

3 types of cardiomyopathy

A
  • hypertrophic
  • dilated
  • restrictive
99
Q

hypertrophic cardiomyopathy

A
  • thickened septum; obstruction of aorta
  • outflow obstruction = dec. CO
  • left ventricle hypertrophy = dec. ventricle size = dec. CO
100
Q

cause of hypertrophic cardiomyopathy

A
  • 50% autosomal dominant

- 50% idiopathic

101
Q

manifestations of hypertrophic cardiomyopathy

A

90% asymptomatic

  • dyspnea
  • angina
  • syncope
  • palpitations
102
Q

treatment of hypertrophic cardiomyopathy

A
  • negative inotrope (dec. workload)
  • surgery (remove obstruction)
  • chemical ablation
103
Q

dilated cardiomyopathy

A

ventricle enlargement (d/t loss of elasticity) = congestion = blood pools

104
Q

causes of dilated cardiomyopathy

A
  • genetic
  • viral infection
  • alcohol abuse
  • chemo drugs
105
Q

manifestations of dilated cardiomyopathy

A
  • decreased ejection fraction

- cardiac failure

106
Q

treatment of dilated cardiomyopathy

A
  • decrease cardiac workload (diuretics, beta blockers)

- symptom management

107
Q

restrictive cardiomyopathy

A
  • worst type, but rare

rigid vessel walls (d/t dec. elasticity) = incomplete filling = decreased CO

108
Q

what is a typical SA node rhythm

A

70 bpm

109
Q

tachycardia rhythm is

A

> 100

110
Q

bradycardia rhythm is

A

< 60

111
Q

problems happen with the conducting system when

A

multiple areas attempt to control the pace

112
Q

what is an arrhythmia

A

abnormal impulse conduction/generation that alters HR and/or rhythm
=> disrupts the cardiac cycle which affects CO and perfusion

113
Q

causes of arrythmia

A
  • congenital defects (ex. foramen ovale closure)
  • electrolyte imbalance (especially K)
  • stimulant drugs
  • myocardial ischemia (reversible)
114
Q

types of arrhythmia

A
  • atrial flutter
  • atrial fibrillation
  • heart block
  • ventricular fibrillation
115
Q

atrial flutter

A
  • regular but rapid rhythm
  • SA node fires repeatedly but ventricles remain slower d/t the refractory period. As the artial rate increases, the ratio will increase
  • atrial and ventricle tachycardia
  • usually 2:1 ratio (300:150 bpm), could be up to 6:1
116
Q

atrial fibrillation

A
  • uncoordinated, spontaneous contractions, irregular rhythm
  • atrial contractions aren’t effective - atria don’t have enough time to fill
  • atrial rate = 300-600 bpm
  • irregular ventricular rate = 80-180 bpm
  • no distinct P wave
117
Q

heart block

A
  • migration of the electrical impulse from atria to ventricle are blocked
  • not a blockage of a vessel
  • 3 types: 1st, 2nd, 3rd degree
118
Q

first degree heart block

A

delayed but regular conduction

= longer PR interval

119
Q

second degree heart block

A

intermittent loss of conduction

some activity passes through, some doesn’t

120
Q

third degree heart block

A

no conduction between artia and ventricle
= safety net activated => ventricles self pace (atria + ventricles are not syncronized)
= independent, regular atrial + ventricle paces

121
Q

ventricular fibrillation

A

worst case, no contractions, heart quivers (no filling/emptying) = no CO
ECG goes flat

122
Q

diagnosis of arrhythmia

A

ECG

123
Q

treatment of arrhythmia

A
  • defibrillation
  • antiarrhythmics
  • pacemaker
  • ablation (part that is blocking conduction)
  • cardioversion
124
Q

what is cardioversion

A

defibrillation that is synchronised to the QRS complex

125
Q

what does defibrillation do

A

extinguishes all existing electrical activity in the heart, allows the pace maker to take on pacing function to establish a sinus rhythm

126
Q

what do valves do

A

ensure unidirectional flow of blood

127
Q

when are atria-ventricular valves open/closed

A

open normally, close during ventricular contraction

128
Q

when are the semilunar valves open/closed

A

normally closed, open during ventricular contraction

129
Q

which valves are most susceptible to damage and why

A

the aortic and mitral valves

d/t the high pressure of the left ventricle

130
Q

2 forms of damage/disease to valves

A
  • regurgitant valve

- stenotic valve

131
Q

causes of valvular disease

A
  • trauma/inflammation
  • ischemia
  • aging
  • congenital defects
132
Q

stenotic valve

A

stiff valve

causes narrowing which impedes flow

133
Q

regurgitant valve

A

floppy valve

improper closure causes regurgitation

134
Q

valvular diseases causes what

A

changes to intra-cardiac blood flow which increases the workload => persistently high workload will cause HF

135
Q

treatment of valvular disease

A
  • pharmacological (maintain fx to prevent failure)

- surgery (repair/replace valve)

136
Q

non modifiable risk factors for coronary heart disease

A
  • men > 45
  • women > 55 (or postmenopausal)
  • family hx CVD: women < 65, men < 55
  • first nations, african, south asian
137
Q

modifiable risk factors for coronary heart disease

A
  • HTN
  • smoking
  • dyslipidemia (low HDL, elevated LDL)
  • diabetes mellitus
  • obesity
  • alcohol
  • low activity
138
Q

target organ damage of coronary heart disease

A
  • LV hypertrophy
  • CAD
  • HF
  • stroke/TIA
  • nephropathy
  • peripheral arterial disease
139
Q

what is infectious endocarditis

A

a bacterial infection of the endocardium and valves causing inflammation

140
Q

what are the 2 requirements of bacteria during infectious endocarditis

A
  • enter and survive the cardiovascular system

- adhere to the intra-cardiac surface

141
Q

what makes it difficult for bacteria to adhere to the intra-cardiac surface

A
  • high pressure
  • smooth surface
  • turbulent flow
142
Q

bacterial adherence to the intra-cardiac surface leads to what

A

proliferation which attracts platelets which will create fibrin strands which bacteria will colonize

143
Q

manifestations of infectious endocarditis

A
  • local + systemic infection
  • manifestations of impaired valve function
  • heart murmur
144
Q

complications of infectious endocarditis

A

distal embolization

145
Q

diagnosis of infectious endocarditis

A
  • history
  • ECG
  • C+S and other labs over 24 hours
  • serology
146
Q

treatment of infectious endocarditis

A
  • antibiotics

- treat the complications

147
Q

what is rheumatic fever

A

an immune-mediated and multi-system inflammatory disease

148
Q

who is affected most by rheumatic fever

A

3% of children aged 5-15

149
Q

rheumatic fever is what kind of genetic abnormality

A

complex trait:

must have strep throat + predisposition

150
Q

rheumatic fever starts as what

A

strep throat

151
Q

how does rheumatic fever cause damage

A

1-4 weeks after having strep throat, antibodies persist and target self-antigens in the heart, joints, CNS, and integument
= molecular mimicry

152
Q

what is rheumatic heart disease

A

the effect rheumatic fever has on the heart

= immune-mediated inflammation of the valves, myocardium and pericardium

153
Q

acute form of RHD

A
  • self-limiting
  • no intervention required
  • monitor and treat symptoms
154
Q

chronic form of RHD

A

leads to severe heart damage

155
Q

manifestations of RHD

A
  • cold/cough symptoms

- valvular dysfunction (SOBOE, weakness, fatigue, edema, chest pain)

156
Q

diagnosis of RHD

A
  • strep throat test
  • CBC, CRP, ESR, serology
  • echo
157
Q

treatment of RHD

A
  • penicillin, erythromycin (strep)
  • anti-inflammatories
  • steroids
  • 4-5 weeks bed rest
  • treat complications

Bio 252 (15 decks)

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