cardiovascular disorders Flashcards
1
Q
hyperlipidemia
A
elevated lipid content in the blood
cholesterol, triglycerides, phospholipids
2
Q
what is a apoprotein
A
a protein that transports lipids
3
Q
what is a lipoprotein
A
a apoprotein + a lipid
4
Q
lipoproteins are named based on
A
density
low density lipid, high density lipid
5
Q
what is a chylomicron
A
lipoproteins that transfer lipids from the digestive tract into circulation
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
7
Q
what is an atheroma
A
a lesion in the intima of the vessel made of lipids and fibrous tissue
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
9
Q
what is the progression of an atheroma lesion
A
- fatty streak
- fibrous atheromatous plaque
- complicated lesion
10
Q
what is a fatty streak made of
A
cells
macrophages, foam cells, smooth muscle cells
11
Q
what is fibrous atheromatous plaque
A
a lesion made of swelling comprised of fibers
accumulation of lipids, scar tissue, calcification
12
Q
what is a complicated lesion
A
hemorrhaging into the plaque
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)
14
Q
an elevated CRP without underlying inflm indicates
A
atherosclerosis
15
Q
4 control mechanisms of BP
A
- baroreceptors (detect pressure change)
- volume regulation (via kidneys)
- vascular autoregulation (vasoconstriction/dilation)
- RAAS (ADH, aldosterone)
16
Q
HTN follows what cycle
A
circadian rhythm
17
Q
when is BP lowest and highest
A
lowest = 2-5am highest = first thing in the morning
18
Q
primary HTN
A
- 90% cases
- idiopathic - can’t eradicate, just manage
- multifactorial (problem w/ several regulatory mechanisms)
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
20
Q
secondary HTN
A
- 5-10%
- renovascular = arteries supplying kidneys occluded
- poor renal perfusion activates RAAS, increases BP systemically
21
Q
malignant HTN
A
- diastolic > 120
- emergency situation
22
Q
manifestations of HTN
A
- BP may be high unknowingly
- AM headaches
- palpitations
- dizziness, fatigue, blurred vision
- organ failure (kidney, heart, brain)
23
Q
treatment of HTN
A
- Lifestyle modification
- DASH diet
- smoking and alcohol cessation
- exercise - 1st line drug = diuretic
- 2nd line drug = add 1/more
- Ca channel blocker (decrease s.m. contraction)
- angiotensin II receptor blocker
- ACE inhibitor
24
Q
what are the types of peripheral vascular disease
A
- acute arterial occlusion
- atherosclerotic occlusive disease
25
what is an acute arterial occlusion caused by
an embolus or thrombus that disrupts perfusion
26
what is an embolus
something that lodges in a vessel (air, clot, malignant cells)
27
what is a thrombus
a stationary blood clot
28
manifestations of acute arterial occlusion
- pain
- pallor
- pistol
- pulselessness
- polar
- paresthesia
- paralysis
29
diagnosis of acute arterial occlusion
- blood flow assessment
| - physical exam
30
treatment of acute arterial occlusion
- surgery (remove clot)
- thrombolytics (dissolve clot)
- anticoagulants (prevention)
31
atherosclerotic occlusive disease
- 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
32
why does diabetes cause atherosclerotic occlusive disease
diabetes causes vascular damage - causes atherosclerosis
33
how does the body compensate for atherosclerotic occlusive disease
- vasodilation
- anaerobic metabolism (d/t hypoxic tissue)
- collateralization
34
manifestations of atherosclerotic occlusive disease
- intermittent claudication
| - complications (ulcers, loss of fx)
35
diagnosis of atherosclerotic occlusive disease
- blood flow assessment
| - physical exam
36
treatment of atherosclerotic occlusive disease
- no clot present - must address manifestations
| know complications, prevent, treat
37
what is an aneurysm
a localized bulge in an artery d/t degenerative change in the vessel wall
(permanent change)
38
most common arteries for aneurysms
femoral, iliac, popliteal arteries
39
highest pressure vessels, likely for aneurysms
thoracic, abdominal aorta
40
risks for aneurysm
- atherosclerosis
- uncontrolled HTN
- congenital defects (weakened vessel walls)
- aging
41
what is a true aneurysm
vessel wall is intact
| 50% increase in vessel diameter
42
what is a false aneurysm
vessel wall is compromised
| supported by external structures
43
what are the types of aneurysms
true
| false
44
what are the forms of aneurysms
fusiform (bilateral)
saccular (unilateral)
dissecting (in vessel walls)
45
a berry aneurysm is what form of aneurysm
saccular
46
complications of aneurysms
- rupture (brain=stroke, aorta=death)
- pressure on adjacent structures
- distal embolization (pooling=thrombus -> dislodges)
47
treatment of aneurysms
- surgery to prevent complications
48
what is coronary artery disease
one or more branches of the coronary circuit has advanced atherosclerosis
49
atherosclerosis in the coronary circuit leads to what
ischemia = MI
50
what are the types of coronary artery disease
- acute coronary syndromes
| - chronic ischemic heart disease
51
characteristics of arteries where aneurysms occur
arteries that:
- bifurcate
- bend
- is not supported externally
52
acute coronary syndromes result in
- unstable angina
| - MI
53
chronic ischemic heart disease results in
- stable angina
- variant angina
- microvascular angina
- silent myocardial ischemia
54
what is microvascular angina
occlusion in smaller branches of the coronary circuit = less pressing
called cardiac syndrome X
55
what is silent myocardial ischemia
myocardial ischemia with no manifestations
56
what is angina pectoris
chest pain d/t myocardial ischemia
| is a manifestation of CAD
57
what is angina pectoris caused by
- atherosclerosis
- vasospasm
- thrombus
- hemorrhage
58
how does angina pectoris occur
inadequate perfusion d/t atherosclerosis = ischemia = chest pain
59
why can't atherosclerotic vessels dilate
b/c they are already compensating by vasodilating and are at max. dilation
60
manifestations of angina pectoris
chest pain
61
types of angina
- stable angina
- unstable angina
- variant/vasospastic/prinzmetals angina
62
what is stable angina
- fixed plaque w/in the wall of the vessel protrudes into the lumen = partial occlusion
63
when does pain from stable angina occur
during exertion
| = transient pain
64
what is transient pain
eliminating the trigger makes the pain subside
65
triggers for stable angina
- physical exertion
- emotional stress
- cold
66
what is variant angina
spasm of an artery in the coronary circuit
67
when does pain from variant angina occur
any time; at rest, nocturnal
68
what causes variant angina
- 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
management of variant angina
is difficult because it cannot be triggered
70
challenges of diagnosing variant angina
ECG must be done during episode (which can't be triggered)
71
what is unstable angina
- 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
when does pain from unstable angina occur
any time; is prolonged, severe, can't withdraw trigger
73
manifestations of unstable angina
- transient and mild-severe chest pain
- squeezing/burning pain
- pain may radiate to left shoulder/arm, neck, jaw
74
treatment of unstable angina
- rest, cease activity
- nitroglycerine (nitric oxide = vasodilator)
- prevention (avoid triggers that will lead to MI)
- cease smoking
75
what is myocardial infarction
an end point/result of CAD
76
% of MI: STEMI vs NSTEMI
70% STEMI
| 30% NSTEMI
77
what is a STEMI
complete occlusion of a larger vessel
78
what is a NSTEMI
partial occlusion of a distal vessel
79
primary vessels affected by MI
- R coronary artery
- L coronary descending artery
- L circumflex artery
80
where does the R coronary artery feed
R atrium + R ventricle
81
where does the L coronary descending artery feed
R ventricle + L ventricle + interventricular septum
82
where does the L circumflex artery feed
L atrium + L ventricle
83
causes of MI
- atherosclerosis
- coronary artery spasms
- hemorrhage
84
patho of MI
- atherosclerosis = ischemia = hypoxia = anaerobic metablism = metabolic acidosis = arrhythmias = infarction
85
why does metabolic acidosis cause arrhythmias
decreased oxygen affects conduction
86
how does arrhythmia affect cardiac output
makes filling/emptying of atria/ventricles off balance
87
what affects the extent of infarction
- affected vessel (proximal vs distal)
- degree of occlusion (partial vs complete)
- duration of ischemia
- cardiac status (rest/exercise)
- HR, BP, rhythm
- collateral vessels
88
types of infarcts
- transmural
| - subendocardial
89
what is a transmural infarct
- result of proximal occlusion of an artery
- the entire ventricle wall is affected
- STEMI
90
what is a subendocardial infarct
- result of distal occlusion
- partial ventricle wall affected (inner 1/2 - 2/3)
- NSTEMI
91
a STEMI will result in what on an ECG
ST elevation
92
a NSTEMI will result in what on an ECG
ST depression
93
manifestations of MI
- crushing chest pain (acute, severe, radiating)
- tachycardia (d/t hypoxia)
- n+v
- anxiety/stress
- dyspnea, dizziness, diaphoresis, palpitations
94
diagnosis of MI
- ECG
- angiogram
- serum markers (troponin I&T, myoglobin, CKmb)
95
no R wave indicates what
ventricles are not contracting
96
treatment of MI
```
stabilization:
- thrombolytics
- anticoagulants
- anti-arrhythmics
- morphine
- oxygen
post stabilization:
- IV diuretic (dec. workload)
- vasodilator
- inotrope
- revascularization surgery (angioplasty, bypass)
```
97
what is cardiomyopathy
defective cardiac muscle
98
3 types of cardiomyopathy
- hypertrophic
- dilated
- restrictive
99
hypertrophic cardiomyopathy
- thickened septum; obstruction of aorta
- outflow obstruction = dec. CO
- left ventricle hypertrophy = dec. ventricle size = dec. CO
100
cause of hypertrophic cardiomyopathy
- 50% autosomal dominant
| - 50% idiopathic
101
manifestations of hypertrophic cardiomyopathy
90% asymptomatic
- dyspnea
- angina
- syncope
- palpitations
102
treatment of hypertrophic cardiomyopathy
- negative inotrope (dec. workload)
- surgery (remove obstruction)
- chemical ablation
103
dilated cardiomyopathy
ventricle enlargement (d/t loss of elasticity) = congestion = blood pools
104
causes of dilated cardiomyopathy
- genetic
- viral infection
- alcohol abuse
- chemo drugs
105
manifestations of dilated cardiomyopathy
- decreased ejection fraction
| - cardiac failure
106
treatment of dilated cardiomyopathy
- decrease cardiac workload (diuretics, beta blockers)
| - symptom management
107
restrictive cardiomyopathy
- worst type, but rare
| rigid vessel walls (d/t dec. elasticity) = incomplete filling = decreased CO
108
what is a typical SA node rhythm
70 bpm
109
tachycardia rhythm is
> 100
110
bradycardia rhythm is
< 60
111
problems happen with the conducting system when
multiple areas attempt to control the pace
112
what is an arrhythmia
abnormal impulse conduction/generation that alters HR and/or rhythm
=> disrupts the cardiac cycle which affects CO and perfusion
113
causes of arrythmia
- congenital defects (ex. foramen ovale closure)
- electrolyte imbalance (especially K)
- stimulant drugs
- myocardial ischemia (reversible)
114
types of arrhythmia
- atrial flutter
- atrial fibrillation
- heart block
- ventricular fibrillation
115
atrial flutter
- 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
atrial fibrillation
- 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
heart block
- migration of the electrical impulse from atria to ventricle are blocked
- not a blockage of a vessel
- 3 types: 1st, 2nd, 3rd degree
118
first degree heart block
delayed but regular conduction
| = longer PR interval
119
second degree heart block
intermittent loss of conduction
| some activity passes through, some doesn't
120
third degree heart block
no conduction between artia and ventricle
= safety net activated => ventricles self pace (atria + ventricles are not syncronized)
= independent, regular atrial + ventricle paces
121
ventricular fibrillation
worst case, no contractions, heart quivers (no filling/emptying) = no CO
ECG goes flat
122
diagnosis of arrhythmia
ECG
123
treatment of arrhythmia
- defibrillation
- antiarrhythmics
- pacemaker
- ablation (part that is blocking conduction)
- cardioversion
124
what is cardioversion
defibrillation that is synchronised to the QRS complex
125
what does defibrillation do
extinguishes all existing electrical activity in the heart, allows the pace maker to take on pacing function to establish a sinus rhythm
126
what do valves do
ensure unidirectional flow of blood
127
when are atria-ventricular valves open/closed
open normally, close during ventricular contraction
128
when are the semilunar valves open/closed
normally closed, open during ventricular contraction
129
which valves are most susceptible to damage and why
the aortic and mitral valves
| d/t the high pressure of the left ventricle
130
2 forms of damage/disease to valves
- regurgitant valve
| - stenotic valve
131
causes of valvular disease
- trauma/inflammation
- ischemia
- aging
- congenital defects
132
stenotic valve
stiff valve
| causes narrowing which impedes flow
133
regurgitant valve
floppy valve
| improper closure causes regurgitation
134
valvular diseases causes what
changes to intra-cardiac blood flow which increases the workload => persistently high workload will cause HF
135
treatment of valvular disease
- pharmacological (maintain fx to prevent failure)
| - surgery (repair/replace valve)
136
non modifiable risk factors for coronary heart disease
- men > 45
- women > 55 (or postmenopausal)
- family hx CVD: women < 65, men < 55
- first nations, african, south asian
137
modifiable risk factors for coronary heart disease
- HTN
- smoking
- dyslipidemia (low HDL, elevated LDL)
- diabetes mellitus
- obesity
- alcohol
- low activity
138
target organ damage of coronary heart disease
- LV hypertrophy
- CAD
- HF
- stroke/TIA
- nephropathy
- peripheral arterial disease
139
what is infectious endocarditis
a bacterial infection of the endocardium and valves causing inflammation
140
what are the 2 requirements of bacteria during infectious endocarditis
- enter and survive the cardiovascular system
| - adhere to the intra-cardiac surface
141
what makes it difficult for bacteria to adhere to the intra-cardiac surface
- high pressure
- smooth surface
- turbulent flow
142
bacterial adherence to the intra-cardiac surface leads to what
proliferation which attracts platelets which will create fibrin strands which bacteria will colonize
143
manifestations of infectious endocarditis
- local + systemic infection
- manifestations of impaired valve function
- heart murmur
144
complications of infectious endocarditis
distal embolization
145
diagnosis of infectious endocarditis
- history
- ECG
- C+S and other labs over 24 hours
- serology
146
treatment of infectious endocarditis
- antibiotics
| - treat the complications
147
what is rheumatic fever
an immune-mediated and multi-system inflammatory disease
148
who is affected most by rheumatic fever
3% of children aged 5-15
149
rheumatic fever is what kind of genetic abnormality
complex trait:
| must have strep throat + predisposition
150
rheumatic fever starts as what
strep throat
151
how does rheumatic fever cause damage
1-4 weeks after having strep throat, antibodies persist and target self-antigens in the heart, joints, CNS, and integument
= molecular mimicry
152
what is rheumatic heart disease
the effect rheumatic fever has on the heart
| = immune-mediated inflammation of the valves, myocardium and pericardium
153
acute form of RHD
- self-limiting
- no intervention required
- monitor and treat symptoms
154
chronic form of RHD
leads to severe heart damage
155
manifestations of RHD
- cold/cough symptoms
| - valvular dysfunction (SOBOE, weakness, fatigue, edema, chest pain)
156
diagnosis of RHD
- strep throat test
- CBC, CRP, ESR, serology
- echo
157
treatment of RHD
- penicillin, erythromycin (strep)
- anti-inflammatories
- steroids
- 4-5 weeks bed rest
- treat complications
