Cardio-pathology-ischemic heart disease Flashcards
(117 cards)
1
Q
Ischemic heart disease (IHD) includes several syndromes caused by .
A
myocardial ischemia
2
Q
Ischemic injury to the myocardium can be caused by which 2 things?
A
- lack of blood flow
- increased demand
or both
3
Q
cardiac myocytes generate energy almost exclusively through
which biochemical process?
A
mitochondrial oxidative phosphorylation,
4
Q
In > percent of cases, IHD is a consequence of reduced coronary blood flow secondary to obstructive atherosclerotic vascular disease
A
90%
5
Q
What is the other name for ischemic heart disease?
A
coronary artery disease, due to the majority of cases being from obstructive atherosclerotic vascular disease.
6
Q
In most cases, the syndromes of IHD are consequences of coronary that has been progressing for decades.
A
atherosclerosis
7
Q
Ischemic heart disease may include one or more of the following 4 cardiac syndromes:
A
- angina pectoris
- MI
- Chronic IHD with congestive heart failure (CHF)*
- Sudden cardiac death (SCD)
8
Q
What is angina pectoris?
A
chest pain
Ischemia induces pain, but is insufficient to cause myocyte death
9
Q
In angina pectoris, Ischemia induces pain, and is insufficient/sufficient to cause myocyte death.
A
insufficient
10
Q
What type of angina occurrs predictably at certain levels of exertion?
A
stable angina
11
Q
Which type angina can be caused by vessel spasm?
A
Prinzmetal angina
12
Q
Which type of angina occurrs with progressively less exertion or even at rest?
A
unstable angina
13
Q
What occurs when the severity or duration of ischemia is sufficient to cause cardiomyocyte death (necrosis)?
A
MI
14
Q
This can occur as a consequence of tissue damage from MI, but most commonly results from a lethal arrhythmia without myocyte necrosis:
A
sudden cardiac death
15
Q
What 4 interventions have greatly diminished cardiac risk factors?
A
smoking cessation programs,
hypertension and diabetes treatment,
and use of cholesterol-lowering agents.
16
Q
IHD is a result of inadequate coronary perfusion relative to myocardial demand, usually due which 3 circumstances:
A
atherosclerotic occlusion of the coronary arteries
and new, superimposed thrombosis
and/or vasospasm.
17
Q
Which coronary arteries can be affected by atherosclerotic narrowing?
A
left anterior descending (LAD), left circumflex (LCX), and right coronary artery (RCA) - singly or in combination.
18
Q
Fixed obstructions that occlude < percent of a coronary vessel lumen typically are asymptomatic, even with exertion.
A
70%
19
Q
Lesions that occlude > percent of a vessel lumen - resulting in a “ stenosis” - generally cause symptoms with increased demand.
A
70%; critical
This patient is said to have stable angina
20
Q
A fixed stenosis that occludes > percent of a vascular lumen can lead to inadequate coronary blood flow with symptoms even at rest - a form of angina.
A
90%; unstable
21
Q
What are some acute coronary syndromes?
A
unstablel angina, MI, sudden cardiac death
22
Q
What can be triggered by thrombosis associated with an eroded or ruptured plaque?
A
acute coronary syndromes, ie, unstable angina, MI, and sudden cardiac death…
23
Q
In most patients, unstable angina, infarction, and sudden cardiac death occur because of abrupt change followed by thrombosis - thus the term acute coronary syndrome.
A
plaque
24
Q
In a majority of cases, the lesion in patients who suffer an MI was/was not critically stenotic or even symptomatic before its rupture.
A
was not (<70% occlusion)
25
It is impossible to predict plaque rupture in any given patient?
T or F
true
26
Angina pectoris is an intermittent chest pain caused by:
transient, reversible myocardial ischemia.
27
The pain associated with angina pectoris is a consequence of the ischemia-induced release of:
adenosine, bradykinin, and other molecules that stimulate autonomic nerves.
28
How many variants of angina pectoris and what are they?
3
typical or stable angina
Prinzmetal (variant) angina
Unstable (crescendo) angina
29
Which angina variant is described?
A predictable episodic chest pain associated with particular levels of exertion, or some other increased demand (eg, tachycardia).
typical or stable angina
30
How is angina pectoris pain described and where is it felt?
crushing or squeezing substernal sensation that often radiates down the left arm or to the left jaw (referred pain).
31
Which variant of angina pectoris is described:
The pain usually is relieved by rest (reducing demand) or by drugs such as nitroglycerin, a vasodilator that increases coronary perfusion.
typical or stable angina
32
What type of angina variant is described:
Occurs at rest, and is caused by coronary artery spasm.
Prinzmetal (variant) angina
33
Concerning prinzmetal (variant) angina, although such spasms typically occur on or near existing atherosclerotic plaques, a completely vessel can be affected.
normal
34
Prinzmetal (variant) angina typically responds promptly to which treatments?
vasodilators such as nitroglycerin, and calcium channel blockers.
35
Which type of angina is described:
Characterized by increasingly frequent pain, precipitated by progressively less exertion or even occurring at rest.
unstable angina (crescendo angina)
36
Which type of angina is described:
It is usually associated with plaque disruption and superimposed thrombosis, and can be a harbinger of MI, portending complete vascular occlusion.
Unstable angina (crescendo angina)
37
What is described as necrosis of the heart muscle resulting from ischemia?
Myocardial infarction (MI) (“heart attack”)
38
What is the major underlying cause of MI?
atherosclerosis
39
The vast majority of MIs are caused by within coronary arteries
acute thrombosis
40
in most intances, what serves as the nidus for thrombus generation, vascular occlusion, and subsequent infarction of the myocardium?
disruption or erosion of preexisting atherosclerotic plaque
41
There a 4 sequential events that take place in a typical MI:
**An atheromatous plaque is eroded**, exposing subendothelial collagen and necrotic plaque contents to the blood.
๏ **Platelets adhere, aggregate, and are activated**, releasing thromboxane A 2 , adenosine diphosphate (ADP), and serotonin - causing further platelet aggregation and vasospasm.
๏ **Activation of coagulation by exposure of tissue factor** and other mechanisms **adds to the growing thrombus.**
๏ Within minutes, the t**hrombus can evolve** to completely **occlude the coronary artery lumen.**
42
Within what amount of time after vascular obstruction does aerobic metabolism cease?
within seconds
43
What is the **functional consequence** occurring within a minute or so of the onset of ischemia?
rapid loss of contractility
44
Prolonged ischemia lasting \> to minutes causes irreversible damage and coagulative necrosis of myocytes
20 - 40
45
What is the goal of **early dx and prompt intervention** by thrombolysis or angioplasty?
blood flow is restored before irreversible injury occurs, myocardium can be preserved
46
Where does Irreversible injury of ischemic myocytes first occur?
subendocardial zone.
47
An infarct usually achieves its full extent within to hours;
3 to 6
48
in the absence of intervention, an infarct caused by occlusion of an epicardial vessel can involve the wall thickness (transmural infarct)
entire
49
The location, size, and morphologic features of an acute myocardial infarct depend on which 4 criteria?
๏ Size and distribution of the involved vessel
๏ Rate of development and duration of the occlusion.
๏ Metabolic demands of the myocardium.
๏ Extent of collateral supply
50
Acute occlusion of the proximal left anterior descending (LAD) artery (40-50% of all MIs) typically results in infarction of the:
anterior wall of the left ventricle, the anterior two thirds of the ventricular septum, and most of the heart apex
51
Acute occlusion of the proximal left circumflex (LCX) artery (15-20% of MIs) causes necrosis of the:
lateral left ventricle.
52
Proximal right coronary artery (RCA) occlusion (30-40% of MIs) affects much of the:
right ventricle, right atrium, SA and AV nodes
53
How can myocardial ischemia possibly result in arrythmias?
causing electrical instability (irritability) of ischemic regions of the heart.
54
Although massive myocardial damage can cause a fatal mechanical failure, sudden cardiac death in the setting of myocardial ischemia most often is due to ventricular caused by myocardial irritability.
fibrillation;
55
The gross and microscopic appearance of an MI depends on the of the injury
age
56
What is the progression of morphologic changes that occur from MI?
coagulative necrosis, to acute and then chronic inflammation, to fibrosis.
57
Myocardial infarcts less than hours old usually are not grossly apparent
12
58
Infarcts over old can be visualized by exposing myocardium to vital stains, such as triphenyl-tetrazolium , a substrate for lactate dehydrogenase.\*
3 hours; chloride
59
What does the yellow, black, and white circled areas of this heart represent?
**yellow** area is area of infarction (lacks enzyme for red staining)
**black** area is an area of hemorrhage
**white** area is fibrosis from a previous MI
60
By **12-24** hrs after MI, an infarct usually can be grossly identified by a discoloration caused by stagnated, trapped blood.
red-blue
61
After 12 to 24 hours, , infarcts become progressively better seen as soft, areas.
yellow-tan
62
By 10-14 days, infarcts are rimmed by:
hyperemic (highly vascularized) granulation tissue.
63
After 10-14 days, the infarcted tissue will gradual evolve to a :
fibrous scar
64
Microscopically, typical features of coagulative necrosis become detectable within hours of infarction.
4-12
65
“Wavy fibers” also can be present at the edges of an infarct, reflecting the stretching and buckling of:
noncontractile dead fibers
notice loss of nuclei
66
Areas of coagulative necrosis with congestion and hemorrhage after MI
67
Necrotic myocardium elicits acute (~1-3 days post-MI), predominantly neutrophils
inflammation
68
When does a wave of macrophages that remove necrotic myocytes and neutrophil fragments show up in damaged heart tissue?
~ 5-10 days post - MI
69
The infarcted zone is progressively replaced by tissue (~ 1-2 wks), which forms the provisional upon which dense collagenous scar forms, usually by the end of the week.
granulation; scaffolding; 6th
**note: slide demonstrates granulation tissue with lots of blood vessels.**
**Trichrome stain -**
**blue= collagen, fibrosis**
70
This trichrome stain heart tissue demonstrates what?
the blue is scar formation with lots of collagen fibrosis
71
What is being described:
severe, crushing substernal chest pain (or pressure) that can radiate to the neck, jaw, epigastrium, or left arm.
MI
72
How are MI symptoms different from angina pectoris?
pain typically lasts several minutes to hours, and is not relieved by nitroglycerin or rest.
73
In a **10-15%** of patients, MIs present with atypical signs and symptoms, and may even be entirely asymptomatic, what is this called:
“silent” infarcts
74
“silent” infarcts are particularly common in which 2 patient populations?
diabetes and older adults
75
What are some signs of MI?
pulse generlly rapid and weak
diaphoretic (sweating) and nausous (especially posterior wall MI)
Dyspnea
cardiogenic shock (with massive MIs)
76
What physical sign accompanies impaired myocardial contractility and/or dysfunction of the **mitral valve apparatus,** with resultant acute pulmonary congestion and edema.
dyspnea
77
What happens as a result of impaired myocardial contractility and/or dysfunction of the mitral valve apparatus?
resultant acute pulmonary congestion and edema.
78
When is a MI considered massive and what can develop as a result?
(\> 40% of the left ventricle), cardiogenic shock develops.
79
What electrocardiographic abnormalities typically show up with transmural MIs?
**ST segment elevations** on the electrocardiogram (ECG) and can have **negative Q waves** with **loss of R wave** amplitude.
80
What is a STEMI?
ST-segment elevated myocardial infarctions (STEMIs)
81
the laboratory evaluation of MI is based on measuring blood levels of what substances?
macromolecules that leak out of injured myocardial cells through damaged cell membranes.
82
What 4 macromolecules leak out of injured myocardial cells through damaged cell membranes, and can be detected through laboratoy evaluation?
myoglobin,
cardiac troponins T and I (TnT, TnI),
creatine kinase (CK; specifically the myocardial isoform, CK-MB),
and lactate dehydrogenase.
83
Which of the 4 macromolecules that leak out of injured myocardial cells through damaged cell membranes have the highest specificity and sensitivity?
**Troponins** (and **CK-MB**) have high specificity and sensitivity for myocardial damage.
84
CK-MB activity begins to rise within to hrs of MI, peaks at to hours, and returns to normal within ~72 hours
2 to 4; 24 to 48
85
TnI and TnT are both detectable within to after acute MI, with levels peaking at hrs, and remaining elevated for 7 to 10 days.
2 to 4 hrs; 48
86
Persistence of elevated levels allows the diagnosis of an acute MI to be made long after CK-MB levels have returned to normal.
troponin
87
~75% of pts experience one or more of the following complications after an acute MI:
• Contractile dysfunction • Arrhythmias • Pericarditis • Myocardial rupture • Ventricular aneurysm • Mural thrombus • Papillary muscle dysfunction • Progressive heart failure
88
In general, MIs affect ventricular pump function in proportion to the volume of damage
left
89
In most cases of MI, there is some degree of left ventricular failure manifested as what 3 conditons?
hypotension, pulmonary congestion, and pulmonary edema.
90
What is severe "pump failure" and how much damage is involved?
cardiogenic shock (10% of patients with transmural MI);
associated with infarcts that damage 40% or more of the left ventricle.
91
Approximately of patients develop some form of rhythm disturbance, with the incidence being higher in STEMIs versus NSTEMIs.
90%
92
MI-associated arrhythmias include: (6)
heart block of variable degree (including asystole), bradycardia,
supraventricular tachyarrhythmias,
ventricular premature contractions or
ventricular tachycardia, and
ventricular fibrillation.
93
The risk for serious arrhythmias is greatest in the hour and decreases thereafter
first
94
What usually develops about the 2nd or 3rd day following a transmural infarct as a result of underlying myocardial inflammation?
A fibrinous or fibrino-hemorrhagic pericarditis
95
When does a fibrinous or fibrino-hemorrhagic pericarditis usually develop after a transmural infarct as a result of underlying myocardial inflammation?
2nd or 3rd day
96
Myocardial rupture complicates only of MIs, but is frequently when it occurs.
1-5%; fatal
97
What is pictured and what are the consequences:
**Left ventricular free wall rupture** is most common, usually resulting in **rapidly fatal hemopericardium and cardiac tamponade**
98
What is pictured and what are the consequences:
Ventricular septal rupture creates a VSD with left-to-right shunting
99
What is pictured and what are the consequences:
Papillary muscle rupture leads to severe mitral regurgitation
100
What is the most common myocardial rupture?
Left ventricular free wall rupture
101
Rupture occurs most commonly within to days after infarction - the time in the healing process when lysis of necrotic myocardium is **maximal/minimal?**
3 - 7; maximal
102
Ventricular aneurysm, a late complication, most commonly results from a large transmural anteroseptal infarct that heals with the formation of which weakness:
thinned wall of scar tissue.
103
Although ventricular aneurysms frequently give rise to formation of mural thrombi, arrhythmias, and heart failure, they **do/do not** rupture.
do not
104
ventricular aneurysms frequently give rise to formation of which 3 conditions/consequences:
mural thrombi, arrhythmias, and heart failure
105
What conditions can lead to a left-sided thromboembolism as concerning MIs?
combination of **decreased myocardial contractility** (causing stasis), **chamber dilation**, and **endocardial damage** (causing a thrombogenic surface) can cause **mural thrombosis,**
106
Large **transmural/subendocardial** infarcts are associated with a higher probability of **cardiogenic shock**, **arrhythmias**, and **late CHF.**
transmural
107
Patients with which type and area of infarct are at greatest risk for **free wall rupture**, **expansion**, **aneurysm formation**, and formation of **mural thrombi**.
anterior transmural MIs
108
Which type of transmural infarcts are more likely to be complicated by **conduction blocks**, **right ventricular involvement**, or both; when **ventricular septal ruptures** occur in this area, they are more difficult to manage.
posterior transmural infarcts
109
Which type and place of infarct has a much more guarded prognosis?
anterior infarcts have a much more guarded prognosis than those with posterior infarcts.
110
Why type of infarct and where does it occur:
thrombi may form on the endocardial surface, but pericarditis, rupture, and aneurysms rarely occur.
subendocardial infarcts,
111
Which 3 conditions rarely occur with subentdothelial infarcts?
pericarditis, rupture, and aneurysms
112
What are the most important factors concerning long-term prognosis after MI?
quality of **left ventricular function**, and the severity of **atherosclerotic narrowing of vessels** perfusing the remaining viable myocardium.
113
The overall mortality rate of MIs within the first year is about percent, including deaths occurring before the patient reaches the hospital.
30%
114
in the majority of cases, cardiac ischemia is due to:
coronary artery atherosclerosis
115
Less common causes of cardiac ischemia are which 3 conditions:
vasopspasm, vasculitis, embolism
116
What typically results from acute thrombosis after plaque disruption (the majority not previously considered critical)?
acute myocardia infarction
117
