Brainscape's Knowledge GenomeTM

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


See full index

Pathology III > Quiz 1 > Flashcards

Quiz 1 Flashcards

1
Q

What is Atherosclerosis?

A

chronic inflammatory response in the walls of arteries, largely due to the deposition of lipoproteins
“hardening of the arteries”

HALLMARK: formation of multiple plaques within the arteries

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

What cellular components are involved in the development of atheroclerosis?

A

endothelial cells, smooth muscle cells, platelets, leukocytes and a wide variety of chemotactic and inflammatory mediators

Atherogenesis is a result of complex and incompletely understood interactions that exist between these cellular elements and other biologic processes

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

What biological processes contribute to atherosclerosis?

A

Vasomotor function, thrombogenicity of the blood vessel wall, activation of the coagulation cascade, the fibrinolytic system, smooth muscle cell migration and proliferation, and adrenergic stimulus are interrelated biological processes that contribute to atherogenesis

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

”response-to-injury” theory

A

the most widely accepted mechanism of action in atherosclerosis

Endothelial injury –> vascular inflammation + fibroproliferative response –> plaque formation

Triggered by by any other number of insults, such as:

  • Physical injury or stress as a result of direct trauma or HTN
  • Turbulent blood flow, esp where arteries branch
  • Circulation of reactive oxygen species (free radicals)
  • Hyperlipidemia
  • Chronically elevated blood glucose levels
  • Homocysteinemia, which is toxic to endothelium
  • infectious agents
  • chemical toxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the atherosclerotic process

A

Circulating monocytes infiltrate the intima of the vessel wall –> monocytes differentiate into macrophages, which ingest oxidized LDL, slowly turning into large “foam cells“ –> Foam cells eventually die, and further propagate the inflammatory process

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

What is the earliest grossly visible pathologic lesion of atherosclerosis? Why does it occur?

A

the fatty streak: occurs as a result of focal accumulation of serum lipoproteins within the intima of the vessel wall
lipid-laden macrophages, T lymphocytes, and smooth muscle cells in varying proportions

Fatty streatks are observed in the aorta and coronary arteries of most individuals by 20 years of age.
*fatty streaks do not impair the lumen size

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

How is smooth muscle involved in atherosclerosis?

A

SM cells migrate to and proliferate in the intima and are responsible for deposition of extracellular connective tissue matrix forming a fibrous cap (plaque) that overlies a core of lipid-laden foam cells, extracellular lipid, and necrotic cellular debris.

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

What is Angina Pectoris? What causes it?

A

Paroxysmal and usu recurrent attacks of chest pain (constricting, squeezing, choking, or knifelike)

Caused by transient (15 seconds to 15 minutes) myocardial ischemia that falls short of inducing the cellular necrosis that defines MIs.

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

Common symptoms of angina

A

• Chest pain: usu across anterior precordium; severe tightness, squeezing pain or intense weight or pressure on the chest; may radiate to the jaw, neck, arms, back, and epigastrium
• Dyspnea: may occur as an isolated complaint; often indicates poor ventricular compliance in the setting of acute ischemia
• Diaphoresis
• Anxiety
• Lightheadedness and syncope
• Cough/wheezing
• Nausea and vomiting or abdominal
*Women (40-50%) do not present with typical cardiac symptoms: dyspnea & SOB are more common presentations

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

Stable Angina

When do Sxs occur?

A

Cardiac ischemia that is usually due to a fixed lesion in a coronary artery
Sxs generally occur only upon exertion and are usu relieved by rest and/or medications which dilate arteries (nitrates)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q 
Variant Angina (Prinzmetal)
When do Sxs occur?
A

Pathophysiology Unknown, but intermittent vasospasm appears to be key to development of sxs

Sxs: Pain often occurs at rest and may be well controlled by vasodilators such as calcium channel blockers

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

Unstable Angina

A

Pattern: increasing frequency or intensity of chest pain; Often includes pain at rest
* Prolonged episode of unstable angina pectoris may precede the development of a myocardial infarction

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

What is an acute myocardial infarction?

A

the development of myocardial necrosis caused by a prolonged critical imbalance between the amount of oxygen supplied to the myocardium and the metabolic demand of the myocardium.

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

What is the most common cause/pathogenesis of an MI

A

plaque rupture within a coronary artery

Subsequent subendothelial exposure results in platelet aggregation, thrombus formation, fibrin accumulation, hemorrhage into the plaque, and varying degrees of vasospasm –> either partial or complete occlusion of the vessel and subsequent myocardial ischemia

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

Less common other causes of MI

A
  • Emboli to coronary arteries (dt cholesterol or infxn)
  • Coronary artery vasospasm
  • Coronary anomalies (irregular/absent coronary arteries or aneurysms)
  • Hypoxia dt underlying pulmonary disease.
  • Hypoxia due to CO poisoning or inhaled toxins.
  • Arteritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Process of an MI

A

Decreased oxygen flow to myocardium → conversion from aerobic to anaerobic metabolism → decreased ATP synthesis (within 1-2 min; reduced to 50% by 10 min) → disruption of the Na+/K+ ATPase membrane channel → marked increase in the membrane permeability of involved cardiac muscle cellsmyocytes swell and metabolic functions deteriorate; Ca activates various degradative enzymes (lipases, proteases and nucleases) → Irreversible cell death approx. 15 to 20 minutes from onset of injury –> possible sudden cardiac death

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

What will dramatically reduce morbidity and mortality from MIs?

A

reperfusion of the affected myocardium within a time period of 1 to 6 hours

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

Describe the gross and histopathology changes S/P Myocardial Infarction at
0 - .5 hours

A

Gross: None
Histopath: None

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

Describe the gross and histopathology changes S/P Myocardial Infarction at 0.5 - 4 hrs

A

Gross: Usu none
Histopath: GLYCOGEN DEPLETION, as seen with a PAS Stain and poss. waviness of myocardial fibers at borders

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

Describe the gross and histopathology changes S/P Myocardial Infarction at 4 - 12 hours

A

Gross: Slight mottling; Edematous, pale to sl. blue in color
Histopath: Initiation of COAGULATION NECROSIS, edema, hemorrhage

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

Describe the gross and histopathology changes S/P Myocardial Infarction at 12 - 24 hours

A

Gross: Dark mottling; Darker areas of hemorrhage appear deep blue or purple
Histopath: Ongoing coagulation necrosis, HYPEREOSINOPHILIA, contraction band necrosis in margins, beginning of neutrophil infiltration

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

Describe the gross and histopathology changes S/P Myocardial Infarction at 1 - 3 days

A

Gross: Infarct center becomes tannish-yellow (bruise-like)
Histopath: Continued coagulation necrosis, Loss of myocardial cell nuclei and striations, increased infiltration of NEUTROPHILS to interstitium

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

Describe the gross and histopathology changes S/P Myocardial Infarction at 3 - 7 days

A

Gross: Hyperemia at border with softening yellow-tan center, with decreased wall thickness and coagulation necrosis
Histopath: Beginning of DISINTEGRATION OF DEAD Mm FIBERS, necrosis of neutrophils, beginning of macrophage removal of dead cells at border

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

Describe the gross and histopathology changes S/P Myocardial Infarction at 10 - 30 days

A

Gross: Red-gray with depressed borders
Histopath: MATURE GRANULATION TISSUE with type I collagen

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

Describe the gross and histopathology changes S/P Myocardial Infarction at 2 - 8 weeks

A

Gross: Gray-white granulation tissue
Histopath: Increased COLLAGEN DEPOSITION, decreased cellularity

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

Describe the gross and histopathology changes S/P Myocardial Infarction at > 2 months

A

Gross: Completed scarring
Histopath: Dense COLLAGENOUS SCAR FORMED

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

How long after a MI are cardiac aneurysms most likely occur?

A

2-8 weeks due to formation of thin scar tissue

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

How does a drop in BP may be due to a massive heart attack cause a Pt to end up with pump failure?

A

With posterior or right sided infarct that is close to the R vagal N (which affects BP)

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

Appearance of an MI Pt

A

Pt may appear normal and entirely asymptomatic; OR quite anxious, agitated, pale and diaphoretic

30
Q

How to HTN and hypoTN relate to MIs?

A
  • Hypertension may precipitate a MI or reflect elevated catecholamines due to pain and anxiety
  • Hypotension: may indicate a large infarct; is frequently seen with R ventricular infarctions
31
Q

What are some risk factors for MIs?

A
  • Prior M.I. Hx
  • Positive fHx for M.I. (45- male or 55- female)
  • Tobacco use
  • HTN
  • Diabetes – pro inflamm endothelium
  • Metabolic syndromes (HTN, hyperglycemia, etc)
  • Sedentary lifestyle
  • Elevated serum homocysteine
  • Hip-to-waist ratio (adipose storage location)
32
Q

Most common age/demographics for MI

A

most frequently in persons > 45 years

At-risk populations < 45 years: cocaine users, insulin-dependent diabetics, pts with hypercholesterolemia, and those with a positive fHx for early coronary disease

33
Q

Fatalaties and MIs

A

> 50% of all deaths dt MI occur in the pre-hospital setting
10 % In-hospital
10% of M.I. related deaths occur in 1st post-infarction year

34
Q

What do ECG changes tell us about MIs?

A

changes may reflect a progression from ischemia to infarction; can reflect the location

MI’s resulting from total coronary occlusion are usu reflected by the Q-wave MI pattern (deeper and wider)

35
Q

What blood tests are used to rule in MI

A
  • Elevated WBC
  • Elevated LDH
  • Elevated cardiac enzymes: ↑Creatine phosphokinase (MB band) and ↑Troponin (esp. Troponins I and T)
36
Q

Describe a transmural infarction. What are the subclassifications?

A

Usu dt acute coronary thrombosis; associated with atherosclerosis involving major coronary artery.
Transmural infarcts extend through the whole thickness of the heart muscle, usu a result of complete occlusion of the area’s blood supply.
Subclassified into anterior, posterior, or inferior.

37
Q

Describe subendothelial (non-transmural) infarctions and a few contributing factors

A

Subendocardial infarcts are thought to be a result of locally decreased blood supply, possibly from a narrowing of the coronary arteries. The subendocardial area is farthest from the heart’s blood supply and more susceptible
o Coronaries narrowed, but patent
o Thrombotic occlusion → thrombolysis
o Limited period of time of ↑oxygen demand and/or decreased oxygen delivery
o HypoTN/HTN
o Anemia

38
Q

What are some potential (cardiac) complications of a myocardial infarction?

A
  • Dysrhythmia
  • Arrhythmia
  • Acute Valvular Dysfunction
  • CHF
  • Abnormalities in LV function
  • Cardiogenic Shock
  • Cardiac Rupture
  • Rupture of Ventricular Free Wall –> hemopericardium –> cardiac tamponade (usu fatal)
  • Ventricular Wall Rupture, VSD and acute mitral regurg
  • Hypotension
  • Hypoxemia
  • Pericarditis
  • Repeat MI
39
Q

Potential Non-cardiac Complications post MI

A
  • Aspiration
  • Infection i.e. pneumonia
  • Complications from prolonged immobilization (DVT or PE)
40
Q

What is an aneurysm

A

“ballooning out” of an a vessel wall due to underlying weakness of the wall and/or the force of increased BP

41
Q

Where do aneurysms occur?
What type of vessel are they most likely to occur in?
Which vessels have the greatest potential for increased morbidity and mortality?

A

may occur in any vessel, but arteries are more common than veins, and they occur often at branching points

Thoracic/Abdominal Aorta and the Circle of Willis = greatest potential for increased morbidity and mortality

42
Q

Where does a Berry aneurysm occur? What might a patient say to alert you?

A

Location: Circle of Willis at the base of the brain

“This is the worst headache of my life”

43
Q

How are aneurysms commonly treated?

A

a catheter is threaded into the area, a spring loaded device releases and occludes the neck to the aneurysm; a clip, collar or “staple” is used to decrease the size

44
Q

Through what layer does aortic dissection occur?

What is it a complication of and why is it important?

A

Dissection usually occurs through the medial tissue layer of the aorta and can affect the ascending aorta, the aortic arch, descending aorta and abdominal aorta. Dissection creates a “double lumen” effect within the aorta.

• Aortic dissection is an extremely severe and potentially life threatening complication of hypertension. If it results in rupture, Pts have an 80% mortality rate, and 50% of patients die before they even reach the hospital.

45
Q

What are a few risk factors for aortic dissection?

What must be achieved in a dissection due to HTN to increase surgical candidacy and likelihood of survival?

A

• Risk Factors: (severe) atherosclerosis, along with cystic medial necrosis and HTN

Dissection due to HTN: immediate BP control must be achieved for the patient to be a surgical candidate and to increase the likelihood of survival.

46
Q

What symptoms or findings might a Pt have with aortic dissection? What might these findings hint to you about location?

A

Sxs/Findings: Pt has excruciating pain resistant to tx with very large doses of morphine
Location:
- severe chest pain (for distal dissection)
- findings that suggest a stroke (with carotid dissection)
- or myocardial ischemia (with coronary dissection)

47
Q

What is CHF?

A

a condition in which the heart is unable to pump enough blood to meet the body’s metabolic requirements for oxygen and nutrients.

48
Q

In what ways does the heart normally try to compensate for increased demands?

A
  • Increasing the heart rate. (Faster)
  • Increasing the contractility of the ventricles. (Harder)

CHF begins to develop as the demands on the heart outstrip the normal range of physiologic compensatory mechanisms.

49
Q

How many Americans does CHF affect each year?

What is the 5 year mortality rate?

A

Congestive heart failure affects over 2 million Americans each year. Of these, some 300,000 will die as a direct or indirect result of their CHF.
The 5 year mortality rate from the time of diagnosis for men with C.H.F. is ~60% and ~45% for women. However, it is estimated that ~50% of patients with advanced cardiac failure will die within one year C.H.F.

50
Q

What is the ejection fraction of a fully functioning heart?

What is the ejection fraction of a person with CHF?

A

Normal: 55% - 70%
CHF: 40% or less

51
Q

How does contractility change in ischemic muscle fibers?

A

Ischemic muscle fibers lose their full elastic recoil forcing healthy muscle fibers to work harder in order to maintain adequate cardiac output.

52
Q

What are heart failure cells? Under what circumstances do you see them?

A

Hemosiderin containing macrophages in the alveoli (assoc with L ventricular failure)

Back flow of blood into the pulmonary circulation and resultant stasis of fluid within the lungs gives rise to heart failure cells

53
Q

Primary disorders of the heart that may result in C.H. F.

A

CAD
valvular disorders
cardiomyopathies

If these are Asx, the signs and symptoms of C.H.F. are often precipitated by an unrelated illness or stress

54
Q

Common precipitating factors to CHF

A
  • Cessation of one or more cardiac drugs such as a diuretic
  • Dysrythmias
  • Tachycardia –> angina

Other systemic factors that can contribute:

  • Increased metabolic rate (i.e. with fever)
  • Anemia
  • Hypoxia and anemia can decrease oxygen supply to the myocardium. (mountain climbing/Denver)
  • Respiratory and/or metabolic acidosis
  • Electrolyte imbalances

Even more “others”: viral and bacterial infections, and environmental, emotional or physical stresses that increase myocardial oxygen demand

55
Q

What type category of cardiac conditions is cardiac failure most common in? What are some of the common underlying conditions?

A

Cardiac failure is most common with cardiac conditions that result in decreased contractile properties of the heart.
Common underlying conditions include:
- inflammatory/degenerative muscle diseases
- atherosclerosis
- HTN
- myocardial ischemia & infarction

56
Q

Classic findings in CHF.

What are some common clinical manifestations?

A

Fatigue, coughing (< lying), peripheral swelling (edema) and weight gain are classic findings in CHF.

o The first manifestation of C.H.F. is usually tachycardia
o SOB or dyspnea: often worse w/ exertion or lying down
o Orthopnea
o paroxysmal nocturnal dyspnea: hallmark of more severe CHF

57
Q

How can you classify CHF?

A
  • Acute vs. chronic
  • Right vs. left
  • Compensated vs. Decompensated
  • Low output vs. High output
58
Q

What does compensated describe in terms of the heart?

A

Compensated = individual is able to bring the pump to a normal or near normal function; usu dt medications

59
Q

What is meant by ACUTE heart failure? (Hours - Days)

What is the mechanism?

A

the sympathetic nervous system and renin-angiotensin system act to maintain blood flow and pressure to the vital organs. Results in:

  • increased myocardial contractility
  • selective peripheral vasoconstriction (increased catecholamine)
  • salt and fluid retention (enhanced by dec hepatic metabolism of aldosterone) –> inc blood volume = inc venous return (preload)
  • and blood pressure maintenance.

• Decreased blood supply to the kidneys serves to activate the renin-angiotensin-aldosterone system.
• The RAA system causes renal arteriolar constriction, decreased glomerular filtration rate (G.F.R.) and increased reabsorption of Na
RESULT: fluid retention!

60
Q

What is meant by CHRONIC heart failure?

A

Myocardial cells eventually die from energy starvation and cytotoxic mechanisms –> necrosis or apoptosis!

NECROSIS/APOP: stimulates fibroblast proliferation –> replacement of myocardial cells with non-contractile collagen fibers –> development of increased ventricular wall thickness

61
Q

What is meant by HIGH-OUTPUT CHF?

A

Anything that causes the heart to maintain an accelerated rate (tachyarrhythmia) and rhythm over a sustained period of time can cause high output failure.
- generally characterized by peripheral VASODILATION and warm extremities.

Certain arrythmias such as atrial fibrillation can cause the heart rate to reach 200 to 300 or more beats a minute. At this rate, blood cannot efficiently empty the chambers.

62
Q

Causes of High-output CHF

A
  • Hyperthyroidism
  • Use of stimulants (cocaine, methamphetamines)
  • Anemia - low oxygen carrying capacty –> compensation
  • Paget’s disease: abnormal bone growth occurs dt greatly increased activity of osteoblasts. New bone has great vascularity and demands more oxygen.
63
Q

What is meant by LOW-OUTPUT CHF?

A

Occurs when heart contractibility has weakened (after MI or continued ischemia); ventricular dilation or hypertrophy.

  • generally characterized by peripheral vasoconstriction and cool extremities.
64
Q

Name a couple of causes of low-output CHF

A

o Infections of the heart (endocarditis and myocarditis)

o Late stage C.H.F.

65
Q

How are right-sided or left-sided CHF characterized in this class?

A

Pure left sided heart failure is generally associated with signs of pulmonary venous congestion
Pure right sided heart failure is associated with signs of systemic venous congestion.
*Failure of either ventricle can affect the function of the other, leading to a combination of both systemic and pulmonary venous congestion.

66
Q

What does the term cor pulmonale mean?

A

Start of the heart problems is from the lungs
• heart failure that occurs as a direct result of pulmonary disease such as emphysema (m/c), chronic bronchitis, pulmonary embolus or pulmonary hypertension.

67
Q

What is left-sided CHF?

A
  • the inability of the left ventricle to produce adequate stroke volume to overcome resistance –> decreased cardiac output
  • Left sided C.H.F. can lead to pulmonary congestion due to increased left ventricular end-diastolic pressure and increased left-atrial pressure.
68
Q

Left sided heart failure is most often caused by…

A

o Ischemic heart disease (LV infarction)
o HTN
o Aortic and mitral valvular disease
o Non-ischemic myocardial diseases

69
Q

What is right-sided CHF? What causes isolated Right CHF?

What is the most common cause of Right-sided CHF?

A

• C.H.F. caused by ineffective right ventricular contraction

Isolated = fairly uncommon. Acute conditions such as right ventricular infarction or pulmonary embolus can result in isolated right sided C.H.F. Cor pulmonale.

M/C cause of right C.H.F. is left sided C.H.F.

70
Q

What causes ACUTE and CHRONIC cor pulmonale?

A

Acute: - Massive pulmonary embolization, Exacerbation of chronic cor pulmonale

Chronic: - COPD, Increased pulmonary BP due to left ventricular insufficiency (backward failure), loss of lung tissue following trauma or surgery, end stage pneumoconiosis, pulmonary sarcoidosis, obstructive sleep apnea and bronchopulmonary dysplasia (in infants)

71
Q

Describe the gross and histopathology changes S/P Myocardial Infarction at 7 - 10 days

A

Gross: Maximally soft lesion with yellow to reddish-tan borders/margins
Histopath: increased PHAGOCYTOSIS OF DEAD CELLS at border, beginning of granulation tissue formation at margins

Pathology III (2 decks)

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