Brainscape's Knowledge GenomeTM

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


See full index

USMLE Pathoma > Cardiac pathology part 1 Angina/MI/CHD > Flashcards

Cardiac pathology part 1 Angina/MI/CHD Flashcards

1
Q

Describe the pathophysiology of a stable angina

A

Chest pain lasting less than 20 minutes that’s triggered by emotional/physical stress

Signs:
- Chest pain radiating to the left arm or jaw
- Diaphoresis
- Shortness of breath
- Depressed ST segments

Rx with rest or nitroglycerin

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

A 45 yr old man with a BMI of 30 took up running for his new years resolution. He suddenly collapsed complaining of chest pain radiating down his left arm.
Upon arrival to the hospital patient has diaphoresis & shortness of breath but he exclaimed he felt “fine now & wanted to go home”. What’s the next best step in treatment? What did the patient likely suffer?

A

Next best step would be to do an ECG to assess whether this patient had an MI or angina

If results show ST depression = Stable angina

If results show ST elevation & significant Q waves = MI

Because the Chest pain was short acting it’s likely the patient has a stable angina

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

Describe the pathophysiology of an unstable angina

A

Chest pain that presents at rest. It usually happens because of an atherosclerotic plaque rupture with thrombosis

Signs:
ST Depression
Chest pain at rest

Rx with nitroglycerin

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

What is a major concern when treating a patient experiencing an unstable angina?

A

There’s a high risk of it progressing to an MI which is irreversible (necrosis)

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

Describe the pathophysiology of a prinzemetal angina

A

Episodic chest pain that happens when platelets release more thromboxane A2 which cause vasospasm in the coronary arteries

Signs:
ST Elevation
Episodic chest pain

Rx Nitroglycerin or Calcium channel blockers

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

What are the causes of an MI?

  • Most common
  • Other
A

MC = Rupture of atherosclerotic plaques

Other:
- Vasospasms (prinzmetal angina, cocaine, emboli, vasculitides i.e Kawasaki’s)

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

Signs of an MI

A
  • Severe & crushing chest pain that lasts longer than 20 minutes (radiates to left arm &/or jaw)
  • Diaphoresis
  • Dyspnea
    (symptoms won’t be relieved with nitroglycerin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

60 yr old woman is brought the ER complaining of crushing chest pain that radiates to her jaw. The team administers nitroglycerin but to no effect. What is the next course of action?

A

No relief of symptoms means this is likely an MI, administer:
- Aspirin/heparin
- Supplemental O2
- Nitrates
- B-blockers
- ACE inhibitors

Team should prep for fibrolysis or angioplasty while confirming the diagnosis with an ECG via ST elevation and significant Q waves

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

Crushing/severe chest pain radiating to the left arm or jaw that lasts longer than 20 minutes (don’t wait to find out though!)
Diaphoresis
Dyspnea
(symptoms won’t be relieved with nitroglycerin)

A

signs of an MI

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

What part of the heart is typically affected in an MI & what are the arteries involved?

A

1. LAD (most common, infarcts the anterior wall of the LV)

Typically, it’s the left ventricle.

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

MI’s can involve complete occlusion of the LAD, RCA & Circumflex artery (most common in that order) what areas of the LV are infarcted in each of these cases?

A

1. LAD (most common, infarcts the anterior wall of the LV)

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

How does an MI present as initially (ECG) then what are the changes as it progresses?

A

Initially MIs have subendocardial necrosis involving less than half of the heart wall & ST Depression

If the ischemic damage progresses to transmural necrosis (all the heart wall) there will be ST Elevation

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

MI Timeline:

What would you expect to see 2-4hrs post MI? What are the potential complications?

A

Elevated troponin

Comps:
- Cardiogenic shock
- Congestive heart failure
- Arrythmia

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

MI Timeline:

What would you expect to see 7-10 days post MI? What are the potential complications?

A

Normalized troponin levels
Granulation tissue (macrophages, fibroblasts, collagen, & blood vessels)

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

MI Timeline:

What would you expect to see 4-6hrs post MI? What are the potential complications?

A

Elevated CK-MB
Dark discoloration
Coagulative necrosis

Comps:
- Arrythmia

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

MI Timeline:

What would you expect to see 4-24hrs post MI? What are the potential complications?

A

Dark discoloration
Coagulative necrosis

Comp:
Arrythmia

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

MI Timeline:

What would you expect to see 1-3 days post MI? What are the potential complications?

A

Lots of neutrophils **
Yellow pallor

Comp:
Fibrous pericarditis (chest pain + friction rub)

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

MI Timeline:

What would you expect to see 4-7 days post MI? What are the potential complications?

A

Lots of macrophages
Yellow pallor

Comp:
- Cardiac tamponade (rupture)
- Shunt (ruptured IV septum)
- Mitral insufficiency (ruptured papillary muscles)

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

How old is the MI?

A

1-2 hrs old the wavy fibers are necrotic myocytes

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

How old is the MI?

A

18-24 hrs

Coagulative necrosis
Eosinophilia
Contraction band necrosis (reperfusion injury)

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

How old is the MI?

A

1-3 days (24-72hrs)

Complete coagulative necrosis with neutrophil infiltration and fragmentation

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

How old is the MI?

A

4-7 days

Macrophages with granulation tissue at the edges of the infarct
No more neutrophils & the walls are weakened at this point

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

How old is the MI?

A

4-7 days old you can see the central pallor & hyperemic border

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

MI Timeline:

What would you expect to see 1-3 weeks post MI? What are the potential complications?

A

A red border with granulation tissue (fibroblasts, collagen, & blood vessels)

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

MI Timeline:

What would you expect to see Months post MI? What are the potential complications?

A

White scar tissue & fibrosis

Comps:
- Aneurysm
- Mural thrombosis
- Dressler’s syndrome

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

What treatment(s) option for an MI would reduce the risk of thrombosis?

A

Aspirin & Heparin

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

What treatment(s) option for an MI would minimalize ischemic damage?

A

Supplemental oxygen

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

What treatment(s) option for an MI would help dilate veins & the coronary artery to reduce BP?

A

Nitrates

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

What treatment(s) option for an MI would reduce heart rate & oxygen demand by the heart?

A

Beta blockers

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

What treatment(s) option for an MI would reduce LV dilation?

A

ACE inhibitors

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

What treatment(s) option for an MI are useful for opening up blockages & what is the major drawback?

A

Fibrinolysis & angioplasty both help open up the occluded blood vessel but have significant risk of a reperfusion injury

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

A young patient with Downs syndrome dies suddenly, the physician suspects a cardiomyopathy… why?

A

Down syndrome is associated with ostium primum defect (whole between the atria) meaning an embolus may have formed & passed into systemic circulation i.e the brain

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

What is sudden cardiac death and what causes it? (most common & other)

A

When death follows within an hour of symptoms onset (chest pain etc)

Common:
- Ventricular arrythmia (Ischemia due to atherosclerosis is a risk)

Other:
- MVP
- Cocaine
- Cardiomyopathy

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

Describe the pathophysiology of Left-sided CHF

A

The heart can’t pump blood into systemic circulation well, so there’s backflow into the pulmonary circulation. Overall there’s not enough blood in systemic & too much in pulmonary. This means pulmonary experiences congestion while systemic organs are at risk of ischemia

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

What are the causes of Left-sided CHF?

A

Ischemic damage to the heart
Hypertension
Dilated cardiomyopathy
MI
Restrictive cardiomyopathy

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

What are the clinical symptoms of someone with left-sided CHF?

A

Pulmonary edema:
- dyspnea
- paroxysmal nocturnal
dyspnea
-Orthopnea
- Cracking lungs

Reduced blood flow to kidneys
- Activated RAAS = high BP

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

What medication is used to treat left-sided CHF?

A

ACE inhibitors to lower BP

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

Describe the pathophysiology of right-sided CHF? What causes it?

A

It’s usually caused by left-sided CHF, which causes congestion in the systemic circulation

It can also be caused by
- Left-to-right shunts
- Chronic lung disease (cor pulmonale)

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

What are the clinical signs of Right-sided CHF?

A

Increased JVD
Painful hepatosplenomegaly
aka Nutmeg liver
Pitting edema (lots of hydrostatic pressure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q
  • Chest pain that radiates to the L.arm or jaw (lasting less than 20min)
  • Triggered by exertion or emotional stress
  • Diaphoresis
  • SOB
A

Stable angina

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

What is the classical presentation of a Stable angina?

A
  • Chest pain that radiates to the L.arm or jaw (lasting less than 20min)
  • Triggered by exertion or emotional stress
  • Diaphoresis
  • SOB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What would you expect on an EKG reading for a stable angina? Why?

A

ST depression, because subendocardial ischemia reduces conductivity in the heart)

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

A 60yr old man presents with chest pain that radiates to his jaw. He said he was gardening in the hot sun. He’s sweating & is short of breath, he states after sitting down he feels better. He recounts he’s experienced brief episodes like this before & that they never last long.

  1. What is the likely diagnosis?
  2. What would his EKG show?
  3. What would you administer to relieve his symptoms?
  4. Which artery is affected & what is the major cause of this condition?
A
  1. Stable angina
  2. ST depression
  3. Nitroglycerin
  4. Narrowing of the Coronary artery likely caused by atherosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the signs of an unstable angina?

A
  • Chest pain at rest that radiates to the L.arm or jaw (<20min)
  • Diaphoresis
  • SOB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What would you expect on an EKG reading for a stable angina? Why?

A

ST depression (subendocardial ischemia)

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

What condition is likely to cause an unstable angina ?

A

Atherosclerosis with thrombosis causing incomplete occlusion of the coronary artery

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

What is a major concern regarding the sequelae of an unstable angina?

A

It has a high risk of progressing to an MI

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

How would you treat an unstable angina?

A

Give nitroglycerin (a vasodilator) to reduce preload/work the heart has to do

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

What is the clinical presentation of a prinzmetal angina?

A
  • Episodic chest pain that radiates to the L.arm/jaw (<20min)
  • Diaphoresis
  • SOB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What would you expect to see on an EKG in a person with Prinzmetal angina?

A

ST elevation because it has transmural ischemia (all layers of the heart)

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

How would you treat a prinzmetal angina?

A

Give nitroglycerin (reduce preload) & Ca2+ channel blockers

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

What causes a prinzmetal angina?

A

Vasospasms of the coronary artery

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

What are the key signs of an MI?

A
  • Crushing/severe chest pain radiating to the L.arm & jaw lasting longer than 20min
  • Diaphoresis
  • SOB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is the most common cause of an MI?

A

Rupture of an atherosclerotic plaque causing complete occlusion of the coronary artery

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

Which part of the heart does an MI typically impact?

A

The left ventricle (other parts are usually spared because the coronary artery feeds the LV most)

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

What are the less common causes of MI’s?

A

MVP
Cardiomyopathies
Cocaine abuse
Vasospasms

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

How do you treat an MI?

A

Aspirin/heparin
ACE inhbitors
B-blockers
Nitrates
Supplemental O2

(Nitroglycerin won’t help)

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

Describe the features of the initial phase of an MI

A

It starts with subendocardial necrosis of less than 50% of the myocardial thickness & the EKG shows ST depression

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

Describe the features of the late phase of an MI

A

It progresses to transmural necrosis affecting the entirety of the myocardial thickness & EKG shows ST elevation, it can cause heart failure!

60
Q

Troponin labs post Mi:

How soon does it rise?
When does it peak?
When does it normalize?

A

rise 2-4hrs
peak 24hrs
lasts7-10 days

61
Q

What surgical procedures can be preformed to treat an MI? What are the major complications associated with each one?

A
  1. Fibrinolysis (risk Ca2+ overload causing contractile band necrosis)
  2. Angioplasty (opening blocked BV risks a reperfusion injury)
62
Q

What can cause left sided heart failure?

A

Ischemia
HTN
Dilated cardiomyopathy
MI
Restrictive cardiomyopathy

63
Q

What are the clinical signs of Left sided heart failure?

A

Decreased forward perfusion(less sys. cir.):

  • Reduced blood to kidneys causing increased RAAS (high renin, aldosterone, & BP)

Pulmonary congestion causing pulmonary edema:

  • Dyspnea
  • Paroxysmal nocturnal dyspnea
  • Orthopnea
  • Crackles
  • Hemoptysis
64
Q

What is a key histological finding of L. HF?

A

Hemosiderin-laden macrophages due to increased alveolar pressure causing rupture & hemoptysis (rusty sputum)

65
Q

How would you treat L. HF?

A

ACE inhibitors

66
Q

What are the causes of Right sided heart failure?

Most common
Less common

A

Most common: L. HF

Less common:
- left-to-right shunt
- chronic lung diseas (cor pulmonale)

67
Q

What are the clinical signs of R. HF?

A

JVD
Nutmeg-hepatosplenomegaly (painful!)
Pitting edema (high hydrostatic pressure)

68
Q

JVD
Nutmeg-hepatosplenomegaly (painful!)
Pitting edema (high hydrostatic pressure)

Are signs of ______

A

Right-sided HF

69
Q

Explain what a ventricular septal defect (VSD) is & what is it associated with?

A

A defect in the intraventricular septum that is associated with FAS.

It causes a right-left shunt between the ventricles that’s usually asymptomatic at birth (except when it’s large)

70
Q

What is a complication of a very large VSD?

A

Eisenmenger syndrome

71
Q

How do you treat/fix a VSD

A

Either surgery or if it’s small it can close on its own

72
Q

What’s the congenital heart defect?

A

VSD

73
Q

What is the most common congenital heart defect?

A

VSD

74
Q

Explain what an Atrial Septal Defect is & what is it associated with?

A

A defect in the atrial septum that present in two ways:

90% of cases = ostium secundum
Down syndrome = ostium primum

Both result in left-to-right shunting & and S2 split (more blood in the right atrial delays the pulmonary artery from closing)

75
Q

What is a major complication of an ASD?

A

A paradoxical embolism

76
Q

What is the congenital heart defect? & what are the findings?

A

ASD

Left-to-right shunting & S2 split

77
Q

Explain what an Patent Ductus Arteriosus (PDA) is & what is it associated with?

A

It’s when the arteriosus didn’t close during development resulting in a left-to-right shunt between the aorta & pulmonary artery

It’s associated with congenital rubella

78
Q

How does PDA clinically present?

A

At birth it is usually asymptomatic with a machine-like murmur that can lead to Eisenmenger syndrome

79
Q

How do you treat/fix PDA?

A

Administer Indomethacin to decrease PGE (to decrease the patency of PDA) & close the PDA opening

80
Q

What’s the congenital heart defect? What condition is it associated with?

A

PDA (machine murmur) & it’s associated with congenital rubella

81
Q

Explain what a Tetralogy of Fallot is & what is it associated with?

A

It’s a combination of many structural defects including:
- R. ventricular stenosis & hypertrophy
- VSD
- Aorta that overrides the VSD

It results in Right-to-left shunting & early cyanosis (depending on the degree of stenosis)

82
Q

What is the congenital heart defect?

A

Tetralogy of Fallot

83
Q

What are the key signs of Tetralogy of Fallot?

A

Boot shaped heart (hypertrophy)
Cyanotic spells

84
Q

How do patients with Tetralogy of Fallot cope with cyanotic spells?

A

They learn to squat, this increases their peripheral arterial resistance to reduce shunting and keep more blood oxygenated

85
Q

Explain what a Truncus Arteriosus is?

A

The truncus didn’t divide so there’s ONE large vessel acting as the aorta & pulmonary artery, this means O2 rich & poor blood mix before reaching systemic or pulmonary circulation (mixer)

Shows early cyanosis

86
Q

What’s the congenital heart defect?

A

Truncus arteriosus

87
Q

Explain what a Tricuspid Atresia is & what is it associated with?

A

It’s when the tricuspid valve orifice doesn’t develop & the right ventricle is hypoplastic,
resulting in a right-to-left shunt.

It’s associated with ASD

A warning sign is early cyanosis

88
Q

What is the congenital heart defect? What is it associated with

A

A Tricuspid Atresia & it’s typically associated with an ASD

89
Q

Explain what a Coarctation of the aorta is?

A

It’s narrowing of the aorta, it presents in two forms:

Infantile= It’s associated with a PDA & the coarctation is after the aortic arch but before a PDA

Adult= It may be associated with a bicuspid aortic valve& the coarctation sits after the aortic arch

90
Q

What are the symptoms of an infantile coarctation of the aorta? What conditions is it associated with?

A

Cyanosis in the lower extremities & it’s associated with PDA & Turners syndrome

91
Q

What are the symptoms of an adult coarctation of the aorta? What condition is it associated with?

A
  1. Hypertension in the upper extremities
  2. Hypotension & weak pulse in the lower extremities
  3. Collateral circulation in the intercostal arteries
  4. Engorged arteries

Associated with a bicuspid aortic valve

92
Q

What’s the congenital heart defect? What is particularly unique about it?

A

Coarctation of the aorta & it has an adult and infantile form!

93
Q

Describe what Acute Rheumatic fever is

A

A systemic complication of strep throat (pharyngitis) caused by group A B-hemolytic streptococci that usually effects 2-3yr olds

94
Q

Describe the MOA of the bacteria involved in Acute Rheumatic fever

A

The group A B-hemolytic streptococci cause ARF via molecular mimicry with their M-proteins to cause the reaction

95
Q

Acute Rheumatic fever is diagnosed by the Jones criteria split into major & minor symptoms. What are the major criteria needed for a diagnosis?

A
  1. The presence of elevated ASO or Anti-DNase B Titres
  2. Migratory polyarthritis (joint swelling that moves aroud)
  3. Pan carditis
    - Endocarditis of mitral valve vegetation + regurgitation
    - Myocarditis with Aschoff bodies
    - Pericarditis with friction rub & chest pain
  4. Subcutaneous nodules
  5. Erythema marginatum (rash on trunk/limbs)
  6. Sydenham chorea (invol movements)
96
Q
  1. The presence of elevated ASO or Anti-DNase B Titres
  2. Migratory polyarthritis (joint swelling that moves around)
  3. Pan carditis
    - Endocarditis of mitral valve vegetation + regurgitation
    - Myocarditis with Aschoff bodies
    - Pericarditis with friction rub & chest pain
  4. Subcutaneous nodules
  5. Erythema marginatum (rash on trunk/limbs)
  6. Sydenham chorea (invol movements)

Are all signs of which cardiac-related condition?

A

Acute rheumatic fever

97
Q

What are the minor symptoms of acute rheumatic fever?

A

Fever & Elevated ESR

98
Q

What is the major COD in acute rheumatic fever?

A

Myocarditis

99
Q

What is the major concern with acute rheumatic fever?

A

With repeated exposure to the bacteria it can progress to chronic rheumatic heart disease

100
Q

Describe what Chronic Rheumatic Heart Disease is

A

It’s when chronic inflammation from the body’s reaction to group A B-hemolytic Strep. causes scarring on the heart valves most commonly the Mitral but sometimes the aortic valve too

101
Q

What happens to the heart if the Mitral valve is scarred by CRHD?

A

The chordae tendinea thicken to compensate

102
Q

What happens to the heart if the Aortic valve is scarred by CRHD?

A

The commissures end up fusing together

103
Q

What is a concerning complication of Chronic Rheumatic HD?

A

Infectious endocarditis

104
Q

What is aortic stenosis? What changes in the heart does it cause?

A

A narrowed/stiff aortic valve that results in less blood being ejected from the LV it causes the following cardiac changes:

  1. LV Hypertrophy (increase EF%)
  2. Angina + Syncope with exercise (less blood flow)
  3. Microangiopathic hemolytic anemia (stiff valve damages RBC’s =schistocytes)
105
Q

What are the causes of aortic stenosis?

Common
Uncommon

A

Common: Fibrosis & Calcification of the valve due to wear & tear from age (60+yrs) or if someone has a bicuspid aortic valve

Uncommon: Chronic Rheumatic valve disease (valve scarring)

106
Q

What are the signs of Aortic stenosis?

A

The compensations from the heart cause:
1. Systolic ejection click followed by a crescendo-decrescendo murmur

107
Q

Explain Aortic regurgitation

A

When the aortic valve “leaks” blood back into the L.ventricle during diastole resulting in LV dilation & hypertrophy (because of volume overload)

108
Q

What are the causes of Aortic regurgitation?

Most common
Other

A

MC: Aortic root dilation (from either syphilis or aortic dissection)

Other: Valve damage (inf. endocarditis)

109
Q

What are the signs of Aortic regurgitation?

A
  1. An early-blowing diastolic murmur
  2. Hyperdynamic Circulation:
  • Different pulse pressures between systolic (higher because increased stroke vol) & diastolic (lower because of regurgitation)
  • Bounding pulse “Water-hammer pulse”
  • Quincke pulse (pulsing nail-beds)
  • Head bobbing
110
Q
  1. An early-blowing diastolic murmur
  2. Hyperdynamic Circulation:
  • Different pulse pressures between systolic (higher because increased stroke vol) & diastolic (lower because of regurgitation)
  • Bounding pulse “Water-hammer pulse”
  • Quincke pulse (pulsing nail-beds)
  • Head bobbing

Are signs of which condition?

A

Aortic regurgitation

111
Q

Patient presents with an early blowing diastolic murmur

What is the condition?

A

Aortic regurgitation

112
Q

A patient presents with a systolic ejection click followed by a crescendo-decrescendo murmur. On exam they have LV hypertrophy & reduced Ejection fraction.

What’s the condition?

A

Aortic stenosis

113
Q

A patient presents with a fish-mouth valve due to stenosis, what is this condition caused by?

A

Chroic rheumatic heart disease

114
Q

How would you treat aortic regurgitation?

A

Replace the valve once there is evidence of L. Ventricular dysfunction

115
Q

Explain what Mitral valve prolapse (MVP) is?

A

There is ballooning of the mitral valve into the L. atrium during systole resulting in a mid-systolic click followed by a regurgitation murmur

116
Q

What are the causes of an MVP?

A

It’s due to myxoid degeneration (accumulation of ground substance) of the valve which makes it very floppy

117
Q

What are the signs of MVP?

A

It’s usually asymptomatic, except for the mid-systolic click followed by a regurgitation murmur

118
Q

What happens to a patient with MVP if they squat down?

A

Their mid-systolic click will be softer sounding because the increase in peripheral resistance decreases the L. ventricular emptying

119
Q

What are the complications of MVP?

A

Infectious endocarditis
Arrythmia
Severe mitral regurgitation

120
Q

How do you treat MVP?

A

Valve replacement

121
Q

Which syndromes are associated with MVP?

A

Marfans & Elher Danlos

122
Q

Patient presents with A mid-systolic click followed by a regurgitation murmur, they otherwise appear normal, what’s the condition?

A

MVP

123
Q

Explain what mitral regurgitation is?

A

When the mitral valve leaks blood back into the L. atrium during systole, resulting in volume overload

124
Q

What causes Mitral regurgitation?

Common
Other

A

Common: A complication of MVP

Other:
Infective endocarditis
Acute rheumatic heart disease
Papillary muscle rupture post MI

125
Q

What are the signs of Mitral regurgitation?

A

Holocystic “blowing” murmur that is LOUDER when squatting (the increase in systemic resistance decreases the L. ventricular emptying)

126
Q

Explain what mitral valve stenosis is?

A

A narrowed mitral valve resulting in an opening snap & diastolic rumble

127
Q

What causes Mitral valve stenosis?

A

Chronic rheumatic valve disease

128
Q

What are the signs of mitral valve stenosis?

A
  1. An opening snap followed by a diastolic rumble
  2. Volume overload causing a dilated L. atrium
    - Pulmonary congestion & edema with alveolar hemorrhaging (hemoptysis)
    - Pulmonary hypertension with right-sided HF
    - A fibrillation with increased risk of a mural thrombi
129
Q
  1. An opening snap followed by a diastolic rumble
  2. Volume overload causing a dilated L. atrium
    - Pulmonary congestion & edema with alveolar hemorrhaging (hemoptysis)
    - Pulmonary hypertension with right-sided HF
    - A fibrillation with increased risk of a mural thrombi

Are all signs of which condition?

A

Mitral stenosis

130
Q

Patient has an opening snap followed by a diastolic rumble

A

Mitral stenosis

131
Q

Explain what you would expect to see 0-4hrs post MI for the following:

Complications

A

Cardiogenic shock (if the infarct was massive)

Congestive heart failure

Arrythmia

132
Q

Cardiogenic shock (if the infarct was massive)

Congestive heart failure

Arrythmia

No changes in gross/microscopic appearance

How old is the MI?

A

0-4hrs

133
Q

Explain what you would expect to see 4-24hrs post MI for the following:

Gross
Microscopic
Complications

A

Gross:
Dark discoloration

Microscopic:
Coagulative necrosis (pyknosis, karyorrhexis, & karyolysis)

Complications:
Arrythmia

134
Q

Gross:
Dark discoloration

Microscopic:
Coagulative necrosis (pyknosis, karyorrhexis, & karyolysis)

Complications:
Arrythmia

How old is the MI?

A

4-24hrs

135
Q

Explain what you would expect to see 1-3 days post MI for the following:

Gross
Microscopic
Complications

A

Gross:
Yellow pallor (WBCs)

Microscopic:
Neutrophils

Complications:
Fibrinous pericarditis (neutrophils trigger inflammation, it presents as friction rub & chest pain)

136
Q

Gross:
Yellow pallor (WBCs)

Microscopic:
Neutrophils

Complications:
Fibrinous pericarditis (neutrophils trigger inflammation, it presents as friction rub & chest pain)

Describes an MI that is how old?

A

1-3 days

137
Q

Explain what you would expect to see 4-7 days post MI for the following:

Gross
Microscopic
Complications

A

Gross:
Yellow pallor (WBCs)

Microscopic:
Macrophages (weakest walls)

Complications = Ruptures!
1. Rupture ventricular wall (cardiac tamponade)
2. IVS rupture (shunt)
3. Papillary muscle rupture (MVP)

138
Q

Gross:
Yellow pallor (WBCs)

Microscopic:
Macrophages (weakest walls)

Complications = Ruptures!
1. Rupture ventricular wall (cardiac tamponade)
2. IVS rupture (shunt)
3. Papillary muscle rupture (MVP)

Describes an MI that is how old?

A

4-7 days

139
Q

Explain what you would expect to see 1-3 wks post MI for the following:

Gross
Microscopic

A

Gross:
Red borders (granulation tissue) along the infarct

Microscopic:
Granulation tissue (fibroblasts, collagen, & blood vessels) aka the scaffold for a scar

140
Q

Gross:
Red borders (granulation tissue) along the infarct

Microscopic:
Granulation tissue (fibroblasts, collagen, & blood vessels) aka the scaffold for a scar

Are indicative of an MI that is how old?

A

1-3wks

141
Q

Explain what you would expect to see 1 month & up post MI for the following:

Gross
Microscopic
Complications

A

Gross:
White scarring (weaker then myocardium)

Microscopic:
Fibrosis

Complications:
1. Aneurysm
2. Mural thrombus (harder wall damaged RBCs)
3. Dressler’s syndrome (Abs vs our own pericardium 6-8wks post MI)

142
Q

Gross:
White scarring (weaker then myocardium)

Microscopic:
Fibrosis

Complications:
1. Aneurysm
2. Mural thrombus (harder wall damaged RBCs)
3. Dressler’s syndrome (Abs vs our own pericardium 6-8wks post MI)

Describes the features of an MI that is how old?

A

1+ months old

143
Q

What is SCD (sudden cardiac death) & what is it associated with?

A

It’s when death happens suddenly without symptoms or within an hour of symptom onset. It’s usually from fatal arrythmia & is often associated with
1. Atherosclerosis (90% cases)
2. MVP
3. Cardiomyopathies- vasospasms
4. Cocaine

144
Q

What are the 3 most common arteries occluded in an MI & what parts of the heart do they effect respectively?

A

1: LAD (L.V ant wall & ant IVS)

145
Q

What’s the difference between the initial phase vs later phase of an MI?

A

Initially there is a subendocardial infarct of <50% of the myocardial thickness causing ST depression

Later there is transmural infarction causing ST elevation

146
Q

CK-MB:

Rises
Peaks
Lasts

A

Rises 4-6hrs
Peaks 24hrs
Normalizes 72hrs

147
Q
A

USMLE Pathoma (20 decks)

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