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DMD 5247 > Bikman - Heart Path > Flashcards

Bikman - Heart Path Flashcards

1
Q

What is heart failure? Early and final stages?

A

Heart cannot pump blood sufficient to meet body’s needs. Generally occurs on one side.

Early stages, compensations can occur:

  • Catecholamines
  • Frank-Starling mechanism
  • Hypertrophy

Eventually:
- Ischemia

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2
Q

What is the Frank-Starling mechanism?

A

The more time the heart has to fill, the stronger it will contract

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3
Q

Where does R heart failure manifest?

A

Below the heart

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4
Q

Where does LHF (left heart failure) manifest?

A

Above the heart

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5
Q

What are some common causes of LHF?

A
  • Systemic hypertension
  • Mitral or aortic valve disease
  • Primary heart diseases
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6
Q

What are some heart changes observed in LHF?

A
  • LV hypertrophy**
  • LV dilation
  • LA may be enlarged
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7
Q

What are some consequences of LHF?

A
  • Dyspnea - hard time breathing
  • Orthopnea - hard time breathing in certain positions
  • Enlarged heart, increased HR
  • Rales - fluid accumulating in lung space
  • Mitral regurgitation, systolic murmur
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8
Q

What are some common causes of RHF (right heart failure)?

A
  • Cor Pulmonale ( HF due to lung failure)

- Some congenital heart diseases

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9
Q

What are some heart changes observed in RHF?

A
  • RV hypertrophy
  • RV dilation
  • RA may be enlarged
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10
Q

What are some consequences of RHF?

A
  • Peripheral edema
  • Hepatomegaly
  • Splenomegaly
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11
Q

Outline the series of events that cause cor pulmonale.

A

HF due to lung failure, causing RHF.
RV enlargement due to pulmonary hypertension (from primary lung disorder).

There is less O2 in the alveolar capillaries, causing alveolar constriction. The R side of the heart has to do more work since the alveoli constriction increases pressure.

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12
Q

What are the 3 categories of congenital heart disease and what diseases fall under each category.

A

Left to right (L2R)

  • ASD
  • VSD
  • PDA

Right to left (R2L)

  • Tetralogy of Fallot
  • Transposition of great arteries

Coactation
- Aortic coarctation

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13
Q

Atrial Septal Defect (ASD)

A

Too much blood going to the lungs

  • May cause pulmonary hypertension
  • Sending too much blood to the lungs
  • Mixing of oxygenated and deoxygenated blood
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14
Q

Ventricular Septal Defect (VSD)

A

Too much blood going to the lungs

  • Most common
  • Most close spontaneously
  • Size and location matters
  • The higher towards the base the defect is, the more problematic it will be with mixing of blood
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15
Q

Patent Ductus Arteriosus (PDA)

A

Too much blood going to the lungs

  • Allows flow from PA to aorta in the fetus
  • Generally closes by day 2 of life
  • Size matters
  • Moving blood from the aorta and into the pulmonary arteries
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16
Q

Tetralogy of Fallot

A

Most common cause of cyanotic congenital heart disease.

  1. VSD
  2. Pulmonary stenosis
  3. Overriding aorta
  4. RV hypertrophy

All 4 of these phenomena happen together

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17
Q

Transposition of great arteries

A

Requires atrial or ventricular shunt to live.

Embryonic lethal in absence of shunt

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18
Q

Coarctation

A

Aortic coarctation.

  • Narrowing of aorta
  • Causes cyanosis and low BP systematically
  • Size of blockage matters
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19
Q

What is Ischemic Heart Disease and what are the 4 conditions associated with it? How is the coronary artery blood flow reduced?

A

Usually a result of reduced coronary artery blood flow.
Myocardial perfusion can’t meet demand.
- By thrombus
- Critical stenosis

  1. Angina pectoris
  2. Acute MI
  3. Chronic IHD
  4. Sudden cardiac death
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20
Q

What is Angina Pectoris and what are the three types?

A

Ischemic heart disease.
Intermittent chest pain.

  1. Stable
    - Most common
    - Pain on exertion
    - Fixed narrowing of CA
  2. Prinzmetal (variant)
    - Pain at rest
    - CA spasm
  3. Unstable (pre-infarction)
21
Q

What is acute MI and what are clinical features?

A

Ischemic heart disease.
Necrosis of myocardium from ischemia.

  • Affects 1.5M/year.
  • Mostly due to CA thrombosis <20-30min
  • Prompt reperfusion can salvage myocardium

Clinical Features:

  • Severe, crushing chest pain
  • Not relieved by nitroglycerin
  • Sweating, nausea
22
Q

Elevation of what molecule precedes acute MI and why?

A

CK-MB increases within 2-4hrs, returns to normal within 72 hours.

Cardiomyocytes have a lot of CK-MB, so if they are damaged, CK-MB spills out of cells.

23
Q

What gross changes may be absorbed with acute MI?

A
  • Mottling - coagulation necrosis
  • Mottling - coagulation necrosis; neutrophils come in
  • Yellow infarct center - Neutrophils die, macrophages come to eat dead cells
  • Yellow center, red borders - granulation tissue
  • Scar - collagen
24
Q

What are the two types of acute MI?

A
  1. Subendocardial infarction
    - Affects 1/3-1/2 of heart wall
    - Inner wall more affected because blood supply goes first to outer wall
  2. Transmural infarction
    - Affects more than 1/2 of heart wall
    - More serious
25
Q

Chronic IHD

A

Ischemic heart disease.

Accumulation of small ischemic insult leads to mechanical failure.

26
Q

Sudden Cardiac Death

A

Ischemia heart disease.

Often a result of a lethal arrhythmia without myocyte necrosis.

27
Q

Hypertensive heart disease

A

Can affect L ventricle (systemic) or R ventricle (pulmonary)

Cor pulmonale is RV enlargement due to pulmonary hypertension (from primary lung disorder)

28
Q

Valvular stenosis

A

Failure to open

29
Q

Valvular insufficiency/regurgitation

A

Failure to close

30
Q

What conditions can valvular heart disease be the cause of?

A
  • Murmurs
  • Angina
  • CHF
  • Fainting
31
Q

What five conditions are associated with valvular heart disease?

A
  1. Valvular stenosis - narrowing of valves
    - Aortic stenosis
    - Mitral stenosis
  2. Valvular regurgitation - leakage of valves
    - Aortic regurgitation
    - Mitral regurgitation
  3. Rheumatic valvular disease
  4. Mitral valve prolapse syndrome
  5. Infective endocarditis
32
Q

What is aortic valve stenosis and what are its manifestations? Do we hear it during systole or diastole?

A

Stiffening and narrowing of the aortic valve.

  • Blood has difficulty exiting the heart
  • Prolonged ejection sound

Clinical Manifestations:

  • Crescendo-decrescendo systolic heart sounds AKA heart murmur
  • Decrease in stroke volume
  • Increased LV pressure
  • Decreased systolic BP
  • Hypertrophy of LV
33
Q

What is aortic regurgitation and what are its manifestations? Do we hear it during systole or diastole?

A

Failure of the aortic valve to properly close.
- Blood leaks back into the ventricle after ventricular contraction

Clinical Manifestations:

  • Diastolic murmur (blowing sound) of high pitch over the LV
  • Hypertrophy of LV
  • LV failure
  • Doppler echocardiography reveals blood flow back through aortic valve

*Aortic valve is not completely closing shut, so the aortic blood is starting to push itself back into the LV which is why we hear it during diastole.

34
Q

What is mitral stenosis and what are its manifestations? Do we hear it during systole or diastole?

A

Narrowing or stiffening of the mitral valve (L AV valve)
- Turbulent blood flow during atrial filling and contraction

Clinical Manifestations:
- Subtle crescendo *diastolic* murmur
- Decreased blood flow from LA to LV
- Increased LA pressure
- Hypertrophy and dilation of LA
- Atrial dysrhythmias (fibrillation)
_ Increases pulmonary BP
_ Pulmonary edema
_ RHF
35
Q

What is mitral regurgitation and what are its clinical manifestations? Does it occur during systole or diastole?

A

Failure of the mitral valve (L AV valve) to properly close
- Blood passing into atrium from ventricle during contraction

Clinical Manifestations:

  • Systolic murmur
  • Hypertrophied LV
  • LHF
  • Pulmonary hypertension and edema
  • Doppler echocardiography reveals blood flow back through mitral valve
36
Q

What is Rheumatic Valvular Disease and how does it develop?

A
  • Diffuse inflammatory disease caused by immune response to infection by the group A beta-hemolytic streptococci
  • Febrile illness
  • – Inflammation of the joints, skin, NS, heart
  • Left untreated, rheumatic fever causes rheumatic heart disease

Strep > Polyarthritis > Mitral Stenosis, LA enlargement

37
Q

Mitral Valve Prolapse

A

Most patients are asymptomatic.

Ballooning of mitral leaflets

38
Q

The presence of what structure is indicative of RVD?

A

Aschoff bodies

39
Q

Which genetic condition is associated with increased risk of valve prolapse?

A

Marfan’s - insufficiency of collagen synthesis, too elastic

40
Q

What is Infective Endocarditis?

A

Microbial invasion of heart valves, endocardium.

Usually mitral and aortic valves.

41
Q

What are the two types of infective endocarditis?

A

Splinter hemorrhages seen with both of these.

  1. Acute
    - Highly virulent infection attacks normal valve
    - 50% patients die within weeks
    - Often requires surgery
  2. Subacute
    - Low virulent infection colonizes abnormal valve
    - Long course, most recover
42
Q

What are cardiomyopathies?

A

Diverse group of disorders in which myocardium dysfunctions.

43
Q

What are the 3 types of cardiomyopathies?

A
  1. Dilated cardiomyopathy
    - Congestive cardiomyopathy
  2. Hypertrophic cardiomyopathy
    - Hypertension is a leading cause
  3. Restrictive cardiomyopathy
    - Deposition of material in myocardium
44
Q

What causes dilated cardiomyopathy?

A

Congestive cardiomyopathy.

Ventricle can’t empty!

Causes:

  • Viral
  • Alcohol/toxin
  • Genetic abnormality

70% of patients dead in 5 years

45
Q

What causes hypertrophic cardiomyopathy?

A

Ventricle can’t fill!

Causes:

  • Hypertension
  • Sarcomere mutation

4% of patients die each year
Can be treated with drugs to relax ventricles

46
Q

What causes restrictive cardiomyopathy?

A

Deposition of material in myocardium.

Heart wall is stiff; can’t fill!

Causes:

  • Idiopathic
  • Amyloidosis or sarcoidosis (too much scar tissue)

70% patients dead in 5 years
Insulin increases the amyloid accrual

47
Q

What are the two disorders of pericardial disease?

A
  1. Acute pericarditis
    - Causes severe chest pain that worsens with respiratory movements and with lying down
    - Dangers: Tamponade, chronic fibrosis
  2. Pericardial effusion
    - Tamponade - Physically pressure compressing the heart
48
Q

What is tamponade?

A

When the heart can’t fill enough because pressure can’t get low enough for that to happen

49
Q

Are primary tumors common?

A

No.

Most are benign. Malignant heart cancers are often metastasized from lung or lymphoma.

DMD 5247 (7 decks)

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