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Patho 1 > 2 - Cardiac Patho > Flashcards

2 - Cardiac Patho Flashcards

1
Q

What is chronic venous insufficiency?

A

Persistent ambulatory lower extremity veous hypertension

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2
Q

Why do venous stasis ulcers occur?

A

Venous hypertension, circulatory stasis and tissue hypoxia create inflammatory reaction that leads to necrosis

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3
Q

What is a thromboembolus?

A

A thrombus that has come detached and is floating freely

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4
Q

Virchow’s Triad

A
  1. Venous Stasis
  2. Venous intimal damage
  3. Hypercoaguable state
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5
Q

Which inpatients are at particularly high risk of DVT?

A

Pts with malignancy (esp ovarian and pancreatic)

Pregnant Women

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6
Q

Why do venous clots occur during stasis?

A

Clotting factors and platelets accumulate around venous valves and form clots

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7
Q

Up to 1/3 of DVT patients develop _______

A

Post-thrombotic Syndrome

chronic, persistent pain, edema and ulceration of affected limb

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8
Q

Superior Vena Cava Syndrome

A

progressive compression of the SVC leads to venous distention in the upper extremities and head

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9
Q

What is an aneurysm?

A

Localized dilation or outpouching of a vessel wall or cardiac chamber

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10
Q

True vs False Aneurysm

A

True: involves all three layers of the vessel wall

False: extravascular hematoma that communicates with the invtravascular space

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11
Q

Why is the aorta particularly prone to aneurysms?

A

constant stress on the vessel wall

absence of vasa vasorum in medial layer

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12
Q

Ventricular wall aneurysms are usually caused by what?

A

Dead portions that are thin and weak and stretch with contraction. Gradually becomes stronger with remodeling, but will continue to bulge and create a resevoir of blood that isn’t ejected with systole

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13
Q

Symptoms of cardiac aneurysms

A

Dysrhythmias

Heart Failure

Embolisms to brain etc

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14
Q

Symptoms of thoracic aneurysms

A

Dysphagia

Dyspnea

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15
Q

What are the goals of aneurysm treatment?

A

Low blood volume

Low blood pressure

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16
Q

Compare Type A and Type B Aortic dissections

A

A: Ascending Aorta

B: Any other portion of the aorta

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17
Q

Which disease are associated with valvular thrombi?

A

Endocarditis

Rheumatic Heart Disease

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18
Q

Where do PEs usually originate?

A

R heart

Lower Extremities

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19
Q

What is Buerger Disease?

A

Thromboangiitis Obliterans

Idiopathic. Autoimmune.

Thrombi filled with inflammatory and immune cells disrupt arterial flow

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20
Q

What is Raynaud Disease?

A

Primary Raynaud’s

Imbalance between endothelial vasodilators and vasoconstrictors

Vasospams in the small arteries and arterioles of the fingers

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21
Q

What is Raynaud Phenomenon?

A

vasospasm 2/2 systemic disease (scleroderma)

chemo, cocaine, pHTN, malignancy

Lots of things that alter endothelial function can cause Raynaud’s Phenomenon

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22
Q

What’s the difference between ateriosclerosis and atherosclerosis?

A

Arteriosclerosis is a hardening of the arterial wall, and has several causes, one of which is Atherosclerosis

Atherosclerosis is caused by accumulation of lipid-saturated macrophages in the arterial wall which form a plaque

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23
Q

When is an atherosclerotic plaque considered unstable?

A

prone to rupture even before they affect blood flow, so will be completely silent until they rupture

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24
Q

What causes plaque rupture?

A

Inflammatory mediators in the matrix are activated

Cells inside the plaque undergo apoptosis

this causes hemorrhaging within the plaque

The plaque ruptures

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25
Q

What are the three lipoprotiens synthesized in the liver?

A

VLDLs (triglyceride and protein)

LDLs (cholesterol and protein)

HDLs (phospholipids and proteins)

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26
Q

What are adipokines?

How are they related to CAD?

A

Hormones released from adipose cells

adiponectin and leptin

Associated with endothelial damage and obesity related disease

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27
Q

Why are CKD patients prone to CAD?

A

Dyslipidemia

Endothelial dysfunction

vascular calcification

Increased levels of growth factors and ROSs

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28
Q

Which drugs can increase risk for CAD?

A

NSAIDs

Antirejection drugs

Protease inhibitors

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29
Q

What percent narrowing of a main coronary artery can alter cellular metabolism?

A

50%

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30
Q

How long does it take for a myocardial cell to become ischemic after occlusion?

A

10 seconds

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31
Q

How long are cardiac cells viable after occlusion?

A

20 minutes

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32
Q

What usually causes stable angina?

A

Chronic atherosclerosis

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33
Q

What causes chest pain?

A

Buildup of lactic acid or abnormal stretching of myocardial cells

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34
Q

Where do the afferent sympathetic fibers of the heart enter the spinal cord?

A

C3-T4

That’s why chest pain can manifest as soooo many different types of radiating pain

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35
Q

What is microvascular angina?

A

50% of women with Myocardial ischemia have this

caused by intramyocardial areteriole spsm

Won’t show any evidence of coronary artery disease on a cath

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36
Q

What is prinzmetal angina?

A

Unpredictable and exclusively at rest

Often occurs during REM

Caused by vasospasm

Tx: Calcium channel blockers, long acting nitrates

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37
Q

What is xanthelasmas?

A

Small fat deposits

If these are found around the eyelids, indicative of CAD

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38
Q

What does it mean if xanthelasmas are found around the arcus senilis of the eyes?

A

yellow lipid ring around the cornea

suggest atherosclerosis/CAD

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39
Q

When does unstable angina occur?

A

when fissuring or superficial erosion of the plaque leads to intermittent thrombotic vessel occlusion and vasoconstriction

It means the plaque has started rupturing and and infarction may follow

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40
Q

Three hallmarks of unstable angina:

A
  1. new onset
  2. occurring at rest
  3. increasing in severity or frequency
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41
Q

What kind of infarction causes an NSTEMI?

A

Subendocardial

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42
Q

What kind of infarction causes a STEMI?

A

Transmural

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43
Q

When are ECG changes visible after hypoxia?

A

30-60 seconds

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44
Q

Ischemic Preconditioning

A

Recurrent smaller episodes of myocardial ischemia actually have a protective/adaptive effect

causes changes in ROS, calcium ions, adenosine, bradykinin and opiods and protects the myocardium!

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45
Q

In hypoxic settings, the cells loses which ions?

A

The ones that have to be pumped in:

K, Ca, Mg

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46
Q

What do ischemic myocardial cells release?

A

Catecholamines (norepi/epi)

causes a lot of the altered sympathetic/parasympathetic symptoms (dysrhythmias etc)

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47
Q

Why do people often have hyperglycemian within an hour of an MI?

A

Catecholamines released by dying myocytes

(particularly norepinephrine)

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48
Q

Why is angiotensin II released during MI?

A

Released locally from the vascular smooth mm cells

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49
Q

What causes myocardial stunning?

A

Can occur in any either MI or cardiac surgery (anytime the heart is hypoxic and then reperfused)

Caused by alterations in electrolyte pumps, calcium homeostasis, and release or ROSs.

50
Q

What is hibernating myocardium?

A

Tissue that is persistently ischemic and actually is able to metabolically adapt and preserve myocytes until perfusion can be restored!

51
Q

What medications are used to treat acute pericarditis?

A

Colchicine (to prevent fibrosis)

NSAIDs

52
Q

What is pulsus paradoxus?

A

ABP during expiration is higher than ABP during inspiration by > 10mmHg

53
Q

What are most common s/s of tamponade?

A

dyspnea, tachycardia, JVD, pulsus paradoxus

CVP EQUAL TO PAD?

54
Q

What is the most accurate and reliable means of diagnosing a pericardial effusion?

A

ECHO

55
Q

Constrictive pericarditis was once synonymous with _________

A

Tuberculosis

56
Q

What happens in constrictive pericarditis?

How is it treated?

A

Pericardial layers become fibrotic and adhere, encasing the heart in a rigid shell

Fluid/Na restriction

Anti-inflammatories

Pericardiectomy

57
Q

Does Dilated cardiomyopathy cause Systolic or Diastolic dysfunction?

A

systolic

58
Q

Hypertrophic Obstructive Cardiomyopathy

A

Most common inherited form of LV Hypertrophy

Thicken septal wall causes LVOT obstruction during exercise or at rest

59
Q

Hypertensive/Vavular Hypertrophic Cardiomyopathy

A

HTN and Ao stenosis cause hypertrophy in LV

Initially diastolic, then systolic dysfunction

60
Q

What causes restrictive cardiomyopathy?

A

Scleroderma, amyloidosis, sarcoidosis, lymphoma

Myocardium becomes rigid and non-compliant d/t pathologic deposits

Usually need LVADs and and heart transplant

61
Q

Why does endocarditis lead to valve problems?

A

The valves are continuous with the endocardium. An infection there leads to an infection of the valves

62
Q

What is the most common valvular abnormality?

A

Aortic Stenosis

63
Q

Top 3 causes of Ao Stenosis

A

Aging

Congential Bicuspid Valve

Rheumatic HD

64
Q

What is the most common form of rheumatic heart disease?

A

Mitral Stenosis

65
Q

Mitral Stenosis Heart Sounds

A

Rumbling decrescendo diastolic murmur

May have an opening snap

66
Q

Aortic Regurgitation Heart Sounds

A

Diastolic Decrescendo Murmur

67
Q

Corrigan Pulses and prominent carotid pulsations are caused by what valve problem?

A

Aortic Regurgitation

68
Q

Regurgitation of the A-V valves causes blood to flow back into the _________

A

Atria

69
Q

Mitral Regurgitation Heart Sounds

A

Loud Pansystolic mumur

Radiates into back and axilla

70
Q

Mitral valve prolapse causes the cusps to billow into the ________ during systole

A

Atria

71
Q

Acute rheumatic fever is most common in what age group?

A

5-15 years

72
Q

The only group A B-hemolytic strep infections that can cause acute rheumatic fever arise from the _______

A

pharynx

Skin infections do not progress to ARF

73
Q

What are aschoff bodies?

A

Fibrinoid necrotic deposits in the myocardium

Caused by RHD

74
Q

What pathogen is most commonly responsible for infective endocarditis?

A

Staph Aureus

75
Q

Altered formation of _________ can lead to ASDs, VSDs, and other defects

A

endocardial cushions

76
Q

Name the three fetal shunts

A

Foramen Ovale

Ductus Arteriosus

Devtus venosus

77
Q

The umbilical arteries carry _____ blood ______ the fetus

A

deoxygenated

away from

78
Q

The umbilical vein carries _______ blood ______ the fetus

A

oxygenated

toward

79
Q

When oxygenated blood exits the umbilical cord, where does it go first?

A

The fetal liver

80
Q

What is the function of the ductus venosus?

A

Blood arrives first in the liver, then half the flow is diverted away from the liver through the ductus venosus and into the IVC

81
Q

What happens when oxygenated blood from the fetal IVC arrives at the RA

A

Since it has a much higher pulsatile pressure than the deoxygenated blood that’s returning to the RA via the SVC, it shunts through the patent foramen ovale into the Left Atrium and then into the LV and Aorta

82
Q

Approximately 2/3 of the blood that exits the fetal Aorta goes to _______

A

The head and upper extremities

83
Q

What happens when deoxygenated blood in the fetal SVC reaches the RA?

A

Lower pressure, so instead of shunting through the foramen ovale it flows into the RV

Some of it flows into the pulmonary artery,

But most flows through the ductus arteriosus and into the descending aorta s

84
Q

What happens to PVR and SVR at a baby’s first breath?

A

PVR decreases

SVR increases

85
Q

Once the umbilical cord is clamped, flow through ________ falls instantly

A

ductus venosus

86
Q

After _____ days, no fetal shunting is noted through the ductus venosus

A

7

87
Q

Once the ductus venosus closes, it forms _______

A

round ligament of the liver

(ligamentum venosum)

88
Q

What causes the foramen ovale to close?

A

Increased L atrial pressure

89
Q

What might cause a PFO?

A

pulmonary HTN

RV failure

Tricuspid atresia

90
Q

What is responsible for closing the ductus arteriosus?

A

Increased oxygen saturation in the systemic arterial blood causes vasoconstriction

91
Q

How long until the ductus arteriosus is completely closed?

A

several weeks after birth

92
Q

What conditions may cause PDA?

A

conditions that cause decreased PaO2

cyanotic heart disease

increased levels of vasodilating substances in the blood

93
Q

What happens to oxygen consumption in a neonate at birth?

A

It doubles

94
Q

Why do neonates have such a small cardiac reserve?

A

Stroke Volume is Fixed

O2 consumption doubles at birth

95
Q

By two months old cardiac reserve increases. Why?

A

Stroke volume increases and heart rate decreases

oxygen consumption is decreased by half

96
Q

How often is the underlying cause of CHD known?`

A

10% of the time

97
Q

What percentage of Downs infants have CHD?

A

50%

Usually VSD or AV canal defect

98
Q

What is the predominant cause of symptoms in pediatric heart failure?

A

pulmonary overcirculation

99
Q

which symptoms commonly manifest in infants with HF?

A

poor feeding/FTT

Dyspnea tahcypnea diaphoresis

retraction grunting nasal flaring

100
Q

Which symptoms will not manifest in infants with HF, no matter how severe the disease?

A

wheezing, coughing, rales

101
Q

Do infants with heart failure develop peripheral edema?

A

No

102
Q

How does H&H affect cyanosis?

A

Anemic infants may not appear cyanotic even when PaO2 is low

Polycythemic infants may appear cyanotic even at normal PaO2

103
Q

Eisenmenger Syndrome

A

Conversion of a L-to-R septal shunt to a R-to-L septal shunt due to increased PVR

104
Q

What are the cyanotic heart defects?

A

Tetralogy of Fallot

Single Ventricle

Transposition of the Great Arteries

105
Q

Which defects increase pulmonary blood flow?

A

PDA

ASD

VSD

AVC defect

106
Q

Which defects decrease pulmonary blood flow?

A

Tetralogy of Fallot

Tricuspid Atresia

107
Q

What kind of shunting occurs with a PDA?

A

L to R

From Aorta to the pulmonary Artery

108
Q

What are the manifestations of a PDA?

A

Continuous machinery murmur

bounding pulses

active precordium with palpable thrill

S/s Of pulmonary overcirculation

109
Q

What are the manifestations of an ASD?

A

Usually asymptomatic

Crescendo-decrescendo systolic ejection murmur

110
Q

What is an Atrioventicular Canal Defect?

A

Nonfusion of the endocardial cushions

Abnormalities in both atrial and ventricular septa and AV valves

111
Q

What are the four defects of ToF?

A

Large VSD

Overriding Aorta

Pulmonary Stenosis

RV hypertrophy

112
Q

List the obstructive defects

A

Coarctation of the Aorta

Aortic Stenosis

Pulmonic Stenosis

113
Q

What is TGA?

A

Transposition of Great Arteries

Aorta comes off the RV

PA comes off the LV

114
Q

What must also be present in order for TGA to be compatible with life?

A

PDA, ASD, or VSD

115
Q

Total Anomalous Pulmonary Venous Connection

A

Pulmonary Veins abnormally connect to the right side of the heart

Must also have an ASD

116
Q

Truncus Arteriosus

A

Failure of the large embryonic artery to divide into the PA and Aorta

Must have a VSD

117
Q

Hypoplastic Left Heart Syndrome

A

L side of the heart is underdeveloped,

Must have a well developed RV and a PDA and ASD

118
Q

Kawasaki Disease

A

Inflammatory vasculitis that leads to scarring of vessels and stenosis of the coronary arteries

119
Q

Systemic HTN in children is defined as:

A

SBP and DBP greater than 95th percentile for age and sex on three occasions

120
Q

What is usually the cause of hypertension in children?

A

Renal disease or CoA

Patho 1 (17 decks)

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