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
What are the three lipoprotiens synthesized in the liver?
VLDLs (triglyceride and protein) LDLs (cholesterol and protein) HDLs (phospholipids and proteins)
26
What are adipokines? How are they related to CAD?
Hormones released from adipose cells adiponectin and leptin Associated with endothelial damage and obesity related disease
27
Why are CKD patients prone to CAD?
Dyslipidemia Endothelial dysfunction vascular calcification Increased levels of growth factors and ROSs
28
Which drugs can increase risk for CAD?
NSAIDs Antirejection drugs Protease inhibitors
29
What percent narrowing of a main coronary artery can alter cellular metabolism?
50%
30
How long does it take for a myocardial cell to become ischemic after occlusion?
10 seconds
31
How long are cardiac cells viable after occlusion?
20 minutes
32
What usually causes stable angina?
Chronic atherosclerosis
33
What causes chest pain?
Buildup of lactic acid or abnormal stretching of myocardial cells
34
Where do the afferent sympathetic fibers of the heart enter the spinal cord?
C3-T4 That's why chest pain can manifest as soooo many different types of radiating pain
35
What is microvascular angina?
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
36
What is prinzmetal angina?
Unpredictable and exclusively at rest Often occurs during REM Caused by vasospasm Tx: Calcium channel blockers, long acting nitrates
37
What is xanthelasmas?
Small fat deposits If these are found around the eyelids, indicative of CAD
38
What does it mean if xanthelasmas are found around the arcus senilis of the eyes?
yellow lipid ring around the cornea suggest atherosclerosis/CAD
39
When does unstable angina occur?
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
40
Three hallmarks of unstable angina:
1. new onset 2. occurring at rest 3. increasing in severity or frequency
41
What kind of infarction causes an NSTEMI?
Subendocardial
42
What kind of infarction causes a STEMI?
Transmural
43
When are ECG changes visible after hypoxia?
30-60 seconds
44
Ischemic Preconditioning
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!
45
In hypoxic settings, the cells loses which ions?
The ones that have to be pumped in: K, Ca, Mg
46
What do ischemic myocardial cells release?
Catecholamines (norepi/epi) causes a lot of the altered sympathetic/parasympathetic symptoms (dysrhythmias etc)
47
Why do people often have hyperglycemian within an hour of an MI?
Catecholamines released by dying myocytes (particularly norepinephrine)
48
Why is angiotensin II released during MI?
Released locally from the vascular smooth mm cells
49
What causes myocardial stunning?
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
What is hibernating myocardium?
Tissue that is persistently ischemic and actually is able to metabolically adapt and preserve myocytes until perfusion can be restored!
51
What medications are used to treat acute pericarditis?
Colchicine (to prevent fibrosis) NSAIDs
52
What is pulsus paradoxus?
ABP during expiration is higher than ABP during inspiration by \> 10mmHg
53
What are most common s/s of tamponade?
dyspnea, tachycardia, JVD, pulsus paradoxus CVP EQUAL TO PAD?
54
What is the most accurate and reliable means of diagnosing a pericardial effusion?
ECHO
55
Constrictive pericarditis was once synonymous with \_\_\_\_\_\_\_\_\_
Tuberculosis
56
What happens in constrictive pericarditis? How is it treated?
Pericardial layers become fibrotic and adhere, encasing the heart in a rigid shell Fluid/Na restriction Anti-inflammatories Pericardiectomy
57
Does Dilated cardiomyopathy cause Systolic or Diastolic dysfunction?
systolic
58
Hypertrophic Obstructive Cardiomyopathy
Most common inherited form of LV Hypertrophy Thicken septal wall causes LVOT obstruction during exercise or at rest
59
Hypertensive/Vavular Hypertrophic Cardiomyopathy
HTN and Ao stenosis cause hypertrophy in LV Initially diastolic, then systolic dysfunction
60
What causes restrictive cardiomyopathy?
Scleroderma, amyloidosis, sarcoidosis, lymphoma Myocardium becomes rigid and non-compliant d/t pathologic deposits Usually need LVADs and and heart transplant
61
Why does endocarditis lead to valve problems?
The valves are continuous with the endocardium. An infection there leads to an infection of the valves
62
What is the most common valvular abnormality?
Aortic Stenosis
63
Top 3 causes of Ao Stenosis
Aging Congential Bicuspid Valve Rheumatic HD
64
What is the most common form of rheumatic heart disease?
Mitral Stenosis
65
Mitral Stenosis Heart Sounds
Rumbling decrescendo diastolic murmur May have an opening snap
66
Aortic Regurgitation Heart Sounds
Diastolic Decrescendo Murmur
67
Corrigan Pulses and prominent carotid pulsations are caused by what valve problem?
Aortic Regurgitation
68
Regurgitation of the A-V valves causes blood to flow back into the \_\_\_\_\_\_\_\_\_
Atria
69
Mitral Regurgitation Heart Sounds
Loud Pansystolic mumur Radiates into back and axilla
70
Mitral valve prolapse causes the cusps to billow into the ________ during systole
Atria
71
Acute rheumatic fever is most common in what age group?
5-15 years
72
The only group A B-hemolytic strep infections that can cause acute rheumatic fever arise from the \_\_\_\_\_\_\_
pharynx Skin infections do not progress to ARF
73
What are aschoff bodies?
Fibrinoid necrotic deposits in the myocardium Caused by RHD
74
What pathogen is most commonly responsible for infective endocarditis?
Staph Aureus
75
Altered formation of _________ can lead to ASDs, VSDs, and other defects
endocardial cushions
76
Name the three fetal shunts
Foramen Ovale Ductus Arteriosus Devtus venosus
77
The umbilical arteries carry _____ blood ______ the fetus
deoxygenated away from
78
The umbilical vein carries _______ blood ______ the fetus
oxygenated toward
79
When oxygenated blood exits the umbilical cord, where does it go first?
The fetal liver
80
What is the function of the ductus venosus?
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
What happens when oxygenated blood from the fetal IVC arrives at the RA
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
Approximately 2/3 of the blood that exits the fetal Aorta goes to \_\_\_\_\_\_\_
The head and upper extremities
83
What happens when deoxygenated blood in the fetal SVC reaches the RA?
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
What happens to PVR and SVR at a baby's first breath?
PVR decreases SVR increases
85
Once the umbilical cord is clamped, flow through ________ falls instantly
ductus venosus
86
After _____ days, no fetal shunting is noted through the ductus venosus
7
87
Once the ductus venosus closes, it forms \_\_\_\_\_\_\_
round ligament of the liver | (ligamentum venosum)
88
What causes the foramen ovale to close?
Increased L atrial pressure
89
What might cause a PFO?
pulmonary HTN RV failure Tricuspid atresia
90
What is responsible for closing the ductus arteriosus?
Increased oxygen saturation in the systemic arterial blood causes vasoconstriction
91
How long until the ductus arteriosus is completely closed?
several weeks after birth
92
What conditions may cause PDA?
conditions that cause decreased PaO2 cyanotic heart disease increased levels of vasodilating substances in the blood
93
What happens to oxygen consumption in a neonate at birth?
It doubles
94
Why do neonates have such a small cardiac reserve?
Stroke Volume is Fixed O2 consumption doubles at birth
95
By two months old cardiac reserve increases. Why?
Stroke volume increases and heart rate decreases oxygen consumption is decreased by half
96
How often is the underlying cause of CHD known?`
10% of the time
97
What percentage of Downs infants have CHD?
50% Usually VSD or AV canal defect
98
What is the predominant cause of symptoms in pediatric heart failure?
pulmonary overcirculation
99
which symptoms commonly manifest in infants with HF?
poor feeding/FTT Dyspnea tahcypnea diaphoresis retraction grunting nasal flaring
100
Which symptoms will not manifest in infants with HF, no matter how severe the disease?
wheezing, coughing, rales
101
Do infants with heart failure develop peripheral edema?
No
102
How does H&H affect cyanosis?
Anemic infants may not appear cyanotic even when PaO2 is low Polycythemic infants may appear cyanotic even at normal PaO2
103
Eisenmenger Syndrome
Conversion of a L-to-R septal shunt to a R-to-L septal shunt due to increased PVR
104
What are the cyanotic heart defects?
Tetralogy of Fallot Single Ventricle Transposition of the Great Arteries
105
Which defects increase pulmonary blood flow?
PDA ASD VSD AVC defect
106
Which defects decrease pulmonary blood flow?
Tetralogy of Fallot Tricuspid Atresia
107
What kind of shunting occurs with a PDA?
L to R From Aorta to the pulmonary Artery
108
What are the manifestations of a PDA?
Continuous machinery murmur bounding pulses active precordium with palpable thrill S/s Of pulmonary overcirculation
109
What are the manifestations of an ASD?
Usually asymptomatic Crescendo-decrescendo systolic ejection murmur
110
What is an Atrioventicular Canal Defect?
Nonfusion of the endocardial cushions Abnormalities in both atrial and ventricular septa and AV valves
111
What are the four defects of ToF?
Large VSD Overriding Aorta Pulmonary Stenosis RV hypertrophy
112
List the obstructive defects
Coarctation of the Aorta Aortic Stenosis Pulmonic Stenosis
113
What is TGA?
Transposition of Great Arteries Aorta comes off the RV PA comes off the LV
114
What must also be present in order for TGA to be compatible with life?
PDA, ASD, or VSD
115
Total Anomalous Pulmonary Venous Connection
Pulmonary Veins abnormally connect to the right side of the heart Must also have an ASD
116
Truncus Arteriosus
Failure of the large embryonic artery to divide into the PA and Aorta Must have a VSD
117
Hypoplastic Left Heart Syndrome
L side of the heart is underdeveloped, Must have a well developed RV and a PDA and ASD
118
Kawasaki Disease
Inflammatory vasculitis that leads to scarring of vessels and stenosis of the coronary arteries
119
Systemic HTN in children is defined as:
SBP and DBP greater than 95th percentile for age and sex on three occasions
120
What is usually the cause of hypertension in children?
Renal disease or CoA