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CPR2 Exam 1 > Cardiac Pathology Part 2 - Dr. Hillard > Flashcards

Cardiac Pathology Part 2 - Dr. Hillard Flashcards

1
Q

congenital heart disease cause

A
  • mostly spontaneous genetics
  • fetal alcohol syndrome
  • most common type if birth defect
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2
Q

most common type of congenital heart disease

A

Ventricular septal defect (VSD)

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3
Q

Left to right shunts causes what and sx

A
  1. high P of left heart or aorta , lower P pulm trunk and right side
  2. Initially asymptomatic and not cyanotic**
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4
Q

right to left shunts what and and sx

A
  1. bypassing pulmonary circulation, usually from right heart hypertrophy or Tetrology of fallot (causing higher P in right side)
  2. symptomatic and cyanotic
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5
Q

left to right shunts top 3

A
  1. ASD
  2. VSD
    3 Patent Ductus Asteriosus
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6
Q

right to left shunt top 3

A
  1. Tetralogy of Fallot
  2. Transposition of Great Arteries
  3. Tricuspid Atresia
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7
Q

ASD most common type

A

Ostium Secundum ASD (90%)

= hole in the middle of septum

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8
Q

ASD sx

A

asymptomatic at birth and until adulthood
= you can here a systolic ejection murmur**
= small hole can close spontaneously

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9
Q

VSD most common sx and most common type

A 
membranous VSD (at the top of septum)**
= asymptomatic until adulthood 
= Holosystolic murmur*
= most close spontaneously
= if child sx then other anomalies usually present
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10
Q

Patent Ductuctus arteriosus happens from

A

increased P on right side or pulmonary P

  1. VSD
  2. hypoxia fetus
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11
Q

Patent Ductuctus arteriosus location and sx

A
  1. Pulmonary A
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12
Q

Patent Ductuctus arteriosus closed how

A

Indomethacin (drug)

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13
Q

Patent Ductuctus arteriosus kept open how and when

A

some congenital malformations like Transposition of Great As you want to keep it open
(PGE E1)

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14
Q

Patent Ductuctus arteriosus causes what to happen over time

A
  1. higher BF to lungs since it goes directly to Pulm A, higher Pulm P, = Pulmonary HTN
  2. Eisenmenger Syndrome
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15
Q

Eisenmenger Syndrome what happens

A

= in long term Left –> Right shunts
1. l–>r increases Pulm BF
2. pulm vascular remodeling (thickening hypertrophy + irreversible)*
3. higher Pulm Resistance –> higher Right side P
4. Right –> Left shunt
5. Eisenmenger syndrome
4.

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16
Q

Eisenmenger Syndrome age and sx

A

around 20-30yo
40% mortality = repare early
SOB, exercise intolerance, cyanosis

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17
Q

Right to left SX

A
  1. Blue babies (blue lips, fingers, toes)

2. clubbing fingers = Hypertrophic ostearthropathy

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18
Q

Tetrology of Fallot includes what

A
  1. VSD
  2. RV hypertrophy
  3. Subpulmonic stenosis
  4. Overriding Aorta (in middle of V so he gets the O2 poor and O2 rich blood
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19
Q

Tetrology of Fallot prevalence and 5 sx

A

most common right to left

  1. cyanotic at birth
  2. holosystic murmur (VSD)
  3. Systolic Ejection murmur (subpulmonic stenosis)
  4. “Tet” Spell = cyanosis, syncope during emotional distress or excitement or high activity
  5. squatting
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20
Q

Tetrology of Fallot prevalence and 5 sx

A

most common right to left

  1. cyanotic at birth
  2. holosystic murmur (VSD)
  3. Systolic Ejection murmur (subpulmonic stenosis)
  4. “Tet” Spell = cyanosis, syncope during emotional distress or excitement or high activity
  5. squatting
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21
Q

Tetrology of Fallot what helps them

A

squatting = increases P on left side = more blood to go l–>r or prevent as much r—>l and allows them to catch breath

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22
Q

imaging Tetrology of Fallot

A

Boot shaped heart
= concave on pulmonary A segment side
= upturned cardiac apex

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23
Q

Transposition of Great Arteries what happens

A

Aorta and Pulm Trunk switch sides
1. Aorta and Right side
2. Pulmonary Trunk and Left side
= NEED shunt to survive

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24
Q

Transposition of Great Arteries how can they survive

A
  1. PDA
  2. VSD
  3. Patent Foca Ovale
    = if not shunt incompatible with life, EM surgery
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25
Q

Tricuspid Atresia what happens

A

X tricuspid valve, no BF from RA to RV

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26
Q

Tricuspid Atresia survival and sx

A
  1. ASD/ PFO + VSD *** needed to survive

2. severe immediate cyanosis after birth, EM surgery

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27
Q

Coarctation of the Aorta what happens and the 2 types

A

narrowing of aorta right before ductes arteriosis

  1. Infantile form : has PDA
  2. Adult form : X PDA
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28
Q

Coarctation of the Aorta infantile and adult sx

A
  1. infantile : BF from RV to PT through PDA to Aorta = cyanosis of lower Extr.
  2. adult : BF from LV to aorta with high P = HTN of upper body and Hypotension and low Pulse lower Extr., pain with exertion (arterial insufficiency)
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29
Q

Coarctation of the Aorta associated with

A
  1. Turners Syndrome XO (check in women)
  2. Bicuspid aortic valve
  3. higher risk in males
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30
Q

Tetrology of Fallot vs Infantile Coarctation of the Aorta

A

Coarctation of the Aorta in infants causes cyanosis of ONLY lower extr.

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31
Q

adult Coarctation of the Aorta can cause what later

A

Rib notching = collateral intercostal Vessles made from and you get pressure erosion of rib margin

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32
Q

Congenital Aortic and Pulmonary Valve Stenosis/Atresia (AORTA) causes what

A
  1. LV hypertrophy

2. hypoplastic Left Heart syndrome = when LV in not developed enough to pump

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33
Q

Congenital Aortic and Pulmonary Valve Stenosis/Atresia (PULMONARY) usually seen when

A
  1. Tet of Fallot

2. Transposition of GAs

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34
Q

Congenital Aortic and Pulmonary Valve Stenosis/Atresia TX

A

EM surgery

preserve PDA*

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35
Q

PE types

A
  1. DVT, thrombus
  2. Bone marrow, fat from trauma
  3. Air from nurse not removing air in syringe
  4. infectious, foreign bodies
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36
Q

Paradoxical Embolism is what

A

when there is some shunt in heart like Tet of Fallot, or VSD, ASD
1. venous thrombi to Rigth heart crossed to left heart
2. to brain or other organ
= RIGHT –> LEFT SHUNT

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37
Q

Paradoxical Embolism in left to right shunt

A

usually to lungs only can cross over during those brief time that it switches to r–>l

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38
Q

when does a l–> r shunt switch briefly to r–>l

A
  1. cough, sneeze
  2. BM
  3. Valsalva (increasing Pulm P)
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39
Q

PFO is what and can open when

A

flap open r–>l only

  1. valsalva
  2. cough, sneeze
  3. BM
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40
Q

Trisomy 21 most common heart conditions

A

Septal defects : Atroventricular septal > VSD > ASD

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41
Q

Marfans Syndrome most common heart problems

A

Aortic aneurysm , Aortic dissection

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42
Q

Marfan Syndrome how it happens

A

Fibrillin-1 mutation = high TGF-B activity**

  1. high metalloprotease,
  2. degrades elastin**
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43
Q

DiGeorge Syndrome mutation and SX

A 
CATCH22
C : cardiac probs
A : Abnormal facies, increased pig levi, streak ovaries
T : thymic aplasia
C : cleft plate
H : hypocalcemia
22 : 22q11
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44
Q

DiGeorge Syndrome heart problems

A

Conotruncal heart abnormalities = tetrology of Fallot ** (transposition of GA, ASD, VSD)

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45
Q

Turner Syndrome heart problems

A

Coarctation of aorta

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46
Q

Hypertensive Heart Disease criteria 2

A
  1. LV concentric hypertrophy (all around LV including septum and wall
  2. HTN other place, organ, peripheral, aortic stenosis = aorta htn)
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47
Q

Hypertensive Heart Diseasesx during systole and diastole

A

S : can’t pump as much, CHF, dilated Atria** (from higher P in A)
D : not relaxing = CHF, Atrial Fib (also from dilation of A) which can cause thrombus (LA)

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48
Q

Hypertensive Heart Disease cells looks like

A

larger and bigger nuclei

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49
Q

Cor Pulmonale is what

A

right side (pulmonary) HTN disease,

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50
Q

Cor Pulmonale can happen how

A

if alveoli is hypoxic then BV constricts there

= diffuse hypoxia –> all BV constrict and ==> high Pulm P

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51
Q

Cor Pulmonale can cause what

A
  1. isolated right side heart failure
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52
Q

Cor Pulmonale can be a cause of what event

A

PE

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53
Q

Cor Pulmonale 4 things causing hypoxia and this to happen

A
  1. pulmonary parenchyma disease
  2. Pulm vessle disease
  3. Chest movement problems
  4. Pulm Arterial constriction (Metabolic acidosis)
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54
Q

right heart hypertrophy causes what to wall

A

thickening of trabaculae, and wall

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55
Q

right CHF SX

A
  1. hepatospenomegally
  2. Distended jugular V
  3. effusions, ascites
  4. edema
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56
Q

most common valve abnormality

A

Calcific Aortic Stenosis

57
Q

Calcific Aortic Stenosis risk and associations

A
  1. age 60yo-80yo
  2. HTN
  3. hyperlipidemia
  4. chronic trauma “wear and tear”
58
Q

Calcific Aortic Stenosis causes what to happen

A
  1. Aortic valves cant open all the way
  2. harder to push blood from LV –>Aorta
  3. LV hypertrophy
59
Q

Calcific Aortic Stenosis made of what

A

osteocalficication = bone can be found

60
Q

heart valves have how many cusps

A

all have 3 except mitral has 2

61
Q

Bicuspid aortic valve (BAV) can cause what 3 things

A
  1. early calcific aortic stenosis
  2. can stop working normal = aortic valve prolapse
  3. infective endocarditis easier to form
62
Q

Bicuspid aortic valve (BAV) causes 2

A
  1. congenital

2. RF

63
Q

any valve problem you have higher chance of

A

infective endocarditis

64
Q

calcific aortic stenosis SX

A
  1. LV hypertrophy
  2. systolic murmur
  3. syncope (5years to live)
  4. Angina (ischemia in heart cells hypertrophy)
  5. left CHF (2 years to live)
65
Q

calcific aortic stenosis TX

A

surgery to replace valves

66
Q

Mitral annular calcification what

A

calcific deposits on fibrous annulus (base of leaflet valves)

67
Q

Mitral annular calcification risk

A

females

over 60yo

68
Q

Mitral annular calcification sx

A
  1. asymp
  2. mild regurgitation
  3. arrhythmia (deep calcification into myocytes) = HEART BLOCK
  4. infectious endocarditis
69
Q

Mitral Valve Prolapse what

A

one of valve leaflets balloon back into LA during SYSTOLE = “floppy valve”

70
Q

Mitral Valve Prolapse risks + associations

A
  1. female
  2. connective tissue problem = Marfan syndrome
  3. past MI, RF
71
Q

Mitral Valve Prolapse valves looks like dont need to know

A
  1. thick rubbery (myxomatous degeneration)

2. Interchordal ballooning (hooding)*

72
Q

Mitral Valve Prolapse auscultation and SX

A
  1. mid systolic click (can also have murmur), MITRAL REGURG
  2. dyspnea
  3. higher A P = atrial dilation —-> Atrial Fib, thrombus
  4. Infective endocarditis
73
Q

rheumatic fever is from what

A

strep pharyngitits Group A

74
Q

Rheumatic fever SX

A
  1. recurrent strep throat —-> CD4+ react with M strep Ag
  2. fever
  3. migratory polyarthritis
  4. pancarditis
  5. Erythma marginatum
  6. Syndenham chorea
  7. subQ noduels
75
Q

Rheumatic fever + rash is what

A

scarlet fever

76
Q

Rheumatic fever DX

A

Ab to streptolysin O + DNaseB

77
Q

Rheumatic fever heart problem

A
  1. Fibrinous pericarditis, myocrditis, endocarditis = if all its pancarditis
  2. Valvulitits (verrucae at mitral V)**
  3. MacCallum Plaques**
  4. Aschoff Body + Antischkow cells*
78
Q

fibrinous pericarditis seen in

A

Rheumatic fever

MI

79
Q

Rheumatic fever most common valves affected

A

mitral** > aortic > tricuspid

80
Q

Antischkow cells

A

macrophage bodies

81
Q

Rheumatic fever chronic does what to heart

A

repeated strep infections

= mitral stenosis (DIASTOLIC rumbling) (looks like a fish mouth)

82
Q

2 valve things that can cause LA dilation

A

mitral stenosis

mitral regurg/ prolapse

83
Q

infective endocarditis from what

A
  1. bacteria at valves (firbinous debri)

2. prosthetic valves

84
Q

infective endocarditis risks

A

dental poor hygiene
IV drugs
Prosthetic heart
valvular disease (Rheumatic heart, stenosis, MVP)

85
Q

acute infective endocarditis sx

A

FAST fever, chills, weak

= STAPH AUREUS

86
Q

subacute infective endocarditis

A

low fever (unknown origin), fatigue
few weeks
STREP, ENTEROCCOCI

87
Q

infective endocarditis major criteria

A

+ Blood culture

mass or abscess on valve (echocardiogram)

88
Q

infective endocarditis minor sx **

A
  1. Roth spots
  2. Splinter hemorrhages
  3. Osler nodes (tips on finger : red nodular painful)
  4. Janeway lesions (red purple dots on sole or palm)
89
Q

subacute infective endocarditis from dental cause

A

strep viridans

90
Q

subacute infective endocarditis from prosthetic valves usually from

A

staph epidermidis

staph aureus if acute

91
Q

subacute infective endocarditis from dental and more rare

A

HACEK (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella)

92
Q

infective endocarditis tricuspid valve cause

A

IV drug use , staph aureus

93
Q

infective endocarditis most common valve effected

A

mitral or aortic

94
Q

Nonbacterial Thrombotic Endocarditis (Hypercoagulable)

A

sterile non-inflammatory valvular thrombi —-> embolizes

95
Q

Nonbacterial Thrombotic Endocarditis (Hypercoagulable) causes

A
  1. cancer releasing procoags (mucinous adenocarcinoma)
  2. primary anti-phospholipid syndrome
  3. SLE
  4. proinflammatory
96
Q

Antiphospholipid syndrome vs SLE

A

APS : auto ABs to endothelial BVs causing thrombus + fetal loss*
SLE : malar rash, ABs to vessel endothelial –>preocoags
====Nonbacterial Thrombotic Endocarditis`

97
Q

Carcinoid heart Disease

A
  1. serotonin secreated from tumor
  2. plaque like endocardial and valvular thickening
  3. RIGTH SIDE heart lesions
98
Q

Carcinoid heart Disease SX and type of tumor

A 
neuroendocrine tumor
1. flushing
2. D
3. Dermatits
4. Bronchoconstriction
==== only after liver is effected and cant breakdown bioactive serotonin
99
Q

Carcinoid heart Disease is right sided why

A

left side has lung vessels that breakdown bioactive serotonin before it gets to heart

100
Q

Prosthetic valves : mechanical vs bioprostheses

A
  1. mechanical : life long life, life long anti-coags (25yrs)

2. Bioprosthetic : need to be replaced, only anticoags first 3-6 months (10-15yrs)

101
Q

Aortic stenosis murmur

A

harsh systolic

creascendo, decrescendo

102
Q

mitral regurgitation murmur

A

holosytisolic (pansystolic) throughout systole

103
Q

VSD murmur

A

holosytisolic (pansystolic) throughout systole

104
Q

aortic regurg vs mitral stenosis murmur

A

diastolic both

  1. A : decreascendo all the way
  2. M : rumbling at the end more
105
Q

PDA murmur

A

continous machine like all the time (crescendo during systole)

106
Q

3 main cardiomyopathies

A
  1. Dilated
  2. Hypertrophic
  3. Restrictive
    (heart structually and functionally abnormal with no congenital or diseases effecting heart)
107
Q

Dilated cardiomyopathy type of problem and what happens to heart

A
  1. Systolic

2. Enlargement in all chambers

108
Q

Hypertrophic cardiomyopathy type of problem and what happens to heart

A
  1. Diastolic
  2. LV thickening of SEPTUM
    = sudden death in young athletes
109
Q

Hypertrophic cardiomyopathy mutation

A

B-myosin heavy chain = involving sarcomere protein *

110
Q

Restrictive cardiomyopathy type of problem and what happens to heart

A
  1. Diastolic

2. Rigid Ventricular walls

111
Q

Restrictive cardiomyopathy usually from

A

amyloidosis

112
Q

Dilated cardiomyopathy familial mutation

A

TTN gene (titin mutation) = sarcomere making

113
Q

Dilated cardiomyopathy causes besides familial 4

A
  1. V overload after birthing child
  2. alcohol
  3. Fe overload (HFE gene, hereditary hemochromatosis)
  4. Takotsubo (catecholamine overload)
114
Q

Dilated cardiomyopathy what is seen

A
  1. hypretrophic (heavy and more muscle from large heart)

2. big dilated chambers

115
Q

Dilated cardiomyopathy SX

A
  1. 20yo-50yo progressive CHF
  2. Systolic prob
  3. arrhythmia sudden death
  4. thrombus formation
116
Q

Dilated cardiomyopathy can be caused by what drug

A

Doxorubicin, daunorubicin (for leukemia, sarcoma, lymphoma)**
= Anthrocyclines*
= important to keep track of medical records

117
Q

HFE iron overload sx

A
  1. Dilated cardiomyopathy
  2. skin bronze pigment
  3. Bronze DM (effects pancreas)
  4. hypogonadism
118
Q

Takotsubo Cardiomyopathy happens how

A
  1. “broken heart syndrome”
  2. from emotional distress = sudden surge of catacholamines
  3. can cause ischemia and death
    = Dilated cardiomyopathy
119
Q

Takotsubo Cardiomyopathy LOOKS LIKE AND PREVALENCE

A

apical (lower) ballooning in LV like a Octopus Pot

= women (90%), 60yo-75yo

120
Q

Hypertrophic Cardiomyopathy looks like

A

myocyte hypertrophy = septal prominance, myocyte disarray** dont line up

121
Q

Hypertrophic Cardiomyopathy prevalence

A

male , genetic

122
Q

Hypertrophic Cardiomyopathy SX

A

none
= early 20s, sudden V arrhythmia
= young athlete sudden death (from such thick septum –> V arrhythmia)

123
Q

Hypertrophic Cardiomyopathy murmur

A

systolic ejection murmur from mitral valve pushed against septum

124
Q

Restrictive Cardiomyopathy what

A

V walls get very stiff
hard to Diastole
= Amylodiosis
= fibrosis from radiation therapy

125
Q

Hypertrophic Cardiomyopathy heart looks like

A

Atrial dilation since Vs cant fill properly

= arrhythmia

126
Q

Amyloid is what

A

apple, green, congo red **
insoluable B-pleated sheets
(myeloma, chronic inflammation, transthyretin)

127
Q

rare causes of Restrictive Cardiomyopathy

A
  1. Endomyocardial fibrosis (Africa)
  2. Loeffler endocarditis (esosinophilic infiltration, AML, CML)
  3. Endocardial fibroelastosis (congenital stenosis aorta)
128
Q

Arrhythmogenic RV cardiomyopathy what is it

A

sudden death young adults

RV wall replaced by fat and fibrosis + dilation

129
Q

Arrhythmogenic RV cardiomyopathy defective what and can cause what sx

A
  1. desmosomes adhesion Proteins

2. V tachy, Premature contractions or fibrillation = sudden death

130
Q

Naxos Syndrome

A 
= Arrhythmogenic RV cardiomyopathy
1. plantar and palmar hyperkeratosis
2. wooly hair
3. mutated plakoglobin
= how it was first seen
131
Q

Myocarditis is what and usually from what

A

inflammation of cardiac muscle

  1. Coxsackie B virus
  2. COVID19
132
Q

Myocarditis sx

A
  1. asymp —-> HF
  2. arrythmia, fever
  3. high troponin
  4. dilated cardiomyopathy can happen
133
Q

Chagas Disease

A

“kissing bug”

  1. releasing Triatomine, Trypanosoma cruzi
  2. can collect in muscle –> BS–> heart = myocarditis
  3. achalasia
134
Q

Trichinosis

A

worm from pork muscle

= can get into heart muscle = myocarditis

135
Q

Lyme disease sx

A
  1. myocarditis with heart block (spirochetes)
  2. migratory erythma
  3. migratory polyarthrtis, fascial palsy, meningitis
136
Q

most common type of myocarditis

A

Lymphocytic myocarditis = from viral or post viral infection

137
Q

Eosinophilic Myocarditis

A

Hypersensitivity myocarditis
from allergy, (usually drug reaction), hypersensitivity
= EXCLUDE parasitic infection first

138
Q

2 Giant Cell myocarditis

A
  1. Idiopathic Giant Cell Myocarditis : agressive and deadly, 3mo life, Giant Cells + inflammation (high E)
  2. Myocardial Sarcoidosis : Giant cells and non-necrotizing granulomas , hiliar lymphadenopathy (AA prevalence)

CPR2 Exam 1 (19 decks)

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