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Cardiovascular > Pathology > Flashcards

Pathology Flashcards

1
Q

What causes congenital right to left shunts? 5 things

A
  1. Tetralogy of Fallot - MCC
  2. Transposition of great vessels
  3. Persistent Truncus arteriosus - failure of truncus arteriosus to divide into pulmonary trunk and aorta - most also have VSD
  4. Tricuspid atresia - characterized by absence of tricuspid valve and hypoplastic RV; requires both ASD and VSD for viability
  5. Total anomalous pulmonary venous return - pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc); associated with ASD and sometimes PDA to allow for right-to-left shunting to maintain CO
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2
Q

What causes congenital left to right shunts? 3 things

A

VSD - most common congenital cardiac anomaly
ASD - loud S1; wide, fixed split S2
PDA - closed with indomethacin

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3
Q

Eisenmenger’s syndrome

A

Uncorrected VSD, ASD, or PDA causes compensatory pulmonary vascular hypertrophy, which results in progressive pulmonary hypertension.
As pulmonary resistance increases, the shunt reverses from left-to-right to right-to-left, which causes late cyanosis, clubbing, and polycythemia

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4
Q 
Tetralogy of Fallot
Cause:
Presents with:
How do you correct sx:
Tx:
A

Caused by anterosuperior displacement of the infundibular septum. Pulmonary infundibular stenosis, RVH, Overriding aorta, VSD (PROVe).
Presents with early cyanosis caused by right to left shunt across the VSD bc pulmonary stenosis forces the right to left shunt and causes RVH (VSD alone is usually left to right).
Older patients learn to squat to relieve cyanotic sx (squatting reduced blood flow to the legs, increase peripheral vascular resistance, and decrease the cyanotic right to left shunt across the VSD).
Tx: primary surgical correction - early

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5
Q

D-transposition of great vessels
Cause:
Looks like:
Tx:

A

Caused by failure of the aorticopulmonary septum to spiral
Aorta leaves RV and pulmonary trunk leaves LV –> separation of systemic and pulmonary circulations –> not compatible with life unless a shunt is present to allow adequate mixing of blood (VSD, PDA, PFO)
Tx with surgical correction and without this most infants die within the first few months of life

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6
Q

Coarctation of the aorta results in:
Infantile type:
Adult type:

A

Aortic regurgitation
Infantile - aortic stenosis proximal to insertion of ductus arteriosus (Turner’s syndrome) –> check femoral pulses
Adult - stenosis is distal to ligamentum arteriosum. Associated with notching of the ribs (due to collateral circulation), hypertension in upper extremities, weak pulses in lower extremities –> bicuspid aortic valve.

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7
Q 
Patent ductus arteriosus
Shunting:
Murmur:
Cause:
If uncorrected: 
Tx:
A

In fetal period - shunt is right to left then in neonatal –> lung resistance decreases and shunt becomes left to right with subsequent RVH and/or LVH and failure.
Murmur: continuous, “machine like” murmur
Cause: patency is maintained by PGE synthesis and ow O2 tension and if uncorrected can result in late cyanosis in the lower extremities
Tx: indomethacin

*Sometimes necessary to maintain life in conditions like transposition of great vessels

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8
Q

22q11 syndromes associated with

A

Truncus arteriosus, tetralogy of Fallot

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9
Q

Down syndrome associated with

A

ASD, VSD, AV septal defect (endocardial cushion defect)

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10
Q

Congenital rubella associated with

A

Septal defects, PDA, pulmonary artery stenosis

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11
Q

Turner syndrome associated with

A

Coarctation of aorta (preductal)

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12
Q

Marfan’s syndrome associated with

A

Aortic insufficiency and dissection (late complication)

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13
Q

Infant of diabetic mother associated with

A

Transposition of great vessels

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14
Q

Hypertension
RF
Features
Predisposition

A
  • BP greater or equal to 140/90 mmHg
  • Increase age, obesity, diabetes, smoking, genetics, black > white > asain
  • 90% of HTN is primary and related to increase CO or TPR; other 10% is secondary to renal disease; malignant htn is severe (>180/120) and rapidly progressing
  • atherosclerosis, LVH, stroke, CHF, renal failure, retinopathy, aortic dissection
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15
Q 
Hyperlipidemia signs:
Atheroma
Xanthomas
Tendinous xanthoma
Corneal arcus
A

Atheromas: plaques in blood vessel walls
Xanthomas: plaques or nodules compsed of lipid-laden histiocytes in the skin, especially eyelids (xanthelasma)
Tendinous xanthoma: lipid deposit in tendon (Achilles)
Corneal arcus: lipid deposit in cornea, nonspecific (arcus senilis)

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16
Q

Atherosclerosis:
Monckeberg
Arterioloscerlosis
Atherosclerosis

A

Monckeberg: calcification in the media of the arteries, especially radial or ulnar (Usually benign, pipestem arteries) - do not obstruct blood flow and intima not involved

Arteriolosclerosis: hyaline (thickening of small arteries in essential htn or dm) and hyperplastic (onion skinning in malig htn)

Atherosclerosis: fibrous plaques and atheromas form in intima of arteries

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17
Q 
Atherosclerosis:
RF
Progression
Complications
Location
Sx
A

Dz of elastic arteries and large and medium sized muscular arteries
- RF: smoking, htn, hyperlipidemia, dm; age, gender, + fmhx
- Progression: inflammation important in pathogenesis; endothelial cell dysfxn –> MO and LDL accum –> foam cell formation –> fatty streaks –> smooth muscle cell migration (PDGF/FGF), proliferation, and ECM deposition –> fibrous plaques, complex atheromas
- Complications: aneurysms, ischemia, infarcts, peripheral vascular dz, thrombus, emobli
Location: Ab aorta > coronary artery > poplitearl artery > carotid artery
Sx: angina, claudication, asymptomatic

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18
Q

Aortic aneurysms

A

Pathologic dilation of blood vessel

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19
Q

Ab aortic aneurysms

Associated with:

A

Associated with atherosclerosis

More frequently with HTN males who smoke >50 yoa

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20
Q

Thoracic aortic aneurysms

Associated with:

A

Associated with htn, cystic medial necrosis (Marfan’s syndrome) and tertiary syphilis

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21
Q 
Aortic dissection
Associated with:
Presents:
CXR:
Result in:
A

Longitudinal intraluminal tear forming a false lumen
Associated with htn, bicuspid aortic valve, cystic medial necrosis, inherited connective tissue disorders
Presents: tearing chest pain radiating to back
CXR: mediastinal widening, false lumen (limited to ascending aorta, propagate from ascending aorta, or propagate from descending aorta)
Results in: pericardial tamponade, aortic rupture, death

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22
Q

Angina

Types:

A

CAD narrowing >75%; no myocyte necrosis
Types:
- Stable: mostly secondary to atherosclerosis, ST depression on ECG (retrosternal chest pain with exertion)
- Prinzmetal’s variant: occurs at rest secondary to coronary artery spasm; ST elevation on ECG
- Unstable: thrombosis with incomplete coronary artery occlusion; ST depression on ECG (worsening chest pain at rest or with minimal exertion)

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23
Q

Coronary steal syndrome

A

Vasodilator may aggravate ischemia by shunting blood from area of critical stenosis to an area of high perfusion

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24
Q

Myocardial infarction

A

Most often acute thrombosis due to coronary artery atherosclerosis with complete occlusion of coronary artery and myoctye necrosis; ECG initially shows ST depression progressing to ST elevation with continued ischemia and transmural necrosis

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25
Q

Sudden cardiac death

A

Death from cardiac causes within 1 hour of onset of symptoms, most commonly due to a lethal arrhythmia (ventricular fibrillation)
Associated with CAD

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26
Q

Chronic ischemic heart disease

A

Progressive onset of CHF over many years due to chronic ischemic myocardial damage

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27
Q

Coronary artery occlusion: MC to LC

A

LAD > RCA > circumflex

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28
Q

MI symptoms

A

diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm and/or jaw, shortness of breath, fatigue

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29
Q

0-4 hr of MI

A

No gross or microscopic signs

Risk: arrhythmia, CHF exacerbation, cardiogenic shock

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30
Q

4-12 hr of MI

A

Gross: Occluded artery, infarct, dark mottling, pale with tetrazolium stain
Microscopic: Early coagulative necrosis, edema, hemorrhage, wavy fibers
Risk: arrhythmia

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31
Q

12-24 hr of MI

A

Gross: Occluded artery, infarct, dark mottling, pale with tetrazolium stain
Microscopic: contraction bands from reperfusion injury, release of necrotic cell content into blood, beginning of PMN migration
Risk: arrhythmia

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32
Q

1-3 days of MI

A

Gross: hyperemia
Microscopic: extensive coagulative necrosis, tissue surrounding infarct shows acute inflammation, PMN migration
Risk: fibrinous pericarditis

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33
Q

3-14 days of MI

A

Gross: hyperemic border; central yellow-brown softening (maximally yellow and soft by 10 days)
Microscopic: macrophage infiltration followed by granulation tissue at the margins
Risk: free wall rupture leading to tamponade, papillary muscle rupture, ventricular aneurysm, interventricular septal rupture due to macrophages that have degraded important structural components

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34
Q

2 weeks of MI

A

Gross: recanalized artery, gray-white
Microscopic: contracted scar complete
Risk: Dressler’s syndrome

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35
Q

Diagnosis of MI in first 6 hours

A

ECG is the gold standard

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36
Q

Diagnosis of MI labs

A

Cardiac troponin I rises after 4 hours and is elevated for 7-10 days
CK-MB is predominantly found in myocardium but can also be released from skeletal muscle (useful in dx reinfarction following acute MI because levels return to normal after 48 hours)

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37
Q

Diagnosis of MI with ECG changes

A

ST elevation (transmural infarct), ST depression (subendocardial infarct), pathologic Q waves (transmural infarct)

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38
Q

Transmural infarct characteristics

A

Increased necrosis
Affects entire wall
ST elevation on ECG, Q waves

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39
Q

Subendocardial infarct characteristics

A

Due to ischemic necrosis of <50% of ventricle wall
Subendocardium especially vulnerable to ischemia
ST depression on ECG

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40
Q

Leads with Q waves in anterior wall infarction (LAD)

A

V1-V4

41
Q

Leads with Q waves in anteroseptal infarction (LAD)

A

V1-V2

42
Q

Leads with Q waves in anterolateral infarction (LCX)

A

V4-V6

43
Q

Leads with Q waves in lateral wall infarction (LCX)

A

I, aVL

44
Q

Leads with Q waves in inferior wall infarction (RCA)

A

II, III, aVF

45
Q

MI complications

A

Cardiac arrhythmia - important cause of death before reaching hospital; common in first few days LV failure and pulmonary edema.
Cardiogenic shock - large infarct (high mortality)
Ventricular free wall rupture –> cardiac tamponade; papillary muscle rupture –> severe mitral regurg; and interventricular septum rupture –> VSD
Ventricular aneurysm formation –> decrease CO, risk of arrhythmia, embolus from mural thrombus; greatest risk approximately 1 week post-MI
Postinfarction fibrinous pericarditis - friction rub (1-3 days post MI)

46
Q

Dressler’s syndrome

A

autoimmune phenomenon resulting in fibrinous pericarditis (several weeks post MI)

47
Q

Dilated Cardiomyopathy
Causes:
Findings:
Tx:

A

Most common cardiomyopathy
Causes: idiopathic, up to 50% familial, chronic alcohol abuse, wet beriberi, coxsackie B virus myocarditis, chronic cocaine use, Chaga’s disease, doxorubicin toxicity, hemochromatosis, peripartum cardiomyopathy (ABCCCD)
Findings: S3, dilated heart on US, balloon appearance on CXR, systolic dysfxn ensues, eccentric hypertophy
Tx: Na+ restriction, ACE-I, diuretics, digoxin, heart transplant

48
Q

Hypertrophic Cardiomyopathy
Causes:
Findings:
Tx:

A

Hypertrophied interventricular septum is “too close” to mitral valve leaflet, leading to outflow tract obstruction (murmur, syncope)
Causes: 60-70% familial (auto dom - B-myosin heavy chain mutation), Friedreich’s ataxia
Findings: disoriented, tangled, hypertrophied myocardial fibers, normal sized heart, S4, apical impulses, systolic murmur, diastolic dysfxn ensues, asymmetric concentric hypertrophy (sarcomeres added parallel)
Tx: b-blocker, non-dihydropyridine calcium channel blocker

49
Q

What leads to sudden death in young athletes?

A

Hypertrophic cardiomyopathy

50
Q

Restrictive/obliterative cardiomyopathy
Causes:
Findings:

A

Causes: sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroeleastosis (thick fibroelastic tissue in endocardium of young children), Loffler’s, hemochromatosis
Diastolic dysfunction ensues (reduced LV compliance)

51
Q

Loffler’s sydnrome

A

endomyocadial fibrosis with a prominent eosinophilic infiltrate

52
Q

CHF

A

Inherited or acquired abnormality of cardiac structure or fxn
Sx: dyspnea, fatigue, edema, rales

53
Q

Right CHF

A

Most often from left heart failure; isolated heart failure from cor pulmonale

54
Q

Tx of CHF

A

ACE-I, B-blocker (not in acute decompensated), angiotensin receptor antag, spironolactone –> reduce mortality
Thiazide or loop diuretics are used mainly for symptomatic relief
Hydralazine with nitrate therapy improves both symptoms and mortality in select patients

55
Q

Cardiac dilation

A

Greater ventricular end-diastolic volume

56
Q

Dyspnea on exertion

A

Failure of cardiac output to increase during exercise

57
Q

Signs of left heart failure

A

Pulmonary edema, paroxysmal nocturnal dyspnea (from increase pulmonary venous pressure –> pulmonary venous distention and transudation of fluid. Presence of hemosiderin-lade MO in the lungs)
Orthopnea –> increase venous return in supine position exacerbates pulmonary vascular congestion

58
Q

Signs of right heart failure

A

Hepatomegaly (nutmeg liver) –> increase central venous pressuer –> increase resistance to portal flow –> rarely leads to cardiac cirrhosis
Peripheral edema –> increase venous pressure –> fluid transudation
Jugular venous distention from increase venous pressure

59
Q

Bacterial endocarditis symptoms

A

Fever, Roth’s spots (round white spots on retina surrounded by hemorrhage), Osler’s nodes (tender raised lesions on finger or toe pads), new murmur, Janeway lesion (small, painless, erythematous lesions on palm or sole), anemia, splinter hemorrhages on nail bed (FROM JANE)

60
Q

Bacterial endocarditis acute cause

A

S. aureus (high virulence)

Large vegetations on previously normal valves (rapid onset)

61
Q

Bacterial endocarditis subacute

A 
Viridans streptococci (low virulence)
Smaller vegetations on congenitally abnormal or diseased valves. Sequela of dental procedures, more insidious onset
62
Q

Non-bacterial endocarditis causes

A

Secondary to malignancy, hypercoaguable state, lupus (marantic/thrombotic endocarditis).

63
Q

Other bacterial causes of endocarditis

A

S. bovis is present in colon cancer

S. epidermidis on prosthetic valves

64
Q

What valve is most frequently involved in bacterial endocarditis?

A

Mitral valve

65
Q

Tricuspid valve endocarditis seen in

A

IVDA - S. aureus, Pseudomonas, Candida

66
Q

Complications of endocarditis

A

chordae rupture, glomerulonephritis, suppurative pericarditis, emboli

67
Q

Rheumatic fever
Cause:
Early:
Late sequalae:

A

Consequence of pharyngeal infection with group A beta-hemolytic streptococci. Early deaths due to myocarditis.
Early: mitral valve regurg
Late sequelae: rheumatic heart disease (affects valves mitral > aortic&raquo_space; tricuspid), mitral stenosis

68
Q

Lab/microscopic findings of Rheumatic fever

A 
Aschoff bodies (granuloma with giant cells), Anitschkow's cells (activated histiocytes), elevated ASO titers
Immune mediated (type II hypersensitivity) - not a direct effect of bacteria but Antibodies to M protein
69
Q

Sx of Rheumatic fever

A 
FEVERSS
Fever
Erythema marginatum
Valvular damage (vegetation/fibrosis)
ESR increase
Red-hot joints (migratory polyarthritis)
Subcutaneous nodules
Sydenham's chorea
70
Q

Acute pericarditis
S/Sx
Three causes

A

Commonly presents with sharp pain, aggravated by inspiration ad relieved by sitting up and learning forward. Friction rub, ECG changes - widespread ST segment elevation and or PR depression
Causes:
1. Fibrinous: caused by Dressler’s syndrome, uremia, radiation, loud friction rub
2. Serous: viral (resolves spontan), noninfectious inflamm dz (RA, SLE)
3. Suppurative/purulent: usually caused by bacterial infxns (pneumo, strepto)

71
Q

Cardiac tamponade

A

Compression of heart by fluid in pericardium, leading to decrease CO
Equilibration of diastolic pressures in all 4 chambers
Findings: hypoTN, increase venous pressure (JVD), distant heart sounds, increase HR, pulsus paradoxus

72
Q

Pulsus paradoxus

A

decrease in amplitude of systolic blood pressure by >10 mmHg during inspiration. Seen in severe cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, croup

73
Q

Syphilitic heart disease

A

Tertiary syphilis disrupts the vasa vasorum of the aorta with consequent atrophy of the vessel wall and dilation of the aorta and valve ring.
May see calcification of the aortic root and ascending aortic arch –> leads to tree bark appearance of the aorta
Can result in aneurysm of the ascending aorta or aortic arch and aortic insufficiency

74
Q

Myxoma

A

most common primary tumor in adults
90% occur in the atria (left atrium)
Ball valve obstruction in the left atrium (multiple syncopal episodes

75
Q

Rhabdomyomas

A

most frequent primary cardiac tumor in children (associated with tuberous sclerosis)

76
Q

Most common heart tumor is

A

A metastasis from melanoma, lymphoma

77
Q

Kussmaul’s sign

A

Increase in JVP on inspiration instead of a normal decrease
Inspiration –> negative intrathoracic pressure not transmitted to heart –> impaired filling of right ventricle –> blood backs up into venae cavae –> JVD
Seen with constrictive pericarditis, restrictive cardiomyopathies, right atrial or ventricular tumors, or cardiac tamponade

78
Q

Raynaud’s phenomenon

A

decreased blood flow to the skin due to arteriolar vasospasm in response to cold temperature or emotional stress
most often in fingers and toes

79
Q

Raynaud’s disease

A

when the phenomenon is idiopathic or primary

80
Q

Raynaud’s syndrome

A

when the phenomenon is secondary to a dz process such as mixed connective tissue disease, SLE, or CREST

81
Q

Temporal arteritis
Clinical: pt population, can lead to, associated with
Morph:
Tx

A

Giant cell (large vessel vasculitis)
Clinical: elderly female, unilateral headache and jaw claudication; may lead to irreversible blindness due to ophthalmic artery occlusion
Associated with polymyalgia rheumatica
Morph: branches of carotid artery, focal granulomatous inflammation, increase ESR
Tx with high dose corticosteroids

82
Q

Takayasu’s arteritis
Clinical: pt population, can lead to
Morph:
Tx

A

Large-vessel arteritis
Asian female <40, pulseless disease (weak upper extremity pulses), fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances
Granulomatous thickening of aortic arch, proximal great vessels, increase ESR
Tx with corticosteroids

83
Q

Polyarteritis nodosa
Clinical: pt population, can lead to, associated with
Morph:
Tx

A

Medium-vessel vasculitis
Young adults; Fever, weight loss, malaise, headache, ab pain, melena, HTN, neurologic dysfxn, cutaneous eruptions, renal damage; Hepatitis B seropositivity in 30% of patients
Renal and visceral vessels, immune complex mediated, transmural inflammation of the arterial wall with fibrinoid necrosis, lesions of diff ages, many aneurysms and constrictions on arteriogram
Tx with corticosteroids, cyclophosphamide

84
Q

Kawasaki disease
Clinical: pt population, can lead to, associated with
Morph:
Tx

A

Medium vessel vasculitis
Asian children MI, rupture
Tx with IV Ig and aspirin

85
Q

Buerger’s disease (thromboangiitis obliterans)
Clinical:
Morph:
Tx:

A

Heavy smokers, males s phenomenon often present
Segmental thrombosing vasculitis
Tx with smoking cessation

86
Q

Microscopic polyangiitis
Clinical:
Morph:
Tx:

A

Necrotizing vasculitis commonly involving lung, kidneys, and skin with pauci-immune glomerulonephritis and palpable purpura
No granulomas, p-ANCA
Tx with cyclophosphamide and corticosteroids

87
Q

Wegener’s granulomatosis (granulomatosis with polyangiitis)
Clinical:
Morph:
Tx:

A

Upper respiratory tract: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis; Lower respiratory tract: hemoptysis, cough, dyspnea; Renal: hematuria, red cell casts
Triad of: focal necrotizing vasculitis, necrotizing granulomas in the lung and upper airway, necrotizing glomerulonephritis
c-ANCA; CXR shoes large nodular densities
Tx cyclophosphamide, corticosteroids

88
Q

Churg Strauss syndrome
Clinical:
Morph:
Tx:

A

Asthma, sinusitis, palpable purpura, peripheral neuropathy (wrist/foot drop)
Can also involve heart, GI, kidneys (pauci-immune glomerulonephritis)
Granuloamtous, necrotizing vasculitis with eosinophilia
p-ANCA, elevated IgE

89
Q

Henoch-Schonlein purpura
Clinical:
Morph:
Tx:

A

MC childhood systemic vasculitis
Follows URI
Triad: skin palpable purpura on buttocks/legs, arthralgia, ab pain/melena/multiple lesions of same age
Vasculitis secondary to IgA complex deposition
Associated with IgA nephropathy

90
Q

Strawberry hemangioma

A

Benign capillary hemangioma of infancy. Appears in first few weeks of life (1/200 births); grows rapidly and regresses spontaneously in 5-8 years of age

91
Q

Cherry hemangioma

A

Benign capillary hemangioma of the eldery; does not regress; frequency increases with age

92
Q

Pyogenic granuloma

A

Polypoid capillary hemangioma that can ulcerate and bleed. Associated with trauma and pregnancy

93
Q

Cystic hygroma

A

Cavernous lymphangioma of the neck. Associated with Turner syndrome

94
Q

Glomus tumor

A

Benign, painful, red-blue tumor under fingernails. Ariese from modified smooth muscle cells of glomus body

95
Q

Bacillary angiomatosis

A

Benign capillary skin papules found in AIDS patients. Caused by Bartonella henselae indfections. Frequently mistaken for Kaposi’s sarcoma.

96
Q

Angiosarcoma

A

Rare blood vessel malignancy typically occurring in the head, neck, breast areas. Associated with patient receiving radiation thearpy, especially for breast cancer and Hodgkin’s lymphoma. Very aggressive and difficult to resect due to delay in dx

97
Q

Lymphangiosarcoma

A

Lymphatic malignancy associated with persistent lymphedema (post-radical masectomy)

98
Q

Kaposi’s sarcoma

A

Endothelial malig most commonly of the skin but also mouth/GI tract/respiratory tract. Associated with HHV-8 and HIV. Frequently mistaken for bacillary angiomatosis

99
Q

Sturge-Weber disease

A

Congenital vascular disorder that affects capillary sized blood vessels. Manifests with port-wine stain (nevus flammeus) on face, ipsilateral leptomeningeal angiomatosis (intracerebral AVM), seizures, and early-onset glaucoma
Affects small vessels

Cardiovascular (8 decks)

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