quiz 2- CV 3-4 Flashcards
1
Q
• what are usual causes of myocardial dysfunction? Cardiomyopathy?
A
- Common: IHD, HTN, valvular heart dz
- Less: intrinsic to myocardium itself: heart inflammatory dos of the heart, immunologic dzs, systemic metabolic dos, muscular dystrophies, myocyte genetic abnormalities, dzs of unknown etiology
- Cardiomyopathy: primary abnormality in myocardium
2
Q
• What are the 3 major categories of cardiomyopathy, and the relative size of the 4 chambers??
A
- Dilated (90% of all cases of non-ischemic cardiomyopathy); all 4 enlarged
- Hypertrophic; very small LV, enlarged LA
- Restrictive; small LV, enlarged LA
3
Q
• What causes dilated cardiomyopathy?
A
- Many unknown etio = idiopathic dilated cardiomyopathy
- Ischemic CM=most commonly identified (60% pts with sx HF)
- Common cause in US is chronic alcoholism
- Viral myocarditis
4
Q
• What is pathophysiology of DCM? Laplace’s Law?
A
- <40% EF (despite enlarged LV vol) , may →systolic dysfunction
- Myocyte injury, necrosis, fibrosis →impaired mechanical function
- Cell failure → chambers dilate
- Laplace’s law: ↑diameter → ↑stress → mechanical disadvantage
- =vicious cycle (adverse ventricular remodeling)
5
Q
• What is prevalence of DCM? Histology? In vivo?
A
- 0.4/1000
- Histo: nonspecific cellular abnormalities, variations in myocyte size, myocyte vacuolation, loss of myofibrillar material, fibrosis
- flabby, hypo-contracting heart
6
Q
• What is shape of a very large heart?
A
• Globoid, bc all chambers are dilated
7
Q
• What is hypertrophic cardiomyopathy (HCM)? Micro?
A
- Aka idiopathic hypertrophic sub-aortic stenosis, hypertrophic obstructive cardiomyopathy
- genetic dz, proteins of sarcomere
- thick-walled, heavy, hyper-contracting
- massive myocardial hypertrophy w/o ventricular dilation; usu only one ventricle
- classic: disproportionate thickening of ventricular septum, compared to free wall of ventricle.
- abnormal diastolic filling, intermittent ventricular outflow obstruction (1/3)
- Micro: hypertrophy of myocardial fibers (prominent dark nuclei) interstitial fibrosis
8
Q
• What is restrictive CM? causes?
A
- Aka: infiltrative CM
- myocardium usu infiltrated w abnormal tissue → impaired/abn ventricular wall contraction/relaxation
- most common causes: amyloidosis and hemochromatosis
- Hemochromatosis (Prussian blue stain for iron): Excessive deposition of iron → heart enlargement and heart failure
- amyloidosis: amorphous deposits of pale pink material bw myocardial fibers
9
Q
• what is Infectious endocarditis?
A
- inflammation on the valve leaflets, or endocardial lining of atrium and ventricles (surgery)
- begin on lines of closure (greatest P): atrial surfaces of AV valves, ventricular surfaces of the semilunar valves
- usu left-sided valves, A=M frequency
- Indwelling devices such as prosthetic valves and pacemakers can also become infected
10
Q
• When is TC valve IE seen? Pulmonic?
A
- Suspicious of IV drug use
- Community-acquired (IV drug abuse)
- Hospital-acquired (implanted devices)
- P: rare, confusing sxs
11
Q
• what are “vegetations” in IE?
A
- colonization by microbes =bulky masses
- =collections of infected thrombotic debris deposited on and around affected valve
- often → destruction of underlying valves and tissue
12
Q
• What are gross and micro appearance of IE?
A
- Gross: aortic valve has large irregular, reddish tan vegetation
- Micro: valve has friable vegetations (easily break off, embolize, spread infxn) of fibrin and platelets (pink) mixed w inflammatory cells and bacterial colonies (blue).
- Gross Mitral: valve destruction and vegetation (destruction at commissure bw anterior and posterior leaflets)
13
Q
• What organisms can cause IE?
A
- Many: all bacteria, fungi, Chlamydia and Rickettsiae.
* Most common is bacterial
14
Q
• What organisms cause IE in community-acquired vs nocosomial?
A
- Staphylococcus aureus: (30-50%, minority MRSA) vs. (60-80%; majority MRSA)
- Alpha-hemolytic Strep (S. viridans): 10-35% vs. < 5%
- Enterococci: 5-10% vs. < 5%
- Culture negative: 5-30% vs. 5%
- Staphylococcus epidermidis (coagulase negative): ?? vs. < 5%
- Misc (Escherichia coli, Klebsiella sp., Corynebacterium) < 5% vs. 5-10%
- Fungi: < 5% vs. 10%
15
Q
• What is culture-neg IE?
A
- 7-33%
- Hi in community-acquired dt abx tx prior to dx
- full work-up: serology and culture for esoteric organisms, PCR → etio dounf in >75% cases w initial negative culture (C burnetii and Bartonella species)
- no assoc bw cult neg and underlying etio
16
Q
• what are the organisms commonly found in initially culture neg. IE?
A
- Fungi (10%)
- Enterococcus (5%)
- Alpha hemolytic streptococci (<5%)
- Misc. others including: E coli, Klebsiella, Corynebacterium; 5-10%
17
Q
• What are portals of entry for organisms that may cause IE?
A
- Poor dental health, dental procedures, pharyngeal infxn
- GU infxns, instrumentation the GU tract
- Skin infections (impetigo)
- Pulm infxns
- IV drug use
- Any infx that can enter blood stream
18
Q
• What is acute IE?
A
- rapidly developing, destructive infxn; usu previously normal heart valve
- usu dt infxn w highly virulent organism
- mb death in days to weeks in ~50%, even w vigorous tx with abx and surgery
- fever most common sign
19
Q
• what is sub-acute IE?
A
- Mostly dt strep viridens
- generally slower and less severe course
- fever common, but not necessarily in elderly (can’t mount fever)
- valve usu already damaged, usu dt infxn w less virulent organism
- usu recover after appropriate tx
- vegetations frequently embolize
20
Q
• what are splinter hemorrhages? Roth’s spots?
A
- S: Microemboli to skin, form petechiae I (mouth, under the tongue, feet, nail beds)
- R: retinal hemorrhages; white center of coagulated firbrin; dt immune complex mediated vasculitis; also seen in leukemia, DM, pernicious anemia, ischemic events, rare HIV
21
Q
• what are sxs of acute IE?
A
- Dramatic onset fever, chills, weakness, fatigue
- Mb new murmur, dt flow over vegetations → commonly embolize
- abscesses in ring of tissue beneath leaflets of infected valve
22
Q
• what are risk factors for IE, and corresponding organisms?
A
- Used to be rheumatic heart dz. Incidence now dec
- artificial valves- staph epidermitis
- damaged native valves: step viridens
- Immunocompromised
- IV drug abuse- staph aureus
- Alcoholics- anaerobes, oral cavity bugs
- indwelling catheters/cystoscopy/prostatectomy: Gram neg like E. coli
- vascular grafts
- colon CA: strep bovis
23
Q
• what is follow-up for strep bovis culture?
A
• Colonoscopy is indicated if cultured from blood, to r/o colon CA
24
Q
• What is follow-up/sig for culture neg IE?
A
- Etio not found on blood culture in 5 - 20% of all IE
- Mb dt abx prior to blood draw, organism not in blood stream at the time, or limitations in culture process in lab
- Mb an endocarditis that is inflammatory in nature rather than infectious
25
• What is Libman-Sachs endocarditis?
* =endocarditis of SLE (systemic lupus erythematosus)
* Inflammatory vegetations can occur w certain collagen vascular dzs like SLE
* Gross: flat, spreading vegetations over mitral valve surface and chordae tendineae.
26
• What is Marantic endocarditis?
* culture neg, vegetations dt hypercoagulable state (lung or pancreatic CA)
* Trousseau's syndrome= paraneoplastic syndrome assoc w malignancies
* =not infectious
* Gross: small pink vegetation on cusp margin; rarely over 0.5 cm
* very prone to embolize
27
• what are outcomes of IE?
* successful tx: affected tissue becomes sterilized, valve more fibrotic and scarred
* cardiac decompensation (CHF dt endocarditis): affected valve must be removed and replaced w artificial/prosthetic valve
28
What is myocarditis?
* =inflammation of heart muscle
| * Dt infxn of heart, or autoimmune (RHD, collagen vascular dzs, SLE, RA, drugs, transplant rejection)
29
• What Infectious agents can cause myocarditis?
* Viral most common
* Coxsackie virus (group B)- most common
* Borrelia burgdorferi (Lyme’s dz)
* Cytomegalic virus (CMV)
* HIV
* Meningococcus
* Rickettsia typhi (typhus)
* Toxoplasmosis
* Trichinosis
* Trypanosoma cruzi (Chaga’s dz)
30
• What is Coxsackie virus?
* Genus Enterovirus (also poliovirus and echovirus), common, fecal-oral
* Group A & B: non-specific fever, rash, UR dz, aseptic meningitis
* A: skin and mucous membrane → herpangia, acute hemorrhagic conjunctivitis, hand foot mouth dz
* B: heart, pleura, pancreas, liver→pleuritis, myocarditis, pericarditis, pericardial effusion, hepatitis
31
• What is Rickettsia typhi?
* Obligate parasite bacteria
| * (Not “typhoid fever”)
32
• What is hallmark of viral myocarditis?
• interstitial lymphocytic infiltrates
33
• what is Valvular disease?
* Valves= CT of cardiac skeleton
* Congetical or acquired; isolated or combined
* stenosis, insufficiency (regurgitation or incompetence), or both
* Stenosis: doesn’t open completely, impedes forward flow
* Insufficiency: doesn’t close completely, allows reverse flow
* slight and physiologically unimportant to severe and rapidly fatal
* severe: Sudden destruction of aortic valve cusp by infxn (IE) → severe regurgitant blood flow → rapidly fatal
* benign: mitral stenosis dt RHD develops over years, well tolerated
* tx: mb meds, or repair/prosthetic
34
• what are the most common heart valve dzs? Rare?
* aortic stenosis (most common*, or mitral prolapse) and mitral regurgitation or insufficiency.
* Tricuspid valve dz rare, 2nd to other heart valve dz
* Mitral stenosis dt rheumatic fever, undeveloped countries
* Pulmonic valve dz is congenital, dx at birth
* Aortic and mitral stenosis: 2/3 of all cases
35
• What are sxs of heart valve dz?
* SOB, palpitations (irregular, rapid HR), weakness, dizziness, fainting, edema (ankles, feet), discomfort in chest
* Can progress slolwly
* Sxs don’t always reflect severity
* heart gradually adjusts, sxs may go unnoticed
* Abd heart sounds: Murmurs and clicks
36
• How is heart valve dz diagnosed?
* W echo
| * St CT-angiography, cardiac MRI
37
• What are the murmurs attributable to left sided valvular dz?
* Normal: S1, softer S2
* Aortic stenosis: long loud systolic
* Mitral regurgitation: soft, holo-systolic
* Aortic regurgitation: holo-diastolic
* Mitral stenosis: S1 and S2 both soft
* PDA: holo-systolic and diastolic, tapers end diastole
38
• What are the most common of all the valve dzs?
* Most: aortic stenosis
* MVP
* Mitral regurg
39
• What causes tricuspid, mitral stenosis, and pulmonic valve dzs?
* T: rare, 2nd to other heat valve dz
* M: RF (unusual in developed countries)
* P: congetial, dx at birth
40
• What causes acquired aortic stenosis? Congenital?
* calcification w age; "wear and tear" of either previously anatomically normal aortic valves or congenitally bicuspid valves (3 is normal)
* 1% in US born w bicuspid aortic valve (raph=cusp w partial fusion at center)
* incidence increasing w rising avg age of pop
41
• what is mitral annular calcification?
* in fibrous ring (annulus) of mitral valve= hard, irregular, ulcerated nodules behind leaflets
* usu doesn’t affect valvular fxn
* but mitral stenosis can occur dt progressive dz
42
• what is Mitral valve prolapse?
* One of the most common forms of valvualr dz
* one or both mitral leaflets are "floppy" and prolapse, or balloon back into LA in systole
* ~3% or more of adults in US; F 20-40
* = “Myxomatous degeneration of the mitral valve”
43
• What is myxomatous degeneration?
* Weak CT, usu in MVP (most common cause of pure M insufficiency)
* Exact mechanism unknown
* CT degenerates, glycosaminoglycan accumulates
* Mb benign, or more severe in Marfan’s, etc
* In valves: mb insufficiency, regurg
44
• What causes MVP? Ssx? Dx?
* Mb cellular defect in CT
* Ssx: most asx, mid-sys click; if mitral regurg: late/holo-sys murmur
* Mb: chest pain (like angina, dyspnea, fatigue)
* Dx: Usu incidental on PE, Echo
45
• What are possible complications of MVP?
* Mostly benign, 3% develop:
* IE- high incidence
* Mitral insufficiency- requires surgery
* Stroke/other infarct: dt embolism or leaflet thrombi
* Arrhythmias: A and V (unknown mechanism for V); st sudden death
46
• What is rheumatic fever? Complications?
* acute, immune mediated, multisystem inflammatory dz
* occurs in few wks after GAS pharyngitis (strep pyogenes)-ONLY
* Acute rheumatic carditis in active phase may → chronic rheumatic heart disease (RHD)
* Mb AI response to anti-strep M protein Abs, cross react w cardiac myosin
* 1/3: →valve insufficiency, HF, pericarditis, or death
47
• What are the major and minor dx criteria for RF?
* Major: Carditis, Polyarthritis, Chorea (Sydenham’s), Subcutaneous nodules, Erythema marginatum
* Minor: Fever, Arthralgias, Prolonged PR interval on EKG , ↑WBC, ESR, CRP
48
• What is incidence of RHD?
* 100 yrs ago: leading cause of death in US, 5-20 yo
* markedly dec since 1940s (developed)
* still common in undeveloped (5-30 million kids, 90,000 die/yr)
* dt penicillin, change in virulence of strep
* median age 10 yrs, 20% in adults
* 2.5 million in US (many contracted 40-50 yrs ago)
49
• how does strep throat progress to RF/RHD?
* GAS spreads by direct contact with oral/resp secretions (↑crowded living)
* attach to epithelium of upper resp tract, make enzymes to invade and damage local tissue
* incubate 2-4 d → acute inflammatory response, 3-7 d of sxs (sore throat, fever, malaise, HA)
50
• how is strep throat diagnosed? Tx? Un-tx?
* Positive throat culture or rapid streptococcal antigen test
* hi strep Ab titer (antistrepotolysin O, ASO titer) (GAS make cytolytic toxins streptolysin S and O. O induces persistently high Ab titers= good marker)
* tx: abx shorten strep throat, reduce infectivity, reduce sequelae of heart damage, but don’t change course of acute RF
* Untx: remain infected/infectious for weeks after symptomatic resolution of pharyngitis
* 0.3-3% untx cases: get RF
51
• What are Aschoff bodies?
* nodules in heart w RF. dt inflammation in heart muscle, characteristic of RHD
* granulomatous: collagen, lymphocytes, plasma cells, M0s, surround necrotic center
* pathognomonic for pan-carditis in RHD (focal inflammation of all 3 layers of heart)
* found in other tissues in RF, but not called Aschoff
* M0s may →multinucleated giant cells, or Anitschkow cells ("caterpillar cells", dt appearance of chromatin)
52
• what is most important cardiac related consequence of RHD?
* Mb chronic valvular deformities, particularly mitral stenosis (65-70%, then aortic valve at 25%)
* have deforming fibrosis → permanent dysfunction and severe, sometimes fatal, cardiac problems decades later
* gross: "fish mouth" shape with chronic rheumatic scarring.
* varying degrees of regurgitation, atrial dilation, arrhythmias, ventricular dysfunction.
* Chronic RHD= leading cause of MSV and valve replacement
* Chronic manifestations: 10-40%
* Fusion of valve develops 2-10 yrs after acute RF, more episodes more damage
53
• What is carditis?
o Inflammation of heart muscle
o 2nd most common complication of RF (50%)
o Sxs: like HF, dyspnea, chest discomfort, pleuritic chest pain, cough, pericarditis/rub
o Often w new murmur, tachycardia (out of proportion to fever)
54
• What are sxs of RF?
```
o Like HF
o Difficulty breathing, exercise intolerance
o Tachycardia (out of proportion to fever)
```
55
• What are Prosthetic heart valves? Complications?
* older ball and cage variety. last indefinitely, require continual anticoagulant tx because of the exposed non-biologic surfaces.
* Thrombosis: so need anticoagulant tx, doesn’t entirely precent
* Infection: vegetations of IE, septic embolization
* Structural failure: leaflets tend to become stiff and calcify
* Dehiscence: right after surgery, suture line leaks= valvular leakage
56
• What are non-cardiac ssx of acute RF?
* often diagnostic
* polyarthritis (most common; transient, large jts, from legs up)
* chorea (Sydenham’s, St. Vitus’ dance), erythema marginatum, subcutaneous nodules (bx if has Aschoff bodies)
* abdominal pain, arthralgias, fever, pneumonia
57
• what are subcutaneous nodules?
* Painless, firm, collagen, over bones or tendons
* back of wrist, outside elbow, front knees
* have Aschoff bodies w RF
58
• what is erythema marginatum?
* Aka erythema annulare
* Rash in 5-13% of acute RF
* Begins trunk/arms 1-3 cm , pink-to-red nonpruritic macules or papules, rarely face
* spread outward → serpiginous ring w red raised margins and central clearing
* worse w heat
59
• Describe presentation of 8 yo boy with RF, chorea, subcutaneous nodules:
* Difficulty writing dt chorea in arms
* Mild sore throat, resolved w/o abx; lo fever, no chills
* Friction rub over heart
* subQ nodules over hands
* bloodword unremarkable, ↑ESR
60
• what are causes of pericarditis/pericardial dz?
* Idiopathic – most common
* Infectious – all microbes, esp viruses
* Inflammatory – post-MI, secondary to uremia
* AI – RF, RA, SLE,
* Drugs: procainamide, hydralazine
* Trauma – penetrating/blunt trauma, post-catheterization, post-cardiac surgery
* Misc. – tumors
61
• What are the types of pericarditis?
* Serous
* Fibrinous
* Hemorrhagic
* Purulent
* Caseous
62
• What are features of Serous pericarditis?
* Usu non-infectious, mb viral
* Uremia (acute)
* AI – RA, SLE
* Normally, minimal fluid in pericardium and less inflammatory response. Often has complete resolution.
63
• What is Fibrinous pericarditis?
* Post-MI or Dressler’s syndrome; Post-cardiac surgery; Trauma; Uremia (chronic); AI– RA, SLE
* Pericardial fluid is mixture of fibrinous exudate in serous fluid
* Pericardial friction rub mb audible
* Gross: surface looks rough, not normal glistening (dt fibrin strands)
* "bread and butter" pericarditis
64
• What is Hemorrhagic pericarditis?
* TB; Tumor; Bacterial; Bleeding dos; Trauma
* =fibrinous pericarditis w blood (w/o inflammation, would be called hemopericardium)
* Pericardial fluid w blood mixed with fibrin, st pus exudate
* Gross: rough and red surface
* usu with metastatic tumors, TB
65
• what is Purulent pericarditis?
* from adjacent infection, septic embolism, septicemia, iatrogenic after heart procedure
* exudative, yellow pericardial fluid, w pus and fibrin.
* Resolution w scarring, may → constrictive pericarditis.
66
• What is incidence of heart tumors?
* Primary: rare, 70% benign, 30% malignant
* Metastatic also uncommon, but most common malignancy in heart
* most common: atrial myxoma (benign)
67
• what are the types of benign and malignant heart tumors?
* B: Fibroma, Hemangioma, Lipoma, Lymphangioma, Myxoma, Neurofibroma, Rhabdomyoma, Teratoma,
* M: Angiosarcoma, Extraskeletal Osteosarcoma, Fibrosarcoma, Leiomyosarcoma, Liposarcoma, Neurogenic Sarcoma, Rhabdomyosarcoma, Malignant Lymphoma, Malignant Teratoma, Mesothelioma, Thymoma,
68
• What is atrial myxoma? Dx?
o benign masses, attached to atrial wall, or valve, ventricle (in chambers)
o usu LA, 80-90%l usu septum
o 1-15 cm, usu 5-6
o 29% all heart tumors
o "ball valve" effect: intermittently occlude valve orifice
o Can embolize (metastasize); esp be careful on surgical removal
o Dx: echo, further confirmation by MRI
69
• What is gross and micro appearance of atrial myxoma?
o Gross: gelatinous ball into LA
o Hypocellular myxoid mass, polygonal/elongated cells
o Mono- or multinuclear
o finely vacuolated eosinophilic cytoplasms.
70
• What is Cardiac rhabdomyoma?
o most common primary pediatric tumor of the heart.
o benign, can’t metastasize, but certain position may cause lethal arrhythmias, chamber obstruction.
o spontaneous regression.
o Mild atypical histology
o Gross: clear cells (not normal myocardium, dt glycogen loss in staining), round/polygonal, enlarged
71
• Which neoplasm has greatest propensity to metastasize to heart? Others?
o Melanoma (64%), but not most common cardiac malig
o Dt hematogenous invasion (like lymphoma, dt myocardium involvement)
o Gross: See brown-black pigment
o Met to heart: 10-12% of autopsies w malignancy, dt hematogenous dissemination
o Bronchogenic 36%, nonsolid 20%, breast 7%, esophagus 6%
72
• What is the most common cardiac malignancy?
o Carcinoma of lung (bronchogenic, 36%)
o involves heart dt proximity/extension or hematogenous spread
o dt lymphatic invasion (dt peri/endocardium involvement)
o Also bc lung CA is so common
