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Pathology > Cardiopulm > Flashcards

Cardiopulm Flashcards

1
Q

Arrhythmias

A

Sudden cardiac death

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2
Q

Hypertensive heart disease

A 
Left sided (systemic)
Car pulmonale (right sided or pulmonary)
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3
Q

Valvular heart disease

A

Calcific valvular degeneration

  • calcific aortic stenosis
  • calcific stenosis of bicuspid aortic valve
  • mitral annular calcification

Mitral valve prolapse

Rheumatic heart disease

Infective endocarditis

Non-infected endocarditis

  • nonbacterial thrombotic endocarditis
  • lupus
  • carcinoid heart disease
  • complications of prosthetic valves
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4
Q

Cardiomyopathies

A

Dilated cardiomyopathy

Arrhythmoegnic right ventricular cardiomyopathy

Hypertrophic cardiomyopathy

Myocarditis

Other causes of myocardial disease

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5
Q

Pericardial disease

A

Pericardial effusion and hemopericardium

Pericarditis
-acute pericarditis

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6
Q

Heart disease associated with rheumatologist

A

Ok

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7
Q

Tumors fo the heart

A

Primary cardiac tumors

Cardiac effects of noncardiac neoplasms

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8
Q

Cardiac transplantation

A

Discuss major complications

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9
Q

Arrhythmia: What is the most common cause of rhythmDOs read pg 550

A

Ischemic injury

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10
Q

Sick sinus syndrome

A

SA node damaged->bradycardia

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11
Q

Atrial fibrillation

A

Myocytes depolarize independently and sporadically (atrial dilation) with variable transmission thru the AV node-> irregular HR=atrial fib

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12
Q

Heart block

A

Dysfunctional AV node

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13
Q

First degree block

A

Prolonged PR interval

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14
Q

Second degree block

A

Intermittent transmission

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15
Q

Third degree block

A

Complete failure

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16
Q

Abnormalities in gap junction structure or spatial relationship

A

Ischemic heart disease , dilated cardiomyopathies, myocytes hypertrophy, inflammation (myocarditis or sarcoidosis), amyloid…

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17
Q

Hereditary conditions arrhythmias

A

AD

Primary electrical DO, Dx thre genetic testing

Chennelopathies: mutations in genes that are required for NL ion channel function
-can be associated with skeletal muscle DOs and diabetes also; most common isolated to heart

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18
Q

Most common inherited arrhythmogenic disease

A

Long QT syndrome

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19
Q

Genes of long QT syndrome

A

KCNQ1 (K channel LOF)

, KCNH2 (K channel LOF)

SCN5A (Na channel LOF)

CAV2 (caveolin Na current GOF)

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20
Q

Short QT syndrome genes

A

KCNQ1 (K channel GOF)

KCNH2 (K channel GOF)

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21
Q

Brigade syndrome genes

A

SCN5A (Na channel)
CACNB2b (Ca channel LOF)

SCN1b (Na channel LOF)*

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22
Q

cPVT syndrome

A

RYR2 (diastolic Ca release )

CASQ2 (diastolic Ca release LOF)

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23
Q

Sudden cardiac death from cardiac cause

A

Unexpected death from cardiac cause, either

  • without symptoms or
  • within 1-24 hours of symptom onset
  • 80-90% of successively resuscitated pts show no lab or ECG changes
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24
Q

Coronary artery disease precipitates sudden cardiac death

A

Usually >75% stenosis or one or more of the 3 main coronary arteries

Unfortunately SCD often the first manifestation of IHD

Healed remote MIs seen in about 40$

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25
Q

Other causes of sudden cardiac death

A

Cardiomyopathies, myocarditis, congenital abnormalities of the conduction system, myocardial hypertrophy

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26
Q

SCD due to a fatal arrhythmia

A

Most often arising from ischemia induced myocardial irritability

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27
Q

Hypertensive heart disease: left sided hypertensive disease

A

Left sided hypertensive disease

  • pressure overload results in left ventricular hypertrophy (LVH)
  • the LV wall is CONCENTRICALLY thickened >1.5 cck, weight >500 gym

Diastolic dysfunction can result in left atrial enlargement
-can lead to atrial fib

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28
Q

Hypertensive left sided heart disease may lead to __- and is a risk factor for ___

A

CHF

SCD

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29
Q

Hypertensive heart disease: right sided hypertensive

A

Isolated right sided hypertensive heart disease arises in the setting of pulmonary hypertension

Acute car pulmonale may arise from a large pulmonary embolus
-marked dilation of RV

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30
Q

Most common cause of pulmonary hypertension is

A

Left sided heart disease

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31
Q

Left sided hypertensive heart disease

A

Systemic

Concentric
LVH

Decrease lumen

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32
Q

Disease of the pulmonary parenchyma that predispose to Cor Pulmonale

A

Chronic obstructive pulmonary disease

Diffuse pulmonary interstitial fibrosis

Pneumoconioses

Cystic fibrosis

Bronchiectasis

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33
Q

Diseases of pulmonary vessels that predispose to Cor pulmonale

A

Recurrent pulmonary thromboembolism

Primary pulmonary HTN

Extensive pulmonary arteritis

Drug toxin or radiation induced vascular obstruction

Extensive pulmonary tumor microembolism

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34
Q

Disorders affecting chest movement predisposing Cor pulmonale

A

Kyphoscoliosis

Marked obesity (sleep apnea, pickwickian syndrome)

Neuromuscular diseases

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35
Q

Disorders including pulmonary arterial constriction predisposing to Cor pulmonale

A

Metabolic acidosis

Hypoxemia

Chronic altitude sickness

Obstruction of major airways

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36
Q

Valvular heart disease

A

Valve disease may present with stenosis and/or insuffiency

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37
Q

Stenosis

A

Valve doesn’t open completely, occurs chronically

  • impedes forward flow
  • chronic stenosis may cause pressure overload hypertrophy->CHF
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38
Q

Insuffiency

A

Valve doesn’t close completely, may occur acutely or chronically

  • allows reversed flow
  • chronic insuffiency may cause volume overload hypertrophy->CHF
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39
Q

Mitral valve stenosis cause

A

Postinflammatory scarring (rheumatic heart disease)

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40
Q

Mitral regurgitation cause

A

Abnormalities of leaflets and commissures

Abnormalities of tensor apparatus

Abnormalities of left ventricle and/or annulus

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41
Q

Abnormalities of leaflets and commissures

A

Postinflammatory scarring

Infective endocarditis

Mitral valve prolapse

Drugs

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42
Q

Aortic stenosis cause

A

Postinflammatory scarring (rheumatic heart disease)

Senile calcific aortic stenosis

Calcification of congenitally deformed valve

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43
Q

Aortic regurgitation cause

A

Postinflammatory scarring (rheumatic heart disease)

Degenerative aortic dilation 
*syphilic aortitis
Ankylosis spondylitis
Rheumatoid arthritis
*marfans
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44
Q

Most common valve abnormality

A

Calcific aortic stenosis

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45
Q

Who gets calcific valvular degeneration

A

60-80 increases with age

Wear a tear associated with chronic HTN, hyperlipidemia, inflammation

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46
Q

In calcific valvular degeneration, ___ valves show na accelerated course

A

Bicuspid

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47
Q

Describe valves in calcific aortic stenosis

A

Osteoblasts like cells, which deposit an osteodystrophy like substance->ossified

Mounded calcification in cusps prevent complete opening of the valve

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48
Q

Symptoms of calcific valvular degeneration

A

Left ventricular hypertrophy (LVH) develops from increased pressure

Most patients with aortic stenosis will die 5 years after developing angina, within 3 years of developing syncope and within 2 years of CHF onset

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49
Q

Mitral annular calcification

A

Calcific deposits in the fibrous annulus

Normally does not affect valve function

Nodules may become sites for thrombus formation or infective endocarditis

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50
Q

Who gets mitral annular calcification

A

Females over 60 with mitral valve prolapse

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51
Q

Bicuspid valve

A

Prone to calcification. Patients can remain relatively asymptomatic until the stenosis reaches a critical point when congestive heart failure rapidly ensues. The dense white nodules of calcification are present on both valve surfaces

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52
Q

Aortic stenosis calcification

A

An aortic valve need not be bicuspid to calcify. Sometimes older adults , a normal aortic valve (three cusps) will undergo calcification, a so called “senile calcific aortic stenosis” nodules of calcification are seen on the cusps

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53
Q

Mitral valve prolapse

A

Valve leaflets prolapse back into LA during systole

Affects 2-3% of adults, mainly female and incidental (mid systolic click**)

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54
Q

Marian syndrome

A

Loss of connective tissue support in the mitral valve leaflets makes them soft and billowy, creating a so called floppy valve

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55
Q

Myxomatosis degeneration

A

MVP leaflets become thickened and rubbery due to proteoglycan deposits (myxomatosis degeneration) and elastic fiber disruption

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56
Q

Why else may MVP occur

A

Complication of other causes of regurgitation (dilated hypertrophy)

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57
Q

Symptoms MVP

A

Most asymptomatic , a minority may experience:
Pain mimicking angina
Dyspnea

Serious (but rare) complications may include

  • infective endocarditis
  • mitral insuffiency
  • thromboembolism
  • arrhythmias
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58
Q

Rheumatic fever

A

Multisystem inflammatory disorder following pharyngeal infection with group A streptococcus

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59
Q

Incidence of rheumatic fever has _ with more rapid diagnosis and treatment of strep infections

A

Decrease

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60
Q

Acute rheumatic fever

A

May include a carditis component, and over time may evolve to chronic rheumatic heart disease

Occurs 10 days to 6 weeks after a group a strep infection
-anti-streptomycin O and anti-DNase B

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61
Q

Pathogenesis rheumatic fever

A

Immune response to streptococcal M proteins cross reacts with cardiac (among other) self -antigen

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62
Q

RF can include:

A

Pancarditis, migratory polyarthritis (large jts), subcutaneous nodules, rash (erythema marginatum)

Sydenham chorea: neurologic disorder with involuntary rapid, purposeless movements

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63
Q

Cardiac features of acute RF

A

Pancarditis, featuring Aschoff bodies

Inflammation and fibrinoid necrosis of endocardium and left sided valves, with verrucae (vegetations)

Repeated streptococcal infections will cause these features to recur

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64
Q

Chronic RHD

A

Mitral leaflet thickening, fusion and shortening of commissures, fusion and thickening of tendinous cords, resultingin mitral

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65
Q

Chronic RF and RHF

A

LA enlargement->atrial fib (arrhythmias), thromboembolic events

Pulmonary congestion/RHF

Infective endocarditis

Surgical repair/prosthetic valve replacement

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66
Q

Infective endocarditis

A

An infection of valves and endocardium, characterized by vegetation’s consisting of microbes and debris, associated with underlying tissue destruction

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67
Q

Acute infective endocarditis

A

Rapidly progressing, destructive infection of a previously normal valve

Requires surgery in addition to antibiotics

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68
Q

Subacute infective endocarditis

A

Slower progressing infection of a previously deformed valve (such as in chronic RHD)
-can often be cured with antibiotics alone

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69
Q

Infective endocarditis predisposing conditions

A

Valvular abnormalities
-HRD, prosthetic valves, MV prolapse, calcific stenosis, bicuspid AV

Bacteremia

  • another site of infection, dental work/surgery
  • contaminated needle
  • compromised epithelium
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70
Q

Classic feature of infective endocarditis

A

Friable, bulky, destructive valvular vegetation’s
-left sided valves are more commonly affected
—right sided valves often involved in IV drug abusers

-friability leads to septic emboli (PE if right side valve)

-vegetation’s are mixtures of fibrin, inflammatory cells, and organisms
—subacute vegetation’s may have a granulation tissue component

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71
Q

Nonspecific symptoms of infective endocarditis

A

Fever, weight loss, fatigue

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72
Q

__ are usually present with left sided lesions

A

Murmurs

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73
Q

Organismsof infective endocarditis

A

S. Viridans (valve abnormalities)

S aureus (normal valves, abnormal valves, IV drug abusers)

S epidermis (prosthetic valves)

HACEK (haemophilus, actinobacillus, cardiobacterium, eikenella, kingella

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74
Q

Acute bacterial endocarditis

A

<6 weeks with 50% mortality

Highly virulent organisms

Normal valves

Necrotizing, ulcerative destructive lesions

Micro: fibrin, inflammatory cells and organisms

Rapid onset of symptoms

Difficult to cure: surgery

Aortic and mitral valves

Right heart valves if IV drug user

Ring abscess: vegetation erode into underlying myocardium

Emboli->septic infarcts or mycotic aneurysm

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75
Q

Subacute infective endocarditis

A

> 6 weeks, most survive with treatment

Less virulent organisms; insidious

Abnormal valves

Less destructive lesions

Micro: granulation tissue, fibrosis, calcification, chronic inflammatory cells

Vague flu like symptoms

Antibiotics

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76
Q

Pathological criteria for diagnostic criteria for infective endocarditis

A

Microorganisms, demonstrated by culture or histologic examination, in a vegetation, embolus from a vegetation or intracardiac abscess

Histologic confirmation of active endocarditis in vegetation or intracardiac abscess

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77
Q

Clinical criteria for endocarditis

A

Blood culture positive for a characteristic organism or persistently positive for an unusual organism

Echocaridiographic identification of a valve related or implant related mass or abscess, or partial separation of artificial valve

New valvular regurgitation

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78
Q

Minor clinical features infective endocarditis

A

Subungual/splinter hemorrhages

Jane way lesions

Oiler nodes, Roth spots

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79
Q

Nonbacterial thrombotic endocarditis

A

Small, sterile thrombi on cardiac valve leaflets, along the line of closure
-loosely attached, not invasive , do not illicit an inflammatory reaction

May be a source of emboli

Associated with malignancies (espicially mucinous adenocarcinomas), sepsis, or catheter induced endocardial trauma

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80
Q

Carcinoid heart syndrome

A

A systemic disorder marked by flushing, diarrhea, dermatitis, and bronchoconstriction; bioactive compounds such as serotonin released by carcinoid tumors

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81
Q

In carcinoid syndrome, what correlates with severely of cardiac lesions

A

Plasma levels of serotonin and urinary excretion of the serotonin metabolite 5-hydroxyindoleacetic acid correlate with the severity of the cardiac lesions

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82
Q

Carcinoid heart disease

A

50% of patients with systemic sx dev cardiac manifestations
-liver normally catabolizes inculcating mediators before they can affect the heart; this usually massive metastatic hepatic burden

-right endocardium and valves*; left side protected due to pulmonary vascular bed degradation of mediators

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83
Q

Carcinoid heart disease similar lesions

A

As patients taking fenfluramine (appetite suppressant) or ergot alkaloids (migraine); affect systemic serotonin metabolism

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84
Q

Complications of cardiac valve prostheses

A

Thrombosis/thromboembolism

Anticoagulant-related hemorrhage

Prosthetic valve endocarditis

  • wear, fracture, poppet failure in ball valves, cuspal tear, calcification
  • other forms of dysfunction

Inadequate healing (paravalvular leak), exuberant healing (obstruction), hemolysis

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85
Q

Cardiomyopathies

A

Dilated cardiomyopathy

Takotsubo cardiomyopathy

Arrhythmogenic right ventricular cardiomyopathy

Hypertrophic cardiomyopathy

Restrictive cardiomyopathy

Amyloid

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86
Q

Dilated functional pattern
Left ventricular ejection fracture, mechanism of heart failure, causes of phenotype, indirect myocardial dysfunction (mimicking cardiomyopathy)

A

,40%

Impairment of contractility (systolic dysfunction)

Genetic, alcohol, peripartum, myocarditis, hemochromatosis, chronic anemia, doxorubicin (adriamycin) toxicity; sarcoidosis; idiopathic

Ischemic heart disease; valvular heart disease; hypertensive heart disease; congenital heart disease

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87
Q

Hypertrophic functional

Left ventricular ejection fraction, mechanism of heart failure, causes of phenotype, indirect myocardial dysfunction (mimicking cardiomyopathy0

A

50-80%

Impairment of compliance (diastolic dysfunction)

Genetic; friedreich ataxia; storage disease; infants of diabetic mother
Hypertensive heart disease; infants of diabetic mother

Hypertensive heart disease; aortic stenosis

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88
Q

Restrictive functional pattern
Left ventricular ejection fraction, mechanism of heart failure

Causes of phenotype

Indirect myocardial dysfunction (mimicking cardiomyopathy0

A

45-90%

Impairment of compliance (diastolic dysfunction)

Amyloidosis; radiation-induced fibrosis;idiopathic

Pericardial constriction

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89
Q

Dilated cardiomyopathy

A

Progressive cardiac dilation and systolic dysfunction, usually with dilated hypertrophy

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90
Q

Pathogenesis dilated cardiomyopathy

A

Thought to be familial in 30-50% of cases (TTN mutations may account for 20% of all cases); usually AD

Alcohol

Myocarditis

Cardiotoxic drugs

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91
Q

Cardiotoxic drugs associated with dilated cardiomyopathy

A

Doxorubicin, cobalt, IRON overload,

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92
Q

Iron overload dilated cardiomyopathy

A

From hereditary hemochromatosis (HFE mutation) or multiple transfusions

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93
Q

Morphology of dilated cardiomyopathy

A

Dilation of all chambers

Mural thrombi are common

Functional regurgitation of valves

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94
Q

Presentation dilated cardiomyopathy

A

Usually manifests between age 20-50

Progressive CHF ->dyspnea , exertional fatigue, decrease EF (<25% end stage)

  • arrhythmias
  • embolism
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95
Q

Takotsubo cardiomyopathy

A

Broken heart syndrome

Excess catecholamines following extreme emotional or psychological stress

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96
Q

Who gets takotsubo cardiomyopathy

A

> 90% women age 58-75

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97
Q

Symptoms takotsubo cardiomyopathy

A

Similar to acute MI

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98
Q

Morph takotsubo cardiomyopathy

A

Apical ballooning of the left ventricle with abnormal wall motion and contractile dysfunction

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99
Q

Hypertrophic cardiomyopathy 1

A

100% genetic causes

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100
Q

Hypertrophic cardiomyopathy phenotype—>leads to heart failure, sudden death, atrial fibrillation, stroke

A

Hypertrophy, marked

Asymmetrical septal hypertrophy

Myofibroblasts disarray

Fibrosis, interstitial and replacement

LV outflow tract plaque

Thickened septal vessel

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101
Q

Arrhythmogenic right ventricular cardiomyopathy

A

Right ventricular failure and arrhythmias

Familial, AD

Naxos syndrome

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102
Q

Right ventricular failure and arrhythmias

A

Myocardium of the right vertncuarl wall replaced by adipose and fibrosis

Causes ventricular tachycardia or fibrillation->sudden death

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103
Q

Familial, autosomal dominant ARVC

A

Defective cell adhesion proteins in the desmosomes that link adjacent cardiac myocyte

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104
Q

Naxos syndrome

A

Arrhythmogenic right ventricular cardiomyopathy with hyperkeratosis of plantar palmar skin surfaces

-mutations int he gene encoding the desmoosme-associated protein plakoglobin

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105
Q

Hypertrophic cardiomyopathy

A

A genetic disorder leading to myocardial hypertrophy and diastolic dysfunction leading to reduced stroke volume and often ventricular outflow obstruction

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106
Q

Mutations of hypertrophic cardiomyopathy

A

Numerous..involving sarcomeric proteins

-most commonly B-myosin heavy chain

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107
Q

Morphology hypertrophic cardiomyopathy

A

Massive myocardial hypertrophy, often with marked septal hypertrophy

Microscopically, myocyte disarray

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108
Q

Consequences of extensive hypertrophy in hypertrophic cardiomyopathy

A

Foci of MI may occur

Left atrial dilation and mural thrombus

Dismissed cardiac output and increased pulmonary congestion leads to exertional dyspnea

Arrhythmias

Sudden death

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109
Q

Restrictive cardiomyopathy

A

Decreased ventricular compliance (increased stiffness), leading to diastolic dysfunction (impaired filling), while systolic function of the LV remains normal

May be secondary to deposition of material with int he wall (amyloid). Or increased fibrosis (radiation)

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110
Q

Heart size and restrictive cardiomyopathy

A

Ventricles are usually of normal size, but both atria can be enlarged

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111
Q

Amyloid with restrictive cardiomyopathy

A

Extracellular deposition of proteins which form an insoluble B pleated sheet

May be systemic (myeloma) or restricted to the heart (usually transthyretin)

  • certain mutated versions of transthyretin are more amyloidogenic
  • amyloid can involve different parts of the heart, but when deposits are in the interstitiium of the myocardium, a restrictive cardiomyopathy results
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112
Q

Amyloid Congo red stain

A

Apple green birefringence

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113
Q

Myocarditis

A

Inflammation of the myocardium , most commonly due to a virus in the US

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114
Q

What viruses cause myocarditis

A

Coxsackie A and B

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115
Q

Infectious causes of myocarditis

A

Tyrpanosome cruzi (chagas)

Bacteria and fungi

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116
Q

Trypanosome cruzi (chagas) and myocarditis

A

10% die during acute attack

May progress to cardiac insuffiency in 10-20 years

Parasitization of scattered myofibroblasts; mixed inflammatory cell infiltrate (PMB, lymph’s, macrophages, occ eosinophils)

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117
Q

Noninfectious causes of myocarditis

A

Immune mediated reactions including RF, DLE, drug hypersensitivity

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118
Q

See table 12-13 p 571

A

Ok

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119
Q

Major causes of myocarditis

A

Infections

Immune mediated reactions

Unknown-sarcoidosis, giant cell myocarditis

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120
Q

Pericardial disease: slow accumulation

A

Normal<50 mL clear, straw colored fluid

Slow accumulation, <500 mL asymptomatic if slow enough
-globular enlargement of heart shadow on CXR

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121
Q

Acute pericardial disease

A

200-300 mL rapid accumulation
—>cardiac tamponade
Normal<50

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122
Q

Fibrinous and serofibrinous pericardial disease most common

A

-AMI, POSTINFARCTION(dressers),Uremia, chest irradiation, RF, SLE, trauma

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123
Q

Fibrinous

A

Dry, finely granular

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124
Q

Serofibrinous

A

Yellow-brown, turbid fliud with WBC, RBC, and fibrin

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125
Q

Symptoms pericardial disease

A

Pain (sharp, pleuritic and position dependent), fever, +/- CHF

LOUD PERICARDIAL FRICTION RUB MOST STRIKING FEATURE

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126
Q

Primary cardiac tumors: top 5

A

All benign

-myxomatosis, fibroma, lipomas, papillary fibroelastomas, rhabdomyomas, and angiosarcomas

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127
Q

Metastatic tumors to heart occur in _% of people dying from cancer

A

5

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128
Q

My MOA

A

Most common primary, pedunculated (sessile), usually in region of fossa ovalis

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129
Q

Genetics myxoma

A

Familial syndromes associated with myxoma have activating mutations in GNAS1, encoding a subunit of G protein a(in association with MCCUNE-ALBRIGHT syndrome) or null mutations in PPKAR1A, encoding a regulatory subunit of a cyclic AMP dependent protein kinase (carney complex)

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130
Q

Morphology myxoma

A

Globular hard mass, mottled with hemorrhage to soft, translucent, papillary or villous with a gelatinous appearance

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131
Q

Symptoms of myxoma

A

Ball valve obstruction, embolization or constitutional symptoms (fever malaise)

132
Q

__ form of myxoma cause intermittent obstruction (position dependent) during systole of AV valve or wrecking ball causing damage to the valve leaflets

A

Pedunculated

133
Q

Constitutional sx of myxoma

A

Elaboration by some myxomas of the IL-6 , a major mediator of the acute-phase response

134
Q

Auscultation myxoma

A

Tumor plop

135
Q

Cardiac transplantation

A

3000 a year worldwide; DCM and IHD most common

136
Q

Major complication of cardiac transplantation

A

Allograft rejection

-routine endomyocardial bx to monitor

137
Q

Allograft arteriopathy

A

Most impt long term limitation

  • late, progressice, diffusely stenosing intima proliferation
  • 50% dev in 5 yr, virtually all pt within 10yr
  • silent MI: enervated transplanted
138
Q

EBV assoc B cell lymphoma

A

Due to chronic T cell immunosuppression

139
Q

Overall survival cardiac transplantation

A

90% at year 1, <60% at 5 year

140
Q

Long QT syndrome

A

Manifests as arrhythmias associated with excessive prolongation of the cardiac depolarization; patients often present with stress induced syncope or sudden cardiac death and some forms are associated with swimming

141
Q

Short QT syndrome

A

Patients have arrhythmias associated with abbreviated depolarization intervals; they can present with palpating, syncope and SCD

142
Q

Brigade syndrome

A

Manifests as ECG abnormalities (ST segment elevations and right bundle branch block) in the absence of structural heart disease; patients classically present with syncope or SCD during rest or sleep or after large meals

143
Q

CPVT

A

Does not have characteristic ECG changes; patients often present in childhood with life threatening arrhythmias due to adrenergic stimulation (stress related)

144
Q

Systemic left sided hypertensive heart disease

A

Marked concentric thickening of the left ventricle wall causing reduction in lumen size. The left ventricle and left atrium are not he right in this apical four chamber view of the heart.

145
Q

Pulmonary right sided hypertensive heart disease (Cor pulmonale)

A

Right ventricle dilated and has a thickened free wall and hypertrophied trabecular. The shape of the left ventricle has been distorted by the enlarged right ventricle

146
Q

Cardiac valvular degeneration

A

Calcific aortic stenosis

Mitral annular calcification

147
Q

Rheumatic aortic stenosis

A

Commissural fusion is not usually seen. The mitral valve is generally normal, although some patients may have direct extension of aortic valve calcified deposits onto the anterior mitral leaflet. In contrast, virtually all patients with rheumatic aortic stenosis also have concomitant and characteristic structural abnormalities

148
Q

Acute carditis

A

Pericardial friction rubs, tachycardia, and arrhythmias

Myocarditis can cause cardiac dilation that may culminate in functional mitral valve insuffiency or even heart failure. Approximately 1% of affected die of fulminant RF involvement of the heart

Arthritis typically begins with migratory polyarthritis in which one large joint after another becomes painful and swollen for a period of days and then subsides spontaneously, leaving no residual disability

149
Q

What are verrucae

A

Vegetation’s=aggregation of fibrin and platelets

Along mitral and/or aortic valvular lines of closure

150
Q

RF histology

A

Anitschow cells pathogenoc for Rheumatic fever; may be multinucleated

Nucleus-central round oval
Chromatin
-central wavy ribbon

151
Q

Most consistent sign of infective endocarditis

A

Fever

152
Q

Acute infective carditis

A

Pt with left sided lesions, 90 % have murmurs
-microemboli give risk to nail bed (splinter) hemorrhages; painless palm or sole erythematous lesions (Jane way); painful fingertip nodules (Oiler); retinal hemorrhages (Roth spots)

153
Q

Jane way lesions

A

Small erythematous or hemorrhagic, macular, nontender lesions not he palms and soles; consequence of septic embolic events

154
Q

Oiler nodes

A

Small tender subcutaneous nodules that develop in the pulp of the digits or occasionally more proximally int he fingers and persists for hours to several days

155
Q

Roth spots

A

Oval retinal hemorrhages with pale centers

156
Q

Sources of mucinous adenocarcinoma??

A

Ok

157
Q

Endocardial fibrotic lesion in carcinoid heart disease

A

Involving the right ventricle and tricuspid valve

158
Q

Dilated cardiomyopathy presentation

A

With slowly progressive signs and symptoms of CHF including dyspnea, easy fatigability, and poor exertional capacity. At the end stage, ejection fractions are typically less than 25% (normal 50-50)

159
Q

Takotsubo

A

Left ventricular contractile dysfunction following extremes physchological stress; affected myocardium may be stunned or show multifocal contraction band necrosis. For unclear reasons, the left ventricular apex is most often affected leading to apical ballooning that resembles a takotsubo Japanese fishing pot for trapping octopus

160
Q

Dilated cardiomyopathy histology

A

Masson trichromatic stain) collagen is highlighted as blue

Four chamber dilation and hypertrophy are evident . No mural thrombus at the apex of the left ventricle the coronary arteries were potent

161
Q

Secondary or primary pericardial disease more common

A

Secondary . Primary usually viral. Secondary; metz from remote neoplasm, s/p surgery, systemic disease

162
Q

Acute suppurative pericarditis

A

Acute suppurative pericarditis arising from direct extension of an adjacent pneumonia. Extensive purple NT exudate is evident

163
Q

Pericarditis

A

Fibrinous/serofibrinous exudate (bread and butter pericarditis) usually resolves

164
Q

Myocarditis

A

Perivascular Aschoff bodies

165
Q

Endocarditis

A

Subendocardial inflammatory foci. May lead to formation of maccallum plaques (causes abnormal blood flow)

166
Q

Valvulitis

A

Inflammation may involve the valves, chordates tendinae

167
Q

Benign masses arising from the mesenchymal components of the atrial wall can produce ___ effect by intermittently occluding the atrioventricular valve orifice. Embolization of tumor fragments may occur. 90% arise from the atrial

A

Ball valve

168
Q

Rheumatic heart disease histology

A

Aschoff bodies

Valvular lesions

169
Q

Chronic rheumatic disease histology

A

Fibrous adhesions

Cardiac valve alterations

Fusion of one or more commissures between adjacent leaflets

170
Q

Mitral stenosis

A

Stenosis and incompetence of the mitral and aortic valve are produced by obstruction of the orifice and regurgitation of blood across the orifice

Right ventricular hypertrophy and dilation and functional tricuspid regurgitation the characteristic opening snap and diastolic rumbling murmur at the cardiac apex

171
Q

SLE heart

A

Atypical verrucae s endocarditis of Libyan and sacks

172
Q

Nonbacterial thrombotic endocarditis

A

Sterile thrombi that form as vegetation’s on the superior surface of the leaflets of the aortic mitral tricuspid and pulmonic valves as a result of mild inflammatory and associated surface endothelial damage

173
Q

Infective endocarditis

A

Results from direct infection of the valvular or mural endocardium by bacteria or other microorganisms including fungi and rickettsia. The bacteria or other microorganisms enter the bloodstream fromt he site of a local infection of the skin, lungs, GU, or oral cavity.

174
Q

Early leasions infective endocarditis

A

Cardiac valves, unless a congenital cardiac defect which predisposes to mural endocar, is present at the site of a jet lesion. As part of a generalized inflammatory reaction to a. Bacteremia, small thrombi form over foci of endothelial damage on the endocardium, producing lesions similar to those of marantic endocarditis.

175
Q

The heart part 1

A

Cardiac specialization

Effects of aging

Heart failure

Congenital heart disease

Ischemic heart disease

176
Q

Heart failure

A

Cardiac hypertrophy
Left sided heart failure
Right sided heart failure

177
Q

Congenital heart disease

A

Left to right shunts
-ASD, VSF, PDA

Right to left shunts
-TOF and TGA

Obstructive lesions
-coarctation of the aorta, pulmonary stenosis, and aortic stenosis

178
Q

What is the number 1 worldwide cause of mortality

A

Heart disease 1/3 of death

179
Q

Does heart weight vary

A

Ya with body habitus, approx .4-.5% body weight

180
Q

Femal heart weight

A

250-320 GN

181
Q

Male heart weight

A

300-360 gm

182
Q

RT ventricular thickness

A

.5-.5 cm thick

183
Q

Left ventricular thickness

A

1.3-1.5 cm

184
Q

Heart hypertrophy

A

Increased ventricular thickness

185
Q

Dilation of heart

A

Enlarged chamber size

186
Q

Cardiomegaly

A

Increased cardiac weight

187
Q

Myocardium

A

Atrial myocytes have storage granules that contain atrial natriuretic peptide which promotes arterial vasodilation and stimulates renal salt and water elimination (natriuresis and diuresis) which is beneficial in the setting of HTN and CHF

188
Q

Valves

A

Due to their thin structure, derive most of their nourishment via diffusion
-normal leaflets and cusps vessels limited to proximal portions

189
Q

3 types of valve damage

A

Collagen (mitral prolapse)

Nodular calcification (calcific aortic stenosis)

Fibrotic thickening (rheumatic heart disease)

190
Q

Conduction

A

SA node, AV node, bundle of His, purkinje network

-normal rate spontaneous depolarization fo SA node (50-100bpm) is faster , thus sets the pace typify

191
Q

Blood supply heart

A

LAD (diagonal branches), LCX (marginal branches) and RCA

-ventricular diastole: closure of aortic valve leads to blood flow to myocardium

192
Q

Cardiac stem cells

A

Bone marrow derived precursors and stem cells present in myocardium; only replaces 1% each year
-no significant recovery in zones of necrosis

193
Q

How does aging effect the myocardium

A

Increase LV chamber size

Increase pericardial fat

Myocardium changes
-lipofuscin and basophillic degeneration

194
Q

How does aging affect valves

A

Aortic and mitral valves annular calcification

Fibrous thickening

Mitral leaflets buckle towards lt atrium -> increase left atrium size

Lambal excrescences: small filiform processes form on the closure lines of aortic and mitral valves, probably resulting from the organization of small thrombi

195
Q

Aging and vascular changes

A

Coronary atherosclerosis

Stiffening of the aorta

196
Q

Lambl excrescences

A

With time small filiform processes (lambl excrescences) form on the closure lines of aortic and mitral valves., probably resulting from the organization of small thrombi

197
Q

Congestive heart failure

A

Occurs when the heart is unable to pump blood at a rate to meet peripheral demand , or can only do so with increased filling pressure

198
Q

What causes CHF

A

Loss of myocardial contractile function (systolic dysfunction)

Loss of ability to fill the ventricles during diastole (diastolic dysfunction)

199
Q

CHF heart on biopsy

A

Heavy and dilated

200
Q

Cardiac hypertrophy

A

Cardiac myocytes become hypertrophic when

  • sustained pressure or volume overload (systemic HTN or aortic stenosis)
  • sustained tropical signals (B adrenergic stimulation)
201
Q

Pressure overload hypertrophy

A

Myocytes become thicker, and LV increases thickness concentrically

202
Q

Volume overload hypertrophy

A

Myocytes elongate and ventricular dilation is seen

Heart weight best ensure of hypertrophy in dilated heart (vs wall thickness

203
Q

Despite an increase in energy deman, hypertrophy of myocytes is not accompanied by ___

A

Increase in blood supple

204
Q

The hypertrophied hear is vulnerable to what

A

Ischemia related decompensation

205
Q

Pressure overload

A

Sarcomeres assemble in parallel

206
Q

Volume overload

A

Sarcomerss arange in series

207
Q

Left sided heart failure

A

Can be systolic do diastolic

208
Q

Most common causes of left sided heart failure

A

Myocardial ischemia

Hypertension

Left sided valve disease

Primary myocardial disease

209
Q

Clinical effects of lest sided heart failure are due to what

A

Congestion in the pulmonary circulation

Decreased tissue perfusion

210
Q

With left sided heart failure there is _ ventricular hypertrophy

A

Left

211
Q

Morphology left sided heart failure

A

Heart failure cells

Some red cells and plasma proteins extravasated into the edema fluids within the alveolar spaces, where they are phagocytosed and digested by macrophages, which store the iron recovered from hemoglobin in the form of hemosiderin. These hemosiderin laden macrophages are called heart failure cells and are telltale signs of precious episodes of pulmonary edema

212
Q

In left sided heart failure, what does left ventricular dysfunction lead to

A

Left atrial dilation

213
Q

In left sided heart failure what does left atrial dilation lead to

A

Atrial fibrillation, stasis, thrombus

214
Q

Pulmonary congestion and edema with left sided heart failure

A

Cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea

215
Q

Decreased ejection fraction with left sided heart failure results in what

A

Decreased glomerular perfusion

Stimulating release of renin->increased volume

Prerenal azotemia

216
Q

Advanced left sided heart failure may lead to what

A

Decreased cerebral perfusion and hypoxic encephalopathy

217
Q

Is right or left sided heart failure more common

A

Right

218
Q

What is right sided heart failure from

A

Isolated right sided heart failure results from any cause of pulmonary hypertension

  • parenchymal lung disease
  • primary pulmonary HTN
  • pulmonary vasoconstriction
219
Q

What happens with right sided heart failure

A

Pulmonary congestion is minimal

The venous system is markedly congested
—liver congestion (nutmeg liver)
—splenic congestion-> splenomegaly
—effusions involving peritoneal, pleural and pericardial spaces
—edema, espicially in dependent areas (ankles)
—renal congestion

220
Q

N*congenital heart disease

A

Sporadic genetic abnormalities are the major causes of congenital heart disease

Turner syndrome and trisomies 13, 18, and 21

221
Q

Most common genetic cause of congenital heart disease

A

Trisomy 21

40% of patients with Down syndrome have at least one heart defect
-usually derived fromt he second heart field (arterioventricular septae)
—most commmonly defects the endocardial cushion, including ostium, ASDs, AV valve malformations, and VSDs

222
Q

Notch pathway and congenital heart disease

A

Associated with a variety of congenital heart defects
-bicuspid aortic valve (NOTCH1)

Tetralogy of fallot (JAH1 and NOTCH2)

223
Q

Why marfans get congenital heart disease

A

Fibrillin mutations underlie marfans-associated with valvular defects and aortic aneurysms

224
Q

Name congenital heart diseases

A

Left to right shunts

Atrial septal defects

Ventricular septal defects

Patent ductus arteriosus (PDA)

Right to left shunts

Obstructive lesions

225
Q

Most commmon heart defects in downs

A

Atrioventricular septal defects, or AV canal defects (45%)

Ventricular septal defects (35%)

Secundum atrial septal defects (8%)

Patent ductus arteriosus (7%)

226
Q

What does fibrill do

A

Structural protein in ECM, also an important negative regulator of TGF-B signaling and hyperactive TGF-B signaling contributes to the cardiovascular abnormalities in marfan and loeys-diets

227
Q

Most common congenital cardiac malformation

A

Ventricular septal defect

228
Q

Genes associated with ASD or conduction defects

A

NKX2.5 transcription factor

229
Q

Genes associated with ASD or VSD

A

GATA4 transcription factor

230
Q

Tetralogy of fallot genes

A

Zfpm2 or NKX2.5 transcription factor

231
Q

Alagille syndrome

A

Pulmonary artery stenosis or tetralogy of fallot

JAG1 or NOTCH2 signaling proteins or receptors

232
Q

Char syndrome

A

PDA

TFAP2B transcription factor

233
Q

CHARGE syndrome

A

ASD, VSD, PDA, or hypoplasia right side of the heart

CHD7 helices binding protein

234
Q

DiGeorge syndrome

A

ASD VAD or outflow tract obstruction

TBX1 transcription factor

235
Q

Holt roam syndrome

A

ASD, VSD, or conduction defect

TBX5 transcription factor

236
Q

Noonan syndome

A

Pulmonary valve stenosis , VSD, or hypertrophiccardiomyopathy

PTPN1, KRAS, SOS1

Signaling proteins

237
Q

Most common congenital heart disease

A

Left to right

  • ASD
  • VSD
  • PDA
238
Q

Presntation of atrial septal defect

A

Asymptomatic until adulthood

But get left to right shunting causing volume overload on the right side, which leads to

  • pulmonary HTN
  • right heart failure
  • paradoxical embolization
  • may be closed surgically , with normal survival
239
Q

What are the atrial septal defects

A

Secundum ASD

Primum anomalies

Sinus venosus defects

240
Q

Secundum ASD

A

90% of all asd; center of atrial septum ; may be multiple of fenestrated

241
Q

Primum anomalies

A

5% of all ASD

Adjacent to AV valves

Often associated with AV valve abnormalities and/or VSD

242
Q

Sinus venosus defects

A

5% of all ASD

Near entrance of SVD

Can be associated with anomalous pulmonary venous return to the R atrium

243
Q

Patent foramen oval

A

80% close by 2

Remaining 20% the flap can open if increase right side pressure
-thus even temporary increase in pressure can produce brief periods of R-L shunting
—pulmonary HTN, bowel movement, coughing, sneezing

Paradoxical embolus

244
Q

Most common congenital heart disease

A

Ventricular septal defect

245
Q

VSD types

A

90% membranous

Infundibulad VSD: below pulmonary cancer or within muscular septum

246
Q

Effects of VSD depend on what

A

Size, and presence of other heart defects

-those that manifest with SX as childre, often associated with other cardiac anomalies

247
Q

Many small VSD do what

A

Close sponataneously

248
Q

Large VSD

A

May cause significant shunting, leading to

  • right ventricular hypertrophy
  • pulmonary HTN, which can ultimately reverse flow through the shunt, leading to cyanosis
249
Q

If VSD symptoms manifest in adulthood

A

Usually a single defect

250
Q

Patent ductus arteriosus

A

May fail to close when infants are hypoxic and/or have defects associated with increased pulmonary vascular reassure

PDA produces a harsh , machinery like murmur

251
Q

Effect of PDA is determined by what

A

Shunts diameter

-large shunts can increase pulmonary pressure and eventually shunt reversal and cyanosis

252
Q

Right to left shunt presentation

A

Cyanosis early in postnatal life (cyanosis congenital heart disease)

253
Q

What causes R to L shunt

A

Tetralogy of fallot, most common

Transposition of great arteries

Persistent truncus arteriosus

Tricuspid atresia

Total anomalous pulmonary venous connection

254
Q

Tetralogy of fallot features

A 
FOUR
VSD
Obstruction of RV outflow tract
Aorta overrides the VSD
RV hypertrophy
255
Q

What does heart look like in TOF

A

Enlarged and boot shaped because of the right ventricular hypertrophy

256
Q

Linical severity of TOF depends on what

A

Degree of subpulmonary stenosis
-mild stenosis: L to R shunt
Classic TOF is R to L shunting with cyanosis
-mst infants cyanosis from birth, or soon after

257
Q

Trnaposion of great vessels results in

A

Two separate circuits, incompatible with life after birth unless a shunt is present for mixing of blood form the two circuits

  • approximately one third have VSD
  • 2/3 have a patent foramen ovale or PSA
  • right ventricle becomes hypertrophic (supports systemic circulation) and the left ventricle atrophied
  • without surgery, patients will die within a few months
258
Q

Coarctation of the aorta

A

Narrowing of the aorta, generally seen with a PDA (infantile) or without a PDA (adult form )

259
Q

Who gets coarctation of aorta

A

Males 2x, Turner syndrome 45 XO

260
Q

Clinical severity of coarctation of the aorta depends on what

A

Clinical severity depends on the degree of stenosis and potency of the ductus arteriosus

261
Q

Coarctation with PDA manifests when

A

At birth; may produce cyanosis in the lower half of the body

262
Q

Coarctation it’s out PDA presented

A

Usually asymptomatic

  • HTN in UE; hypotension in LE
  • claudication and cold lower extremities
  • may eventually see concentric LV hypertrophy
263
Q

What can get from coarctation of aorta

A

Pulmonary stenosis and atresia

Aortic stenosis and atresia

264
Q

Turner syndrome

A

Complete or partial monosomy of the X chromosome and is characterized primarily by hypogonadism in the phenotypic females. Bilateral neck webbing and persistent looseness of skin on the back of the neck, left sided cardiovascular abnormalities, particularly predictable coarctation of the aorta an bicuspid aortic calve, are seen most frequently. Cardiovascular abnormalities are the most important cause of increased mortality in kids with turner

265
Q

Ischemic heart disease results from

A

Insufficient perfusion to meet the metabolic of the myocardium

266
Q

Blood to the myocardium is supplied by what

A

Coronary arteries, so any disruption of coronary flow may result in ischemia

267
Q

Ischemia results in what

A

Myocardial infarction

Angina pectoris

Chronic ischemic heart disease, with heart failure

Sudden cardiac death

268
Q

Ischemic heart disease is leading cause of death in US and >90% are secondary to ___

A

Atherosclerosis

-chronic vascular occlusion
-acute plaque change
—thrombus

269
Q

Angina pectoris

A

Transient, often recurrent chest pain induced by myocardial ischemia insufficient to induce myocardial infarction

270
Q

Three clinical variants of angina pectoris

A

Stable angina

Prinzmetal variant angina

Unstable (crescendo) angina

271
Q

Stable angina

A

Stenosis occlusion of coronary artery

Squeezing or burning sensation, relieved by rest or vasodilator

Induced by physical activity, stress

272
Q

Prinzmetal variant angina

A

Episodic coronary artery spasm, relieved with vasodilator

Unrelated to physical activity, HR or BP

273
Q

Unstable crescendo angina

A

Frank pain, increasing in frequency, duration and severity; at progressively lower levels of physical activity, eventually even at rest

Usually rupture of atherosclerotic plaque, with partial thrombus

50% may have evidence of myocardial necrosis, acute MI may be imminent

274
Q

MI

A

Age distribution and risk factors mirror those atherosclerosis in general, because nearly 90% of infarcts are caused by an atheromatous plaque

Or embolus, vasospasm, ischemia secondary to vasculitis, shock, hematologic abnormalities

275
Q

Classic presentation MI

A

Prolonged chest pain >30 min

  • crushing, stabbing , squeezing, tightness
  • radiating down left arm

Diaphoresis

Dyspnea

Nausea-vomiting

Up to 25% are asymptomatic

276
Q

MI the location , size and features of acute MI depend on what

A

Site, degree and rate of occlusion of artery, size of the area perfused, duration of occlusion, metabolic and oxygen needs of the area at risk, extend of collateral blood flow, presence of arterial spasm

277
Q

Ischemia of myocytes

Seconds, 2 min, 10 min, 40 min, 20-40 min, >1 hour

A

Onset of ATP depletion

Loss of contractility

ATP reduced 50%

10%

Irreversible cell injury
Microvascular injury

278
Q

Coronary vessels and areas of infarction

A

LAD (40-50%)
-apex, LV anterior wall, anterior two thirds of septum

RCA (30-40%)
-RV free wall, LV posterior wall, posterior third of septum

LCX (15-20%)
-LV lateral wall

279
Q

Transmural infarcts RV

A

Permanent occlusion of the left anterior descending branch

Permanent occlusion of left circumflex

Permanent occlusion of right coronary artery (or its posterior descending branch)

280
Q

Non transmural infarcts LV

A

Transient/partial obstruction-> regional subendocardial infarct

Global hypotension->circumferential subendocardial infarct

Small intramural vessel occlusions->microinfarcts

281
Q

Distribution of MI necrosis correlated with the location and nature of decreased perfusion. Left, the positions of transmural acute infarcts resulting from occlusions of the major coronary arteries; top to bottom, left anterior descending, left circumflex, and right coronary arteries. IGH, the types of infarcts that result from a partial or transient occlusion, global hypotension, or intramural small vessel occlusion

A

Ok

282
Q

0-1 hours MI

A

Reversible..no gross features, no light microscope,

EM relaxation of myofibroblasts, glycogen loss, mitochondrial swelling

283
Q

1/2 4 hours MI

A

No gross features,
LM variable waviness of fibers at border

EM sarcolemmal disrutpion, mitochondrial amorphous densities

284
Q

4-12 hours MI

A

Dark mottling

LM early coagulation necrosis; edema, hemorrhage

285
Q

12-24 hours

A

Dark mottling

LM ongoing coagulation necrosis; pyknosis of nuclei; myocyte hypereosinophilia; marginal contraction band necrosis; early neutrophilic infiltrate

286
Q

1-2 days MI * note after 4 hours irreversible

A

Mottling with yellow tan infarct

LM coagulation necrosis, with loss of nuclei and striations; brisk interstitial infiltrate of neutrophils

287
Q

3-7 days MI

A

Hyperemic border; central yellow tan softening

LM beginning disintegration of dead myofibroblasts, with dying neutrophils l early phagocytosis of dead cells by MACROPHAGES at infarct border

288
Q

7-10 days MI

A

Maximally yellow tan and soft, with depressed red tan margins

LM well developed phagocytosis of dead cells; granulation tissue at margins

289
Q

10-14 days MI

A

Red gray depressed infarct borders

Well established granulation tissue with new blood vessels and collagen deposition

290
Q

2-8 weeks MI

A

Gray white scar progressive from border toward core of infarct

LM increased collagen deposition, with decreased callularity

291
Q

> 2 months MI

A

Scarring complete

Dense collagenous scar

292
Q

Acute MI over 24 hours

A

Coagulation necrosis, pyknotic nuclei, loss of cross striations

293
Q

MI 1-3 days

A

Loss of striations

Neutrophilic infiltration

294
Q

Repercussion

A

Restoring blood flow to an area of ischemia and impending infarction
-an attempt to limit the infarct size by rescuing at risk myocardium

Thrombolysis, angioplasty and stent placement, CABG

295
Q

Effects of reperfusion

A

Following coronary occlusion, contractile function is lost within 2 minutes and viability begins to dismiss after 20 minutes . If perfusion is not restored then nearly all myocardium int he affected region suffers death
If flow is restored, then some necrosis is prevented, myocardium is salvages and at least some function can return. The earlier reperfusion occurs, the greater the degree of salvage. However, the process of reperfusion itself may inducesome damage and return of function of salvaged myocardium may be delayed for hours to days (postischemic ventricular dysfunction or stunning)

296
Q

Release of myocyte proteins in MI

A

Troponin I or tropoini T, and creatine kinase, MB fraction (CK-MB) are routinely used as diagnostic biomarkers

297
Q

Measuring the blood levels of proteins that leak out of irreversibly damaged myocytes; the most useful are cardiac specific proteins. What are they

A

Cardiac specific troponin T and I CTnT and CTnI

MB fraction of creatinine kinase CK-MB

298
Q

The most sensitive and specific biomarkers of myocardial damage are what

A

Cardiac specific proteins, particularly cnTnT and cTnI (proteins that regulate calcium mediated contraction of cardiac and skeletal muscle )

299
Q

Are troponin I and T normally in circulation

A

No not normally

Following an MI, levels of both begin to rise at 3-12 hours

CTnT levels peak somewhere between 12-48 hours while cTnI levels are maximal at 24 hours

300
Q

Creatine kinase

A

Enzyme expressed in brain, myocardium and skeletal muscle; it is a dimer composed of two isoforms designated M and B

301
Q

MM and BB diners creatine kinase

A

MM home dimer s are found predominantly inc Adrian and skeletal msucle, and BB home dimer s in brain, lung, and many other tissues. MB heterodimer are principally localized to cardiac muscle (with considerably lesser amounts found in skeletal msucle)

Thus MB form of CK (CK-MB) is sensitive but not specific , since it can also be elevated after skeletal muscle injury

302
Q

CK-MB begins to rise when

A

Within three to twelve hours of onset of MI, peaks at twenty four hours, and returns to normal within forty eight to seventy two hours

303
Q

Time to elevation of CKMB, CTnT and cTnI

A

Three to twelve hours

304
Q

CKMB and cTnI peak

A

Twenty four hours

305
Q

CKMB returns to normal

A

Forty eight to seventy two hours

Five to ten days

Five to fourteen days

306
Q

Arrhythmia

A

Half of all MI deaths occur within one hour of onset and are usually secondary to arrhythmia

Arrhythmia can be a longer term complication of MI, depending on the site and extent of the lesion
-can result from permanent damage to the conducting system, or from myocardial irritability following the infarct

307
Q

Contractile dysfunction

A

Dependent on size of the infarct and associated loss of function

308
Q

Fibrous pericarditis

A

Ok

309
Q

Myocardial rupture

A

Typically requires a transmural infarct

2-4 days post MI, when inflammation and necrosis have weakened the wall

310
Q

Risk factors myocardial rupture

A

Increased age, large transmural anterior MI, first MI, absence of LV hypertrophy

311
Q

Infarct expansio

A

Muscle necrosis->weakening, stretching and thinning of the wall

Mural thrombus often seen

312
Q

Ventricular aneurysm

A

Late complication of large transmural infarcts with early expansion

Composed of thinned wall of scarred myocardium

Also associated with mural thrombus

Rupture does not ususallly occur

313
Q

Myocardial necrosis

A

Being after forty five minutes of severe ischemia and extends from the subendocardium into the subepicardium in a wave front fashion over a period of approximately three to four hours

314
Q

Subendocardial (intramural) myocardial infarcts

A

Limited to the inner half of the wall

315
Q

Transmural MI

A

Extend into the outer half of the wall

316
Q

Lesions of the left anterior descending coronary system give rise to what

A

Anterior and anteromedial MI

317
Q

Lesiosn of the right coronary artery give rise to

A

Inferior (posteroapical) and posterior MI

318
Q

Lesions of the left circumflex coronary artery give rise to l

A

Lateral MI

319
Q

Acute MI may result in death due to pump failure or

A

Ventricular fibrillation

If patient survives, the infarct undergoes organizationa Nd healing. During the first 2-3 weeks, the necrosis myocardium is gradually replaced by granulation tissue; during the nex two to three months, the granulation tissue is converted to fibrous scar.

320
Q

TRANSMURAL MI

A

MAY RUPTURE DURING FIRST SEVEN TO TEN DAYS AFTER ONSET. PATIENTS AT HIGH RISK ARE THOSE WITH PERSISTENT HTN DURING THEIR INFARCTS AND THOSE WITH INFARCTS IN REGIONS WITHOUT FIBROSIS; DURING THEIR INFARCTS AND THOSE WITH INFARCTS INR EGIONS WITHOUT FIBROSIS; TYPICLLY THESE ARE FIRST INFARCTS. OVER TIME A DISSECTION TRACK DEVELOPS FROM THE LEFT VENTRICULAR CHAMBER THROUGH THE NECROTIC MYOCARDIUM AND THE COMPLETED PROCESS RESULTS IN ABRUPT DEVELOPMENT OF HEMOPERICARDIUM, CARDIAC TAMPONADE, AND ELECTROMECHANICAL DISSOCIATION. THIS GENERALLY FATAL, IN SOME CASES THE INTRAMURAL DISSECTIONR OCCURS SLOWLY ENOUGH FOR A PERICARDIAL INFLAMMATORY RECTION TO OCCUR AND SEAL OFF A REGION OF PERICARDIUM , CONTAINING THE RUPTURE. THIS GIVES RISE TO A WIDE MOUTHED PSEUDOANEURYSM THAT, UNLIKE TRU ANEURYSMS IS PRONE TO LATE RUPTURE. OTHER SEVERE COMPLCIATIONS OF ACUTE MI INVLVE RUPTURE OF INFARCTED INTERVENTRICULAT SEPTUM TO PRODUCE A VSD AND RUPTURE OF THE HEAD OR ENTIRE TRUNK OF AN INFARCTED PAPILALRY MUSCLE. THESE COMPLCIATIONS LEAD TO SYSTOLIC MURMURS AND CARDIAC FIALURE

321
Q

Concentric hypertrophy hypertension

A

Leads rapidly to cardiac hypertrophy, a compensatory increase of mass of the LV. The typical pattern of concentric hypertrophy of the LV, characterized by a thick wall and a relatively small chamber columns, is produced by a pressure load (afterload) on the ventricle. The heart size on cardiac silhouette is relatively normal, but the ECG shows increased voltage. When the limits of compensation are reached, the patient may have progressive cardiac decompensation accompanied by cardiac dilation. Cardiac hypertrophy is an independent risk factor for ventricular arrhythmias and sudden cardiac death

322
Q

Heart failure

A

A state in which the heart fails as a pump to provide sufficient volume of circulating blood to meet the metabolic demands of the body. Bc the dominant symptoms usually result from pulmonary or systemic venous congestion, the condition is termed CHF
Most commonly, heart failure is of the low cardiac output , but some including thiamine defiency (beriberi), thyrotoxicosis and severe anemia, produce cardiac failure with an increased circulating blood volume (high output cardiac failure) as shown here. The failure may be left sided right sided, or combined left and right sided heart failure. This illustration shows the major manifestations of failure of the left and right ventricles. Cardiac transplantation or an artificial heart is the last therapeutic option. The most common conditions necessitating cardiac transplantation are end stage ischemic heart disease and dilated cardiomyopathy

323
Q

Eccentric hypertrophy

A

Heart failure results in progressive ventricular dilation superimposed on the hypertrophy, which produces a pattern of eccentric hypertrophy

Left sided heart failure-most commonly from HTN and CAD

324
Q

Right sided heart failure

A

Cor pulmonale
Due to HTN int he pulmonary circulation, is caused by pulmonary vascular or parenchymal disease
Thromboembolism -may cause sudden death bc the obstruction of the pulmonary vasculature produces pulmonary HTN and acute right sided failure with an impaired return of blood to the left heart with consequent decreased systemic and coronary perfusion and secondary left sided heart failure

Segmental thromboembolism- do not make infarcts bc dual circulation from th epulmnonary arterues and bronchial arteries. Pulmonary infarcts do occur int he presence of thromboemboli and impaired systemic circulation associated with preexistent CHF

325
Q

Chronic Cor pulmonale

A

Typically develops in response to recurring pulmonary thromboembolic disease or chronic pulmonary parenchymal diseases, particularly chronic bronchitis and emphysema. The heart exhibits significant hypertrophy and dilation of the RV with a normal sized LV

Pathology (36 decks)

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