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CPR II Exam 1 > Lecture 3: Cardiac Pathology Part 2 (Hillard) > Flashcards

Lecture 3: Cardiac Pathology Part 2 (Hillard) Flashcards

1
Q

What is the most common cause of arrythmias?

A

Ischemic Heart Disease

  • also caused by cardiomyopathies, myocarditis, valvular disease, congenital disorders

almost ANY structural change can cause an arrhythmia

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2
Q

What is Sick Sinus Syndrome and Atrial Fibrillation?

A

SSS: SA node damage causing bradycardia
- AV node takes over –> < 50-60 BPM

AF: myocytes depolarize independently and sporadically w/variable transmission in AV node (can be seen with atrial dilation)

  • irregular HR = atrial fibrillation
  • can cause thrombus formation/thromboembolism
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3
Q

What is Heart Block and what is the difference between first, second, and third degree?

A
  • dysfunctional AV node

First Degree: prolonged PR interval
Second Degree: intermittent transmission
Third Degree: complete failure

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4
Q

Hereditary Channelopathies

What is Long QT Syndrome?

What is the classical presentation of disease?

A
  • due to hereditary abnormal ion channels which cause arrhythmogenic disease (K+ LOF/Na+ GOF)
    • Long QT is most common form
    • cause of SUDDEN DEATH after EXERTION

Classic Pt: strong swimmer that drowns due to arrhythmia

  • shows Torsades de Pointes on ECG
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5
Q

What is Hypertensive Heart Disease?

What can it lead to the development of and what is another organ finding common in patients with disease?

A
  • left ventricular hypertrophy (typically concentric, > 500 grams) with clinical history or evidence of hypertension in other organs (myocytes are larger and thicker)
  • diastolic dysfunction leading to left atrial enlargement –> atrial fibrillation (can cause CHF or Sudden Cardiac Death)

look for granular kidneys with hyaline atherosclerosis

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6
Q

What is Cor Pulmonale?

A
  • isolated Right-sided Pulmonary hypertensive heart disease in the setting of Pulmonary Hypertension
  • can arise due to disease of pulmonary parenchyma, vessels, or disorders of chest movements; also large pulmonary embolus

Left Heart Failure is MOST common cause of Right-sided Heart Failure

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7
Q

What is Calcific Aortic Stenosis?

What are three common conditions it is associated with? (H/H/I)

A
  • MOST COMMON VALVULAR ABNORMALITY (inc. risk with age - 60-80 yo)
  • due to “wear and tear” associated with chronic HTN, hyperlipidemia, and inflammation
  • see mounded calcifications in CUSPS that prevent complete opening of valve
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8
Q

What is a Bicuspid Aortic Valve?

What is a complication that is frequently found with this disease?

A
  • a congenital condition that shows accelerated course of aortic stenosis (shows symptoms 1-2 decades earlier)
  • can become incompetent leading to valve dilation and prolapse
  • bacterial endocarditis is commonly seen with this condition
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9
Q

How does Calcific Aortic Stenosis commonly present?

A
  • leads to inc. LV pressure and concentric LV hypertrophy (muscle becomes ischemic –> angina)
    signs: systolic murmur, angina (die within 5 yrs), syncope (die within 3 yrs), and CHF (die within 2 yrs)
  • treat with SURGICAL REPLACEMENT
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10
Q

What is Mitral Annular Calcification?

Who is it commonly seen in?

A
  • calcific deposits in fibrous annulus (base of leaflets) of mitral valve that is usually asymptomatic
  • can lead to regurgitation, stenosis, arrhythmias with deep calcifications; acts as nidus for thrombus and infective endocarditis
  • commonly seen in WOMEN > 60 yo
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11
Q

What is Mitral Valve Prolapse?

What genetic disease is it commonly seen in?

What do the leaflets look like in this disease?

A
  • valve prolapse back into left atrium during systole (“floppy valve”) –> more common in WOMEN
  • can be seen in MARFAN SYNDROME; also MI and rheumatic fever
  • leaflets are thick and rubbery (Myxomatous Degeneration due to inc. proteoglycan deposits) and “hooding” (interchordal ballooning)
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12
Q

How does Mitral Valve Prolapse present clinically?

A
  • most asymptomatic with mid-systolic CLICK and is the most common cause of mitral regurgitation in developed countries; chronic can cause dyspnea
  • can cause (rare): infective endocarditis, mitral insufficiency, arrhythmias (atrial), and thromboembolism
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13
Q

What is Rheumatic Fever and what is used to confirm diagnosis?

A
  • multisystem inflammatory disorder following GROUP A STREP pharyngitis (“SCARLET FEVER”)
    • typically occurs 10 days-6 wks AFTER infection
    • cannot culture active infection from blood
  • caused by Abs and CD4+ T cell rxn against M Streptococcal Ag that causes rxn to heart/joint/skin/soft tissue/nervous system antigens (MIMICRY)

Confirm: Abs to STREPTOLYSIN O and DNase B

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14
Q

What are 6 common signs of Acute Rheumatic Fever? (F/MP/P/SN/EM/SC)

A
  • Fever (101 F+)
  • migratory polyarthritis (large joints)
  • pancarditis
  • subQ nodules
  • erythema marginatum (curved, ring-shaped macules)
  • Sydenham Chorea (basal ganglia damage)
    • hopping, halting gait, grimacing, asymmetric jerking
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15
Q

What are 4 common heart findings in pts. with Acute Rheumatic Fever? (P/VV/MP/AB)

What valves does Rheumatic Heart Disease affect?

A
  • pericarditis (fibrinous), myocarditis, endocarditis
  • verrucae formation (valvulitis w/vegetations)
  • MacCallum Plaques
    • irregular thickening in Left Atrium due to regurg.

Histo: Aschoff Bodies w/Anitschkow cells
- PATHOMNEUMONIC

affects: mitral > aortic > tricuspid valves
- mitral valves have “fish mouth”/”buttonhole” stenosis

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16
Q

How does Chronic Rheumatic Heart Disease present?

A
  • valvular leaflet thickening, short chordae tendinae, fusion, and regurg. –> VALVULAR STENOSIS causing DIASTOLIC “rumbling” MURMUR
  • structural changes predisposes valve to infective endocarditis
  • can cause left atrial enlargement –> atrial fibrillation and thromboembolic events
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17
Q

What are the most likely causes of infective endocarditis in patients with:

  1. native, structurally abnormal valves
  2. poor dentition/invasive dental procedures
  3. prosthetic valves
  4. IV drug use
A
  1. Streptococcus viridans
  2. HACEK organisms
  3. Staph epidermidis
  4. Stap. aureus
    • causes RIGHT-SIDED endocarditis if injected

most infective endocarditis is LEF-SIDED

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18
Q

What are the HACEK organisms associated with infective endocarditis in patients with poor dentition?

A 
H - hemophilus
A - actinobacillus
C - cardiobacterium
E - eikenella
K - kingella
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19
Q

What are 4 physical findings of infective endocarditis?

What are they all caused by?

A
  • Subungal Splinter Hemorrhages
  • Janeway Lesions (spots on palms/soles)
  • Osler Nodes (tender nodules w/pale center)
  • Roth Spots (retinal hemorrhage)

all are caused by small septic emboli that flake off of left-sided endocarditis

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20
Q

What are 4 common causes of Nonbacterial Thrombotic Endocarditis? (S/C/AS/SLE)

A
  • sepsis, cancer (procoagulant release), antiphospholipid syndrome (APS), and systemic lupus erythematous (LIBMAN-SACKS ENDOCARDITIS)
  • all cause sterile, non-inflammatory valvular thrombi and are asymptomatic until embolization occurs
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21
Q

What are Antiphospholipid Syndrome and Libman-Sacks Endocarditis?

A

APS: autoantibodies to endothelial membrane (ANTICARDIOLIPIN, lupus anticoagulant)

  • manifests as fetal loss during pregnancy
  • can also be associated with lupus

LSE: endocarditis caused by systemic lupus
- nonbacterial

22
Q

What is Carcinoid Heart Disease?

What side of the heart does it occur on and what are common signs of disease?

A
  • bioactive compounds (SEROTONIN) from carcinoid tumors induce plaque-like endocardial/valvular thickening
  • lesions are usually seen during massive metastatic liver burden and ONLY on RIGHT-SIDE of heart (lung vasculature degrades the mediators)

Signs: flushing, diarrhea, dermatitis, bronchoconstriction

23
Q

What is the difference between use of Mechanical Prosthetic valves and Tissue Prosthetic valves?

A

M: usually long lasting (>25 yrs)

  • inc. risk of thromboembolism
  • pts. on life-long anticoagulant therapy

T: made from cow or pig valves

  • inc. risk of mechanical failure (usually 10-15 yrs)
  • only on anticoagulants for 1st 3-6 months

both types have INCREASED risk of infective endocarditis

24
Q

What conditions are associated with:

  1. crescendo-decrescendo systolic murmurs
  2. holosystolic murmurs (2)
  3. diastolic decrescendo murmur
  4. diastolic rumbling murmur
  5. continuous “machine-like” murmur
A
  1. calcific aortic stenosis
  2. mitral regurgitation and VSD
  3. aortic regurgitation
  4. Rheumatic Heart Disease (mitral prolapse)
  5. patent ductus arteriosus
25
Q

What is Cardiomyopathy and what are the three major types?

A
  • structurally and functionally ABNORMAL heart with mechanical and/or electrical dysfunction in ABSENCE of coronary artery disease, HTN, valvular disease, and congenital heart disease
  • Dilated (90% of cases), Hypertrophic, Restrictive
26
Q

What are 5 common causes of Dilated Cardiomyopathy? (F/P/A/D/IO)

A
  • familial (30-50%) due to TITIN AD mutation (TTN gene)
  • peripartum (multifactorial) - late in pregnancy
    • volume overload
  • alcohol: wet beri-beri (thiamine deficiency)
  • DOXORUBICIN (chemo drug)
  • IRON OVERLOAD due to Hereditary Hemochromatosis (HFE gene) or multiple transfusions
27
Q

What is morphology of Dilated Cardiomyopathy?

How does it present clinically?

A

M: dilation of ALL CHAMBERS and is often hypertrophic (inc. weight without thickened ventricle walls) and functional regurgitation

C: manifests between 20-50 yo with progressive CHF
- arrhythmias and thrombi formation

SYSTOLIC DYSFUNCTION

28
Q

What is Takotsubo Cardiomyopathy?

Who does it commonly affect and what is it described as looking like?

A
  • form of Dilated Cardiomyopathy associated with emotional distress (“broken heart syndrome”)
  • sudden catecholamine surge causes apical ballooning of LV, as well as inc. contractility and Coronary A. constriction (acute MI)
  • common in 60-75 yo FEMALES; looks like Japanese Octopus Pot
29
Q

What is Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)?

A
  • defective cell adhesion proteins in desmosomes linking myocytes cause RIGHT ventricular failure and arrhythmias (myocytes replaced by adipose and fibrosis w/dilation)
  • classically familial and Auto Dominant
  • causes ventricular tachycardia or fibrillation leading to sudden death
30
Q

What is Naxos Syndrome?

A
  • variant of ARVC with plantar and palmar hyperkeratosis and wooly hair
  • caused by mutation in gene encoding PLAKOGLOBIN (desmosome-associated protein); adipose and fibrosis of right ventricular wall (SUDDEN DEATH)
  • Auto RECESSIVE; presents as heart disease after 12 yo (need defib implant)
31
Q

What is Hypertrophic Cardiomyopathy?

What is its histological appearance?

What mutation is most commonly implicated?

A
  • relative common genetic disorder w/MALE prominence characterized by marked myocyte hypertrophy/disarray of SEPTAL PROMINENCE (no dilation)
  • mutation is commonly Beta-Myosin heavy chain (B-MHC)

histo shows irregular and whorled myocytes

DIASTOLIC DYSFUNCTION

32
Q

How does Hypertrophic Cardiomyopathy present clinically?

What is the classic presentation?

A
  • usually asymptomatic
  • ventricular arrhythmias = sudden death, mitral valve regurg. (systolic ejection murmur), exertional dyspnea and chest pain; palpitations

Classically: young teenage athlete dies while exercising

33
Q

What is Restrictive Cardiomyopathy and what is it caused by? (A/F)

A
  • dec. ventricular compliance leading to DIASTOLIC DYSFUNCTION (impaired filling)
  • can be caused by amyloid deposition or increased fibrosis due to radiation
  • ventricles are usually NORMAL size while both atria are ENLARGED –> congestive heart failure
34
Q

What is Amyloid-associated Restrictive Cardiomyopathy?

What staining is done to test for it?

What are two common causes of this?

A
  • extracellular deposition of proteins forming insoluble B-pleated sheets with APPLE GREEN birefringence on CONGO RED STAIN
  • can be caused by mutated Transthyretin or Senile Amyloidosis (normal transthyretin)
35
Q

Other Forms of Restrictive Cardiomyopathy

  1. Endomyocardial Fibrosis
  2. Loeffler Endocarditis (two cancer association)
  3. Endocardial Fibroelastosis
A
  1. children in tropical regions (Africa)
    • fibrosis of endocardium and subendocardium
  2. seen in tropical regions
    • EOSINOPHILIC infiltration
    • associated with leukemia and lymphoma
  3. fibroelastic thickening of LV endocardium in 1st 2 YEARS of LIFE
    • associated w/congenital heart defects
36
Q

What is the most common infection associated with Myocarditis?

A

COXSACKIEVIRUS B

viral infection is the most common cause of myocarditis

37
Q

What does infectious myocarditis due to Chagas Disease look like?

What is used to visualize it?

A
  • caused by triatomine bug or “Kissing Bug”
  • can see AMASTIGOTES on lower power imaging of myocytes
  • use GIEMSA-stain to visualize Trypanosoma cruzi
38
Q

How do Trichinosis and Lyme Syndrome cause infectious myocarditis?

A

T: helminthic infection due to eating undercooked pork
- larvae enter bloodstream and create cysts in muscle

LS: caused by spirochetes and is associated with Erythema Migrans (Bulls Eye rash) and polyarthritis/neurological issue
- carditis with TRANSIENT HEART BLOCK

39
Q

What is is the difference between Lymphocystic and Eosinophilic Myocarditis?

A

L: most common form
- due to viral/post viral infection, autoimmune, idiopathic

E: marked inc. eosinophils

  • due Hypersensitivity Myocarditis (allergy/hypersens)
  • also idiopathic: methyl dopa and sulfonamides
  • EXCLUDE PARASITIC INFECTION
40
Q

Myocarditis with Giant Cells

What is the difference between Idiopathic Giant Cell Myocarditis and Myocardial Sarcoidosis?

A

IGC: aggressive with poor prognosis (< 3 months)
- admixed w/variable inflammation (eosinophils)

MS: immune-mediated granulomatous reaction
- giant cells w/non-necrotizing granulomas

41
Q

What are two common cardiotoxic drugs (D/D) and what condition do they lead to?

What are 3 additional drugs that rarely cause serious injury? (L/P/C)

A
  • Doxorubicin and Daunorubicin (chemo drugs)
  • cause Dilated Cardiomyopathy and heart failure (dose-dependent lifetime toxicity)

also lithium (moods), phenothiazines (psychotics), and chloroquine (antimalarial) can occasionally cause reversible injury

42
Q

What is the difference between Slow Accumulation and Acute Pericardial effusions?

A

SA: < 500 mL that’s asymptomatic and has “heart shadowing” on CXR

A: 200-300 mL rapid accumulation (< 1 wk) that can cause symptomatic (or fatal) cardiac tamponade

**normal: < 50 mL clear, straw colored fluid

43
Q

What is the difference between Fibrinous/Serofibrinous, Serous, and Purulent pericarditis?

A

F/S: MOST COMMON; “bread and butter” apperance

  • Acute MI, Dressler’s Syndrome
  • see with uremia (chronic kidney disease, inc BUN)

S: viral or noninfectious inflammatory disease

P: ACTIVE infection via microbial invasion

44
Q

What is Pericarditis and how does it present?

What does an ECG of a pt. with Pericarditis look like and what positions do they experience less pain?

A
  • inflammation of pericardial sac
    signs: chest pain (worse w/breathing), pericardial FRICTION RUB and effusion, fever

ECG: ST elevation (concave) and PR depression

  • pt. has less pain sitting up, more pain lying down
45
Q

What is the difference between Caseous, Hemorrhagic, and Constrictive pericarditis?

A

Ca: tuberculosis in origin, sometimes fungal
- looks “cheese-like” w/necrotizing granuloma

H: most commonly due to spread of malignant neoplasm; also TRAUMA

Co: dense, fibrous/fibrocalcific scar that limits diastolic expansion and cardiac output
- mimics restrictive cardiomyopathy

46
Q

What is the most common cardiac tumor of adults and children?

A

Adults: myxoma

Children: rhabdomyoma

metastatic tumors are MORE COMMON than primary tumors

47
Q

What is a Cardiac Myxoma and where does it typically occur?

What are common signs of Myxoma? (BV/F/P)

A
  • stromal tumor of mesenchymal origin (gelatinous –> solid) located on LEFT ATRIUM in septal region of FOSSA OVALIS
    signs: causes “Ball-Valve” obstruction that does mechanical valve damage (wrecking ball) –> embolization; fever (IL-6 inc. via tumor), and “plop” sound on ascultation
48
Q

What are the differences between Cardiac Lipoma and Papillary Fibroelastoma?

A

L: localized mature lobulated fat mass
- can occur throughout the heart

PF: usually incidental; looks like “sea-anemone”; > 80% are located on the VALVES

  • look like LAMBL EXCRESCENCES
  • have avascular core
49
Q

What are the differences between Cardiac Rhabdomyoma and Angiosarcoma?

What are the two genetic components of Rhabdomyoma?

A

R: most frequent benign tumor of pediatric heart

  • hamartoma of developing cardiac myocytes
  • 50% sporadic, 50% due tuberous sclerosis
  • mutations in TSC1 (hamartin)/TSC2 (Tuberin)

see large, vacuolated cells; “spider cells”

A: malignant endothelial neoplasm that typically affects older adults

50
Q

What is the difference between Cellular Mediated and Antibody Mediated Allograft Rejection after heart transplant?

A

CM: T cells; lymphocytic response

AM: antibodies; vascular neutrophilic inflammation
- reactive endothelium and macrophages

51
Q

What is Allograft Vasculopathy?

What is a major clinical problem it leads to and why?

A
  • late, progressive, diffusely stenosing intimal proliferation (50% in 5 yrs, all pts. within 10 yrs)
  • causes concentric intimal thickening of BVs
  • leads to SILENT MI; due to denervated transplanted heart (NO ANGINA)

CPR II Exam 1 (15 decks)

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