patho3

Question 1

What is ischemic heart disease?

Answer 1

• An imblance between myocardial oxygen demand and supply from coronary arteries
  
  • the coronary arteries provide oxygen and nutrients to the myocardium
  • The coronary arteries usually fill during diastole
• Tachycardia can also cause ischemic heart disease. Tachycardia over 180bpm decreases filling time that leads to ischemia

Question 2

What are the coronary artery differences when it comes to supplying the SA node.

Answer 2

• Right coronary artery supplies the SA node 60% of the time
• Circumflex supplies the SA node 40% of the time.

Question 3

What are the dominant coronary artery variants? How do you determine which side is dominant?

Answer 3

• right coronary artery dominant occurs 70% of the time.
• Left coronary artery is dominant 10-15% of the time
• Remainder is co-dominatn 15-20% of the itme.
• Dominance can be determined in two different ways.
  
  • One way is determined by what artery supplies the posterior descending artery
  • Another way is which artery supplies the AV node.

Question 4

EKG review, which leads correlate with which artery, and distribution?

Answer 4

• V1 & V2 - Septal, - LAD
• V3 V4 V5 - Anterior - LAD
• I, aVL, V5, V6 - lateral - circumflex
• II, III, aVF- inferior - RCA

Question 5

What is the distribution of the LAD? What percentage of coronary artery infarcts occur here?

Answer 5

• Anterior portion of the left ventricle
• anterior two thirds of the interventricular septum
• apex of the heart
• 40% of coronary artery infarcts occur here.

Question 6

Distribution of the RCA? What % of infarcts occur here?

Answer 6

• Posterobasal wall of the left ventricle
• Posterior one third of the interventricular septum in the right coronary dominant hearts.
  
  • This is supplied by the circumflex in left coronary dominant hearts
• Right ventricle in 80% of individuals
• Posteromedial papillary muscle in the left ventricle
• AV and SA nodes
• 45% of coronary artery infarcts occur here.

Question 7

Distribution of the left circumflex? % of coronary artery infarcts occur here?

Answer 7

• Lateral wall of the left ventricle in 80% of individuals
• Also could supply the posterior 1/3 of the interventricular septum in left dominant hearts
• 15% of coronary artery infarcts occur here.

Question 8

What happens if there is slow occlusion of a coronary artery?

Answer 8

Collateral circulation can occur. However, this is usually not as good or not as effective as the original circulation. Restoration of regular circulation can be attempted.

Question 9

What is the epidemiology of IHD? What is often the first symptom of cardiovascular disease?

Answer 9

• IHA is a major cause of death in the united states
• More common in men than women
  
  • For men 65%
  • 47% women
    
    • First symptom of cardiovascular disease is AMI or sudden death.

Question 10

What are the different types of IHD? (4)

Answer 10

• Angina pectoris - Most common
• chronic ischemic heart disease CIHD
• sudden cardiac death
• acute myocardial infarction AMI

Question 11

What are the most common risk factors for IHD (5)? What is most important? What is protective against IHD?

Answer 11

• Age is most important. Men over 44, and women over 55
• Lipid abnormalities
  
  • LDL low density lipoproteins > 160 mg/dl
  • HDL high density lipoproteins < 40 mg/dl
• Smoking
• hypertension
• diabetes mellitus
• HDL is protective.

Question 12

What is the underlying disease in IHD?

Answer 12

• The underlying disease in the vast majority of ischmemic heart disease is atherosclerosis (hardening of the gruel) also known as atherosclerotic cardiovascular disease ASCVD and ateriosclerosis (hardening of the arteries).

Question 13

What is angina pectoris? Is it correlated with degree of ischemia? what are the different types?

Answer 13

• Degree of angina is weakly related to the degree of ischemia.
• Within one year of the onset of angina, there is 10-20% chance of developing an AMI or unstable angina.
• Most common in middle aged and elderly males
• Women- mostly post-menopausal

3 different types - stable, unstable, prinzmetal

Question 14

What is stable (chronic angina)? What is its most common cause? Other causes? What is the severity of stenosis in vessels that correlates with angina? What would a stress test EKG show?

Answer 14

• Chronic (Stable) anigna is also called effort angina. chest discomfort and associated symptoms (pressure, squeezing, diaphoresis, referred pain, SOB) occurs with effort. (also occurs with heavy meals, emotional stress, and cold temperatures)
  
  • It abates with rest or nitroglycerin. Then reccurs with exercise. Similar to intermittent claudication
• It is the most common variant
• Fixed ASVD is the most common cause
  
  • other causes include
    
    • hypertension with concentric hypertrophy
    • aortic valvular stenosis
  • Fixed ASVD can occur in single or multiple vessels
    
    • severity of stenosis in vessels is usually 70%
    • Stress test can show ST segment depression of greater than 1mm

Question 15

What is the pathogenesis of stable angina?

Answer 15

• Subendocardial ischemia due to decreased coronary blood flow. This is the most common.
  
  • Plaque builds up and coronary blood flow decreases.
• Other cause would be concentric hypertrophy
  
  • remember C - P vs E - V
    
    • Concentric associated with pressure changes (hypertension)
    • Essentric associated with volume changes (volume overload)

Question 16

What is unstable angina? What is the pathogenesis? What can this progress to?

Answer 16

• Unstable angina is chest pain that occurs at rest or with minimal exertion.
  
  • Clinical features include
    
    • a significant change from before, angina that changes or worsens
    • occurs at rest or with minimal exertion of 3-5 minutes or longer
    • severe and of new onset
    • cresecnedo pattern, more severe, prolonged or frequent from before.
• Unstable angina occurs from severe, fixed multivessel ASCVD.
  
  • Reduction of coronary blood flow due to transient platelet aggregation on the apparently normal epithelium, coronary artery spasms, or coronary artery thrombosis.
  • Disrupted plaques with or without non-occlusive thrombi invariably present
• This can progress to AMI

Question 17

What is prinzmetal angina? Pathogenesis? What would an stress test EKG show?

Answer 17

• Prinzmetal angina is an angina that occurs at rest in cycles secondary to vasospasm
• Pathogenesis
  
  • intermittant coronary artery vasospasm at rest with or without ASCVD
  • Vasoconstriction can be due to an increase in platelet thromboxane A2 originating from thrombus material, or increase in endothelin
• Stress test would show ST segment elevation secondary to transmural ischemia.

Question 18

What is the process of atherosclerosis?

Answer 18

1. Initially, leukokcytes adhere to the endotheluim, migrate into the intima and mature into macrophages.
2. Macrophages uptake lipids and become foam cells.
3. Smooth muscle cells then migrate from the media to the intima and there is synthesis of extracellular matrix in the intima with collagen, elastin, proteoglycans.
4. Lipids from dead macropahges and cholesterol accumulate into plaque.
5. Eventually thrombus can form.

Question 19

What are plaques that are stable vs unstable?

Answer 19

1. Plaques that are stable are not as likely to rupture. They have a small lipid pool and a thick fibrous cap. They also have a preserved lumen
2. Unstable plaques have a thin fibrous cap, a large lipid pool, and many inflammatory cells.

Question 20

What are the different locations that athersclerosis occurs?

Answer 20

Technically occurs anywhere.

• Signs and symptoms can show up depending on where it occurs though
• Brain
  
  • chronic ischemia leads to mental deteroriation, syncope.
  • Acute occlusion -> infarction, rupture –> hemorrhage.
• Kidney
  
  • Renal artery stenosis can cause hypertension
• Aorta
  
  • Can get stenosis or aneurysm. Can lead to occlusion or rupture
• Heart
  
  • Intermittent ischemia –> angina pectoris
  • chronic ischemia –> myocardial fibrosis
  • Acute occlusion –> myocardial infarction.

Question 21

What is the most common type of hypertension? What % of hypertension does it account for? What is the other type of hypertension?

Answer 21

• Essential hypertension is the most common hypertension: accounts for 85% of cases of hypertension
• Remaining 15% represents secondary hypertension. –> potentially curable
• In the united states 25% of the adult population has hypertension.

Question 22

Staging of hypertension

Answer 22

• Normal Blood Pressure: <120/<80.
• Prehypertension: 120-139/80-90.
• Stage 1 Hypertension: 140-159/90-99.
• Stage 2 Hypertension: >160/100.

Question 23

Systolic blood pressure correlates with _______ & ______?

What are the primary determinants of stroke volume? (3)

Answer 23

• Stroke volume and compliance of the aorta.
• Primary determinants of stroke volume include
  
  • Preload (correlates to the volume of the blood in the ventricle at the end of diastole)
  • Afterload (correlates to the resistance that the left ventricle has to contract against to eject blood from the heart
  • Contractility of the heart.

Question 24

Vessel elasticity determines the _____ of the aorta, or the ability of the aorta to expand with systole?

Compliance _______ with age because of the reduced elasticity of the aorta

______ compliance is a common mechanism causing systolic hypertension in patients over the age of 60.

Answer 24

• Vessel elasticity determines the compliance of the aorta, or the ability of the arota to expand with systole
• Compliance decreases with age because of the reduced elasticity of the aorta
• Decreased compliance is a common mechanism causing systolic hypertension in patients over 60 years old

Question 25

What causes an increase in systolic pressure? What causes a decrease in systolic pressure?

Answer 25

• Increased
  
  • Increased stroke volume
  • increased preload
  • increased contractility
  • decreased compliance of the aorta
• decreased
  
  • decreased stroke volume
  • decreased preload
  • decreased contractility
  • increased afterload (severe aortic stenosis)

Question 26

What does diastolic blood pressure correlate with? What is it primarily related to ?

Answer 26

• Diastolic blood pressure correlates with the volume of blood in the aorta during diastole
• Thus, DBP is primarily related to peripheral vascular resistance which is related to the tonicitiy (state of contraction) of the smooth muscle of the peripheral arterioles, the viscosity of the blood and the heart rate.

Question 27

What can cause an increase and a decrease to DBP? (4), (3)

Answer 27

• increased DBP
  
  • vasoconstriction of the arterioles (alpha adrenergics, catecholamines, angiotensin II, vasopressin, endothelin, and increased total body sodium)
  • volume of the intravascular blood
  • increased blood viscosity
  • increase in HR
• decreased DBP
  
  • vasodilation of the peripheral arteries
  • severe anemia
  • decreasing HR

Question 28

What is the role of sodium in systolic and diastolic blood pressures?

Answer 28

• Sodium increases both systolic and diastolic blood pressures
  
  • excess sodium increases plasma volume
  • excess sodium increases stroke volume
  • increased stroke volume increases systolic blood pressure
• Excess sodium produces vasoconstriction in the peripheral arterioles smooth muscles increasing total vascular resistance. This is caused by calcium mediated contraction of the smooth muscle causing an increased diastolic blood pressure.

Question 29

What is the pathogenesis of essential hypertension? Who is it more common in?

Answer 29

1. More common in african americans than whites
2. Pathogenesis
   
   1. Genetic factors reduce renal sodium excretion
   2. Decreased sodium excretion increases plasma volume, which increases stroke volume, increased stroke volume leads to increase in systolic blood pressure.
   3. Decreased sodium excretion increases vasoconstriction of the perphieral vascular resistance arterioles, which increases diastolic blood pressure.
   4. Obesity, stress, smoking, increased salt intake, and lack of physical exercise compound the problem.

Question 30

What are the complications of hypertension? Most common? (4 systems)

Answer 30

1. Cardiovascular
   
   1. left ventricular hypertrophy- concentric hypertrophy - most common complication
      
      1. remember C - P, E -V
   2. acute myocardial infarction - most common cause of death
   3. atherosclerosis
2. CNS
   
   1. intracerebral hemorrhage
   2. berry aneurysm
   3. lacunar infarction, infarction dementia
3. Renal
   
   1. Hypertensive nephrosclerosis - due to hyaline arteriolosclerosis. Atrophy of tubules and sclerosis of glomeruli progressing to renal failure
4. Eyes: Hypertensive retinopathy: AV nicking, retinal hemorrhages, exudates (increased vascular permeability), papilledema.

Question 31

What is malignant hypertension?

Answer 31

1. another complication of HTN
2. Occurs when there is a rapid increase in blood pressure accompnaied by renal failure and cerebral edema.

Question 32

What causes concentric hypertrophy? What is the disease process?

Answer 32

1. Concentric hypertrophy occurs from chronic pressure overload
   
   1. The ventricular chamber radius may decrease somewhat in size.
   2. Cardiac muscle wall thickens, capable of generating greater forces and higher pressures
   3. Decreased compliance of LV with diastolic dysfunction.

Question 33

What is secondary hypertension? What might cause it? (7)

Answer 33

1. This is hypertension secondary to another condition and is not a complication of essential hypertension
2. Adrenal gland
   
   1. cushing syndrome: increased glucocorticoids – can have mineralcorticoid effect of increasing BP
   2. pheochromocytoma: increased catecholamines
   3. neuroblastoma : increased catecholamines - primarily in children
   4. primary hyperaldosteronism (conn syndrome): increased aldosterone
      
      1. usually from a conn tumor.
3. Aorta
   
   1. post-ductal coarctation: activates the RAAS
   2. Decreased elasticity of the elderly aorta
4. CNS:
   
   1. increased intracranial hypertension: increased catecholamines
5. Drugs
   
   1. oral contraceptives: increased synthesis of angiotensinogen (MCC of htn in young women) - resolves with discontinuation of oral contraceptives
6. pregnancy:
   
   1. pre-eclampsia: increased angiotensinogen II
7. Renal
   
   1. renovascular disease: epigastirc bruit and activation of RAAS
      
      1. atherosclerosis
      2. fibromuscualr hyperplasia
8. Thyroid disease
   
   1. graves disease: systolic HTN from increased cardiac contraction
   2. hypothyroidism: diastolic HTN due to retention of sodium

Question 34

Epidemiology of Rhematic fever? What are the bacteria that can cause this? What else can they cause?

Answer 34

• Epidemiology
  
  • first attack between 5 and 15 years
  • develops over 1-5 weeks after a group A streptococcal (streptococcus pyogenes) pharyngitis
  • Pharynx is the only site for infection leading to RF
• Nephrogenic strains of group A streptococcus that proeduce poststreptococcal glomerulonephritis lack virulence factors present in pharngeal strains, and don’t produce RF

Question 35

What are the risk factors for rheumatic fever?

Answer 35

1. RF
   
   1. Crowding, Poverty
   2. Young age
   3. Salt Lake City, Utah- highet incidence and prevalence in the U

Question 36

What is the pathogenesis behind rheumatic fever? What type of hypersensitivity reaction is it?

Answer 36

• Antibody mediated disease that follows group A streptococcal pharyngeal infection
• Host develops antibodies against group A strep M proteins
• These antibodies cross react with similar proteins in human tissue (molecular mimicry) with a type II antibody mediated hypersensitivity reaction

Question 37

What are the clinical findings in RF?

Answer 37

1. Migratory polyarthritis - 75%
   
   1. Most common initial presentation
   2. large joints - knees, ankles, wrists
   3. no permanent joint damage
2. Carditis 35%
   
   1. Most serious complication -
   2. Fibrinous pericarditis presents with percoridal chest pain, some with pericardial friction rubs
   3. Myocarditis with left herat failure may present with CHF
   4. Most common cause of death in RF
   5. Endocarditis with inflammation of cardiac valves
   6. Most common is the mitral valve, then the aortic valve - regurgitation may occur. Eventually stenosis may occur
   7. Sterile verrucous vegetations develop along line of closure of valve.
3. Subcutaneous nodules on extensor surfaces of forearms
4. Erythema marginatum
5. Evaescent C or ring shaped erythema
6. Syndeham’s chorea, - reversible rapid, involuntary choreiform movements.

Question 38

What is the Jones Criteria? What is needed for diagnosis of RF? Major and minor criteria?

Answer 38

1. Jones criteria is diagnostic criteria for RF
   
   1. One major and two minor criteria if supported by evidence of a prior gorup A streptococcal pharyngitis
2. Major criteria:
   
   1. Carditis, migratory polyarthritis, chorea, erythema marginatum or subcutaneous nodules
3. minor criteria
   
   1. previous RF, arthalgia, fever, increased phase reactants (ESR, CRP, absolute neutrophilic leukocytosis), prolonged PR interval on EKG.

Question 39

What are the laboratory tests that you can run to diagnose someone with RF?

Answer 39

1. Increased ASO (antistreptolysin O) titers
2. Increased anti Dnase B titers
3. Throat culutres possible positive.

Question 40

What is the cardiac skeleton? How does it relate to the valves?

Answer 40

1. The cardiac skeleton is a high density collagenous connective tissue that forms and anchors the valves, anulus fibrosus cordis
2. Composed of the right and left fibrous rings of the heart, left stronger than the right
3. These rings can stretch in cardiomegaly

Question 41

Mitral valve stenosis, MCC? What is the typical narrowing? What does it lead to? Clinical findings (6)

Answer 41

1. Most commonly secondary to recurrent RF
2. Women>Men
3. Narrowing of the mitral valve orifice <2.5cm (normally 4-6cm)
4. **Leads to a dilated and hypertrophied left atrium**
5. Clinical findings
   
   1. Murmur of MV stenosis is an opening snap (valves are thick) followed by an early to mid diastolic rumble. Remember about 70% of the filling of the left ventricle is passive filling during diastole. Left atrium must exert a lot of pressure to open fibrosed and calcified valves
   2. Dyspnea and hemopytsis with rust colored sputum (heart failiure)
   3. Secondary to pulmonary capillary congestion and hemorrhage into alveoli pulmonary venous hypertension occurs as blood builds up behind left atrium.
   4. Atrial fibrillation secondary to dilated and hypertrophied left atrium
      
      1. intra-antrial thrombi seondary to blood stasis in afib
   5. systemic emoboli occur in 80% with atrial thrombi
   6. Dysphagia secondary to enlarged left atrium encroaching on esoohagus.

Question 42

Mitral valve regurgitation:Definition, MCC, pathophys, clincial features (3)

Answer 42

• Mitral valve regurgitation is due to an incompetent closure of the valve (insufficiency)
  
  • Secondary to
    
    • Mitral valve prolapse - MCC
    • Ruptured posteromedial papillayr muscle from posterior myocardial infarction
    • functional MV regurgitation secondary to stretching of the MV ring in left ventricular hypertrophy
    • Infective carditis
    • Acute Rheumatic fever, dilated cardiomyopathy, Mycocarditis, SLE.
• Pathophys
  
  • Regurgitation occurs during sytole
  • decreases cardiac output actuely
  • if uncorrected, left atrium becomes dilated and hypertorphied- secondary to volume overload and there is elevated pulmonary venous pressure and CHF
  • Can lead to right ventricular hypertrophy and right heart failure.
• Clinical
  
  • Dysnpnea, CHF
  • Murmur: Pansystolic murmur with S3 and S4
  • Crackles in lungs

Question 43

Mitral Valve Prolapse MCC, epidemiology, pathophys, clinical findings? What murmur is associated with it?

Answer 43

• Epidemiology
  
  • Most common MV lesion and cause of MV regurgitation
  • Women>men
  • efective embryogenesis
• Pathophysiology
  
  • bulging of the nateiror and or posterior leaflets into the left atrium during systole.
  • Redundancy of mitral valve tissue
• Clinical findings
  
  • Most patients are asymptomatic
  • Heart mumur of MV prolapse
    
    • Midsystolic click - secondary to sudden restraint by chordae tendinae of the prolapsed mv
    • Mid to late systolic MV regugitnat murmur follows the click
• Murmur inside baseball
  
  • Decresed preload causes the click and the murmur to move closer to the S2 heart sound because the length of systole is decreased.
    
    • Causes are
      
      • increased venous return to the heart - reclining
      • increased peripheral vascular resistance - squatting.

Question 44

Aortic valve stenosis: epidemiology, etiology, patho, clinical findings

Answer 44

1. Most common valve lesion of adults in western countries
2. Etiology
   
   1. Calcific aortic valve stenosis is the most common cuase in persons over 60 years old
   2. Calcification may involve a normal or congenital bicuspid valve (1-2% of pop)
   3. Congenital form most common findings are around age 30
3. Patho
   
   1. Normal valve oriface area is 3 cm^2
   2. Symptoms and sign appear at 1cm^2, severe at 0.5cm^2
   3. Cause obstructin of the left ventricular outflow during systole
   4. Causes concentric hypertrophy and post stenotic dilation of the aorta
   5. Cardiac output can be normal at rest, compromised with exercise
4. Clinical findings
   
   1. Harsh systolic ejection murmur in the right second intercostal space with radiation to the neck
      
      1. the murmurs intensity is proportional to the preload (volume the LV must eject)
   2. Angina with exercise secondary to filling of the coronary arteries
   3. sub-endocardium of the concentrically hypertrophied heart receives less blood
   4. Syncope with exercise secondary to decreased blood flow to the brain
   5. decreased pulse pressure
   6. decreased cardiac output
   7. a hemolytic anemia with damaged red cells (shistocytes)

Question 45

Aortic valve regurgitation, MCC, other causes, patho, clinical findings

Answer 45

1. Most common cause of isolated AV regurg is aortic root dilation
2. Other causes
   
   1. Infective endocarditis
   2. chronic rheumatic fever
   3. aortic dissection
   4. coarctation of the aorta
   5. dilated AV ring, Syphilitic Aortitis, ankylosing spondylitis, takayasu arteritis,
   6. cystic medial necrosis
   7. marfan syndrome
3. Pathophysiology
   
   1. Incomplete closure of the AV leading to regurgitation of blood from the aorta back into the left ventricle
   2. Acutely can occur with infective endocarditis
   3. There will be marked increase of left ventricular end diastolic pressure and volume, decreased stroke volume, decreased cardiac output
   4. Chronically, the left ventricular size increases, stroke volume increases, cardiac output is normal and systolic blood pressure increases and diastolic blood pressure decreases
   5. Volume overload in the left ventricle –> eccentric left ventricular hypertrophy (wall thickness increases in proportion to the increase in the chamber radius
4. Clinically
   
   1. Early diastolic murmur
   2. S3 and S4 sounds are present
   3. Austin flint murmur
   4. diastolic murmur secondary to regurgitant stream hitting anterior mitral valve leaflet
   5. widened pulse pressure
   6. head nodding with systole (deMusset sign)
   7. Quincke Pulse pulsating nail bed.

Question 46

Tricuspid valve regurgitation, MCC, what occurs in 70% of adults?

Answer 46

1. Etiology
   
   1. Most common cause is functional, stretching of the cardiac ring in right heart failure
   2. In younger paitents, cause is congential heart disease
   3. Normally, there is a small degree of TVR in 70% of adults
   4. other causes, infective endocarditis, pulmonary htn,, dilated cardiomyopathy, RV infarction, carcinoid heart disease.
2. Patho
   
   1. Causes right atrial dilatin and hypertrophy, increased backup in venous pressure
3. Clinical
   
   1. pulsating liver, can be seen on ultrasound
   2. dependent edema
   3. ascities
   4. increased JVP with C-V wave
   5. Pansystolic murmur heard best along left parasternal border.

Question 47

Pulmonary valve stenosis, etiology, Murmur?

Answer 47

1. Uncommon
2. Seen with congential heart disease and carcinoid heart disease
3. Systolic ejection murmur with concentric right ventricular hypertrophy

Question 48

Pulmonary valve regurgitation. MCC, patho

Answer 48

• Most often functional murmur from stretching of the pulmonary valve ring secondary to pulmonary hypertension
• volume overload of the right ventricle
• diastolic murmur heart after S2

Question 49

What is infective endocarditis? Risk factors?

Answer 49

1. def: infection of the endocardial surfaces of the heart
   
   1. may include one ore more valves or septal defects
2. Adults 45-65 years old
3. Risk factors
   
   1. Diabetes mellitus
   2. congential heart disease
   3. HIV infection
   4. Poor dental hygiene
   5. Mitral valve prolapse
   6. aortic valve stenosis
   7. intravenous drug use - staph aureus
   8. intravenous catheters
   9. hemodialysis
   10. prosthetic heart valves - staphlococcus epidermidids and aureus

Question 50

What are the pathogens associated with infective endocarditis?

Answer 50

1. Infection of the endocardial surfaecs of the heart, may include one or more vlaves or septal defects
2. Assocaited pathogens
   
   1. acute
      
      1. staphylococcus auerues - mc
      2. streptococcoal species
      3. haemophilus influenza
      4. streptococcus pneumoniae.
   2. IV drug use
      
      1. staphylococcus aureus most common, psuedomonas, candida, enterococci
   3. Subacute endocarditis
      
      1. streptococcus viridans, S bovis, enteroccci, straphylococcus aureus
      2. nosocomial endocarditis
      3. staph aureus with indwelling iv catheters
      4. enteroccci with urinary catheters.

Question 51

What valves are usually involved in endocarditis? Pathophysiology behind it?

Answer 51

• Most commonly the left sided valves are involved 90%
  
  • most commonly the mitral valve
  • IV drug users affect tricuspid valve and the aortic valve
• Patho
  
  • Adherence of fibrin and paltelets on damaged valves –> bacteria set up shop on damaged valves –> bacterial growth damages valves and creates vegetations.
  • Vegetations break off and cause septic emboli, causing infarcts in brain, fingers.

Question 52

Clinical findings of infective endocarditis?

Answer 52

• Clinical findings
  
  • fever - 90% often of unkown origin
  • Microembolization
    
    • splinter hemorrhages in nail beds
    • janeway lesions: painles areas of hemorrhage on palms and soles of feet 10%
    • osler nodes: painful hemorrhagic nodules on the pads of fingers or toes 10-20%
  • Damaged valves may cause heart murmurs

Question 53

What do the lab findings show for infective endocarditis?

Answer 53

• Positive blood cultures in 80%. Take three sets in first 24 hours
• Neutrophil leukocytosis
• mild anemia.

Question 54

Myocarditis is the major cause of ______ 15-20% of cases in adults <40 years.

Answer 54

Major cause of sudden death in 15-20% of cases in adults younger than 40 years old

Question 55

Myocarditis etiology

Answer 55

• Microbial
  
  • Viruses: adenovirus most common, coxsackie B, HIV, Parovirus B19, Herpes virus 6
  • Parasites: trypansomo cruzi (Chaga’s disease), trichinella spiralis (Trichinosis), and toxoplasma gondii (ttoxoplasmosis)
  • Bacteria: borrelia burgdorferi, mycoplasma, rickettsia rickettsii
  • Fungi: candida, mucor, aspergillus
• Other
  
  • Rheumatic heart disease
  • toxins: diptheria, carbon monoxide, venom from black widows and scorpions,
  • Drugs: doxorubicin, cocaine, zidovudine, sulfas
  • collagen vascular disease, SLE systemic sclerosis, kawasaki disease
  • sarcoidosis
    *

Question 56

myocarditis pathology and pathophysiology?

Answer 56

• global enlargement of the heart
• lymphocytic infiltration with areas of necrosis
• cardiac dysfunction depends on location and extent of disease.

Question 57

clinical findings of myocarditis?

Answer 57

1. dysnpnea - b/c of heart failure, build up of fluid in lungs
2. fever 20%
3. chest pain 35%
4. Arrhythmias - persistant tachycardia out of proportion to fever is a characteristic finding. The conduction system is damaged.
5. Pericardial friction rub
6. Biventricular failure with S3 and s4 sounds
7. heart murmurs - mitral valve regurgitation secondary to dilation of mitral valve anulus.

Question 58

What is cardiac remodeling? What are the different kinds? Is it reversible?

Answer 58

1. Occurs in response to stresses on the heart
2. These stresses can be physiological (ie normal stresses such as exercise or pregnancy) or pathological (secondary to disease)
3. Generally, there is enlargement of the heart, ie cardiac hypertrophy
4. Eccentric hypertorphy is secondary to the stress of volume overload, E V
5. Concentric hypertrophy is secondary to the stress of pressure overload - C P
6. Physiological remodeling is reversibel, whereas pathological remodeling is less reversible

Question 59

Hypertrophy of the heart classifications/causes

Answer 59

Concentric or Eccentric. C=P, E=V

Physiological or pathological

Question 60

What causes eccentric hypertrophy?

Answer 60

1. Occurs with volume overload
   
   1. non-pathological eccentric (exercise or pregnancy) is characterized by an increase in ventricular volume with growth in wall thickness, individiual cardiomyoctyes sarcomeres grow in both length and width
   2. pathological eccentiric (myocardial infarction or dilated cardiomypahthy, valvular regurgitation - aortic or mitral) - Can lead to wall dilated with preferentiral lengthening of the cardiomyocytes/sarcomeres.

Question 61

Concentric remodeling: cause?

Answer 61

1. Concentric occurs with pressure overload
   
   1. characterized by a redution in left ventricular chamber dimension and increase in wall thickness as cardiomyocytes grow more in thickness than length
   2. concentric usually occurs with pathological conditions (chronic htn, or aortic valvular stenosis) characterized by pressure overload of the left ventricle
   3. concentric hypertrophy can be physiological with isometric exercise training.

Question 62

Pericarditis, MCC? Pathology? Clinical presentation?

Answer 62

1. Inflammation of the pericardium
2. most are idiopathic
3. other forms are similar in cause to myocarditis (viruses)
4. Pathology
   
   1. fibrinous pericardial exudate, often with pericardial effusoin
   2. chronically can lead to dense scar and sytrophic calcificatoin with constrictive pericarditis
5. Clinical
   
   1. fever
   2. tachycardia
   3. chest pain: precordial, relieved when leading forward
   4. pericardial frictoin rub: three components, systole, early and late diastole - heard in about 50%

Question 63

What is pericardial effusion? What are the clincial signs? what is the Kussmual sign?

Answer 63

• Pericardial effusion is a complicatoin of pericarditis
  
  • Heart sound muffled
  • decreased cardiac output
  • neck vein distension especially on inspiratoin
    
    • Kussmaul sign - blood refluxing back into the neck veins on inspiration)
  • Hypotension with pulsus paradoxus
    
    • Drop in systolic blood pressure during inspiration
      
      • With inspiration there is a decrease in intrathoracic pressure with an increase in venous return to the right ventricle. This increase in blood in the RV dispalces the intraventricular septum to the left and decreases the LV volume and thus stroke volume.
      • Also with negative intrathoracic pressure there is an expansion of pulmonary vasculature and relative pooling of blood in the lungs and decreased pulmolnary venous return to the left heart.

Question 64

What is Beck’s triad of acute cardiac tamponade?

Answer 64

• Hypotension, distended neck veins, muffled heart sounds.

Question 65

When does tamponade occur?

Answer 65

Beck’s Triad of Acute Cardiac Tamponade: Low arterial blood pressure Distended neck veins Muffled heart sounds

• Tamponade occurs when the pericardial effusion compromisses the blood return back to the heart with the resulting pathophysiolgic changes of becks triad.

Question 66

What does pericardial effusion look like on x-ray?

Answer 66

water bottle heart.

Question 67

What does pericardial effusion look like on echo?

Answer 67

Can see the fluid surrounding the hearts and compomising the ventricles.

Question 68

What happens in aortic dissection? What causes it?

Answer 68

• Tear in the intima of the aorta with dissection of blood between the intima nad the media and adventitia
• Rupture of aorta may result. May occur in peripheral vessels, carotid dissection can cause stroke
• Causes
  
  • Hypertension - 80%
  • Connective tissue disorders: marfans, cystic meidal necrosis, ehlers andlos syndrome
  • trauma: occurs at ligamentum arteriosum.

Question 69

Aortic dissection complications?

Answer 69

• rupture and death
• aortic insufficiency
• myocardial infarction
• pleural effusion - hemorrhage
  *

Question 70

What does aortic dissection look like on x-ray

Answer 70

widening of the aorta and mediastinum on chest film. Loss of outline of the aortic knob - indistinct.

Question 71

What are the types of dissection?

Answer 71

See image

Question 72

What is the test of choice for aortic dissection?

Answer 72

CT test is choice for diagnosis - use contrast.

Question 73

What defines an aortic aneurysm? Where are the most common? Screening? What type is more prone to rupturing?

Answer 73

1. Enlargement of aortic diameter to greater than 1.5 times normal size
2. More common in the abdomen than thorax
3. May rupture and cause death
4. Screening ultrasound
   
   1. greater thatn 5 cm in diameter means that the risk of rupture is greater than the risk for surgical repair
   2. fusiform aneuryssm have less chance of rupture than saccular aneurysms
5. Clinically may present as large pulsatile mass above the umbilicus
6. Abdominal pain, severe constant, radiating to the back.

Question 74

What are the 3 types of aortic aneurysm?

Answer 74

Saccular, fusiform, dissecting.

Fusiform aneurysms have less chance of rupture than saccular aneurysms.

Question 75

What are the surgical cautions that need to take place when repairing an aortic aneurysm.

Answer 75

1. surgical caution to save renal arteries and also avoid artery of adamkiewicz supplying the spinal cord.

Question 76

What is ALCAPA? What occurs in ALCAPA?

Answer 76

• Anomalous left coronary artery from the pulmonary artery.
  
  • Multiple small heart attacks create extensively damaged left ventricle with chamber enlargement