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52 Cards in this Set

  • Front
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1. Pulmonary Hypertension

a.	^ pressure in the lungs dt COPD, scleroderma, fibrotic dz
b.	Hypoxia -> pulm vasoconstriction
c.	Course: severe resp distress → cyanosis & RVH → RHF → death from decompensated cor pulmonale
a. ^ pressure in the lungs dt COPD, scleroderma, fibrotic dz
b. Hypoxia -> pulm vasoconstriction
c. Course: severe resp distress → cyanosis & RVH → RHF → death from decompensated cor pulmonale
2. Systemic hypertension
a.	BP > 140/90
b.	Risk factors: ^ age, obesity, smoking, genetics, 
c.	90% Primary causes (essential) ^ CO and ^ TPR
d.	10% Secondary causes – Renal disease
e.	Predisposes to : atherosclerosis, LVH, stroke, CHF, RF, retinopathy, and aortic dissection
a. BP > 140/90
b. Risk factors: ^ age, obesity, smoking, genetics,
c. 90% Primary causes (essential) ^ CO and ^ TPR
d. 10% Secondary causes – Renal disease
e. Predisposes to : atherosclerosis, LVH, stroke, CHF, RF, retinopathy, and aortic dissection
3. Left sided Hypertension
a.	Causes:  Ischemic heart disease (MI) 
b.	HTN and aortic and mitral valvular disease causes LVH
c.	Myocardial diseases such as pulmonary congestion and myocarditis
d.	Clinical Manifestations: Dyspnea and orthopnea caused by pulmonary congestion and e
a. Causes: Ischemic heart disease (MI)
b. HTN and aortic and mitral valvular disease causes LVH
c. Myocardial diseases such as pulmonary congestion and myocarditis
d. Clinical Manifestations: Dyspnea and orthopnea caused by pulmonary congestion and edema
e. Reduction in renal perfusion (→ ^ RAAS system)
4. Right Sided Heart Failure
a.	MCC is LHF or left sided lesions (mitral stenosis)
b.	COPD → Pulmonary HTN → RHF
c.	Clinical Manifestations: Renal hypoxia → fluid retention → pitting edema ankles
d.	Enlarged and congested liver (nutmeg liver) and spleen
e.	Distention of the neck

a. MCC is LHF or left sided lesions (mitral stenosis)
b. COPD → Pulmonary HTN → RHF
c. Clinical Manifestations: Renal hypoxia → fluid retention → pitting edema ankles
d. Enlarged and congested liver (nutmeg liver) and spleen
e. Distention of the neck veins (JVD)

5. Angina Pectoris
a.	Occurs when CAD narrowing is > 75% and the O2 demand is > blood supply
b.	Extremely large meal→ Then Shovel! (Low CFR predisposes)
c.	Stable: dt atherosclerosis -> rest relieves pain
d.	Prinzmetal’s variant: dt coronary artery spasms
e.	Unstable: t
a. Occurs when CAD narrowing is > 75% and the O2 demand is > blood supply
b. Extremely large meal→ Then Shovel! (Low CFR predisposes)
c. Stable: dt atherosclerosis -> rest relieves pain
d. Prinzmetal’s variant: dt coronary artery spasms
e. Unstable: thrombosis but no necrosis (worsening chest pain at rest)
6. Chronic Ischemic heart disease
a.	progressive onset of CHF over years dt chronic ischemic myocardial damage
b.	Inc. Risks: Smokers, High Cholesterol, DM, HTN -usually males. 
c.	Can present itself as a long-standing Unstable Angina Pectoris. 
d.	Dx: ECG, Blood markers, cardiac stres
a. progressive onset of CHF over years dt chronic ischemic myocardial damage
b. Inc. Risks: Smokers, High Cholesterol, DM, HTN -usually males.
c. Can present itself as a long-standing Unstable Angina Pectoris.
d. Dx: ECG, Blood markers, cardiac stress testing.
7. Myocardial Infarction
a.	Elephant on my chest pressure
b.	Embolism -> Dec in blood flow -> ischemia -> necrosis
c.	MC is LAD (anterior septum) > RCA (inferior /posterior) > circumflex
d.	EKG: ST segment elevation & Q wave changes 
e.	Cardiac enzymes: 1st troponin 3-6 hrs,
a. Elephant on my chest pressure
b. Embolism -> Dec in blood flow -> ischemia -> necrosis
c. MC is LAD (anterior septum) > RCA (inferior /posterior) > circumflex
d. EKG: ST segment elevation & Q wave changes
e. Cardiac enzymes: 1st troponin 3-6 hrs, 2nd CK/MB 6-10 hrs post MI
f. Complications: 90% develop arrhythmias, 50% mortality, 2/3 Heart failure.
8. Aortic Stenosis/ Insufficiency
a.	Causes: Congenital bicuspid (2 cusps) valve→  calcification by 40-50yo
b.	Age related valve (3 cusps) degeneration and calcification mc > 70yo
c.	Rheumatic heart disease: LVH→diastolic dysfunction → LHF →SOB, chest pain, syncope with exertion
d.	TX:
a. Causes: Congenital bicuspid (2 cusps) valve→ calcification by 40-50yo
b. Age related valve (3 cusps) degeneration and calcification mc > 70yo
c. Rheumatic heart disease: LVH→diastolic dysfunction → LHF →SOB, chest pain, syncope with exertion
d. TX: valve replacement or Often results in SUDDEN DEATH
e. Murmur: crescendo-decresendo systolic ejection murmur following ejection click.
9. Mitral Stenosis (MS)/ Insufficiency can lead to MVP
a.	Calcification of mitral valve → Narrowing of valve ↓ blood to body
b.	Causes: rheumatic fever, congenital, carcinoid heart dz, Chronic MS → can result in LA dilation 
c.	Murmur: follows opening snap (dt tensing of chordae tendinae) delayed rumbling l
a. Calcification of mitral valve → Narrowing of valve ↓ blood to body
b. Causes: rheumatic fever, congenital, carcinoid heart dz, Chronic MS → can result in LA dilation
c. Murmur: follows opening snap (dt tensing of chordae tendinae) delayed rumbling late diastolic murmur
10. Mitral Valve prolapse
a.	Assoc w/Marfan and Ehlers-Danlos syndromes
b.	Can be caused by Myxomatous degeneration, rheumatic fever, or chordae rupture
c.	Most frequent valvular lesion, usually benign
d.	Predisposes to infective endocarditis
e.	Murmur: Systolic click heard lo
a. Assoc w/Marfan and Ehlers-Danlos syndromes
b. Can be caused by Myxomatous degeneration, rheumatic fever, or chordae rupture
c. Most frequent valvular lesion, usually benign
d. Predisposes to infective endocarditis
e. Murmur: Systolic click heard loudest @ S2 followed by blowing murmur
11. Endocarditis
a.	Mitral valve is most frequently involved
b.	Can be bacterial, viral, or unknown
c.	S/Sx: Duke criteria: Fever, Roth spots, Osler’s nodes, Janeway lesions, splinter hemorrhages, new murmur
d.	Complications: chordae rupture, glomerulonephritis, suppur
a. Mitral valve is most frequently involved
b. Can be bacterial, viral, or unknown
c. S/Sx: Duke criteria: Fever, Roth spots, Osler’s nodes, Janeway lesions, splinter hemorrhages, new murmur
d. Complications: chordae rupture, glomerulonephritis, suppurative pericarditis, emboli
e. Acute: Staph. aureus OR Subacute: Strep
12. Rheumatic heart Disease
a.	Occur after group A strep pharyngitis
b.	Immune mediated type II hypersensitivity rxn
c.	Migratory polyarthritis MC presentation; myocarditis MCC death.
d.	MV involved first→AV. Mitral regurgitation in acute attack; mitral stenosis in chronic Dz.
e
a. Occur after group A strep pharyngitis
b. Immune mediated type II hypersensitivity rxn
c. Migratory polyarthritis MC presentation; myocarditis MCC death.
d. MV involved first→AV. Mitral regurgitation in acute attack; mitral stenosis in chronic Dz.
e. Jones criteria DDx→major criteria: carditis, arthritis, chorea, erythema marginatum, subcutaneous nodules.
13. Carcinoid heart disease
a.	Caused by tumors (usually in the liver) that secrete functional hormones. 
b.	VERY slow growing tumors up to 20 yrs presents 50-70's
c.	secretes serotonin, histamine, tachykinins, and prostaglandins released by the malignant cells –>vasoactive substa
a. Caused by tumors (usually in the liver) that secrete functional hormones.
b. VERY slow growing tumors up to 20 yrs presents 50-70's
c. secretes serotonin, histamine, tachykinins, and prostaglandins released by the malignant cells –>vasoactive substances (cause vasoconstriction) → ^ pressure in Right heart
d. The preferential right heart involvement is most likely related to inactivation of the vasoactive substances by the lungs
e. The fibrous tissue in the plaques results in distortion of the valves leading to either stenosis, regurgitation, or both.
14. Dilated cardiomyopathy
a.	MC cardiomyopathy ( 90%)
b.	Systolic dysfunction (Left Ventricle enlarged and floppy -> not working properly → Dec LV ejection fraction)
c.	Eccentric hypertrophy
d.	Causes: Alcohol, Coxsackie, cocaine use, & chaga’s dz
e.	Findings: hear a S3, displ
a. MC cardiomyopathy ( 90%)
b. Systolic dysfunction (Left Ventricle enlarged and floppy -> not working properly → Dec LV ejection fraction)
c. Eccentric hypertrophy
d. Causes: Alcohol, Coxsackie, cocaine use, & chaga’s dz
e. Findings: hear a S3, displaced PMI, and on xray see a balloon heart
15. Hypertrophic cardiomyopathy
a.	Diastolic Dysfunction
b.	Concentric hypertrophy
c.	Causes: familial, AD
d.	The septum hypertrophies and blocks mitral leaflets obstructing outflow → systolic murmur & syncope
e.	Findings: normal sized heart, S4, systolic murmur 
f.	Think young ath
a. Diastolic Dysfunction
b. Concentric hypertrophy
c. Causes: familial, AD
d. The septum hypertrophies and blocks mitral leaflets obstructing outflow → systolic murmur & syncope
e. Findings: normal sized heart, S4, systolic murmur
f. Think young athletes and sudden death
16. Restrictive Cardiomyopathy
a.	Diastolic dysfunction
b.	Heart becomes stiff because of infiltrates in the muscle
c.	Major causes of infiltrates are sarcoidosis, any fibrosis, hemochromatosis
a. Diastolic dysfunction
b. Heart becomes stiff because of infiltrates in the muscle
c. Major causes of infiltrates are sarcoidosis, any fibrosis, hemochromatosis
17. Myocarditis
a.	inflammation of the myocardium w/ myocyte necrosis
b.	Causes: Viral (coxsackie, influenza), Toxic or Autoimmune
c.	Had an illness 2 wks prior → signs of ventricular dysfunction → LV dilation → can get murmurs
d.	1st: initial insult, 2nd early subacu
a. inflammation of the myocardium w/ myocyte necrosis
b. Causes: Viral (coxsackie, influenza), Toxic or Autoimmune
c. Had an illness 2 wks prior → signs of ventricular dysfunction → LV dilation → can get murmurs
d. 1st: initial insult, 2nd early subacute viral clearing phase, 3rd late subacute viral clearing & lysis of myocytes, 4th Chronic phase – immune response of too much XS loss of myocytes
e. 1/3 resolve, 1/3 develop mild scarring, 1/3 progress to dilated cardiomyopathy
18. Metastatic pericardial disease aka hemorrhagic pericarditis
a.	Malignant Tumors can metastasize and deposit in the pericardial space (ex: melanoma, carcinoma of the bronchus, breast cancer, Hodgkin’s lymphoma, leukemia)
b.	Can be an accumulation of blood and suppurative effusion in the pericardial space
c.	Findi
a. Malignant Tumors can metastasize and deposit in the pericardial space (ex: melanoma, carcinoma of the bronchus, breast cancer, Hodgkin’s lymphoma, leukemia)
b. Can be an accumulation of blood and suppurative effusion in the pericardial space
c. Findings: pericardial pain, friction rub, pulsus paradoxus, distant heart sounds, ECG changes, ST segment elevation in several leads
d. Can lead to chronic adhesive or chronic constrictive pericarditis
19. Pericardial effusions
a.	The pericardial space normally has 30-50mL of thin, clear and straw colored pericardial fluid. 
b.	Under various circumstances the parietal pericardium may be distended by serous fluid = pericardial effusion.  (blood = hemopericardium, or pus = purule
a. The pericardial space normally has 30-50mL of thin, clear and straw colored pericardial fluid.
b. Under various circumstances the parietal pericardium may be distended by serous fluid = pericardial effusion. (blood = hemopericardium, or pus = purulent pericarditis)
c. With long standing pressure the pericardium will dilate to accomadate the volume overload in the space. Slowly accumulating pericardial effusion can stretch a lot w/o affecting cardiac fxn.
d. Rapidly developing fluid collections such as due to hemorrhage caused by a ruptured MI or aortic dissection may → compression of the thin walled atria or ventricles --? Potentially fatal cardiac tamponade
20. Pericarditis
a.	Definiton - It is usually secondary to infections, cardiac diseases, immune-mediated diseases, or systemic disorders
i.	1. Serous pericarditis- a noninfectious inflammation, such as RF, SLE, scleroderma, tumors, uremia, etc
b.	Morphology - inflammato
a. Definiton - It is usually secondary to infections, cardiac diseases, immune-mediated diseases, or systemic disorders
i. 1. Serous pericarditis- a noninfectious inflammation, such as RF, SLE, scleroderma, tumors, uremia, etc
b. Morphology - inflammatory reaction in pericardium with scant number of inflammatory cells; fluid 50-200ml, that accumulates slowly
i. 2. Fibrinous and serofibrinous pericarditis ( MC) and causes: Acute MI is the MCC, uremia, chest radiation, SLE, RF, cardiac surgery, trauma
c. Morphology
(1) Fibrinous pericarditis - surface is dry, with a fine granular roughening
(2) Serofibrinous pericarditis - thicker fluid, yellow and claudy, leukocytes and erythrocytes are present, and fibrin
d. Clinical feature: Pain, fever, cardiac failure, loud pericardial friction rub
e. can develop constrictive pericarditis b/c of scarring
21. Bicuspid aortic valve
a.	2 flaps instead of 3 may not cause symptoms
b.	MC associated w/ coarctation of the aorta and aortic stenosis
c.	Coarctation of the aorta
a.	Narrowing just distal to origin of left subclavian artery.  BP in arms will be > than in the legs
b.	Symptom
a. 2 flaps instead of 3 may not cause symptoms
b. MC associated w/ coarctation of the aorta and aortic stenosis
c. Coarctation of the aorta
a. Narrowing just distal to origin of left subclavian artery. BP in arms will be > than in the legs
b. Symptoms of severe coarctation à Pulm HTN
c. Symptoms of mild coarctation (asym as kids as get older HTN, leg cramps w/exercise)
d. Systemic Complications: ^ risk aortic dissection and systemic HTN → Extensive development of collateral circulation w/ dilation of intercostal arteries → Rib notching 3-8 on inferior border
22. Patent Ductus Arteriosis
a.	Causes a R→L shunting of blood in utero
b.	After birth lung pressures are low and shunt becomes L → R
c.	PDA or Failure of DA to close after birth can lead to RVH and failure. 
d.	Continuous machine like murmur. Uncorrected PDA may eventually result
a. Causes a R→L shunting of blood in utero
b. After birth lung pressures are low and shunt becomes L → R
c. PDA or Failure of DA to close after birth can lead to RVH and failure.
d. Continuous machine like murmur. Uncorrected PDA may eventually result in late cyanosis in lower extremities (blue kids)
23. Ventricular Septal Defect
a.	Common congenital anomaly causing L → R shunt 
b.	Will cause R sided CHF and/or pulmonary HTN if very large. 
c.	If small, the infant may be asymptomatic at first and as they get older around 15-18 months begin to see Sx.  (blue kids)
a. Common congenital anomaly causing L → R shunt
b. Will cause R sided CHF and/or pulmonary HTN if very large.
c. If small, the infant may be asymptomatic at first and as they get older around 15-18 months begin to see Sx. (blue kids)
24. Atrial septal defect
a.	The R ventricle will fill during diastole ^ R ventricular volume. → ^ blood on the R → causes a wide fixed split  S2
b.	L → R shunt, → pulm HTN → late cyanosis  → blue kids
a. The R ventricle will fill during diastole ^ R ventricular volume. → ^ blood on the R → causes a wide fixed split S2
b. L → R shunt, → pulm HTN → late cyanosis → blue kids
25. Tetralogy of Fallot
a.	Most common cyanotic heart defect (right to left shunt) early cyanosis = Blue babies
b.	* Must have all four of these * (PROVe)
   	1. Pulmonary Valve stenosis (narrowed)
   	2. RVH (Right Ventricular Hypertrophy)
3. Overriding Aorta  
	4. VSD (Ve
a. Most common cyanotic heart defect (right to left shunt) early cyanosis = Blue babies
b. * Must have all four of these * (PROVe)
1. Pulmonary Valve stenosis (narrowed)
2. RVH (Right Ventricular Hypertrophy)
3. Overriding Aorta
4. VSD (Ventricular Septal Defect)
c. early cyanosis is caused by the R → L shunt across the VSD.
d. R → L shunt exists b/c ^ pressure from stenotic pulm valve.
e. Findings: “boot shaped heart” on x-ray. Tet Spells (infant) - blue crying baby
Squatting to alleviate DOE (toddler)
Metabolic & Resp Acidosis w/ hypoxemia
Harsh Systolic Heart Murmur
Hemodynamic Conditions
26. Embolism
a.	Passage and trapping of blood clot
b.	Most frequent place of origin is the lungs.
a. Passage and trapping of blood clot
b. Most frequent place of origin is the lungs.
Hemodynamic Conditions
27. Hemorrhage
a.	Escape of blood from the vasculature to the surrounding tissues. 
b.	Cz: Trauma. 
c.	Results; Hematoma, Hemothroax, hemopericardium, hemoperitoneum, hemarthrosis.
a. Escape of blood from the vasculature to the surrounding tissues.
b. Cz: Trauma.
c. Results; Hematoma, Hemothroax, hemopericardium, hemoperitoneum, hemarthrosis.
Hemodynamic Conditions
28. Edema
a.	Abnormal Accumulation of fluid in interstitial tissue spaces or body cavities
b.	Cz: Inc Hydrostatis pressure 
i.	Eg CHF, RSHF Eg. Periferal Edema, LSHF Eg. Pulmonary edema. 
c.	Dec. oncotic pressure
i.	Eg. Nephrotic syndrome, Cirrhosis of Liver
d
a. Abnormal Accumulation of fluid in interstitial tissue spaces or body cavities
b. Cz: Inc Hydrostatis pressure
i. Eg CHF, RSHF Eg. Periferal Edema, LSHF Eg. Pulmonary edema.
c. Dec. oncotic pressure
i. Eg. Nephrotic syndrome, Cirrhosis of Liver
d. Inc. sodium retention
i. Eg. Primary: Renal disorders
ii. Secondary: CHF
Hemodynamic Conditions
29. Shock
a.	Circulatory collapse results in hypoperfusion and dec. oxygenation of tissues.
b.	Cz: Dec. CO, Wide spread peripheral vasodilation. 
c.	Types: Hypovolemic shock, Cardiogenic shock, Septic Shock. Neurogenic shock. 
d.	Stages: Nonprogressive stage, pr
a. Circulatory collapse results in hypoperfusion and dec. oxygenation of tissues.
b. Cz: Dec. CO, Wide spread peripheral vasodilation.
c. Types: Hypovolemic shock, Cardiogenic shock, Septic Shock. Neurogenic shock.
d. Stages: Nonprogressive stage, progressive stage, irreversible stage.
Hemodynamic Conditions
30. Thrombosis
a.	Intravascular coagulation of blood. 
b.	Cz: Significant interruption of blood flow. 
c.	Et: Venous stasis, CHF, polycythemia, sickle cell disease, OCB, cigarette smoking.
a. Intravascular coagulation of blood.
b. Cz: Significant interruption of blood flow.
c. Et: Venous stasis, CHF, polycythemia, sickle cell disease, OCB, cigarette smoking.
Vascular conditions
31. Aneurysms
a.	Abnormal Dilations arteries or veins. 
b.	Cz: 
i.	Atherosclerotic: Descending, abdominal aorta. 
ii.	Berry: Circle of Willis, not atherosclerosis. 
iii.	Syhilitic: Tertiary syphilis: Obliterative endarteritis of the vasa vasorum ‘tree-bark’ aorta.
a. Abnormal Dilations arteries or veins.
b. Cz:
i. Atherosclerotic: Descending, abdominal aorta.
ii. Berry: Circle of Willis, not atherosclerosis.
iii. Syhilitic: Tertiary syphilis: Obliterative endarteritis of the vasa vasorum ‘tree-bark’ aorta. Ascending aorta.
iv. Dissecting aneurysms: Lonitudinal intraluminal tear. Ass w/HTN, cystic medial necrosis (Marfan syndrome) not athrosclerosis.
Vascular conditions
32. Aortic dissection
a.	60-70y/o, complication of High BP. Constant Chronic Pain. 
b.	Def: Lonitudinal Intraluminal tear. Not atherosclerosis, ass. w/Marfan Syndrome. 
c.	S/SE: Severe, tearing ripping, chest pain radiates to back. 
d.	Ddx: MI: Negative ECG and heart enzyme
a. 60-70y/o, complication of High BP. Constant Chronic Pain.
b. Def: Lonitudinal Intraluminal tear. Not atherosclerosis, ass. w/Marfan Syndrome.
c. S/SE: Severe, tearing ripping, chest pain radiates to back.
d. Ddx: MI: Negative ECG and heart enzymes, Ultrasound positive.
e. Results: Cystic Medial Degenration, Aortic Rupture/Cardiac Tamponade.
Vascular conditions


33. Arteriosclerosis
a.	General term for three types of vascular disease w.rigidity, thickening, of blood vesseles. 
i.	Monckeberg arteriosclerosis: 50y/o, medial calcific sclerosis: Radial and ulnar arteries. 
ii.	Arteriolosclerosis: hyaline thickening of small arteries es
a. General term for three types of vascular disease w.rigidity, thickening, of blood vesseles.
i. Monckeberg arteriosclerosis: 50y/o, medial calcific sclerosis: Radial and ulnar arteries.
ii. Arteriolosclerosis: hyaline thickening of small arteries esp. kidneys.
1. Ass. HTN and DM
2. Two variants: Hyaline arteriolosclerosis: Hyaline thickening.
3. Hyperplastic arteriolosclerosis: concentric, laminated, onionskin.
Vascular conditions
34. Atherosclerosis
a.	MC cause of death bc. of vascular dz. In developed countries. 
b.	Cz: Fibrous atheromas in intima of arteries with central core of cholesterol and lipid-laden macrophages ‘foam cells’, covered by a fibrous cap. 
c.	Plaques may: 
i.	Ulcerate, hemorrh
a. MC cause of death bc. of vascular dz. In developed countries.
b. Cz: Fibrous atheromas in intima of arteries with central core of cholesterol and lipid-laden macrophages ‘foam cells’, covered by a fibrous cap.
c. Plaques may:
i. Ulcerate, hemorrhage or calcify.
ii. Thrombus formation
iii. Embolization.
d. Atheromas develop from fatty streaks→ Appear very early in life→ Ischemic heart disease, MI or aneurysm.
Vascular conditions
35. Familial hypercholesterolemia
a.	Et: Autosomal dominant genetic disorder heterozygous. (LDLR gene of chromosome 19)
b.	Result: Absence of LDL cholesterol receptors-→ Absent hepatic clearance→ premature atherosclerosis. 
c.	Clinical: xanthomatois, arcus senilis corneae.
a. Et: Autosomal dominant genetic disorder heterozygous. (LDLR gene of chromosome 19)
b. Result: Absence of LDL cholesterol receptors-→ Absent hepatic clearance→ premature atherosclerosis.
c. Clinical: xanthomatois, arcus senilis corneae.
Vascular conditions
36. Giant cell arteritis (temporal arteritis)
a.	Medium to large arteries, granuloma formation
b.	Giant Cells w/mononuclear cells, neutrophils, and eosinophils
c.	Location: Branches of carotid artery
d.	Visual impairment- ophthalmic artery, Inc. ESR.
a. Medium to large arteries, granuloma formation
b. Giant Cells w/mononuclear cells, neutrophils, and eosinophils
c. Location: Branches of carotid artery
d. Visual impairment- ophthalmic artery, Inc. ESR.
Vascular conditions
37. Peripheral arterial disease (PAD)
a.	Arterialsclerosis of leg arteries. 
b.	Inc. smoking, , high intake of processed foods and animal products. 
c.	High risk of thromboembolism and death. 
d.	Intermittent claudication w/peripheral pulses obscured.
a. Arterialsclerosis of leg arteries.
b. Inc. smoking, , high intake of processed foods and animal products.
c. High risk of thromboembolism and death.
d. Intermittent claudication w/peripheral pulses obscured.
Vascular conditions
38. Pulmonary embolism (PE)
a.	Et: Based on Virchow’s triad: Hypercoagulability, Hemodynamic changes (stasis, turbulence), Endothelial injury/dysfunction.
b.	Originates: lower extremities or pelvis.  
c.	Predisposing Factors: Venous stasis, CHF, Cancer, fractures, OBC.
d.	Results
a. Et: Based on Virchow’s triad: Hypercoagulability, Hemodynamic changes (stasis, turbulence), Endothelial injury/dysfunction.
b. Originates: lower extremities or pelvis.
c. Predisposing Factors: Venous stasis, CHF, Cancer, fractures, OBC.
d. Results: hemorrhagic, or red infarcts (bc. lungs have dual blood supply). ASYM to Death.
Vascular conditions
39. Raynaud’s phenomenon (primary and secondary)
a.	Primary: Raynaud disease
i.	Young Women
ii.	Recurrent vasospasm small arteries. 
iii.	Cyanosis Fingers and Toes
iv.	S/SE: Chilling
b.	Seondary: Raynaud Phenomenon
i.	Secondary bc. of an underlying disorder
ii.	MC Cz: Systemic Lupis Erythmatosis
a. Primary: Raynaud disease
i. Young Women
ii. Recurrent vasospasm small arteries.
iii. Cyanosis Fingers and Toes
iv. S/SE: Chilling
b. Seondary: Raynaud Phenomenon
i. Secondary bc. of an underlying disorder
ii. MC Cz: Systemic Lupis Erythmatosis
iii. Second MC Cz: Scleroderma
c. Results (Primary and Secondary): Ulceration and gangrene.
Vascular conditions
40. Thromboangiitis obliterans (Bueger’s Disease)
a.	Young Jewish Men
b.	Acute Inflammatory Dz: Affects- small to medium arteries/veins of extremities. 
c.	Results: Painful ischemic disease, gangrene, distal claudication/necrosis of digits. 
d.	Major Risk Factor: Heavy Smoking, even smokeless tobacco.
a. Young Jewish Men
b. Acute Inflammatory Dz: Affects- small to medium arteries/veins of extremities.
c. Results: Painful ischemic disease, gangrene, distal claudication/necrosis of digits.
d. Major Risk Factor: Heavy Smoking, even smokeless tobacco.
Vascular conditions
41. Thrombosis –deep vein (DVT)
a.	Lead to Embolism, deep veins of Legs. 
b.	Et: Based on Virchow’s triad: Hypercoagulability, Hemodynamic changes (stasis, turbulence), Endothelial injury/dysfunction.
a. Lead to Embolism, deep veins of Legs.
b. Et: Based on Virchow’s triad: Hypercoagulability, Hemodynamic changes (stasis, turbulence), Endothelial injury/dysfunction.
Vascular conditions
42. Varicose vein
a.	Abnormally dilated and tortuous veins
b.	Superficial veins in lower extremities. 
c.	Predisposition: Inc. venous pressure Eg. Pregnancy, thrombophlebitis or prolonged standing.
a. Abnormally dilated and tortuous veins
b. Superficial veins in lower extremities.
c. Predisposition: Inc. venous pressure Eg. Pregnancy, thrombophlebitis or prolonged standing.
Vascular conditions
43. Vasculitis
a.	Inflammatory & Necrotizing
b.	Often immune mediated (HepB, surface AG’s, Hep C RNA, DNA)
c.	Classified: Polyarthritis nodosa,  henoch-Schonlein purpura.
a. Inflammatory & Necrotizing
b. Often immune mediated (HepB, surface AG’s, Hep C RNA, DNA)
c. Classified: Polyarthritis nodosa, henoch-Schonlein purpura.
Vascular neoplasms
44. Hemangiomas
a.	MC Tumor of Infancy. Inc. number of normal/abnormal BV’s
b.	Cz: Port-wine Stains (Flat Lesions)
c.	Types: 
1) Capillary (Birthmark/Stawberry Type)- BV’s represent capillaries in subq tissues→ Resolve by 7y/o. 
2) Vavernous- Larger dilated vascular
a. MC Tumor of Infancy. Inc. number of normal/abnormal BV’s
b. Cz: Port-wine Stains (Flat Lesions)
c. Types:
1) Capillary (Birthmark/Stawberry Type)- BV’s represent capillaries in subq tissues→ Resolve by 7y/o.
2) Vavernous- Larger dilated vascular channels in internal organs. Damage nerves. Require Tx ass w/VonHippel-Lindaw Disease: AD, hemangioblastomas of brain, retina, internal organs, Inc. Risk Renal Cell Carcinoma.
Vascular neoplasms
45. Kaposi’s sarcoma
a.	HHV-8 Malignant vascular tumor that occurs in several forms. 
b.	Morph: Reddish-purple to dark-blue cutaneous macules, plaques, or nodules. 
i.	Classic: Ashkenazic Jewish or Mediterranean origin. 
ii.	Endemic (African): Young African men and childre
a. HHV-8 Malignant vascular tumor that occurs in several forms.
b. Morph: Reddish-purple to dark-blue cutaneous macules, plaques, or nodules.
i. Classic: Ashkenazic Jewish or Mediterranean origin.
ii. Endemic (African): Young African men and children. Effects Jaw.
iii. Epidemic : Ass. With AIDS.
Infectious vascular diseases
46. bacterial endocarditis
a.	Inflammation of the endocardium of the heart. 
b.	Acute: Staphylococcus auresus
c.	Subacute: Streptococcus viridans (Rheumatic Related)
d.	Cz: Rheumatic endocarditis (Group A Beta-hemolytic streptococci). 
i.	Occurs in valves, posterior left atrium
a. Inflammation of the endocardium of the heart.
b. Acute: Staphylococcus auresus
c. Subacute: Streptococcus viridans (Rheumatic Related)
d. Cz: Rheumatic endocarditis (Group A Beta-hemolytic streptococci).
i. Occurs in valves, posterior left atrium creates MacCallum plaque.
ii. Valve Leaflets are red and swollen and tiny warty, bead-like rubbery vegetations.
iii. Healing of valves causes thickening→ Cz’s: Rheumatic Heart Disease (RHD) and valvular prolapse.
Infectious vascular diseases
47. Chagas disease
a.	Protazoa Infection: Trypanomasoma cruzi. 
b.	Transmission: Kissing Bug, painless bite. Can enter placenta. 
c.	Attack macrophages and enter heart nervous, reticuloendothelial, and muscle tissue. 
d.	Tx: Nifurtimox
a. Protazoa Infection: Trypanomasoma cruzi.
b. Transmission: Kissing Bug, painless bite. Can enter placenta.
c. Attack macrophages and enter heart nervous, reticuloendothelial, and muscle tissue.
d. Tx: Nifurtimox
Infectious vascular diseases
48. Lyme Disease
a.	Et: Borrelia burgdorferi from Tick. 
b.	Morph: Bull’s eye red rash with central clearing. 
i.	Stage 1: Erythema chronicum migrans, flulike symtooms. 
ii.	Stage 2: neurologic (Bell’s palsy) and cardiac (AV nodal block) manifestations. 
iii.	Stage 3:
a. Et: Borrelia burgdorferi from Tick.
b. Morph: Bull’s eye red rash with central clearing.
i. Stage 1: Erythema chronicum migrans, flulike symtooms.
ii. Stage 2: neurologic (Bell’s palsy) and cardiac (AV nodal block) manifestations.
iii. Stage 3: Chronic monoarthritis and migratory polyarthritis.
c. Dx: IgM or IgG antibody to spirochete. PCR of DNA.
Infectious vascular diseases
49. Rocky Mountain Spotted Fever
c.	Et: Rickettsia rickettsia from Tick. 
d.	Ca; Vasculitis→ Coronary vessels. 
e.	Clinical: Flu-like, prupural rash, petechiae, GI pain arthralgia’s. Rashes start on limbs and move towards trunk.
c. Et: Rickettsia rickettsia from Tick.
d. Ca; Vasculitis→ Coronary vessels.
e. Clinical: Flu-like, prupural rash, petechiae, GI pain arthralgia’s. Rashes start on limbs and move towards trunk.
Infectious vascular diseases
50. Viral hemorrhagic fever (Yellow fever ~ Dengue fever, filoviruses)
b. Dengue
a.	Yellow fever Virus
i.	Et: Flavivirus (arbovirus) from mosquitos
ii.	Monkey or human reservoir
iii.	S/SE: High fever, black vomitus, and jaundice.
a. Yellow fever Virus
i. Et: Flavivirus (arbovirus) from mosquitos
ii. Monkey or human reservoir
iii. S/SE: High fever, black vomitus, and jaundice.
Dengue:
i. Et: A. aegypti mosquite
ii. Clinical: Flu-like, severe pain in muscles and joints, maculopapular rash, and leukopenia.
iii. Hemorrhagic fever results in shock and hemorrhaging that progresses to death.
Infectious vascular diseases
52. Viral myocarditis
i.	Et: A. aegypti mosquite
ii.	Clinical: Flu-like, severe pain in muscles and joints, maculopapular rash, and leukopenia. 
iii.	Hemorrhagic fever results in shock and hemorrhaging that progresses to death.
a. Presents Young persons, w/biventricular heart failure.
b. Et: Coxsakievirus
c. Morph: Diffuse myocardial degeneration and necrosis w inflammatory infiltrate.
d. Ass. With Chagas disease of South America.
Myocardial infarction
1. partial interruption of blood supply to heart, causing tissue damage
2. Elevated ST segment
3. s/s dyspnea, chest pain, sweating, pain in left arm
4. risk factors: stress, DM, HTN, smoking, diet
5. damage to myocardium
1. partial interruption of blood supply to heart, causing tissue damage
2. Elevated ST segment
3. s/s dyspnea, chest pain, sweating, pain in left arm
4. risk factors: stress, DM, HTN, smoking, diet
5. damage to myocardium