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pathology
CONGENITAL HEART DISEASES
Cyanotic = right-to-left shunt.
Acyanotic = left-to-right shunt.
CYANOTIC CONGENITAL HEART
DISEASES
Early cyanosisblue babies.
Often diagnosed prenatally or become
evident immediately after birth.
Usually require urgent surgical treatment
and/or maintenance of a PDA.
cyanosis
CYANOTIC CONGENITAL HEART
DISEASES
The 5 Ts:
1. Truncus arteriosus (1 vessel)
2. Transposition (2 switched vessels)
3. Tricuspid atresia (3 = Tri)
4. Tetralogy of Fallot (4 = Tetra)
5. TAPVR (5 letters in the name)
+ Ebstein anomaly
Tetralogy of Fallot
Most common cause of early childhood
cyanosis.
AGE !!
HTN
HTN
Hypertensive urgencysevere ( 180/ 120 mm
Hg) hypertension without acute end-organ
damage.
Hypertensive emergencysevere hypertension
with evidence of acute end-organ damage (eg,
encephalopathy, stroke, retinal hemorrhages and
exudates, papilledema, MI, HF, aortic dissection,
kidney injury, microangiopathic hemolytic
anemia, eclampsia).
HTN
Complications :
CAD, LVH, HF, AF; aortic dissection, aortic
aneurysm; stroke; chronic kidney disease
(hypertensive nephropathy) ; retinopathy.
HTN
TREATMENT :
Diuretics , ACEI , ARBs, BB, CCB.
HYPERLIPIDEMIA
LDL < 130.
HDL > 40 males, > 50 females
TRIGLYCERIDE < 200.
HYPERLIPIDEMIA
XANTHOMA :
Composed of lipid-laden histeocytes .
HYPERLIPIDEMIA
On eyelids >>> xanthalesma.
HYPERLIPIDEMIA
Corneal arcus (arcus senilis).
Age ?
ARTERIOLOSCLEROSIS
Hardening of arteries, with arterial wall
thickening and loss of elasticity.
ARTERIOLOSCLEROSIS
1. Arteriolosclerosis:
Affects small arteries and arterioles
Two types:
hyaline (thickening of vessel walls in essential
hypertension or diabetes mellitus (non-enzymetic
glycosylation) )
Consequences ? Kidney ischemia >>
glomerulosclerosis and shrunken kidneys >> CKD
ARTERIOLOSCLEROSIS
hyperplastic (onion skinning in severe
hypertension , with proliferation of smooth
muscle cells).
Consequences ? ARF >>> FLEA-BITTEN
APPEARANCE (PIN-POINT HMG)
ARTERIOLOSCLEROSIS
ARTERIOLOSCLEROSIS
2. M nckeberg sclerosis(medial calcific
sclerosis)
Affects medium-sized arteries
Calcification of internal elastic lamina and
media of arteries >>>vascular stiffening
without obstruction.
Pipestem appearance on x-ray . Does not
obstruct blood flow; intima not involved.
ARTERIOLOSCLEROSIS
ARTERIOLOSCLEROSIS
3. ATHEROSCLEROSIS :
Disease of elastic arteries and large- and
medium-sized muscular arteries;
a form of arteriosclerosis caused by buildup of
cholesterol plaques >>> THICK INTIMA.
ARTERIOLOSCLEROSIS
Abdominal aorta > coronary artery > popliteal
artery > carotid artery.
ARTERIOLOSCLEROSIS
RF:
Modifiable: smoking, hypertension,
hyperlipidemia (LDL), diabetes.
Nonmodifiable: age, sex (in men and
postmenopausal women), family history.
ARTERIOLOSCLEROSIS
PATHGOGENSIS :
Inflammation is important in pathogenesis:
endothelial cell dysfunction >>> macrophage
and LDL accumulation >>>foam cell formation
>>> fatty streaks* >>>> smooth muscle cell
migration (involves PDGF ( FROM PLATTLETS )
and FGF), proliferation, and extracellular
matrix deposition >>>fibrous plaque >>>
complex atheromas .
ARTERIOLOSCLEROSIS
PRESENTATION : SITE !!
Angina, claudication, but can be asymptomatic.
ARTERIOLOSCLEROSIS
COMPLICATION :
Aneurysms, ischemia, infarcts, peripheral
vascular disease, thrombus, emboli.
AORTIC ANEURYSM
Localized pathologic dilatation of the aorta.
AORTIC ANEURYSM
AORTIC ANEURYSM
Sx :
May cause abdominal and/or back pain
which is a sign of leaking, dissection, or
imminent rupture.
AORTIC ANEURYSM
1. Abdominal Aortic Aneurysm (AAA)
Associated with atherosclerosis.
Risk factors include history of tobacco use, age,
male sex, family history.
May present as palpable pulsatile abdominal
mass
Mostly INFRARENAL .
SIZE 5 cm ??!
Screening ??!
AORTIC ANEURYSM
1. Thoracic aortic aneurysm:
Associated with cystic medial degeneration.
Risk factors include hypertension, bicuspid
aortic valve, connective tissue disease (eg,
Marfan syndrome).
Also historically associated with 3syphilis
(obliterative endarteritis of the vasa vasorum).
AORTIC ANEURYSM
Mycotic aneurysm :
Due to septic emboli
Inflamatory aneurysm :
Associated with vasculitis .
AORTIC ANEURYSM
Treatment :
SURGERY when indicated.
Aortic dissection
Longitudinal intimal tear forming a false
lumen.
Aortic dissection
Associated with hypertension, bicuspid aortic
valve, inherited connective tissue disorders
(eg, Marfan syndrome).
Complicaions :
Free wall rupture tamponade;
papillary muscle rupturemitral regurgitation;
interventricular septal rupture
due to macrophage-mediated structural
degradation.
LV pseudoaneurysm (risk of rupture).
ISCHEMIC HEART DISEASE
2 weeks to several months:
Contracted scar complete.
Complications :
Dressler syndrome,
HF,
arrhythmias,
true ventricular aneurysm (risk of mural
thrombus).
ISCHEMIC HEART DISEASE
COMPLICATIONS OF MI:
Cardiac arrhythmia:
Occurs within the first few days after MI.
Important cause of death before reaching the
hospital and within the first 24 hours post-MI.
ISCHEMIC HEART DISEASE
Postinfarction fibrinous pericarditis
Occurs 13 days after MI ( only transmural )
Friction rub.
Ttt : aspirin.
ISCHEMIC HEART DISEASE
Papillary muscle rupture:
Occurs 27 days after MI.
Posteromedial papillary muscle rupture
risk due to single blood supply from posterior
descending artery.
Can result in severe mitral regurgitation.
Treatment: surgery.
ISCHEMIC HEART DISEASE
Papillary muscle rupture:
ISCHEMIC HEART DISEASE
Interventricular septal rupture:
Occurs 35 days after MI.
Macrophage-mediated degradation
VSD.
ISCHEMIC HEART DISEASE
Ventricular pseudoaneurysm formation:
Occurs 314 days after MI.
Contained free wall rupture ;
low CO, risk of arrhythmia, embolus from
mural thrombus.
ISCHEMIC HEART DISEASE
Ventricular pseudoaneurysm formation:
ISCHEMIC HEART DISEASE
Ventricular free wall rupture:
Occurs 514 days after MI.
Free wall rupture may lead tocardiac
tamponade.
ISCHEMIC HEART DISEASE
True ventricular aneurysm:
Occurs 2 weeks to several months after MI.
Outward bulge with contraction
dyskinesia),associated with fibrosis.
ISCHEMIC HEART DISEASE
Dressler syndrome
Occurs several weeks after MI.
Autoimmune phenomenon resulting in
fibrinous pericarditis ( diffused ).
Pericardial antigens get exposed to immune
system.
ISCHEMIC HEART DISEASE
LV failure and pulmonary edema
Can occur 2 to LV infarction, VSD, free wall
rupture, papillary muscle rupture with mitral
regurgitation.
ISCHEMIC HEART DISEASE
Acute coronary syndrome treatments:
Unstable angina/NSTEMIAnticoagulation (eg,
heparin), antiplatelet therapy (eg, aspirin+ ADP
receptor inhibitors (eg, clopidogrel), -blockers,
ACE inhibitors, statins. Symptom control with
nitroglycerin and morphine.
STEMIIn addition to above, reperfusion therapy
most important (percutaneous coronary
intervention preferred over fibrinolysis).
HEART FAILURE
Clinical syndrome of cardiac pump dysfunction
congestion and low perfusion.
Symptoms: include dyspnea, orthopnea,
fatigue;
signs: include rales, jugular venous distention
(JVD), pitting edema.
HEART FAILURE
Systolic dysfunctionreduced EF, increased
EDV; due to decrease contractility often 2 to
ischemia/MI or dilated cardiomyopathy.