Pathology Flashcards
Congenital heart diseases
2 groups
Special names
Reasons
- R to L shunts-early cyanosis-blue babies
2. L to R shunts-late cyanosis with Eisenmengers phenomenon-blue kids
R to L shunts
Cyanosis when
Diagnosed when
Compatibility with life unless
Early cyanosis—“blue babies.”
Often diagnosed prenatally or become evident immediately after birth.
Usually require urgent surgical correction and/or maintenance of a PDA.
What are the R to L shunt disorders
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)
Persistsnt Truncus arteriosus
Causes
Pathology
Also have what
Truncus arteriosus fails to divide into pulmonary trunk and aorta due to lack of aorticopulmonary septum formation
most patients have accompanying VSD.
TGV Means what Due to Shunts present Prognosis
Aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior)
Due to failure of the aorticopulmonary septum to spiral.
VSD
ASD
PDA
If no sx die within weeks
Tricuspid atresia
Pathology
Shunts
Absence of tricuspid valve and hypoplastic RV
requires both ASD and VSD for viability.
TOF Commonest what Cause Components 4 Factor determining the prognosis Shape of the heart,due to Special symptom Relieved how RX
Most common cause of early childhood cyanosis.
Caused by anterosuperior displacement of the infundibular septum
Pulmonary infundibular stenosis (most important determinant for prognosis)
Right ventricular hypertrophy (RVH)— boot-shaped heart on CXR
A Overriding aorta
VSD
early cyanotic “tet spells”
Squatting: SVR, right-to-left shunt, improves
cyanosis.
Treatment: early surgical correction.
TAPVD
Means
Via
Shunts 2
Pulmonary veins drain into right heart circulation
SVC, coronary sinus
associated with ASD and sometimes PDA to allow for right-to-left shunting to maintain CO.
L to R shunt diseases
Cyanosis when
Why
VSD>ASD>PDA
Late cyanosis
Eisenmengers
VSD Common Symptoms at birth Symptoms appear when Resolve how Larger ones can causes
Most common congenital cardiac defect.
Asymptomatic at birth.
May manifest weeks later or remain asymptomatic throughout life.
Most self resolve
larger lesions may lead to LV overload and HF.
ASD Pathology Clinical signs Two types/common/associated abnormalities Symptoms Difference from patent f.ovale
Defect in interatrial septum
loud S1/wide, fixed split S2.
Ostium secundum defects most common and usually occur as isolated findings
ostium primum defects rarer yet usually occur with other cardiac anomalies.
Symptoms range from none to HF.
Distinct from patent foramen ovale in that septa are missing tissue rather than unfused.
PDA Function in fetal period Neonatal period function Later on what happens Diagnostic sign
In fetal period, shunt is right to left (normal).
In neonatal period, lung resistance shunt becomes left to right
progressive RVH and/or LVH and HF-Eisenmengers
Lower extremity cyanosis
Eisenmengers syndrome Caused by How Clinical signs 3 Age of onset
Uncorrected left-to-right shunt (VSD, ASD, PDA)
pulmonary blood flow pathologic remodeling of vasculature pulmonary arterial hypertension. RVH occurs to compensate -shunt becomes right to
left
Causes late cyanosis, clubbing and polycythemia.
Age of onset varies.
Congenital COA Pathology Site Associated conditions 2 Symtopms and signs
Later on CXR changes,due to
Aortic narrowing near insertion of ductus arteriosus (“juxtaductal”).
Associated with
bicuspid aortic valve
Turner syndrome.
Hypertension in upper extremities and weak, delayed pulse in lower extremities (brachial-femoral delay).
With age, collateral arteries erode ribs (notched appearance on CXR).
Congenital cardiac defect s associations
Alcohol exposure in utero (fetal alcohol syndrome)
Congenital rubella
Down syndrome
Infant of diabetic mother
Marfan syndrome
Prenatal lithium exposure Turner syndrome Williams syndrome
22q11 syndromes
Alcohol exposure in utero (fetal alcohol syndrome)-ASD/VSD/PDA/TOF
Congenital rubella-ASD/VSD/PDA/PS
Down syndrome-AV canal defects/ASD/VSD
Infant of diabetic mother-TPGV
Marfan syndrome-MVP/AR/thoracic aorta aneurysms and dissections
Prenatal lithium exposure -Ebstein anomaly(TV defect)
Turner syndrome -COA/bicuspid aortic v
Williams syndrome-supravalvular AS
22q11 syndromes-TA,TOF
HTN
Definition Risk factors Ethnic frequency Types and % Causes for both contrast X-ray in fibromyscular dysplasia What's HT urgency What's HT emergency/eg Complications Explain high renin HT
Defined as persistent systolic BP ≥ 140 mmHg and/or diastolic BP ≥ 90 mmHg
age, obesity, diabetes, physical inactivity, excess salt intake, excess alcohol intake, family history
black > white > Asian
90% -1° (essential) and related to CO or TPR
10% -2°
-renal/renovascular disease-renal artery stenosis (e.g., fibromuscular dysplasia -usually found in younger women-string of beads appearance)
-1° hyperaldosteronism.
Hypertensive urgency—severe (≥ 180/≥ 120 mmHg) hypertension without acute end-organ damage.
Hypertensive emergency—severe hypertension with evidence of acute end-organ damage
(e.g., encephalopathy, stroke, retinal hemorrhages and exudates, papilledema, MI, HF, aortic dissection, kidney injury, microangiopathic hemolytic anemia, eclampsia)
Complications
1.CVS-CAD, LVH, HF, atrial fibrillation
aortic dissection, aortic aneurysm
- CNS-stroke
- Renal-chronic kidney disease (hypertensive nephropathy)
- retinopathy.
B. Renal artery stenosis is a common cause (renovascular hypertension).
Stenosis decreases blood flow to glomerulus.
Juxtaglomerular apparatus (JGA) responds by secreting renin, which converts angiotensinogen to angiotensin 1.
Angiotensin I is converted to angiotensin 11 (ATII) by angiotensin converting enzyme (ACE).
ATII raises blood pressure by (I) contracting arteriolar smooth muscle, increasing total peripheral resistance and (2) promoting adrenal release of aldosterone, which increases resorption of sodium in the distal convoluted tubule (expanding plasma volume).
Leads to HTN with increased plasma renin and unilateral atrophy (due to low blood flow) of the affected kidney; neither feature is seen in primary hypertension
Important causes of stenosis include atherosclerosis (elderly males) and fibromuscular dysplasia (young females).
HLD signs 3
Xanthelesma-
lipid deposited in histiocytes
Seen as plaque sin eye lids
Tendinous xanthomata-
Lipid deposited on tendons
Common Archillies
Corneal arcus-
Deposit in cornea
Old age-senile arcus
Premature if high cholesterol
Arteriosclerosis What types 3 How common Affects which vessels
Thickening of vessel walls-hardening and loss of elasticity
Ateriolosclerosis-
common
Aterioles
Medial calcific sclerosis-
uncommon
Medium size arteries
Atherosclerosis-
very common
Elastic and medium and large muscular arteries
Ateriolosclerosis Common Affect which vessels Types 2 Eg Hyper plastic Appearance on histo,due to Classically seen when
Common.
Affects small arteries and arterioles.
Two types:
1.hyaline (thickening of vessel walls in essential hypertension or diabetes mellitus
classically produces glomerular scarring (arteriolonephrosclerosis)that slowly progresses to
chronic renal failure
2.hyperplastic (“onion skinning” in severe hypertension with proliferation of smooth muscle cells).
fibrinoid necrosis of the vessel wall with hemorrhage
classically causes acute renal failure with a characteristic ‘flea-bitten’ appearance
Medial calcific sclerosis Common Affects Pathology Effect Involves what Not involves Blood flow affected X-ray appearance
Uncommon.
Affects medium-sized arteries.
Calcification of elastic lamina of arteries vascular stiffening without obstruction.
“Pipestem” appearance on x-ray
Does not obstruct blood flow
intima not involved
Atherosclerosis Common Affects what What's it Risk factors Pathophysio Complications Vessels affecting frequency Symptoms
Very common.
elastic arteries and large- and medium-sized muscular arteries
a form of arteriosclerosis caused by buildup of cholesterol plaques.
Risk factors-
Modifiable: smoking, hypertension, hyperlipidemia, diabetes.
Nonmodifiable: age, sex ( in men and postmenopausal women), family history.
Pathophysio Inflammation important in pathogenesis: endothelial cell dysfunction macrophage and LDL accumulation foam cell formation fatty streaks smooth muscle cell migration (involves PDGF and FGF), proliferation extracellular matrix deposition fibrous plaque complex atheromas
Complications Aneurysms ischemia infarcts peripheral vascular disease thrombus emboli.
Frequency-
Abdominal aorta > coronary artery > popliteal artery > carotid artery B .
Symptoms-
Angina, claudication, but can be asymptomatic.
Aortic aneurysms What Symptom of complications Complication Two types. Causes Risk factors Tertiary syphillis causes what ,special name Abdominal aortic aneurysm site High risk of rupture when Abdominal aneurysms occure in who
Localized pathologic dilatation of the aorta.
May cause abdominal and/or back pain
which is a sign of leaking, dissection, or imminent rupture.
Abdominal
Associated with atherosclerosis
Risk factors include history of tobacco use, age, male sex, family history.
May present as palpable pulsatile abdominal mass .
Thoracic
Associated with cystic medial degeneration.
Risk factors include hypertension, bicuspid aortic valve, connective tissue disease (e.g., Marfan syndrome)
Also historically associated with 3° syphilis (obliterative endarteritis of the vasa vasorum).
Below renal vessels above bifurcation
Diameter >5cm
Males >60y,HT
Flank pain/hypotension/pulsatile mass
Aortic dissection What Pathology Risk factors Symtopms Special sign CXR finding Complications 3 Types 2 Involve which parts Treatment If ascending aorta and descending both involves which type
Longitudinal intimal tear forming a false lumen
hypertension
bicuspid aortic valve
inherited connective tissue disorders (e.g., Marfan syndrome).
Can present with tearing chest pain, of sudden onset, radiating to the back +/− markedly unequal BP in arms.
CXR shows mediastinal widening.
Can result in
rupture
pericardial tamponade
death.
Two types:
Stanford type A (proximal):
involves Ascending aorta.
May extend to aortic arch
or descending aorta.
Treatment is surgery.
Stanford type B (distal):
involves descending aorta and/or aortic arch.
No ascending aorta involvement.
Treat medically with β-blockers, then vasodilators.
Stanford A
Ischemic artery disease types
Angina Infarction Coronary steal syndrome SCD Chronic IHD
Angina Means Due to Myocytes damage? Types
Chest pain due to ischemic myocardium
2° to coronary artery narrowing or spasm
no myocyte necrosis
Stable angina
Prinzemetal(variant) angina
Unstable angina
What's stable angina Symptoms Occures when Acute ECG changes Resolves with
Stable—usually 2° to atherosclerosis
exertional chest pain in classic distribution
ST depression on ECG
resolving with rest or nitroglycerin.
Prinze metal angina What's Occurs when Due to Triggers ECG changes RX 3
Chest painoccurs 2° to coronary artery spasm
Occurs at rest
transient ST elevation on ECG
Known triggers include tobacco, cocaine, and triptans, but trigger is often unknown.
Treat with Ca2+ channel blockers, nitrates, and smoking cessation (if applicable).
Unstable angina What's? Due to ECG changes Difference to NSTEMI
Increase in frequency or intensity of chest pain or any chest pain at rest.
thrombosis with incomplete coronary artery occlusion
+/− ST depression and/or
T-wave inversion on ECG
no cardiac biomarker elevation (unlike NSTEMI)
Coronary steal syndrome
Explain
Basis of what
Distal to coronary stenosis, vessels are maximally dilated at baseline.
Administration of vasodilators (e.g., dipyridamole, regadenoson) dilates normal vessels and shunts blood toward well-perfused areas flow and ischemia in poststenotic region.
Principle behind pharmacologic stress tests.
MI Due to what Symtopms Types 2 ECG in both Diagnostic ix
Most often acute thrombosis due to rupture of coronary artery atherosclerotic plaque.
Acute onset typical chest pain
Autonomic symptoms
Lasting more than1/2hr
Not responding to rest or GTN
transmural, ECG may show ST elevations (STEMI)
subendocardial, ECG may show ST depressions (NSTEMI)
Cardiac biomarkers are diagnostic.
Sudden cardiac death Means Usually due to Causes-common,% Other causes
Death from cardiac causes within 1 hour of onset of symptoms
most commonly due to a lethal arrhythmia (e.g., ventricular fibrillation).
Associated with CAD (up to 70% of cases), cardiomyopathy (hypertrophic, dilated),
hereditary ion channelopathies (e.g., long QT syndrome, Brugada syndrome).
Chronic IHD
What
Progressive onset of HF over many years due to chronic ischemic myocardial damage
MI
Arteries affected frequency 3
Evolution periods
LAD>RCA>LCX
0-4hrs 4-24hrs 1-3days 3-14days 2wks -several months
0-4hrs
Gross changes
LM changes
Complications
None
None
Arrythmias
HF
Cardiogenic shock
4-24hrs
Gross
LM
Complications
Gross-
Dark mottling
Pale with Tetrazonium stain
LM- Early coagulative necrosis- release of necrotic cell contents into blood edema hemorrhage wavy fibers. Neutrophils appear.
Reperfusion injury may cause contraction bands (due to free radical damage and hyper contraction from high Ca influx)
Complications
Arrythmia
HF
Cardiogenic shock
1-3days
Gross
LM
Complications
Gross-
Hyperaemia
LM-
Extensive coagulative necrosis.
Tissue surrounding infarct shows acute inflammation with neutrophils.
Complications -post MI fibrinous pericarditis
3-14 days
Gross
LM
Complications
Gross-
Hypereamic border
Pale yellow soft middle
Softest on day 10(high risk of rupture)
LM-
Macrophages cause phagocytosis
Granulation tissue formation in the border
Complications -
Free wall rupture -tamponade
papillary muscle rupture -mitral regurgitation
interventricular septal rupture - VSD
LV pseudoaneurysm (risk of rupture).
2wks to months
Gross
LM
Complications
Gross-
Re canalized vessel
White gray area
LM-
Contracted scar complete
Complications - Dressler syndrome(AI pericarditis) HF arrhythmias true ventricular aneurysm (risk of mural thrombus).
MI diagnosis
Gold standerd ix in first 6 hours
ECG changes
What indicates evolving or old infarct
Important cardiac enzymes 2
Which is more specific
Trop I rises when
Keeps elevated till
CK-MB rises when Reduces when Useful for what Disadvntg
ECG
ST elevation (STEMI, transmural infarct) ST depression (NSTEMI) hyperacute (peaked) T waves T-wave inversion new left bundle branch block pathologic Q waves or poor R wave progression (evolving or old transmural infarct).
Trop I- more specific
CK-MB
Cardiac troponin I rises after 4 hours
High for 7–10 days
CK-MB rises after 6–12 hours
Normal in 48 hours
predominantly found in myocardium but can also be released from skeletal muscle.
Useful in diagnosing reinfarction following acute MI because levels return to normal
to normal after 48 hours.
Types of infarcts
Amount of necrosis
Area involved
ECG Changes
STEMI
More necrosis
Affects entire wall
ST elevation on ECG, Q waves
NSTEMI
Subendocardial infarcts
Due to ischemic necrosis of
MI sites
Vessels involved
ECG leads
Anteroseptal (LAD)-V1-V2
Anteroapical (distal LAD) -V3-V4
Anterolateral (LAD or LCX) -V5-V6
Lateral (LCX)-aVL,I
InFerior (RCA)-II,III,aVF
Post MI complications
Arrythmia important cause of what
Most common during when
Cardiogenic shock occurs with what
Risk of what
Pseudo aneurysm means
Risks of 3
True v aneurysm means
Associated with
Cardiac arrhythmia—
important cause of death before reaching hospital
common in first few days.
LV failure and pulmonary edema.
Cardiogenic shock (large infarct high risk of mortality).
Ventricular free wall rupture -cardiac tamponade
papillary muscle rupture -severe mitral
regurgitation
interventricular septum rupture -VSD
Ventricular pseudoaneurysm formation (contained free wall rupture)— CO, risk of arrhythmia, embolus from mural thrombus;
greatest risk approximately 3–14 days post-MI (as with rupture).
True ventricular aneurysm—outward bulge during contraction (“dyskinesia”),
associated with fibrosis
arises 2 weeks to several months after MI.
Postinfarction fibrinous pericarditis—friction rub (1–3 days post-MI).
Dressler syndrome—autoimmune phenomenon resulting in fibrinous pericarditis (several weeks
post-MI).
RX for MI For STEMI which is most important Two methods of reperfusion Better one Do how soon Types of fibrinolytic SK side effects
Unstable angina/NSTEMI—
Anticoagulation (e.g., heparin)
antiplatelet therapy (e.g., aspirin + clopidogrel),
β-blockers,
ACE inhibitors,
statins.
Symptom control with nitroglycerin and morphine.
STEMI—In addition to above, reperfusion therapy most important (percutaneous coronary intervention preferred over fibrinolysis).
PCI better
Within
Three types of cardiomyopathies
Dilated -most common
Hypertrophic
Restrictive
Dilated cardiomyopathy Common Common etiology 2 Other causes Unlikely causes physiological causes Clinical signs 2 Complication -type Echo feature CXR feature RX-drugs/life style/sx Dilatation occures how with fibers
Most common cardiomyopathy (90% of cases)
Often idiopathic or familial. Other etiologies include A-Alcohol abuse B-Beriberi C-Coxsackie B virus myocarditis C-chronic Cocaine use C-Chagas disease, D-Doxorubicin toxicity hemochromatosis sarcoidosis peripartum cardiomyopathy.
Findings: S3, systolic regurgitant murmur
HF-systolic
dilated heart on echocardiogram
balloon appearance of heart on CXR.
Treatment: Na+ restriction, ACE inhibitors, β-blockers, diuretics, digoxin, ICD, heart transplant.
Eccentric hypertrophy (sarcomeres added in
series
Hypertrophic cardiomyopathy Cause% Inheritance Due to want mutation Associated disease Symtopms ,when Complication 2,due to Finding 3 RX-drugs 2 Life style If high risk Gross appearance HOCM what, pathophysio ,symptoms
60–70% of cases are familial
autosomal dominant
commonly a β-myosin heavy-chain mutation
Can be associated with Friedreich ataxia.
Causes syncope during exercise
Diastolic HF
sudden death in young athletes due to ventricular arrhythmia.
Findings: S4, systolic murmur. May see mitral regurgitation due to impaired mitral valve closure.
Treatment:
cessation of high-intensity athletics
use of β-blocker
non-dihydropyridine Ca2+ channel blockers (e.g., verapamil)
ICD if patient is high risk.
Marked ventricular hypertrophy often septal
predominance
Obstructive hypertrophic cardiomyopathy
(subset)—asymmetric septal hypertrophy and systolic anterior motion of mitral valve outflow obstruction
dyspnea, possible syncope.
Restrictive cardiomyopathy Causes 6 What's endo myocardial fibroelastosis,occures in who Loefflers syndrome what's complication ECG change ,especially in
sarcoidosis
amyloidosis
postradiation fibrosis
endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children)
Löffler syndrome (endomyocardial fibrosis with a prominent eosinophilic infiltrate)
hemochromatosis (dilated cardiomyopathy can also occur).
Diastolic dysfunction ensues.
Can have low- voltage ECG despite thick myocardium (especially amyloid).
What's heart failure 2 main pathologies Types-sides LHF-2types Systolic HF-pathology/EF/EDV/cause-2 Diastolic HF-pathology/EF/EDV/cause RHF-results from or due to RX-reduce mortality 4 Symtopm relieve only 2 Both by2 ,in who Bblockers not given when Symptoms in LHF,RHF LHF pathophysio
Clinical syndrome of cardiac pump dysfunction
congestion and low perfusion.
LHF/RHF LHF Systolic dysfunction— low contractility reduced EF, high EDV often 2° to ischemia/MI or dilated cardiomyopathy.
Diastolic dysfunction—
low compliance
2° to myocardial hypertrophy
preserved EF, normal EDV
RHF most often results from left HF.
Isolated right HF -due to cor pulmonale.
ACE inhibitors or angiotensin II receptor blockers, β-blockers (except in acute decompensated HF),
and spironolactone reduce mortality.
Thiazide or loop diuretics are used mainly for symptomatic relief.
Hydralazine with nitrate therapy improves both symptoms and mortality in select patients.
LHF
1.Orthopnea-
Shortness of breath when supine: venous return from redistribution of blood (immediate gravity effect) exacerbates pulmonary vascular congestion.
2.PND-
Breathless awakening from sleep: venous return from redistribution of blood, reabsorption of edema, etc.
3.Pulmonary oedema-
pulmonary venous pressure pulmonary venous distention and transudation of fluid.
Presence of hemosiderin-laden macrophages (“HF” cells) in lungs.
RHF
1.Hepatomegaly(Nutmeg liver)-
central venous pressure resistance to portal flow. Rarely, leads to “cardiac cirrhosis.”
2.JVD-
High venous pressure.
3.High central venous pressure -fluid transudation
Refer book
Types of shocks 4 Causes for each Main pathology Changes to CO/CVP/SVR Treatment
Hypovolemic
Cardiogenic
Obstructive
Distributive
SIRS- What Components First sign of shock Last result of shock
Systemic inflammatory response syndrome ≥ 2: fever/hypothermia tachycardia tachypnea leukocytosis/leukopenia
First sign of shock is tachycardia.
Multiple organ dysfunction syndrome (MODS) is the end result of shock.
Bacterial endocarditis- Symptoms Most common symptoms Diagnostic crtiteria What's necessary for diagnosis Two main types-onset/cause/virulence/vegetations/valve status/association Strep.bovis when Strep.epiderdimis Commonly affect which valve TV affected in who/organisms Culture neg causes Non bacterial causes of IE-name/ Other special ix
bacteria FROM JANE
Fever (most common symptom)
new murmur
Roth spots (round white spots on retina surrounded by hemorrhage)
Osler nodes (tender raised lesions on finger or toe pads)
Janeway lesions (small,painless,erythematous lesions on palm or sole)
glomerulonephritis
septic arterial or pulmonary emboli
splinter hemorrhages on nail bed
Multiple blood cultures necessary for diagnosis.
Acute—S. aureus (high virulence).
Large vegetations on previously normal valves Rapid onset.
Subacute—viridans streptococci (low
virulence).
Smaller vegetations on congenitally abnormal or diseased valves.
Sequela of dental procedures. Gradual onset.
S. bovis (gallolyticus) is present in colon cancer,
S. epidermidis on prosthetic valves.
Mitral valve is most frequently involved.
Tricuspid valve - associated with IV drug abuse (don’t “tri” drugs).
Associated with S. aureus, Pseudomonas, and Candida.
Culture ⊝—most likely Coxiella burnetii, Bartonella spp., HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella,
Kingella)
Endocarditis may also be nonbacterial (marantic/thrombotic)
2° to malignancy, hypercoagulable state, or lupus(Libermann sacks)
Transeosophageal Echo to see valves
Rheumatic fever What Infection where,by,when Late sequele Affects which valves frequency MV-early and late lesions Histological feature-and special cells Diagnostic ix pathophysiology-hypersen type /due Diagnostic criteria Major criteria Minor criteria Other must have thing for diagnosis Carditis which type Endocarditis involve what /vegetation type Myocarditis Histological feature Most common cause of death in acute disease Repeat exposure to bacteria risk What's chronic RHD Major pathology to valve-appearance Change in MV/AV Complication
A consequence of pharyngeal infection with group A β-hemolytic streptococci.
After2-3 weeks
Late sequelae include rheumatic heart disease, which affects heart valves—mitral > aortic»_space; tricuspid (high-pressure valves affected most).
Early lesion is mitral valve regurgitation;
late lesion is mitral stenosis.
Rheumatic granuloma-
Aschoff bodies -giant cells
Anitschkow cells -enlarged macrophages with ovoid, wavy, rod-like nucleus
anti- streptolysin O (ASO) titers.
Anti DNAse B titres
Immune mediated (type II hypersensitivity) not a direct effect of bacteria.
Antibodies to M protein cross-react with self antigens (molecular mimicry).
Treatment/prophylaxis: penicillin.
J♥NES (major criteria):
Joint (migratory polyarthritis) -large joints
♥ (carditis)-pan carditis
Nodules in skin (subcutaneous)
Erythema marginatum
Sydenham chorea
Minor-
None specific-fever /ESR high
Prior group a infection-ASOT/anti DNAse b titres
Pan carditis
Endocarditis involve valves-small vegetations
Aschoff bodies in myocardium
Death due to myocarditis
High risk of chronic disease
CHRONIC RHEUMATIC HEART DISEASE
A. Valve scarring that arises as a consequence of rheumatic fever
B.Results in stenosis with a classic ‘fish mouth’ appearance
1. Almost always involves the mitral valve;thickening of chordae tendineae and cusps
- Occasionally involves the aortic valve; fusion of the commissures
- Other valves are less commonly involved.
C. Complications include infectious endocarditis.
Acute pericarditis Symptoms-increased by/relieved by/ Sign ECG changes Causes-commonest
Commonly presents with sharp pain, aggravated by inspiration,
relieved -sitting up and leaning forward.
Presents with friction rub.
ECG changes include widespread ST-segment elevation and/or PR depression.
Causes include idiopathic (most common-presumed viral),
confirmed infection (e.g., Coxsackievirus), neoplasia,
autoimmune (e.g., SLE, rheumatoid arthritis), uremia
cardiovascular (acute STEMI or Dressler syndrome), radiation therapy.
Cardiac tamponade Means Results in 2 Clinical signs-main,other ECG Changes 2 Pulsus paradox-explain/causes-CVS,RS
Compression of heart by fluid (e.g., blood, effusions) in pericardial space
Low CO.
Equilibration of diastolic pressures in all 4 chambers.
Findings: Beck triad (hypotension, distended neck veins, distant heart sounds),
High HR
pulsus paradoxus.
ECG shows low-voltage QRS electrical alternans (due to “swinging” movement of heart in large effusion).
Pulsus paradoxus— in amplitude of systolic BP by > 10 mmHg during inspiration.
Seen in cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, croup.
Which syphillis affects the aorta? Pathology X Ray feature Gross appearance Complications 2
3° syphilis disrupts the vasa vasorum of the aorta(end arteritis obliterans) -atrophy of vessel wall -dilatation of aorta and valve ring.
calcification of aortic root and ascending aortic arch.
Leads to “tree bark” appearance of aorta.
Can result in aneurysm of ascending aorta or aortic arch, aortic insufficiency.
What’s the commonest tumour in heart
Mets from where,
Deposit where
Other types of cardiac Tumors 2
Myxomatosis -who/where-side/effect/symptoms/sign
Rhabdomyomas-who/associated with other diseases/benign or not /site
Most common heart tumor is a metastasis.
Lung/breast/lymphomas/melanomas
Mostly affect the pericardium-effusions
Myxomas
Rhabdomyomas
Myxomas-
Most common 1° cardiac tumor in adults
90% occur in the atria (mostly left
atrium)
“ball valve” obstruction in the left atrium
associated with multiple syncopal episodes
early diastolic “tumor plop” sound.
Rhabdomyomas-
Most frequent 1° cardiac tumor in children associated with tuberous sclerosis
Benign
Ventricles
Kusmmauls sign
What’s
Pathology
Seen when 4
Increased JVP on inspiration instead of a normal reduction
Inspiration -negative intrathoracic pressure not transmitted to heart -impaired filling of right
ventricle -blood backs up into venae cavae -JVD.
constrictive pericarditis
restrictive cardiomyopathies
right atrial or ventricular tumors.
Angiosarcoma Common Malignant Of what tissue Age Site 3 Risk factors 3hepatic angiosarcoma-severity/risk/prognosis/why
Rare
blood vessel malignancy
in the head, neck, and breast areas.
Usually in elderly
on sun-exposed areas.
Associated with radiation therapy
chronic postmastectomy lymphedema.
Hepatic angiosarcoma associated with vinyl chloride and arsenic exposures.
Very aggressive and difficult to resect due to delay in diagnosis.
Bacillary angiomatosis benign What tissue Lesion Who Caused by Similar to Difference
Benign
capillary skin papules
found in AIDS patients
Caused by Bartonella henselae infections. Frequently mistaken for Kaposi sarcoma, but has neutrophilic infiltrate.
Cherry haemangiomas Benign Tissue Who Frequency with age Regression
Benign capillary hemangioma elderly Does not regress Frequency increase with age.
Cystic hygroma
What
Site
Associated disease
Cavernous lymphangioma
neck
Associated with Turner syndrome.
Glomus tumour Benign Painful Tissue Site colour
Benign painful red-blue tumor under fingernails Arises from modified smooth muscle cells of the thermoregulatory glomus body.
Kaposi sarcoma Benign Tissue of origin Sites -common ,also Risk factor Similar to Difference
Endothelial malignancy
most commonly of the skin
but also mouth, GI tract, and respiratory tract. Associated with HHV-8 and HIV.
Frequently mistaken for bacillary angiomatosis, but has lymphocytic infiltrate.
Pyogenic granuloma Tissue Shape Complications Seen in who 2
Polypoid capillary hemangioma
ulcerate and bleed.
Associated with trauma and pregnancy
Strawberry haemangiomas What tissue In who Appears when Growth Regression when
Benign capillary hemangioma of infancy Appears in first few weeks of life (1/200 births)
grows rapidly
regresses spontaneously by 5–8 years old.
Reynaudes phenomenon Due to what Who exposed to Site Color change Two types /causes RX
Reduction in blood flow to the skin due to arteriolar (small vessel) vasospasm
response to cold or stress
color change from white (ischemia) to blue (hypoxia) to red (reperfusion).
Most often in the fingers A and toes.
Raynaud disease when 1° (idiopathic)
Raynaud syndrome when 2° to a disease process such as mixed connective tissue disease, SLE, or CREST (limited form of systemic sclerosis) syndrome.
Treat with Ca2+ channel blockers.
Types of vasculitis according to affecting vessels
Large-
Temporal
Takayasu
Medium-
Polyarteritis nodosa
Kawasaki dis
Buergers dis(pollyangitis obliterance)
Small- Granulomatosis with polyangitis(wegners) Microscopic polyangitis Eosinophilic Granulomatosis with polyangitis HSP
Temporal arteritis Affects who commonly Main symptoms 2 Complication-due to Affect which arteries Pathology Ix 2 RX RX before what-why
Usually elderly females.
Unilateral headache (temporal artery)
jaw claudication.
May lead to irreversible blindness due to
ophthalmic artery occlusion.
Associated with polymyalgia rheumatica.
commonly affects branches of carotid artery.
Focal granulomatous inflammation
ESR-high
Temporal artery bx
Treat with high-dose corticosteroids prior to
temporal artery biopsy to prevent blindness.
Polyarteritis nodosa Affects who Associated diseas Symptoms -non specific,specif Vessels affected/not Pathology -caused by Ix-see what RX-2
Young adults.
Hepatitis B seropositivity in 30% of patients.
Fever, weight loss, malaise, headache.
GI: abdominal pain, melena.
Hypertension, neurologic dysfunction,
cutaneous eruptions, renal damage.
Typically involves renal and visceral vessels
not pulmonary arteries.
Immune complex mediated.
Transmural inflammation of the arterial wall
with fibrinoid necrosis.
Innumerable renal microaneurysms and spasms
on arteriogram.
Treat with corticosteroids, cyclophosphamide.
Granulomatosis with polyangitis Other name Symptoms affect with systems-they are Special symtopms Pathology triad Proteins associated CXR RX
Wegners Granulomatosis
Upper respiratory tract: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis.
Lower respiratory tract:
hemoptysis, cough, dyspnea.
Renal: hematuria, red cell casts.
Triad:
Focal necrotizing vasculitis
Necrotizing granulomas in the lung and
upper airway
Necrotizing glomerulonephritis
PR3-ANCA
c-ANCA (anti-proteinase 3).
CXR: large nodular densities.
Treat with cyclophosphamide, corticosteroids.
Microscopic polyangitis Pathology Sites Symptoms,except Renal pathology Skin pathology Histology absence of Proteins associated RX
Necrotizing vasculitis
lung, kidneys, and skin
pauci-immune glomerulonephritis
palpable purpura.
Presentation similar to granulomatosis with polyangiitis but without nasopharyngeal involvement.
No granulomas.
MPO-ANCA/p-ANCA H (anti- myeloperoxidase).
Treat with cyclophosphamide, corticosteroids.
Eosinophilia Granulomatosis with polyangitis Systems affects Nerve symtop-due to Pathology -speciality Proteins imvolved Ix
Asthma, sinusitis, skin nodules or purpura, peripheral neuropathy (e.g., wrist/foot drop).
Can also involve heart, GI, kidneys (pauci- immune glomerulonephritis).
Granulomatous, necrotizing vasculitis with eosinophilia
MPO-ANCA/p-ANCA,
IgE level high
HSP-in who Following what Classical traid Pathology Associated with what
Most common childhood systemic vasculitis.
Often follows URI.
Classic triad:
Skin: palpable purpura on buttocks/legs J Arthralgias
GI: abdominal pain
Vasculitis 2° to IgA immune complex deposition.
Associated with IgA nephropathy (Berger disease).
Beurgers disease Who-age,risk f Symptoms Sign Pathology RX
Refer book
Kawasaki dis Who Race Symptoms Complication RX
Refer book
Takayuki arteritis Who-age/sex Other name Symtopms Pathology Vessels affects Ix RX
Usually Asian females
