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Flashcards in Pathology Deck (76):
1

Congenital heart diseases
2 groups
Special names
Reasons

1.R to L shunts-early cyanosis-blue babies
2.L to R shunts-late cyanosis with Eisenmengers phenomenon-blue kids

2

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.

3

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)

4

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.

5

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

6

Tricuspid atresia
Pathology
Shunts

Absence of tricuspid valve and hypoplastic RV

requires both ASD and VSD for viability.

7

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.







8

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.

9

L to R shunt diseases
Cyanosis when
Why

VSD>ASD>PDA
Late cyanosis
Eisenmengers

10

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.

11

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.

12

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 Ž shunt becomes left to right Ž

progressive RVH and/or LVH and HF-Eisenmengers

Lower extremity cyanosis

13

Eisenmengers syndrome
Caused by
How
Clinical signs 3
Age of onset

Uncorrected left-to-right shunt (VSD, ASD, PDA) Ž 

pulmonary blood flow Ž pathologic remodeling of vasculature Ž pulmonary arterial hypertension. RVH occurs to compensate Ž -shunt becomes right to
left

Causes late cyanosis, clubbing and polycythemia.

Age of onset varies.

14

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).

15

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

16

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

2.CNS-stroke

3.Renal-chronic kidney disease (hypertensive nephropathy)

4.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).

17

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

18

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

19

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

20

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 Ž vascular stiffening without obstruction.

“Pipestem” appearance on x-ray

Does not obstruct blood flow
intima not involved

21

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 Ž
macrophage and LDL accumulation Ž
foam cell formation Ž
fatty streaks Ž
smooth muscle cell migration (involves PDGF and FGF), proliferation
extracellular matrix deposition Ž
fibrous plaque Ž
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.

22

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

23

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:
ƒ
Stanford type A (proximal):
involves Ascending aorta.
May extend to aortic arch
or descending aorta.

Treatment is surgery.


ƒ Stanford type B (distal):
involves descending aorta and/or aortic arch.
No ascending aorta involvement.

Treat medically with β-blockers, then vasodilators.

Stanford A

24

Ischemic artery disease types

Angina
Infarction
Coronary steal syndrome
SCD
Chronic IHD

25

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

26

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.

27

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).

28

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)

29

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 Ž  flow and ischemia in poststenotic region.

Principle behind pharmacologic stress tests.

30

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.

31

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).

32

Chronic IHD
What


Progressive onset of HF over many years due to chronic ischemic myocardial damage

33

MI
Arteries affected frequency 3
Evolution periods

LAD>RCA>LCX

0-4hrs
4-24hrs
1-3days
3-14days
2wks -several months

34

0-4hrs

Gross changes
LM changes
Complications

None
None

Arrythmias
HF
Cardiogenic shock

35

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

36

1-3days
Gross
LM
Complications

Gross-
Hyperaemia

LM-
Extensive coagulative necrosis.
Tissue surrounding infarct shows acute inflammation with neutrophils.

Complications -post MI fibrinous pericarditis

37

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 Ž -mitral regurgitation
interventricular septal rupture - VSD
LV pseudoaneurysm (risk of rupture).

38

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).

39

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.

40

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

41

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

42

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 Ž high risk of mortality).

Ventricular free wall rupture Ž -cardiac tamponade
papillary muscle rupture -severe mitral
regurgitation
interventricular septum rupture Ž-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).

43

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

44

Three types of cardiomyopathies

Dilated -most common
Hypertrophic
Restrictive

45

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

46

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 Ž outflow obstruction Ž
dyspnea, possible syncope.

47

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).

48

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 Ž pulmonary venous distention and transudation of fluid.
Presence of hemosiderin-laden macrophages (“HF” cells) in lungs.

RHF
1.Hepatomegaly(Nutmeg liver)-
central venous pressure Ž  resistance to portal flow. Rarely, leads to “cardiac cirrhosis.”

 2.JVD-
High venous pressure.

 3.High central venous pressure Ž -fluid transudation

Refer book

49

Types of shocks 4
Causes for each
Main pathology
Changes to CO/CVP/SVR
Treatment

Hypovolemic
Cardiogenic
Obstructive
Distributive

50

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.

51

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.


ƒ Acute—S. aureus (high virulence).
Large vegetations on previously normal valves Rapid onset.

ƒ 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




52

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 >> 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

2. Occasionally involves the aortic valve; fusion of the commissures
3. Other valves are less commonly involved.

C. Complications include infectious endocarditis.

53

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.

54

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.

55

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.

56

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


57

Kusmmauls sign
What's
Pathology
Seen when 4

Increased JVP on inspiration instead of a normal reduction

Inspiration Ž -negative intrathoracic pressure not transmitted to heart Ž -impaired filling of right
ventricle Ž -blood backs up into venae cavae Ž -JVD.

constrictive pericarditis
restrictive cardiomyopathies
right atrial or ventricular tumors.

58

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.

59

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.

60

Cherry haemangiomas
Benign
Tissue
Who
Frequency with age
Regression

Benign
capillary hemangioma
elderly
Does not regress
Frequency  increase with age.

61

Cystic hygroma
What
Site
Associated disease

Cavernous lymphangioma
neck
Associated with Turner syndrome.

62

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.

63

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.

64

Pyogenic granuloma
Tissue
Shape
Complications
Seen in who 2

Polypoid capillary hemangioma
ulcerate and bleed.
Associated with trauma and pregnancy

65

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.

66

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.

67

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

68

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.

69

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.



70

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:
ƒ Focal necrotizing vasculitis
ƒ Necrotizing granulomas in the lung and
upper airway
ƒ Necrotizing glomerulonephritis


PR3-ANCA
c-ANCA (anti-proteinase 3).

CXR: large nodular densities.
Treat with cyclophosphamide, corticosteroids.

71

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.

72

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

73

HSP-in who
Following what
Classical traid
Pathology
Associated with what

Most common childhood systemic vasculitis.

Often follows URI.


Classic triad:
ƒ Skin: palpable purpura on buttocks/legs J ƒ Arthralgias
ƒ GI: abdominal pain


Vasculitis 2° to IgA immune complex deposition.

Associated with IgA nephropathy (Berger disease).

74

Beurgers disease
Who-age,risk f
Symptoms
Sign
Pathology
RX

Refer book

75

Kawasaki dis
Who
Race
Symptoms
Complication
RX

Refer book

76

Takayuki arteritis
Who-age/sex
Other name
Symtopms
Pathology
Vessels affects
Ix
RX

Usually Asian females