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CardioVascularSystems > CVS Pathology > Flashcards

CVS Pathology Flashcards

Based on Devesh Mishra book and class notes.

1
Q

Histological layers of a Blood Vessel?

What are each made of?

A

T. intima - single layer of endothelium
T. media - smooth muscles, elastic tissue
T. adventitia - collagen, elastic fibres.

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2
Q

Types of capillaries?

A

Continuous type - No gaps
Sinusoidal type - gaps + in endothelium and BM.
Fenestrated type - gaps + only in BM.

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3
Q

Veins which are valveless are?

A

Common Iliac. V

Vena cava

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4
Q

Diff b/w arteries and Veins?

A

Thin wall
have valves
scanty elastic tissue

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5
Q

Neoinitima?

A

seen after vascular injuries.
combination of intima and media.
intima will have smooth muscles derived from medial hyperplasia.

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6
Q

Vasuclar pathologies in HTN?

A

Hyaline arteriolosclerosis

Hyperplastic arteriolosclerosis

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7
Q

Hyaline arteriolosclerosis?

A

Diabetic angiopathy, Benign nephrosclerosis, Benign HTN.

diffuse pink hyaline thickening - luminal stenosis.

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8
Q

Hyperplastic arteriolosclerosis?

A

Malignant HTN.
Concentric laminated/Onion-skin app.
Hyperplasia of smooth muscles and
Fibrinoid necrosis/ necrotising arteriolitis.

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9
Q

Arteriosclerosis?

A

Wall thickening

Loss of elasticity.

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10
Q

Patterns of arteriosclerosis?

A

ARTERIOLOSCLEROSIS - small, medium arteries and arterioles.
DM, HTN - as hyperplastic and hyaline types.

MONCKEBERG MEDIAL SCLEROSIS - medial calcification in muscular arteries.
>50yrs
Non obstructive, no clinical significance.

ATHEROSCLEROSIS - MC pattern with clinical significance.
due to intimal damage.

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11
Q

Modifiable R/f for atherosclerosis?

A

Other than being fat and having all bad habits :p

Lipoprotein A
Trans unsaturated FA
Chlamydia, pneumonia, CMV, HSV

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12
Q

Non- modifiable R/f for atherosclerosis?

A

Male
Old
Stress - Type A personality
Hyper- homocysteinemia

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13
Q

Theory of Atherosclerosis?

A

Inflammatory response to endothelial injury.

monocyte, platelet adhesion - growth factor release - smooth muscle proliferation in intimal and matrix synthesis.

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14
Q

what are foam cells?

A

when macrophages and smooth muscle cells accumulate oxidised LDL.

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15
Q

Fatty streaks

A

Earliest lesions.

Intimal collections of foamy macrophages and smooth muscle cells.

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16
Q

Mature atherosclerotic plaque?

A

Fibrous cap - smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans.

Necrtoic core - dead cells, lipid, cholesterol, foam cells, plasma proteins.

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17
Q

complications of plaque?

A

Rupture, ulceration, erosion
Hemorrhage
Aneurysmal dilatation
Thrombus formation.

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18
Q

MC blood vessel affected in atherosclerosis?

LC affected blood vessel?

A

Abdominal aorta (below renal.A and above iliac bifurcation).

Circle of Willis

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19
Q

what is an Aneurysm?

A

Localised abnormal dilatation of blood vessel or wall of heart.

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20
Q

Types of Aneurysm?

A

True
Pseudo-
Mycotic
Syphylitic and so on

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21
Q

True aneurysm?

A

covered by all 3 vessel wall layers.

ass. with atherosclerosis, post-MI ventricular aneurysm.

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22
Q

Pseudo-aneurysm?

A

Extravascular hematoma.

MCC - Post-MI rupture.

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23
Q

Mycotic aneurysm?

A

due to bacterial infection weakening vessel wall.
MCC - Staph
MC site - Femoral.A

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24
Q

Syphilitic aneurysm?

A 
a/k/a Leutic aneurysm.
Tertiary stage of syphilis.
MC site- Ascending aorta.
Linear calcification - characteristic.
Tree barking app. - Intimal wrinkling
Cor Bovium/ cow's heart - cardiac hypertrophy - due to AR.
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25
Q

Syndromes ass. with Aortic dissection?

A

Marfan’s

Ehlers Danlos. S

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26
Q

MCC of Aortic dissection?

A

HTN

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27
Q

MC pre existing Histologic change for Aortic Diss.?

A

Cystic medial degeneration.

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28
Q

Types of classification of Aortic diss.?

A

2 Types:
De baker classification (Anatomical) - not used now
Stanford’s classification (Prognostic) - commonly used.

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29
Q

Cystic medial necrosis occurs in which conditions?

A 
Marfan's
Ehlers danlos. S
Pregnancy (3rd tri)
Congenital Bicuspid aortic valve
Familial thoracic aortic aneurysm. S
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30
Q

Large vessel vasculitis?

A 
GCA (Temporal arteritis)
Takayasu Arteritis (TA) (Pulseless disease)
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31
Q

Medium vessel vasculitis?

A 
PAN (immune cell-mediated)
Kawasaki disease (KD) (Anti-endothelial cell Ab's)
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32
Q

Small vessel vasculitis?

A

Immune complex mediated- SLE
HSP
Good Pasteur’s disease(GPD)

Pauci immune mediated - Miscroscopic polyangitis (MP) (vasculitis w/o asthma/granuloma)
Granulomatosis with polyangitis (Wegners granulomatosis)
Churg strauss. S (CSS) (asthma+Granuloma+eosinophilia)

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33
Q

What is ANCA?

A

They are group of auto-Ab’s directed against components of Neutrophils.
2 types- p-ANCA
c-ANCA

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34
Q

p-ANCA?

A 
Perinuclear ANCA.
Target Ag- MPO (Anti-MPO)
seen in- 
CSS
MP
GPS
IBD
Wegners. G(25%)
Idiopathic cresentric GN
Drug- Hydralazine
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35
Q

c-ANCA?

A

Cytoplasmic location/staining.
target Ag- cytoplasm protein- Pr3
seen in- Wegners..G (70%)

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36
Q

Giant cell/Temporal arteritis?

A

MC vasculitis- adults
Focal granulomatous inflammation - cranial vessels
MC-Superficial temporal.A

Segmental nodular thickening with narrowing of lumen
vessel wall- Granulomatous inflammation+ langhans giant cells
Fragmentation of internal elastic lamina

MC symptom- Localised temporal headache
MS symptom- Jaw claudication
Most feared complication - permanent blindness (ophthalmic.A)

Raised ESR
ass. with Polymyalgia Rheumatica
Normocytic normochromic.A

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37
Q

Takayasu’s Arteritis?

A

a/k/a Aortic Arch. S
Granulomatous vasculitis of Aortic arch and its branches.

Thick wall- narrow lumen
filling-defect on fluoroscopy distal to stenotic/obstructed area.

<50yrs
same features in>50yrs- Giant cell Aortitis

MC- subclavian vessels (pulseless disease)
LC- Coronary vessels
elevated ESR
Anemia

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38
Q

Intermediate vessel vasculitis?

A

Behcet’s disease.

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39
Q

PAN?

A

Systemic necrotising vasculitis- Medium sized arteries.
Varying age of lesions- in same biopsy
Classical PAN- Non-Granulomatous

MC- affects kidneys(arcuate.A), but no GN
spares- Lungs

ANCA (-ve)
ass. with chronic Hep-B (30%)- HbSAg +ve
MC vasculitis ass. with Mononeuritis multiplex

Segmental transmural fibrinoid necrosis
elastic lamina fragmentation

MCC of death- Renal failure

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40
Q

MCC - Mononeuritis multiplex?

A

Overall - DM

amongst vasculitis- PAN

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41
Q

MC vasculitis in Paeds?

A

HSP

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42
Q

MC vasculitis causing death in paeds?

A

KD (Coronary arteries)

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43
Q

MC vasculitis in adults?

A

GCA

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44
Q

Kawasaki disease?

A

a/k/a Mucocutaneous LN syndrome
children <5yrs
100% clinical diagnosis

Etiology- Anti-endothelial Ab’s
coronary vasculitis- coronary ectasia- aneurysm
MCC of death- MI- due to Aneurysmal rupture

elevated ESR & CRP
Thrombocytosis

treatment- IV-IG

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45
Q

Diagnosis of KD?

A

Fever>/= 5days + any 4/5 :

  • b/l non-exudative conjunctivitis (red eye)
  • strawberry tongue, cracked lips, throat redness
  • Palmar and plantar erythema——- } diff. from
  • polymorphous rash (MC-trunk)——} pharyngitis
  • Large LN in neck (>1.5cm)

Diagnosis also confirmed, if:
fever + only 3 of the above are present with documented 2DECHO or angio evidence of CAD.

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46
Q

TAO

A

Buerger’s disease
R/f- smoking, >35yrs age
HLA-A-9, HLA-B5 associated

HLA-B12 is protective for TAO

Segmental, thrombosing, inflammation with secondary extension into veins & nerves.
Thrombus will have Neutrophilic mmicroabscesses surrounded by granulomatous inflammation.

Early feature- Raynaud’s
Intermittent claudication
excruciating pain even at rest- due to neural involvement.

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47
Q

where all micro abscesses are seen?

A

[TIPS]

TAO
Sezary.S
Psoriasis
IBD

48
Q

Microscopic Polyangitis?

A

a/k/a Hypersensitivity vasculitis/ Leukocytoclastic vasculitis.
similar to PAN, but involves small vessels.
have p-ANCA
all lesions- of same age.

segmental fibrinoid necrosis - media
focal transmural necrotising lesions.
No granuomatous inflammation.

Necrotising GN (90%)
Pulmonary capillaritis- common

hemoptysis, hematuria, proteinuria,purpura, bowel pain/bleeding.

49
Q

Leukocytoclastic meaning?

A

fragmented neutrophilic nuclei within and around vessel walls.

50
Q

Wegner’s Granulomatosis?

A

Triad-
* Necrotising/ granulomatous vasculitis of small vessels of lung & airway.
* Necrotising granulomas of upper & lower RT
Focal Necrotising & cresentric GN.

granulomas - fuse - nodules & cavities.
Renal lesions - FSGS & scarring to Proliferative(crescentic) GN.

c-ANCA (70%) & p-ANCA(25%) +ve

males
around 40yrs.

features- b/l persistent pneumonitis. (nodules & cavities)-95%
chronic sinusitis- 90%
mucosal ulcerations of nasopharynx- 75%
Renal lesions- 80%

treatment- steroids, Cyclophoshamide, TNF antagonists.

51
Q

what is limited Wegner’s?

A

disease involving only RS.

52
Q

Churg- Strauss syndrome?

A

Vasculitis + eosinophilis
Can be a side effect of Motelukast/ Zafirlukast use.
small vessel necrotising vasculitis with asthma
allergic rhinitis
peripheral eosinophilia
granulomas.
resemble PAN, but with eosinophils and granulomas.

p-ANCA +ve <50%

eosinophilic infiltrates - ass. with cardiomyopathy.
MCC of death - Cardiac involvement.

53
Q

HSP?

A

Mc vasculitis- children
a/k/a Anaphylactoid purpura.
IgA deposits

Tetrad-

  • Palpable purpura (due to vasculitis)
  • Arthritis
  • GN
  • Abdominal pain.

Renal involvement - 10-50% of HSP.

Thrombocytosis
Raised IgA & ESR
Mild leukocytosis.

54
Q

Hypersensitivity Angitis?

A

due to Hypersensitivity
Leukocytoclastic vasculitis
Palpable purpura of LL

Criteria for diagnosis:

  • > 16yrs
  • Maculopapular skin rash
  • use of any drug prior to symptoms
  • purpura
  • biopsy - rash- neutrophils around small vessels.
55
Q

Behcet’s disease?

A

Anti-endothelial cell Ab’s.
Target Ag- human alpha enolase.
small vessel neutrophilic vasculitis.

Triad:

  • Recurrent oral aphthous ulcers
  • genital ulcers
  • uveitis

Ass. with HLA-B5, B51.
also TH-17 cells- recruit neutrophils

56
Q

Tumors of Blood vessels?

A

Benign- Hemangioma - Capillary.H
Cavernous.H
Pyogenic.H
Intermediate(Boderline)- Kaposi Sarcoma
Malignant - Angiosarcoma

57
Q

Capillary.H?

A

MC type - vascular tumor
affects skin & mucous.M
Unencapsulated, > 1mm

closely packed aggregates of capillaries
partially/completely thrombosed.

a/k/a juvenile strawberry.H
variant present at birth
MC- face
Reddish/pinkish
regresses as child grows. (by 7yrs)
58
Q

Cavernous.H?

A 
Unencapsulated
1-2 cm
MC sites - Skin,Liver
Locally destructive, do not regress
Thrombosis &amp; dystrophic calcification- common

VON HIPPEL LINDAU. S- chromosome 3p
cavernous.H in cerebellum ,brain stem, eye + angiomatous cystic neoplasms in pancreas & liver.

59
Q

Pyogenic.H?

A

Ulcerated polypoid variant of capillary.H
occurs following trauma.

proliferating capillaries, interspersed with edema
inflammatory infiltrates- resemble granulation tissue.

a/k/a pregnancy tumor- Granuloma Gravidarum
occurring in- gingiva of 1% of pregnant women
regress spontaneously after pregnancy.

60
Q

Kaposi Sarcoma?

A 
HHV 8
2nd MC malignancy in HIV.
MC site - Skin of feet
MC extracutaneous site - LN
MC site in GIT- Duodenum

Gross- 3 stages- patch, plaque, nodule.
Nodular stage- sheets of plump, proliferative spindle cells & endothelial in the dermis/ s/c tissue
Attempted vessel formation.

61
Q

Diagnosis of Vascular tumors?

A

IHC

  • CD31 (PECAM)
  • CD34
  • Factor VIII (weibel palade bodies)
62
Q

what are weibel palade bodies?

A

vWF + Pselectin

63
Q

Epidemiological types of KS?

A 
Chronic/Classic/European KS:
  elderly 
  men
  Not ass. with HIV
  red-purple plaques on LL
  visceral involvement- rare
Endemic/Lymphoadenopathic/African KS:
     Not ass. with HIV
     cutaneous lesions- rare
     Aggressive form
     occasional- visceral involvement
     MC- LN

Transient/Immunodeficiency ass. KS:
Transplant ass.
Chronic immunosuppression
Nodal, mucosal, visceral involvement- fatal & rare.
lesion regresses when immunosuppression is discontinued.

Epidemic/ AIDS ass. KS:
Skin, Mucous.M, LN, GIT, Viscera
wide visceral dissemination- early.

64
Q

Cavernous lymphangioma neck seen in?

A

Turner’s syndrome

65
Q

Gloms tumor?

A

Gloms body - Specialised A-V structure - involved in thermoregulation.
Glomangioma
benign
Extremely painful
Modified smooth muscle cells arising from gloms body.
MC site - distal phalanges (under nail beds)
Excision - curative

66
Q

Angiosarcoma?

A 
Malignant endothelial neoplasma.
Common sites- skin, soft tissue, breast, liver.
Aggressive
early mets
all degrees of differentiation are seen
Diagnosis - Immunosaining for CD31, vWF.
67
Q

Hepatic angiosarcoma are ass. with exposures to?

A

Arsenic (pesticides)
PVC (plastics)
Thorotrast (Radio-contrast agent)

68
Q

Hemangiopericytoma?

A

tumors of pericyte (myofibroblast like cells ass. with capillaries and venules).
MC site- LL/ retroperitoneum.
painless
slow- growing.

69
Q

MC congenital cardiac anomaly?

A

VSD

70
Q

MC genetic cause of congenital heart disease?

A

Trisomy 21- Downs syndrome

71
Q

what is the main mode of cardiac adaptation?

A

Hypertrophy

Never hyperplasia.

72
Q

Cardiac Adaptations in pressure overload?

A

Increase in transverse diameter of myocyte.
length remains same.
concentric hypertrophy of LV.
seen in - HTN, AS.

73
Q

Cardiac Adaptations in Volume overload?

A

Both transverse diameter & length of myocyte increase.
Eccentric hypertrophy- dilatation of LV chamber
increased thickness of ventricular wall.
seen in - AR, CCF.

74
Q

Left Heart Failure features?

A

Wet lung- pulmonary congestion.
Kerly B & C lines - Perivascular & interstitial edema.
Siderophages - heart failure cells- hemosiderin laden macrophages - indicate current and previous episodes of pulmonary edema.

75
Q

Right Heart failure features?

A

Nutmeg liver - Hepatomegaly with centrilobar congestion & atrophy - chronic passive congestion.
Cardiac cirrhosis.
Peripheral edema of dependent parts.
Pleural effusion.

76
Q

Calcific Aortic Stenosis features?

A

Age related degeneration.
>70yrs.
MC R/f- Congenital bicuspid aortic valves.
Valve fibrosis + concentric LVH. (pressure overload).

77
Q

Mitral Valve Prolapse?

A 
Barlow syndrome.
young females.
Due to - Abnormal matrix synthesis - dysregualtion in TGF-beta signalling.
Ass with Marfan's . S
Mitral valve leaflets- myxomatous change
Prolapse back into atrium during systole.
thickened ventricular endocardium.
Asymptomatic
Mid- systolic click +
78
Q

MC affected artery in atherosclerosis?

LC affected artery in atherosclerosis?

A

LAD

LEft circumflex. A

79
Q

Earliest enzymes to raise in MI?

A

Myoglobin

80
Q

Most sensitive & specific marker in MI?

A

Troponin (I > T)

81
Q

Best marker for reinfarctiron?

A

CK-MB

82
Q

Flipping of LDH meaning?

A

Normally, LDH2 > LDH1

in MI, LDH1 > LDH2.

83
Q

Complications of MI?

A

Contractile dysfunction - Pul. edema, shock.
Arrhythmia
Myocardial rupture
-MC- ventricular free wall
-MC site- Anterolateral wall @ mid-vent. level.
-MC 2-4 days after MI.
Ventricular aneurysm- late - after 7days.
Dressler.S.

84
Q

what is Dressler.S?

A 
Fibrinous pericarditis.
a/k/a- Post-MI syndrome.
a/k/a- Post-cardiotomy pericarditis.
Auto immune rxn.
manifest after 2-3 weeks after MI
can be seen after 2-3days also- rare.
85
Q

Dialated Cardiomyopathy (DCM)?

A

Gradual 4 chamber hypertrophy & dilation.
Systolic dysfunction
Progressive CCF.
MC aetiology- idiopathic.
Others- Genetic
Alcohol toxicity
Peri-partum
Myocarditis- flabby heart weighing 900g.
Diffuse myocyte hypertrophy with variable interstitial fibrosis.

86
Q

Genetic causes of DCM?

A

20-50%- familial.
MC- AD
20%- have mutations in “TITIN”.

87
Q

which is X-linked Cardiomyopathy?

A

Duchenne & becker muscular dystrophy.

88
Q

what is TITIN?

A

Largest known human protein with 30,000 AA.

89
Q

Hypertrophic CM?

A

MC- AD
MC mutation- beta- myosin heavy chain (beta-MHC).
Poor diastolic relaxation- heavy, muscular, hyper contractile heart.
Asymmetrical inter ventricular septal hypertrophy.
Banana-shaped - LV
HOCM.

Myofiber hypertrophy with helter-skelter pattern.
MCC of sudden death in young athletes.

90
Q

Arrhythmogenic RV CM?

A

AD.
predominantly RHF and arrhythmia.
MCC- defective adhesive molecules in desmosomes.
RV- wall - severely thinned out with myocyte loss, fatty infiltration.

91
Q

Gene involved in LVH?

A

Osteoglycin (OGN)

92
Q

Restrictive CM?

A

Impaired ventricular filling - Diastolic dysfunction.
Ventricle size- normal.
Dialation of both atrium.
Non-specific interstitial myocardial fibrosis.
causes- Amyloidosis, radiation, hemochromatosis, sarcoidosis, scleroderma, neoplasm.

93
Q

Myocarditis?

A

Inflammation of myocardium.
MCC - viral - Herpes.V > Coksackie.V
MC helminth - Trichinella spiralis.

94
Q

MCC of constrictive pericarditis?

A

TB

95
Q

MCC of hemorrhagic pericarditis?

A

Malignancy - MC - lungs.

96
Q

Cardiac tumors are?

A

Myxoma

Rhabdomyoma

97
Q

MC tumors of heart?

A

secondries.

98
Q

MC primary of cardiac secondaries?

MC primary tumors of heart?

A

lung cancer> breast cancer (MC involve pericardium)

Myxomas.

99
Q

Myxomas

A

MC site- left atrium (fossa ovale)
arise from- primitive multipotent mesenchymal cells.
MC- females >60yrs.

100
Q

Types of myxomas?

A

Sporadic - MC type, mostly solitary.

Familial myxomas- B/l, multi centric, affects young ppl.
- ass. with mutations in GNAS1 gene
(McCune Albright.S).

Microscopy- stellate multi potential mesenchymal myxoma cells (Lepidic cells)- in an acid mucopolysaccharide matrix.

10% myxoma are ass. with AD Carney.S :

  • Cardiac & extra- cardiac myxomas.
  • Pigmented skin lesions.
  • Endocrine hyperactivity.
101
Q

MC primary heart tumor in children?

A

Rhabdomyoma.

102
Q

Rhabdomyoma

A

most are harmatomas ass. with tuberous sclerosis- defects in TSC1, TSC2 tumor suppressor genes.

Microscopy - large rounded-polygonal cells rich in glycogen containing myofibrils.

Spider cells are seen- artefacts seen on histology- cytoplasmic stranding radiating from central nucleus to plasma membrane.

103
Q

Carcinoid syndrome

A

Systemic disorder.
Flushing, diarrhoea, dermatitis, bronchoconstriction.
caused by serotonin released by carcinoid tumors.

MC- right heart
MC cardiac manifestation- TR.
Left heart lesions- uncommon, as serotonin is metabolised in lungs, and left heart is supplied by pulmonary circulation.

104
Q

When is left heart affected in carcinoid?

A

Primary/ metastatic carcinoid - lung.
ASD & Right to left flow.
Drugs with ergotogenic activity - Ergotamine, Fenfluramine, Phenteramine, Methylsergide.

105
Q

Morphology of carcinoid?

A

Glistening white intimal plaque like thickening of - endocardial surfaces - cardiac chambers & valve leaflets.
composed of- smooth muscles, few collagen fibres in acid mucopolysaccharide matrix.

Severity- correlates with

    * Plasma levels of serotonin.
    * Urinary excretion of metabolite (5-HIAA).
106
Q

Serous pericarditis

A

Unkown etiology.
Non- bacterial
seen in - RF, SLE, tumors, uraemia, primary viral infections.

107
Q

Fibrinous & serofibrinous pericarditis

A

MC type
serous fluid + fibrinous exudates.
seen in- MI, Dressler.S, cardiac surgery, uraemia, irradiation, RF, SLE, trauma.

108
Q

Purulent (supparative) pericarditis

A

due to - bacterial, fungal, parasitic infection reaching pericardium.

109
Q

Hemorrhagic pericarditis

A

cardiac surgery

ass. with TB/ malignancy.

110
Q

Caseous pericarditis

A

TB
less commonly mycotic infections.
precedes fibrocalcific constrictive pericarditis.

111
Q

Milk spots/ soldier’s plaque

A

seen in healing pericarditis.

Pericardial fibrosis- thick, pearly, non- adherent epicardial plaque.

112
Q

Cardiac polyp

A

Not a tumor.

Postmortem fibrinous clot.

113
Q

De Bakey’s classification of aortic dissection ?

A

DeBakey 1 - from root of aorta to its bifurcation
DeBakey 2 - from root of aorta to its 1st branching
DeBakey 3 - beyond subclavian. A

114
Q

Stanford’s classification?

A

DeBakey 1 & 2 - Stanford’s type A
DeBakey 3 - Stanford type B

type A- worse prognosis
type B - better prognosis

115
Q

D/D for aortic dissection?

A

Acute Pancreatitis (pain in lower abdomen radiating to the back).

CardioVascularSystems (2 decks)

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