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Year 3 > Pathology > Flashcards

Pathology Flashcards

1
Q

Fibroadenoma

A

Common in young women <30
“breast mice” - discrete, non-tender, firm lumps
Benign

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2
Q

Abscess

A

Common in lactating women.
Red, hot, tender swelling
More common in smokers

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3
Q

Pagets disease of the breast

A

Ca of the nipple-areolar complex presenting as an eczematous lesion of the nipple
Most associated with invasive BC
Usually unilateral

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4
Q

Fat necrosis

A

Obese W with large breasts
May follow trauma
Firm and round but may become irregular/hard

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5
Q

Fibrocystic breast

A

Breast pain - sx may fluctuate with menstrual cycles
Middle aged
Rubbery, well circumscribed, mobile mass

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6
Q

Intraductal papilloma

A

Bloody nipple discharge

Younger

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7
Q

Mammary duct ectasia

A

Dilatation of breast ducts
Common in meno W
Smokers
Thick + green discharge

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8
Q

Consequences of acute inflammation

A

Resolution
Scarring/fibrosis
Progression to chronic

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9
Q

Vascular changes in acute inflammation

A

Vasodilation (arterioles)

Increased permeability (capillary bed/venules)

Leukocyte margination

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10
Q

Leukocyte emigration

A

Margination - (stasis) movement to the periphery of the BV

Rolling - weak binding to endo by selectins

Adhesion - firm adhesion to endo by integrins

Transmigration

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11
Q

Clinical aspects of acute inflammation

A

Calor Rubor Tumour Dolor

Heat, redness, swelling, pain

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12
Q

Anti-inflammatory therapy

A

Broad spectrum e.g. NSAIDs - inhibit COX1/2 involved with arachidonic acid metabolism

Targeted treatments e.g. Anti-TNF antibodies, Anti-ICAM1

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13
Q

Stages of phagocytosis

A

Recognition + attachment of particle to leukocyte

Engulfment

Killing + degradation

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14
Q

Causes of chronic inflammation

A

Progression from acute e.g. repeated episodes of cholecystitis

Primary chronic e.g.micro-organisms associated with intracellular infections ( hep C, TB) or foreign body reactions (silica, atherosclerosis), or autoimmune diseases or unknown aetiology e.g. chronic IBD, sarcoidosis

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15
Q

Ratio of fat to haemopoietic cells in the BM?

A

30:70

Fat tissue is an important diagnostic criterion as it is increased in marrow aplastic states + decreased in myeloproliferative disorders

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16
Q

Erythrocyte in a BM sample

A

Looks purple + round

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17
Q

Granulocyte in BM sample

A

Looks pink with purple shaped thing inside

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18
Q

What does a megakaryocyte become?

A

A platelet

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19
Q

Megakaryocyte on a BM sample

A

Quite large - pink with purple in the middle (like granulocyte but a lot bigger)

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20
Q

Diagnosis of CLL on a BM film

A

Tumour cells express CD20 and CD23

Marrow shows nodular + diffuse infiltration by small lymphocytes with scanty cytoplasm, clumped chromatin and low mitotic activity

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21
Q

Diagnosis of CML on a BM film

A

BM is hyper cellular as attested by decrease in fat cells

and shows majority of mature (hyper segmented) neutrophil granulocytes

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22
Q

Diagnosis of AML on BM film

A

Hyper cellular marrow with monotonous proliferation of undifferentiated cells

High rate of proliferation as attested by expression of Ki67 molecule within nuclei of tumour cells

Proliferating blasts express CD34

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23
Q

More than 90% of causes of transmural MI are due to..

A

Acute thrombosis of a ruptured atherosclerotic plaque

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24
Q

What precipitates angina in patients with underlying coronary artery atherosclerosis

A

An increase in HR - increases demand for energy + decreases duration of diastole relative to systole therefore decreases time of myocardial perfusion

Reduced BP - less pressure to overcome resistance of stenotic arteries + there is associated increased in HR which increases the myocardial energy requirements and decrease time for perfusion of heart

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25
Q

What does the RCA supply?

A

RV free wall, posterobasal wall of LV and posterior third of ventricular septum

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26
Q

What does the L circumflex supply?

A

Lateral wall of L ventricle

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27
Q

What does the LAD supply?

A

Anterior wall of LV, apex of heart + anterior 2/3 of interventricular septum

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28
Q

Occlusion of the LAD artery produces a …. infarct

A

Anterior

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29
Q

Occlusion of the L CFX artery produces a …. infarct

A

Lateral

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30
Q

Occlusion of the RCA produces a …. infarct

A

Posterior

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31
Q

Pulmonary HTN results in which sided HF?

A

Right

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32
Q

Which type of HF causes congestion of the liver with a nutmeg liver

A

Right

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33
Q

Which type of HF causes impairment of renal function due to hypoperfusion of the kidneys?

A

Left

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34
Q

Which type of HF causes impairment of renal function due to congestion of the kidneys?

A

Right

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35
Q

Is rheumatic heart disease related to RA?

A

Yes - occurs in 20-40% of severe prolonged RA. Most common finding is fibrinous pericarditis

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36
Q

Most common long term problem of rheumatic heart disease?

A

Mitral stenosis

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37
Q

Does rheumatic heart disease predispose to infective endocarditis?

A

Yes - deforming fibrotic valvular disease is a feature of chronic rheumatic heart disease. Valve abnormalities predispose to infective endocarditis

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38
Q

Most common cause of sudden explained death in young athletes

A

Hypertrophic cardiomyopathy

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39
Q

3 types of cardiomyopathy

A

Dilated cardiomyopathy

Hypertrophic cardiomyopathy

Restrictive cardiomyopathy

There are overlaps of features between the groups

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40
Q

Most common primary tumour of the heart

A

Atrial myxoma

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41
Q

What is bronchopneumonia?

A

Inflammation of the lung beginning as inflammation of bronchi and bronchioles with extension into adjacent alveolar spaces

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42
Q

What is lobar pneumonia?

A

Acute inflammation of the lung in which a large part of a lobe or an entire lobe is involved (acute bronchi pneumonia is different because it is patchy)

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43
Q

4 classic stages of lobar pneumonia

A

Congestion in the first 24h
Red hepatisation or consolidation
Grey hepatisation
Resolution

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44
Q

Complications of acute pneumonia

A 
Death
Lung abscess
Empyema 
Spread of infection - meningitis, arthritis, IE
Fibrosis of lung
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45
Q

Causes of lung abscesses

A

Acute pneumonia
Septic emboli
Puncture wounds of the chest

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46
Q

What are opportunistic infections that HIV pts may develop in the lung?

A 
TB
pneumocystis carinii 
Cytomegalovirus
Herpes simplex virus
Varicella-zoster
Atypical mycobacteria
Aspergillus
47
Q

What conditions predispose to PE?

A 
Immobility
Pregnancy
COCP
CHF
Thrombosing disorders
48
Q

Consequences of PE?

A

Many have no effect as undergo fibrinolysis + disappear

Large emboli may cause sudden death

Repeated small emboli may lead to fibrous narrowing of small pulmonary arteries causing pulmonary HTN

An embolism may cause pulmonary infarction but only if there is HF with a rise in pressure in the pulmonary circulation

49
Q

Changes seen in bronchial lining of smokers?

A

Squamous metaplasia
Increased no. of mucous glands
Epithelial atypia leading to carcinoma in situ

50
Q

What may be local effects of a bronchial carcinoma?

A
  • Bleeding into a bronchus
  • Obstruction of a bronchus causing bronchopneumonia, lung abscess, bronchiectasis or collapse of lobe
  • Pleural effusion
  • Invasion of recurrent laryngeal nerve causing hoarseness
  • Invasion of ribs, oesophagus, phrenic nerve, SVC or pericardium
  • Invasion of symp chain causing Horner’s syndrome
51
Q

Common patterns of metastatic neoplasia in the lung?

A

Multiple small masses

Few large masses = cannon ball

52
Q

What is ARDS?

A

Defined clinically as acute respiratory failure with decreased arterial oxygen content, decreased lung compliance so lungs are stiff and diffuse lung infiltrates on XR.

Pathologically - diffuse alveolar damage with oedema, haemorrhage and hyaline membranes in alveolar ducts in early stages with fibrosis later

53
Q

What is pneumoconiosis?

A

Non-neoplastic lung condition caused by inhalation or inorganic or organic particles

54
Q

Most common cancer in the kidney?

A

Renal cell carcinoma - don’t confirm with biopsy because of risk of dissemination of cancer along needle track - yellowish mash with degenerate, cystic areas

Transitional neoplasia much less common

Kidney is unusual site for metastatic carcinoma

55
Q

Spread of renal cell carcinoma

A

May be local invasion of kidney, fat around kidney + renal pelvis that leads to haematuria. Main route of spread is into renal vein + then dissemination to lungs, bones + sometimes unusual sites e.g. skin

Lymph node spread is not common

56
Q

Investigations for MS

A

MRI - plaques of demyelination and exclude other diagnoses

Oligoclonal bands in the CSF

Visual evoked potentials (VEPs) on an EEG

57
Q

Pathology of MS

A

Multiple, discrete areas in white matter where axons have lost myelin sheaths + early active stage - inflammatory changes

Lesions scattered through the CNS and can appear anywhere but certain sites: optic nerves, SC and periventricular sites such as corpus callosum

58
Q

Huntington disease pathology

A

Atrophy of corpus striatum (caudate nucleus + putamen) with some compensatory dilatation of the lateral ventricles

59
Q

Huntingtons

A

Repeat of CAG in gene for protein huntingtin. 38+ repeats in individuals with HD.

Anticipation occurs in children as number of repeats can increase at meiosis

60
Q

How is HSV encephalitis in the immunocompetent managed?

A

If acyclovir is given in early stages - both mortality + morbidity are reduced

61
Q

Which heart murmur presents with pulsatile hepatomegaly?

A

Tricuspid regurgitation - backflow of blood into liver during cardiac cycle

62
Q

where does LDL build up in atherosclerosis?

A

Tunica intima

63
Q

which arteries are more prone to atherosclerosis?

A 
Abdo aorta
Coronary ateries
Popliteal arteries
Thoracic aorta
Internal carotids 
Circle of Willis
64
Q

Most common cause of ischaemic heart disease?

A

90% is due to atherosclerosis

65
Q

What is critical stenosis?

A

> 75% reduction in diameter of the artery

Leads to compensatory vasodilation but not enough to meet increased demands

66
Q

Consequences of atherosclerosis

A

Narrowing - plaque size protrudes into lumen, overlying thrombus, haemorrhage into plaque

Dilation (aneurysm) - rupture, mural thrombi which can embolise

Thrombosis
Plaque rupture
Haemorrhage
Wall weakening
Calcification
67
Q

Stable v unstable plaque

A

Stable = thick fibrous cap

Unstable = no thick cap, risk of rupture/fissure, emboli +/- thrombosis

68
Q

What aggravates ischaemic heart disease?

A

Hypertrophy - more muscle so need more oxygen

Hypotension - less pressure to overcome resistance in arteries + compensatory rise in HR

Hypoxaemia

Increased HR

69
Q

Difference between angina + MI ?

A

Cell death (necrosis)

70
Q

Transmural MI

A

Full thickness of the wall

Usually associated with acute thrombosis/occlusion of vessel. Occasionally related to vasospasm or emboli

71
Q

Subendocardial MI

A

inner 1/3 to 1/2 myocardium

Usually critical stenosis but no acute plaque change

72
Q

At how many hours do you see MI?

A

Histologically - 4hrs

Macroscopically - 12h

73
Q

Preconditioning

A

Repetitive short lived ischaemia may be protective

74
Q

Complications of MI?

A 
Cardiogenic shock
Arrhythmias
Myocardial rupture - tamponade, 
Pericarditis 
Ventricular aneurysm
75
Q

Compensatory mechanisms of heart in HF

A

Dilatation - increased preload
Hypertrophy - increase in size of myocytes
Neurohumoral mechanisms

76
Q

L sided HF

A

Pulmonary oedema

Organ ischemia - impaired renal function (high creatinine)

77
Q

R sided HF

A

Peripheral oedema

Congestion of organs

Ascites/pleural effusion

78
Q

What is pure R sided HF called?

A

Cor pulmonale (uncommon)

79
Q

How does systemic HTN affect the L V?

A

LV hypertrophy
No dilation of LV
Increased heart weight
Thick wall

Impaired diastolic filling

80
Q

Histological features of hypertrophy

A

Increased size of myocyte
Increased nuclear size
Interstitial fibrosis

81
Q

Valvular heart disease - stenosis

A

failure of valve to open completely - impedes forward flow of blood

82
Q

Valvular heart disease - incompetence

A

Regurgitation - failure of valve to close so allows reverse flow of blood

83
Q

What is functional regurgitation?

A

valves become imcompetent due to dilation of ventricles (valve gets stretched so ends can’t touch)

84
Q

Most common functional valvular lesions

A

Mitral stenosis
Mitral incompetence
Aortic stenosis
Aortic incompetence

85
Q

Mitral stenosis

A

From rheumatic heart disease

86
Q

Mitral incompetence

A

Floppy mitral valve

87
Q

Aortic stenosis

A

Calcification of normal + congenitally bicuspid aortic valves

88
Q

Aortic incompetence

A

Dilation of ascending aorta related to HTN + age + connective tissue disorders

89
Q

Most common type of valvular heart disease?

A

Mitral regurgitation due to floppy mitral valve

90
Q

What is rheumatic fever?

A

Occurs a few weeks after group A b-haemolytic streptococcal pharyngitis

Thought to by hypersensitivity reaction induced by group A strep

91
Q

Signs and symptoms of rheumatic fever

A

Fever
Painful joints
Involuntary muscle movements
Non itchy rash - erhythema marginatum

92
Q

Most important complication of rheumatic heart disease

A

Chronic rheumatic heart disease - characterised by:

  • Deforming fibrotic valvular disease (especially mitral stenosis)
  • Fish mouth/button hole stenosis
  • Chordea tendinae become fibrotic + stick togther
93
Q

How many cases of mitral stenosis are caused by rheumatic heart disease?

A

99%

94
Q

What does infective endocarditis cause on the heart?

A

Thrombotic debris

Organisms

95
Q

Types of infective endocarditis

A

Acute - previously normal valve, acute onsent, 50% mortality, necrotising + ulcerative destruction

Subacute - abnormal valve, insidious onset, most recover, less destructive

96
Q

Which organisms cause acute endocarditis?

A

S aureus
Pneumococcus
S pyogenes

97
Q

Which organisms cause subacute endocarditis?

A

Strep viridans

Enterococci

98
Q

Which organism causes IE on prosthetic valves?

A

Staph epidermis

99
Q

Which valves are most commonly affected in IE?

A

Aortic + mitral

Tricuspid in IVDU

100
Q

Complications of IE?

A 
Myocardial abscess
Valve rupture/perforation
Systemic emboli 
Septic emboli
Immune complexes e.g. in kidney
101
Q

What is nonbacterial thrombotic endocarditis?

A

Deposition of fibrin/plt thrombi on valve - quite small

on a normal valve
non-destructive

102
Q

3 types of cardiomyopathy

A

Dilated (90%)
Hypertrophic
Restrictive (least common)

Overlap of features in each group + spectrum of severity

103
Q

Causes of dilated cardiomyopathy

A 
Most idiopathic
Alcohol
Genetics
Haemachromatosis
Drugs
Sarcoidosis
104
Q

EF in dilated cardiomyopathy

A

25%

105
Q

Hypertrophic cardiomyopathy

A

Myocardial hypertrophy - wall thick + assymetric with IV septum thicker than LV wall
No ventricular dilation
Interstitial fibrosis

106
Q

When does the septum become wider than the wall?

A

Hypertrophic cardiomyopathy

107
Q

Restrictive cardiomyopathy

A

Normal sized ventricles + chambers
Both atrial dilated
Firm myocardium

Get decreased ventricular compliance so impaired filling

108
Q

Most common cause of myocarditis

A

Viruses

109
Q

What is myocarditis

A

Inflammatory process of the myocardium which results in injury to cardiac myocytes

110
Q

Causes of pericarditis

A

Infections, immune mediated, MI, uraemia, trauma

111
Q

Types of pericarditis

A 
Serous - clear fluid
Fibrinous - fibrin 
Purulent - pus 
Haemorrhagic - blood
Caseous - TB
112
Q

What does metastatic melanoma in heart look like?

A

Black dots through myocardium

113
Q

Right to left shunt

A 
Blood shunted from pulmonary to systemic circulation 
Cyanotic 
5 't's: 
- Tetralogy of fallot
- Transposition of great arteries
- Perisistent Truncus arteriosus
- Tricuspid atresia
- Total anomalous pulmonary venous connection
114
Q

L to R shunt

A

Get pulmonary HTN

ASD
VSD
Patent ductus arteriosus
AV septal defect

Year 3 (14 decks)

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