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Meeran Histopath Flashcards

1
Q

What is the most likely causative organism of acute infective endocarditis?

A

Staphylococcus aureus

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2
Q

What is the most likely causative organism of subacute infective endocarditis?

A

Streptococcus viridans (after dental procedures)

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3
Q

What are causes of aortic stenosis?

A

Age-related degenerative calcification
Rheumatic heart disease
Congenital malformations (bicuspid valve)

*LVH can develop as a consequence of chronic pressure overload

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4
Q

What causes left heart failure?

A

Two types - high output failure (increased demand) or low output failure (reduced supply)

High output failure - severe anaemia, hyperthyroidism
Low output failure - Ischaemic heard disease, hypertension, aortic/mitral valve defects

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5
Q

What are histological findings of left heart failure?

A

Dilated ventricles
Thin walls
Nutmeg liver
Haemosiderin macrophages in the lungs

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6
Q

What is Dressler’s syndrome?

A

Autoimmune complication of myocardial infarction - occurs around 4 weeks post-infarction

Characteristics: chest pain, fever, pericardial rub

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7
Q

What is dilated cardiomyopathy?

A

LVEF <40% due to progressive loss of myocytes

Caused by: alcohol, chemotherapy and viral mycoarditis

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8
Q

What is bronchiectasis and what are the causes?

A

Permanent dilation of the bronchi and bronchioles secondary to chronic inflammation

Causes: chronic pneumonia (S. aureus, H. infleunzae), obstructing tumours, cystic fibrosis

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9
Q

What are the histological findings in bronchiectasis?

What is the diagnostic imaging modality?

A

Bronchial wall destruction & transmural inflammation

High resolution CT

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10
Q

What are small cell carcinomas?

A

Also known as “oat-cell” carcinoma under microscopy - they are nests of small, round, hyperchromatic cells and possess nuclear moulding.

These are very agressive with 80% metastasising. They can express neuroendocrine markers and cause paraneoplastic syndromes like Lamber-Eaton muasthenic syndrome

On CXR these cancers arise centrally

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11
Q

What are the important inflammatory markers in sarcoidosis?

A

TNF-alpha
IFN-gamma
IL-12

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12
Q

What are the dermatological signs in dermatomyositis?

A

Heliotrope rash (violet erythema around the periorbital region)
Gottron papules (violet scaly plaques over hands)

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13
Q

What are the characteristics of a subdural haemorrhage?

A

Slow bleeding (usually up to 48hrs) with a clear history of trauma - bleed between the dura and arachnoid due to an acute tear in bridging veins

Patients will present with an altered mental state

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14
Q

What are clinical features of multiple sclerosis?

A

Optic neuritis
Intranuclear opthalmoplegia
Cerebellar signs
Spasticity and weakness of limbs

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15
Q

What are histological features of multiple sclerosis?

A

Active and inactive plaques on the CNS:
Active - lymphocytes and macrophages
Inactive - reduced nuclei and myelin

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16
Q

What are the main features of gastric carcinoma?

A

Signet ring cells - cells with compressed nuclei
Linitis plastica - stomach becomes thick and rigiid resembling a leather bottle

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17
Q

What is the histological change in Barrett’s osephagus?

A

Metaplastic change of squamous epithelial cells to columnar epithelial cells (which produce intestinal mucin)

This predisposes Barrett’s oesophagus patients to an increased risk of adenocarcinoma

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18
Q

What is the most common oesphageal cancer?

A

Squamous cell carcinoma (90%) due to smoking or alcohol

Adenocarcinoma (10%) due to Barrett’s oesophagus

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19
Q

What is Gardener’s syndrome?

A

Similar to familial adenomatous polyposis (presence of adenomas in the GIT caused by a defect in the APC gene) AND extra-intestinal growth (osteomas, epidermoid cysts and desmoid tumours)

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20
Q

What is cirrhosis and how is it classified?

A

Diffuse fibrosis of the liver with abnormal architecture characterised by nodules secondary to chronic hepatic disease

Micronodular (<3mm) - usually alcohol aetiology
Macronodular (>3mm) - usually viral aetiology

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21
Q

What is the pathophysiology behind cirrhosis?

A

Fibrosis results from stellate cell activation –> increased collagen deposition

Nodules represent proliferating hepatocytes that lack normal acinar structure and hence have a haphazard blood supply –> shunt formation and portal hypertension

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22
Q

What can copper accumulation (Wilson’s disease) in the brain cause?

A

Parkinsonism
Seizures
Dementia
Psychological changes - behavioural changes, depression, psychosis

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23
Q

What is haemochromatosis?

A

Autosomal recessive condition in a mutation of the HFE gene. HFE protein generally regulated iron absorption which is then stored as haemosiderin.

Histological features: golden-brown haemosiderin deposition in the parenchyma of many organs (leading to subsequent inflammation and fibrosis). These samples will stain blue with Perl’s Prussian blue

Organs affected: liver (cirrhosis), pancreas (diabetes), skin (bronzed pigmentation), heart (cardiomyopathy), gonads (atrophy and impotence)

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24
Q

What is aflatoxin associated with?

A

Hepatocellular carcinoma

Aflatoxin is a carcinogen produced by aspergillus - it contaminates many crops in the developing world (mainly cereals and nuts)

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25
Q

What is the difference between haemosiderosis and haemochromatosis?

A

Haemosiderosis is excessive iron deposition due to an acquired cause (alcohol and blood transfusions) - there is no architectural change and development of cirrhosis (unless really severe)

Haeomochromatosis is an inherited disorder characterised by excessive absorption and iron accumulation in the body

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26
Q

What is pemphigoid?

A

Autoimmune deep bullous (blisters >0.5cm) condition that occurs in the elderly.

Bullae are fluid-filled and do not rupture easily. They are Nikolsky sign negative.

Pathophysiology - IgG binding to hemi-desmosomes which causes activation and recruition of eosinophils.

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27
Q

What is pemphigus?

A

Autoimmune bullous disease affecting middle-aged patients. There is superficial bullae on the kin (Nikolsky positive)

Pathophysiology: IgG bind to desmosomes in the intra-epidermal region resulting in acantholysis

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28
Q

What are the histological features of psoriasis?

A

Parakeratosis - corneum nuclei mixed with keratin to form a thick keratin layer creating “silvery scales”
Munro-abscesses - white blood cells entering the corneum
Loss of the granular layer leading to pin-point bleeding (Auspitz sign)
Clubbing of the rete ridges - grow downwards leading to a “test-tubes in a rack” appearance

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29
Q

What is actinic keratosis?

A

Also known as solar keratosis - epidermal dysplasia that occurs secondary to sunlight and presents as a brow-red warty lesion with sandpaper-like consistency

Histological features - solar elastosis, focal parakeratosis, atypical cells, inflammatory cell infiltrates

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30
Q

What is lichen planus?

A

Inflammation at the epidermal-dermal junction - lymphocytic infiltrate creates a saw-tooth pattern

7 Ps:
* Pruritic
* Purple
* Polygonal
* Planar
* Popular
* Plaques
* Pearl sheen

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31
Q

What are the characteristics of nephritis syndrome?

A

Haematuria, oliguria, red cell and white cell casts, dysmorphic red cells, hypertension

Pathogenesis: inflammation of glomerular vessels –> red cells enter renal tubule and cause damange –> slow of renal blood flow –> oliguria and hypertension secondary to water retention

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32
Q

What is seen on renal biopsy of rapidly progressive glomerulonephritis (RPGN)?

A

Crescent sign - due to proliferation of macrophages and parietal cells in the Bowman’s space

Causes include:
Goodpasture’s syndrome (anti-GBM)
Immune complex-mediated glomerulonephritis (SLE, IgA nephropathy, post-infectious glomerulonephritis)
Pauci-immune glomerulonephritis (Wegener’s polyangiitis and microscopic polyangiitis)

33
Q

How is membranous glomerulonephritis defined histologically?

A

Thickened glomerular basement membrane, spike/dome protusions, sub-epithelial immunoglobulin and granular staining pattern

34
Q

How is minimal change glomerulonephritis defined histologically?

A

Normal on light microscopy
Podocyte effacement on electron microscopy

*Most cases will respond to steroids

35
Q

How is focal segmental glomerulonephritis defined histologically?

A

Obliterated lumen and podocyte effacement

*Not responsive to steroids

36
Q

What is duct ectasia?

A

Chronic ductal inflammation due to acini secretions –> prone to clogging –> dilate and rupture

This leads to green/white discharge. It is common in women >40yo who have had children.

37
Q

What is a fibroadenoma?

A

Common benign breast tumour that arise from stroma and lobules (mixed tumours)

They grow rapidly in pregnancy and during menstraul cycles as they are oestrogen driven. Conversely, they regress during menopause.

Examination: very mobile, well circumscribed, discrete and usually <5cm. Soft in young female and firm in elderly (as stroma becomes more fibrous)

38
Q

What are ductal carcinomas in situ?

A

These occur in pre- or post-menopausal women and are usually unilateral and unifocal.

Mammogram findings: microcalcification secondary to central necrosis

Microscopy: presence of central necrosis and pleomorphic nuclei

*Differentiates from lobar carcinoma in situ which is usually pre-menopausal, bilateral and multifocal - no calcification and no necrosis with uniform nuclei

39
Q

What are phylloides tumours?

A

Similar to fibroadenomas as they are mixed - arise from stroma and duct epithelium.

Discrete, well-circumscribed and mobile

Usually >5cm, in women over 40yo and can be malignant.

Hisotlogy: “artichoke-like” appearance as the stroma pushes up on the epithelium

40
Q

What is an infiltrating ductal carcinoma?

A

Invasive cancer tha penetrates the basement membrane - usually results from DCIS

Macroscopically - scirrhous look with a very fibrous centre (giving a white appearance)

Worst prognosis of all breast cancers

Features: peau d’orange, Paget’s disease of the breast, tethering, nipple retraction, lymphadenopathy, ulceration of the mass, pain

41
Q

What is the presentation of mastitis?

A

Breast-feding mothers
Cracked nipples, tender, erythematous and oedematous

42
Q

What are causes of gynaecomastia?

A

Malnutrition
Spironolactone
Ketoconazole
Cirrhosis

43
Q

What is fibrocystic disease?

A

Benign lumps and cysts in the breast due to irregular menstrual cycles with unbalanced oestrogen

Peri-menopausal disease that regresses after menopause

Treatment is symptomatic

44
Q

What is fat necrosis?

A

Tender lump of necorsed fat surrounded by macrophages - usually due to breast trauma

45
Q

What is a giant cell tumour?

A

Malignant tumour of giant osteoclast cells - they cause lytic lesions on the epiphyses (especially around knees).

Visible on XR with “soap bubble” appearance

Histology - multinucleated giant osteoclasts with surrrounding ovoid and spindle cells

46
Q

What is the pathophysiology behind osteoporosis?

A

It is reduced bone density (reduced quantity) with normal quality

Reduced oestrogen concetration –> raise in IL-1 and IL-6 –> increased osteoclastic activity

47
Q

What are causes of osteoporosis?

A

Primary - post-menopausal women
Secondary - lifestyle (smoking, alcohol, inactivity), drugs (steroids, goserelin), low BMI, thyroid and parathyroid disease

48
Q

What is fibrous dysplasia?

A

Fibrous dysplasia occurs when there is a developmental arrest of normal bone structures secondary to an osteoblast maturation defect - most commonly affects the proximal femur and ribs

XR: ground-glass or soap bubble appearance
Histology - trabeculae that lack osteoblastic rimming

Assocaited with 2 syndromes: Mono-ostotic and McCune-Albright syndrome

49
Q

What is Paget’s disease?

A

Disease of bone remodelling whereby new bone is larger but weaker and more prone to fractures

Initial lytic phase - giant osteoclasts with multiple nuclei resorb bone
Mixed phase - osteoblast activity leads to increased bone mass
Osteosclerotic phase - bone formation continues but is woven and weak - collagen arranged haphazardly in a mosaic pattern

50
Q

What is non-bacterial thrombotic endocarditis (NBTE)?

A

Commonly affects patients >40yo and often characterised the absence of inflammation or bacteria

You can see sterile fibrin and platelet vegetations affecting the left heart (mitral > aortic).

NBTE is associated with recurrent thromboembolism to the brain, heart and kidneys

51
Q

What is cystic medical necrosis?

A

Focal degeneration of the elastic tissue and muscle fibres in the media with accumulation of basophilic ground substance –> more common aneurysm formation –> aortic dissection (common in Marfan’s)

52
Q

Where is “onion skin” syndrome?

A

Fibrosis with intimal thickening of small arteries which is due to arteriosclerosis.

Seen is limited and diffuse scleroderma.

53
Q

Polymyositis vs dermatomyositis?

A

Polymyositis = weakness, pain and swelling of the proximal limb muscles and facial muscles - often with ptosis and dysphagia.

Dermatomyositis = polymyositis with periorbital oedema and purple “heliotrope” rash on the upper eyelids. Also get erythematous cutaenous rash on the face, shoulders, upper arm, knuckes, elbow and knees

anti-SRP = poly
anti-Jo1 = dermato
anti-Mi2 = mixed but more dermato

54
Q

What is familial Parkinson’s disease?

A

Mutation in gene coding for alpha-synuclein which causes alpha synuclein proteins to aggregate to form insoluble fibrils (Lewy Bodies).

It has a worse prognosis with earlier onset and non-responsiveness to Levodopa

55
Q

What are the different classifications of plaques in multiple sclerosis according to the International Classification of Diseases?

A

Acute plaque - minor changes (e.g. oedema) and often difficult to recognise

Early chronic active plaque - oedema and macrophages, indicative of an inflammatory disorder of the central nervous system, with some myelin breakdown. Reactive astrocytosis is present

Late chronic active plaque - complete loss of myelin. Some macrophages will contain myelin debris and there will be often very mild perivascular inflammation at this stage with enlarged perivascular spaces

Chronic inactive plaque - Complete loss of myelin with the absecne of macrophages

Shadow plaque - Nearly complete remyelination as a thin myelin with some scattered macrophages. and a mild microglial up-regulation

56
Q

What do these four characteristic pathological features indicate:

Severe severe brain atrophy, loss of neurons, senile plaques and neuro- fibllirary tangles.

A

Alzheimer’s

57
Q

What is the pathological feature of Huntington’s disease in the brain?

A

Cerebral atrophy in the caudate nucleis and putamen and several changes in neurotransmitters

58
Q

What is multiple system atrophy associated with?

A

Glical cytoplasmic inclusion bodies (i.e. Papp-Lantos bodies)

59
Q

What is the Z line?

A

Irregular white line which indicates the squamo-columnar junction. It is 2cm above the gastro-oesophageal junction

60
Q

Histology of chronic pancreatitis?

A

Chronic inflammation with parenchymal fibrosis, loss of pancreatic parenchymal elements and duct strictures with formation of intrapancreatic calculi.

In short terms, the pancreas is replaced by firm fibrous tissue within which are dilated ducts and areas of calcification.

*This is different to acute pancreatitis where there is only acute inflammation and necrotic changes

61
Q

What is hydrosalpinx?

A

A complication of salpingitis (pelvic inflammatory disease).

Damage to the tube causes dilation making it thin-walled and contains clear fluid.

62
Q

What is COPD characterised by?

A

Chronic bronchitis - productive cough wtih copious amounts of sputum caused by damage to airways. Histology shows hypertrophy of mucous glands and goblet cell hyperplasia. These patients are also prone to infections
+
Emphysema - dyspnoea with no cough. Histology shows alveolar parenchymal damage by elastase that is activated by neutrophil/macrophage action secondary to cigarette smoking

63
Q

What is the definition of asthma?

A

Reversible inflammation and narrowing of airways which leads to recurring episodes of wheezing, coughing, chest tightness, and shortness of breath

64
Q

What is the definition of bronchiectasis?

A

Chronic condition characterized by permanent abnormal widening and inflammation of the bronchial tubes, which are the airways that carry air to and from the lungs. The bronchial tubes become permanently damaged and lose their elasticity. This can lead to the buildup of mucus, recurrent infections, and persistent coughing.

65
Q

What are the stages of lobar pneumonia?

A

Fibrinosuppurative consolidation.
Stages:
1. Consolidation
2. Red Hepatisation (neutrophilia)
3. Grey Hepatisation (Fibrosis)
4. Resolution

66
Q

What is acute respiratory distress syndrome?

A

Severe lung disease often 24-48hrs post-trauma, burns or sepsis

Characterised by inflammation in the lung parenchyma impairing gas exchange.

It is a less severe form of acute lung injury

67
Q

What is a mesothelioma?

A

Malignant tumour of the pleura and is associated with asbestos exposure decades earlier

68
Q

What is pneumoconiosis?

A

Type of fibrosing lung disease (‘dusty lung’) caused by inorganic dust inhalation. It is an alteration of the lung structure rather neoplastic differentiation of cells. It commonly affects the upper lobes whereas asbestosis affects the lower lobes more severely.

69
Q

What are classical X-ray features of rheumatoid arthritis?

A

LESS

Loss of joint space
Erosions
Soft tissue swelling
See-through bones (osteopenia)

70
Q

What are white cell casts characteristic of?

A

Acute pyelonephritis

71
Q

What are red cell casts characteristic of?

A

Glomerulonephritis

72
Q

What is eosinophiluria suggestive of?

A

Tubulointerstitial nephritis

73
Q

What tumour suppressor gene is involved Wilm’s tumour?

A

WT1 gene on chromosome 11

74
Q

What are the microscopic characteristics of Wilm’s tumour?

A

Immature-looking glomerular structures
Primitive small cell blastaematous tissue
Epithelial tubules and stroma composed of spindle cells
Striated muscle

75
Q

What are the histology core biopsy codes (breast)?

A

B1 = normal breast tissue
B2 = benign abnormality
B3 = lesion of uncertain malignant potential
B4 = Suspicious of malignancy
B5 = malignant
B5a = ductal carcinoma in situ
B6a = invasive carcinoma

76
Q

What are the associations of multiple endocrine neoplasia?

A

MEN1 (3 Ps): Pituitary, Pancreatic (e.g. insulinoma), Parathyroid (hyperparathyroidism)

MEN2a (2Ps 1M): Parathyroid, Phaeocromocytoma, Medullary thyroid

MEN2b (1P 2Ms): Pharocromocytoma, Medullary thyroid, Mucocutaneous neuromas (& Marfanoid)

77
Q

What cells are seen in Hashimoto’s thyroiditis?

A

Hurthle cells

78
Q

Which of the following describes an adaptation of mucosal surfaces which helps them prevent infection?

A

Lactoferrin - starves invading bacteria of iron

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