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MRCS > 2 - Surgical Pathology > Flashcards

2 - Surgical Pathology Flashcards

1
Q

What is a neoplasm?

A

An abnormal mass of tissue, the growth of which:

  • is uncoordinated
  • exceeds that of normal tissues
  • persists in the same excessive manner after cessation of the stimulus which evoked change
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2
Q

How may neoplasms be classified?

A
  • Benign or malignant (primary or secondary)
  • 1 cell type of origin (epithelial, mesenchymal, lymphoma)
  • > 1 cell type from 1 germ layer (pleomorphic adenoma, fibroadenoma breast)
  • > 1 cell type from >1 germ layer (teratomas)
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3
Q

What is hyperplasia? Give examples

A

An increase in size of an organ or tissue through an increase in cell numbers

  • physiological: breast, thyroid in pregnancy
  • pathological: adrenal’s in Cushings, Grave’s disease
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4
Q

What is hypertrophy? Give examples

A

An increase in the size of an organ or tissue through an increase in the size of cells

  • physiological: skeletal muscle with exercise, uterus in pregnancy
  • pathological: HOCM cardiomyopathy
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5
Q

What is a harmatoma? Give examples

A

A tumour-like malformation composed of a haphazard arrangement of the different amount of tissues normally found at the site
- Peutz-Jadher’s polyps of bowel, haemangiomas

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6
Q

What is metaplasia? Give examples

A

A reversible replacement of one fully differentiated cell type with another differentiated cell type - an adaptive change in response to injury, irritation, altered cell function. Has greater susceptibility to malignant transformation

  • Barret’s oesophagus (stratified squamous to glandular, columnar type epithelium)
  • Bronchus (pseudo stratified ciliated columnar to stratified squamous epithelium)
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7
Q

What is dysplasia?

A

Disordered cellular development characterised by increased mitosis and pleomorphism BUT without the ability to invade throughout the basement membrane and metastasise to distant sites.
Severe dysplasia = carcinoma in situ

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8
Q

What is carcinoma?

A

A malignant tumour of epithelial cells

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9
Q

What is sarcoma?

A

A malignant tumour of connective tissue

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10
Q

How to carcinomas and sarcomas typically spread?

A

Carcinomas via the lymphatics
Sarcomas via the haematogenous route
There are exceptions e.g. follicular thyroid carcinoma - haematogenous

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11
Q

What makes a tumour malignant?

A
  • invasion through the basement membrane

- ability to metastasise to distant sites

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12
Q

What is a metastasis?

A

The survival and growth of cells that have migrated or have otherwise been transferred from a malignant tumour to a site or sites distant from the primary

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13
Q

What are the routes by which tumours spread?

A
  • local invasion
  • lymphatics
  • blood
  • transcoelomic (carcinoma stomach, ovary, colon, pancreas)
  • CSF
  • peri-neural (adenoid cystic parotid)
  • iatrogenic (implantation / seeding during surgery)
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14
Q

Which tumours typically spread to bone?

A 
Carcinoma of
- breast
- bronchus
- thyroid
- kidney
- prostate
Myeloma
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15
Q

What are the cytological features of malignancy?

A
  • hyperchromatism
  • pleomorphism
  • cellular atypia
  • increased nuclear-cytoplasmic ratio
  • large and prominent nucleoli
  • increased mitotic index and abnormal mitoses
  • loss of differentiation and/or failure of cellular maturation
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16
Q

What are the histological features of malignancy?

A
  • loss of normal tissue architecture
  • invasion beyond basement membrane
  • necrosis
  • haemorrhage
  • infiltrate borders
  • cell shedding
  • lymphovascular invasion
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17
Q

What is the difference between staging and grading?

A 
Staging = extent of growth (size and spread)
Grading = how well differentiated a tumour is
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18
Q

What is Dukes’ staging?

A

A - in the wall: 95-100% 5 yr survival
B - through the wall: 65-75%
C - lymph node mets: 30-40%
D - distant mets: 5-10%

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19
Q

How is TNM applied to breast cancer?

A

Tx - tumour cannot be assessed
T0 - no evidence of primary tumour
Tis - carcinoma in situ
T1 - <2cm
T2 - >2cm but <5cm
T3 - >5cm
T4 - any size with direct extension to chest wall and/or skin
N0 - no regional lymph mets
N1 - mets to ipsilateral, mobile axillary lymph nodes
N2 - mets to ipsilateral, fixed axillary or internal mammary nodes
N3 - mets to infra/supraclavicular nodes or both axillary and internal mammary nodes
M0 - no clinical or radiological evidence of mets
M1 - distant detectable mets

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20
Q

Which viruses cause cancer?

A 
DNA
- EBV (nasopharyngeal carcinoma, Burkitt's and Hodgkin's lymphoma)
- Hep B (Hepatocellular carcinoma)
- HPV 16/18/31 (cervical cancer, anal carcinoma)
- HHV-8 (Kaposi's sarcoma)
RNA
- HTLV-1 (leukaemia/lymphoma)
- Hep C - Hepatocellular carcinoma)
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21
Q

How do viruses cause cancer?

A
  • inappropriate activation of cellular oncogenes
  • expression of viral oncogene
  • production of viral proteins promoting growth / inhibiting cell death
  • chronic inflammation
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22
Q

What types of thyroid neoplasms are there?

A
  • Papillary
  • Folicular
  • Medullary
  • Anaplastic
  • Lymphoma
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23
Q

What are the risk factors for thyroid cancer?

A

Radiation exposure

Family history

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24
Q

What is multiple endocrine neoplasia?

A

A group of related conditions, inherited as AD traits, characterised by hyperplasias and/or neoplasms of several endocrine organs.

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25
Q

What does MEN 1 consist of?

A
  • Pituitary adenomas (prolactinomas most commonly)
  • Pancreatic islet cell tumours (gastronomes most commonly)
  • Parathyroids (four-gland hyperplasia most commonly)
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26
Q

What does MEN 2a consist of?

A
  • Medullary thyroid carcinoma
  • Pheochromocytoma
  • Parathyroid hyperplasia (four-gland hyperplasia most commonly)
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27
Q

What does MEN 2b consist of?

A
  • Medullary thyroid carcinoma
  • Pheochromocytoma
  • Marfanoid-type body habitus
  • Mucosal neuromastosis
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28
Q

What is acute inflammation?

A

Stereotypical response to tissue injury characterised by calor, dolor, rubor and tumour (heat, pain, redness, swelling)

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29
Q

What are the stages of acute inflammation?

A
  • vasodilation
  • increased vascular permeability
  • diapedesis / extravasation
  • phagocytosis
  • resolution or progression to chronic inflammation
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30
Q

Name some chemical mediators that participate in acute inflammation

A
  • vasoactive amines (histamine, 5-HT / serotonin)
  • kinin system (bradykinin)
  • complement cascade (C3a, C5a)
  • coagulation cascade and fibrinolytic system
  • arachidonic acid metabolites (leukotrienes, prostaglandins, thromboxane A2)
  • cytokines (interleukins, TNF-alpha, TGF-beta)
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31
Q

What are the possible outcomes of acute inflammation?

A
  • resolution
  • progression to chronic inflammation
  • organisation and repair culmination in scar formation
  • death (e.g. meningitis)
  • abscess formation
32
Q

How does chronic inflammation differ from acute inflammation?

A

Chronic inflammation is defined by the cell types present
- macrophages
- lymphocytes
Typically, longer time course

33
Q

What are the causes of chronic inflammation?

A
  • persistant infections that evade host defence mechanisms (TB, syphilis, leprosy, H.pylori)
  • endogenous injurious agent (acid in stomach in PUD)
  • persistant / non-degradable toxins (silica dust, asbestos, lipid in arterial walls)
  • autoimmune diseases
  • immunodeficiency
  • unknown/idiopathic (sarcoidosis, IBD)
34
Q

What are the pathological consequences of chronic inflammation?

A
  • tissue destruction and scaring
  • malignant transformation
  • amyloidosis (e.g. in RA, UC)
35
Q

What is amyloidosis and how is it classified?

A

A condition that results from the aggregation of beta-pleated, insoluble amyloid protein that gets deposited in organs and tissues thereby disrupting their normal function.
Can be localised or systemic
Can be primary or secondary (RA, IBD)
Subtypes: AL (light chains), AA (inflammatory), A-beta (Alzheimer’s), ATTR (familial)

36
Q

What special histological properties does amyloidosis exhibit?

A

Amyloid may be stained with Congo red and exhibits

‘apple-green birefringence’ under plane-polarised light

37
Q

What is wound healing?

A

The process by which tissue restoration of structure and function occurs, with restitution of tissue integrity and tensile strength.

38
Q

How does a wound heal?

A
  • Primary, secondary (granulation) or delayed primary (tertiary) intention
  • Resolution (no scar) or organisation and repair (scar)
    Stages
  • haemostats / coagulation
  • acute inflammation
  • formation of granulation tissue (endothelial cells, fibroblasts, macrophages)
  • angiogenesis
  • epithelialisation, fibroplasia, wound contraction (myofibroblasts)
  • maturation and remodelling
39
Q

What factors affect wound healing?

A

Local factors
- poor blood supply, haematoma, infection, FBs, surgical technique (wound tension, suture material), radiotherapy
Systemic factors
- DM, steroids, immunodeficiency, heart/renal/liver failure, hypoxia, malnutrition, chemotherapy, malignancy

40
Q

What is the key difference between hypertrophic and keloid scarring?

A

Hypertrophic
- confined to wound margins
- often across flexor surfaces and skin creases
Keloid
- scar extends beyond wound margins.
- more common in Black and Hispanic ethnic groups
- Earlobe, chin, neck, shoulder, chest, deltoid regions

41
Q

What is an abscess?

A

A localised collection of pus surrounded by granulation tissue / fibrous tissue

42
Q

What is pus?

A

A collection of neutrophils, together with dead and dying microorganisms

43
Q

What is a sinus?

A

A blind ending tract lined by granulation tissue

44
Q

What is a fistula?

A

An abnormal communication between two epithelial or endothelial (AV) surfaces.
Commonest - ear piercing

45
Q

What is a stoma? How can they be classified?

A

A surgical opening into a hollow viscus.

  • Anatomical site or output (colostomy, ileostomy, urostomy, tracheostomy, gastrostomy etc)
  • Indication (temporary vs permanent)
  • No. openings (end vs loop)
46
Q

How may fistulae be classified?

A
  • congenital vs acquired
  • aetiology (infections, inflammation, malignancy, radiotherapy etc)
  • internal vs external
  • simple vs complex
  • anatomical - by-site (entero-enteric, entero-cutaneous, colo-vaginal, vesicle-colic etc)
  • physiological - high vs low output
47
Q

What factors prevent an intestinal fistula from healing spontaneously?

A
  • distal obstruction
  • malignancy
  • FB
  • associated undrained infection
  • radiation injury to tissues
  • underlying inflammatory condition (e.g. Crohn’s)
  • mucocutaneous continuity
  • high output
  • malnutrition
48
Q

How are fistulae managed?

A

SNAP

  • sepsis control
  • nutritional suport
  • anatomical assessment, adequate fluid and electrolyte replacement
  • plan, protect skin to prevent excoriation

60% close spontaneously within 1 month when sepsis is controlled and distal obstruction is relieved

49
Q

What are the macroscopic and microscopic differences between Crohn’s and UC?

A

Macro
- Crohn’s: any part of GI tract, ‘skip’ lesions, rectal sparing, full thickness, fistulae & sinuses, strictures
- UC: confined to colon (+/- backwash ileitis) starting at rectum, contiguous, mucosal, pseudopolyps
Micro
- Crohn’s: non-caseating granulomas, ‘cobblestone’ mucosa
- UC: no granulomas, Crypt abscesses (UC>CD), dysplasia

50
Q

What are the extra-intestinal manifestations of IBD?

A
  • Integument: clubbing, erythema nodosum, pyoderma gangrenosum, aphthous ulcers
  • Eyes: conjunctivitis, episcleritis, scleritis, anterior, uveitis
  • Liver: Fatty liver, chronic active hepatitis, cirrhosis, gallstones, PSC, cholangiocarcinoma
  • Renal: calculi
  • Joints: peripheral arthropathy, sacroilitis, ankylosing spondylitis
  • Amyloidosis
51
Q

What is a granuloma? Give examples

A

A focal area of chronic inflammation consisting of a microscopic aggregation of activation macrophages that are transformed into epithelium-like cells surrounded by a collar of mononuclear leukocytes.

  • Infections: TB, leprosy, syphilis, actinomycosis
  • Inflammation: sarcoidosis, Crohn’s, PBC, Wegener’s
  • Foreign bodies: Beryllium, silicosis, talc, sutures
  • Malignancy: e.g Hodgkin’s lymphoma
52
Q

What is an aneurysm? How are they classified?

A

An abnormal, permanent, locatlised dilation of a blood vessel to 1.5-2x its normal diameter

  • Aetiology: atherosclerotic, inflammatory etc
  • Congenital vs acquired
  • True vs False
  • Site: thoracic, abdominal, intracranial
  • Size: giant, berry
  • Shape: fusiform, saccular, dissecting etc
53
Q

What are the complications of aneurysms?

A
  • rupture
  • thrombosis
  • embolism
  • local compressive effects
  • infection (mycotic)
  • fistula (e.g. aorta-enteric fistula)
54
Q

What is a polyp? How are they classified?

A

A pedunculated mass of tissue arising from an epithelial surface

  • Non-neoplastic: hyperplastic, hamartomatous, inflammatory pesudopolyps, lymphoid hyperplasia
  • Neoplastic: tubular, tubulo-villous, villous
55
Q

What complications might polyps undergo?

A
  • malignant transformation
  • ulceration
  • bleeding
  • infection
  • intussusception
  • protein and potassium loss
56
Q

What is a diverticulum? How are they classified?

A

An abnormal out pouching go a hollow viscus into the surrounding tissues

  • congenital vs acquired
  • pulsion vs traction (rare)
  • anatomical site
  • mesenteric (small intestine) vs anti-mesenteric
  • true (Meckel’s) vs false (sigmoid, pharyngeal)
57
Q

What complications might diverticula undergo?

A
  • perforation
  • inflammation +/- infection
  • bleeding
  • fistulae
  • strictures
  • malignancy (e.g. bladder diverticulula)
58
Q

What is the difference between a clot, thrombus and embolus?

A
  • Thrombus: ‘solid material formed from the constituents of blood in FLOWING blood’
  • Clot: ‘solid material formed from the constituents of blood in STATIONARY blood
  • Embolus: an abnormal mass of undissolved material that is carried in the bloodstream from one place to another
59
Q

What causes a thrombus?

A

Vichow’s triad

  • damage to vessel wall / endothelial injury
  • abnormal blood flow
  • alteration in constituents of blood / hypercoagulable state
60
Q

What are the different types of emboli?

A

Can be solid, liquid or gas

  • thrombus
  • fat
  • air
  • atheromatous material
  • amniotic fluid
  • tumour cells
  • foreign material e.g. broken cannula
61
Q

What are the complications of atherosclerosis?

A
  • distal ischaemia
  • vessel occulation
  • plaque ulceration & rupture
  • thrombosis
  • haemorrage into plaque
  • embolism - lipid or thrombus
  • calcification
  • aneurysm formation
62
Q

What is necrosis? What are the different types?

A

Abnormal tissue death during life, always pathological and accompanied by inflammation.

  • coagulative / structured: from interruption of blood supply, tissue architecture preserved
  • liquefactive / colliquative: in lipid-rich tissues lysosomal enzymes denature fat, characteristically occurs in brain
  • caseous / unstructured: tissue architecture destroyed, TB
  • fat necrosis: post trauma (breast) or enzymatic lipolysis (pancreatitis)
  • fibrinoid: in arterial walls subjected to high pressures in malignant hypertension
  • gangrenous: characterised by putrefaction. Wet, dry or gaseous.
63
Q

What is the difference between apoptosis and necrosis?

A
  • Apoptosis: energy dependent, internally programmed, affects single cells, no inflammation, physiological or pathological, intact plasma membrane, formation of apoptotic bodies
  • Necrosis: energy independent, response to external injury, affects groups of cells, inflammation, pathological, loss of plasma membrane, cell swelling and lysis
64
Q

What is a hypersensitivity reaction? How are they classified?

A

A condition in which undesirable tissue damage follows the development of humeral or cell mediated immunity. An exaggerated host immune response to a stimulus.

  • Type I: mast cell degranulation (anaphylaxis, atopic allergies)
  • Type II: antibodies (transfusion reactions, autoimmune haemolytic anaemia, Goodpasture’s syndrome)
  • Type III: antibody-antigen complexes (serum sickness, systemic lupus erythematousus)
  • Type IV: cell-mediated, granulomatous conditions
  • Type V: stimulatory autoantibodies in autoimmune conditions (Grave’s disease, Myasthenia gravis)
65
Q

What is an ulcer? What are the types / causes?

A

A break in an epithelia surface

  • venous (70%)
  • arterial
  • neuropathic
  • infection (TB, leprosy, syphilis)
  • malignancy (SCC, BCC, melanoma, Marjolin’s, Karposi’s)
  • haematological conditions (sickle cell, polycythaemia ruby vera, thalassaemia)
  • vasculitides (RA, polyarteritis nodosa)
  • metabolic (pyoderma gangrenosum)
  • trauma (lacerations, burns, radiation, self-inflicted)
  • iatrogenic (over-tight bandaging, ill-fitting cast)
  • idiopathic
66
Q

What is a tumour marker? Give examples

A

A substance reliable found in the circulation of a patient with neoplasia which is directly related to the presence of the neoplasm, disappears when the neoplasm is treated and reappears when the neoplasm returns.

  • Hormones (beta HCG, calcitonin)
  • Enzymes (PSA, placental ALP, LDH)
  • Oncofetal antigens (alpha-fetoprotein, CEA, CA-125, CA19-9)
  • Serum and tissue proteins (thyroglobulin)
67
Q

What are the possible uses of tumour markers?

A
  • diagnostic purposes
  • prognostic information (tumour load)
  • monitoring response to treatment
  • surveillance to detect recurrence
  • screening
68
Q

What is colitis? How can it be classified?

A

Inflammation of the colon.

  • Inflammatory: UC, CD, indeterminate colitis
  • Infective
  • Ischaemic
  • Radiation
  • Collagenous
  • Microscopic (and lymphocytic/eosinophilic colitis)
69
Q

What is malignant melanoma? What are the different types?

A

A malignant neoplasm of melanocytes

  • superficial spreading (70%)
  • nodular
  • lentigo malignant melanoma (Hutchinon’s freckle)
  • aural lentiginous
  • amelanotic
70
Q

What macroscopic features in naevi are suggestive of melanoma?

A
  • Asymmetry
  • Border irregularity
  • Colour variation
  • Diameter >6mm
  • Elevation
  • Tingling, itching, crusting, discharge, satellite lesions
  • Only 10-20% form in pre-exisiting naevi, remainder de novo.
71
Q

What are the risk factors for developing melanoma?

A 
Congenital
- xeroderma pigmentosum
- dysplastic nevus sundrome
- BRAF gene mutations
- Giant congenital pigmented nevus
Acquired
- UV exposure, sunburn
- Past history of melanomas
- Red hair
- Freckles
- Pre-exisiting skin lesions (lentigo maligna)
- >20 naevi
- immunocompromise (HIV, Hodgkin's, Cycclosporin A therapy)
72
Q

How is malignant melanoma staged?

A 
Breslow's thickness - tumour invasion depth from top of granular layer of epidermis to deepest point of tumour
I <0.75 mm
II 0.76-1.5 mm
III 1.51 - 2.25 mm
IV 2.26 - 3.00 mm
V > 3.00 mm
73
Q

What is the difference between cytology and histology?

A

Cytology - study of individual cells and cell morphology obtained from FNA or brushings
Histology - study of cells within the context of tissues and their architecture, obtained by biopsy

74
Q

What are the advantages and disadvantages of cytology?

A 
Advantages
- simple to perform, rapid
- minimally invasive
- cheap, requires minimal equipment
Disadvantages
- no info r.e. tissue architechture
- large, poorly defined field sampled leading to sampling error or insufficient material for diagnosis
- need experiences cytologist
- operator dependent
- potential for spread of malignant cells
- less amenable to further studies
75
Q

What are the advantages and disadvantages of histology?

A

Advantages
- defined lesion sampled
- provides info on tissue architecture and definitive diagnosis of invasion - staging of cancers
Disadvantages
- technically more difficult
- required fixation and processing (time)
- invasive
- painful
- expensive
- potential for spread of malignant cells
- may alter morphology of lesion for subsequent imaging

76
Q

When would you refer a death to the coroner?

A
  • cause of death unknown
  • Dr not attended deceased within 14 days of death or in terminal illness
  • all sudden deaths
  • violent,, unnatural, or suspicious death
  • if may be due to an accident
  • if may be due to see-neglect or neglect by others
  • if may be due to industrial disease or related to employment
  • if may be due to abortion
  • if occurred during an operation or before recovery from the effects of anaesthesia
  • if may be due to suicide
  • if death during or shortly after detention in police or prison custody

MRCS (6 decks)

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