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MRCS B > Pathology > Flashcards

Pathology Flashcards

1
Q

Describe this

A
  • 2x2cm nodular lesion
  • Raised
  • Rolled edge
  • Central ulcerated crater
  • Visible telangiectasia
  • Shiny surface
  • Clinical features suggestive of basal cell carcinoma
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2
Q

What is basal cell carcinoma?

A
  • Malignant proliferation of basal cells of epidermis
  • Most common skin cancer (80%)
  • M > W
  • Sun exposed areas (head and neck)
  • Locally invasive and rarely metastasise
  • Subtypes: Nodular (most common), superficial, morphoeic (scar like with indistinct borders), basosquamous
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3
Q

Why is there erythema associated with BCC

A
  • Telangictasia: dilated blood vessels in epidermis (directly due to BCC or as a result of sun damage)
  • Local inflammatory response?
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4
Q

Histological classification BCC

A
  • Localised: nodular, nodulocystic, pigmented
  • Superficial: superficial spreading
  • Infiltrative: morphoeic
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5
Q

DDX BCC

A
  • NODULAR: SCC, skin appendage tumour, dermatofibroma
  • PIGMENTED: Melanoma, compound naevus
  • MORPHEAFORM: Scar, trichoepithlioma
  • SUPERFICIAL: psoriasis, eczema, Bowen’s disease
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6
Q

How does BCC spread

A
  • Rarely metastasises
  • Locally invasive
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7
Q

How can you ensure complete intra-operative resection for BCC?

A
  • Moh’s micrographic surgery
  • Sequential horizontal excision with immediate intra-operative frozen section examination
  • Resection until adequate margins
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8
Q
A
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9
Q

BCC risk factors

A
  • Congenital: Fitzpatrick skin type I, Xeroderma pigmentosum (AR, XPA gene)
  • Acquired: UV exposusure, age
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10
Q

BCC management

A
  • Conservative: sun protection
  • Medical: 5-FU cream, imiquimod cream (activation of TLRs = local immune response), photodynamic therapy, cryotherapy
  • Surgical: Excision, Moh’s micrographic surgery
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11
Q

Excision margins BCC

A
  • Primary <2cm: 5mm
  • Primary >2cm or morphoeic: 10-15mm
  • Recurrent: 5-10mm
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12
Q

Define metastasis

A
  • Process by which a primary malignant neoplasm gives rise to secondary tumours at distant sites through lymphatic, haematogenous or transoleomic (penetrating visceral surface e.g. peritoneal) spread
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13
Q

Management of MRSA colonisation?

A
  • Isolation side room
  • Contact precautions
  • Nasal mucopuricin 2%
  • Chlorhexidine 4% daily body wash (hibiscrub)
  • Rescreen after 5 days
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14
Q

What is PVL staph?

A
  • Panton valentine leucocidin
  • Exotoxin comprising two subunits
  • Forms pores in membrane of leucocytes  cell lysis and death by necrosis
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15
Q

What other staph aureus toxins are there?

A
  • TSST-1 > Binds MHC-II with high affinity  cytokine storm  toxic shock syndrome
  • Haemolysin
  • Exfoliatin
  • Enterotoxin
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16
Q

What is rheumatic fever?

A
  • Systemic complications of pharyngitis due to group A beta-haemolytic strep
  • T2HSR caused by molecular mimicry
  • Bacterial M protein resembles protein found in normal tissues
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17
Q

How does acute rheumatic fever lead to chronic rheumatic heart disease?

A
  • Repeat attacks of ARF lead to valve scarring
  • Thickening of valve leaflets and cordae tindinae
  • Fusion of valve commissures
  • Increased risk of infective endocarditis: Strep Viridans (previously damaged valve)
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18
Q

How can you diagnose acute rhematic fever?

A
  • JONES criteria
  • Joint pain (migratory polyarthritis)
  • Pancarditis (endocarditis most commonly affects MV, myocarditis (aschoff bodies and anitschkow cells), pericarditis)
  • Nodules
  • Erythema marginatum
  • Sydneham’s chorea (TS2HR affecting basal ganglia)
  • + positive ASOT titre
  • Minor criteria: Fever, elevated ESR
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19
Q

What is a GIST?

Histopathology report below:

  • Large, well circumscribed. Fleshy, tan pink lesion in the muscularis propria of the stomach.
  • Ulceration
  • CD 117
  • Nodal involvement
  • No metastasis
A
  • MC mesenchymal cell of the GIT
  • Arises from interstitial cells of Cajal in myenteric plexus of muscularis propria (pacemakers cells of GIT for peristalsis and segmentation)
  • Stomach (80%) > jejunum/ileum > duodenum > colorectal
  • Most form due to activating mutations in proto-oncogene KIT
  • Positive stains: CD117 (tyrosine kinase growth factor receptor for KIT)
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20
Q

Difference between GIST and gastric adenocarcinoma

A
  • GIST = Mesenchymal cell tumour from interstial cells of cajal
  • Gastric adenocarcinoma due to malignant proliferation of surface epithelial cells
  • Intestinal type: MC, associated with H. Pylori and nitrosamines. Large ulcer with heaped margins
  • Diffuse type: signet ring cells with diffuse infiltration and thickening of stomach wall (linitis plastica).
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21
Q

How do GISTs behave?

A
  • Peritoneal spread with liver metastasis
  • Rarely metastasise via lymphatics
  • Size and mitotic rate predictive of behaviour
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22
Q

Management GIST

A
  • Surgical resection
  • Chemotherapy: imatinib (tyrosine kinase inhibitor)
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23
Q

What is jaundice?

A
  • Yellow discolouration of skin, sclera and mucous membranes
  • Serum bilirubin binds to elastin
  • Pre-, intra- and post-hepatic causes
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24
Q

Patient develops ascites, how would you investigate?

A
  • Broadly: transudative (<30g protein /L) and exudative (>30g protein/L) causes of ascites
  • Full Hx and examination
  • Bloods: LFTs (hepatocellular damage), clotting/INR (impaired synthetic function), FB, UE, CRP
  • USS: Confirm presence of ascites, examine for portal HTN (splenomegaly, collaterals)
  • Paracentesis: Chemistry (SAAG, tryglycerides, amylase), microscopy and culture (PMN >250 = SBP, gram stain), cytology
  • Cross-sectional imaging
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25
Q

Definition of a polyp

A
  • Raised protrusions of colonic mucosa
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26
Q

Types of colonic polyp?

A
  • Adenomatous polyps arise due to neoplastic proliferation of glands. Benign but may progress through adenoma-carcinoma sequence
    • Subclassified on growth pattern:
      • Tubular
      • Tubulovillous
      • Villous (highest rate of malignant transformation)
  • Hyperplastic arise due to hyperplasia of glands
  • Inflammatory pseudopolyps (not protrusions of colonic mucosa, inflammatory debris)
  • Hamartomatous: disordered growth of tissue native to site of origin. A/W PJS
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27
Q

Hyperplasia vs dysplasia?

A
  • Hyperplasia = increase in cell number
  • Dysplasia = disordered cellular growth. May arise due to longstanding hyperplasia
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28
Q

22M multiple polyps all throughout colon

DDX?

A
  • FAP
  • Gardner’s syndrome
  • Turcot’s syndrome
  • Peutz Jegher
  • IBD with pseudo polyps
  • C. diff
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29
Q

Treatment FAP

A
  • Genetic counselling
  • Surveillance colonoscopy
  • Colectomy with IRA
  • Colectomy with J-pouch formation
  • Panproctocolectomy + ileostomy
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30
Q

What is FAP?

A

Familial adenomatous polyposis

  • Autosomal dominant
  • APC gene mutation chromosome 5
  • APC = Tumour suppressor gene
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31
Q

What is HNPCC?

A

Hereditary non-polyposis colorectal carcinoma

Lynch syndrome

  • Autosomal dominant
  • Mutations in genes that are involved in mismatch repair
  • MLH1 and MSH2
  • Amsterdam criteria: 3 family members with CRC, 2 generations, 1 <50
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32
Q

Peutz Jegher Syndrome

A
  • Autosomal dominant
  • Hamartomatous polyps through GI tract
  • Oromucosal hyperpigmentation
  • STK11 gene
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33
Q

Extra-intestinal features of FAP

A
  • Gardner’s syndrome: fibromatosis and osteomas
  • Turcot’s syndrome: glial tumours and medulloblastoma
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34
Q

What is APC

A
  • TSG
  • Chromosome 5
  • Mutated in FAP
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35
Q

What is KRAS

A
  • Proto-oncogene
  • Chr 12
  • RAS/MAPK pathway
  • Mutation = oncogene = uninhibited cell growth
  • Secretes growth factors that permit anchorage independence > adenoma formation
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36
Q

What is P53

A
  • Tumour suppressor gene
  • Chr 17
  • Regulates progression through G1/S
  • Upregulates DNA repair enzymes, if not possible then induces apoptosis
  • Knudson two hit hypothesis > both copies have to be mutated
37
Q

Modified Duke’s

A
  • A: Confined to mucosa (90%)
  • B1: Extends to muscularis propria (80%)
  • B2: Extends through muscularis propria, no nodes (70%)
  • C1: Not through muscularis propria, nodes involved (30%)
  • C2: Extends through muscularis propria, nodes involved
  • D: Distant metastasis (<10%)
38
Q

TNM colorectal

A
  • T1: Mucosa
  • T2: Muscularis propria
  • T3: Through muscularis to serosa
  • T4A: Full thickness
  • T4B: Grown into nearby organs
  • N0: No nodes
  • N1: <3
  • N2: >3
  • M0
  • M1
39
Q

Adenoma-carcinoma sequence FAP

A

Mutated FAP > Hyperplasia > KRAS mutation > Dysplasia > loss of P53 > Adenocarcinoma

40
Q

What is a carcinoid tumour?

A
  • Neuroendocrine tumour that arises from AUPD cells (cells which share common function in producing low molecular weight polypeptide hormones)
  • MC tumour of appendix
  • 20% of GI carcinoids found in appendix (appendix > ileum > rectum)
  • Also found in lung, ovaries, testes
41
Q

Management of carcinoid tumour?

A
  • Medical: octreotide (somatostatin analogue to reduce serotonin) and antihistamines
  • <2cm: Appendicectomy is curative
  • >2cm or involving base: Right hemicolectomy
42
Q

What is carcinoid syndrome?

A
  • Collection of clinical features seen following metastasis of carcinoid tumours to the liver
  • Occur due to overproduction of serotonin, histamine and secretin
  • Flushing and diarrhoea
  • Bronchospasm
  • Pulmonary stenosis and TR
  • 10% of patients with carcinoid tumours
43
Q

Investigations of carcinoid syndrome

A
  • 24h urinary 5-HIAA (serotonin metabolite)
  • Octreoscan: PET with radiolabelled octreotide (somatostatin analogue) binds NETs.
  • CT/MRI
44
Q

Describe this

A
  • Endoscopic image
  • Hyperaemic mucosa
  • Numerous yellow-white mucosal plaques throughout
  • Pseudomembranous colitis
45
Q

What is c. diff?

A

Clostridium dificille

  • Gram positive spore forming rod
  • Facultative anaerobe
46
Q

Pathophysiology of pseudomembranous colitis?

A
  • Broad spectrum antibiotics (clindamycin) eradicate microbial flora favouring growth of c. diff
  • C. diff toxin A = enterotoxin, c. diff toxin B = cytotoxin
  • Pseudomembrane = mucopurulent exudate from crypts
  • necrosis
  • Adherent layers of inflammatory cells and cellular debris at site of colonic mucousal injury
  • Excess fibrin deposition
47
Q

How does C. diff spread?

A
  • Spore forming bacteria
  • Metabolically dormant form of bacteria, resistant to environmental stressors (extremes of temperature, ethanol, pH)
  • C. diff cannot cause disease unless spores germinate into metabolically active toxin producing cells (germination)
  • Spores spread through nosocomial infection
48
Q

Management of c. diff?

A
  • Isolation room
  • Contact precautions (apron and gloves)
  • Cessation of causative ABx if appropriate
  • PO Vancomycin 125mg QDS/ Fidaxomicin/ Metronidazole
  • Tigecycline/ IVIG if no response
  • Faecal transplantation in recurrent episodes
49
Q

What is toxic megacolon?

A
  • Colitis with colonic dilation >6cm
  • IBD, infectious colitis (c. diff)
50
Q

Management of toxic megacolon?

A
  • Resuscitation
  • ABX/steroids
  • NG decompression
  • Laparotomy + subtotal colectomy with end ileostomy formation
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MRCS B (6 decks)

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