MRCS B > Pathology > Flashcards

Pathology Flashcards

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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
Definition of a polyp
* Raised protrusions of colonic mucosa
26
Types of colonic polyp?
* **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
27
Hyperplasia vs dysplasia?
* Hyperplasia = increase in cell number * Dysplasia = disordered cellular growth. May arise due to longstanding hyperplasia
28
22M multiple polyps all throughout colon DDX?
* FAP * Gardner’s syndrome * Turcot’s syndrome * Peutz Jegher * IBD with pseudo polyps * C. diff
29
Treatment FAP
* Genetic counselling * Surveillance colonoscopy * Colectomy with IRA * Colectomy with J-pouch formation * Panproctocolectomy + ileostomy
30
What is FAP?
Familial adenomatous polyposis * Autosomal dominant * APC gene mutation chromosome 5 * APC = Tumour suppressor gene
31
What is HNPCC?
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
32
Peutz Jegher Syndrome
* Autosomal dominant * Hamartomatous polyps through GI tract * Oromucosal hyperpigmentation * STK11 gene
33
Extra-intestinal features of FAP
* Gardner’s syndrome: fibromatosis and osteomas * Turcot’s syndrome: glial tumours and medulloblastoma
34
What is APC
* TSG * Chromosome 5 * Mutated in FAP
35
What is KRAS
* Proto-oncogene * Chr 12 * RAS/MAPK pathway * Mutation = oncogene = uninhibited cell growth * Secretes growth factors that permit anchorage independence \> adenoma formation
36
What is P53
* 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
Modified Duke’s
* 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
TNM colorectal
* 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
Adenoma-carcinoma sequence FAP
Mutated FAP \> Hyperplasia \> KRAS mutation \> Dysplasia \> loss of P53 \> Adenocarcinoma
40
**What is a carcinoid tumour?**
* 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
**Management of carcinoid tumour?**
* Medical: octreotide (somatostatin analogue to reduce serotonin) and antihistamines * \<2cm: Appendicectomy is curative * \>2cm or involving base: Right hemicolectomy
42
**What is carcinoid syndrome?**
* 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
**Investigations of carcinoid syndrome**
* 24h urinary 5-HIAA (serotonin metabolite) * Octreoscan: PET with radiolabelled octreotide (somatostatin analogue) binds NETs. * CT/MRI
44
Describe this
* Endoscopic image * Hyperaemic mucosa * Numerous yellow-white mucosal plaques throughout * Pseudomembranous colitis
45
**What is c. diff?**
Clostridium dificille * Gram positive spore forming rod * Facultative anaerobe
46
**Pathophysiology of pseudomembranous colitis?**
* 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
**How does C. diff spread?**
* 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
**Management of c. diff?**
* 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
**What is toxic megacolon?**
* Colitis with colonic dilation \>6cm * IBD, infectious colitis (c. diff)
50
**Management of toxic megacolon?**
* Resuscitation * ABX/steroids * NG decompression * Laparotomy + subtotal colectomy with end ileostomy formation
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MRCS B
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