CPC's - surgical Flashcards

1
Q

Where is the appendix located?

A
  • The base of the appendix extends from the caecum.
  • It is contained within the visceral peritoneum.
  • Its exterior layer is dervived from the taenia coli where the 3 tenaia coli meet at the base of the caecum.
  • 2cm from the ileo caecal vavlve
  • Average length 8-10 cms
  • Can sit:
    • Retro-caecal (65-70%)
    • Pelvic (25-30%)
    • Pre- or post-ileal (5%)
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2
Q

How does inflammation of the appendix cause pain?

Where is the pain felt and why?

A
  • Obstruction causes pressure within the lumen, if continued the presssures oversomes that oft he appendiceal vein, leading to venous outflow obstruction.
  • Ischemia begins, if this worsends, thrombosis of the appendicular artery and vein leading to perforation and gangrene
  • Midgut visceral discomfort = periumbilical
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3
Q

What are the common symtpoms of appendicitis in addition to pain?

A
  • Periumbilical colic
  • Pain shifting to the right iliac fossa from periumbilical region
  • Anorexia and Nausea - from dismotility of the gut
  • Tenismus: a continual or recurrent inclincation to evacute the bowels
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4
Q

What findings on physical examination suggest a diagnosis of appendicitis?

A
  • General: Fetor (foul odor), fever, tachycardia
  • Right iliac fossa: tnederness and guarding maximal over McBurney;s point, rebound tenderness
  • Rectal exam: tender anteriorly and to the right in 30%
  • Other: pressure in the left iliac fossa produces pain in the right iliac fossa (Rovsings sign)
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5
Q

What are the DDx for Right Iliac Fossa pain?

Should be able to come up with 15.

A
  • Things that kill you: Ectopic pregnancy (young), AAA (old)
  • Most likely diagnosis: Appendicitis, mesenteric adenitis, gastroenteritis, Meckel’s diverticulitis
  • Renal: UTI, renal colic, acute pyelonephritis
  • GIT: Crohns disease, bowel obstruction, cholecystitis, peforated peptic ulcer
  • Gynae: Salingitis, ovarian cyst, ovarian torsion (testicular torsion), pelvic inflammatory disease
  • Other: Right lower lobe pneumonia, shingles
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6
Q

What questions need to be ask when a patient presents with RIF pain?

A
  • SOCRATES
  • Other symptoms: nausea and/or vomiting, changes in bowel habit
  • Surigcal and medical Hx: esp previous operations, IBD
  • Gynae: sexual activity, last period
  • Preparation for surgery: (5 important questions)
    • Medications
    • Last ate or drunk?
    • Bleeding disorders
    • Significant cardioresp illness
    • Consent
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7
Q

What investigations would you order to confirm a diagnosis of acute appendicitis and rule out DDx of RIF pain?

A
  • UECs: dehydration and renal function
  • FBC: leucocytosis, bleeding risk, anaemia
  • Serum ßHCG: pregnancy
  • Urine analysis: blood, proteint, leucocyte esterase (UTI) and ßHCG (note +ve urinalysis may be found in appendicitis due to secondary ureteruc inflammation)
  • US RIF
  • CT Abdo
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8
Q

What are the similarities and differences between the appendix and large bowel?

A
  • Similarities: presence of large bowel mucosa, submucosa, lamina propria, muscularis mucosae, muscularis and adventitia.
  • Differences: adolescent appendix has prominent lymphoid tissue, there are no Peyer’s patches in the infantile appendix
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9
Q

Desscribe what an acute appendix looks like microscopicaly?

A
  • Exudate in the lumen
  • Focal ulceration of the mucosa
  • Neutrophilic infiltrate within the wall
  • Serosal inflammation
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10
Q

How do you differentiate between acute and chronic inflammation?

A
  • Acute inflammation = presence of neutrophils
  • Chronic inflammation = presence of lymphocytes, plasma cells, macrophages.
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11
Q

Define:

  • Perforation
  • Necrosis
A
  • Perforation: an abnormal opening, especially in a hallow organ
  • Necrosis: death of cells in a restricted portion of tissue due to irreversible damage, recognisable by autolytic changes. Histologically this appears as eosinophilic amorphous material, as all of the nuclear details is lost in the dead cells.
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12
Q

What are the possible outcomes of acute inflammation?

A
  • Resolution with or without fibrosis
  • Progression to gangrenous appendicitis with necrosis, perforation and peritonitis
  • Abscess formation
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13
Q

What it the management of acute appendicitis?

A
  • Do nothing
  • Medical:
    • If uncomplicated can treat with Abx and delay surgery for 24-48Hrs
      • Benefit: establish dx, exclude differentials
      • Risk: perforation → peritonitis → long term complications (e.g. infertility, adhesions, retroperitoneal fibrosis)
  • Surgical:
    • Surgical drainage
    • Appendectomy
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14
Q

What are the neoplastic and non neoplastic tumours of the appendix?

(Draw table)

A
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15
Q

Describe what can been seen in this microscopic picture?
What is it?

A

Normal appendix

  1. Mucosa
  2. Submucosa
  3. Muscularis propria
  4. Adventitia/serosa
  5. Arrows: lymphoid tissue in the mucosa and submucosa
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16
Q

What are the arrows pointing to?
What is this a picture of?

A

Normal appendix

  • Top arrow: large bowel type glandular epithelium
  • Bottom arrow: lymphoid follicle
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17
Q

What is this and why?

A

Normal appendix of a 3 month old.

Lymphoid tissue not seen in infantile bowel.

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18
Q

What is occuring in this appendix?

A

Wall thickening due to haemorrhage, oedema and a neutrophilic infiltrate.

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19
Q

What are the differential of right upper quadrant pain?

(At leat 15 DDx)

A
  • Things that will kill you: MI, perforated duodenal/gastric ulcer, AAA dissection, pancreatitis
  • Most likely diagnosis: Acute or chronic cholecystitis,
  • Anatomicaly:
    • GIT: Cholelithiasis, cholangitis, cholecystitis, biliary colic, acute hepatitis, bowel obstruction, appendicitis, liver abcess
    • Resp: RLL pneumonia, pleurisy, tension pneuothorax, subdiaphragmatic abscess, PE
    • MSK: muscle injury
    • Renal: Pyelonephritis, renal colic
    • Gynae: endometriosis
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20
Q

What information would you like to know from a patient who presents with RUQ pain?

A
  • SOCRATES
  • PMHx:
    • gallstones, cholecytectomy IBD, small bowel resection, dyslipidaemia, haemolytic anaemia, sickle cell disease
    • Smoking, alcohol, meds (OCP, HRT, fibrates), allergies
  • FHx
  • POSH
  • Preparation for surgery:
    • medications
    • late ate or drank
    • bleeding disorder
    • significant cardiorespiratory illness
    • consent
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21
Q

What investiagtions would you order for RUQ pain?

A
  • FBC: leucoytosis, anaemia, platelets for bleeding risk and inflammation
  • UECs: renal function, dehydration
  • LFTs: Cholestatic pattern?, hepatitis?, NAFLD?
  • Lipase/amylase: pancreatitis
  • Coags: rule out coagulopathies
  • AXR: to rule out bowel obstruction, calcified AAA
  • US: gallbladdder, liver and biliary tree
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22
Q

What are the consequences and complications of inflammation in the gallbaldder?

A
  • Consequences: resolution, chronic inflammation, abscess formation, necrosis/gangrene
  • Complcations: empyema, perforation of the gallbladder, peritonitis, fistula formatiopn, gallstone ileus, septicaemia, adhesions, death
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23
Q

How do you manage a patient who has acute cholecystitis secondary to cholelithiasis?

A
  • IV access: IV fluids and IV Abx - ceftriaxone or gent + amoxy
  • Nil by mouth
  • Oxygen
  • Analgesia: paracetamol 1g PO or oxycodene 5-10mg PO
  • Monitor change in vitals or pain and fluid loss
  • Consent and book for surgery
  • DVT prophylaxis
  • Medical: Oral dissolution therapy to dissolve gallstones
    • Limted success high recurrence of gallstones
    • Medications may have SE on liver
  • Surgical: Cholecystecomy
    • Benefits (laproscopic): better cosmesis, earlier return to work, shorter hospital stays, lower costs, lower mortality, less post-operative pain
    • Relative contraindications (laproscopic): Obesity, pregnancy, end-stage cirrhosis, previous surgery, sepsis.
    • Complications of cholecystecomy:
      • Leakage of bile
      • injury to surrounding structures
      • Missed stones - jaundice
      • Cholangitis or associated pancreatitis, haemorrhage
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24
Q

Describe the histology of a normal gallbadder?

A

Layers:

  1. Mucosa: thrown into folds and bearing short irregular microvilli = uneven surface
  2. Submucosa
  3. Muscular layer (not forming distinct layers as in the bowel
  4. Serosa
  5. Epithelial lining consists of columnar cells with basally orientated nuclei
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25
Q

What does this gallbladder show? and how does it differ from a normal gallbladder?

A

The gallbladder demonstrates features of acute inflammation, necrosis and perforation.

  • The gallbladder wall is thickenedby fibrosis, in areas there is full thickness necrosis of the wall, an acute inflammatory infiltrate of neutrophils is seen, the mucosa is mostly replaced by necrotic debris.
  • The findings that differ from anormal gallbladder are the thickness of the wall, presence of an inflammatory infiltrate and necrosis.
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26
Q

Define metasplasia.

A

An adaptive transformation of one type of adult fully differentiated tissue into another type of differentiated tissue, not native to the site. Usually induced by a noxious stimulus and represents an adaptive change. May be physiologic as in the uterine cervix, or pathologic as in Barrett’s oesophagus.

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27
Q

Define dysplasia.

A

Atypical cellular differentiation occuring as a response to chronic noxious stimulus; neoplastic bu pre-invasive; may be observed in the sequence of cellular responses to a potential carcinogen.

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28
Q

What are the potential complications of cholelithiasis?

A
  • Cholecystitis - acute or chronic
  • Choledocholithiasis
  • Pancreatitis
  • Fistula formation
  • Gallstone ileus
  • Carcinoma of the gallbladder
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29
Q

What is cholangitis? and what can cause it?

A

Inflammation of the biliary tree. Common causes include:

  • Primary: sclerosing cholangitis
  • Secondary:
    • Biliary obstruction
    • Postoperative stricture
    • Chronic pancreatitis
    • Infections
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30
Q

What are the different tumours of the gallbladder?

(Write up table)

A
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31
Q

What is Calot’s triangle? Why is it important?

A

Calot’s triangle is a triangle space, bordered superiorly by the inferior edge of the liver medially by the common hepatic duct and laterally by the cystic duct, where the cystic artery may be found. It helps the surgeon to identify the cystic artery.

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32
Q

What is the pathogenesis of cholesterol stone? and what are the risk factors?

A

Bile supersaturated with cholesterol leads to precipitation of choelsterol into crystals, which then form gallstones. Pigmented stones are associated with cirrhosis, haemolysis and biliary tract infection.

Risk factors: female, fat, forty and fertile

Also: oral contraceptives, bile stasis, chronic haemolysis, cirrhosis, infection, rapid weight loss, inflammatory bowel disease, terminal ileum resection, total parenteral nutrition, hyperlipidemia, somatostatin therapy.

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33
Q

What are the differential for central colicky abdominal pain?

A
  • Things that kill: AAA, ischaemic gut
  • Most likely DDx: gastroenterititis, intestinal obstruction
  • Midgut structures: - intraluminal, luminal, and extraluminal causes.
    • Gastroenteritis, dulcer ulcer, pancreatitis, intestinal obstruction, ischaemic small or large bowel, inflammatory bowel disease.
  • Referred pain: appendix
  • Expanded differential:
    • renal colic, UTI with pyelonephritis, ectopic pregnancy, twisted or ruptured ovarian cyst, endometriosis.
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34
Q

What further information would you need on a patient with RUQ pain?

A
  • SOCRATES for pain
  • Changes in bowel habits - diarrhoea, with blood /mucus, constipation, obstipation, colour of stool, pain on defication, difficulty in defaecation
  • Vomiting: fresh blood, coffee ground, bile, feculent, quantity, frequency.
  • Fevors, rigors, sweating
  • Weight loss, anorexia
  • O&G Hx: last menstruation cycle, ?pregnancy
  • PHx: previous abdominal surgery, inflammatory bowel disease, renal colic, hernia
  • FHx: colonic tumours
  • Smoking, alcohol, medications (NSAIDs, corticosteroids, ACE inhibitors)
  • Fitness for surgery:
    • When last ate or drank
    • medications - allergies
    • significant medical disorders esp cardiorespiratory illness
    • bleeding risks
    • blood test results
    • is hte patient stable - ie have they been resuscutated re fluids etc.
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35
Q

What would you look for on physical examination in a patient with potential small bowel obstruction?

A
  • Signs of obstruction:
    • Crampy abdominal pain
    • Vomiting
    • Reduced bowel sounds
    • Loss of appetite
    • Constipation/ unable to pass gas
    • Swelling of abdomen
  • Signs of the cause of the obstruction:
    • Previous surgery: postsurgical adhesions
    • Incarcerated groin hernia
    • malignant tumour (20%)
    • Hernia (10%)
    • IBD (5%)
    • Volvulus (3%)
  • Degree of hydration
  • Signs that the obstruction has become complicated
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36
Q

What investigations would you order if you suspect a small bowel obstruction? and why?

A
  • EUC: hydration status, renal function for surgery
    • if patient has been vomiting: metabolic acidosis - hypochloremic alkalosis, sometimes hypokalemic too.
  • FBC: Hct dehydration, infection, anaemia
  • ßHCG: rule out pregnancy
  • Amylase/lipase: rule out pancreatitis
  • Lactate: non specific for tissue damage
  • CXR supine and upright
  • Contrast enema
  • CT abdo
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37
Q

How do you tell at what level the bowel has been obstructed?
Clinically
Radiologically

A
  • Clinically: location of pain, frequency of colic, history to explain of obstruction.
  • Radiologically:
    • Small bowel obstruction: central location of distened loops of bowel, complete plicae circulares.
    • Large bowel obstruction: plicae semilunares of the large bowel are only partially around the inner circumferes
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38
Q

What does a closed loop obstruction lead to?

A

Strangulation of the bowel with subsequent necrosis.

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39
Q

What is the management of a small bowel obstruction? 7 points

A
  1. IV cannulation
  2. IV fluid and electrolyte resuscitation - lots of vomiting = K+ replacement
  3. NBM
  4. monitor fluid losses:
    1. NGTinsertion and suction or
    2. Urinary catheter
  5. Monitor vital signs, changes in character of pain
  6. Analgesia
  7. Consent for surgery
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40
Q

What part of the body is this?

A

Normal small bowel

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41
Q

What part of the body is this and what is the pathology?

A

Carcinoid tumour of small bowel.

Cytological features: The cells of the carcinoid ttumour are relatively uniform, with small amounts of pink finely granular cytoplasm. The nuclei are round and contain strippled chromatin.

Architectural features: Characteristically carcinoid tumours grow in small nests or trabeculae of cells. Glandular structures and sheets of cells may also be seen.

A Dx of a carcinoid tumour and decides to order immunohistochemistry (IPX’s)

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42
Q

What is a carcinoid tumour?

A

A tumour arising from neuroendocrine cells.

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43
Q

What are the principles of immunohistrochemistry? What is the role of immunohistochemistry in a carcinoid tumour?

A
  • Immunohistochemistry aims to demonstrate specific tissue antigens, e.g. cytokeratin filaments of epithelial cells, with peroxidase or fluorescent markers
  • Specific antibodies are manufactured against specific tissue antigens, and then these antibodies are bound to colour-marking-systems (peroxidase or fluorescence) that allow detection of positive cases on tissue sections.
  • Immunohistochemistry is principally used when light microscopy and histochemical stains are unable to illustrate sufficient features to confidently diagnoise a lesion.
  • Immunohistochemistry is employed in the case of a carcinoid tumour to allow for an accurate diagnosis.
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44
Q

What colour do tumour cells stain? Carcinoid tumour.

Where is the stain located - in the cytoplasm or nucleus of cells?

What colour are the mucosal epithelial cells of the small bowel?

A
  • Tumour cell stain brown and the positive staining is located within the cytoplasm.
  • Cytoplasmic staining occurs as this is where the neurosecretory granules, identified by immunohistochemistry, are located.
  • The mucosal epithelial cells stain blue, due to the presence of hamatoxylin only counter stain. This allows the pathologist to see the basic cytological and archicetural features of the underlying tissue when interpreting the immunohistochemical staining pattern.
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45
Q

What are the clinical features of someone with a carcinoid tumour?

A

ABCDEF

  • Abdominal pain
  • Bronchospasm
  • Cardiac features (valvular disease)
  • Diarrhoea
  • Elevated urninary 5-HIAA
  • Flushing
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46
Q

Typically where are carcinoid tumours found?

A

In order of frequency, carcinoids may occur in the appendix (35%), ileum (28%), rectum (13%), and bronchi (13%). Incidence is less than 1% in the pancreas, gallbladder, liver, larynx, testes, and ovaries; however, tumors in these locations frequently metastasize and spread through the mesenteric lymph nodes and portal vein.

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47
Q

What test can be used to monitor carcinoid syndrome?

A

Urinary 5-HIAA

Carcinoid tumours secrete seratonin and the metabolite of this, 5-hydroxyoxyindole acetic acid, and is excreted in urine and is one means of confirming a suspected diagnosis of carcinoid tumour.

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48
Q

What are the surgical and medical treatments of a carcinoid tumour?

A
  • Surgical: resection of the tumour is the best treatment if feasible, this will reduce tumour mass and obtain symptom remission.
  • Medical:
    • Somatostatin analog such as octrotide (serotonin antagoist) can ne considered. This relieves the symptoms in 85% of cases and may lead to tumour shrinkage in a small number of patients.
    • Chemoembolisation and embolisation with spheres can be used
    • In non-resectable tumours chemotherapy can be used

Patients with metastatic disease or carcinoid syndrome there is a 50% 3 year survival.

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49
Q

What features are important in determining the prognosis of a carcinoid tumour?

A
  • No reliable histologic or molecular markers exist to distinguish benign and malignant behaving carcinoid tumours. Metastatic disease is the only true marker of malignacy. Vascular invasion and destructive growth into adjacent organs are also considered markers of malignancy.
  • In some carcinoid tumours the behaviour can not be predicted from hte morphologic findgins, these tumours may then be designates as having ‘uncertain malignancy potential’
  • However, a tendency for aggressive behaviour correlates with: tumour site and size, depth of invasion, presence of necrosis and mitoses.
  • Bad prgnostic factors = ileal/gastric/colonic tumour, >2cm, increased mitosis and presence of necrosis.
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50
Q

Are all carcinoid tumours malignant?

A

No, in particular those occuring in the appendix and rectum usualy have a benign course and are cured by local exicison.

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51
Q

What other tumours occur in the small intestine?

Draw table

A
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52
Q

What are the DDx of a breast lump?

A
  • Mastitis
  • Breast abscess
  • Cyst: galactocele, fibrocystic disease
  • Solid lumps: Fibroadenoma, fat necrosis, lipoma, cystosarcoma phylloides
  • Malignant: Carcinoma
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53
Q

What further information would you seek from a history in a patient with a breast lump?

A
  • Lump history
  • Period history: info about pre, post or peri menopause, menarche
  • Children history: number of children, breast feeding?
  • FHx: breast disease, other disease
  • PMHx: risk factors for surgery
  • Meds: OCP, aspirin, NSAIDs and natural products such as fish oil (bleeding risk)
  • SHx: occupation, supports
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54
Q

What features would you look for on physical examination in a patient with a brest lump?

A
  • Look at both breasts - sitting/lying +/- manoeuvres
  • Feel other breast and feel lump and note:
    • Site, size, shape of lesion, skin changes including peau d’Orange, breast and/or nipple asymmetry, nipple changes, inversion, retraction.
  • Squeeze nipple: for discharge
  • Examine both axillary and supraclavicular lymph nodes, +/- liver
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55
Q

What investigations are appropriate for a breast lump?

A
  • US for younger patients (<35 yo)
  • Mammogram for older patients (>35 yo)
  • MRI may be useful in patients with breast implants
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56
Q

What is fine needle aspirate cytology?

Who performs a FNAC?

How helpful is it in the diagnosis of a breast lump?

A
  • FNAC is the microscopic study of single cells obtained by sampling a lesion with a narrow gauge (23 or 25) needle. Usually several passes are madwe into the lesion and the aspirated contents are smear onto a slide. The slide is then stained and the cells examined using a light microscope.
  • Pathologists, radiologists or surgeons usually perform FNAC
  • FNAC is helpful as it may provide a diagnosis. Needs to be taken in light of the clinical and radiological findings, as false positives and false negative diagnoses accur. It allows for triaging of the lesion, neoplastic vs non neoplastic, benign vs malignant, cell type.
  • Because of the limitations of FNAc it forms paret of the triple test (clinical, radiological and pathological assessment) and the result should be interpreted in light of the results of these other investigations.
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57
Q

WHat should you tell the patient about FNAC?

A

Patient needs to know:

  • Why the test is being done
  • What the test involves
  • Risks and complications of the test
  • Limitations of the test
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58
Q

What are the risks and limitations of FNAC?

A
  • Risk: Bleeding, pneumothorax, pain, infection
  • Limitations: leading to no diagnostic, false positive or false negative results.
    • Operator: does not hit lesion
    • Technical: non-diagnostic, too much blood, crushed cells, problems with staining
    • Pathologist: incorrect interpretation
    • Nature of lesion: unable to differentiate between in situ vs invasive malignancy, papillary lesions, mucinous lesions.
    • Other traps: mimica - fat necrosis, nodular fasciitis, cellular fibroadenoma.
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59
Q

How does FNAC differ from core biopsy?

A
  • FNAC gives cytological information, but is limited in that it does not give information about the surrounding structures.
  • Core biopsy takes a sample of tissue, where both cytology and surrounding architecture is available for examination.
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60
Q

What is this tissue?

A

Normal breast tissue

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61
Q

What type of tumour of the breast is this?

A

Fibroadenoma

Benign neoplasm. Proliferation of both glands and stroma. Stromal proliferation frequently distorts the glands into complex anastomosing, ribbon-like profiles as above.

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62
Q

What tumour of the breast is this?

A

Fibroadenoma

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63
Q

What tumour of the breast is this?

A

Lobular carcinoma in situ.

Neoplastic proliferation of epithelial cells confined to the termial duct lobular unit. Has a distinctive “bags of marbles” appearance. Cells are small, uniform, bland and distend the acinar units

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64
Q

What tumour of the breast is this?

A

Ductal carcinoma in situ

Ducts distended by large malignant cells with central necxrosis and calcification (comedo necrosis).

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65
Q

What tumour of the breast is this?

A

Invasive lobular carcinoma.

Invasive malignant tumour of breast epithelial cells. Small and uniform malignant cells, showing minimal nuclear atypia. Note “file pattern of infiltration and absence of gland formation.

66
Q

What is carcinoma in situ? What might be the clinical consequence of a diagnosis of lobular carcinoma in situ?

A

Carcinom in situ (CIS) is breast carcinoma that is confined by the basement membrane to the duct or lobule and is therefore not invasive. The importance of this is that due to the absence of invasion, the neoplastic cells will not have metastasied and therefore CIS carries a better prognosis than invasive carcinoma.

Lobular carcinoma in situ (LCIS) refers to CIS found within the terminal duct-lobular unit (the breast lobules as opposed to the ducts). It has a distinctive morphology and comprises lobules expanded by atypical cells, which are usually small and loosely cohesive. LCIS is mutlicentric in ~85% of patients and bilateral in ~30% of patients.

The relative risk of development of invasive cancer in patients with LCIS is approximately 12 times that of the background population. The subsequent cancer may demonstrate either lobular or ductal morphology. Both the ipsilateral and contralateral breast show a similar risk of developing invasive carcinoma.

67
Q

What is a sentinel node biopsy?

A

Sentinel node biopsy is where the primary drainage lymph node is identified by a dye (usually methylene blue) and/or a radioactive substance, and examined to see if it contains metastatic disease. the node is localised by injecting dye into the primary breast tumour, dye then travels via the lymphatics to the sentinel node.

68
Q

What is the sentinel nodes roles in breast cancer management?

A

The sentinel node needs to be processed and examined carefully to ensure small metastases are identified. A disease-free sentinel node assumes that the cancer is confined to the breast and axillary clearance is therefore not performed.

69
Q

What are the risk factors for developiong breast cancer?

A
  • Increasing age
  • Young age at first menarche or late menapause (total oestrogen time)
  • Nulliparous or older than 35 yo for first live birth
  • First degree relative with breast cancer
  • BRCA1 or BRCA2 gene mutations
  • HRT or OCP use
  • Radiation exposure
  • PMHx of atypical proliferative breast disease
  • Lifestyle factors – Adult weight gain, sedentary lifestyle, alcohol consumption
70
Q

What is a clinical multidisciplinary team?

Who is in the team for the management of breast cancer?

A

A team of health professionals from diverse backgrounds that come together and combine their expertise, to most effectively manage the disease of an individual patient.

  • Radiologist
  • Surgeon
  • Pathologist
  • Oncologist (medical and radiation)
  • Specialist nursing staff
  • GP
71
Q

What are the DDx of a neck lump?

A

Best to think of these is 3 broad categories: Congenital, inflammatory, neoplastic.

Congenital:

  • Branchial cleft cyst
  • Thyroglossal duct cyst
  • Vascular anomalies: Haemangiomas, vascular tumour.
  • Laryngocele
  • Ranula
  • Teratoma
  • Dermoid cyst
  • Thymic cyst

Inflammatory:

  • Reactive viral lymphadenopathy
  • Bacterial lymphadenopathy
  • Parasitic lymphadenopathy
  • Non-infectious disorders: Sarcoidosis, Kawasaki disease

Neoplastic:

  • Metastases: Squamous cell carcinoma
  • Thyroid/parathyroid cancers
  • Salivary gland neoplasm
  • Carotid body tumour
  • Paragangliomas
  • Schwannoma
  • Lymphoma
  • Lipoma and beign skin cysts
72
Q

What information would you seek from a patient who presents with a neck lump?

A
  • Local effects of the lump: pain, hoarseness, rapid growth, dysphagia, pressure, discomfort.
  • Symptoms of hyperthyroidism: decrease weight, increase appetite, tremor, irritability, increase sweating.
  • Symptoms of hypothyroidism: increase weight, constipation, menorrhagia, hoarse voice, lethary, depression and dementia
  • FHx: MEN, non-MEN medullary cancers, familial papillary cancer, familial hyperparathyroidism.
  • SHx: smoking?
  • PMHx: previous malignancy, radiation therapy, surgery
  • Fitness for surgery.
73
Q

What features would you look for on physical examination?

A
  • Characteristics of lump: size, site, consistency, mobile or fixed, moves with swallowing, moves with protruding tongue.
  • Signs of hyper and hypothyroidism
74
Q

What investigations would you order for a patient with a neck lump?

What follow up tests would you order?

A

Inital:

  • Thyroid function tests: check thryroid function
  • Parathyroid hormone: check parathyroid function
  • Serum calcium: check parathyroid function
  • US lump
  • FNAC if needed

Follow up: Depending on results

  • Non contrast CT
  • MRI
  • PET for malignancy
  • Radio-iodine
  • Vit D
  • 24 hour calcium excretion
  • Serum and urinary catecholamines if paraganglioma is suspected
75
Q

How helpful is a FNA in the diagnosis of a thyroid lesion?

A

FNA is a simple test that will provide information regarding the nature of the mass. It out performs US, TFTs, clinical evaluation and radioactive iodine scans in determining a diagnosis.

76
Q

What do you need to tell a patient about FNA of a thyroid lesion?

A

Patients need to know:

  • Why the test is being done
  • What the test involves
  • Risks and complications of the test
  • Limitations of the test

Risks:

  • Haematoma formation with possible tracheal compression
  • Puncture of the carotid: requires compression for at least 5 mins
  • Puncture of the trachea: generally leads to transient coughing
  • Temporal laryngeal nerve paresis
  • Haemorrhagic necrosis of tumours esp, adenomas, meaning histological examination is limited
  • Needle tract implanatation is rare
  • Infection is rare

Limitations:

  • Non diagnostic: blood/paucity of cells
  • False negative: does not sample lesion, unable to distinguisj follicular adenoma vs carcinoma
  • False positive: multinodular goitre vs follicular neoplasm
77
Q

What further investigations are needed of a thyroid mass before surgery?

A
  • Radioactive iodine scan may be considered to show whether the lesion is functioning (hot nodule) or non functioning (cold nodule)
  • CT scan may be performed to look for any obvious metastatic disease prior to surgery.
78
Q

Describe what is involved in producing a frozen section.

A

A frozen section is produced by freezing a small amount of tissue in a mixture of dry ice and acetone. The tissue is then sectioned on a special microtome called a cryostat, which keeps the tissue frozen. Frozen sections are used to give an intraoperative diagnosis while hte patient is anaesthetised. they are performed when the surgical management depends on what the diagnosis is i.e. follicular lesion vs papillary carcinoma.

79
Q

What tissue is this?

A

Normal thyroid

Composed of follicles. Each follicle appears as an irregular circle of cells lined by simple cuboidal epithelium. Follicles are filled with a colloid. Between these follicles are the parafollicular cells which produce calcitonin.

80
Q

What type of pathology is this?

A

Follicular adenoma

Follicles of varying size, compresses surrounding tissues, increased cellularity.

81
Q

Can FNA destinguish between follicular adenoma vs follicular carcinoma of the thyroid?

A

No, it can only diagnose a follicular neoplasm.

82
Q

What histological information is needed to distinguish between a follicular adenoma and a follicular carcinoma of the thyroid?

A

For a diagnosis of carcinoma you need:

  • Capsular invasion
  • Vascular invasion
  • Metastatic spread

Therefore histological analysis of the excised specimen is necessary to differentiate adenoma from carcinoma.

83
Q

What type of pathology is this?

A

Papillary carcinoma

The tumour is composed of papillary fronds and monolayered sheets surrounded by a thick fibrous capsule.

Cellular features of papillary carcinoma:

  • Overlapping nuclei
  • Nuclear inclusions
  • Nuclear grooves
84
Q

What are the differences between frozen and paraffin sections?

A

Frozen section causes:

  • Ice artefact: water within the tissues expands when frozen, distorting some cellular and architectural features.
  • Shattering of the section: as frozen sections are technically harder to cut than paraffin sections.
85
Q

What key macro and microscopic features should be present in a pathology report of a thyroid neoplasm?

A
  • Macro: Location and size of nodule, ?circumscribed, appearance if the cut surface, ?calcification, appearance of the adjacent thyroid, ?parathyroid tissue present.
  • Micro: Growth patterns, +/- capsular invasion, +/- vascular invasion, appearance of the adjacent thyroid parenchyma, excision margins.
86
Q

What are the common indications for a frozen section?

A
  • Determine adequacy of resection (surgical margins) during resection of organs with malignancy.
  • Staging: evaluate spread to regional lymph nodes (sentinel nodes in breast).
  • Determine if the tissue with the pathology is sampled. This can be importnat in case of tissue with extensive fibrosis or a diffuse pathology.
  • Distinguish between benign and malignant
  • Primary diagnosis occasionally.
87
Q

How do patients with parathyroid adenoma commonly present?

A

Primary hyperparathyroidism: “Bones, stones, abdominal groans, and psychic moans.”

  • With a raised serum calcium
  • Muscle weakness
  • Bone pain
  • Lethargy
  • Vague pain
  • Depression
  • Disturbance of mental functions
  • Osteopenia or osteoporosis
88
Q

What is the surgical management of parathyroid hyperplasia?

A

Removal of all glands and placement of at least 30 mg of parathyroid tissue within the forearm muscles of the non-dominant arm or into the sternomastoid muscle. This proceduyre retains the function of the parathyroid and allow easy access in the future, if the transplanted gland again becomes hyperplastic.

89
Q

What are the causes of primary, secondary and tertiary hyperparathyroidism?

A

Primary hyperparathyroidism:

  • Increased secretion of parathyroid hormone by the parathyroid gland due to:
    • Adenoma (84%)
    • Primary parathyroid hyperplasia (15%)
    • Parathyroid carcinoma (1%)

Secondary hyperparathyroidism:

  • Increased serum PTH due to chronically low serum calcium, with resulting compensatory hyperplasia of the glands:
    • Renal failure
    • Vit D deficiency

Tertiary hyperparathyroidism:

  • Arises in the setting of longstanding secondary hyperparathyroidism, where there is continued secretion of PTH when the cause of the secondary hyperparathyroidism has been removed:
    • I.e. parathyroids are now acting autonomously
90
Q

What are the DDx for hirsute, central obesity and striae?

A
  • Cushings syndrome (excessive cortisol production) - pituitary adenoma (Cushing’s disease), adrenal hyperplasia with hyperfunction, adenocortical tumours, ectopic source of ACTH (small cell lung carcinoma, islet cell tumours), exogenous/idiopathic source of corticosteroids.
  • Diabetes mellitus
  • Polystic ovary syndrome
  • Liver disease
  • Paraneoplastic disease
  • Androgen produce tumour
91
Q

What further information would you like to know about a patient who presents with:

  • Bruising
  • Increase wright
  • Increase weakness
A
  • Bruising: site, onset, duration of bruising, level of trauma associated, other sites of bleeding e.g. gum, epistaxis, menorrhagia, PR bleeding, melena, FHx, anticoagulants
  • Weight: current weight, any increase in weight and rate of increase, appetite, dietary history
  • Weakness: timing of onset, ?worse at the end of the day, proximal or distal weakness, does it affect ADLs?
  • Other associated features: thirst, infections, visual problems, polyuria
  • PMHx: liver disease, hepatitis, diabetes
  • FHx: esp diabetes, muscular dystrophies, myasethenia gravis
  • Medications: warfarin, NSAIDs, Corticosteroids
  • SHx
  • Fitness for surgery
92
Q

What investigations should be ordered in someone who is suspected to have Cushings Syndrome?

A
  • FBC, platelets, APTT, PT, LFTs: check for coagulation abnormalities for the bruising.
  • HbA1c: rule out diabetes
  • UECs: electrolytes for arrythmias, kidney function for surgery
  • Plasma testosterone/oestrogen and sex hormone binding globulin (SHBG): rule out differentials
  • 24h urine free cortisol levels : diagnostic of Cushings syndrome
  • Low-dosedexamethasone suppression test, evening serum and salivary cortisol level, and dexamethasone–corticotropin-releasing hormone test: diagnostic of Cushings syndrome
  • CT abdo/chest: lesions
  • CT or MRI brain: pituitary tumour
93
Q

What do these results indicate?

What is the next step?

A
  • Hypersecretion of cortisol
  • The next step is imaging studies (CT abdo) to determine whether it is pituitary production og ACTH driving adrenal cortisol secretion or autonomous adrenal cortisol secretion or autonomous adrenal cortisol secretion which is responsible.
94
Q

What tissue type is this?

A

Normal adrenal gland.

95
Q

What tumour type is this?

A

Adrenal cortical adenoma.

The tumour is composed of sheets and cords of eosinophilic and clear cells separated by firbous stroma. The tumour is circumscribed and encapsulated.

96
Q

What tumour is this?

A

Adrenal cortical adenoma.

The cells resemble those seen in the zona fasciculata. Clear, finely granular cells and eosinophilic cells arranged in trabecular. Regular nuclei.

97
Q

What is the organ and what tumour is this?

A

Adrenal cortical adenoma

98
Q

What tumour type is this?

A

Phaeochromocytoma

The tumour is composed of clusters of cells separated by highly vascular stroma. The tumour is encapsulated and haemorrhagic.

99
Q

What tumour type is this?

A

Phaeochromocytoma.

The tumour cells have pleomorphoc nuclei with a prominent nucleolus, moderate amount of finely granular cytoplasm. There is mitotic activity.

100
Q

What are the 7 steps for consent? and how would you gain consent in a patient who needs an malignant adrenal tumour removed?

A
  1. Competent
  2. Explain provisional diagnosis and DDx
  3. Management options:
    1. Do nothing: explain natural history of disease, consequence of no treatment
    2. Do something
  4. Do something: medical or surgical
    1. need to be tailored to the individual patient, taking into consideration, age, size of tumour, renal function, fitness for surgery, patients wishes
    2. laparoscopic versus open
    3. Partial or total removal
  5. Risks of surgery
    1. General surgery: PAIN, wound infection, bleeding, wound dehiscence, DVT/PE, atelectasis, pneumonia
    2. Specific surgical: to that operation damage of adjacent structures especially major vessels including the inferior vena cava
    3. Anaesthetic: death, MI, stroke, aspiration, reaction to drugs (allergy, amaphylaxis), sore throat, damage teeth
    4. Others: blood transfusion, finding something unexpected
  6. Questions patient might have?
  7. Financial consent if private patient
101
Q

Describe the difference between biliary colic, cholecystitis, cholangitis in terms of pain, fever and jaundice?

A
102
Q

Describe the normal histology of the adrenal gland? And what are what hormones are made in which areas?

A
103
Q

Define a non-functional from a functional tumour?

A
  • Non-functional: not actively producing hormones, found incidentially i.e. biochem not normal or found on imaging.
  • Functional: actively producing hormones.
104
Q

A patient with a pituitary or lung tumour could have a similar clinical presentation. Why would this be?

A

Pituitary adenomas and some lung cancers may secrete ACTH, which in turn stimulates steroid production from the adrneal glands. The pituitary may be affcted by an ACTH-secreting adenoma and the lung cancer (usually a small cell carcinoma) may produce ACTH as a paraneoplastic syndrome.

105
Q

What are the key macroscopic and microscopic features that should be present in a pathology report of a surgical specimen?

A
  • Name, age, UR number and clinical history
  • Operation performed and nature of specimen
  • Gross features of specimen: size, site, shape, surface and cut surface, consistency, colour, adjacent/attached structures
  • Microscopic features: tumour type, vascular invasion, extent of invasion and excision margins, ?confirmed metastatic disease, cytologic features e.g. nuclear to cytoplasmic ratio, mitotic figures, necrosis
  • IPX results
106
Q

What is Addison’s disease? What is it caused by?

A

Disease of the adrenal glands leading to destruction of the adrenal glands and adrenocortical insufficiency.

Causes: 80% idiopathic with a propbable autoimmune bases, metastatic disease, TB.

107
Q

Pituitary tumours can secrete other hormones. What are they and what are the names given to the clinical disease they produce?

A
108
Q

What are the different tumour types of the adrenal glands?

(Draw table)

A
109
Q

What are the DDx for a suspicious mole?

A

Most likely:

  • Melanoma
  • Seborrhoeic keratosis
  • Pigmented basal cell carcinoma

Others:

  • Dysplasic naevus
  • Blue naevus
  • Benign melanocytic lesion (mole): e.g. junctional, compound and intradermal
  • Vascular tumour: e.g. haemangioma
  • Spitz naevus (more likely in children)
110
Q

What further information would you like to know about someone who present with a suspicous mole?

A
  • SOCRATES for mole cancer, immnunosuppression
  • POSHx:
    • Lifestyle - sun exposure, occupational, episodes of severe sun damage (especially innm childhood)
  • FHx: of melanoma
  • Age, fair skin that burns easily freckles and doesn’t tan
111
Q

How do you examin a skin lesion?

A
  • Asymmetrical
  • Border
  • Colour
  • Diameter
  • Elevated
  • Firm to touch
  • Growth vertically
  • Ulceration
112
Q

What are some other warning signs of a skin lesion?

A
  • A sore that does not heal
  • A new growth
  • Spread of pigment from the border of a spot to surrounding skin
  • Redness of a new swelling beyond the border
  • Change in sensation: itchiness, tenderness or pain
  • Change in the surface of a mole - scaling, oozing, bleeding, or the appearance of a bump or nodule
113
Q

Once you have looked at a suspicious skin lesion, what else would you need to do on physical exam?

A
  • Full body exam
    • Lynph nodes - drainage area
    • Abdo exam for mets (liver and small bowel)
  • Examine skin type and amount of sun damage
114
Q

What investigation would you consider for a melanocytic lesion? What are the problems associated with partial excision of a melanocytic lesion?

A
  • Melanocytic lesion need to full excision.
  • Punch biopsy and shave excisions are not recommended as they can interfere with pathology analysis.
    • Punch biopsy: risk of false positive or false negatives
    • Shave excision: only part of the lesion is examined and accurate assessment is not possible.
  • Consider lymph node investigation
115
Q

Describe the normal histology of skin.

A
116
Q

Describe the layer of the epidermis.

A
117
Q

Describe the microscopic histological features of a melanocytic lesion that are describe in a pathology report?

A
  • Breslow thickness
  • Clark level
  • Cytological features:
    • High N:C ratio
    • Tumour giant cells
    • Hyperchromatic nucleus
    • Increased mitosis
    • Irregular nucleus size
    • Pleomorphic cells
  • Lymphovascular invasion
  • Perineural invasion
  • Excised margins
  • Prognostic factors:
    • ulceration
    • regression
    • intradermal mitotic rate
118
Q

What type of lesion is this?

A

Melanoma, superficial spreading type.

Malignant tumour of melanocytes. This slide shows a prolieration of malignant melanocytes within the epidermis and dermis associated with brown pigment.

119
Q

What are the key macro and microscopic features should be present in a pathology report?

Particularly for a melanoma

A
  • The patient name, hospital number and specimen site
  • Clinical history
  • Macroscopic description:
    • Orientation
    • Margins
    • Insertion of suture to orientate lesions
  • Type of melanoma
  • Breslow’s thickness
  • Clark level
  • Margin clearance
  • Cellular morphology i.e. spindled vs epithelioid
  • Presence or absence of tumour infiltrating lymphocytes
  • Vascular or perineural invasion
  • Mitotic rate
  • Presence or absence of ulceration
  • Presence or absence of tumour regression
  • Overall diagnosis/summary
120
Q

What are the key features in a pathologty report in terms of prognosis for a melanoma?

A
  • Thickness of the primary lesion
  • Stage of the disease at the time of prognosis
  • Other factors: ulceration, mitotic rate, lymphoid host response, regression, satellite lesions, vascular/lymphatic invasion, tumour cell morphology, age, sex, anatomic site are also taken into consideration.
121
Q

What additional procedures may be helpful in determining if a melanoma has metastasised?

A
  • FNA of an enlarged lymph node
  • Surgical excision of the enlarged lymph node
  • Sentinel node biopsy
  • PET scan for mets - melanoma had the highest glycolytic rate of any neoplasm in humans and whole body PET scanning can demonstrate unsuspected hypermetabolic melanoma mets leading to early therapy.
122
Q

What are the common causes of melanoma?

A
  • Ultra violet light exposure: either through sun exposure or artifical UV sources.
  • High socioeconomic status
  • Phenotypic factors:
    • Fair skin, freckles, fair or red hair.
    • Number of melanocytic naevi
  • Genetic factors:
    • Familial melanoma
    • Xeroderma pigmentosum
123
Q

What are the current theories as to the aetiology of malignant melanoma?

A

It is thought that melanoma evolves from benign naevi via a pathway of hyperplasia and dysplasia. Progressive damage to DNA primarily from UV light leads to genetic mutations resulting in altered cell growth.

124
Q

What are the treatment options for melanoma?

A
  • Surgical excision of primary lesion, sentinel node biopsy and excision of metastatoc deposits
  • Chemotherapy and radiotherapy
  • Interferon and immunotherapy
125
Q

What are the types of melanocytic lesion of the skin?

(Draw table)

A
126
Q

What are the DDx for a ulcer near the eye?

A
  • Basal cell carcinoma
  • SCC
  • Ulcerated actinic keratosis
  • Traumatic lesion
  • Infectious lesion
  • ORF: viral infection causing ulcer
  • Viral wart
  • Merckle cell carcinoma
127
Q

What further information would you like to know about an ulcer near the eye?

A
  • SOCRATES:
    • Timeframe: BCCs grow slow and SCCs groe slightly more quickly
    • Changes over time
      Hx of bleeding and ulceration (has it healed and recurred)
  • PMHx: of non-melanocytic skin cancers
  • FHx:
  • POSHx: occupation
  • Risk factor analysis: radiation exposure, cumulative sun exposure, exposure to trivalent arsenic or tar (increased risk of SCC)
128
Q

What features would you look for on physical examination?

A
  • ABCDEFGU: of skin lesion
  • Examine the rest of the skin
  • Lymph nodes
129
Q

What investigations are appropriate for an SCC or BCC?

A
  • Punch biopsy
  • Shave biopsy
  • If suspicous of melanoma full excision
  • Mohs surgery for removal if cosmetic result needed - referral to plastic surgeon.
130
Q

What are some risk factors for surgical removal of a lesion near the eye?

A

Specific risks of surgery:

  • Cosmetic outcome may be unacceptable to the patient
  • risk of nerve injury
  • To achieve adequate/complete resection of the tumour sacrifice of major structures may be involved (ee.g. underlying bone or glands)
  • May require further reconstructive surgery

General risk of surgery:

  • Haematoma, infection, PAIN, wound dehiscence
131
Q

What are the common causes of SCC?

A
  • Sun exposure
  • Immunosupression
  • Human papilloma virus infection
  • Chronic inflammation i.e. draining sinuses
132
Q

What other organs (besides skin) can develop squamous cell carcinoma?

A

Any organ usually lined by stratified squamous epithelium or that may undergo squamous metaplasia:

  • Oropharynx
  • Oesophagus
  • Anus
  • Vulva/vagina/cervix/uterus
  • Bronchus
  • Conjunctiva
  • Bladder
133
Q

What is PSA a measure of?

What common conditions could results in a slightly elevated PSA?

A
  • Prostate specific antigen, which is a protein produced by prostatic epithelium.
  • PSA is a measure of the amount of prostate specific antigen found within the serum of a patients blood. NOrmally only very small amounts are present, however, in certain disease states the PSA may be elevated.
  • The 1/2 life of PSA is about 3 weeks
  • Normal levels of PSA are defined 0-0.4ng per ml.
  • An elevated PSA can occur due to:
    • Prostate cancer
    • Prostate infection
    • Irritation
    • Benign prostatic hypertrophy
  • PSA may be within normal range in patients with prostatic cancer
134
Q

What factors can influence an accurate PSA result?

A
  • Age: PSA needs to be age specific levels
  • Recent Hx or infection/prostatic instrumentation/ejaculation: can lead to raised levels

PSA results measured over time (PSA velocity) can give valubale information; a change of 0.75ng/ml per year is worrisome, note that there may be substantial short term variation → Interpretation in light of the clinical findings.

135
Q

How do patients with prostate cancer commonly present?

A
  • In the pre-PSA era, patients with prostate cancer commonly presented with symptoms that included:
    • Urinary complaints or retention
    • Back pain
    • Haematuria.
  • With PSA screening, most prostate cancers are diagnosed at an asymptomatic stage.
  • When symptoms do occur, diseases other than prostate cancer may be the cause e.g. benign prostatic hyperplasia:
    • Urinary frequency
    • Urinary urgency
    • Decreased urine stream
  • Incidental findings on Transurethral resection of the prostate (TURP)
  • As the majority of tumours arise in the periphery of the gland obstructive symptoms occur late in the disease.
136
Q

What information would you want from Hx and exam in a patient who has a slightly elevated PSA?

A

Hx:

  • Urinary symptoms: urgency, frequency, dysuria, haematuria, trouble starting or stopping flow, terminal dribbling, reduced stream
  • General wellbeing: weight loss, energy, bone pain
  • PMHx: including prior investigations
  • FHx: particularly father, number of first degree relatives with prostate cancer.
  • Social Hx
  • Assessment for surgery

O/E:

  • Digital rectal examination
  • General examination: ?metastatic disease, fitness for surgery
137
Q

What investigations would you order for a suspected prostate cancer?

A
  • Free PSA and calculate the ratio of free PSA to total PSA: men with prostate cancer the ratio of free PSA to total PSA is decreased. The lower the ratio the greater the probability of prostate cancer.
  • Digital rectal exam: looking for palpable abnormalities of the peripheral aspect of the gland.
  • US guided transrectal biopsies of the protate: should be performed on a aread of palpable or US abnormality, together with random systematic biopsies. Number of biopsies depends on the size of the gland. Important that the peripheral zone is targeted.
138
Q

What are the complications of having a transrectal US biopsy (TRUS)?

A
  • PR bleeding
  • Blood in ejaculate
  • Urinary retention
139
Q

How are Gleason grade and score determined?

A

The Gleason grading system is based on the glandular growth pattern of hte tumour (i.e. the architecture) as identified on a relatively low power magnification. It does not utilise cytological features.

The primary Gleason grade is the moninant pattern of tumour growth, while the second Gleason grade is the second most prevalent growth pattern. As both the primary and the secondary patterns have been found to influence outcome, these are combined to give the Gleason Score.

Primary grade + secondary grade = Gleason Score

i.e. 4 + 3 = 7

140
Q

What information does the Gleason score indicate about the disease?

A
  • The higher the Gleason score the more liekly there is to be metastatic disease, particulalry >8.
  • The Gleason score along with the stage is the best marker for predicitng prognosis.
141
Q

Besides the Gleason score what other factors are associated with metastatic prostate cancer?

A
  • High inital PSA
  • Multiple core biopsies containing cancer
  • Approx 40% of patients have metastatic disease at presentation.
142
Q

How would you investigate for metastatic disease in a patient with prostate cancer?

A
  • Bone scan
  • PET scan
  • CT chest and abdo
  • MRI pelvis in some cases
143
Q

What are the risks and benifits of having a radial prostatectomy?

A

Risks:

  • Specific risks:
    • Incontinence (1-2%): leakage often subsides after 6-12 months
    • Erectile dysfunction (50%): this is getting better with surgical advances
    • Damage to the adjacent structures
  • General surgical:
    • PAIN
    • Wound infection
    • Bleeding
    • Wound dehiscence
    • DVT/PE
    • Atelectasis, pneumonia
  • Anasthetic risks:
    • Grave: death, MI, stroke, aspiration, reaction to drugs (allergy, anaphylaxis)
    • Less grave: sore throat, damage teeth
  • Other risks:
    • Blood transfusion
    • Finding something unexpected - what to do

Benefits:

  • Potential cure
  • Control of local disease
144
Q

What organ is this from?

A

Normal prostate gland

Comprises prostatic glands and fibromuscular stroma.

145
Q

What organ is this from?

A

Normal prostate gland

Note the two layers of epithelial cells lining the glands and smooth muscle within the stroma. Basal layer = myoepithelial cells.

146
Q

What type of tumour is this?

A

Prostatic adenocarcinoma.

Shows prostate gland within which prostate acinar adenocarcinoma is seen. Small well defined glands (Gleason grade 3) and cribriform areas (Gleason 4) are present.

147
Q

What are the other treatment modalities available for the treatment of prostate cancer, including metastatic prostate cancer?

A
  • Active surveillance v watchful waiting
  • Hormonal therapy:
    • Medical: androgen blockade with oestrogen diethylstilbesterol (DES) or Luteinizing hormone-releasing hormone (LHRH) agonists
    • Surgical: castration (orchidectomy)
  • Radiation therapy:
    • External beam: may be used at any stage of cancer, if localised then treatment is given with intent of sure (T1-3). Can relieve symptoms in metastatic disease.
    • Brachytherapy: involves implanting radioactive seeds directly into the prostate.
148
Q

What are the risk factors associated with prostate cancer?

A

The exact cause in unknown.

  • Race: Higher in African Americans than Caucasians
  • Age: increased incidence with age, increases in men over 70
  • FHx: the risk is proportional to the number of close relative with prostate cancer
  • Hormone levels: testosterone levels, unknown how this increases risk
  • Environmental influences: many candidates none yet proven to be causative
149
Q

List the zones within the prostate and the zone more susceptible to developing malignancy.

A
  • Peripheral zone: acinar prostatic adenocarcinoma
  • Transitional zone: ductal prostatic adenocarcinoma
  • Central zone: BPH
150
Q

What factors are thought to be protective for prostate cancer?

A

Dietary factors - lycopenes (found in tomatoes), Vit A, Vit E, selenium, soy products.

151
Q

What would you say to a patient wanting to know if there is anything they can do to prevent prostate cancer?

A

Current research has not shown any particular avoidable risk factors associated with prostatic carcinoma. However, it is suspected that certain dietary habits may be associated with the development of cancer in general. Fats especially those from animala sources, increase the risk of several cancers. On the other hand, foods such as green vegetables and fresh fruit may protect people against developing some cancers. The following advice could be given:

  • Enjoy a variety of foods
  • emphasise cereals, breads and other grain products, vegetables and fruits
  • lower fat dairy products, leaner meats, and foods prepared with little or no fat
  • Regular exercise and maintaine a healthy weight.
152
Q

Why is the PSA not recommended as a screening test for prostate cancer?

A

PSA testing is of unknown value as population-screening test. Although there is good evidence that it increases the detection rate of early stage, clinically significant prostate cancer, there is little evidence to date that such early detection leads to reduced mortality; the “gold standard” for evaluating screening tests.

153
Q

Patient presents with change in urine colour and vague lower back pain.

What information would you like from the history?

A
  • SOCRATES - pain/urine changes
    • macro vs microscopic haematuria
    • painful vs non painful haematuria
    • timing of the bleeding ? fresh or old blood
  • Urinary symptoms: duration and timing of colour change, nature or colour change, difficulty initiating micturition, poor flow, terminal dribble, dysuria.
  • General symptoms associated with malignancy: weight loss, fever, bone pain, paraneoplastic syndromes.
  • Features of anaemia: SOB, palpitations, conjunctival and palmar pallor
  • PMHx and Meds: rifamycin, isoniazid (causing colour change in urine)
  • FHx: especially of renal cancer, Von Hippel-Lindau syndrome
  • SHx: smoking, exposure to chemicals and dyes
154
Q

What investigations would you order for someone with haematuria?

A
  • FBC
  • UECs
  • Coags
  • Mid stream urine MCS
  • Urinary cytology: mid morning voided urine sample x3 on different days, can not be the first void of the day
  • 24 hour creatinine clearance
  • CT abdo with contrast
  • urogram noncontrast - detect stones
  • US guided renal biopsy
155
Q

What tissue type is this?

A

Normal kidney

The renal parenchyma is composed of functional units called hte nephron, and connective tissue, the interstitium. The cortex contains the glomeruli, the medulla contains the tubules. The proximal tubule is lined by tall cuboidal-to-columnar epithelial cells contianing many mitochondria (stained pink) and a prominent brush border. The distal tubule is lined by cuboidal epithelium that lacks a brush border.

156
Q

What type of tumour is this?

A

Renal cell carcinoma

This tumour arises from tubular epithelium. It is solid and cystic. in the solid areas the tumour cells form sheets, cords and solid ducts.

157
Q

What type of tumour is this?

A

Transitional cell carcinoma.

The tumour arises from the transitional epithelium lining the collecting system. It has a papillary architecture and is non invasive.

The tumour cells have irregular nuclei with usually small nucleoli. The cytoplasm is relatively abundant and solid, not clear. Variable numbers of mitosis are seen. Necrosis and haemorrhae are uncommon unless the tumour is high grade.

Unlike renal cell carcinoma this tumour is not cystic and its cytoplasm is usually more sold.

158
Q

What are some risk factors for developing renal cell and transitional cell carcinomas?

A

Renal cell carcinoma: Most are sporadic

  • smoking = main risk factor
  • carcinogenic arsenic compounds (industry or drinking water)
  • increased BMI
  • hypertension

Transitional cell carcinoma:

  • smoking = main risk factor
  • industrial exposure to aromatic amines, commonly encountered in dyestuff workers
  • chronic abuse of analgesics containing phenacetin
  • drinking water containing arsenic
159
Q

What syndromes are associated with renal cell carcinomas?

A
  • Clear cell renal cell carcinoma: Von Hippel-Lindau syndrome, hereditary (familial) clear cell carcinoma syndrome
  • Papillary carcinoma: Hereditary papillary carcinoma syndrome
  • Angiomyolipoma: Tuberous sclerosis
160
Q

What are the common types of renal stones in our community?

A
  • Calcium oxalate - 49% associated with hyperoxaluria, hypercalciuria, dehydration, renal tubular acidosis, medullary sponge kidney, UTI
  • Calcium phosphate - 25%
  • Struvite - 15%
  • Urate - 8%
  • Cystine - 5%

Stones form when there is an increased urinary concentration of the stones constituents. when the urine is supersaturated and the substance is no longer soluble, precipitation occurs and stones are formed.