Papillary carcinoma of the thyroid

Papillary carcinoma constitutes about two thirds of thyroid malignancies in adults and nearly all thyroid malignancies in children. Females are affected at least three times as often as males and the peak incidence is between 30y and 45y.

Histologically, the tumour forms a complex branching papillary structure with a fibrovascular stroma, often containing calcified 'psammoma bodies'.

Tumours vary over a wide range of epithelial dysplasia between apparently benign and obviously malignant.

Whatever the degree of dysplasia, the tumours grow slowly.

Papillary carcinomas are microscopically multicentric in about 80% of cases and about one third affect both lobes; this is important in planning treatment.

The tumour occasionally invades locally into trachea or oesophagus. Metastasis is to central cervical and later lateral cervical LNs and only rarely to distant sites such as lung or bone.

By presentation, LN are involved in about 40% of patients (90% in children).

LN enlargement is often the sole presenting feature and the histology of involved LNs is so close to normal thyroid tissue that at one time this condition was known as 'lateral aberrant thyroid'.

The prognosis of papillary carcinoma is the best of all thyroid carcinomas with only about 10% of patients dying of the tumour after 10y; it is remarkable that survival is hardly prejudiced by the presence of LN mets.

Symptoms and signs

Papillary ca presents as a slow-growing thyroid nodule.......... incomplete

Management

Total thyroidectomy because of the high risk of other foci within the gland.

Palpable cervical nodes are removed at the same operation. The operation is no more difficult than subtotal thyroidectomy but carries a higher risk of post-op hypoparathyroidism.

Total thyroidectomy has the added advantage that recurrent local disease, LN or distant mets can then effectively be treated with radioiodine (131I). This requires a very high TSH level which only occurs if no normal thyroid tissue remains.

A further advantage is that plasma thyroglobulin can then be used as a tumour marker to detect recurrent disease.

After treatment, hormone replacement is necessary to keep TSH close to zero to minimise the risk of stimulating any residual malignant cells.

Since papillary ca progress so slowly and only 15% develop contralateral lobe recurrence, some surgeons prefer to retain one thyroid lobe if the primary tumour is small and there are no palpable or isotope-detectable nodules. Their reasoning is that any further tumours can be removed later without reducing life expectancy.

Follicular carcinoma of the thyroid

Info from Burkitt pg 720

Follicular carcinoma is another well-differentiated thyroid malignancy.

Histologically, the neoplastic cells form a well-developed follicular pattern which is impossible to distinguish from benign adenomatous hyperplasia on FNA cytology; even on histology of the surgical specimen, it may also be difficult to diagnose malignancy unless there is evident capsular or vascular invasion.

Unlike papillary carcinoma, multicentricity is common.

The peak incidence of follicular carcinoma is between 40y and 50y, older than for papillary ca, but it is still three times more common in women. Generally, follicular carcinoma grows slowly and metastasises at a late stage.

In contrast to papillary carcinoma, metastasis tends to occur via the bloodstream to the lungs, bone and other remote sites rather than to local lymph nodes.

Since follicular carcinoma is rarely multicentric, management depends on the extent of local invasion. A tumour with only microinvasion of the capsule has a very good prognosis and only requires removal of the thyroid lobe containing the tumour. If, however, there is gross capsular invasion or vascular invasion (or known remote mets), total thyroidectomy is performed.

The purpose of total thyroidectomy is not to treat the local tumour but to enhance radioiodine uptake by metastatic lesions should this be required later for diagnosis, or any consequent Rx with high-dose radioiodine (as with papillary carcinoma).

Prognosis can be predicted by the degree of capsular and vascular invasion by the primary lesion and on histology. If there is no invasion, 10y survival is close to 100% but this falls to 30% if there is extensive local invasion.

ERCP

Procedure

A catheter is advanced from a side-viewing duodenoscope into the CBD. Contrast medium is injected and x-rays taken to show lesions in the biliary tree and pancreatic ducts.

Diagnostic indications

1. Cholangitis.
2. Jaundice with dilated intrahepatic ducts.
3. Jaundice with normal calibre ducts and a non-diagnostic liver biopsy.
4. Recurrent pancreatitis.
5. Post-cholecystectomy pain.

Therapeutic indications

1. Sphincterotomy for CBD stones.
2. Stenting of malignant strictures.

Pre-procedure

1. LFT, clotting, platelet count.
2. Antibiotic prophylaxis e.g. ciprofloxacin 750mg PO 2h before.
3. Analgesia e.g. pethidine.
4. Sedation e.g. midazolam 2.5-10mg IV.

Complications

1. Pancreatitis.
2. Bleeding.
3. Cholangitis.
4. Perforation.
5. Mortality less 0.2% overall; 0.4% if performing stone removal.

Complications of bowel stoma

Early complications

• Mucosal sloughing or necrosis of the terminal bowel due to ischaemia.
  Rx = Reoperation and refashioning.
  
  
• Obstruction of stoma due to oedema/faecal impaction/adhesions.
  Rx = Exploration with a gloved finger and sometimes glycerol suppositories or softening enemas.
  
  
• Persistent leak between skin and appliance causing skin erosion and patient distress, often due to inappropriate location of stoma (e.g. over skin crease).
  Rx = May respond to stoma nursing care or require a resiting operation.
  
  
• Haemorrhage at stoma site.
  
  
• Stoma ischaemia - colour progresses from dusky grey to black.
  
  
• High output - can lead to hypokalaemia. Consider loperamide +/- codeine to thicken the output.
  

Late complications

• Obstruction (failure at operation to close the lateral space around stoma).
  
  
• Parastomal hernia due to abdominal wall weakness. Risk increases with time.
  Rx = Resiting.
  
  
• Prolapse of bowel.
  Rx = refashioning.
  
  
• Parastomal fistula.
  Rx = refashioning.
  
  
• Retraction of spout ileostomy
  Rx = refashioning.
  
  
• Stenosis of stomal orifice.
  Rx = refashioning.
  
  
• Perforation after colonic irrigation.
  Rx = emergency operation.
  
  
• Dermatitis around stoma site (worse with ileostomy).
  
  
• Psychological and psychosexual dysfunction.
  Rx = Counselling or measures to reverse stoma.
  

Causes of haematuria

Renal causes TTP PING

• Tubulointerstitial nephritis
• Trauma
• PCKD
• Papillary necrosis
• Neoplasia
• Infection (pyelonephritis)
• GN

Extrarenal CINT

• Calculi
• Infection (cystitis, prostatitis, urethritis)
• Neoplasia (bladder, prostate, urethra)
• Trauma (E.g. from catheter)

Causes of false +ve dipstick haematuria

• Haemoglobinuria
• Myoglobin e.g. in rhabdomyolysis
• Beetroot
• Porphyria
• Alkaptonuria
• Rifampicin
• Phenindione
• Phenolphthalein

Tests
Urine MC&S
CBC
ESR & CRP
U&E
Clotting
...
AXR/KUB
Urine cytology
Estimation of proteinuria
Renal US +/- renal biopsy

What is liver fibrosis?

1. Activated stellate cells ('myofibroblast').
   
   
2. Dense ECM in the space of Disse (types I and III collagen are deposited... normal liver has type IV collagen in the space of Disse).
   
   
3. Loss of fenestrations between sinusoidal endothelial cells.
   
   
4. Hepatocytes lose their microvilli (which normally project into the space of Disse).
   
   
5. Kupffer cells are activated and produce plenty a cytokine.

Information from Robbins diagram on pg 636.

What is cirrhosis?

1) Diffuse loss of normal hepatic architecture.
2) Fibrosis.
3) Nodular regeneration.