Pathology Flashcards
What are the histological features of amyloidosis?
Bright pink hyaline material on microscopy
Characteristic staining with ‘Congo red’ shows apple green membranes under polarized light.
Stages of acute inflammation
Haemostasis Increased vascular permeability Recruitment and extravasation of white cells Phagocytosis Resolution or chronic inflammation
Chemical mediators involved in acute inflammation
Vasoactive mediators- histamine and serotonin
Bradykinin
Complement/coagulation/fibrinolytic cascade
Arachidonic acid metabolites- thromboxaneA2, leukotrienes, prostaglandins
Cytokines- TNF-a, interleukins
What is the complement cascade?
Part of innate immune system
Results in formation of membrane attack complex which promotes inflammation via opsonisation and facilitation of phagocytosis
Classical pathway triggered by antigen-antibody complex
Alternative pathway triggered by cell wall of micro-organism
Possible outcomes of acute inflammation
Resolution
Repair, organisation and scar formation
Chronic inflammation
Abscess formation
What is chronic inflammation?
Simultaneous processes of tissue healing, inflammation and injury
Characterised by presence of macrophages and lymphocytes rather than neutrophils (as in acute inflammation)
Usually lasts longer than acute inflammation
What is a granuloma?
Isolation of foreign body/infection/area of necrosis by the immune system. Surrounded by epithelioid macrophages which may converge to form Langerhans giant cells
How can you classify granulomatous inflammation?
Caseating- TB
Non caseating- IBD or sarcoid
What causes chronic inflammation?
Infection that cannot be eliminated by the body- TB
Persistence of insult to mucosa- eg peptic ulcer disease
Auto-immune conditions eg RA
Unknown- eg IBD
Duke’s classification
Stage A: Limited to muscularis propria; nodes not involved
Stage B: Extending beyond muscularis propria; nodes not involved
Stage C: Nodes involved but highest (apical) node spared
Stage D: Distant metastatic spread
Layers of the gastrointestinal tract
Mucosa (epithelium, lamina propria and muscularis mucosa) - internal
Submucosa
Muscularis propria
Adventitia/Serosa - external
To where does colorectal cancer commonly metastasize?
Liver, Lung, Brain, Bone
How would you monitor your patient for disease recurrence following a colorectal resection?
CT colon & CEA monitoring
Describe constituent of malignant ascites
Exudate, with a protein count >30g/L (as opposed to transudate, with a low protein content)
Causes of hepatomegaly
Physiological
Tumour- benign/malignant
Infective (e.g. parasitic/bacterial/viral abscesses)
Metabolic (acromegaly, alcohol)
Infiltrative (amyloid)
Vascular (right heart failure, Budd-Chiari syndrome)
Haematological- sickle cell, thalassaemia
What is the cytological classification of thyroid nodule biopsy?
- Benign
- Indeterminate or suspicious
- Malignant
- Inadequate specimen
What is the difference between primary, secondary and tertiary hyperparathyroidism?
- Primary hyperparathyroidism: due to excess parathyroid hormone secretion from parathyroid adenomas, hyperplasia, or carcinoma.
- Secondary hyperparathyroidism: Increase in parathyroid hormone in response to low plasma ionised calcium secondary to renal disease or malabsorption.
- Tertiary hyperparathyroidism: development of autonomous hyperplastic parathyroid glands in a patient with secondary hyperparathyroidism resulting in profound hypercalcaemia.
Causes of hypoparathyroidism?
- Post-thyroidectomy
- Idiopathic (autoimmune)
- After radioactive iodine therapy for Graves
What is the difference between primary and secondary hyperaldosteronism?
- Primary hyperaldosteronism: elevated aldosterone, suppressed renin levels. Causes include aldosterone producing adenoma, adrenal hyperplasia, aldosterone producing adrenocortical carcinoma, familial hyperaldosteronism.
- Secondary hyperaldosteronism: elevated aldosterone AND renin. Causes include renal vascular disease, renin-secreting tumours, liver cirrhosis
What are the commonest risk factors for cholangiocarcinoma?
The commonest cause is Primary Sclerosing Cholangitis, followed by chronic liver disease, HIV and congenital liver disease.