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RLH MRCS > CL Pathology > Flashcards

CL Pathology Flashcards

1
Q

What are the histological features of amyloidosis?

A

Bright pink hyaline material on microscopy

Characteristic staining with ‘Congo red’ shows apple green membranes under polarized light.

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2
Q

Stages of acute inflammation

A 
Haemostasis
Increased vascular permeability
Recruitment and extravasation of white cells
Phagocytosis
Resolution or chronic inflammation
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3
Q

Chemical mediators involved in acute inflammation

A

Vasoactive mediators- histamine and serotonin
Bradykinin
Complement/coagulation/fibrinolytic cascade
Arachidonic acid metabolites- thromboxaneA2, leukotrienes, prostaglandins
Cytokines- TNF-a, interleukins

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4
Q

What is the complement cascade?

A

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

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5
Q

Possible outcomes of acute inflammation

A

Resolution
Repair, organisation and scar formation
Chronic inflammation
Abscess formation

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6
Q

What is chronic inflammation?

A

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

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7
Q

What is a granuloma?

A

Isolation of foreign body/infection/area of necrosis by the immune system. Surrounded by epithelioid macrophages which may converge to form Langerhans giant cells

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8
Q

How can you classify granulomatous inflammation?

A

Caseating- TB

Non caseating- IBD or sarcoid

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9
Q

What causes chronic inflammation?

A

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

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10
Q

Duke’s classification

A

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

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11
Q

Layers of the gastrointestinal tract

A

Mucosa (epithelium, lamina propria and muscularis mucosa) - internal
Submucosa
Muscularis propria
Adventitia/Serosa - external

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12
Q

To where does colorectal cancer commonly metastasize?

A

Liver, Lung, Brain, Bone

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13
Q

How would you monitor your patient for disease recurrence following a colorectal resection?

A

CT colon & CEA monitoring

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14
Q

Describe constituent of malignant ascites

A

Exudate, with a protein count >30g/L (as opposed to transudate, with a low protein content)

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15
Q

Causes of hepatomegaly

A

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

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16
Q

What is the cytological classification of thyroid nodule biopsy?

A
  • Benign
  • Indeterminate or suspicious
  • Malignant
  • Inadequate specimen
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17
Q

What is the difference between primary, secondary and tertiary hyperparathyroidism?

A
  • 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.
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18
Q

Causes of hypoparathyroidism?

A
  • Post-thyroidectomy
  • Idiopathic (autoimmune)
  • After radioactive iodine therapy for Graves
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19
Q

What is the difference between primary and secondary hyperaldosteronism?

A
  • 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
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20
Q

What are the commonest risk factors for cholangiocarcinoma?

A

The commonest cause is Primary Sclerosing Cholangitis, followed by chronic liver disease, HIV and congenital liver disease.

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21
Q

What tests would you request in order to diagnose a cholangiocarcinoma?

A

Imaging: USS of the liver and biliary tree/ ERCP (for biopsy)/MRCP
If unable to obtain a biopsy via ERCP, an open biopsy should be performed

Staging: CT (full body)

Immunohistochemistry can be employed to distinguish between hepatocellular carcinoma and cholangiocarcinoma.

22
Q

Management of cholangiocarcinoma

A

Cholangiocarcinoma is incurable and rapidly lethal unless the tumour is completely resected. An open approach is usually employed.

If tumour is unresectable, adjuvant therapy, hepatectomy and liver transplantation is advisable.

Overall median survival is less than 6 months.

23
Q

How does clostridium difficile form a pseudomembrane?

A

C Diff. produces a toxin that helps it to colonize the gut. This toxin causes an inflammation of the bowel, there is production of grey-white exudate that is thin and adherent onto the bowel wall. The membrane is composed of necrotic epithelium, debris, fibrin, bacteria and neutrophils merging with the mucosa.

24
Q

What criteria must a donor meet?

A

The patient should meet the requirements for brainstem death, have consent from the next of kin or be on the organ donor register, and be ABO compatibility with the recipient. They should also be free of malignancy, HIV, hepatitis and acute infection.

25
Q

What are the criteria that must be met for brainstem death?

A

The pupils must be fixed and unresponsive to light.
There must be no corneal reflex
Vestibulo-ocular reflexes must be absent – ie no eye movement on injection of 50ml of ice cold water into the external auditory meatus
No motor response to supraorbital pressure
No gag reflex
No cough in response to bronchial stimulation down the endotracheal tube
No respiratory movements in response to disconnection from a ventilator, despite allowing the PaCO2 to rise to 6.65kPA on ABG

Brainstem testing must be carried out by two doctors who have held registration with the GMC for more than 5 years; two sets of tests should be carried out.

26
Q

What cells mediate type 1 hypersensitivity reaction?

A

B cells, Helper T lymphocytes and mast cells mediate a type one hypersensitivity reaction

The initial exposure to the antigen leads the sensitization of the T and B cells. As a result primed IgE binds to mast cells. If exposed to the antigen again, cross linking of the IgE on mast cells occurs, leading to degranulation and release of histamine.

27
Q

What causes graft-vs-host disease?

A

Graft-versus-host disease occurs when donor T cells recognizes and react against the hosts HLA antigens.

28
Q

Complications of steroids

A 
General Cushingoid features:
Central obesity
Muscle wasting in limbs
Thin skin
Bruising
Buffalo hump
Striae
Hirsutism

Cardiovascular system:
Hypertension
Fluid retention

GI system:
Fatty liver
Pancreatitis

Neurological system:
Depression
Psychosis
Insomnia

Locomotor system:
Osteoporosis
Avascular necrosis
Proximal myopathy

Immune system:
Immunosuppression

Endocrine system:
Diabetes mellitus

29
Q

What is H Pylori?

A

Gram-negative, microaerophilic spiral bacterium found in the stomach

30
Q

How does H Pylori colonise the stomach?

A

H pylori is able to detect pH and uses its flagella to swim away from the acidic contents of the lumen and adheres to the more neutral epithelial lining of the stomach.

31
Q

How does H Pylori survive the acidic conditions in the stomach?

A

H. pylori produces the enzyme urease. This converts urea to carbon dioxide and ammonia. The ammonia then binds with H+ to form ammonium which neutralizes gastric acid.

32
Q

How is H Pylori diagnosed?

A

Via the CLO campylobacter-like organism) test which is dependent on urease production by H Pylori
A gastric mucosal biopsy is taken during gastroscopy and is placed into a medium consisting of urea and an indicator such as phenol red. Urease produced by H Pylori converts urea to ammonia which increases the pH changing the colour from yellow to red, hence a positive test.

33
Q

Eradication therapy for H Pylori?

A

7-day twice-daily course of treatment consisting of a:
Full-dose PPI
+
amoxicillin/clarithromycin AND metronidazole

80% of patients infected with H pylori are asymptomatic

34
Q

Other tests for H Pylori other than mucosal biopsy?

A

Urease breath test: By having the patient drink radiolabelled urea, the carbon dioxide produced will also be labelled and can be collected and measured.

Stool antigen test

Serum antibody test

35
Q

How is hydrochloric acid produced in the stomach?

A

There is nervous stimulation via the cephalic phase (thinking about food) and gastric phase (having food in the stomach). G cells in the stomach are stimulated to produce gastrin. Gastrin travels in the circulation to stimulate enterochromaffin-like cells to produce histamine. The histamine and gastrin both stimulate parietal cells to produce hydrochloric acid.

36
Q

What are hypersensitivity reactions?

A

Exaggerated response of host’s immune system to stimulus

Undesirable tissue damage follows the humeral (mediated by antibodies) or cell-mediated immunity.

37
Q

What is the pathophysiology behind a type 2 hypersensitivity reaction and can you give some examples?

A

Antibodies vs antigens on surface of cells

Eg transfusion reactions and autoimmune haemolytic anaemia

38
Q

What is the pathophysiology behind a type 3 hypersensitivity reaction and can you give some examples?

A

The formation of antibody-antigen complexes (immune complex mediated)
Eg SLE

39
Q

What is the pathophysiology behind a type 4 hypersensitivity reaction and can you give some examples?

A

Delayed hypersensitivity reaction mediated by T-lymphocytes. Takes 48-72 hours to see the effects.
Eg contact dermatitis

40
Q

What is the pathophysiology behind a type 5 hypersensitivity reaction and can you give some examples?

A

Formation of stimulatory autoantibodies in autoimmune conditions Eg Graves’ disease and myasthenia gravis.

41
Q

What is actinic keratosis?

A

Premalignant skin condition provoked by UV light. It can progress to squamous cell carcinoma

42
Q

What histological feature characterizes a squamous cell carcinoma?

A

Proliferation of atypical keratinocytes, invasion of the dermis and keratin pearls

43
Q

Signs of systemic toxicity of local anaesthetic?

A

Perioral tingling and parasthesia progressing to drowsiness, seizures, coma, apnoea, paralysis, arrhythmias and shock (LAs are negative inotropes and vasodilators).

44
Q

Organisms causing rheumatic fever

A

Group A beta haemolytic strep

45
Q

Diagnostic criteria name for rheumatic fever

A

Jones Criteria

46
Q

How to diagnose rheumatic fever with Jones criteria

A

Evidence of infection 3 major or 1 major 2 minor

47
Q

Describe the Jones criteria

A 
Evidence: +ve blood culture/antigen/ASOT
Major: 
-Arthritis (migratory), 
-Bulky elbows (subcutaneous nodules), 
-Carditis, 
-Dancing (Sydenham's chorea), 
-Erythema marginatum

Minor:

  • Arthralgia
  • Block (heart block)
  • CRP elevated
  • Temperature
48
Q

What is the diagnostic criteria for infective endocarditis?

A

Modified Duke criteria

49
Q

How do you diagnose infective endocarditis with modified Duke criteria?

A

2 major
1 major 3 minor
5 minor

50
Q

Describe the modified Duke criteria

A

BETI MVP
Major:
-Blood cultures (2 separate, IE known organisms, >24h apart),
-Endocarditis on echo

Minor:

  • Temperature,
  • Immune phenomena (Oslers nodes, glomerulonephritis, roth spots)
  • Microbiology not meeting major criteria (non diagnostic/non IE organisms)
  • Vascular phenomena (aneurysms, septic emboli, splinter haemorrhages, Janeway lesions)
  • Predisposing factors (artificial valve, IVDU)

RLH MRCS (22 decks)

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