Formative Flashcards

1
Q

During ischaemia cells swell. Why is this? Is this change reversible or
irreversible?

A

Loss of function of energy-dependant membrane pumps, therefore
sodium and water accumulate in cytoplasm.

The change is reversible.

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2
Q

Describe the differences between oncosis/necrosis & apoptosis

A
Oncosis/Necrosis:         
Sheets of cells affected  
Associated inflammation  
Cell swelling    
Always pathological  
Membrane breaks down  
Diffuse/random DNA cleavage 
Apoptosis:
Single cells affected 
No associated inflammation 
Cell shrinkage
Can be pathological or physiological 
Membrane remains intact 
Internucleosomal DNA  cleavage
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3
Q

Name the 4 “cardinal” clinical features of acute inflammation.

A

Pain (dolor)
Swelling (tumor)
Redness (rubor)
Heat (color)

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4
Q

Why is swelling seen in an acutely inflamed area

A

Chemical mediators, such as histamine, serotonin and bradykinin, are
released and formed.
They cause arterioles to dilate and endothelial cells to contract (resulting in the formation of spaces between the endothelial cells).

Arteriolar dilatation results in increased hydrostatic pressure within the
capillaries and venules and fluid (with the plasma proteins that it contains) is pushed out of the venules through the gaps between the endothelial cells into the tissue spaces.

As the concentration of protein within the tissue spaces is increased, the osmotic pressure of the tissue spaces increases which serves to pull further fluid into the tissue spaces and to hold it there.

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5
Q

Give some functions of the complement system

A

Killing bacteria by forming the membrane attack complex which punches holes in them

Some components act as chemical mediators. C5a and C3a are
chemotaxins.

Opsonisation. C3b is an opsonin.

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6
Q

What is the molecular abnormality in inherited angio-oedema? Briefly
describe the main clinical features.

A

Absence of C1 esterase inhibitor (a component of the complement
system).

Attacks of non-itchy cutaneous angio-oedema (rapid oedema of the dermis, subcutaneous tissue, mucosa and submucosal tissues) especially of the face and airway.

Recurrent abdominal pain which is due to intestinal oedema.
Often a family history of sudden death due to laryngeal involvement.

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7
Q

Give some functions of macrophages in chronic inflammation

A

Phagocytosis of bacteria and other particles

Secretion of chemical mediators

Presenting antigens to the immune system and initiation of the immune response

Stimulating angiogenesis

Inducing fibrosis

Inducing fever, acute phase reaction and cachexia (loss weight, musc atrophy, weakness)

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8
Q

What is a granuloma?

Name the types of multinucleated giant cell that can be found in a granuloma and describe each.

A

A granuloma is a chronic inflammatory response.
It is a collection of cells (macrophages (some of which are modified to form epithelioid histiocytes), giant cells, fibroblasts and sometimes lymphocytes) which surrounds and attempts to destroy difficult to eliminate microorganisms and particles.

Multinucleated cells seen in granulomas:
Langhans giant cells – nuclei arranged around the periphery of the giant cell

Foreign body giant cells – nuclei arranged randomly in the cell,

Touton giant cells – nuclei arranged in a ring towards the centre of the cell.

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9
Q

What is sarcoidosis?

Name 2 organs that are commonly affected

A

Sarcoidosis is an inflammatory disease with an unknown cause in which granulomas are formed in organs throughout the body.

It commonly affects the lungs and lymph nodes.

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10
Q

Name some ways that sarcoidosis can be distinguished from TB (microscopically or in lab tests)

A

• Tuberculous granulomas often show central caseous necrosis and more frequently contain Langhans type giant cells than do sarcoid granulomas
• Mycobacteria may be seen in tuberculous granulomas with Ziehl-Neelsen stain
• Mycobacterial DNA can be identified from tuberculous granulomas using PCR (polymerase chain reaction)
• Mycobacterium tuberculosis may be cultured from infected tissues
• Hypercalcaemia is often seen in sarcoidosis
• Serum angiotensin converting enzyme (ACE) levels are often raised in
sarcoidosis

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11
Q

Why must the myocardium always heal with a scar

A

Cardiac myocytes are permanent cells and no stem cells are present in the myocardium, therefore no regeneration is possible.

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12
Q

Granulation tissue is important in the healing of the myocardium. Name its principal cellular constituents.

A

Fibroblasts and myofibroblasts

Endothelial cells/capillaries

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13
Q

List some local factors that can impair the healing of a wound

A
  • Large size of wound
  • Poor blood supply
  • Local infection
  • Presence of foreign bodies
  • Large haematoma or large amount of necrotic tissue
  • Mechanical stress on the healing tissue
  • Poor surgical technique
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14
Q

Give 2 important functions of (myo)fibroblasts in the healing of a wound

A

Production of extracellular matrix

Wound contraction

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15
Q

Describe the route of a typical thrombo-embolism from the leg veins to the lungs taking care to give vessel types i.e. artery or vein. Detailed vessel names are not needed.

A
Deep veins of calf
iliac veins 
inferior vena cava
right atrium
right ventricle 
pulmonary artery
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16
Q

How does a thrombosis differ from clotting?

A

Thrombosis is a pathological process. It is the inappropriate formation of a solid mass from the constituents of the blood within a vessel during life.

Clotting is the physiological process whereby blood forms a solid mass which controls bleeding when blood vessels are severed. It occurs outside of vessels.

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17
Q

Describe Virchov’s Triad

A

Abnormal flow (e.g. peri-operative immobility)

Abnormal blood constituents (e.g. Smoking, post-partum, post-operative hypercoagulability)

Abnormal vessel wall (e.g. Atheroma)

18
Q

What are the 2 possible mechanisms of death from a pulmonary embolism

A

Respiratory compromise – there is a non-perfused but ventilated area of lung, i.e. a ventilation-perfusion mismatch which results in hypoxaemia.

Haemodynamic compromise – there is an increased resistance to pulmonary blood flow due to obstruction of the pulmonary vessels by the embolus. This results in acute right sided heart failure (acute cor pulmonale).

19
Q

What is the name given to an abnormal dilation & atherosclerosis in the abdominal aorta ?
Briefly describe the most likely pathogenesis of the dilatation

A

Abdominal Aortic Aneurysm

Atherosclerosis: weakens media

20
Q

Give some major complications of an abdominal aortic aneurysm

A
  • Rupture and haemorrhage
  • Thromboembolism to the legs causing acute ischaemia
  • Aortic dissection causing acute aortic occlusion or aortic rupture
  • Aorto-caval or aorto-duodenal fistulae
21
Q

Name some modifiable & non-modifiable risk factors for developing atherosclerosis

A
Modifiable: 
 Diabetes mellitus   
 Smoking   
 Hyperlipidaemia   
 Hypertension 
 Obesity 
 Lack of exercise 
 Unhealthy diet 

Non-modifiable:
Age
Family history
Sex

22
Q

Name some clinical features seen on external examination of a patient that suggest hyperlipidaemia.

A

Corneal arcus
Xanthoma
Xanthelasma

23
Q

What is the difference between hyperplasia & hypertrophy?
Why is it that some organs can only undergo hypertrophy & not hyperplasia?

A

Hyperplasia is an increase in tissue or organ size due to increased cell numbers.
Hypertrophy is an increase in tissue or organ size due to an increase in cell size without an increase in cell numbers.

Permanent tissues can only undergo hypertrophy as these cell populations have little or no replicative potential and so any increase in organ size must occur via hypertrophy.

24
Q

Give some causes of ventricular hypertrophy

A
  • Systemic hypertension
  • Valvular heart disease – aortic stenosis, aortic regurgitation, mitral regurgitation
  • Ischaemic heart disease
  • Hypertrophic cardiomyopathy
  • Exercise
25
Q

Give some causes of atrophy

A
Inadequate nutrition
• Reduced functional demand/workload (atrophy of disuse) 
• Loss of innervation (denervation atrophy) 
• Inadequate blood supply 
• Loss of endocrine stimulation 
• Persistent injury 
• Aging (senile atrophy) 
• Pressure
26
Q

Rudolf Virchow believed that in metaplasia one cell type turned directly into that of another cell type. We now know that this doesn’t happen. What does happen?

A

Stem cells within the tissue are reprogrammed and express different genes resulting in a switch from producing one type of cell to the production of cells with a different phenotype. Therefore cells of one type are eliminated and replaced by those of another type.

27
Q

Why is it that both alleles of a tumour suppressor gene need to be mutated in order for cancer to develop but only one allele of a proto-oncogene needs to be mutated?

A

Mutations in tumour suppressor genes are inactivating and so both alleles need to be mutated in order for tumour suppressor proteins which act as brakes on the cell cycle to be ineffective.

Mutations in proto-oncogenes are activating and therefore mutation in only one allele is needed for the proteins which act as neoplastic growth enhancers to favour neoplastic growth.

28
Q

With reference to the colonic adenoma-carcinoma sequence, briefly describe what is meant by the term ‘progression’ in cancer.

A

Malignant tumours require alterations affecting a combination of multiple tumour suppressor genes and proto-oncogenes.

This has been demonstrated by the colonic adenoma-carcinoma sequence.

Early adenomas, later adenomas, primary carcinomas and metastatic carcinomas showed that step-wise accumulation of mutations occurs during this sequence over time. This steady accumulation of multiple mutations is called cancer progression.

29
Q

Give some types of cancer that frequently metastasise to bone

A
  • Breast carcinoma
  • Bronchial carcinoma
  • Renal carcinoma
  • Prostate carcinoma
  • Thyroid carcinoma
30
Q

Give some examples of tumour markers, and tumours associated with that marker

A

Human chorionic gonadotropin:
Trophoblastic tumours
Nonseminomatous germ cell tumours of the testes

Calcitonin:
Medullary carcinoma of the thyroid

Catecholamine and metabolites:
Pheochromocytoma and related tumours

α-fetoprotein:
Liver cell cancer
Nonseminomatous germ cell tumours of the testes

Carcinoembryonic antigen:
Colon cancer

Prostate-specific antigen:
Prostate cancer

CA-125:
Ovarian cancer

CA-19-9:
Pancreatic cancer

31
Q

What is the most common type of cervical cancer?

A

Squamous cell carcinoma

32
Q

Cervical cancer usually arises in areas of the cervical epithelium that show cervical intraepithelial neoplasia (CIN). What is the difference between CIN and cervical cancer?

A

In CIN dysplastic cells are confined to the epithelium and no stromal invasion is seen.
In cervical cancer malignant cells have invaded through the basement
membrane and are present in the sub-epithelial tissue.

33
Q

The HPV virus is known to play an important causative role in CIN and cervical cancer. By what means is this virus known to cause cancer?

A

HPV produces two proteins (E6 and E7) that inactivate tumour suppressor proteins (RB protein and p53), speed the cell through the cell cycle (activate cyclins), inhibit apoptosis (p53) and combat cellular senescence (activate telomerase).

34
Q

Which types of cancer currently have screening programs in the UK

A

Cervix
Breast
Bowel

35
Q

A 52 year old man with a long history of alcohol abuse is diagnosed with liver cirrhosis. Which of the following best describe how this man’s liver would appear histologically?

A. Accumulation of bile pigment both within bile canaliculi and hepatocytes.

B. Accumulation of round eosinophilic globules within hepatocytes.

C. Focal hepatocyte necrosis, formation of Mallory bodies and an infiltrate of
neutrophils.

D. Large clear vacuoles with hepatocytes that compress and displace the
nucleus of the hepatocyte.

E. Micronodules of hepatocytes surrounded by bands of collagen.

A

E

36
Q

An eight year old falls off his bike and grazes his knee. He sits and
watches the blood clot. Which is the correct sequence of events in
haemostasis?

A. A platelet plug forms, arteries contact, fibrin filaments accumulate and trap red blood cells.

B. A platelet plug forms, fibrin filaments accumulate and trap red blood cells, arteries contract.

C. Arteries contract, a platelet plug forms, fibrin filaments accumulate and trap red blood cells.

D. Arteries contract, fibrin filaments accumulate and trap red blood cells, a platelet plug forms.

E. Fibrin filaments accumulate and trap red blood cells, a platelet plug forms, arteries contract.

A

C

37
Q

A 79 year old woman presents with a 3 cm mass in her right breast
which after biopsy is confirmed to be a breast cancer. On examination
she is found to have enlarged right axillary lymph nodes. A CT scan
reveals a number of nodules in her right lung. Which of the following is
most likely to represent the stage of her disease?

A. T1 N1 M0

B. T2 N0 M1

C. T2 N1 M0

D. T2 N1 M1

E. T3 N0 M0

A

D

38
Q

A 25 year old woman is found to have an ovarian mass. It is removed
surgically and when it is opened it is found to contain hair and sebum. On microscopic examination squamous epithelium with hair follicles,
cartilage and neural tissue are identified. Which of the following
statements about this type of neoplasm is true?

A. Infection with human papillomavirus (HPV) predisposes to this type of
tumour.

B. Metastases are unlikely to be present.

C. Patients with these tumours often present with irregular menstrual bleeding.

D. Primitive mature tissue resembling that from an embryo can usually be seen.

E. These tumours are associated with BRCA1 mutations.

A

B

39
Q

A 47 year old woman has had menorrhagia (heavy periods) for 6 years.
She undergoes a hysterectomy and a firm, pale tumour measuring 10 cm in diameter is seen within the body of the uterus. Histological examination of the tumour shows that it is composed of spindled cells. Which of the following neoplasms is she most likely to have?

A. Endometrial adenocarcinoma.

B. Leiomyoma of the myometrium.

C. Leiomyosarcoma of the myometrium.

D. Metastatic ovarian carcinoma.

E. Squamous cell carcinoma of the cervix.

A

B

40
Q

A 64 year old with a known malignancy is found to have
hypercalcaemia. A blood test reveals a high level of parathyroid hormone related protein. Which of the following neoplasms is he most likely to have?

A. Adenocarcinoma of the prostate.

B. Bronchial small cell carcinoma.

C. Bronchial squamous cell carcinoma.

D. Clear cell carcinoma of the kidney.

E. Medullary carcinoma of the thyroid.

A

C

41
Q

What pattern of necrosis would you expect to find following a myocardial infarction? Briefly describe its histological appearance.

What colour would you expect the infarction to be and why?

A

Coagulative necrosis
Loss of cell detail but ghost outline of tissue architecture endures

White.
In this case there is occlusion of an “end” artery, which causes a death with only very slight haemorrhage