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Pathology Flashcards

1
Q

What are the possible reasons for an inflammatory response?

A

Trauma, Infection, foreign bodies, immune reaction, necrosis of any cause.

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2
Q

Explain the vascular changes that take place in inflammation

A

There will be changes in flow and vessel calibre which will result in vasodilation. This is mediated by histamine and nitric oxide. There is increased heat and redness.

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3
Q

Explain the cellular changes that take place in inflammation

A

Things slow down, white cell margination takes place (white cells move peripherally),. Vessels express selectins and integrins that are complementary to receptors on white cell surface. Selection-Integrin interactions with white cells results in rolling. The white cells will then be able to migrate into surrounding tissues as the vessel walls are leaky. The leaky vessels will lose proteins and there will be a change in osmotic pressure.

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4
Q

Describe what happens in chemotaxis

A

After penetration of the vessel wall, the subsequent movement of the leucocytes is controlled by chemotaxis. The cell moves in response to an increasing concentration gradient of the particular chemotactic agent, usually a protein or a polypeptide.

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5
Q

How do neutrophils and macrophages clear the injurious agent?

A

Through phagocytosis

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6
Q

What type of cell characterises acute inflammation?

A

The neutrophil

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7
Q

What happens in resolution?

A
  • This involves the complete restoration of the tissue to normal after removal of inflammatory components as well as complete return to function.
  • Resolution can occur if there has been minimal cell death, the tissue has capacity to repair, there is a good vascular supply and the injurious agent can be easily removed.
  • Erosions and abrasions describe injury with basement membrane intact. Heal rapidly with complete resolution.
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8
Q

What happens in suppuration?

A

• This is the process of pus forming which contains living, dying and dead cells. These include neutrophils, bacteria and inflammatory debris.

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9
Q

What are potential reasons for repair, organisation and fibrosis happening?

A
  • This occurs if an injury produces lots of necrosis or it produces lots of fibrin that isn’t easily cleared.
  • This may be caused by a poor blood supply resulting in difficulty in removing debris.
  • In mucosa where damage goes beyond the basement membrane favours healing by organisation and repair and not resolution. This is because many mucosae are complex structures and when injury is severe enough they can’t be easily rebuilt.
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10
Q

Explain granulation tissue formation

A
  • The wound begins to be built with new healthy granulation tissue.
  • The defect is slowly infiltrated by capillaries and then by myofibroblasts.
  • Collagen is deposited and smooth muscle cells move in from the side.
  • After granulation comes fibrosis (thickening and scarring of connective tissue).
  • Scarring and fibrosis plugs holes but results in loss of function.
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11
Q

Why would chronic inflammation occur?

A
  • There is suppuration with walled off pus and scarring.
  • The injury is persistent e.g. foreign material or keratin from skin.
  • If there is a persistent infectious agent e.g. viruses.
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12
Q

What is chronic inflammation characterised by?

A

The lymphocyte

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13
Q

Explain Granulomatous Inflammation

A
  • This is the term given to forms of chronic inflammation in which modified macrophages (epithelioid cells) accumulate in small clusters surrounded by lymphocytes.
  • The small clusters are called granulomas.
  • The system attempts to wall of substances it sees as foreign but is unable to eliminate.

Doesn’t happen with viruses

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14
Q

What are the different adaptions to changes in demand?

A
  • Increased Demand (lots of stress)- hyperplasia or hypertrophy
  • Decrease Demand- atrophy
  • Altered Stimulus (different kind of stress)- metaplasia
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15
Q

What is hyperplasia?

A

Growth of tissue by increasing more cells. This is reversible growth and will be reversed on withdrawal of the stimulus.

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16
Q

What is hypertrophy?

A

Growth of tissue by cells getting bigger

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17
Q

What is atrophy?

A

Reduction in cell size

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18
Q

Name six reasons why pathological atrophy can occur

A

1) Decreased workload e.g. broken leg in cast
2) Loss of innervation (loss of function after nerve supply is removed)
3) Blocked Blood Supply
4) Loss of hormonal stimulation e.g. post-menopausal uterus
5) Inadequate nutrition
6) Pressure due to endogenous or exogenous structures. Can be seen in normal tissue adjacent to tumours.

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19
Q

What is metaplasia?

A

Reversible change from one mature cell type to another mature (fully differentiated) cell type (response to stress, not more work but different work). Squamous metaplasia is often encountered in injury to lungs as squamous epithelia are very resistant and usually line the skin.

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20
Q

What are the signs of inflammation?

A

Rubor, calor, dolor, tumor and loss of function

21
Q

Define cancer

A

Uncontrolled cell proliferation and growth that can invade other tissues.

22
Q

Define Tumour

A

A descriptive term, swelling, it can be benign or malignant, may be inflammatory, could be a foreign body.

23
Q

Define Neoplasia

A

New growth, not in response to a stimulus. Can be benign, premalignant or malignant

24
Q

Define Malignant

A

It has metastatic potential (potential to spread). For something to be malignant it must have grown beyond the basement membrane.

25
Q

Define metastases

A

Spread to other sites.

26
Q

Define Dysplasia

A

Disordered Growth

27
Q

Give examples of things that increase risk of developing cancer

A 
Genetic dispositions
Chemical carcinogenesis
Radiation
Microbial Carcinogenesis e.g. HPV
Chronic Inflammation as this can cause metaplasia
Obesity
28
Q

What are the hallmarks of cancer?

A

Sustained Growth Signalling (permanent oncogenes)
Loss of Growth Inhibition (deletion of tumour suppressors)
Unlimited Replicative Potential (renewal of telomeres)
Resisting Apoptosis (mutations in apoptotic pathway)
Inducing Angiogenesis (up regulate growth factors for creating blood supply)
Disordered Repair Mechanisms (repair mechanisms mutated resulting in more DNA abnormalities)
Evasion of Immune System (Inhibition of T cell proliferation etc)
Activating Invasion and Metastasis (must be able to chew up surrounding tissue to make way into blood vessels)

29
Q

Describe how you would tell that a tumour is benign

A

– Looks small, round and smooth, often symmetrical.
– Homogenous, cut surface is uniform, one area looks the same as another.
– Often is encapsulated, this takes time and infers that slow growing lesions are often benign.
– Benign tumours are in general well differentiated meaning they mimic the structure of the parent tissue and resemble the cells of their tissue of origin.
– Histologically in benign tumours the nucleus will look small compared to the cytoplasm.

30
Q

Describe how you would tell that a tumour is malignant

A

– These don’t look natural, they are irregular, infiltrative and destructive.
– Heterogenous, there will be different areas.
– May be evidence of haemorrhage and necrosis (this can be seen histogically or macroscopically
– Malignant tumours are in general poorly differentiated and will bear less resemblance to the cells of origin.
– Histologically the cells will show pleomorphism (variation in shape and size) and a high nucleus to cytoplasm ratio.
– Histologically they will show hyperchromasia (lots of colour as malignant cells have high amounts of DNA so will stain dark)
– Histologically they will also show frequent mitoses often of abnormal type.

31
Q

Name 3 groups of tumours

A

1) Epithelia
2) Mesenchymal tissues (including fibrous tissue, bone, cartilage and vessels)
3) Haemopoietic and lymphoid cells

32
Q

Benign epithelial tumours of squamous cells and of glands?

A
  • Papilloma (squamous cell tumour)

* Adenoma (Glandular epithelia)

33
Q

Malignant epithelial tumours of glands?

A

• Adenocarcinoma (malignant glandular epithelium)

34
Q

Examples of benign mesenchymal tumours?

A
  • Lipoma (mass of fat)
  • Chondroma (cartillage)
  • Osteoma (tumour of bones)
  • Leiomyoma (tumour of smooth muscle)
  • Rhadbdomyoma (tumour of skeletal muscle)
35
Q

Examples of malignant mesenchymal tumours?

A
  • Chondrosarcoma (malignant cartilage tumour)
  • Osteosarcoma (malignant bone tumour)
  • Leiomyosarcoma (malignant smooth muscle tumour)
  • Rhabdomyosarcoma (malignant skeletal muscle tumour)
36
Q

Haemopoietic and Lymphoid Cell tumours?

A

All are malignant as they are in the blood so are already systemic

  • Leukaemias (abnormal cells in the blood)
  • Lymphomas (abnormal cells in the lymphnodes)
  • Haemangioma (benign tumour of blood vessels)
  • Angiosarcoma (malignant tumour of blood vessels)
37
Q

What are tumours in the CNS?

A

Gliomas

38
Q

What can melanocytic tumours be?

A

Moles (benign) or melanoma (malignant)

39
Q

Describe staging and grading of a tumour

A

Staging describes the tumour size and whether it has spread beyond the area it first started and grading describes how it looks under the microscope compared to normal cells.

40
Q

Describe the different effects of tumours

A

Compression of structures, blocking of structures (e.g. airways and blood vessels), may result in loss of function.
Infection due to things not draining
Energy and weight loss due to requirement from tumour and also tumours produce molecules that result in increased metabolism
Invasion of other structures and organs can result in nerve function loss or risk of haemorrhaging in blood vessels.
Paraneoplastic syndrome is when tumours do things they shouldn’t and is usually hormonal or neurological e.g. fever or electrolyte disturbance
Immunosuppression as tumours attempt to evade the immune system
Metastases to bone, makes bone weaker and get pathological fractures and calcium metabolism is impacted.

41
Q

What is another word for a neutrophil?

A

Polymorph

42
Q

Describe the difference between the two forms of cell death

A

Necrosis:
• Does not require energy
• Necrosis is always pathological and never occurs as a physiological phenomenon. No physiological example.

Apoptosis:
• Programmed cell death in response to specific signals
• This requires energy.
• Sometimes cell death is physiological and we need cells to die off.

43
Q

Describe coagulative necrosis

A
  • Frequently caused by lack of blood supply.
  • Most common type in sudden injury
  • Preservation of cell outline
  • Dead cells are consumed by various enzymatic processes and cells.
  • Microenvironment too toxic for proteolysis
44
Q

Describe liquefactive necrosis

A
  • Death of cells in the brain.
  • Liquid viscous mass, complete loss of structure (hole where structure was previously).
  • Pus.
  • Associated with localised and fungal infections.
  • This is the necrosis that occurs in the brain.
45
Q

Describe caseous necrosis

A
  • Microscopic
  • Usually associated with Tuberculosis
  • The necrotic tissue has a ‘cream-cheesy’ appearance.
46
Q

Describe the extrinsic apoptotic pathway

A
  • All cells have a death receptor in the membrane and all those receptors have a death domain associated with them.
  • Death receptors – Tumour necrosis factor (TNF) or Fas
  • These result in the activation of initiator caspases.
47
Q

Describe the intrinsic apoptotic pathway

A
  • Known as mitochondrial pathway
  • Growth signals promote anti-apoptotic molecules in mitochondrial membrane
  • When removed they are replaced by Bax, Bak resulting in an increase in permeability of mitochondria
  • This causes release of pro-apoptotic molecules e.g. Cytochrome C which activate initiator caspases.
48
Q

What is carcinoma in situ?

A

Carcinoma in-situ is dysplasia affecting the whole of the epithelium, this applies to non-glandular epithelium.

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