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1
Q

List 3 features to take into account when grading cancer

A
  • Degree of differentiation
  • Mitotic rate
  • Nuclear grade
  • Necrosis
  • Pleomorphism
  • Integrity of cells
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2
Q

List 4 characteristics used in the staging of cancer

A
  • Site of the primary tumour
  • Local spread into surrounding tissue
  • Spread into lymphatics or veins
  • Spread to local and distant lymph nodes
  • Metastatic spread
  • Involvement of excision margins
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3
Q

Describe the sequence of example events during carcinogenesis

A

Loss of response to growth control signals
Ability to promote angiogenesis
Ability to evade apoptosis

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4
Q

How does PTEN promote apoptosis?

A

PL3 kinase inhibition. PTEN dephosphorylates PIP2 -> PIP3. PIP3 activates Akt which blocks FOXO activity by phosphorylation resulting in decreased cell death.

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5
Q

What is a tumour suppressor gene, and give example.

A

Inhibitory genes regulating proliferation

p53, PTEN, BRCA1/2, APC, pRB, p27KIP1, p16INK4a

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6
Q

What is an oncogene, and give an example.

A

A gene that stimulates cell growth and proliferation, that is aberrantly expressed and insensitive to growth control signals. E.g. HER2, Ras, Raf, EGFR, CyclinD1, cMyc

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7
Q

Describe 2 differences between benign and malignant tumours

A 
Malignant:
Invades + Metastasises
Fast Growth
Less differentiated
NOT encapsulated
Abnormal mitoses
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8
Q

4 types of protozoa and examples of each

A

Amoeba - entamoeba histolyca
Coccidia - toxoplasma gondii
Flagellate - leishmania
Ciliate - balantidium coli (immunosuppressed, diarrhoea)

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9
Q

What are the two types of leishmaniasis and give features of each

A

Visceral - affects internal organs
BLACK FEVER: irregular fever, hepatosplenomegaly, weight loss

Cutaneous (e.g. localised cutaneous) - crusted lesions/scars

Worsened with HIV co-infection

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10
Q

What is hypersensitivity?

A

Tissue damaging immune responses mounted against harmless foreign antigens, autoantigens or alloantigens

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11
Q

Give the 4 types of hypersensitivity, with mechanisms and examples of each

A

Type I = immediate, IgE mediated. Need sensitisation - primary exposure to form IgE. Then secondary exposure antigen can cross link IgE -> mast cell degranulation, eosinophil and basophil recruitment. An aphylaxis, asthma, rhinitis, food allergy

Type 2 = Ab-dependent cytotoxicity. Tissue damage. e.g. Pernicious anemia. Hemolytic anemia.

Type 3 = Immune complex. Antigen-antibody complexes form in blood - deposition in tissue. Complement, cell activation/recruitment, activation of other cascades Causes vasculitis. SLE

Type 4= T-cell, delayed. Transient/persistent antigen causes T cell activation of macrophages, CTLs causes tissue damage - dependant on TNF alpha. Th1 or CTLs release TNFa. Contact dermatitis, chronic graft rejection

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12
Q

What are 6 ways in which pathogenic infections can contribute to the onset of autoimmune disease?

A
  1. Molecular mimicry of self molecules
  2. Induce changes in the expression and recognition of self proteins
  3. Induction of costimulatory molecules or inappropriate MHC class II expression: pro-inflammatory environment
  4. Effects on regulatory T-cells (failure of regulation)
  5. Immune deviation: shift in type of immune response e.g. Th1-Th2
  6. Tissue damage at immunologically privileged sites
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13
Q

A man presents with your surgery with a raised haematocrit and Hb. He is a smoker. Imaging shows a mass in his right kidney. List 4 possible causes for his raised Hb and haematocrit.

A

Renal tumour secreting erythropoeitin
Blood doping
Polycythaemia vera
Pseudo-polycythaemia (reduced plasma volume)
Increased EPO due to hypoxia (CO in smoke binds to Hb, O2 binding availability decreased, kidney secretes more EPO)

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14
Q

A man presents with your surgery with a raised haematocrit and Hb. He is a smoker. Imaging shows a mass in his right kidney. List 4 possible causes for his raised Hb/Hct and their mechanisms.

A

Renal tumour secreting EPO

Blood doping

Polycythaemia vera - bone marrow disorder producing too many red cells regardless of EPO

Increased EPO due to hypoxia (CO in smoke binds to Hb, O2 binding availability decreased, kidney secretes more EPO)

Pseudo-polycythaemia (reduced plasma volume)

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15
Q

Give 5 causes of normocytic normochromic anaemia

A
  1. Recent blood loss
  2. Early IDA/ACD
  3. Renal failure (low EPO)
  4. Bone marrow failure
  5. Hypersplenism - pooling of RBCs
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16
Q

What would you see on blood film of haemolytic anemia

A

Reticulocytosis

17
Q

Why does G6PD deficiency lead to anaemia? What would you see on blood film?

A

G6PD important in protection from oxidants (pentose phosphate shunt)
No G6PD -> Hb denatured by oxidants

Forms HEINZ bodies which are removed by spleen
Results in IRREGULARLY CONTRACTED CELLS

18
Q

Why does G6PD deficiency lead to anaemia? What would you see on blood film?

A

G6PD important in protection from oxidants (pentose phosphate shunt)
No G6PD -> Hb denatured by oxidants

Forms HEINZ bodies which are removed by spleen
Results in IRREGULARLY CONTRACTED CELLS

19
Q
  1. Two types of viruses with genetic drift and we have vaccines for them
  2. Genetic drift vs Genetic shift.
  3. How do viruses evade interferon detection? Give 4 examples.
  4. Give three examples of cytoplasmic sensors for viruses and how they work
A

Influenza, Polio
Genetic drift = Continued rapid evolution driven by antigenic pressure from host
Genetic shift = Introduction of new subtypes from animal source

Hep C - cleaves Mavs
Influenza - Binds Rig-I/RNA complex + goes to nucleus and inhibits translation
Ebola: Inhibits Rig-I, stops IFN signalling in neighbour cells
Pox - Soluble cytokines receptors ‘mop up’ cytokines

TLR3/7 -> detects foregin RNA -> downstream signals -> Irf3

Rig-I -> abnormal nucleic acid in cytoplasm -> activates MAVS (mitochondria) -> Irf3/7 -> IFN

cGas -> detects DNA -> makes cGAMP -> phosphorylates STING (RER) -> Irf7 -> Type 1 IFNs

20
Q

What is immunological tolerance? (3A’s) In what kind of immune cells does immunological tolerance occur?

A

Acquired inability to respond with an immune reaction to an antigenic stimulus which organism normally responds.

  1. Acquired - involves cells of the acquired immune system
  2. Antigen specific
  3. Active processes in neonates, effects maintained throughout life

Involves cells of the acquired/adaptive immune system - B and T cells.

21
Q

What is the difference between central and peripheral tolerance? Explain the mechanisms involved in each

A

Central tolerance - presentation of self-peptides by MHC during lymphocyte devleopment

Peripheral tolerance

  1. Anergy
  2. Immunological ignorance
  3. Suppression/regulation by T reg cells
22
Q

What are three causes of a prolonged APTT?

A

Problem with intrinsic or common pathway

Heparin administration, haemophilia A/B, vWD

23
Q

Name three physiological inhibitors of the clotting cascade and explain their mechanisms.

A

Antithrombin
Plasminogen activator
Protein c

24
Q

Name four functions of tumour suppressor genes

A 
Control cell cycle progression
DNA repair
Regulate apoptosis
Regulate cell proliferation and growth
Controls growth factors/transcription factors
25
Q

Why do you only need one mutated oncogene to cause neoplasia, but need two mutated tumour suppressor genes to cause neoplasia?

A

TSG are recessive. So even if one copy fails the other can still continue to do an adequate job

Oncogenes are dominant, so they only need one mutation

Cancer (18 decks)

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