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ED Primary Exam > Week 3 Pathology - Immunity and Neoplasia > Flashcards

Week 3 Pathology - Immunity and Neoplasia Flashcards

1
Q

What is innate immunity? Components?

A

Mechanisms to fight infection before they occur - rapid response within the first 12 hours

Epithelial barriers, phagocytes, dendritic cells, NK cells, complement

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2
Q

What is adaptive immunity? What are the two types?

A

Mechanisms stimulated by specific infection, generated targeted response against inciting pathogen.

1) Humoral –> extracellular pathogens

2) Cell mediated –> intracellular pathogens

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3
Q

What is the role of macrophages?

A

Digestion of microbes and protein antigens, allowing them to be presented as peptide fragments on MHC II molecules to T cells (function as antigen presenting cells)

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4
Q

What are the two pathways by which phagocytosis occurs for macrophages?

A
  1. Non-opsonic: scavenger receptors, c-type lectin receptor (direct recognition)
  2. Opsonic: Fc receptor + Ab or complement (indirect recognition)
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5
Q

What is the role of B cells?

A

Mediator of humeral response, production of antibodies (plasma cells).

Begin life as ‘naive’ B cells, with membrane bound antibodies, which after stimulation with an antigen, cause them to develop into plasma cells capable of producing antibodies against the antigen

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6
Q

What is the role of MHC-I molecules?

A

Expressed on all nucleated cells, recognised by CD8-T cells, (cytotoxic T lymphocytes) derived from intracellular proteins/peptides

i.e. are useful for INTRAcellular pathogens

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7
Q

What is the role of MHC-II molecules?

A

Expressed on antigen presenting cells (macrophages, B cells, dendritic cells)

Presenting antigens that have been phagocytosed/internalised into vesicles/lysosomes and combined with MH-II to be presented on membrane for recognition by CD4 positive T cells

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8
Q

For repetition, difference between MHC I and II?

A

I = intracellular pathogens, all nucleated cells produce them, allow recognition by CD8 T cells

II = extracellular pathogens, expressed by APC, for CD4 recognition

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9
Q

What cells predominantly secrete cytokines?

A

Dendritic cells, activated lymphocytes and macrophages

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10
Q

What are the cytokines involved in chemotaxis?

A

TNF, IL-1, IL-2, Type I IFNs

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11
Q

What are the cytokines involved in adaptive immunity?

A

IL-2, IL-4, IL-5, IL-17, IFN-gamma

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12
Q

What are the cytokines involved in limiting adaptive immune response?

A

IL-10, TGF - beta

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13
Q

Where is complement formed? Where is it found?

A

Synthesised in the liver, found in plasma in inactive form

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14
Q

What are the 3 different pathways of complement activation?

A
  1. Classical pathway: C1 fixation to Ab/Ag complex
  2. Alternate pathway: microbial surface molecule, in absence of Ab
  3. MB-Lectin Pathway: trigger by mannose binding lectin protein binding to carbohydrates on microbes, directly activating C1
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15
Q

What is the critical step in complement activation?

A

Activation of C3 - most abundant

All pathways converge on a common pathway step which is formation of C3 convertase, splitting C3 into C3a and C3b.

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16
Q

Regarding As and Bs, memory aid for recalling function?

A

In general, B sticks to the membrane like honey to a B.

A is released, and goes to get more help (C3a and C5a stimulate histamine release from mast cells, and chemotaxis of monocytes, granulocytes to site of inflammation)

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17
Q

What is the result of C3b binding to membrane of pathogen?

A

Formation of C5 convertase, cleaves C5 into C5a and B.

C5b remains attached to cell surface and binds ‘late components’ C6-9 which form MAC –> direct cell lysis via making cells permeable to water and ions

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18
Q

What are the most important opsonins?

A

Fc portion of IgG
C3b
Lectin

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19
Q

What is Type I Hypersensitivity characterised by?

A

“IgE mediated hypersensitivity”

Also known as immediate hypersensitivity

The “traditional” allergic reaction, responsible for allergy/anaphylaxis/asthma.

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20
Q

What are the two phases involved in Type I hypersensitivity?

A

Sensitisation phase
- Exposure to allergen leads to production of IgE specific antibodies to allergen (after APC present to T helper cells), which then coat the surface of mast cells and basophils

Allergy Phase
- second exposure leads to allergen bound by surface IgE, cross linking and degranulation of mast cells –> increased vascular permeability, bronchoconstriction, vasodilation, increased mucosal secretion

21
Q

What is Type II hypersensitivity?

A

Antibody dependent cytotoxic hypersensitivity

IgM or IgG: can be intrinsic (made by cells) or extrinsic (attaches to host cell, i.e. haemolytic disease of the newborn)

22
Q

What is the mechanism of Type II hypersensitivity>?

A

Antibodies bind to self cell, and then trigger a complement reaction that opsonises the cell for destruction

23
Q

What are some examples of Type II hypersensitivity?

A

Blood transfusion reaction/ABO incompatibility, haemolytic anaemia, Goodpasture’s Syndrome

24
Q

What is the fundamental cause of Type III hypersensitivity reactions?

A

Deposition of Antigen-Antibody complexes within vessel walls (i.e. the antibody is not to a specific tissue, like in Type II hypersensitivity, it is more indiscriminate, and is more about where these complexes end up)

25
Q

What types of antigens are commonly involved in Type III?

A

DNA
Nucleoproteins

26
Q

How does Type III cause inflammation?

A

Soluble immune complexes are deposited within vessel walls, and activate complement –> which then opsonises and causes chemotaxis of immune cells to area, leading to more damage, as well as increased vascular permeability and oedema

27
Q

What are examples of Type III hypersensitivity?

A

SLE
Rheumatoid arthritis
PSGN
Serum sickness

28
Q

Regarding complement, how does it differentiate between Type II and III hypersensitivity?

A

Type III = significant activation of complement, and so low levels indicate high activity and also used to track progression of disease

29
Q

What is type IV hypersensitivity?

A

“T cell mediated hypersensivity”

CD4 or CD8 T cells that recognise antigens on APC and attack (meant to be helpful in intracellular infection or malignancy) –> not involving antibodies

Examples = T1DM, IBD, contact dermatitis

30
Q

What is a broad definition of scleroderma?

A

Multisystem autoimmune disorder characterised by functional and structural abnormalities of small blood vessels, fibrosis of skin and internal organs, and production of autoantibodies

31
Q

What is the CREST acronym for recalling features of cutaneous scleroderma?

A

C = Calcinosis
R = Reynauds
E = Oesophageal dysmotility
S = Sclerodacytyly
T = telangiectasia

32
Q

What auto-antibodies are generally present in SLE?

A

ANA (anti-nuclear antibody), dsDNA, anti-Rho, anti-SM

33
Q

What are the most common symptoms of lupus?

A

Skin and joint manifestations:
- Arthritis, symmetrical small joints
- Malar rash
- Photosensitive rash

34
Q

What other systems can be affected by lupus?

A

Resp: effusions, restrictive lung disease, pneumonitis/fibrosis

Card: myopericarditis, valvular disease, cardiomyopathy

Renal: GN

35
Q

What cells are first to become infected in HIV?

A

Via mucosal tissues, T cells and dendritic cells and macrophages

36
Q

Where does infection initially become established in HIV?

A

Lymphoid tissue

37
Q

What receptor does HIV target/show tropism for?

A

CD4 molecules - present on monocytes, macrophages, densities cells

38
Q

What co-receptors are required for HIV infection to occur?

A

CCR5 and CXCR4

39
Q

What is the life cycle of HIV once inside infected cell?

A

RNA genome of HIV undergoes reverse transcription into complementary DNA, which circularises and incorporates into host genome.

Latent infection means can remain dormant for years. Active infection occurs when genome is transcribed and viral particles form which bud from membrane of infected cell.

Because immune cells are activated in infection, HIV particles undergo increased transcription with activation by cytokines, inducing increased cell activation and lysis –> infection

40
Q

What are the 3 broad stages of HIV infection?

A
  1. Active infection: CD4 >500, 4-8 weeks, increased HIV RNA load
  2. Latency: CD4 200-500, count gradually decreases every approx 10 years
  3. AIDS: CD4<200, progression to opportunistic infections, malignancy, neurological symptoms
41
Q

What are AIDS defining illnesses?

A

Cryptococcal meningitis, TB, PJ pneumonia, Kaposi sarcoma

42
Q

Define neoplasm:

A

Abnormal mass of tissue, with uncoordinated growth that persists in excessive manner after stimulus removed - triggered by acquired mutations in single cell

43
Q

What is the major difference between benign vs malignant tumours RE local invasion?

A

Benign tissues grow as cohesive expansive mass, remains localised to site of origin, lack ability to invade and metastasise to distant sites

**Malignant tumours tend to invade and destroy surrounding tissues

44
Q

What defines metastasis?

A

Spread of tumour to a site physically discontinuous with primary tumour

45
Q

What are the different routes of metastatic spread from a localised cancer?

A
  1. Direct seeding of body cavity/surface (i.e. ovarian to peritoneum
  2. Lymphatic spread
  3. Haematogenous spread (typically following invasion of veins)
46
Q

What factors of normal cells/tissues prevent malignancy/metastasis?

A

division of tissues into their own compartments by ECM (basement and interstitial connective tissue)

47
Q

Broadly describe process of metastasis from primary malignancy to secondary site:

A
  • Loosening of cell-cell connections, and degradation via enzyme of ECM and basement membrane
  • Attachment of tumour cell to disrupted BM and migration across ECM cytoskeleton
  • Invasion into bloodstream and adhesion to platelets, and then deposition and attachment to BM at distant site (tumour emboli)
  • Angiogenesis and growth, as tumour cells secrete cytokines and growth factors that act on resident stromal cells to make the new site a habitable environment
48
Q

Define paraneoplastic syndrome:

A

Development of signs and symptoms that can’t be explained by anatomical distribution of tumour or hormones indigenous to tissue it arose

49
Q

What are some examples of paraneoplastic syndrome?

A

Hypercortisolism in SCLC, pancreatic cancer
Hypogylcaemia in Ovarian Ca, HCC
Acanthosis nigricans in Gastric, lung and uterine cancer

ED Primary Exam (46 decks)

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