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Phase 2a > ICS 1 > Flashcards

ICS 1 Flashcards

Immunology & Pathology

1
Q

What are the 3 tissues that can’t regenerate?

A

Cardiac Muscle, Nerve, Skeletal Muscle fibres

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2
Q
  1. Difference between hypertrophy and hyperplasia?
  2. Do they generally occur together? Example?
  3. Exceptions to this rule?
A
  1. Hypertrophy = size of cell, Hyperplasia = number of cells
  2. Yes. Eg, uterus in pregnancy
  3. Permanent tissues, eg. heart (only hypertrophy)
    Endometrium - only hyperplasia
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3
Q

What does pathogenic hyperplasia lead to? Exception to this rule?

A

Dysplasia (abnormal cells) possibly leading to cancer

Exception: Benign prostatic hyperplasia

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4
Q

Why does atrophy occur? Defintion? Mechanism?

A

Decrease in stress on an organ
Decrease in both size cell and nunber
Via apoptosis (ubiquitin or autophagy)

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5
Q

Metaplasia definition? Example? Lead to? Is it reversible?

A

Change in cell type (usually surface epithelium)
Example: Barrett’s Oesophagus, Bronchii of a smoker
It IS reversible (remove the stimulus)
Can lead to dysplasia and cancer

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6
Q

What are the two options after tissue damage has occurred? What determines which of these occurs?

A

Regeneration or Repair

Determined by tissue type and whether the damaging stimulus is removed

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7
Q

When does tissue regeneration occur? Example? Mechanism?

A

Occurs with acute inflammation, with removal of damaging stimulus. Eg, liver regenerates using stem cells after tumour

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8
Q

When does tissue repair occur? Example? Mechanism?

A

Occurs with chronic inflammation, with sustained damaging stimulus. Eg, liver with cirrhosis after excessive alcohol, fibrosis occurs

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9
Q

What occurs in the brain instead of fibrosis?

A

Gliosis

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10
Q

Healing by 1st intention mechanism? Skin wounds

A

Sutures - bring skin close together.

Weak fibrin joins wound. Replaced by collagen. Replaced by normal cells with remodelling.

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11
Q

Healing by 2nd intention mechanism? Skin wounds

A

Skin can’t be brought together. Granulation tissue formed, heals from the bottom up. Larger scar formed.

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12
Q

Two types of blood flow? How does this affect clotting?

A

Laminar flow: cells move through centre of blood vessel

Turbulent flow: cells move chaotically all around the blood vessel

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13
Q

What is Virchow’s Triad? Definition & categories

A

3 categories contributing to thrombosis
Endothelial cell damage (endothelial dysfunction)
Change in blood flow (stasis or turbulence)
Change in blood constituents (hypercoagubility)

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14
Q

Define thrombosis

A

solid mass of blood constituents formed within the vascular system during life

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15
Q

Differences of venous thrombosis?

A

More commonly due to slow blood flow - especially without muscle use.

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16
Q

5 possible outcomes from thrombosis?

A
  1. Lysis and resolution (plasmin)
  2. Organisation (fibrosis, grows within vessel layer)
  3. Recanalisation (holes)
  4. Embolism (dislodges)
  5. Propagation (growing along the vessel)
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17
Q

Define embolism. Causes? (4)

A

Mass of material in the vascular system: lodging and blocking a blood vessel:
thrombo-embolism, fat, tumour, air

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18
Q

Definitions of ischaemia and infarction?

A

Ischaemia: reduction in blood flow
Infarction: cell death due to reduction in blood flow

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19
Q

What is reperfusion injury? Basic mechanism?

A

Tissue damage caused when blood supply returns to tissue after ischaemia
Lack of antioxidants, ROS released, Damaged further

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20
Q

End-artery vs Dual-artery - definitions and significance

A

End-artery: artery that is only supply of oxygenated blood to tissue (most organs)
Dual-artery: tissue with two supplies of oxygenated blood (lungs, liver, parts of brain)

End-artery far more likely to undergo infarction and ischaemia

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21
Q

Two classes of anti-thrombotic drugs? Mechanism? 2 examples of each?

A

ANTICOAGULANTS: slow down clotting
eg:
Heparin - blocks thrombin from allowing: ‘fibrin to fibrinogen’
Warfarin - inhibits production of Vitamin K dependent clotting (10, 9, 7, 2)

ANTIPLATELETS: stop platelet aggregation
eg:
Aspirin - stops thromboxane formation
Clopidogrel - binds to P2Y12 ADP receptors

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22
Q

5 signs of inflammation? (local)

A 
Heat (calor)
Redness (rubor)
Swelling (tumor)
Pain (dolor)
Joint Immobility
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23
Q

Acute inflammation: characteristics? main cell involved?

A

Sudden onset, short duration, usually resolves

Main cell: Neutrophil polymorph

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24
Q

Chronic inflammation: characteristics? cells involved?

A

Slow onset, long duration, usually doesn’t resolve

Cells: Plasma, Macrophage, Lymphocyte, Giant cells (granuloma)

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25
Q

Granulomas: name of cell, how the cell is made, disease list

A

Giant cells - made from epitheliod cells (macrophage) and lymphocytes.
Eg: TB, Sarcoidosis, Leprosy, Crohn’s Disease, Rheumatic Fever

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26
Q

Acute Inflammation: 4 outcomes

A

Resolution
Suppuration (abcess/pus)
Repair and Organisation
Chronic Inflammamtion

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27
Q

How do you treat inflammation? 2 methods and mechanism

A
  1. NSAIDS - aspirin, ibuprofen, inhibit prostaglandin synthesis
  2. Corticosteroids: upregulate inhibitors and down regulate chemical mediators by binding to DNA
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28
Q

Two parts of the definition of atherosclerosis?

A

Hardening of arteries

Narrowing due to plaque

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29
Q

Atherosclerosis mechanism steps.

A

Endothelium damage due to irritants, causes LDL deposition, where it is oxidised

oxLDL is taken in by macrophage, becomes FOAM cells

FOAM cells promote migration of smooth muscle from media and more WBC migration

Plaque forms with FOAM cells, collagen, dead cell centre - RUPTURES and causes THROMBOSIS

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30
Q

Apoptosis - mechanism

A

Cell shrinkage, caspases act, vesicles formed (apoptotic vesicles), phagocytes clean up

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31
Q

Apoptosis - how is it regulated control

A

BAX (+ve)
Bcl2 (-ve)
Fas receptor and ligand

32
Q

6 types of necrosis

A

Coagulative necrosis (infarction)

Liquefactive necrosis
(bacteria, fungal, infection)

Caseous necrosis
(mycobacteria - TB)

Fat necrosis
(lipases)

Fibrinoid necrosis.
(immune complexes)

Gangrenous necrosis
(gangrene)

33
Q

Difference between thrombosis and a clot?

A

Thrombosis: within the vascular system during life
Clot: blood coagulation outside of the vascular system or after death

34
Q

Carcinogenesis definition?

Difference between carcinogenesis and oncogenesis?

A

Carcinogenesis: ‘the transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations’

Oncogenesis: ‘benign and malignant’

35
Q

3 characteristics of a neoplasm?

Structure of a neoplastic tumour?

A

Neoplasms (new growths) are autonomous, abnormal, persistent.

Contain neoplastic cells (monoclonal, nucleated, secreting) and stroma (mechanical support, nutrition, fibroblasts/collagen)

36
Q

How big can tumour get before angiogenesis/blood vessel recruitment is needed?

A

1-2mm^3

37
Q

Carcinogen definition and categories (+ examples)

A

Carcinogens - ‘agents known or suspected to cause tumours’

Chemical (polycyclic aromatic hydrocarbons)
Viral (HPV)
Radiation (UV light)
Hormones/Parasities/Mycotoxins
Miscellaneous (asbestos)
38
Q

Most common cancers in UK?

Which cancers kill the most?

A

Breast (F) / Prostate (M)
Lung
Bowel

Lung
Bowel
Breast/Prostate

39
Q

Which carcinomas most commonly spread to bone? (5)

A 
Breast
Prostate
Lung
Thyroid
Kidney
40
Q

3 types/stages of a carcinoma?

A

Carcinoma in situ
Micro-invasive carcinoma
Invasive carcinoma

41
Q

Stages of metastasis?

A 
• Invasion of basement 
  membrane
• Tumour cell motility
• Intravasation
• Evasion host immune 
  defence
• Extravasation
• Growth at metastatic site
• Angiogenesis
42
Q

Two types of chemotherapy? Mechanism? Example?

A

Conventional chemotherapy:
Antimicrotubule, topoisomerase inhibitors, DNA synthesis inhibitors
Non-selective - cause myelosuppresion, hair loss, diarrhoea
Good for fast dividing tumours (leukaemia, lymphoma, choriocarcinoma)

Targeted chemotherapy:
exploits difference between cancer cells and normal cells, often blocking growth factor receptors
Herceptin in breast cancer, CetuxiMAB (monoclonal antibody)

43
Q

Benign epithelial cell neoplasm nomenclature? Examples

A

Papilloma: benign tumour of non-glandular, non-secretory epithelium
Example: squamous cell papilloma and transitional cell papilloma

Adenoma: benign tumour of glandular or secretory epithelium
Example: colonic adenoma, thyroid adenoma

44
Q

Malignant epithelial cell neoplasm nomenclature? Examples?

A

Carcinoma: malignant tumour of epithelial cells
Example: transitional cell carcinoma

Adenocarcinoma: malignant tumour of glandular epithelum
Example: adenocarcinoma of prostate, adenocarcinoma of breast

45
Q

Connective tissue neoplasm nomenclature? Examples (7)

A 
Lipoma, Liposarcoma (adipocytes)
Rhabdomyoma, Rhabdomyosarcoma (skeletal/striated muscle)
Leiomyoma, Leiomyosarcoma
(smooth muscle)
Chondroma/Chondrosarcoma
(cartilage)
Osteoma/Osteosarcoma
(bone)
Angioma/Angiosarcoma
(vascular)
46
Q

Exceptions to neoplasm nomenclature?

Have ‘-oma’ but are malignant

A

Melanoma - malignant neoplasm of melanocytes
Mesothelioma: malignant tumour of mesothelial cells, eg pleura or peritoneum
Lymphoma: malignant neoplasm of lymphoid cells

47
Q

TNM classification of tumours? Will lead to?

A

T - primary tumour size
N - number of lymph nodes affected
M - amount and distance of metastases

Will lead to a cancer STAGE

48
Q

Significance of p53 protein? What chromosome?

Significance of RB1 gene?

A

p53: Gatekeeper to the cell: inhibits proliferation or promotes cell death, responds to DNA damage
Chromosome 17

RB1: transcriptional regular, controlling G1/S checkpoint.
Association with retinoblastoma

49
Q

TUMOUR SUPPRESSOR GENES:

Two types?

A

Gatekeepers: p53, RB1
(inhibits proliferation or promotes cell death)
Caretaker: BRCA1/2
(maintain the integrity of the genome, by repairing DNA damage)

50
Q

Tumour grade: what is it?

A

Assessment of its degree of malignancy or aggressiveness, from histology (mitotic activity, nuclear size, differentiation)

51
Q

What would come out of centrifuged blood?

A

Plasma 55% - water, electrolytes, proteins
Buffy Coat <1% - leukocytes + proteins
Erythrocytes 45% - haematocrit

52
Q

How are bradykinin’s formed?

A

Activated factor XII (Hageman factor)
Prekallikrein turns to Kallikrein
Kinninogen to Bradykinin

53
Q

How does damaged cells lead to inflammatory cytokines?

A

Damage to lipid membrane
Arachadonic acid goes through:
1. Lipoxygenase: Leukotrienes
2. COX 1,2: Prostaglandins

54
Q

3 endothelial cell receptors presented to enhance margination of WBC? When are they shown?

A

P-selectins (initially)
E-selectins (IL-1/TNF-alpha)
ICAMs, VCAMs (IL-1/TNF-alpha)

55
Q

Systemic signs of inflammation? (due to TNF-alpha, IL-1)

A

Fever (via hypothalamus and PGE2)
Leukocytosis (in bone marrow)
Liver acute phase reactants due to IL6
(CRP, complement, fibrinogen)

56
Q

Two mechanisms of killing in phagocytosis?

4 free radicals

A
  1. Oxygen independent (lysozymes, defensins, pH)

2. Oxygen-dependent (O2-, H2O2, OH-, HOCl)

57
Q

What does PRRs stand for?
What do they do?
Two main types and examples

A

Pattern Recognition Receptors
Recognise PAMPs and DAMPs
Cell associated: TLRs, NLRs, RLRs
Secreted + circulating: Defensins, Cathepsins, Lectins, Collectins, Pentraxins (CRP)

58
Q

Primary and Secondary lymphoid tissues?

A

Primary:
Thymus (t-cells)
Bone marrow (b-cells)

Secondary:
Spleen/Lymph nodes/MALT

59
Q

3 types of antigen presenting cells? What receptor do they present specifically?

A

• Dendritic Cells
• Macrophages
• B Cells
Will have Major Histocompatibility Complex II

60
Q

How do antibodies act? (4)

A

Neutralisation
Opsonisation
Complement Activation
Agglutination

61
Q

3 actions of complement?

A

Cause lysis of pathogens using ‘membrane attack complex’ (MAC)
Increases chemotaxis via C3a, C5a
Opsonisation via C3b

62
Q

3 complement pathways? What complement proteins binds first in each pathway?

A

Classical pathway - antibody-antigen immune complexes (C1)
Alternative pathway - foreign surfaces, directly to antigen (C3b)
Lectin pathway - mannose-binding lectin on pathogen surface (C4)

63
Q

What are interferons?
What cells make them?
Different types?
What is their action?

A

Signalling molecules
Made by infected host cells
Alpha, Beta (platelets), Gamma (immune cells)
Enhance inflammation and tell healthy cells to produce anti-viral peptides

64
Q

Basic humoral immunity process?

A

Free antigen uptaken by naive B-cell, becomes activated.
Naive CD4+ T-helper is activated my APC with MHC II via co-stimulation
T-helper 2 cells, produce cytokines to allow B-cells to undergo clonal expansion and differentiation. Memory cells formed
Plasma cells with produce antibodies.

65
Q

T-helper 1 vs T-helper 2 model:
What determines which is produced?
What do each perform?

A

T-helper 1: high IL-12
Help cell-mediated immunity
T-helper 2: low IL-12
Help humoral immunity

66
Q

Basic cell mediated immunity process?

A

CD8+ cytotoxic T-cell recognize non-self antigens, and viral antigens on MHC I. Kill via perforins and granzymes.

67
Q

Function of T-reg cells

Function of NK cells.

A

T-regulatory cells:
Suppresses autoimmunity, down-regulates other T-cells
Natural Killer Cells:
Innate immunity, killing pathogens via perforins and granzymes

68
Q

Antibody structure? Draw and then mark on:

Structure of antigen-antibody complex

A

Heavy Chains, Light Chains
Disulfide bonds
Variable Region, Constant Region

FAB fragment: region on antibody that binds
Epitope: region on antigen that binds

69
Q

How do B-cells and T-cells randomly assemble genes?

A

Somatic (VDJ) recombination:

Forms massive variety of TCRs and BCRs

70
Q 
IgG antibody:
How abundant?
Monomer, Dimer, Pentamer?
Can it cross placenta?
Normal role?
A 
IgG antibody:
80% in plasma
Monomer
Can cross placenta
Normal antibody functions
71
Q 
IgA antibody:
How abundant?
Monomer, Dimer, Pentamer?
Where is it found?
Can it cross placenta?
A 
IgA antibody:
10% in plasma
Dimer
Found in secretions and mucosa
No. Transferred in breast milk
72
Q 
IgM antibody:
Monomer, Dimer, Pentamer?
How is it linked?
When is it made?
Main roles?
A

IgM antibody:
Pentamer
Linked by J protein
Made in primary immune response (first exposure)
Good at fixing complement and agglutination

73
Q 
IgE antibody:
Monomer, Dimer, Pentamer?
Where is it found? On what cell?
Roles?
Abundant?
A 
IgE antibody:
Monomer
Found in respiratory mucosa, urogential, lymphatic tissue
Binds to mast cells, for inflammation.
Allergy and anti-parasitic activity
Very rare - not abundant
74
Q

IgD antibody:
Monomer, Dimer, Pentamer?
Role?

A

IgD antibody:
Monomer
Acts as a B cell receptor (BCL) - binds to antigens in humoral immunity

75
Q

5 kinds of arteries affected by atherosclerosis?

A 
Carotid
Aorta
Coronary
Cerebral
Common Iliac/Femoral
76
Q

3 routes of metastasis?

A

Haematogenous (blood)
Lymphatic (lymph)
Transcoelomic (cavities - abdo, chest)

77
Q

Histological findings of a malignant tumour? (3)

A

Pleomorphism
Hyperchromatic nuclei
Poorly defined border

Phase 2a (9 decks)

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