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ICS 1 Flashcards

Immunology & Pathology (77 cards)

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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
Granulomas: name of cell, how the cell is made, disease list
Giant cells - made from epitheliod cells (macrophage) and lymphocytes. Eg: TB, Sarcoidosis, Leprosy, Crohn's Disease, Rheumatic Fever
26
Acute Inflammation: 4 outcomes
Resolution Suppuration (abcess/pus) Repair and Organisation Chronic Inflammamtion
27
How do you treat inflammation? 2 methods and mechanism
1. NSAIDS - aspirin, ibuprofen, inhibit prostaglandin synthesis 2. Corticosteroids: upregulate inhibitors and down regulate chemical mediators by binding to DNA
28
Two parts of the definition of atherosclerosis?
Hardening of arteries | Narrowing due to plaque
29
Atherosclerosis mechanism steps.
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
30
Apoptosis - mechanism
Cell shrinkage, caspases act, vesicles formed (apoptotic vesicles), phagocytes clean up
31
Apoptosis - how is it regulated control
BAX (+ve) Bcl2 (-ve) Fas receptor and ligand
32
6 types of necrosis
Coagulative necrosis (infarction) Liquefactive necrosis (bacteria, fungal, infection) Caseous necrosis (mycobacteria - TB) Fat necrosis (lipases) Fibrinoid necrosis. (immune complexes) Gangrenous necrosis (gangrene)
33
Difference between thrombosis and a clot?
Thrombosis: within the vascular system during life Clot: blood coagulation outside of the vascular system or after death
34
Carcinogenesis definition? | Difference between carcinogenesis and oncogenesis?
Carcinogenesis: 'the transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations' Oncogenesis: 'benign and malignant'
35
3 characteristics of a neoplasm? Structure of a neoplastic tumour?
Neoplasms (new growths) are autonomous, abnormal, persistent. Contain neoplastic cells (monoclonal, nucleated, secreting) and stroma (mechanical support, nutrition, fibroblasts/collagen)
36
How big can tumour get before angiogenesis/blood vessel recruitment is needed?
1-2mm^3
37
Carcinogen definition and categories (+ examples)
Carcinogens - 'agents known or suspected to cause tumours' ``` Chemical (polycyclic aromatic hydrocarbons) Viral (HPV) Radiation (UV light) Hormones/Parasities/Mycotoxins Miscellaneous (asbestos) ```
38
Most common cancers in UK? | Which cancers kill the most?
Breast (F) / Prostate (M) Lung Bowel Lung Bowel Breast/Prostate
39
Which carcinomas most commonly spread to bone? (5)
``` Breast Prostate Lung Thyroid Kidney ```
40
3 types/stages of a carcinoma?
Carcinoma in situ Micro-invasive carcinoma Invasive carcinoma
41
Stages of metastasis?
``` • Invasion of basement membrane • Tumour cell motility • Intravasation • Evasion host immune defence • Extravasation • Growth at metastatic site • Angiogenesis ```
42
Two types of chemotherapy? Mechanism? Example?
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
Benign epithelial cell neoplasm nomenclature? Examples
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
Malignant epithelial cell neoplasm nomenclature? Examples?
Carcinoma: malignant tumour of epithelial cells Example: transitional cell carcinoma Adenocarcinoma: malignant tumour of glandular epithelum Example: adenocarcinoma of prostate, adenocarcinoma of breast
45
Connective tissue neoplasm nomenclature? Examples (7)
``` Lipoma, Liposarcoma (adipocytes) Rhabdomyoma, Rhabdomyosarcoma (skeletal/striated muscle) Leiomyoma, Leiomyosarcoma (smooth muscle) Chondroma/Chondrosarcoma (cartilage) Osteoma/Osteosarcoma (bone) Angioma/Angiosarcoma (vascular) ```
46
Exceptions to neoplasm nomenclature? | Have '-oma' but are malignant
Melanoma - malignant neoplasm of melanocytes Mesothelioma: malignant tumour of mesothelial cells, eg pleura or peritoneum Lymphoma: malignant neoplasm of lymphoid cells
47
TNM classification of tumours? Will lead to?
T - primary tumour size N - number of lymph nodes affected M - amount and distance of metastases Will lead to a cancer STAGE
48
Significance of p53 protein? What chromosome? | Significance of RB1 gene?
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
TUMOUR SUPPRESSOR GENES: | Two types?
Gatekeepers: p53, RB1 (inhibits proliferation or promotes cell death) Caretaker: BRCA1/2 (maintain the integrity of the genome, by repairing DNA damage)
50
Tumour grade: what is it?
Assessment of its degree of malignancy or aggressiveness, from histology (mitotic activity, nuclear size, differentiation)
51
What would come out of centrifuged blood?
Plasma 55% - water, electrolytes, proteins Buffy Coat <1% - leukocytes + proteins Erythrocytes 45% - haematocrit
52
How are bradykinin's formed?
Activated factor XII (Hageman factor) Prekallikrein turns to Kallikrein Kinninogen to Bradykinin
53
How does damaged cells lead to inflammatory cytokines?
Damage to lipid membrane Arachadonic acid goes through: 1. Lipoxygenase: Leukotrienes 2. COX 1,2: Prostaglandins
54
3 endothelial cell receptors presented to enhance margination of WBC? When are they shown?
P-selectins (initially) E-selectins (IL-1/TNF-alpha) ICAMs, VCAMs (IL-1/TNF-alpha)
55
Systemic signs of inflammation? (due to TNF-alpha, IL-1)
Fever (via hypothalamus and PGE2) Leukocytosis (in bone marrow) Liver acute phase reactants due to IL6 (CRP, complement, fibrinogen)
56
Two mechanisms of killing in phagocytosis? | 4 free radicals
1. Oxygen independent (lysozymes, defensins, pH) | 2. Oxygen-dependent (O2-, H2O2, OH-, HOCl)
57
What does PRRs stand for? What do they do? Two main types and examples
Pattern Recognition Receptors Recognise PAMPs and DAMPs Cell associated: TLRs, NLRs, RLRs Secreted + circulating: Defensins, Cathepsins, Lectins, Collectins, Pentraxins (CRP)
58
Primary and Secondary lymphoid tissues?
Primary: Thymus (t-cells) Bone marrow (b-cells) Secondary: Spleen/Lymph nodes/MALT
59
3 types of antigen presenting cells? What receptor do they present specifically?
• Dendritic Cells • Macrophages • B Cells Will have Major Histocompatibility Complex II
60
How do antibodies act? (4)
Neutralisation Opsonisation Complement Activation Agglutination
61
3 actions of complement?
Cause lysis of pathogens using 'membrane attack complex' (MAC) Increases chemotaxis via C3a, C5a Opsonisation via C3b
62
3 complement pathways? What complement proteins binds first in each pathway?
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
What are interferons? What cells make them? Different types? What is their action?
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
Basic humoral immunity process?
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
T-helper 1 vs T-helper 2 model: What determines which is produced? What do each perform?
T-helper 1: high IL-12 Help cell-mediated immunity T-helper 2: low IL-12 Help humoral immunity
66
Basic cell mediated immunity process?
CD8+ cytotoxic T-cell recognize non-self antigens, and viral antigens on MHC I. Kill via perforins and granzymes.
67
Function of T-reg cells | Function of NK cells.
T-regulatory cells: Suppresses autoimmunity, down-regulates other T-cells Natural Killer Cells: Innate immunity, killing pathogens via perforins and granzymes
68
Antibody structure? Draw and then mark on: | Structure of antigen-antibody complex
Heavy Chains, Light Chains Disulfide bonds Variable Region, Constant Region FAB fragment: region on antibody that binds Epitope: region on antigen that binds
69
How do B-cells and T-cells randomly assemble genes?
Somatic (VDJ) recombination: | Forms massive variety of TCRs and BCRs
70
``` IgG antibody: How abundant? Monomer, Dimer, Pentamer? Can it cross placenta? Normal role? ```
``` IgG antibody: 80% in plasma Monomer Can cross placenta Normal antibody functions ```
71
``` IgA antibody: How abundant? Monomer, Dimer, Pentamer? Where is it found? Can it cross placenta? ```
``` IgA antibody: 10% in plasma Dimer Found in secretions and mucosa No. Transferred in breast milk ```
72
``` IgM antibody: Monomer, Dimer, Pentamer? How is it linked? When is it made? Main roles? ```
IgM antibody: Pentamer Linked by J protein Made in primary immune response (first exposure) Good at fixing complement and agglutination
73
``` IgE antibody: Monomer, Dimer, Pentamer? Where is it found? On what cell? Roles? Abundant? ```
``` 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
IgD antibody: Monomer, Dimer, Pentamer? Role?
IgD antibody: Monomer Acts as a B cell receptor (BCL) - binds to antigens in humoral immunity
75
5 kinds of arteries affected by atherosclerosis?
``` Carotid Aorta Coronary Cerebral Common Iliac/Femoral ```
76
3 routes of metastasis?
Haematogenous (blood) Lymphatic (lymph) Transcoelomic (cavities - abdo, chest)
77
Histological findings of a malignant tumour? (3)
Pleomorphism Hyperchromatic nuclei Poorly defined border

Phase 2a (9 decks)

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