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Human Pathology > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

3 layers of host defence against pathogens

A
  1. Physical barriers
    • Mechanical barriers; epidermis, ciliated cells
    • Chemical barriers; protective proteins and chemical secretions
    • Properdin in plasma activates complement system
    • Lysozymes in body fluids (saliva, tears, respiratory tract), kill bacteria
  2. Innate immune response
    • Phagocytic cells (neutrophils, macrophages, dendritic cells, natural killer cells)
  3. Adaptive immune response
    •Lymphocytes (T and B cells
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2
Q

Lymphoid lineage

A

Natural killer cells
T lymphocytes
B lymphocytes

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3
Q

Myeloid lineage

A

Mast cell
Basophil
Neutrophil
Eosinophil
Monocytes > Macrophages

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4
Q

Innate Immunity

A

• Inherited and operational at birth
• Fast to act and nonspecific
• Recognizes conserved pathogen patterns (PAMPs)
• Response to repeat infection remains relatively the same
• Trained immunity (epigenetic changes)

Protects the body via 3 mechanisms:
1. Initiating inflammation
2. Combating infections (bacterial, fungal etc.)
3. General response to damaged cell

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5
Q

Innate immune cells

A

Neutrophils
Basophils
Eosinophils
Mast cells
Macrophages
Natural killer cells
Dendritic cells

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6
Q

Adaptive (acquired) immunity

A

• Ability to distinguish “self” from “non-self”
• Specific response elicited by antigens requires time (5-7 days): “Lock and key” receptor-antigen interactions
• Immunological memory
• Rapid and effective response upon subsequent exposure to the same pathogen
• Mediated by T and B cells; antigen specific receptors and antibodies

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7
Q

Maturation of T & B lymphocytes

A

T cells: the thymus
B cells: the bone marrow

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8
Q

Primary lymphoid organs

A

Sites of lymphoid maturation (thymus and bone marrow)

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9
Q

Secondary lymphoid tissue

A

Site of lymphoid cell activation (spleen, lymph nodes, Peyers patches, adenoids, tonsils)

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10
Q

Cluster Differentiation (CD) Antigens

A

• T and B cells cannot be distinguished based on morphological differences
• CD antigens – unique markers on the cell surface
• Expressed during lymphocyte development and when mature
• Markers specific to T cells (CD3, CD4, CD8) and B cells (CD19)
• Characterized via fluorescence-activated cell sorting

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11
Q

T helper cells

A

• CD4+
• Responsible for cytokine release that coordinates the immune response
• Help B cells secrete antibodies
• TH1 – Stimulate macrophages to become phagocytotic, formation of granulomas
• TH2 – IgE antibody production, activation of eosinophils, basophils, mast cells

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12
Q

Cytotoxic T cells

A

• CD8+
• Mediate killing of virus infecte

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13
Q

Natural Killer Cells

A

• Similar surface markers to T cells but do not have T cell receptor gene rearrangement
• Mediate innate immune functions and are not involved in T/B cell reactions
• Similar function to T cells – react to virus infected cells and kill tumor cells/transplanted cells
• Contain lytic granules to destroy foreign substances

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14
Q

B Lymphocytes

A

• Essential for the production of antibodies
• Activated B-cells differentiate into plasma cells
• Plasma cells have increased ribosomes and RER for protein production/release

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15
Q

Antibodies

A

• Serum proteins secreted by plasma cells
• Comprised of 4 polypeptide chains: 2 light chains & 2 heavy chains
• Fab (variable) region is antigen specific: contain hypervariable regions that directly contact antigens and undergo frequent mutations
• Fc (constant) region: binds specific receptors on various immune cells – Fc receptors

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16
Q

IgM antibodies

A

Neutralizes microorganisms, activates the complement system
- Natural antibody against ABO blood antigens
- First to appear after immunizationIgG: Most abu

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17
Q

IgG antibodies

A

Most abundant, boosted by re-exposure to an antigen
- Receptors on macrophages, PMNs, lymphocytes etc., and placenta, helps facilitate phagocytosis

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18
Q

IgA antibodies

A

most in mucosa, found in bodily secretions (tears), breast milk

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19
Q

IgE antibodies

A

trace amounts in serum
- Attach to mast cells, basophils, eosinophils (Fc-epsilon-RI)
- Mediate allergic type I hypersensitivity reaction

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20
Q

IgD antibodies

A

Function not fully understood, found exclusively on B cells, antigenic activation of B cells

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21
Q

Antibody functions

A
  1. B cell receptors
  2. Opsonin – increase phagocytosis
  3. Neutralizes antigen by binding
  4. Directs immune cell effector function
  5. Activates mast cells during allergy
  6. Activates complement
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22
Q

T Cell activation

A

Requires antigen-presenting cells
Immune cells such as macrophages, dendritic cells and B cells internalize and process antigens
Present antigens to T cells via major histocompatibility complexes

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23
Q

Major histocompatibility complexes

A

• Essential for presentation of antigens to T-cells
• Mediates cell-to-cell contact during antigen presentation

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24
Q

MHC Class I

A

Expressed by all nucleated cells,
receptors for CD8 activation – presents intracellular antigens (viruses, cancer)

25
MHC Class II
present on specialized cells to bind to CD4 Links macrophages to helper T cells
26
Type 1 hypersensitivity
Primarily mediated by IgE antibodies & Mast cells (also basophils and eosinophils) Two step process: 1. Primary exposure (sensitization): primes the immune response to produce IgE antibodies that bind to mast cells 2. Secondary (subsequent exposure): Results in mast cell activation 1.Immediate response i.e., mast cell degranulation (histamine) 2.Late phase (6-9 hours) cytokines, arachidonic acid (leukotrienes, prostaglandins)
27
Hay fever
Type 1 hypersensitivity reaction • Typically seasonal allergy to pollens & other substances such as dander and dust • Allergens are inhaled and result in nasal itching and sneezing • Swelling and inflammation of the nasal mucosa • Symptoms attributed to histamine & can be neutralized with antihistamine
28
Atopic dermatitis
Type 1 hypersensitivity reaction • Typically a disease of childhood that causes chronic skin irritation • Eczema: 10% of all children, 50% genetic predisposition • Hyperproduction of IgE in response to allergens • Exposures to allergen usually through direct skin contact
29
Allergic asthma
• Hypersensitivity to inhaled allergens • Mediated primarily by leukotrienes and prostaglandins (bronchoconstriction) • Affects the bronchi (*severe forms of asthma) • Usually affecting children • Coughing/wheezing due to constriction of the bronchi and increased mucus
30
Anaphylactic shock
• Life threatening systemic response to a previously sensitized allergen•nuts, bee sting, shellfish • Shock develops as a massive release of histamine – results in significant systemic edema • Symptoms/side effects: stridor, choking due to laryngeal edema & narrowing, bronchial spasm (wheezing), pulmonary edema, systemic circulatory collapse and hypotension
31
Type 2 hypersensitivity
• Mediated by cytotoxic antibodies that react with antigens in cells or tissue components • Antigen can be extrinsic or intrinsic • Extrinsic: microbes, drugs, animal products • Intrinsic: macromolecules such as proteins, nucleic acids that become autoantigenic • Mediated by IgG or IgM antibodies that form antigen-antibody complexes on membranes Ex. Transfusion of mismatched blood
32
Hemolytic anemia
Type 2 hypersensitivity • Cytotoxic antibody-mediated reaction • RBC antigens are recognized as foreign
33
Graves’ disease
• Hyperthyroidism, typically in women • Autoantibodies to TSH receptor of the thyroid leads to overproduction of thyroid hormones • Swelling of the neck, protrusion of the eyes, weight loss, muscle weakness
34
Myasthenia gravis
Type II hypersensitivity • Muscle disease, severe muscle weakness • Antibodies to acetylcholine receptors on striated muscle cells, blocks receptors Acetylcholine is a neurotransmitter required for muscle movemen
35
Goodpasture’s syndrome
• Autoimmunity to a component of collagen type IV in the glomeruli (kidney) and alveoli (lung) • Antigenic epitope becomes exposed allowing circulating antibodies to attack • Renal failure • Pulmonary hemorrhage
36
Type 3 Hypersensitivity
Mediated by immune complexes between antigens and appropriate antibodies Antigen-antibody complexes 1.System reactions (complexes in circulation): Serum sickness 2. Localized reactions (complexes deposit in tissues)
37
Systemic lupus erythmatosus
Type 3 hypersensitivity • Autoimmune disease of unknown origin • Several circulating immune complexes to autoantigens
38
Poststreptococcal glomerulonephritis
Type 3 hypersensitivity Acute renal disease, follows an upper respiratory tract infection caused by streptococci, deposited in glomerular basement membrane
39
Polyarteritis nodosa
Type 3 hypersensitivity • Antigen-antibody-mediated inflammatory disease • Small to medium arteries, destruction of vessel walls leads to thrombus, ischemia, infarct
40
Type 4 hypersensitivity
• Cell-mediated or delayed-type immune reaction • Initiated by antigens taken up by macrophages or APC • Macrophages transform into epithelioid cells & multinucleated giant cells > phagocytic • T-lymphocyte and macrophages aggregate to form granulomas
41
Type 4 hypersensitivity diseases that lead to granuloma formation
1. Infections in response to complex antigens such as: Mycobacterium tuberculosis or Mycobacterium leprae 2. Reaction to tumours 3. Sarcoidosis – inflammatory disease (autoimmune) that affects multiple organs (mostly lungs and lymph)
42
Acute contact dermatitis
Type 4 hypersensitivity • Most common clinical form • NOT associated with granuloma formation • Infiltration of T-lymphocytes and macrophages • Can be caused by things like laundry detergent, poison ivy etc
43
Autograft
Patient is both the donor and recipient
44
Isograft
Transplantation between genetically identical individuals
45
Allograft
Transplantation between individuals who are not genetically identical.
46
Xenograft
Transplant from non-human species (like porcine heart valves)
47
Hyperacute reaction transplant rejection
• Recipient has preformed antibodies to the donors antigens • Typically occurs during operation • Recipients blood enters the graft, preformed antibodies react with endothelial cells leading to thrombosis formation and reduced perfusion • Transplant must be removed immediately Hypersensitivity type 2
48
Acute reaction transplant rejection
(first few weeks) • Antibody and cell mediated immune reaction • Antibodies damage blood vessels and activate complement • T-cell mediated rejection: T cells bind to endothelial cells of tubules and cause fibrinoid necrosis • B-cells: appear in the interstitial spaces between the tubules resulting in tubulitis Hypersensitivity types 2 and 4
49
Chronic reaction transplant rejection
• Evolves slowly over months to years • Antibody and cell mediated responses • Vascular changes to arterial lumen leads to hypoperfusion of tissues and chronic ischemia • Interstitial tissue inflammation deteriorates tissues Types 2 and 4 hypersensitivity
50
How to prevent transplant rejection
• Match donor and recipient (MHC, blood type etc.) • Immunosuppression (drugs cyclosporine – inhibits IL-2 and T-cell response
51
Clinical features of Rh factor incompatibility
• Hydrops Fetalis: abnormal accumulation of fluid • Erythroblastosis fetalis: hemolytic anemia in the fetus • Icterus gravis neonatorum: Severe jaundice & kernicterus (bilirubin induced brain dysfunction) Occurs during second pregnancy Rhogam binds D antigen on fetal RBCs to prevent the production of anti Rh antibodies
52
Autoimmune disorders
• Failure to protect the host from self-reactive lymphocytes • T or B cells can attack self tissues • May involve antibodies, T cells, immune complexes or any combination of elements • Familial: genetic predisposition • Sex differences: more common in women than men because X chromosome contains a large number of genes, increases the likelihood of mutations occurring & X chromosome contains a large number of immune related and immunoregulatory gene
53
Systemic autoimmune diseases
Systemic lupus erythematosus, rheumatic fever, rheumatoid arthritis, polyarteritis nodosa
54
Autoimmune disorders limited to a single organ
• Multiple sclerosis: CNS • Graves disease: thyroid • Autoimmune hemolytic anemia: blood • Myasthenia gravis: muscle
55
Systemic lupus erythematosus
• More common in women (9:1) • Malfunction of T cells • Polyclonal activation of B cells • B-cells secrete antibodies • Antibodies against DNA, RNA, nuclear proteins • Antibody forms complexes in circulation which deposit in membranes
56
Type 1 diabetes mellitus
Cause by an autoimmune attack against insulin producing beta cells in the pancreas
57
Primary immunodeficiency diseases
Congenital Affect differentiation of T- and B- cells 1. Severe combined immunodeficiency: defect of lymphoid stem cells (pre-B and pre-T cells). Typically, in children, small lymph nodes 2. IgA deficiency: most common; often asymptomatic. Block in B cell to IgA producing plasma cells 3. DiGeorge’s syndrome: T cell deficiency related to block in thymus formation, unable to have a cell-mediated immune response
58
Secondary immunodeficiency disorders
Acquired Result of infections, metabolic disorders, cancer Most prevalent is AIDS
59
AIDS
• Human immunodeficiency virus (HIV), RNA retrovirus (DNA incorporated into host cells) • Transmitted in bodily fluids (blood, sperm) • Infects CD4+ T cells (T helper cells) and monocytes • Stored in macrophages and related phagocytic cells • Cytotoxic and results in depletion of helper T cells and other infected cells

Human Pathology (9 decks)

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