Immunity & Inflammation Flashcards

1
Q

Features of AIDS?

A

Pneumonia, nausea, diarrhoea, weight loss, meningitis, encephalitis, brain abscesses, neurological deteriroration, skin eruptions, lymphadenopathy, tumours

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2
Q

How is HIV spread?

A

Contaminated needle, sexual contact, mother-child ( placenta, childbirth, breast feeding)

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3
Q

WHat is AIDS?

A

HIV - RNA virus - enzyme reverse transcriptase inside host cells - transfroms viral RNA to DNA - new DNA (provirus) incorporated into host DNA - new copies of virus into tissue fluid & blood - infect Helper T cells - suppression of antibody mediated & cell mediated immunity - infections

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4
Q

What are the 2 classes of immunodeficiency?

A

Primary - genetically mediated
Secondary - acquired - protein deficiency, AIDS, bone marrow diseases, splenectomy, infection

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5
Q

What is myasthenia gravis?

A

Antibodies bind to & block acetylcholine receptors of neuromuscular junction - transmission of nerve impulses to muscle blocked - progressive muscle weakness - eyelid muscle, neck, limbs

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6
Q

What is autoimmune haemolytic anaemia?

A

Antibodies to antigens on RBC, destruction of RBC

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7
Q

What is Grave’s disease?

A

Antibodies to thyroid cells - stimulates glands - increased BMR, anxiety, restlessness, palpitations, warm sweaty skin, heat intolerance, diarrhoea

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8
Q

What is Hashimoto’s disease?

A

Antibodies against thyroglobulin & cells of thyroid - prevent T3 & T4 synthesis - hypothyroidism - decreased BMR, weight gain, depression, lethargy, dry cold skin, constipation

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9
Q

What is rheumatoid arthritis?

A

Antibodies to synovial membrane in ball & socket, hinge, & condyloid joints - Ig detected in blood - Ig + rheumatoid factor -chronicallly inflames joint , stiff, painful, swollen

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10
Q

What are examples of autoimmune disorders?

A

Rheumatoid arthiritis, Hashimoto’s disease, Grave’s disease, autoimmune haemolytic anaemia, myasthenia gravis

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11
Q

What are the stages of hypersensitivity?

A
  1. anaphylactic
  2. cytotoxic
  3. immune complex mediated
  4. delayed type
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12
Q

What is delayed type hypersenitivity?

A

Overreaction of T lymphocytes - antigen detected by memory t lymphocytes causes clonal expansion & large numbers of cytotoxic T lymphocytes released to eliminate antigen - damge to normal tissue e.g. skin graft rejection

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13
Q

What is immune complex mediates hypersensitivity?

A

Ag-Ab form insoluble complexes -usually bacterial toxins - broken down by complement and transported to spleen for destruction - problems iwth pagocytes - complexes deposited in tissue - kidneys, skin, joints, eye causin inflammation & tiisue damage - block glomeruli in kidney causing glomerlurinephritis

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14
Q

What is cytotoxic hypersensitivity?

A

Antibody reacts with antigen on cell surface - marked for destruction via complement activation, phagocytosis, antibody dependent cell mediated cytoxicity - usual process for bacteria, HDNB, transfusion reaction - ocuurs with IgM & IgG antibodies

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15
Q

What is anaphylactic hypersentivity?

A

Overproduction of IgE in response to allergen - mast cells & basophils have receptors for IgE - release granules of histamine (constricts smooth muscle - vasodilation & increased vascular permeability) - heart under severe pressure, bronchoconstriction & shock - eosinophils have a late response

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16
Q

Progression of hypersensitivity (Hay Fever).

A

IgE - mast cells -histamine

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17
Q

What is hypersensitivity?

A

Allergy - powerful immune response to allergen (non-harmful) - immune response = harmful
1st exposure - sensitised - subsequent exposure - exaggerated immune response

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18
Q

What are the 3 types of abnormal immune function?

A

Hypersensitivity, autoimmune disease, immunodefiency

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19
Q

What is latency?

A

M/O infect and remain dormant for many years - mycobacterium tuberculosis resides in macrophages in granulomas resume replication if immune system is compromised or repressed
HIV - dormant for up to 15 years

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20
Q

What is replication inside the host cells?

A

Plasmodium falciparum replicates in RBCs
Trinchinella replicates inside cysts

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21
Q

What is shedding of surface antigens?

A

Plasmodium parasite (malaria) - shed large quantities of surface antigens that bind to antibodies - block interaction with parasite

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22
Q

What is antigen masking?

A

Parasite worms coat themselves in host molecules - not recognised as foreign

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23
Q

What is antigenic variation?

A

HIV, influenza, & rhinovirus change surface antigens due to mutations - new strains - large changes result in pandemics as T & B memory cells don’t recognise antigens

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24
Q

What are examples of viruses that infect & destroy immune cells?

A

HIV - infects T cells
Epstein Barr virus - infects B cells

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25
Q

What are example of toxins that kill or inhibit immune cells?

A

Streptococcus - streptolysin kills neutrophils & inhibits chemotaxis
Leishmania prevents cytokine production by T cells
Viruses - toxin that downregualte inflammation

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26
Q

Examples of substances that degrade proteins of the immune system?

A

Menigococcus - enzymes that destroy antibodies
Herpes simplex virus & leishmania parasite - proteins that degrade complement

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27
Q

How do microorganisms evade the immune system?

A

Suppress immune system & evasion

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28
Q

How does the innate immune system recognise pathogens?

A

Viruses - nucleic acid in genome
Bacteria - flagellin
Fungus - mannan (oligosaccharide in cell wall)

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29
Q

How can past infection/immunity be tested?

A

Viral peptides - test antibodies in blood - agglutination (positive result) - DNA sequencing

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30
Q

What is passive artificial acquired immunity?

A

Antibodies processed in biopharma plants/ inoculated animals - prophylaxis to prevent worsening of disease

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31
Q

What can be given to preterm babies to raise their immune system?

A

Frozen (avoid immunoglobulin denaturation) breast milk donated - provides antibodies & nutrition (underdeveloped digestive system)

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32
Q

What is passive natural acquired immunity?

A

Via placenta & breast milk - lymphocytes not stimulated - immunity short lived until exposure

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33
Q

What is active artificial acquired immunity?

A

Vaccination - dead, live artificially weakened microbes, toxoids (inactive toxins) - retain antigens

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34
Q

What is active natural acquired immunity?

A

Illness (memory B cells formed) - subclinical infection (sufficient response for immunity but asymptomatic)

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35
Q

What is passive immunity?

A

Given antibodies - broken down - brief immunity

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36
Q

What is active immunity?

A

Individuals responds to antigen- lymphocytes activated - memory cells formed

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37
Q

What are the types of acquired immunity?

A

Active & passive (natural & artificial)

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38
Q

What are memory b cells?

A

Long-lasting - rapid response to repeat infection - stimulate plasma cells

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39
Q

What are plasma cells?

A

Secrete immunoglobulins - carried to tissue via blood - only react to one antigen - binds to target cell (neutalisation/agglutination) - binds to toxins, activate complement, attracts cytotoxic t cells & macrophages

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40
Q

What are the 2 type of B cells?

A

Plasma cells & Memory B cells

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41
Q

How does antibody mediated immunity differ from cell mediated immunity?

A

Don’t need APC - produce antibodies to detect & bind antigens

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42
Q

Where are B lymphocytes stored?

A

lymphoid tissue e.g. spleen & lymph node

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43
Q

What type of immunity do B lymphocytes cause?

A

Antibody Mediated/Humoral Immunity

44
Q

What type of immunity do T lymphocytes cause?

A

Cell mediated immunity

45
Q

What are helper T cells?

A

Produce cytokines (interleukins & interferons) which call immune cells - enable B cells to produce antibodies

46
Q

What are suppressor T cells?

A

Inactivate T & B lymphocytes after initial immune response

47
Q

What are cytotoxic T cells?

A

Inactivate cells carrying foreign antigens - attach & release toxins

48
Q

What are memory T cells?

A

Long living cells - survive after infection - more rapid response to repeat infection

49
Q

What are antigen presenting cells?

A

Macrophages that engulf foreign material and transport antigen fragments to T lymphocytes, APC destroyed & T lymphocytes sensitised to antigen

50
Q

What are the 4 types of T lymphocytes?

A

Memory T cells, Cytotoxic T cells, Helper T cells, Suppressor T cells

51
Q

What are B lymphocytes

A

Mature in bone marrow - produce immunoglobulins which bind to antigen - Antibody Mediated Immunity

52
Q

What are T lymphocytes?

A

Mature in the thymus gland with a hormone called thymosin - 1 specific antigen - elicit specific immune response - Cell Mediated Immunity

53
Q

What is the abundance of each type of lymphocytes?

A

70-80% T lymphocytes
20-30% B lymphocytes

54
Q

How does the adaptive immunity differ from innate immunity?

A

Slower, specific, controlled by lymphocytes

55
Q

What is SCID/ “Bubble Boy Syndrome”?

A

Absence of functional T-lymphocytes - defective antibody response - B&T lymphocytes don’t function due to non functional helper T lymphocytes

56
Q

What are the effects of fibrosis?

A

1) Adhesions - fibrous tissue, may affect movement (peristalsis, loops of bowels)
2) Fibrosis of Infarcts - thrombi block blood vessels - infarction (tissue death due to starvation of blood supply) - varying degrees of organ damage
3) Tissue shrinkage - aging of fibrous tissue - may cause restriction of air passages, ureters, blood vessels

57
Q

What is fibrosis?

A

Scar formation - fibrous tissue formed from granulation tissue - new capillaries & inflammatory material removed leaving behind collagen fibres (fibroblasts secrete this)

58
Q

What disease can cause granulomas?

A

Tuberculosis (mycobacterium tuberculosis) - resistant to body’s defence - granulomas form in lungs

59
Q

What cells are active in chronic inflammation?

A

Lymphocytes mainly - fibroblasts activate & lay down collagen (fibrosis) - inflamed site may be walled off to form granulomas (collection of immune cells)

60
Q

What is chronic inflammation?

A

Causative agent cannot be removed - immune deficiency, m/o’s that evade initial immune response - similar symptoms to acute inflammation without resolution - wider scale tissue damage

61
Q

What are the outcomes of acute inflammation?

A

Resolution (damaged cells removed - healthy tissue/scar tissue) & chronic inflammation

62
Q

What is suppuration?

A

Pus formation - pus = dead phagocytes, dead cells, cell debris, fibrin, living & dead microbes - pyogenic (pus forming) bacteria = streptococcus pyogenes & staphylococcus aureus - small amounts form boils & large amounts form abscess

63
Q

What is pain in inflammation?

A

Local swelling compresses sensory nerve endings - exacerbated by bradykinin & prostaglandins (chemical mediators that potentiate the sensitivity of the sensory nerve endings to pain stimuli) - promotes healing

64
Q

What is pyrexia in inflammation?

A

Body temp rises - interleukins released from macrophages & granulocytes in response to infection - increase metabolic rate - increase need for oxygen & nutrients

65
Q

What is pyrexia?

A

Increased core body temperature

66
Q

What is chemotaxis?

A

Chemotaxins released from damaged cells, WBCs attracted to site of injury

67
Q

Describe the migration of leucocytes in inflammation.

A

Neutrophils adhere to blood vessel linings via binding to adhesion molecules & squeezing between endothelial cells - phagocytosis
Macrophages - persist if issue not resolved (chronic) - live longer than neutrophils

68
Q

Describe increased tissue fluid in inflammation.

A

Swelling of tissue (oedema) - leaking of fluid from blood vessels & enter interstitial spaces - prevents spread of infection - harmful (obstruct breathing & pain) & helpful (cushion joints & limit movement)

69
Q

Describe increased blood flow in inflammation.

A

Arterioles & capillaries near the injured site dilate - dilatation caused by release of chemicals (histamine & serotonin) from damaged cells - provide more O2 & nutrients - increased temperature, redding, oedema

70
Q

What are the overlapping actions of inflammation?

A

Increased blood flow, accumulation of tissue fluid, migration of leucocytes, increased core temp., pain & suppuration

71
Q

What is acute inflammation?

A

Immediate response to cell injury - short duration - mild/severe reactions

72
Q

What are the signs of acute inflammation?

A
  1. Redness
  2. Heat
  3. Pain
  4. Swelling
  5. Loss of function
73
Q

What causes inflammation

A

Microbes & their toxins, physical agents (heat, cold mechanical injury, UV, radiation), & chemical agents ( weed killers, poisons, acids, alkalis)

74
Q

What is the inflammatory response

A

Non-specific response to tissues damage - series of local events at cellular & tissue level - protective (isolates, inactivates & removes causative agent & damaged tissue) - removes causative agents, microbes, toxins, dead tissue & replaced with scar tissue or healthy tissue

75
Q

What suffix indicates inflammatory disease?

A

Itis

76
Q

Immunodeficiency disorders?

A

Severe combined immunodeficiency (SCID), temporary acquired immunodeficiency, & AIDS (HIV infection(

77
Q

Limitations of innate immunity?

A

Pathogens can evade phagocytes & complement, immune response starts afresh if repeat infection occurs

78
Q

What is immunological surveillance?

A

NK cells constantly patrol the body for abnormal cells - malignant/infected cells have unusual markers on membrane recognised by NK cells (reduction is major histocompatibility complex) - attempt to kill it - non-specific

79
Q

What are examples of acute phase proteins?

A

Complement, C reactive protein, serum amyloid A, fibrinogen, anti-trypsin, caeruloplasmin, haptoglobins

80
Q

What are acute phase proteins?

A

Liver produces in response to cytokines - causes fever & leucocytosis (increased WBC)

81
Q

What is complement?

A

Plasma protein - binds to bacterial cell wall & stimulates phagocytosis & attract more phagocytes by chemotaxis

82
Q

What are cytokines?

A

Proteins secreted by macrophages & T lymphocytes

83
Q

What are interferons?

A

Produced by T lymphocytes & viral infected cells - prevent viral replication within infected cells & spread of virus to healthy cells

84
Q

What is saliva?

A

Slightly acidic substances - antibacterial

85
Q

What is lysozyme?

A

Bactericidal enzyme in mucous, sweat, tears

86
Q

Where is HCL found?

A

Gastric juices

87
Q

What are some natural antimicrobial substances?

A

HCL, lysozyme, saliva, interferons, cytokines, complement, acute phase proteins

88
Q

What are eosinophils?

A

WBC - defence against parasites - granules of major basic protein (damage outer surface of parasite), cationic protein (neurotoxin affects parasite), peroxidase (produces hydrochlorus acid) - allergic reaction

89
Q

What are basophils & mast cells?

A

Basophils (WBC) in blood & mast cells in tissue - discharge granules of histamine, heparin, chemotactic factors, & peroxidase - allergic reactions (asthma & peanuts)

90
Q

What are macrophages?

A

Last for many years - phagocytose - secrete cytokines, hydrolytic acid & bactericidal substances into extracellular space - act as antigen presenting cell (APC)

91
Q

What are monocytes?

A

Largest WBC - circulate in blood for 8 hours - enter tissue and differentiate into macrophages

92
Q

What are neutrophils?

A

Arrive quickly at the site of infection - kill pathogens - move via chemotaxis - phagocytes allow neutrophils to engulf specific materials - dead neutrophils found in pus

93
Q

What are phagocytes?

A

Macrophages in tissue, monocytes & neutrophils in blood

94
Q

What is phagocytosis?

A

Cell eating - phagocytes move to infection/inflammation site via chemotaxis - pseudopodia engulf foreign substances - enzymes destroy invading organism - cytokines released to attract other cells

95
Q

What cells are involved in innate immunity?

A

Neutrophils, eosinophils, basophils, tissue mast cells, monocytes in blood/macrophages in tissue, NK cells

96
Q

How does sweat cause immunity?

A

Contain antibacterial and antifungal substances

97
Q

How does nasal hair cause immunity?

A

Coarse filter - cilia in respiratory tract moves mucous containing microbes out of the throat via the mouth

98
Q

How does mucous cause immunity?

A

Traps microbes

99
Q

How does skin and the mucosa cause immunity?

A

Physical barrier to entry of substances

100
Q

What defences exist at the body surface?

A

Skin, mucous, sweat, nasal hair

101
Q

What are 5 types of non-specific immunity?

A

Defence at body surfaces, phagocytosis, natural antimicrobial defences, NK cells, inflammatory response

102
Q

What is the specific immune system?

A

Specific to 1 invader - long term immunity against specific antigen - adaptive immunity

103
Q

What is the non-specific defence system?

A

1st line of defence - prevents entry & inhibits further passage of microbes & foreign substances (proteins & chemicals) - quick & non-specific - innate immunity

104
Q

What are the 2 types of defence mechanisms?

A

Specific & non-specific

105
Q

What are the threats to the body?

A

Bacteria, viruses, parasites, fungi, protozoa, cancer cells, non-self cells (blood transfusion & transplantation)

106
Q

What is the function of the immune system?

A

Protect the body from infection (caused by pathogens) & non-self bodies