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MEDI > immunology > Flashcards

immunology Flashcards

1
Q

Clinica infection

A

Infections with signs and symptoms

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2
Q

Subclinical infection

A

Infection with pathogen but no symptoms

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3
Q

Localised infection

A

Confined to one area of body

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4
Q

Systemic infection

A

Spread to different areas of body

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5
Q

Iatrogenic (nosocomial) infection

A

From a medical practitioner / intervention (hospital)

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6
Q

Exogenous infection

A

from external environment

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7
Q

Endogenous

A

From within the human host

Congenital disease is a type of endogenous (from mother to fetus)

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8
Q

modes of disease transmission

A
  • Contact transmission(direct & indirect physical contact)
  • Common vehicle transmission (air-borne, food- & water-borne)
  • Vectors (mechanical & biological)
  • Direct inoculation (parenteral)
  • Intra-placental
contact by droplet 
blood and wounds
sexual trans
oral-faecal route
respiratory-salivary route
zoonoses
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9
Q

Reservoirs of Infectious Agents + e.g

A

Animate (carriers)
• healthy
•. active disease
• convalescent

Inanimate eg. air, dust, soil, food etc.

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10
Q

epidemiology

A

The study of the spread, frequency, distribution of disease
– Specific source
– Factors determining spread

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11
Q

epidemiology types

A

• Descriptive epidemiology
– Data relating to location, ages, time, occupation, etc to track disease

• Analytical epidemiology
– Disease in detail to identify cause, transmission and prevention

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12
Q

classifications of disease

A

endemic
epidemic
pandemic
sporadic

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13
Q

Endemic

A

Disease present in a community (region) all the time, usually only clinical in a few

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14
Q

Epidemic

A

Wide spread disease within a community (region), affecting many people but only occasionally present

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15
Q

Pandemic

A

Wide spread epidemic, not confined to a single community or region (more than one continent)

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16
Q

Sporadic

A

Widely scattered disease, occurring singly, irregularly, infrequently

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17
Q

Aetiology

A

Cause of the disease

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18
Q

Outbreak of Infection

A

Occurrence of number of cases of disease over the expected in a given time & place

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19
Q

Morbidity

A

Number made ill by infective agent

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20
Q

Mortality

A

Number of deaths caused by infective agent

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21
Q

Incidence

A

Number of new cases over specific period

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22
Q

Prevalence

A

Number of cases (infected or diseased) at a given time (old and new cases)

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23
Q

first epi study

A

• Dr John Snow (1813 – 1858), investigated a cholera outbreak in London in 1854
• Mapped cases which centered around a water pump on Broad street
– water was thought to be curative by locals
• Had the handle removed and well blocked
• Sewage was contaminating water
• Stopped outbreak!
• Bacterial cause of cholera was unknown at the time.

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24
Q

how to control epidemic disease

A
  • Prevent contamination of water supplies
  • Proper treatment of water supplies
  • Proper sewage treatment and disposal
  • Immunization
  • Health personnel and community workers
  • Educate the public
  • Eliminate reservoirs of infection
  • isolate diseased persons
  • immunization programs
  • treat sick persons

SARS good example of successful controls used to prevent spread of disease

25
Q

factors influencing the disease spread

A

• Virulence of the pathogen
• Pathogen transmission mode
• Population susceptibility
– Immunity

26
Q

immune system is and does

A

Loose collection of cells, tissues, proteins and organs widely distributed throughout the body
– Homeostatic mechanism
– Surveillance (detect changes)
– Discriminate between self and non-self
– Destroy non-self (defend against attack)

27
Q

immune system response type and description

A

• Innate:
– Non specific defences which do not require previous exposure to foreign agent

• Adaptive:
– Response based on specific recognition of invader (foreign agent)
• Antibody mediated (humoral)
• Cell mediated

28
Q

non specific innate defence types

A

Inflammation – complex response to tissue injury (vasodilation, cytokines, coagulation, attraction & adhesion of WBC - fever from pyrogens)
Phagocytosis – engulfing and destroying invaders NK cells

29
Q

specific adaptive defense types

A

– B- lymphocytes – antibody production

– T-lymphocytes – help antibody production, cell mediated cytotoxicity

30
Q

inflammation response + effects and signs

A

Response to injury
– Trauma, chemical, infection, heat

• Effects
– Prevents spread
– Removal of debris / infectious agent – Repair

• Four “Cardinal signs”
– Redness, heat, swelling, pain,
• limitation of joint movement (if joint involved)

31
Q

inflammatory chemical released

A

Release of chemicals mediators
(from damaged cells and resident Mast cells)

  • Histamine, complement, kinins, prostaglandins
  • Release of Leukotactic (chemotactic) agents
  • Leukocytosis inducing factor
32
Q

chemical mediators what do

A

• Increase vaso-dialation
– Increase blood to area
• Increaseoxygen,nutrients,temperature
• Increasemetabolicrateofcells
• HeatandRedness

• Increase capillary permeability
– Capillaries leak fluid
• Proteinfluidintotissuespaces
• Clottingfactors,complement,(antibodies)
• Clot forms a barrier prevents spread
• Painandswelling

33
Q

innate non-specific defences - first line defense

A

Mechanical barriers
intact mucous membrane
intact skin

Normal flora
Competition

Secretions
        Mechanical removal and Germicidal 
        action Sebum (oil) pH 5
        antimicrobial peptides
        Acid in gastric juice
        Spermine and zinc in semen
        Lactoperoxidase in milk
        Lysozyme in tears, nasal secretions and saliva 
    Mucus in digestive and respiratory tracts
34
Q

innate non-specific defence - second line

A

Serum
– Complement, a series of 20 proteins, adhere, initiate inflammation, kill cells
• membrane lesions by attaching to bacterial cells directly or via antibodies
– Other anti-microbial peptides
• Interferon
• acute phase proteins

White Blood Cells (leucocytes)
– Phagocytic
• Neutrophils, monocytes + eosinophils are (eosinophils also destroy large parasites)
• Basophils (mast cells) release inflammatory chemicals
– Natural killer cells (NK)

35
Q

Antigen Presenting Cells - APC

A
  • Professional antigen presenting cells move around detecting foreign antigens
  • Phagocytose infectious invader (antigen)
  • Digest and present bits of antigen on its surface travel to local lymphnode
  • Present antigen to T-helper cells
  • T-h then stimulates adaptive immune response
36
Q

lymphocytes cells and the immune system they involved in

A 
t cells (adaptive)
b cells (adaptive)
NK cells (innate and adaptive)
37
Q

t cells

A

(adaptive)
• Cytotoxic T cells (T-C), T helper (T-H), T regulator (T-reg)
• 80% of lymphocytes

38
Q

B cells

A

(adaptive)
• Ig on surface, become plasma cells to produce antibody
• 15% of lymphocytes

39
Q

NK cells

A

(innate and adaptive)
• Natural killer cells (Kill virus infected cells and cancer cells)
• 5% of lymphocytes

40
Q

T cell types

A

T-h
T-reg
T-c

41
Q

T-h

A

– Detect antigen on antigen presenting cells
– Activate macrophages, Tc and B cells
– Stimulates adaptive immune response

42
Q

T-reg

A

Suppress the immune response

43
Q

T-c

A

Cytotoxic T cells that kill virus infected cells and cancer cells

44
Q

Adaptive immunity

A

Adaptive immunity fight invaders once innate system breached
• More specific than innate system
• Has memory
• Mediated by lymphocytes

45
Q

Adaptive immunity division

A

Divided into two, although there is overlap and communication

  1. Humoral Immunity
  2. Cell Mediated Immunity (CMI)
46
Q

Humoral Immunity

A

• Antibody mediated immunity
• Antibodies made by B cells (turn into plasma cells)
• Antibodies are specialised proteins that recognise and attach to antigen
• Recognise antigen on a foreign invader
– Antibodies stick to antigen
Action against extracellular invader

47
Q

Antibodies

A
  • Belong to Immunoglobulin group of proteins
  • They have two heavy and two light chains linked by disulfide bonds
  • Constant region and two variable region (end of Y shape)
48
Q

Antigens

A
  • Antigens stimulate the generation of antibodies
  • Antibodies have specific binding (variable region) regions to specific antigens
  • Foreign objects have proteins, carbohydrates that act as antigens.
49
Q

Epitopes or Antigenic determinants are

A

Specific region on antigens where Antibodies bind

50
Q

Primary response

A
  • Initial exposure to antigen stimulates a primary humoral response
  • Primary response has a lag of several days while B cells proliferate (time for invader to do harm)
  • Antibody levels peaks and falls as antigen is removed
  • The type of antibody is IgM (Immunoglobulin M)
51
Q

secondary response

A
  • Second exposure to the same antigen stimulates the secondary immune response
  • The response is much quicker and larger with a rapid rise in antibody levels
  • Lasts longer
  • Memory cells require fewer cycles to become plasma cells (shorter reaction time)

• The antibody type is IgG (Immunoglobulin G)

52
Q

Cell Mediated Immunity

A

Lymphocytes directly / indirectly kill infected cells
Act against intracellular invaders (also cancer)

• Humoral immunity only effective against extracellular antigen
• Viruses and mycobacteria are intracellular infections (out of reach of humoral response)
• Cancer cells also need to be removed
• The mechanism for protection against these attacks is the Cell Mediated Immune (CMI) response
• Two populations of T cells involved:
– Cytotoxic T cells (TC)
– Natural Killer cells (NK cells)

53
Q

Cytotoxic T-cells (Tc)

A

• Wide range of surface receptors against antigen called T cell receptors (TCR)
• Each TC is specific for one receptor
• Infected cells express the antigen (of the invader) on their surface
• TC via T cell receptor binds and destroys cells expressing the specific antigen
• Kill by release of toxic molecules
– effect membrane causing lysis,
– initiate apoptosis

54
Q

Natural Killer cells

A

• Natural Killer cells (NK cells) recognise reduced MHC 1 (protein on surface of cells) and kill the cell
– Cancer cells and many virus infected cells have reduced MHC 1

• NK cells kill by Antibody Dependant Cell Cytotoxicity (ADCC)
– NK cells have receptors that recognise antibodies
– Can bind and kill cells that have antibodies on them

• Killing is similar to TC cells – release of cytotoxic molecules

55
Q

Regulation of immune response

A

• The activation of B and Tc cells is regulated by T lymphocytes (T cells)
– T helper cells (TH) stimulate
– T regulator cells (TReg) inhibit
– TH specific for the antigen stimulate B cells to proliferate to plasma cells producing antibody, once antigen removed TReg inhibit TH and stop production

56
Q

Passive immunity

A

– Rely on administration of antibodies (already directed against an antigen)
– Often after infection or toxin
– The recipient does not produce an immune response of their own
– Short term

57
Q

active immunity

A

– Administration of antigen
– Prophylaxis (prevent future infection)
– The recipient mounts a response producing own antibodies and memory
– Long term

58
Q

Autoimmune disease (what, who)

A

• When Immune system attacks self.
– Antigen on a microbe similar to self antigen
– T cells and antibodies made against microbe cross react with self

Who:
Mostly western society - women - adults
Genetic component?

Insulin Dependent Diabetes Mellitus (IDDM)
– Type 1
– Destruction of the β-cells of islets of langerhans in pancreas
– β-cells responsible for insulin production
– Cytotoxic T cells followed by auto-antibodies
– Anti-Islet cell antibodies (ICA)
58

MEDI (7 decks)

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