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Pathophysiology Year 2 > Week 2- Immune System > Flashcards

Week 2- Immune System Flashcards

1
Q

Describe innate immunity (3)

A

First line of defence against invading pathogens
Fast acting
Non-specific, no memory
Doesn’t improve after exposure to antigen
Always present
Activates adaptive immune system

Components:
Physical barriers, chemical barriers , cellular components (macrophages, neutrophils and dendritic cells, NK, mast cells)
Soluble factors like cytokines

Steps:
Pathogen recognition
Release of mediators like cytokines and chemo lines are released to recruit immune cells to site of infection and promote inflammation

Phagocytosis
Inflammatory rep isn’t where vasodilation occurs
Destruction of pathogen
Links to adaptive immunity

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2
Q

List physical barriers

A

Skin and mucous membrane

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3
Q

List chemical barriers

A

Gastric acid
Lysosome
Lactoferin
Nitric acid

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4
Q

List cell barriers

A

Phagocyte and natural killer

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5
Q

List protein defence barriers

A

Complement, acute phase proteins and interferons

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6
Q

List mechanical removals

A

Sneezing
Coughing
Secretions
Urine
Perisatalsis
Ciliary escalator
Respiratory mucosa

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7
Q

List colonisation resistance barrier

A

Skin
Gut micro biome

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8
Q

List types of host defence mechanisms

A

Physical barrier
Chemical barriers
Cell
Protein
Mechanical removal
Colonisation resistance

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9
Q

List certain factors which reduce the effectiveness of this protection

A

• Breach of physical barrier (i.e. trauma, burns, eczema)

• Loss of chemical barriers (i.e. drugs which inhibit gastric secretion)

• Suppression of the cough reflex (i.e. opiates, neurological disease)

• Failure of respiratory mucus clearance (i.e. smoking, asthma, cystic fibrosis)

• Failure of washing mechanism (i.e. urinary stasis)

• Loss of colonization resistance (i.e. broad spectrum antibiotic use

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10
Q

List factors that influence the level of innate immunity

A

Age
• Very old or very young are more susceptible to infectious disease

Hormones
• Endocrine disorders such as Diabetes Mellitus, hypothyroidism and adrenal dysfunctions create
enhanced susceptibility to infection.
• Increased corticosteroid - decreased anti-inflammatory effect.

Nutrition
• Immune response is reduced in malnourished patient

Medications
Detox immune system

Diet

Stress

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11
Q

In recombination, what protein is called upon to alter dna

A

Major histamine compatibility

MCH2

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12
Q

Why does recombinbantion occur

A

In order for an antigen to be presented on the phagosomes cell surface

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13
Q

Why do monocytes undergo exocytosis

A

Monocytes are not antigen presenting cells

Instead they transport the pathogen out of the cell by vesicle docking at plasma membrane, fusing with the cel membrane and are released outside the cell in apoptic bodies

Once exocytosis is undergpon, an antigen is also released from the cell

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14
Q

What are apoptotic bodies

A

A controlled for of cell death
Small fragments contain cellular components and are packaged by cuytosplasm of ‘monocyte’ type cell to ensure safely packaged cells.

Doesn’t cause inflammatory response of cause damage

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15
Q

List the 4 functions of complement system

A
  1. Lysis of infectious organisms
  2. Activation of inflammation
  3. Opsonisation
  4. Immune clearance
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16
Q

Once antigens are presented/ floating where do they move to

A

Lymph nodes

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17
Q

Once antigens are presented/ floating where do they move to

A

Lymph nodes

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18
Q

In lymph nodes what occurs to the antigen involving a B-cell

A

B-cell rejectors on a b-cell binds to the antigen.
Recombination occurs
The MCH2 molecule presents the antigen

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19
Q

In lymph nodes what occurs with the antigen and a t-cell

A

Antigen contacts t-cell receptor which activates cd4. T-cell locks on to the antigen on the macrophage’s presented antigen.

T-cell needs to be activated to stimulate the b-cell
Cell turns from naive to mature and active via interlukin cell 2,4,5,6. Undergoes colonial expansion by creating other b-cells presenting this antigen (Memory cells)

Differentiation occurs where some cells are plasma cells and some are antibodies, memory cells.

T-cells create t helper cells

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20
Q

Describe t-cytotoxic cells

A

Activated when there is a virus, cancer or infection

It has CD8 as detection

It releases preferin which creates gaps in these cell walls.

Releases granuloysin which can induce apoptosis in target cells.
Destroying intracellular pathogens such as bacteria or paracytes with infected cells,

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21
Q

In t-cell what is released to activate the b-cell

A

Interleukins 2,4,5,6

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22
Q

CD4 role

A

CD4= helper t-cells.
Recognsises antigens presented by MHC2 which further helps activate B-cells to produce antibodies
Stimulates cytoxic t-cells and macrophages to destroy infected or cancerous cells

Release cytokines to amplify immune repose

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23
Q

CD8 role

A

A receptor Found on cytoxic t-cells
Kil infected or abnormal cells

24
Q

What is innate immunity

A

Genetically determine

No prior exposure or antibody production involved

25
Q

What is acquired immunity

A

Produced by prior exposure or antibody production

26
Q

Describe innate immunity

A

Bacteria with antigen on surface releases endotoxins
Endotoxins act on mast cell nucleus to release inflammatory cytokines
Stimulating P-selectin on endothelial cells to initiate extravasation

Transmigration, margination, adhesion, diapedeasis and positive chemotaxis occurs

The inflammatory cytokines act on endothelial cells causing them to contract and increase permeability (swelling)
Smooth muscle cells are acted on and they relax leading to vasodilation and heat and redness

Neutrophils undergo exocytosis of free antigens. Apoptosis

Macrophages undergo phagocytosis forming a phagolysosome
MCH2 recombination and attach to specific antigen and present on cell membrane
Macrophage turns into antigen presenting cell

Complimentary pathway is activated
Classical
Alternative
Lectin

Allowing chemoattract more neutrophils and macrophages to the area
Opsonisation(pathogens are marked for destruction)
Cell lysis
Inflammation enhances by activation of mast cells

Interferential Alpha, beta, gamma stimulate neighbouring cells / macrophage toi increase in size and number

27
Q

Describe adaptive immunity

A

Viral or cancer infected cell exposes viral protein on self antigen

Cytoxic t clell bind to viral protein on viral cell with a CD8 receptor

Cytoxic T cell releases performing
Granzymes we hitch move through pores and activate pro-apoptosis genes

28
Q

Describe adaptive immunity

A

Viral or cancer infected cell exposes viral protein on self antigen

Cytoxic t clell bind to viral protein on viral cell with a CD8 receptor

Cytoxic T cell releases performing
Granzymes we hitch move through pores and activate pro-apoptosis genes

29
Q

Name complimentary pathway steps

A

Classical

  1. Alternative
  2. Lectin
30
Q

Name the cells which stimulate neighbours cels and macrophages to increase in size and number

A

Interferential alpha, beta, game

31
Q

Describe the process of humoral response

A

Free antigen binds to b lymph
MCH2 and b cell receptor form an antigen presenting cell

Macrophage binds to t-h cell via CD4 protein and tcell receptor

Differentiation of th cell into
Th1
Th2 (IL 2,4,5)

IL 4 + 5 send chemical messages to b lymph to stimulate cell proliferation = clinal expansion

B cell differentiation into memory b cells for long term protection
Plasma cells which secrete antibodies which cause neutralisation or opsonisation

32
Q

What is opsonisation

A

Where pathogens are marked for destruction by immune cells via tagging

33
Q

What is the role of P-selectin

A

Cell adhesion molecule found on the surface of endothelial cells.

When there is inflammation or damage, it appears on the blood vessel wall, helping wbc stick and roll along the surface of the vessel. This allows slowing of the cells so they can exit the bloodstream and reach the affected tissue.

34
Q

What activates pain in inflammatory response

A

Plasma leaks out of the blood via intracellular clefts which causes swelling in this space pressure of excess fluid stimulates nociceptors causing pain

Bradykinins activate nociceptors causing pain

35
Q

Function of inflammatory mediators, name them

A

Histamines, leukotrienes, prostoglandins, bradykinins bind to smooth muscle causing them to vasodilate leading to hyperaemia (redness and heat)> speeding up metabolism to attract more wbc to area

36
Q

Mast cell function

A

WBC
When allergens enter body, mast cells release histamines and other chemicals from their granules, Degranulation occurs.

This helps to increase blood flow to affected area
Attract other immune cells to the site
Promote healing

37
Q

How many granules are on the cytoplasm of the mast cell

A

50-200

38
Q

Leukotrienes function

A

Promote mucus production
Blood vessel leafiness
Narrowing of airways

Can worse’s respiratory inflammation and asthma

39
Q

Why do inflammatory mediates send chemicals signals- positive chemotaxis

A

To attract macrophages to gram negative bacteria

40
Q

What do macrophages secrete

A

Interlukin 1 and 8

Tumour necrotic factor alpha

41
Q

Functions of interlukin

A

Recruit inflammotary cells to site

Attract and activate neutrophils buy activating protein by endo9thelial cell which facilitates diapedesis

42
Q

What is clonal expansion

A

Immune cell t/b cell recognsises a specific antigen and undergoes rapid division producing many identical copies.

43
Q

Cellular vs humerol response

A

C= targets and destroys infected/ abnormal cells.
H= targets pathogens in body fluid

C= key cels are t-cells ct cells, ht cells
H= b cells, plasma cells

C= targets intracellular pathogens
H=targets extracellular pathogens

C=mechanism is cytoxic T cells destroy infected cells
H= b cels produce antibodies that neutralise or mark pathogens

44
Q

What is the role of the compliment system

A

Proteins and immune cells in our body have a specific shape which is complimentary to other pathogens. When they bind, it formes a complimentary complex. It ensures that the correct cell is destructed, complimatry memory cells to be made to ensure upon re infection it will be able to fight it off faster, pathogen destruction and promote inflammation.

Without this, any cells could bind to one another ands the correct immune response would jot be undergone. It bridges the innate and adaptive immune response increasing the effectiveness of immune response

45
Q

Innate vs adaptive

A

Innate is non-specific and targets all pathogens whereas adaptive is highly specific

Innate immunity response is immediate within minutes to hours. Adaptive is delayed and days to weeks

Innate there is no memory as same response is repeated to exposure whereas adaptive has memory so is faster, stronger response

Duration of innate is short term defence, adaptive is long lasting

Key cells innate is phagocytes (macrophages, neutrophils), natural killer. Adaptive is B-cells, t-cells

46
Q

Name 3 cells involved in immune response and their roles

A

Macrophages engulf and digest pathogens and are antigen presenting allowing T cells to be activated in adaptive immune repsonse

TH cells- release cytokines that activate other immune cells like B cells to produc antibodies and CT cells to kill infected cells

B cells for humoral immune response. Differentiate to plasma when activates which produce antibodies to neutralise pathogen or marking them for destruction by other immune cells

47
Q

Name 3 antigen presenting cells

A

Macrophage-phagocyte
Dendritic cells- activate T cells
B-cells-present to ht cells

48
Q

Identify and describe the role of t-cells in the inflammatory response

A

Th cells release cytokines IL-2,4,6 which activate other immune cells like macrophages, b cells and cytoxic T cells

Cytoxic T cells kill infected or abnormal cells by releasing perferin and granzymes which leads to cell death and pro-inflammatory signals that attract other immune cells to the site of infection or injury.

T-cells suppress excess inflammation. They release anti-inflammatory cytokines to prevent tissue damage

49
Q

Describe extravasation anfd its 5 stages

A

Margination. Neutrophil loosely binds to endothelial cells lining blood vessel. Mediated by p-selectin

Rolling, weak interactions between selectins allow it to roll along the serfuce to slow them down

Adhesion neutrophil adhere to wall facilitated by inter grins

Transmigration. Neutrophil squeeze between endothelial cells into surrounding tissue

Diapedesis- follow chemical signals via positive chemotaxis to site of infalammation

50
Q

Describe the humeral response

A

B cell receptors bind to angiotensin receptors
However they require activation

Helper T cells with CD4 receptors provide activation signals by releaseing cytokines after interacting with this antigen. It involves MHC2 molecules to bind antigen to b cell

Activated B cells undergo rapid division to produce clones of themselves
Plasma cells (antibodies)
Memory B cells

Plasma release antibodies into blood stream and lymph fluid.
They can neutralise, opsonise, agglutinate these antigens as well as activate the compliment system.

Vaccines stimulate humeral response
Leading to productive of memory b cells and antibodies

Autoimmune disease, allergic reaction and immunodeficiencuieds can affect the humeral response

51
Q

Describe the cell mediated humeral response

A

Defends against intracellular pathogens like virus and bacteria and cancer cells

Macropgeas and dendritic cells ingest pathogens and present their receptors.
Naive T cells are activated upon binding it antigfen complex
They mature,

Activated T cells proliferate and differentiate into effector T cells and memory T cells

Cytoxic T cells kill infected cells performing and granny ears
Helper T cells secrete cytokines interlukin 2,4,5,6 to activate B cells for humeral repose
Recruit other immune cells

Most effector T cells undergo apoptosis

52
Q

Describe adaptive immunity

A

Second line of defence
Highly specific
Long lasting, memory
Specific
Delayed response

Components:
Humoral immunity

Defends against extracellular pathogens (e.g., bacteria, toxins, viruses in the bloodstream).
Mediated by B cells and antibodies.
2. Cell-Mediated Immunity

Defends against intracellular pathogens (e.g., viruses inside cells) and abnormal cells (e.g., cancer cells).
Mediated by T cells.

Main molecules:

Lymphocytes:
B cells: Responsible for antibody production in humoral immunity.
T cells: Responsible for cellular responses in cell-mediated immunity.
Helper T cells (CD4+): Coordinate immune responses by releasing cytokines.
Cytotoxic T cells (CD8+): Kill infected or abnormal cells directly.
Antigen-Presenting Cells (APCs):
Includes dendritic cells, macrophages, and B cells.

53
Q

Compare and contrast addaptive and innate immunity

A

I= Immediate. Min-hours
A= delayed. Days-weeks

I=non-spec
A=highly spec

I= no memory. Same response
A=has memory. Stronger and faster upon re exposure

I=limited diversity.
A=highly diverse can recognise millions of antigens

I=short-lived. Active whilst pathogen is present
A=long lasting. Sustained immunity through memory cells

I=Majorly cells= phagocytes like macrophages, neutrophils, NK, Dendritic cells
A= lymphocytes, b cells and T cells

I= effector molecule is compliment proteins, cytokines and interferons,
A=antibodies produced by B cells
Cytokines, interlukin from T cell

I=effective against extracellular pathogens
A=effective against extracellular and intracellular pathogens

I= Limited mechanisms for self-recognition
A=highly developed mechanisms to distinguish self from non-self

I= First line of defense: Prevents pathogens from spreading
A=Second line of defense: Clears infection and builds long term immunity

54
Q

Cigarette smoke is an irritant which can lead to inflammation in the lungs, resulting in excessive sputum production. Name the cellular adaptation that occurs in the cells of the airway. In your answer, identify the specific tissue type that normally lines the airways and the tissue type that occurs because of cellular adaptation to chronic exposure to cigarette smoke.

A

The tissue which normally lines the airways is cilia which performs a cilia escalator to remove pathogens and bacteria using mucus.

Smoke can damage the cilia, altering the tissue structure, undergoing metaplasia.

Metaplasia is reversible reaction forming more resilient cells which can withstand mechanical stress and chemical irritation. These cells are less functional and affect the ciliary escalator

These cells are called tratified squamous epithelium.

Leading to build up of mucus and inflammation.

Goblet cells often become hyperplastic (increase in number) as well, further increasing mucus production in response to irritation.

55
Q

Functions of cells in humeral response

A

Macrophages: Engulf and digest pathogens and debris.
Neutrophils: Rapidly recruited to infection sites; phagocytose and kill pathogens.
Dendritic Cells: Capture pathogens and present antigens to adaptive immune cells (link between innate and adaptive immunity).

Macrophages: Engulf and digest pathogens and debris.
Neutrophils: Rapidly recruited to infection sites; phagocytose and kill pathogens.
Dendritic Cells: Capture pathogens and present antigens to adaptive immune cells (link between innate and adaptive immunity).

Pathophysiology Year 2 (20 decks)

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