Case 5

Front 1

describe the classification of myeloid cells and name them.

Back 1

mononuclear - macrophages, monocytes, dendritic cells.

granulocytes - neutrophils, eosinophils, basophils, mast cells.

Front 2

what is innate immunity?

Back 2

all plants and animals have it, it provides rapid defence against infection in a non-specific manner.

Front 3

what is adaptive immunity?

Back 3

Has a memory, involves lymphocytes which recognise the antigens of specific pathogens and produce antibodies to combat them. Only in vertebrates.

Front 4

describe the different types of immune response.

Back 4

adaptive and innate.

Adaptive - humoral (B lymphocytes, bacterial infection) and cell-mediated (T cell, viral infection).

Innate - bloodborne (complement cascade and phagocytes), physical barriers.

Front 5

name the lymphoid cells/ lymphocytes.

Back 5

B cell, T cell, natural killer cell.

Front 6

Which cells can act as antigen presenting cells?

Back 6

macrophages, dendritic cells, monocytes, B cells.

Front 7

Explain the humoral response.

Back 7

1. A bacterium gets into tissue and starts replicating.

2. The bacterium is phagocytosed by a macrophage, which releases cytokines that trigger inflammation.

3. Dendritic cells phagocytose bacteria and present the antigens on class 2 MHCs as they migrate to a lymph node.

4. A CD4+ Th cell binds to the antigen and MHC gets activated, and undergoes clonal expansion to produce active Th cells and T memory cells.

5. Th cells release cytokines which stimulate B cells to differentiate into plasma cells and memory cells.

The B plasma cells secrete antibodies, which fight infection by: facilitating phagocytosis, preventing toxins from entering cells, and activating complement.

Front 8

What are the 5 major classes of antibody/immunoglobulin?

Back 8

IgG, IgA, IgM, IgE, IgD

(GAMED)

Front 9

Function of IgG

Back 9

Blood and tissue antibody, it is the only one that can pass across the placenta to foetus. It fixes complement, binds phagocytes, and neutralises toxins.

Front 10

Function of IgM

Back 10

Blood antibody. It fixes complement and acts as a B cell receptor

Front 11

Function of IgA

Back 11

secretory antibody, it agglutinates/clumps bacterial cells together and provides protection at mucosal surfaces.

Front 12

Function of IgE

Back 12

Binds to mast cells and basophils, important in multicellular parasite infections.

Front 13

IgD function

Back 13

membrane receptor.

Front 14

Describe the structure of an immunoglobulin.

Back 14

Consists of heavy and light chains connected by disulphide bridges. There are 2 variable regions where antigens attach, and 1 constant region where complement or other immune cells attach.

Front 15

Where on the antibody does the effector function occur?

Back 15

The constant region.

Front 16

If the heavy chains in 2 antibodies differ, what will this result in?

Back 16

different functions.

Front 17

What does high avidity mean?

Back 17

Binds well to antigens.

Front 18

how do antibodies facilitate phagocytosis?

Back 18

they opsonise/coat bacteria and the constant region of the antibody is available to bind to receptors on macrophages and neutrophils for faster digestion.

Front 19

How do antibodies activate complement and thus kill bacteria?

Back 19

They opsonise bacteria and bind to complement with their constant regions. Complement has a cascade effect and the end product is a membrane attack complex which punctures holes in the surface of cells and destroys them.

Front 20

What disease is caused by a lack of lymphocyte precursor cells / progenitor cells?

Back 20

SCID - severe combined immunodeficiency disease.

Front 21

What is Bruton's disease?

Back 21

Absence of circulating B cells and B plasma cells, resulting in reduced/absent antibodies.

Front 22

Humoral response:

1. A bacterium gets into tissue and ______.

2. The bacterium is phagocytosed by a _____, which releases cytokines that _______ .

3. _______ phagocytose bacteria and present the antigens on _____ as they migrate to a lymph node.

4. A ______ cell binds to the antigen and MHC gets activated, and undergoes clonal expansion to produce ____ and ____ .

5. Th cells release cytokines which stimulate __________ .

6. The B _____ cells secrete antibodies, which fight infection by: facilitating phagocytosis, preventing ________, and activating _______.

Back 22

1. starts replicating

2.macrophage, trigger inflammation

3. Dendritic cells, class 2 MHCs

4.CD4+ Th, active Th cells, T memory cells

5.B cells to differentiate into plasma cells and memory cells

6. plasma, toxins from entering cells, complement.

Front 23

Explain the cell-mediated response.

Back 23

1. A virus infects a body cell.

2. A dendritic cell phagocytoses the infected cell and presents it antigens on MHC II.

3. A Tc cell gets primed by binding to an antigen-MHC complex.

4. A CD4+ Th cell also binds to an antigen-MHC complex and secretes IL-2, which stimulates the Tc cell to proliferate and differentiate into effector cells and memory cells.

5. Effector cells hunt for infected body cells, bind to their antigen-MHC complex and release perforins which puncture holes in the membrane and cause cell lysis.

Front 24

Cell-mediated response:

1. A _____ infects a body cell.

2. A _______ phagocytoses the infected cell and ________ .

3. A ____ gets primed by binding to an antigen-MHC complex.

4. A _____ cell also binds to an antigen-MHC complex and ______ , which stimulates the ___________________________ .

5. _____ cells hunt for infected body cells, bind to their antigen-MHC complex and _______________.

Back 24

1. virus

2. dendritic cell, presents it antigens on MHC I

3. Tc cell,

4. CD4+ Th, secretes IL-2, Tc cell to proliferate and differentiate into effector cells and memory cells

5. Effector, release perforins which puncture holes in the membrane and cause cell lysis.

Front 25

Describe a major difference in B and T cell function.

Back 25

B cells can bind to soluble antigens, T cells can only bind to antigens on an MHC.

Front 26

What are cytotoxic cells also known as?

Back 26

T killer cells

Front 27

Give 2 differences between cytotoxic T cells and T helper cells.

Back 27

Cytotoxic have CD8 receptors, T helper have CD4 receptors.

Cytotoxic kill cells with antigens on MHC I, T helper cells only recognise antigens on MHC II.

Front 28

If there is a viral/intracellular infection, describe how the immune response is altered.

Back 28

Th 1 cells produce IL-2 and IFN-gamma.

Front 29

If there is a fungal infection, describe how the immune response is altered.

Back 29

Th17 cells produce IL-17 and IL-22.

Front 30

If there is a bacterial infection, describe how the immune response is altered.

Back 30

Th2 cells produce IL-4, IL-5, IL-10, and IL-13.

Front 31

what is IFN-gamma and what does it do?

Back 31

A cytokine, it activates macrophages and causes MHC II molecule expression.

Front 32

Name the physical barriers in the skin and the respiratory system.

Back 32

Skin: barrier itself, sebum, sweat

Resp: mucus, ciliated epithelium

Front 33

Name the physical barriers in the GI tract and the eyes.

Back 33

GI: microbiome, stomach acid, mechanical flushing

Eye: tears, lysozyme.

Front 34

Complement is a series of _____ produced by hepatocytes. They remain inactive in the blood until ______ bind to an antigen and _________ for complement protein 1. Binding = activation.

Back 34

proteins, hepatocytes, IgG or IgM, expose a binding domain

Front 35

What are interferons and what is their function?

Back 35

Cytokines. They are released by lymphocytes and virally infected cells. Interferons bind to receptors on nearby healthy cells and cause them to produce antiviral proteins which interfere with viral replication in the cell.

Front 36

Give an example of an iron-binding protein and how it is involved in the immune system.

Back 36

Lactoferrin, it binds to iron, thus removing an essential substrate required for bacterial growth.

Front 37

Give an example of an AMP and how it is involved in the immune system.

Back 37

Antimicrobial peptide such as defensin. It is found in phagocytes and can directly kill a wide range of pathogens, even cancer cells.

Front 38

Explain the process of inflammation.

Back 38

1. Pathogen enters tissue, starts replicating, which damages tissue.

2. Macrophages, mast cells, and damaged cells in tissue secrete histamine, chemokines (e.g. leukotrienes that attract neutrophils), and cytokines.

3. Histamine causes vasodilation to increase blood flow to site, as well as increased vascular permeability. It does this by binding to receptors on endothelial cells in capillaries, causing them to shrink.

4. Clotting proteins from blood enter tissue and seal off the site of infection from rest of body.

5. IL-1 causes production of adhesion molecules on endothelial cells and neutrophils so that they adhere to endothelial cells in capillary wall.

6. Neutrophils enter the tissue down a chemokine gradient (high conc of IL-8 at site). They phagocytose pathogens, recruit macrophages, then die.

7. Pus is a collection of alive/dead microbes/phagocytes/tissue cells.

8. Tissue repair.

Front 39

INFLAMMATION

1. Pathogen enters tissue, starts ______, which damages tissue.

2. ____, _____, and damaged cells in tissue secrete ______, chemokines (e.g. ______ that attract neutrophils), and ______.

3. _____ causes vasodilation to increase blood flow to site, as well as _______ . It does this by _________, causing them to ____.

4. _____ proteins from blood enter tissue and ________ body.

5. ___ causes production of _______ on endothelial cells and neutrophils so that they __________. 6. ______ enter the tissue down a chemokine gradient (high conc of ____ at site). They phagocytose pathogens,_______ , then ___.

7. Pus is a _____________

8. Tissue _____.

Back 39

1. replicating

2. macrophages, mast cells, histamine, leukotrienes, cytokines.

3.Histamine, increased vascular permeability, binding to receptors on endothelial cells in capillaries, shrink.

4.Clotting, seal off the site of infection from rest of

5. IL-1, adhesion molecules, adhere to endothelial cells in capillary wall.

6.Neutrophils, IL-8 ,recruit macrophages, die.

7.collection of alive/dead microbes/phagocytes/tissue cells.

8. repair.

Front 40

what triggers fever and why is fever beneficial?

Back 40

IL-1beta and TNF-alpha

It causes higher body temperature so bacterial growth is inhibited.

Front 41

Explain the replication cycle of HIV.

Back 41

1. HIV infects CD4+ cells (mainly), monocytes and dendritic cells.

2. The gp120 glycoprotein on HIV membrane binds to the CD4 receptor.

3. The gp41 protein binds to a co-receptor (either CCR5 or CXCR4), bringing HIV close enough for the membranes to fuse.

4. The viral nucleocapsid enters the cell and releases its contents.

5. Reverse transcriptase copies viral RNA into DNA.

6. Integrase removes a dinucleotide from each end of viral DNA and inserts it into host cell DNA. It lies dormant here during latent stage.

7. Upon activation, translation occurs and viral productions are produced, which are cut into smaller core proteins by protease.

8. The viral RNA and proteins form a new HIV which buds out of cell using part of the host cell's membrane as its lipid membrane.

Front 42

What are the stages of HIV infection?

Back 42

Primary infection, latent stage, development of AIDS.

Front 43

Describe what happens during the infection stage of HIV.

Back 43

High levels of virus in the blood, usually asymptomatic but some people experience seroconversion illness or acute HIV syndrome which has severe flu symptoms. The immune response occurs: CD8 cells recognise cells that have the viral antigens on their MHC 1 and kill them. Antibodies for gp120 and p24 are produced, they activate complement and facilitate phagocytosis.

Front 44

How is AIDS diagnosed?

Back 44

When the CD4 cell count dips below 200 cells/microlitre of blood.

Front 45

What happens during latent stage of HIV infection?

Back 45

Generally asymptomatic, the viral DNA lies dormant as provirus, CD4 cell count decreases slowly. Usually lasts around 10 years.

Front 46

How is AIDS clinically defined?

Back 46

1. CD4 cell count below 200

2. Appearance of major opportunistic infections.

Front 47

What are the symptoms of AIDS?

Back 47

Swollen lymph nodes, rapid weight loss, night sweats, fever, diarrhoea.

Front 48

How is HIV transmitted?

Back 48

Through unprotected sex, sharing needles, across the placenta, or breastfeeding

Front 49

How is HIV screened?

Back 49

Using ELISA to screen for anti-gp120 antibodies.

Front 50

How is a HIV diagnosis confirmed if the HIV antibody screen is positive?

Back 50

Western blot tests for p24 antigen, gp120 and gp41 antibodies.

Front 51

What helps the doctor decide when a patient should start antiretroviral treatment?

Back 51

when the CD4 cell count falls below 350.

Front 52

Can HIV be prevented?

Back 52

Yes, by having protected sex, not sharing needles, and getting tested regularly for STIs and HIV, and getting your partner to do the same.

People at high risk of getting HIV should consider taking PrEP

Front 53

What does PEP and PrEP stand for?

Back 53

Post exposure prophylaxis (prevention)

Pre exposure prophylaxis.

Front 54

What does HAART stand for?

Back 54

Highly Active Antiretroviral Therapy

Front 55

Difference between NRTIs and NNRTIs?

Back 55

Nucleoside Reverse Transcriptase Inhibitors need intracellular phosphorylation to be activated.

Non-nucleoside RTIs don't, they bind straight to reverse transcriptase.

Front 56

Name the 5 types of antiretroviral treatment.

Back 56

- Fusion inhibitors

- nucleoside reverse transcriptase inhibitors

- non-nucleoside reverse transcriptase inhibitors

- protease inhibitors

- integrase inhibitors.

Front 57

Which antiretroviral treatment acts as a competitive inhibitor?

Back 57

Integrase inhibitors

Front 58

what is the prognosis for HIV positive patients?

Back 58

dependent on treatment and management but people with controlled HIV tend to live into their 70s, dying with HIV and not because of it.

Front 59

what does the standard genotypic drug-resistance profile involve?

Back 59

testing people who have never had antiretroviral therapy before for mutations in the reverse transcriptase and protease genes. This tells the doctor which ART to avoid as it will be ineffective in that particular patient.

Front 60

What is a serodiscordant couple?

Back 60

Where one partner is HIV positive, the other is HIV negative.

Front 61

What is a differential white blood cell count?

Back 61

Determines the percentage of each type of WBC present in the blood, as well as immature WBCs and abnormalities.

Front 62

What is bilateral diffuse interstitial shadowing?

Back 62

Normally the interstitial space is so thin that it can't be seen on a chest x-ray but when it becomes inflamed due to an infection, it thickens due to oedema and therefore creates a shadow on the x-ray.

Front 63

What are diffuse crackles?

Back 63

crackles are caused by the "popping open" of small airways and alveoli collapsed by fluid. Diffuse means the crackles aren't localised.

Front 64

difference between tachypnoeic and tachycardia?

Back 64

Tachypnoeic - high breathing rate

Tachycardia - high heart rate.

Front 65

What is the Mantoux test?

Back 65

Test for TB - a small amount of PPD tuberculin is injected into the skin of the forearm and if a red bump develops, this indicates that the person has latent TB.

Front 66

What is IGRA?

Back 66

The TB blood test, stands for Interferon Gamma Release Assay. People infected with mycobacterium tuberculosis will release interferon-gamma when mixed with antigens from mycobacterium tuberculosis.

Front 67

What is AAFB and what does its/their presence indicate?

Back 67

Alcohol and acid fast bacilli, can indicate pulmonary tuberculosis.

Front 68

Colours of gram-positive and negative bacteria?

Back 68

Positive - blue/purple

Negative - pink.

Front 69

Difference between pharmacokinetics and pharmacodynamics?

Back 69

kinetics is what the body does to drug

dynamics is what the drug does to body.

Front 70

bioavailability

Back 70

the fraction of administered dose of drug that reaches the systemic circulation.

Front 71

oral administration leads to ___ bioavailability.

Back 71

low

Front 72

why do most drugs recirculate instead of being excreted straight away?

Back 72

they are lipophilic.

Front 73

drug metabolism

Back 73

the enzyme-mediated conversion of a lipid-soluble compound into a more water-soluble one.

Front 74

What metabolises the majority of drugs?

Back 74

Cytochrome p450 enzyme in the smooth ER of liver.

Front 75

What are the 2 phases of drug metabolism?

Back 75

pharmacological activation - addition of functional groups to make drug more chemically reactive.

pharmacological inactivation - conjugation (small hydrophilic molecules added to make the drug water-soluble and eliminate biological activity).

Front 76

Function of the health belief model?

Back 76

Used to predict/explain/change a variety of behaviours, both good and bad.

Front 77

Downside of the health belief model?

Back 77

assumes that humans are always rational, with no focus on emotion or habit.

Front 78

compliance

Back 78

the degree to which the patient follows the advice of a medical professional

Front 79

concordance

Back 79

doctors and patients making decisions together

Front 80

adherence

Back 80

extent to which a person's behaviours are aligned with treatment plans agreed with medical professional.

Front 81

3 reasons for non-adherence?

Back 81

capability - patient understanding/recall of infomotivation - patient motivation to adhereopportunity - provision of resources to facilitate adherence.