Pathp Test 2

Front 1

What is meant by hypersensitivity with respect to an immune response

Back 1

hypersensitivity is an immune response that is inappropriately triggered or excessive that produces undesirable effects on the body

Front 2

What are the four types of hypersensitive reactions

Back 2

Type 1--IgE mediated reactions

Type 2 - tissue-specific reactions

Type 3 - immune complex mediated reactions

Type 4 - t cell-mediated reactions

Front 3

How do the 4 types of hypersensitivity differ with respect to their time course

Back 3

Types 1 2 3 are immediate

Type 4 is delayed

Front 4

What types of antigens are involved in development of allergic autoimmune and a low immune hypersensitivity reaction

Back 4

Allergies involve an environmental antigen

Autoimmunity is a self antigen

Alloimmunity is an antigen from another individual

Front 5

Describe the sensitization process of type 1 hypersensitivity

Back 5

The first exposure to allergen leads to sensitization of mast cells

During sensitization allergen-specific ige moleculesare produced and then attach to receptors on the cell membrane of mast cells or basophils

subsequent exposure to allergen cause binding to ige molecules located on mast cells and basophils which caused degranulation and leads to an early response occurs within 5 to 30 minutes

Front 6

What happens during the subsequent exposure to type 1 hypersensitivity reaction

Back 6

Subsequent exposure to allergen causes binding to ige molecule located on the mast cells basophils which causes degranulation and leads to early response. Occurs within 5 to 30 minutes

Granules contain the chemical mediators of the allergy

Front 7

What are the chemicals involved with early and late response of a type 1 hypersensitivity

Back 7

Early response

Histamine, bradykinin, chemotactic factors in other chemicals

Late response

Leukotrienes, prostaglandins, chemotactic factors

Front 8

Histamine

Back 8

A potent vasodilator increases permeability of capillaries bronchoconstrictor.

Front 9

Kinins eg bradykinin

Back 9

Pro-inflammatory proteins causes vasodilation, smooth muscle contraction, leukocyte chemotaxis, and increased vascular permeability

Front 10

Leukotrienes and prostaglandins

Back 10

These have a similar effect of histamine

Front 11

Describes the signs and symptoms of allergic rhinitis? What are the typical allergens that trigger this condition

Back 11

Symptoms include sneezing itching and watery discharge from eyes and nose

Can also produce sinusitis and bronchial asthma

Severe attacks may be accompanied by systemic malaise and fatigue

Headaches may be present due to sinus obstruction

Typical allergens are Polynesians from ragweed, grasses, trees and weeds, fungal spores, house dust mites, animal dander and feathers.

Reactions can occur year-round or appear seasonally

Front 12

Desensitization

Back 12

Involves frequent injections of the allergen in increasing doses. high levels of IGG are produced which bind to allergen and prevent their interaction with ige molecules.

Front 13

What are the signs and symptoms of food allergies. What are the common allergens for food allergies

Back 13

Can produce reactions in the skin gastrointestinal or respiratory tracts

the most common allergens in children include milk eggs peanuts soy tree nuts fish and shellfish. In adults peanuts shellfish and fish

An acute reaction would be hives systemic anaphylaxis or chronic reactions such as asthma atopic dermatitis and GI disorders

Front 14

Describe how systemic anaphylaxis develops. what are the major signs and symptoms

Back 14

Large amounts of the chemical mediators are released from mast cells into general circulation.

Systemic vasodilation leads to a sudden severe decrease in blood pressure

Bronchoconstriction and edema can occur in the lungs reducing air flow

decrease in oxygen within tissues can cause loss of consciousness within minutes

signs and symptoms include generalized itching or tingling all over the body, difficulty in breathing followed by feelings of weakness dizziness or fainting and sense of fear and panic

Hives may appear on the skin

Edema may be found around eyes lips tongues hands and feet

Front 15

What is the treatment for systemic anaphylaxis. How does it work

Back 15

Emergency treatment includes injection of epinephrine

this leads to vasoconstriction in an increase in blood pressure and increases heart rate

Relaxes bronchiolar smooth muscle to restore air flow

Front 16

Vasculitis

Back 16

Inflammation of blood vessels causes changes in blood vessel walls including thickening weakening narrowing or scarring. These changes can restrict blood flow resulting in organ and tissue damage.

Front 17

Indicate the location of antigens in a type 2 and type 3 hypersensitivity reaction

Back 17

The location of the antigens would be within the body.

Front 18

What is meant by the ABO and Rh blood groups

Back 18

ABO. Blood groups can be O, A, B, or AB.

The serum of blood group O contain IGM antibodies against both A&B carbohydrates.

The serum of blood group A some of the h antigens have been modified into a antigens. The serum has antibodies against the B antigen

in the serum of blood group b some of the age antigens have been modified into B antigens. The serum has antibodies against the a antigen

Those with AB blood have h antigens which I've been modified into both A and B antigens. These individuals do not have antibodies to either A or B antigens

The RH blood group is a group of antigens expressed only on red blood cells. It consists of at least 45 separate antigens but the most important is the d antigen. those who Express the d antigen are RH positive where's individuals who do not express the d antigen are RH negative

Front 19

Systemic lupus erythematous sle

Back 19

It's a condition with unknown cause that can affect almost any organ system genetics play a role

It is a common and serious condition

Antibodies are produced against several self antigens including nucleic acids, RBCs, phospholipids ect

Possible manifestations include arthritis, arthralgias, butterfly rashes on skin of nose and cheek call my hair loss, kidney damage, pleuritis, as well as others

as with most autoimmune diseases is severity of manifestations will vary between flares and remission

Occurs more commonly in women

Front 20

What type of cells mediate type 4 hypersensitivity

Back 20

T cytotoxic cells or t helper cells

Front 21

Allergic contact dermatitis

Back 21

An allergic inflammatory response confined to skin

Can be caused by cosmetics hair dyes topical drugs poison ivy

Signs and symptoms include blisters reading spots and elevation of skin

Other signs can include a demonic resting and development of secondary infection

Severity of reaction depends on allergen and person

Reactions do not become a parent for 12 to 24 hours or moreremoval of irritant and application of ointments or corticosteroid creams can clear reactions

More serious reactions are treated with systemic corticosteroid therapy

Front 22

Latex allergies

Back 22

Can elicit a type 1 or type 4 response

type one response is normally a reaction toward the latex proteins and can lead to anaphylaxis

most common type of reaction with latex is type for response to the additives used in the manufacturing process. This leads to contact dermatitis and rashes

Front 23

Describe how Central and peripheral tolerance is achieved within the immune system

Back 23

Central tolerance refers to deletion of t and B cells that react to self antigens during maturation of Central lymphoid organs

peripheral tolerance refers to deletion or inactivation of self reactive t and B cells that escaped elimination in central lymphoid organs. Performed by the t regulatory cells

Front 24

Describe the factors that are involved with the development of an autoimmune disease

Back 24

1 - genetics

2 - environmental factors including infectious agents

3 - molecular mimicry. Scene in rheumatic fever

4 - breakdown of tolerance

Front 25

Why do autoimmune diseases arise

Back 25

They arise due to inappropriate reactions between the immune system and self peptides. these reactions lead to the production of antibodies against the host tissue and cells antibodies are called autoantibodies

Front 26

How are autoimmune diseases treated

Back 26

Treatment include administering immunosuppressive therapy - methotrexate or corticosteroids

Since the causes unknown the treatment is to reduce symptoms

Front 27

Allograft

Back 27

Introduction of foreign tissue from one human into the body of another human

Front 28

Autografts

Back 28

Tissue transferred from one part of the body to another part on the same individual

Front 29

Xenograft

Back 29

Tissue transferred from a member of one species to a different species

Front 30

Isograft

Back 30

Tissue transfer between two genetically identical bodies like identical twins

Front 31

How is a successful transplant achieved

Back 31

A successful transfer of tissue or organs occurs with matching MHC (HLA) molecules between donor and recipient

Front 32

Why is immunosuppressive therapy used on someone receiving a transplant

Back 32

Immunosuppressant drugs keep the bodies immune system from attacking the new organ

Front 33

List three different patterns of graft rejection

Back 33

Hyperacute--occurs immediately after transplant when circulation is re-established

Acute - develops after several weeks when unmatched antigens cause a reaction

cronic Dodge occurs after months or years with gradual degeneration of the blood vessels. develops due to a weak immune response against minor MHC molecules on the grafted tissue

Front 34

What is the difference between a primary and secondary immunodeficiency disorder

Back 34

A primary immunodeficiency disorder is congenital or inherited

A secondary immunodeficiency disorder is acquired later in life

Front 35

Examples of primary immunodeficiency disorders

Back 35

X-linked agammaglobulinemia which is low antibody production because of a b-cell defect

DiGeorge's syndrome hypoplasia of the thymus and therefore impaired t cell immunity

SCIDS severe combined immunodeficiency syndrome. A severe genetic mutation that leads to absence of all immune function. Children usually die by age 2 from opportunistic infections

Front 36

List examples of secondary immunodeficiency disorders

Back 36

AIDS acquired immunodeficiency syndrome.

Cancer. Example Hodgkin's lymphoma. Cancer of B cells leading to a reduction in normal function

Immunosuppressive therapy. Corticosteroid or transplant rejection medications.

Front 37

Indicate the common modes of transmission for HIV infection

Back 37

Transmitted person-to-person via blood semen or vaginal fluids. Through sexual intercourse or sharing of needles or from mother to fetus through the placenta.

Front 38

Which cells are targeted by HIV

Back 38

T helper cells

Front 39

How does HIV replicate

Back 39

it infects cells by entering a host cell and stimulating the host cell to produce new viral components in order for the virus to replicate

in some cells replication occurs for years before release of new virus and other cells replication leads to cell death and release of new virus to infect other cells

Front 40

How long does it take most individuals infected with HIV to progress to AIDS

Back 40

It can take several years

Front 41

What are the three stages of HIV infection. What is occurring during each stage

Back 41

Primary infection. Leads to signs and symptoms of fever fatigue rash headache myalgia GI problems etc. Appears 2 to 4 weeks after exposure and last for a few days to two weeks. The immune system reduces viral numbers but does not completely eliminate them

Latent period. There are no real signs or symptoms of illness as viral numbers climb this can last for several years

AIDS. Persons t helper cell count has dropped to less than 200 cells per microliter. Person develops opportunistic infections in malignancies. Without medication death occurs within two to three years

Front 42

Nociception

Back 42

Pain sense. Activation of nociceptors and the subsequent feeling of pain

Front 43

Nociceptors

Back 43

Pain receptors. Non encapsulated free nerve endings.

Front 44

What type of stimuli activate pain receptors

Back 44

In the unimodal nociceptors. They respond to a single stimulus mechanical or thermal. They are found primarily in the skin and mucous membranes

The polymodal nociceptors respond to a variety of stimuli. Thermal chemical and mechanical

Front 45

Which area of the body contains the majority of nociceptors

Back 45

The skin has many more nociceptors than internal structures and is therefore more sensitive to pain

Front 46

Nociceptors adaptation

Back 46

Nociceptors do not adapt to stimulation. Adaptation means that it would become less sensitive over time

Front 47

Neuropathic pain

Back 47

Occurs when there is damage or dysfunction in the peripheral or central nervous system

Front 48

Types of nerve fibres a fibres

Back 48

Alpha fibres transmit motor impulses and proprioceptive information

Beta fibres transmit touch and pressure sensation

Gamma fibres transmit touching motor excitation of muscle spindles

Delta fibres transmit pain heat cold and pressure sensations

Front 49

What is the difference between a Delta and c fibres in terms of transmission of pain information

Back 49

A Delta fibres conduct pain impulses at a speed of 10 to 30 metres per second. Fast pain fibres. Pain conducted along these fibres usually described as sharp stabbing and localized

c fibres are small and unmyelinated fibres which transmit pain and itch sensations at a speed of .5 to 2.5 metres per second. they are called slow pain fibres and comprise more than half of the sensory fibres in the peripheral nerves and all postganglionic fibres of the autonomic nervous system. Pain along these fibres are as described as diffused all an aching.

Front 50

Describe the two function of acute pain transmitted to the central nervous system

Back 50

Acute pain information travelling to the central nervous system from the gnosis sceptre is involved with two functions

Reflex motor response

Alerting the brain that tissue damage is occurring or about to occur

Front 51

Alerting the brain

Back 51

Primary order neurons enter the spinal cord via the dorsal root of a spinal nerve.

Once in the dorsal Horn of the spinal cord sn1 releases neurotransmitters. Glutamate released by a Delta fibres. Glutamate and substance p release by small c fibres

second-order neurons carry the pain impulses to the opposite side of the spinal cord these are interneurons

Front 52

What is the difference between Neospinothalamic and paleospinothalamic tracts

Back 52

The Neospinothalamic tract is for fast pain

The Paleospinothalamic tract is for slow pain