Pathophysiology Module 3

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dendritic cells

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recruite t-cells

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mast cells

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release histamine which makes blood vessels more pourous (vasodilate) so the white blood cells, neutrophils, and phagocytes can come out. Initiates inflammatory response

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type I hypersensitivity reaction

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normal type of allergy. immune globulin IgE attaches to a recognized antigen. Mast cells release histamine when antigen-antibody complex binds with it. vasodilation and capillary leakage occurs. causes urdicaria and hives and swelling in larynx (if really bad), and anaphylactic shock (because of the dramatic drop in BP because of vasodilation)

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type II hypersensitivity reaction

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tissue specific reaction. ciliac disease

gluten binds with walls of bowel and immunoglobulins bind to the gluten on cell wall. . complement reactions occur which leads to inflammation which calls neutrophils which phagocize portions of cells which lead to cell death.

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type III hypersensitivity reaction

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antibody antigen complex reaction

caused by IgM instead of IgE. IgM has five components so it is really efficient at causing agglutination. quickly becomes ball of antigen antibody complexes which create huge molecules. lead to problems in kidneys- glomerulonephritis. this is because it is really large and sticky and will get stuck in the glomerulus.

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type IV hypersensitivity

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delayed hypersensitivity reaction. poison ivy.

poison ivy molecules bind with proteins in skin activate t cells which cause inflammatory reaction in tissues (dermititis)

also can be from medicine or from medicine/ sunlight photoreaction. something about UV light causes proteins to bind with NSAID molecules which leads to a similar dermititis as poison ivy

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systemic lupus erythematosus

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related to inheritance and acquired environmental factors (viruses)- leads to hightened activity of B cells and plasma cells

loss of self tolerance and increased activity of helper t cells. decreased activity of suppressor t cells. abnormal cell break down (apoptosis) (all of the parts are not broken down completely so a lot of phospholipids and nucleic acids enter blood stream)

anti-nuclear antibodies and antiphospholipid antibodies are created. can't differentiate between self and non self. inflammation in many systems through out the body. this makes it autoimmune.

rash, arthritis, lung lesions, raynauds disease, and nephritis

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endothelial cell derived immunity

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provide a tight seal so other things can't get through. involved in antigen recognition so endothelial cells can detect when cells are not self. interact with platelets and leukocytes to allow these cells to migrate to an area of intrusion. produce antimicrobial peptides. has a pH that won't allow certain bacteria and produces secretions to catch foreign antigens.

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bacteria defense (biochemical barriers)

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normal flora in body forms immune function in skin, oral, conjunctiva, gi tract. aids digestion and metabolizes complex sugars.

lacto bacillus creates acidic pH in vagina which is hostile to some antigens

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cathelicidins and defensin

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drill holes in membrane and affect protein synthesis of microbes.

antibiotics

attracted to bacteria and virus through charge (they are positively charged and membranes are negatively charged) electrostatic interaction

strong broad spectrum antibiotics

bind to and inhibit protein and enzyme synthesis and DNA and RNA synthesis

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collectins

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innate immune system. defense lectins that are proteins that bind to carbohydrates. pattern recognition receptors of patterns of carbohydrates of antigens. form aggregate which activates immune response and trigger interleukins and cytokines. disrupt cell membrane, deactivate toxins (endotoxins), enhance phagocytosis. another form of antibiotic which is innate

defence lectins- bind to carbohydrates- recognize patterns of carbohydrates and bind to pathogen associated molecular patterns- allow immune cells to recognize as dangerous

form aggregate to activate immune response

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bradykinins

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inflammatory molecule released during inflammation

peptides that result in pain and swelling

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pathways for complement plasma proteins

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complement immune response

1. classic pathway-activated by antibodies

2. alternative pathway- responds to surface products of antigens (endotoxins)

3. lectin pathway- responds to mannose residues (sugar residues) on antigen

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opsonization

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process of attaching opsonins on antigen surface. negates negative charge on membrane surface so immune cells (phagocytes) can interact with them (which are normally negatively charged as well)

allows them to react

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chemotaxis

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attract cells to a certain area. complement proteins are cleaved to act as a signal for the area

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cell lysis/ MAC

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complement proteins bind to antigen to form membrane attack complex (MAC). causes osmotic lysis of the cell by forming channels in membrane

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overactivation of C3A leads to

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asthma- stimulates interleuken 13

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angiodema

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swelling of subcutaneous tissue (lips)

can be from deficiency of C1 Esterase which disintegrates complement protein C1

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rheumatoid arthritis

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toll-like receptors leads to inflammatory response in joints

overactivation of toll like receptors

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coagulation and clotting purpose

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stop bleeding, trap foreign molecules, repair and healing

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activation of coagulation

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tissue factor activates enzymes and cofactors of coagulation cascade leading to insoluble cross linked fiber net (clot)

or by platelet activation from collagen which blinds to glycoprotein on platelets. soluble protein binds and strengthens this bond so the platelet can change it's shape and release molecules which draw more platelets to the area to create plug. also accumulates fibrin to form stronger clot

vonwillenbran factor binds and strengthens bond of platelet and fibrin also creates platelet plug. forms fibrin net

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fibrinolysis

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destruction of clot. dissolves bond between fibrin, platelet, and other clot molecules

involves enzymes- fibrinolytics (TPA)

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hemophilia

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disorder with lack of cofators needed to clot blood.

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von willebrand disease

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lack of von willebrand factor so can't clot

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antiphospholipid syndrome

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procoagulant syndrome-

antibodies lead to inactivation of anticoagulants so embolisms can occur

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how does aspirin help prevent formation of clots

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platelet inhibitor. inhibits thromboxin A2

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warfarin

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anticoagulant medication.

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margination

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phagocytes leave circulation and enter tissue

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antigen

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has ability to provoke immune response by binding to antibody or MHC

epitopes- key like complex that fits in with antibody to provoke response- complex protein structures

exogenous- inhaled/ ingested bacteria or virus

endogenous- part of bacteria or virus that is put onto surface membrane for recognition

autoantigen- ability to recognize self and nonself is disrupted

tumors- abnormal rapidly growing cells that are recognized as hostile invaders

hapten is something too small to provoke response but can attach to a larger protein to provoke response (poison ivy)- urshiol must bind with molecules in skin to provoke response

allergens- not always pathogenic but can produce immune reaction

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antibodies

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produced by b cells

y shaped

immunoglobulins

tag antigen for attack

can be soluble and circulate through blood stream

or surface bound on b- cells

identify epitopes of antigens and tag for attack

b cell receptor allows them to react to antigens

types: immunoglobulins (antibodies)

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immunoglobulins

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antibodies

IgA- tears, saliva, respiratory endothelium,

first line defense- weak activator of compliment- some bacteria overcome it

IgG- most abundant, activates classic complement pathway, neutralizes antigens and toxins- sticks around for life and can be rebound to antigen if another exposure- presence of IgG indicates exposure to an antigen

IgM- natural antibody- can respond even if no previous exposure- first to appear in early infection

IgE- allergens and parasites

IgB- b-cell activation

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lymphocytes

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lymphocytes- type of white blood cell- differentiate to b cells or t cells

3 types of lymphocytes - natural killer cells, t-cells, b-cells

type of white blood cell

natural killer cells- rapidly respond, don't require antibody but identify MHC in stressed cells- release porforins to degrade membrane

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natural killer cells

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large lymphocytes, rapidly respond to cells infected or in distress.

do not require antibody to be activated, but bind to MHC on surface. release porforins and proteases to degrade membrane leading to apoptosis.

identify tumor cells

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t- cells

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differentiate in thymus gland

CD4- t helper cells- activate immune response, no phagocytic activity, HIV uses to gain entry

CD8 t cells- cytotoxic, bind to MHC and induce apoptosis when signaled by CD4, has memory to create rapid response upon reexposure

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b-cells

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develop in bone marrow and produce surface and soluble antibody. then become memory cells for subsequent exposure

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infection

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when immune system fails to respond to antigen

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pathogen

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agent capable of causing disease. depends on factors

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communicability

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ability to spread between individuals

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immunogenicity

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ability to induce or avoid immune response, used for vaccines- present inactivated antigen to provoke an immune response

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infectivity

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how quickly it multiplies in a host

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MOA

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mechanism of action- what it does to a host

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portal of entry

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how it gets into a host.

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toxigenicity

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ability to produce toxins to enhance its effects

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virulence

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severity of the disease. measured by case fatality.

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prokaryotes

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no cell nucleus- bacteria, unicellular

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gram +

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thick cell wall with thecoic acid

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gram -

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thin cell wall surrounded by lipid membrane

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endospores

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hibernation. able to live in inactive state for long time

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yeasts

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unicellular eukaryotes. ferment carbs to CO2 and alcohols.

earliest domesticated microbe

commensal- benefit from host without affecting it (generally)

opportunistic pathogen

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parasites

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symbiotic- benefit at expense of host

require vector to survive

unicellular

produce toxins or cause direct tissue damage

sometimes immune can't get rid of it