immunopathology

sorry about spelling errors but not that sorry this is a mc test lol

types of innate immunity

types of innate immunity

mechanical barriers, cellular responses, protective proteins

examples of mechanical barriers

skin (best defense), spit, mucus etc

types of cellular responses in innate immunity

phagocytes, macrophages, compliment, lysosomes

which immunity are you born with (nonspecific)

innate

which immunity has a concept of self vs non-self (specific)

acquired

what is the first line of defense, what do they do

mechanical and chemical barriers, prevent invaders from entering

what is the second line of defense

inflammatory, innate, phagocytosis, immediate

what is the third line of defense

specific, acquired, only done if pathogen is recognized and 1st and 2nd lines already engaged

types of lymphocytes

helper T cells (CD4), cytotoxic t cells (CD8), B lymphocytes, NK cells, Plasma cells

what do helper T cells (CD4) do

activate phagocytes to kill microbes

what do cytotoxic T cells do (cd8)

destroy infected cells w microbes in them, will eliminate any infected cell

what do B lymphocytes differentiate into

NK cells and plasma cells

what to nk cells attack

literally anything

what do plasma cells do

produce antibodies incase invader ever returns, initiate ability to kill invader

what do macrophages do

provide long standing inflammatory response

what do macrophages come from

monocytes

what is the same between antibody types

light chain (constant, Fc) (k and λ) and hinge area

what varies between each antibody

heavy chain (variable chain, Fab)

what does IgM do

neutralize microorganisms, activate compliment

which antibody is most prevalent

IgG

what does IgG do

acts as opsonin (season antigens) so phagocytes can eat better

what does IgE do

mediate allergic rxns

what does IgA do

primary protective antibody of mucosal surfaces

what does IgD do

activated B cells

what does major histocompatability complex (MHC) do

regulates cell to cell contact during antigen presentation, is essential for presentation of antigens to T cells to initiate immune response

patient presents to clinic with 10/10 back pain for weeks with no clear physical signs why, what test could you as the best PA ever do to see if they may have an underlying immune problem causing inflammation (like ankylosing spondylitis) and what would be a bad sign on that test

MHC test (aka HLA test), see if its too high

what are the two groups of MHC

type 1 (receptors for CD8, viral) and type 2 (react w CD4, Helper T cells, macrophages)

what is scenario 1 for antigen-antibody reactions

antibodies for soluble complexes that may be found in circulation

what is scenario 2 fro antigen-antibody reactions

antibodies bind to fixed antigens on cells and coat their surface (osponization)

what is the third scenario for antigen-antibody reactions

antigen-antibody complex binds to active compliment, triggers T cells to engadge CD8 or CD4, initiates cell lysis

what is a hypersensitivity rxn

an abnormal rxn to exogenous antigens or endogenous rxns to own cells

what is a type 1 hypersensitivity rxn

anaphylactic

which hypersensitivity rxn is the only true allergic rxn

type 1

what is a type 2 hypersensitivity rxn

cytotoxic antibody mediated

what is a type 3 hypersensitivity rxn

immune complex mediated

what is a type 4 hypersensitivity rxn

cell mediated, delayed hypersensitivity rxn

what happens in a type 1 hypersensitivity rnx

mast cell primed w too much IgE (oversensitized) → during second exposure to antigen it freaks out → mast cell degranulates → releases histamine → leads to localized or systemic edema, inc blood vessel permeability, vasodilation

what diseases are caused by type 1 hypersensitivity rxns

Allergic rhinitis, asthma, atopic dermatitis, anaphylactic shock

describe allergic rhinitis

itchy eyes, runny nose, histamine regional response (type 1)

describe asthma

regional histamine release in lungs (type 1)

describe atopic dermatitis

when you go outside and get a rash, itchy skin on flexors (type 1)

how do you treat atopic dermatits

topical steroids and antihistamines

which antibody is involved in type 2 hypersensitivity

IgG

what happens in type 2 hypersensitivity

IgG coat target cell (opsonization) → leads to lysis or cytotoxicity → end up w tissue damage or loss of function

what diseases are from type 2 hypersensitivity reactions

hemolytic anemia, goodpastures syndrome, graves disease, myasthenia gravis

describe hemolytic anemia and its signs

lifespan of RBCs cut short, bone marrow cant make enough new RBCs fast enough. high reticulocyte count, anemic, hepatosplenomegaly, pale, tired, SOB, type 2 hypersensitivity

describe goodpastures syndrome and its signs

kidney issue, rapidly progressing kidney inflammation, type 2 hypersensitivity. may have protein and blood in urine, swelling, trouble pissing. most often seen in young men

describe graves disease

thyroid problem (hyperthyroidism), immunoglobulin embedded in thyroid stimulating hormone and thyroid is going nuts, type 2 hypersensitivity. high HR, weight loss, exophthalmos (bug eyes)

how is goodpastures treated

ace inhibitors

how is graves disease treated

beta blockers and thyroidectomy

describe myasthenia gravis and its signs

muscle issue at the junction between nerves and muscles, type 2 hypersensitivity. have episodic weakness, fragility, paleness, double vision, progressive weakness. often seen in women 20-40

what happens in type 3 hypersensitivity reactions

antigen-antibody relationship busted, antigen-antibody complexes are embedded in regions across body and fuck up shit everywhere. often multisystemic autoimmune issue w chronic inflammation

what diseases are caused by type 3 hypersensitivity reactions

lupus, poststreptococcal glomerulonephritis, polyarteritis nodosa

describe lupus

body makes antibodies to its own nuclei, inflammatory response body wide, type 3 hypersensitivity (POTS is a form of lupus).

signs of lupus

BUTTERFLY FACE RASH, fatigue, weightloss, hairloss, arthritis, raynauds phenomenon, osteoporosis

how is lupus diagnosed and treated

need a biopsy and ANA (95% sensitive), use steroids and NSAIDS

describe poststreptococcal glomerulonephritis and its symptoms

immune complex mediated type 3 hypersensitivity. often preceeded by several weeks of upper resp infection (strep) → immune system attacks kidneys → acute nephritis. cant piss, swelling, hypertensive. often seen in younger ppl. treated w steroids

describe polyarteritis nodosa

get booster shot (tetnis)→ develop response to antigens 4-12 hrs later → antigen-antibody complex coelesses and gets overaggressive → inflammation. caused by IgG deposits. attacks arteries (type 3 hypersensitivity)

polyarteritis nodosa symptoms and treatment

ischemia of tissues supplied by arteries that were attacked, fever, abdominal pain, neuropathy, weight loss, high wbc, protein and blood in urine. need long term immunosupressents

what happens in a type 4 hypersensitivity rxn

basophils, macrophages, t cells migrate out of capillaries and put parameter over foreign body. infiltration of basophils/ lymphocytes/macrophages at exposure site results from actions of effected helper T cells and macrophages.

which hypersensitivity type doesnt involve antibodies

type 4

which hypersensitivity type is delayed

type 4

what is the hallmark of presentation in type 4 hypersensitivity rxns

caseous necrosis (granuloma)

what disease are caused by type 4 hypersensitivity rxns

TB, mycobacterium leprae infection, histoplasmosis, reactions to tumors, sarcoidosis, contact dermatitis

symptoms of sarcoidosis

tender red nodules on tibia, arms, or both, looks like ground glass in x-ray, bilateral paratracheal adenopathy. seen more in african americans 20-40yo

patient presents to clinic w a slightly red and dry patch on their wrist where they normally wear their metal watch, what type 4 hypersensitivity rxn is this

contact dermatitis

what is an autograft transplant

you are the donor and recipient (you gave blood and its used later in surgery, your gracilis is used to craft your new asshole), no rejection chance

what is an isograft transplant

transplant between identical twins, no reaction chance

what is a homograft (allograft) transplant

transplant between patients not genetically identical but histocompatability complexes have been matched as close as possible, low rxn chance

what is a xenograft transplant

transplant between species, histocompatability matched to minimize rxn chance

types of transplant rejection

hyperacute rxn, acure rxn, chronic

what is a hyperacute transplant rxn

happens during transplant operation, person receiving has preformed antigens and body immediately reacts and makes thrombosis. tissue hypoprofuses and transplant fails

what is an acute transplant reaction

reaction within 2 weeks after transplant, severe inflammation in area, hypoprofusion and transplant fails

what is a chronic transplant rejection

rejection happens months to years after transplant, tissue slowly becomes necrotic adn dies (more w allografts), must minimize w immunosuppresants

what is a graft v host reaction

tissue rejects the host

what mediates a graft v host reaction

t lymphocytes

what is often affected in a graft v host rxn

skin, intestines, liver, and bone marrow (marrow one often fatal)

what blood type should you give in an emergency if the host blood type is unknown

O neg

what is the universal blood donor type

O neg

what is the universal recipient blood type

AB

what can happen if a mother and fetus are Rh incompatable

maternal antibodies in Rh- mom can activate against Rh+ fetus and attack the fetus, killing the fetus

how can Rh+ erythroblastosis fetalis be prevented

inject the mother with anti Rh immunoglobulin before she gives birth, IgG will bind and stop the mother from developing anti Rh antibodies

what should you look for to make an autoimmune disorder diagnosis

antibodies in blood, evidence that immune mechanisms have caused the pathologic lesions, direct or indirect evidence that the disease has an immune nature (ex: steroids help)

examples of systemic autoimmune disorders

lupus, rheumatic fever, rheumatoid arthritis, systemic sclerosis, polyarteritis nodosa

CNS specific autoimmune disease

multiple sclerosis

thyroid specific autoimmune disorders

hashimotos thyroiditis, graves disease

blood specific autoimmune disease

autoimmune hemolytic anemia

skin specific autoimmune disease

pemphigus vulgaris

muscle specific autoimmune disease

myasthenia gravis

types of immunodeficiency diseases

primary (congenital) and secondary (acquired)

types of primary immunodeficiency diseases

severe combines immunodeficiency, isolated deficiency of IgA, DiGeorge syndrome

characteristics of severe combined immunodeficiency

defect of lymphoid stem cells: Pre-B, Pre-T cells. extremely poor immune system, young kids at high risk of death from infection, often have to be kept in isolation to prevent infection (bubble boy)

characteristics of isolated deficiency of IgA

most common primary immunodeficiency disease, often asymptomatic

characteristics of DiGeorge syndrome

T cell deficiency, caused by congenital defect of thymus and parathyroid glands, often have thymic aplasia, heart disease, craniofacial abnormalities, recurrent viral and fungal infections, and tetanic bc hypocalcemic in first few days of life

characteristics of acquired immunodeficiency syndrome (AIDS)

starts as HIV (RNA retrovirus), infects/kills helper T cells (CD4), macrophages and related phagocytic cells can also become infected, patients often die of secondary infections

pathologic changes associated w AIDS

patients get many weird infections or severe common infections, profuse interstitial pneumonia→ Pneumocystis carinii, fungal and protozoal infections lead to encephalitis, epstine barr virus, mouth thrush, TB