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Chapter 5 Immunity

Additional Physiology Flashcards




Nonspecific/Natural Immunity

Defense mechanisms that do not depend on prior exposure include:


1. physical barriers: skin, mucus


2. antibacterial agents: GI acid, lysozyme in tears, vagina, urinary tract


3. commendal microorganism


4. phagocytes: macrophages, natural killer (NK) cells


5. inflammatory reponse


6. fever


Acquired/adaptive/specific immunity

involves recognition of specific antigen, increased response to subsequent exposure of same antigen (learning), long-term retention of improved response (memory), ability to discriminate between self and foreign antigen

List the main cells and organs that participate in specific immune reponse

Primary lymphoid Organs: thymus, bone marrow


Secondary lymphoid Organs: lymph nodes, spleen, tonsils, Peyer's patches


Presence in other locations: MALT in GI, bronchial mucosa



T-cells develop in thymus

B-cells develop in bone marrow

plasma cells: differentiated B cells

T and B cells are stored in secondary lymphoid organs 


antigen (Ag)

particle recognized by specific immune system, provokes response


example: antigen could be a surface protein on a bacterium, foreign particle or cancer cell

epitopes/ antigenic determinants

parts of an antigen, antigenic sites to which antibody can bind


example: epitope is a certain part of a surface protein


What are the main differences between T cell and B lympohocytes?


T cells: produced in bone marrow and thymus, mature in the thymus, many surface proteins, these proteins are T cell receptors which recognize surfaces of foreign antigen. 

T cell DNA has hundreds of genes that can reaarange to form new populations of T cells, with receptors that can ever better recognize a specific foreign antigen


B cells: produced and mature in bone marrow, differentiate into plasma cells, which produce Ab and differentiate into memory B cells

B cells have many surface proteins/cell receptors, plasma cells also have coating of own antibodies which repsond to specific antigen, more production of Ab

What is the difference between CD4- and CD8-positve lymphocytes?

CD-4 surface protein is a characteristic of Thelper (Th1 or Th2) cells: these cells enhance the function of B cells and other cells


CD-8 surface protein is characteristiuc of Tsuppressor/cytotoxic (Ts/c): these cells inhibit function of B cells to provide regulation and fine-tuning of function, and can also directly kill foreign cells

What is self-tolerance and how does it occur?

Self-tolerance: usually immune cells will not attack their own body cells. 


It is believed that T cells recognizing self antigen (MHC) on thymus cells (even though they also can recognize foreign antigen) undergo apoptosis (negative selection), while T cells with little or no affinity for MHC (and can recognize foreign antigen) will proliferate (positive selection).  Autoimmune disease occurs if this mechanism fails.  It is believed that B cells undergo a similar process in bone marrow.

Describe the basic features of antibodies/immunoglobins and their reaction with antigen

Antibodies/Immunoglobins are Y shaped protein molecules produced by plasma cells (a type B cell).


Fab portion: "branches" of Y, each branch can bind to epitope of antigen, specificity is coded for by DNA of B cell, structure of this portion varies among antibodies according to specificity for a particular antigen.


Fc portion: "stem" of Y, fixed structure, the same in every antibody of same type in the same individual.


-can bind to macrophages, PMN's, eosinophils, allowing to phagocytize or kill antigen attached to branches of Y


-can bind to platelets, mast cells, causing release of mediators


-can bind to complement: causing activation of complement

What are the most important common features of IgG, IgM, IgA, IgE, and IgD, and what features distinguish one from another

These are all types of antibodies/immunoglobins, all are made by plasma cells.


IgM: largest, 5 "Y" units bound together, arranged like "flower", first Ab to appear in immune response, neutralizes microorganisms, these are the Ab against blood groups Ags, 5 Fc parts to bind complement or other cells.


IgG: smallest, most abundant in body, greater levels with subsequent exposure to Ag, Fc parts bind to receptors on macrophages, PMNs, lymphocytes, eosinophils, platelets, placental cells can pass into fetus.  Fab parts can bind to Ag on microorganisms


IgA: usually 2 "Y" units bound together, in mucosal secretions and milk, protected from digestion so can pass to blood of baby


IgE: made by attaches to mast cells, mediates Type I hypersensitivity/allergic reactions


IgD: only on surfaces of B cells, involved in Ag activation of B cells by antigen presenting cells (APC) 

What are natural killer cells?

Part of the natural/nonspecific immunity, not directly involved in specific immunity as are T and B and plasma cells.  These are large, non-T, non-B lymphocytres, kill foreign cells in 3 ways:


ADCC: NK cells attach to Fc part of Ab attached to foreign cell and kill cell


Tumor surveillance: recognition of cell that is becoming abnormal due to decreased MHC, killing cell


lysis of cells infected by virus, since these cells have decreased MHC


Describe the antigen presenting cells (APCs) and what are the 2 possible responses of immune cells to presentation of antigen


Role of antigen presenting cells: a few Ag can directly stimulate T cells to produce lymphokines and proliferate, or B cells to differentiate into plasma cells which produce Ab, but most Ag must be "presented" to T and B cells by APCs


APC cells may be macrophages, Langerhans cells in skin, follicular dendritic cells of lymph nodes, microglia in brain, Kupffer cells in liver


APC phagocytizes antigen and presents antigen


2 possible responses of immune cells:

-T cell proliferation response

-antibody/humoral response


Describe the role of MHC in antigen (Ag) presentation by APCs


APC phagocytizes Ag.


APC expresses MHC Type II on surface which is holding Ag, CD4 protein/receptor on T helper cells (Th1 or Th2) then binds to Ag which is "held" by MHC Type II


APC also expresses MHC Type I on surface which is "holding Ag, CD8 protein/receptor on Tsuppressor/cytotoxic cells (Ts/c) cells then binds to Ag which is "held" by MHC Type I



Describe the T cell proliferation response when APC presents antigen

T cell proliferation response


Only Th1 cells with receptors specific for the antigen will bind to APC (this is clonal selection)


Bound Th1 cells release IL-2 and IFN-g stimulates macrophages, NK cells, Tsuppressor/cytotoxic cells, destruction of foreign cell, also bound Th1 cells will proliferate to form more activated Th1 cells with receptors specific for that antigen and T memory cells specific for that antigen


Describe the antibody/humoral response when APC presents antigen


-only Th2 cells and Ts/c cells with receptors specific for the antigen will bind to APC (clonal selection)


-Binding of Th2 cells involves Type II MHC-Ag complex on APC cells, Ag binds specific T cell receptor for antigen (TCR) PLUS CD4 on Th2 cell


-Binding of Ts/c cells involves Type I MHC on APC cells-Ag binds to specific T cell receptor for antigen (TCR) PLUS CD8 on Ts/c cell


-Binding of B cell to APC involves IgD on B cell, Fc portion on IgD binds to Fc receptor on B cell and eventual antibody production


-B cell divides into antibody producing plasma and memory B cells


primary challenge: plasma cell makes IgM, switches to IgG


secondary challenge: plasma cell makes mainly IgG

Describe functions of lymphokines

Lymphokines produced by APCs and T cells include Interleukins (ILs), interferons (IFNs), tumor necrosis factors (TNFs) and colony stimulating factors (CSFs).


These all regulate and promote the interaction of cells of the immune system

How do immunization and use of antisera produce therapeutic effects in treatment or prevention of diseases

a) Immunization: prophylactic induction of immune response to prevent an infection by virus, bacteria, etc., involves preparation of antigens (Ag) of a microorganisms or its toxins and introduction into a body called a vaccine


vaccine: induces active immunity, Ab are formed against Ag


examples: flu vaccine, strep vaccine


b) use of antisera: involves injection of ready-made Ab from outside of the body, injected serum containing these outside Ab is called antiserum



rabies antiserum: to neutralize rabies virus before it can replicate


antibotulinum toxin antiserum: to neutralize toxin before neuromuscular effects occur


What is the Rh factor fetal blood group incompatibility and how is it prevented by use of antiserum?


This can occur if Rh- mother becomes pregnant with Rh+ fetus (Rh+ father).


If fetus is Rh+ : 1st preganancy is OK, but mother is exposed to Rh+ blood during childbirth or abortion, mother's immune system will make Ab to Rh+.


If subsequent pregnancy with Rh+ fetus, the mother's Ab will attack fetal RBCs, since these Ab are small IgG and can pass across placenta, anemia and jaundice called erythroblastosis fetalis or hemolytic disease of newborns, can possibly result in fetal death before birth.


To prevent this, -Rh mother is injected with Ab to Rh+ Ag called RhoD immunoglobin (Rhogamm), within 48 hours of delivery of Rh+ baby Abs bind to any Rh+Ag during delivery to hide these Ag from mother's immune system so that the mother will not make her own Ab to Rh+

List 4 mechanisms of hypersensitivity reactions, in which "self" cells and tissues are damaged or destroyed

Type I: anaphylactic-type reaction


Type II: cytotoxic Ab-mediated reaction


Type III: immune complex-mediated reaction


Type IV: cell-mediated, delayed-type reaction

Describe type I hypersensitivity reaction and how it induces hay fever and asthma

Type I: anaphylactic type-mediated by IgE and mast cells or basophils, mediators (especially histamine) are released immediately which affect blood vessels and smooth muscle.


First exposure to antigen: Ag-APC-B cells-plasma cells-Abs-Fc part attaches to mast cells


Second exposure: Ag binds to Fab parts of Ab (AgAb combination), release of histamine, LTs stimulate mast cells and other mediators


Type I reactions involve 2 phases of response, but not always.

1. early phase: mainly due to histamine release bronchoconstriction, mucus, increased permeability of blood vessels, edema, accumulation of inflammatory cells, occurs 5-30 min and may be finished in 1 hour


2. late phase: 2-8 hours later, casued by mediators that take longer to be released or become active, PGs, LTs, PAF, etc., more bronchoconstriction, mucus, increased permeability of blood vessels, edema, accumulation of inflammatory cells typical of asthma attack


Results in allergic rhinitis/hay fever, can be seasonal, swelling of nasal mucosa, nasal itching and sneezing, conjunctivitis, due to histamine release


Results in asthma, early and late phase problems: coughing, wheezing due to bronchoconstriction, and excessive mucus production

Which diseases are caused by Type I hypersensitivity reactions?
  • bronchial asthma
  • hay fever
  • atopic dermatitis
  • anaphylactic shock
What is anaphylactic shock and what is its pathogenesis?

Anaphylactic shock is life threatening, severe systemic response to an allergen to which the body has been previously sensitized.


medical emergency


type I hypersensitivity


a) first exposure to antigen: Ag-APC-B cells-plasma cells-IgEAb-Fc attaches to mast cells


b) second exposure: Fab part of IgEAb-Ag attaches to IgE Ab on mast cells, histamine and other mediators


Shock develops as a result of massive release of histamine and other vasoactive mediators into the circulation, which causes vasodilation.  Histamine also causes other effects such as bronchspasm.  Typical symptoms of anaphylaxis include choking secondary to laryngeal edema; wheezing and shortness of breath resulting from bronchospasm; and pulmonary edema and systemic shock and leakage of fluid from the hyperpermeable blood vessels.  Extreme vasodilation occurs in anaphylactic shock.


What are the 2 basic mechanisms of Type II hypersensitivity?

1st mechanism: Cytotoxic antibody-mediated reactions: antibodies attach to antigens on body cell surfaces forming AgAb complex on cell surface, IgG or IgM Abs are involved, cells are then susceptible to phagocytosis or lysis.


Possible results: Either or Both of the following:

a) complement is activated: binds to exposed Fc part of Ab attached to Ag on cell surface, lysis of cell


b) Antibody-dependent, cellular, cytotoxic (ADCC) reaction is initiated: IgG Abs involved, Fab end binds to Ag on cell, Fc end binds to macrophages, PMNs, NK cells or others, phagocytosis or lysis of cell


2nd mechanism: antibody mediated cellular dysfunction, no cell injury but disrupted function of cell due to bonding of Ab


examples: Graves' disease, myasthenia gravis

Which diseases are caused by Type II hypersensitivity reaction
  • Hemolytic anemia
  • Graves' disease
  • Myasthenia gravis
  • Goodpasture's syndrome
Describe how Type II hypersensitivity induces hemolytic anemia, myasthenia gravis, and Graves' disease

a) hemolytic anemia: can be caused by foreign chemicals or Ag.  Ag on RBCs activates complement and/or ADCC reaction


b) Graves' disease: antibody mediated cellular dysfunction: no cell injury but cell function is disrupted: Ab are formed to TSH receptors (acting as self Ag) on thyroid cells, Ab binding stimulates excessive production of T3, T4.


c) myasthenia gravis: antibody mediated cellular dysfunction-no cell injury.  Ab are formed to N2 Ach receptors (acting as self Ag) at NMJ on skeletal muscle cells, receptors are blocked, muscles cannot contract when Ach is released.

Describe Type III hypersensitivity

Type III: immune complex mediated reactions: exposure to Ag (exogenous or self) causes Ab formation


a) with exposure to exogenous Ag such as drug, Abs are formed.  With 2nd exposure to exogenours Ag, AgAb complexes form.  Smaller circulating AgAb complexes are not removed from blood, may become "stuck" in blood vessel walls and/or blood filtration areas

-activates complement, which then attacks neutriphils, which release lysozymes or free radicals, can cause inflammation and tissue damage, can be localized or systemic


b) Abs may also develop to self-tissue Ag-AbAg complexes remain in tissue, inflammation and tissue damage, as in autoimmune diseases

Which diseases are caused by Type III hypersensitivity reaction?

Autoimmune diseases such as:

  • Systemic Lupus Erythematosus
  • Polyarteritis nodosa
  • Scleroderma
  • Sjogren's syndrome
  • Rheumatoid arthritis
  • Post strepoccal glomerulo nephritis

arthus phenomenon


Arthus phenomenon, Polyarteritis nodosa and SLE all result in antigen-antibody (AgAb) complexes being deposited in the tissues


a) Arthus: involves injection of foreign Ag, Abs are formed to this Ag, with subsequent Ag injection at another site Ab in blood travel to site and complex with Ag, these complexes become stuck in walls of blood vessels in the area and activate complement, which then attacts leukocytes including PMNs and sets up acute inflammation in blood vessels.


This can cause fibrinoid necrosis of blood vessel walls and fibrin forms at this injured area, which can lead to localized clotting blood vessel walls.


This is a localized reaction similar to naturally occurring autoimmune disease polyarteritis nodosa.  Unlike autoimmune polyarteritis nodosa, this is temporary and is resolved with discontinuation of foreign Ag

Polyarteritis nodosa

Like Arthus phenomenon but chronic, same events occur, but since self Ag cannot be eliminated, there is continuing inflammation and tissue destruction. 


Pathologic changes:

a) early: inflammation leads to plasma protein infiltration and fibrinoid necrosis of blood vessel walls, which can lead to localized clotting in blood vessel walls


b) chronic: destruction of blood vessel walls, formation of microaneurysms, thrombosis and occlusion of these vessels, infarcts and ischemias results

Systemic Lupus Erythematosus (SLE)

Abs form to self antigens in body, and form complexes with self Ag, these complexes travel to various sites in the body: kidney, skin, joints, spleen, lymph, bone marrow and set up inflammation and fibrinoid necrosis of blood vessels in affected areas. 


This is chronic systemic problem

What is pathogenesis of poststreptocoocal glomerulo nephritis

May occur after upper respiratory strep infection, Abs form to Ag (strep bacteria and possibly selfAg that look like streg Ag), AgAb complexes circulate and become deposited in glomerulu, causes complement activation, which attracts PMNs, leading to inflammation.


This is usually a temporary condition, but chronic renal insufficiency can occur in some cases.


Localized condition involving Type III hypersensitivity

Strep throat MUST be treated

What is pathogenesis of rheumatoid arthritis

Abs form against Ag of synovial tissues, AgAb complexes accumulate in joints, tissue damage, a chronic condition


Localized condition involving Type III hypersensitivity


Describe the Type IV hypersensitivity reaction and how it induces granuloma formation


Type IV: cell mediated or delayed type hypersensivity: sensitized Th1 cells are the cause of cell and tissue injury, macrophages, Ts/c, NK cells are also involved


Body is trying to fight resistant, intrcellular bacteria (TB, leprosy), or persistent immune complexes (contact dermatitis), or foreign tissue (transplantation)


Ag taken up by APCs, activation of Th 1 cells, attract macrophages, epitheloid cells, and giant cell on inside, produce inflammatory cytokine, possible necrosis or organ cells in center of inside (caseous necrosis in TB)


Granulomas are not always formed in Type IV

What diseases involve Type IV hypersensitivity reaction?
  • TB
  • leprosy
  • fungal infections
  • sarcoidosis
  • contact dermatitis
  • syphilis
What is pathogenesis of contact dermatitis and give examples

This is a Type IV hypersensitivity. 


There are T cells and macrophages in skin lesions.

No granulomas are formed. 

There is wheal formation and edema of affected skin


examples: poison ivy, latex allergy, gold allergy

What is the Major Histocompatibility Complex (MHC) and how is it involved in antiviral activity of Ts/c cells?

MHC are proteins expressed on surface of body cells, cell "fingerprint" identifying cell as "self", MHC is inherited and important in tissue matching for transplation


MHC is involved in antiviral activity of Ts/c cells: body cells infected with virus express viral Ag on surface, Ts/c cells bind to specific viral Ag presented by normal MHC I on cells, destroy cell

What are the main forms of transplants





from self
from identical twin
from another individual-most common

from another species: poorly tolerated, except for avascular tissue such as a pig heart valves and corneas

Discuss the medical uses of transplantation and give 3 examples

a) skin grafts, autografts: are done for burns


b) allografts: are done to replace damaged organs

heart, lung, liver, pancreas, kidneys


c)bone marrow transplants: usually autografts

sometimes allografts are done to treat aplastic anemia, leukemia, bone marrow failure

hyperacute transplant rejection

recipient has preformed Abs to donor Ag, due to childbirth, blood transfusions, etc.


Immediate rejection: AbAg complexes become deposited in vascular endothelium of the new organ


A Type III, Arthus-like reaction

Acute transplant rejection

more usual, within days, first few weeks, or later


involves Type II antibody, mediated immune reactions and/ or type IV cell-mediated as follows:


1. cellular-cell mediated-Type IV:

Ag-APC-Th1 cells activated, attract and activate Ts/c cells, Ts/c travel to graft and kill graft cells


2. cellular-cell mediated-Type IV:

Ag-APC-Th1 cells activated and travel to graft, release cytokines, attract and activate Ts/c cells and macrophages, kill graft cells


3. rejection vasculitis: Type II

Ab formed to graft Ag, attach to vascular endothelial cells out of graft blood vessels, complement or ADCC damage to blood vessels


Chronic Transplant Rejection

Involves same processes as acute but evolves over moths or years.


Wtih regard to kidney transplant (most common transplant): serum creatine levels increase over 4-6 months, vascular changes (ischemia), loss of glomeruli, tubular atrophy, interstitial inflammation, destruction of parenchymal cells

What is the pathogenesis and clinical features of graft-versus-host (GVH) reaction?

This reaction results when immunocompetent donor cells are transplanted to immunosuppressed receipient.  In response to antigens on the recipient;s tissues, the donor lymphocytes (Th cells) initiate a cell-mediated Type IV immune reaction.


Clinical features:

acute reaction, within a few days or weeks, results in infection (immune cells are attacked), dermatitis (skin cells), diarrhea (intestinal epithelial cells), jaundice (liver cells)


Chronic  GVH reaction: intensified effects of acute-severe infections, liver disease, esophageal strictures, death to infection

How may graft survival be improved?

Objective is to avoid Th cell sensitization


a) tissue matching: MHC/HLA testing


b) immunosuppresive drug therapy


c) depletion of donor T cells before transplant

Describe 5 primary/congenital immunodeficiency diseases.

These are caused by deficiency of T or B cells, congenital problems, seen in babies.


a) isolated deficiency of IgA: most common, probably due to inability to make IgA, producing plasma cells, decreased resistance to intestinal infection


b)Bruton's agammaglobulinemia: sex-linked, seen mostly in males, B-cell deficiency with variable or depressed level of Ab, T cell levels are normal, lymphoid tissues, except in thymus, are poorly developed, decreased resistance to bacterial infections, increased incidence of RA or SLE


c) Di George syndrome: deficiency of T cells due to small or absent thymus, usually children die of infections

small cheeks, heart defects, small parathyroid, hypocalcemia, severe spastic convulsions


d) Chronic mucocutaneous candidiasis: absence of T cells with receptors for Candida, usually candidiasis of oral cavity  and vagina, rarely-esophagus


e) severe combined immunodeficiency (SCID): defect of lymphoid stem cells, small thymus and lymph nodes, death in early infancy unless isolated

What is secondary immune deficiency?
Individual is born with normal immune system but immune system is depressed due to "secondary" causes, such as nutritional deficiences, extensive burns, diabetes, malignancies, infections, immunosuppressive drugs including corticosterod, chemotherapeutic drugs, surgery and anesthesia, stress, HIV infection
Which body cells can become infected by HIV?

Th and some other cells:


  • monocytes
  • macrophages
  • microglia of nervous system
  • follicular dendritic cells in lymph nodes
  • Langerhans cells


How does the HIV-1 virus bind to host cells

GP 120 knbs on surface of HIV particle bind to CD4 protein on surface of Th and some other cells: monocytes, macrophages, microglia of nervous system, follicular dendritic cells in lymph nodes, langerhans cells


GP 120 knobs also bind to chemokine receptors (R5 and R4) on the above cells


GP 120 binds to CD4 , another GP120 knob binds to R5 or R4, close interaction enables merging with host cell and emptying of viral contents into host cell


Early in detection, HIV is mostly R5 selective and infects monocytes, spreading the HIV, later HIV is mostly R4 selective and infects Th cells


This probably accounts for delay between HIV infection and AIDS

How does HIV replicate in host cells

-core of HIV contains RNA and 2 molecules of reverse transcriptase


-in host cell, reverse transcriptase converts HIV RNA to HIV DNA, this becomes incorporated into host DNA and starts making parts of the HIV virion


-HIV-1 protease cleaves proteins to final form


-Virion is shed from cell by "budding", assembled viral core forms sheath of host cell membrance studded with GP120

How is HIV transmitted

HIV is a retrovirus (RNA is its genetic material) that cannot survive outside of human cells, humans are the only source of infection.


Transmission via saliva, tears, blood, urine, CSF, Th, macrophages, and not by casual contact.


a) adults: gay men, IV drug abusers, hemophiliacs, transfusion recipients, heterosexual contact, unknown


b) children: infected in utero, during delivery, via breast milk

C-section reduces chance of infection by 50%, perinatal use of ARV drugs also reduces chance of infection

Describe clinical phases of HIV infection

a) acute illness: seen in 40-70% of exposed patients.  About a week after exposure, lasts 2-3 weeks: fever, night sweats, nausea, myalgia, headache, sore throat, rash, swelling of lymph nodes.


b) chronic phase of asymptomatic infection: last few months to few years, possibly minor opportunistic infections such as thrush, shingles, patient is a cearrier of virus, can infect others.

During this time, Ts/c cells, with help from healthy Th cells, are destroying infected cells and keeping viral levels relatively low.  This is called HIV set point.


c)persistent generalized lymphadenopathy: stimulation of B cells, may develop early during chronic, asymtomatic phase and last for months or years, or may develop later: fever, rash, fatigue, gradual decrease in T4 cells


d) crisis phase and AIDS:

-AIDS according to CD4 count: CD4 cell <200/ul : usually 7-10 years after diagnosis

-AIDS defining illness: FUO and diarrhea for more than 2-4 weeks, >10% unexplained weight loss, develops, persistent candidiasis of oral cavity and vagina, also seen are persistent night sweats, fatigue, herpes simplex infections

-appearance of opportunistic infections that are rare in immunocompetent: pneumocystis jiroveci pneumonia (PJP/PCP), toxoplasma gondii, mycoplasma avium complex (MAC), cryptococcus, cytomegalovirus (CMV), epstein-barr virus (EBV), also neoplasms, Kaposi's sarcoma


What is seroconversion with regard to HIV infection, when does it occur and how is HIV detected?

Seroconversion means that HIV proteins are now present in blood, occurs between 3-7 weeks after infection. 


These HIV proteins can be detected by ELISA, then if ELISA is positive, a Western blot assay is done

What is chronic HIV encephalopathy/AIDS dementia complex?, when does it occur, and how does this progress during the course of HIV infection?

This is a decline in CNS and neuromuscular function and the cause is not understood.


First appears in 2-3% of asymptomatic HIV+ patients during chronic phase and 50% of pateints with lymphadenopathy in chronic phase.  Symptoms are difficulty concentrating, slowing of verbal and motor responses.


With progression of HIV, increasing symptoms withdrawal, personality changes, mutism, psychosis, partial paralysis, seizures, incontinence, unresponsiveness

How is HIV infection treated?

a) ARVT- CDC guidelines for treatment of HIV infection: CD4 <350/ul, History of AIDS defining illness, HIV associated with nephropathy, HBV coinfection, pregnancy


b) ARV drugs:





salvage drugs: fusion inhibitor (FI) and others


c) also for Tx and Px of opportunistic infections antibacterials, antimycobacterials, antifungals, antivirals

What is chief source of risk for HIV infection in health care workers and how is this treated?

Accidental puncture with needle, wire, bone, scalpel, eye exposure


Recommendations if accidental puncture: Cleanse site of exposure and begin ARV Px therapy with 3 ARV drugs immediately and continue for 1 month

What are the most common autoimmune diseases?
  • SLE
  • Rheumatoid fever
  • Rheumatoid arthritis
  • scleroderma
  • Polyarteritis nodosa
How is SLE diagnosed?

This disease uslaly occurs in women 20-64 years old


a) typical patient: young woman with butterfly rash, fever, joint pain


b) symptoms are variable: malar rash "butterly or lupoid", discoid rash, photosensivity, oral ulcers, arthritis, serositis, renal disorder such as glomerulonephritis, neurologic disorder, blood disorder such as anemia, immune disorder, presence of ANA


Disease assumed to present with 4 or more of above symptoms

What is the pathogenesis of SLE and how does the disease progress?

Believed to be a Type III hypersensitivity reaction


a) Theory: malfunction of Ts/c cells leads to excessive activity of B cells, formation of many B cell clones, leading to plasma cells that secrete a variety of Ab


b) Abs react with self-antigens of tissues, antigens in blood form complexes with antibodies in blood and are deposited in certain areas of body, these deposits activate complement and initiate inflammation


Progression: course is variable and unpredictable

rarely: death within weeks or months

most often: flareups and remissions over many years


Common causes of death: Renal failure, recurrent infections, CNS disease, CAD

How does Drug-Induced Systemic Lupus Erythematosus occur?

Probably due to a genetic lack of enzyme to metabo.lize drug


Accumulation of drug causes changes in self antigens, setting off production of various Abs


This is reversible when drug is discontinued.

Describe Progressive Systemic Sclerosis (PSS, Scleroderma) and what is its pathogenesis?

This is an autoimmune disease that involves fibrosis of skin, GIT, kidneys, heart, muscles, lungs


Mainly occurs in women with peak incidence in 50-60 year age group.


Pathogenesis: Theory:

Th cells respond to unknown antigen, release cytokines which attract other inflammatory cells, a Type IV hypersensitivity.  These other cells release mediators that increase collagen production by fibroblasts, excessive fibrosis throughout body.

Describe polymyositis-dermatomyositis

Chronic inflammation of multiple skeletal muscles (polymyoitis), sometimes skin is also involved (dermamyoitis)


Symtoms: Pain, weakness, impaired movement: All of this is more prominent in proximal rather distal part of limbs, difficulty in swallowing


If skin is involved: heliotropic rash of eyelids and extensor surfaces of skin & muscles symptoms.


This disease usually has a prolonged course.

What is polymyoitis-dermatomyositis pathogenesis?

Muscles are infiltrated with T and B cells, macrophages, sometimes plasma cells


Loss of fibers, replacement with fibrous tissue, hypertrophy of remaining fibers.


May occur with SLE: due to a Type III hypersensitivity reaction, myositis mainly around blood vessels, perifasicular atrophy


May occur with sarcoidodid: due to Type IV hypersensitivity reaction, noncaseating granulomas in affected tissues

Describe Sjogren's syndrome and what is its pathogenesis

Immune destruction of lacrimal and salivary glands

May be primary problem, or secondary to RA, SLE, scleroderma, thyroiditis, etc.


90% of patients are women between 35-45 years


Clinical features:

  • lack of tears: keratoconjunctivitis, blurred vision, burning, itching
  • xerostomia: taste problems, cracks in mouth, gland enlargement
  • extraglandular: nasal dryness, recurrent bronchitis, synovitis, pulmonary fibrosis, peripheral neuropathy


Pathogenesis not completely known, probably due to excessive # of Th cells


Theory: A self-Ag cause this

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