Disorders Associated with the Immune System Flashcards
what happens if we have an OVERACTIVE IMMUNE RESPONSE?
- HYPERSENSITIVITY/ALLERGY
- AUTOIMMUNITY
- POSSIBILITY OF TRANSPLANT/GRAFT REJECTION
what happens if we have DEFECTIVE IMMUNE RESPONSE?
- due to OLD AGE
- can be CONGENITAL
- can be INFECTION – ex. HIV
describe HYPERSENSITIVITY
- where our IMMUNE RESPONSE goes BEYOND NORMAL
- have SENSITIZATION; previous exposure is needed for hypersensitivity to occur
- has ALLERGEN; the ANTIGEN ELICITING RESPONSE
what are our FOUR TYPES OF HYPERSENSITIVITY?
- TYPE I (ANAPHYLACTIC)
- TYPE II (CYTOXIC)
- TYPE III (IMMUNE COMPLEX)
- TYPE IV (DELAYED CELL-MEDIATED)
describe TYPE I - ANAPHYLACTIC REACTION
- around only 2 - 30 min to occur
- needs SENSITIZATION
- results in FORMATION of IgE ANTIBODIES–binds to MAST CELLS
- MAST CELLS - releases HISTAMINE
what are our TWO TYPES OF ANAPHYLACTIC REACTIONS?
- SYSTEMIC – anaphylactic shock
- LOCALIZED – hay fever, asthma, hives
describe HISTAMINES
- pre-stored in GRANULES
- helps to INCREASE PERMEABILITY & DILATION of CAPILLARIES (can lead to EDEMA and SWELLING)
- increases MUCUS SECRETION
- allows for SMOOTH MUSCLE CONTRACTION
describe LEUKOTRIENES + PROSTAGLANDINS
LEUKOTRIENES:
- allows for PROLONGED CONTRACTION OF SMOOTH MUSCLES (ASTHMA)
PROSTAGLANDINS:
- INCREASES MUCUS SECRETION from smooth muscles of our respiratory system
describe SYSTEMIC ANAPHYLAXIS
- seen in ANAPHYLACTIC SHOCK
- often commonly caused by INJECTED ANTIGENS
- needs SENSITIZATION–only a small dose can already cause a massive response
- treatment; EPINEPHRINE – allows to CONSTRICTS BV (BV dilates in reaction and our BP drops)
describe PENICILLIN ALLERGY
- PENICILLIN combines with CARRIER PROTEIN in SERUM – becomes IMMUNOGENIC
- around 2% have allergy + tested with SKIN TEST
describe LOCALIZED ANAPHYLAXIS
- often seen in INGESTED or INHALED ANTIGENS
- using SKIN TESTS to identity allergens
- symptoms depend on HOW ANTIGEN GETS IN
describe HAY FEVER
- involves MAST CELLS in MUCUS MEMBRANES OF RESPIRATORY TRACT
- ALLERGENS; pollen, dander, spores, mite feces
- SYMPTOMS; watery eyes, sneezing, congestion
- ANTIHISTAMINES; competes with HISTAMINE RECEPTOR SITES (allows for a reduced response)
describe ASTHMA
- in the LOWER RESPIRATORY SYSTEM
- has WHEEZING + SHORTNESS OF BREATH
- have CONTRACTION of SMOOTH MUSCLES of the BRONCHIAL TUBES
- INHALANTS – allows to BLOCK IgE (by blocking – HISTAMINE RELEASE IS NOT INDUCED)
describe INGESTED ANTIGENS
- seen often in FOOD INTOLERANCE–this is NOT AN ALLERGY
- just means the BODY CANNOT PROCESS FOOD
- can not be reliably tested by SKIN TEST
- around RIGHT FOODS cause over 90% of FOOD ALLERGIES
SYMPTOMS: - HIVES
- GI UPSET
what are the TWO WAYS TO PREVENT ANAPHYLATIC SHOCK?
- SKIN TEST
- DESENSITIZATION
describe SKIN TEST
- helps to DETERMINE what an INDIVIDUAL is ALLERGIC TO
- uses a SMALL AMOUNT OF ANTIGEN – inserted under the EPIDERMIS of the SKIN
- looking for a RAPID INFLAMMATORY RESPONSE
describe DESENSITIZATION
- series of using GRADUAL INCREASING DOSES injected under the skin
- around 65 - 75% effective VS. INHALED ANTIGENS
describe HYGIENE HYPOTHESIS
living conditions might be TOO CLEAN–kids are NOT EXPOSED TO GERMS = NO TRAINING FOR IMMUNE SYSTEM
- upsets the BALANCE BETWEEN TWO TYPES OF HELPER T CELLS; Th1 & Th2
- Th1 RESPONSE – helps to DOWN REGULATE Th2-RESPONSE; produces IMMUNOGLOBULIN IgE
- IgE: important to react to COMMON ALLERGENS
- lower STIMULATION OF TH1 RESPONSE = NO DAMPENING of OVERACTIVE Th2 RESPONSE
describe TYPE II - CYTOTOXIC REACTION
- have IgG & IgM antibodies interact with ANTIGENIC CELLS
- looks for FOREIGN CELLS that DISPLAY UNKNOWN/FOREIGN ANTIGENS
- will LYSE the cell; activates the COMPLEMENT SYSTEM / CYTOTOXIC T CELLS
examples;
- TRANSFUSION REACTION
- HEMOLYTIC DISEASE OF NEWBORN
- DRUG INDUCED CYTOTOXIC REACTIONS
describe ABO BLOOD GROUPS
- determines our BLOOD TYPE
- looking for ABSENCE or PRESENCE of CARBOHYDRATE ANTIGENS on the CELL SURFACE of RBCs
- TYPE A – has A TYPE CARBS + ANTI B ANTIBODIES
- TYPE B – has B TYPE CARBS + ANTI A ANTIBODIES
- TYPE AB – has both A + B TYPE CARBS + NO ANTI-A or ANTI-B ANTIBODIES
- TYPE O – has NO A + B TYPE CARBS + HAS BOTH ANTI-A + ANTI-B ANTIBODIES
what happens if we get the WRONG BLOOD TYPE?
- a TRANSFUSION REACTION
- opposing antibodies of blood begin AGGLUTINATION (clumping) + HEMOLYSIS
describe RH GROUPS
- RH FACTOR: protein that is found on the SURFACE of human RBCs
- around 85% (are RH+ — have Rh factor + NO ANTI-RH FACTOR)
- around 15% (have ANTI RH FACTOR ANTIBODY)
what happens if we have a TRANSFUSION with the WRONG RH TYPE CELL?
- needs FIRST-TIME SENSITIZATION
- creation of RAPID SERIOUS RESPONSE LYSING the TRANSFUSED CELLS (within SECOND EXPOSURE)
How is the RH factor inherited?
- if the DOMININANT GENE (D) – has Rh factor is present vs. the RECESSIVE GENE (d) – does not have Rh factor
what happens if we have an RH- MOTHER that is pregnant with an RH+ fetus?
- causation of HEMOLYTIC DISEASE of the NEWBORN
- blood of both mother and fetus are CONSTANTLY BEING EXCHANGED
- RH- MOTHER will receive RH ANTIGENS from RH+ FETUS (will start producing ANTI-RH ANTIBODIES)
- during SECOND EXPOSURE/BABY (if by chance the second baby is RH+)–the ANTI-RH ANTIBODIES will start to attack the baby
- this all OCCURS ONCE THE BABY IS BORN –effects of JAUNDICE, ANEMIA, and need of a TRANSFUSION
- within the UTERUS–BABY IS STILL OK because toxic produces are filters out by the PLACENTA
how do we TREAT HEMOYLTIC DISEASE OF NEWBORNS?
- make sure we PREVENT MOTHER from BUILDING UP ANTI RH ANTIBODIES
- injection of ANTI-RH ANTIBODIES at TIME OF DELIVERY
- allows for the BINDING OF THE RH FACTOR – as a RESULT OF DELIVERY = no interaction with mom’s immune system
describe TYPE III - IMMUNE COMPLEX REACTION
- where ANTIBODY-ANTIGEN REACTIONS – cleared RAPIDLY by PHAGOCYTIC CELLS
- sometimes SMALL AB-ANTIGEN COMPLEXES are able to ESCAPE PHAGOCYTOSIS
- allows to go through BV ENDOTHELIAL CELLS – attaches to the BASEMENT MEMBRANE OF VESSELS
- activates the COMPLEMENT; causes INFLAMMATION + ATTRACTION OF NEUTROPHILS
describe GLOMERULONEPHRITIS
- a type of IMMUNE COMPLEX CONDITION
- due to an INFECTION
- see DAMAGE to the KIDNEY GLOMERULI + SITE OF BLOOD FILTRATION
describe TYPE IV - DELAYED CELL MEDIATED REACTION
- does NOT INVOLVE ANTIBODIES
- takes around 2 - 3 days to KICK IN
- caused by our T CELLS
- mediated by CYTOTOXIC T CELLS + NK CELLS
what is an EXAMPLE of DELAYED CELL-MEDIATED HYPERSENSITIVITY OF SKIN?
- the TB TEST – looking for Mycobacterium tuberculosis –often seen in MACROPHAGES
- stimulation of DELAYED CELL-MEDIATED IMMUNE RESPONSE
- test involves; INJECTION OF PROTEIN COMP. of BACTERIA INTO SKIN
- if you had a PREVIOUS INFECTION; memory cells will occur = shows 1-2 day INFLAMMATORY RESPONSE
describe AUTOIMMUNE DISEASES
- where our IMMUNE SYSTEM begins to INTERACT with SELF-ANTIGENS causing DAMAGE to OWN TISSUES + ORGANS
- around 75% of autoimmune cases – affects WOMEN
what CAUSES AUTOIMMUNE DISEASES?
- the LOSS OF SELF TOLERANCE
**- T CELLS mature in the THYMUS – any cells that start to RECOGNIZE THEIR OWN PROTEINS are removed by THYMIC SELECTION - also occurs in B CELLS
what are the THREE TYPES OF AUTOIMMUNE DISEASES?
- CYTOTOXIC
- IMMUNE COMPLEX
- CELL MEDIATED IN NATURE
what are our CYTOTOXIC AUTOIMMUNE REACTIONS?
- GRAVES DISEASE
- MYASTHENIA GRAVIS
describe GRAVES DISEASE
- stimulation of THYROID GLAND (by TSH) to produce THYROID HORMONES
- the IMMUNE SYSTEM; starts to CREATE ANTIBODIES that MIMICK TSH – INCREASES THYROID ACTIVITY = INCREASE OF THYROID HORMONES
SYMPTOMS:
- HEART POUNDING
- TREMBLING
- SWEATING
- SWELLING OF THYROID GLAND
- BULGING EYES
describe MYASTHENIA AGRAVIS
- muscles start to become more PROGESSIVELY WEAKER
- due to ANTIBODY COATING OF ACETYLCHOLINE RECEPTORS within the NEUROMUSCULAR JUNCTION – starts to BLOCK SIGNAL OF MUSCLES
- any MUSCLES that CONTROL RIB CAGE or DIAPHRAGM – can FAIL LEADING TO DEATH
what are our IMMUNE COMPLEX AUTOIMMUNE REACTIONS?
- SYSTEMIC LUPUS ERYTHEMATOSUS
- RHEUMATOID ARTHRITIS
describe SYSTEMIC LUPUS ERYTHEMATOSUS
- mainly AFFECTS WOMEN
- ETIOLOGY (cause) still NOT UNDERSTOOD
- production of ANTIBODIES that are DIRECTED AGAINST THEIR OWN COMPONENTS/CELLS/DNA
- has WORSENING SYMPTOMS over TIME / alternates between mild & severe
describe RHEUMATOID ARTHRITIS
- where our IMMUNE COMPLEXES are DEPOSITED in the JOINTS
- IMMUNE COMPLEXES – known as RHEUMATOID FACTORS
- causes CHRONIC INFLAMMATION – due to DEPOSITION OF FACTORS
- damage to JOINTS AND CARTILAGE
what are OUR CELL-MEDIATED AUTOIMMUNE REACTIONS?
- MULTIPLE SCLEROSIS
- INSULIN DEPENDENT DIABETES (TYPE 1)
- PSORIASIS
describe MULTIPLE SCLEROSIS
- women 2x more LIKELY TO GET
- have the T CELLS + MACROPHAGES ATTACKS THE MYELIN SHEATH OF NERVES
- has a SLOW PROGRESSION with PERIODS OF REMISSION
- has EVIDENCE OF GENETIC PREDISPOSITION (of multiple genes)
- UNKNOWN ETIOLOGY
- possible is TRIGGERED BY EPSTEIN-BARR VIRUS INFECTION
describe INSULIN DEPENDENT DIABETES (TYPE 1)
- the IMMUNOLOGICAL DESTRUCTION of INSULIN SECRETING CELLS within the PANCREAS
- T CELLS are implicated
- has GENETIC COMPONENTS
describe PSORIASIS
- have ITCHY RED PATCHES OF THICK SKIN
- have DENDRITIC CELLS (IL-17) + Th1 CELLS = creates ABUNDANT PSORIATIC CYTOKINES (IFN-y / TNF)
- TREATMENT; IMMUNOSUPPRESSANT FOR T CELLS + TNF
- around over 25% of cases lead to PSORIATIC ARTHRITIS
what is the HUMAN LEUKOCYTE ANTIGEN (HLA) COMPLEX?
- codes within HUMAN GENES that code for the MAJOR HISTOCOMPATIBILITY COMPLEXES
- the MHCs interact with ANTIGENS and PRESENTS THEM TO OUR IMMUNE SYSTEM
- found in MOLECULES OF OUR CELL SURFACES – part of our INHERITED GENETIC CHARACTERISITC
define HLA TYPING
- used to COMPARE + IDENTIFY HLAs
- can look for CERTAIN HLAS – that can INDICATE INCREASED SUSCEPTIBILITY to a SPECIFIC DISEASE
why is HLA TYPING SO IMPORTANT?
- important for IDENTIFYING COMPATIBLE DONOR ORGANS
- must be MATCHED WITH TISSUE TYPING
- cont. of PCR to AMPLIFY + COMPARE HLA GENES of RECIPIENT + DONOR
- ABO BLOOD TYPE MATCH + DNA MATCH = GREATER TRANSPLANT SUCCESS RATE :) !
what are SOME REACTIONS TO TRANSPLANTATION?
- the TRANSPLANTED TISSUE can be NOT RECOGNIZED AS SELF – attacking by IMMUNE SYSTEM
- attacked by T CELLS + MACROPHAGES + ANTIBODIES = TRANSPLANT REJECTION
definition of PRIVILEDGED SITE
- able to TOLERATE INTRODUCTION OF FOREIGN ANTIGENS – does not INDUCE IMMUNE RESPONSE
- there is NO CIRCULATING ANTIBODIES in these areas
- ex. EYES, PLACENTA/FETUS, and TESTICLES
describe PRIVILEGED TISSUE
- tissue that DOES NOT ELICIT IMMUNE RESPONSE
- ex. PIG HEARTS
describe PREGNANCY and reactions
- have TISSUE OF TWO COMPLETLY GENETICALLY DIFFERENT PEOPLE in DIRECT CONTACT = but still NO DIRE REACTION TO FETUS
- IMPORTANT FACTOR; MHCI + MHCII COMPLEXES of PLACENTA – does not STIMULATE CELLULAR IMMUNE RESPONSE
- the FETUS IS PROTECTED by PROTEINS that has IMMUNOSUPPRESSANT PROPERTIES
describe STEM CELLS
- can DEVELOP INTO OVER 200 DIFFERENT CELL TYPES
- has transformed TRANSPLANTATION MEDICINE
- has NO MORE REJECTION as these EXPRESSES OWN SELF ANTIGENS
- have EMBRYONIC STEM CELLS + ADULT STEM CELLS
describe EMBRYONIC STEM CELLS
- harvested from BLASTOCYSTS
- PLURIPOTENT; can be used to GENERATE any KIND OF CELL
describe ADULT STEM CELLS
- type of SPECIALIZED STEM CELLS
- gives rise to SPECIFIC FAMILIES of CALL TYPES (ex. BLOOD CELLS)
- called MULTIPOTENT
- replenishes ORGANS and TISSUES as NEEDED
- ex. SKIN CELLS + CARDIAC CELLS + BRAIN CELLS
describe GRAFTS and what are OUR FOUR TYPES?
- transplanted LIVING TISSUE
- AUTOGRAFT
- ISOGRAFT
- ALLOGRAFT
- XENOGRAFT
definition of AUTOGRAFT
- one’s OWN TISSUE is USED in TRANSPLANT
- NO REJECTION – can be used for BURN PATIENTS – used to GROW NEW SKIN to COVER DAMAGED AREA
describe ISOGRAFT
- a GENETICALLY IDENTICAL GRAFT
- used typically in TWINS
describe ALLOGRAFTS
- graft between PEOPLE WHO ARE NOT GENETICALLY IDENTICAL
- usage of TISSUE TYPING to MATCH HLAs – to REDUCE CHANCE OF REJECTION
- often seen in CLOSE RELATIVES – SIBLINGS
describe XENOGRAFT
- usage of ANIMAL TISSUE being TRANSPLANTED
- causes SEVERE IMMUNE REACTION
- greater research to make HUMANIZED PIGS (less reactive) – creation of BETTER DONORS
- main concern is ANIMAL VIRUSES
describe BONE MARROW TRANSPLANTS
- type of HEMATOPOIETIC STEM CELL TRANSPLANT
- given when PATIENTS CANNOT PRODUCE B CELLS + T CELLS / or have LEUKEMIA
- allows to TRANSPLANT produces HEALTHY RBC IMMUNE SYSTEM CELLS
- can cause GRAFT vs. HOST DISEASE
describe GRAFT vs HOST DISEASE
- where TRANSPLANTED BONE MARROW has IMMUNOCOMPETENT CELLS – CREATION OF CELL MEDIATED IMMUNE RESPONSE in TISSUE
- can be FATAL
- seen as EPITHELIAL CELL DEATH in the SKIN, GI TRACT, and LIVER
describe UMBILICAL CORD BLOOD
- full of MULTIPOTENT STEM CELLS - develops into a NUMBER OF BLOOD CELLS
- harvested from PLACENTA + UMBILICAL CORD of NEWBORNS
- allows for LESS IMMUNE REACTION - cells are LESS MATURE
- LESS RISK FOR GRAFT v. HOST DISEASE
describe IMMUNOSUPPRESSION in TRANSPLANT PATIENTS
- have a more SUPPRESSED CELL-MEDIATED IMMUNITY
- leaves the HUMORAL IMMUNITY intact to deal with INFECTIONS
describe CYCLOSPORINE
- the FIRST DRUG USED FOR IMMUNOSUPPRESSION
- isolated from a FUNGUS
- suppresses Il-2 DISRUPTING CYTOTOXIC T CELLS
- does NOT AFFECT Ab PRODUCTION
describe SIROLIMUS
- inhibits BOTH HUMORAL + CELL MEDIATED IMMUNITY
- HYPERACUTE REJECTION
- is TAKEN FOR LIFE
Can we AVOID IMMUNOSUPPRESSANT DRUGS ?
- sometimes! – ex. KIDNEY TRANSPLANT PATIENT
- usage of BONE MARROW from PATIENT and TRANSPLANTS BOTH KIDNEY AND BONE MARROW TOGETHER–creation of a REBUILT IMMUNE SYSTEM
- creation of CHIMERA; the MIX OF IMMUNE MARKERS of the DONATED KIDNEY + PATIENT’S OWN CELLS
- acceptance of ORGAN + stops drugs less than a year after surgery
- CHIMERA STATE NOT PERMANENT HOWEVER
what happens to our IMMUNE SYSTEM AS WE GET OLDER?
- thymus cannot EFFICIENTLY MATURE and DIFF. T-LYMPHOCYTES
- LOWER ABILITY to FIGHT DISEASE
- more SUSCEPTIBILITY to DISEASE
describe CANCER
- the FAILURE within the BODY’S NORMAL FUNCTION
- cells transform and GROW WITHOUT CONTROL – cancerous growth
- NORMAL CELLS KNOW WHEN TO STOP GROWING – has CONTACT INHIBITION (creates only a MONOLAYER OF CELLS)
are cancer cells always popping up in the body?
YES!
- eliminated by the immune system through IMMUNE SURVEILLANCE; a type of CELL MEDIATED IMMUNE RESPONSE
- looks for TUMOR ASSOCIATED ANTIGENS – marks cancer cells as NON-SELF
- then is ATTACKED BY THE CELL MEDIATED IMMUNE SYSTEM - CYTOTOXIC T CELLS
describe Dr. William Coley’s cancer research
- noted that CANCER PATIENTS that get TYPHOID FEVER – cancer is DIMINISHED
- injection of TYPHOID FEVER (Streptococci + Serratia) into CANCER PATIENTS
- had mixed results
- NOW USE ENDOTOXINS from BACTERIA – to create TUMOR NECROSIS FACTOR (TNFalpha)
definition of SPONTANEOUS REMISSION
- the ACTIVATION OF THE IMMUNE SYSTEM
- apoptosis/tumor microenvironment
describe VACCINES
- THERAPEUTIC
- treats EXISTING CANCER
- 2010; first approved vaccines for METASTATIC PROSTATE CANCER
describe PROPHYLACTIC IMMUNOTHERAPY
- prevents the DEVELOPMENT OF CANCER
- have TWO;
- HUMAN PAPILLOMAVIRUS VACCINE HPV (GARDASIL)
- cervical, rectal, head, and neck cancer - HEPATITIS B VIRUS VACCINES
- liver cancer
describe MONOCLONAL ANTIBODIES
- new promising tool to FIGHT CANCER
- interferes with CANCER CELL FUNCTION
- ex. HERCEPTIN – neutralizes GF HER2 (seen in around 25 - 30% of cancer)
- also is COMBINED WITH TOXIC AGENTS - IMMUNOTOXINS
- able to TARGET CANCER CELLS where the TOXIN WORKS
- ex. ADCETRIS - for HODGKIN’S LYMPHOMA
describe IMMUNODEFICIENCY
- the ABSENCE OF A ROBUST IMMUNE SYSTEM
- can have ACQUIRED or CONGENITAL IMMUNODEFICIENCY
describe CONGENITAL IMMUNODEFICIENCY and DIGEORGES SYNDROME
- is BORN with DEFECTS to IMMUNE SYSTEM
- syndrome where we have a SMALL DELETION in CHROMOSOME 22
- causes ABNORMAL THYMUS DEVELOPMENT
- have POOR T CELL PRODUCTION = INCREASES SUSCEPTIBILITY for INFECTIONS
describe ACQUIRED IMMUNODEFICIENCY
- CANCER
- DRUGS
- INFECTION
describe ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS)
- was originated of symptoms of Pneumocystis pneumonia
- development of rare skin cancer - Kaposi’s sarcoma (seen in several homosex. men)
- thought to be correlated to SEXUALITY – named GRID (gay-related immune deficiency)
- 1983; discovered correlation of NOVEL RETROVIRUS HIV + AIDS
describe HIV - ORIGin
- mutation from VIRUS ENDEMIC in PRIMATES in AFRICA
- from the SIMIAN IMMUNODEFICIENCY VIRUS SIV – consumed BUSHMEAT by humans (got SIV)
- began to MUTATE into HIV
- starts to SPREAD after URBANIZATION OF AFRICA
what type of VIRUS is HIV?
- RETROVIRUS (Lentivirus)
- has TWO IDENTICAL STRANDS of RNA
- has REVERSE TRANSCRIPTASE
- has ENVELOPE with GLYCOPROTEIN SPIKES (gp120)
how does HIV infect people?
infects our T HELPER CELLS
- usage of path; ATTACHMENT, FUSION and then ENTRY
- usage of REVERSE TRANSCRIPTION of its VIRAL RNA into cDNA
- is able to INTEGRATE INTO THE HOST CHROMOSOMAL DNA
- and stays HIDDEN (LATENT) !!
what are the FACTORS that AFFECT HIV SURIVIVAL with the ABSENCE of TREATMENT?
- OLD AGE
(harder to replace T helper cells) - IMMATURE IMMUNE SYSTEM
- SUBSET – you are exposed but not INFECTED
(T cells don’t have co-receptor for HIV binding) - NO PROGRESSION into FULL AIDS
(very active CTLs)
what are the MEANS of HIV TRANSMISSION?
- UNPROTECTED SEX
- SHARING NEEDLES
- TRANSMISSION FROM MOTHER TO FETUS
- INFECTION FROM BLOOD PRODUCTS
how does HIV hide from our IMMUNE SYSTEM?
- a POOL of LATENT INFECTED T CELLS – very hard to remove
- REVERSE TRANSCRIPTASE – very HIGH MUTATION RATE
- very hard to MAKE VACCINE
- only good model is PRIMATES–ethically questionable