Which are primary lymphoid organs?	Bone marroy - Thymus.
What is Bone marrow function ?	Immune cell production - B cell MATURATION
What is Thymus function?	T cell MATURATION.
Which are secondary lymphoid organs?	Spleen - Lymph nodes - Tonsils - Peyer patches.
What is secondaty organs function?	Interaction of immune cells with antigens.
What is a LYMPH NODE?	Secondary lymphoid organ - Encapsulated - It fuction is: NONspecific filtration by MECROPHAGES - Storage of B & T cells & Immune response activation.
Which are the parts of a LYMPH NODE?	Follicle - Medulla - Paracortex.
What is a follicle?	Site of B-CELL localization & PROLIFERATION. Located in OUTER CORTEX. There are two types - 1° & 2°.
What is the diference between 1° & 2° Follicles?	PRIMARY: Dense and dormant SECONDARY: With a PALE CENTRAL GERMINAL and is ACTIVE.
What is the medulla?	Composed by: MEDULLARY CORDS (Packed lymphocytes & PLASMA cells) & MEDULLARY SINUSES (Communicate with efferent lymphatics & contain RETICULAR cells & MACROPHAGES)
What is the paracortex?	House of T CELLS - Regions between follicles & medulla.
Which disease is associated with not well developing of PARACORTEX?	DiGeorge syndrome
What diseases can enlarge PARACORTEX in a extreme cellular immune response?	EBV - Viral infections.
Which immune cells are derivative from MYELOID CELL LINE?	1. PMN Cells // Neutrophils (Phagocytic oxidative burst) - Eosinophils (Hystamine - Paracytes ) - Basophils & Mast Cells (NON phago - Asthma - Allergies ) // 2. MONOCYTES // Macrophages & Dendritic cells. (Antigen presenting cells, Phagocyte, release cytokines and attract other immune cells)
Which immune cells are derivative from LYMPHOID CELL LINE?	1. NATURAL KILLERS ( BM developed, Granules create pores = Apoptosis - Intracellular VIRUSES & TUMOR cells // 2. B CELLS ( Does NOT need a MCH to identify an antigen ) 3. T CELLS ( Thymus developed, All CD3 response; CD4 helper (Coordinates MCH II ) CD8 Cytotoxic (Kill target only MCH I)
What area is drain by the CERVICAL & SUPRACLAVICULAR lymph node cluster?	Head and Neck
What pathology is related with this cluster	Upper respiratory track infections - MONONUCLEOSIS - KAWASAKI disease.
What area is drain by the MEDIASTINAL lymph node cluster?	Trachea & Esophagus
What pathology is related with this cluster	PRIMARY LUNG CANDER - GRANULOMATOUS DISEASE
What area is drain by the HILAR lymph node cluster?	Lungs
What pathology is related with this cluster	GRANULOMATOUS DISEASE
What area is drain by the AXILLARY lymph node cluster?	Upper limb - Breast - Skin above UMBILICUS
What pathology is related with this cluster	MASTITIS - METASTASIS (Breast cancer)
What area is drain by the CELIAC lymph node cluster?	Liver - Stomach Spleen - Pancreas - Upper Duodenum.
What area is drain by the SUPERIOR MESENTERIC lymph node cluster?	Lower Duodenum - Jejunum - Ileum - Colon to slenic flexure.
What area is drain by the INFERIOR MESENTERIC lymph node cluster?	Colon from splanic flexure to upper rectum
What pathology is related with Celiac - Sup & Inferior mesenteric clusters?	MESENTERIC LYMPHADENITIS - TYPHOID FEVER - ULCERATIVE COLITIS - CELIAC DISEASE
What area is drain by the PARA - AORTIC lymph node cluster?	Testes - Ovaries - Kidneys - Uterus.
What pathology is related with this cluster	METASTASIS
What area is drain by the EXTERNAL ILIAC lymph node cluster?	Cervix - Superior bladder & body of the Uterus.
What area is drain by the CERVICAL & SUPRACLAVICULAR lymph node cluster?	Lower rectum to Anal canal (Above pectinate line), Bladder, Vagina (middle third), Cervix & Prostate.
What area is drain by the CERVICAL & SUPRACLAVICULAR lymph node cluster?	Anal canal (Below pectinate line) Skin below umbilicus (except popliteal area) Scroum - Vulva.
What pathology is related with this cluster	SEXUALLY TRANSMITED INFECTION / Mefial foot, leg CELLULITIS (superficial inguinal).
What area is drain by the CERVICAL & SUPRACLAVICULAR lymph node cluster?	Dorsolateral foot - Posterior calf
What pathology is related with this cluster	Lateral foot / Leg CELLULITIS.
Which are the lymphatic trunks ?	2 Lumbar - 2 Bromchomediastinal - 2 Subclavian trunks - 2 Jugular trunks - 1 Intestinal trunk
Which are the TONSILs?	Adeoid - Tubal - Palatine & Lingual tonsils.
What and where does the RIGHT LYMPHATIC DUCT drains?	Drains RIGHT side of the body above the diaphragm into JUNCTION OF THE RIGHT SUBCLAVIAN AND INTERNAL JUGULAR VEIN.
What and where does the THORACIC DUCT drains?	Below de diaphragm and left thorax and upper limb into the JUNCTION OF LEFT SUBCLAVIA AND INTERNAL JUGULAR veins.
What is caused if Throracic duct ruptures?	CHILOTHORAX.
Where is SPLEEN located ?	LUQ - Anterolateral to L Kidney - Protected by 9 to 11 ribs.
What are the compounds of the Spleen ?	Capsule - Trabecule - RED & WHITE PULP - Marginal zone.
What is in the RED PULP	RBCs
What are the sinusoids?	Long vascular channels in RED PULP -
What is in the WHITE PULP?	Follille (B cells) Periarteriolar lymphoid sheat (PALS - T cells)
What is in the MARGINAL ZONE	It is between red and white pulp, contains MACROPHAGES (Removes encapsulated bacteria) & SPECIALIZED B CELLS. It is the place where APC (Antigen presenting cells) capture blood borne antigens for recognition by Lymphocytes.
What situations can cause SPLENIC DISFUNCTION?	Postsplenectomy state - SICKLE CELL DISEASE = L: Low IgM, Complement activation = H: Susceptibility to encapsulated organisms.
What are the findings in blood after SPLENECTOMY?	Howell Jolly bodies (Nuclear remnants) - Target cells - Thrombocytosis & Lymphocytosis (Loss of sequestration and removal).
What VACCINES are needed after splenectomy	PNEUMOCOCCAL - HiB - MENIGOCOCCAL.
Where is THYMUS located?	In the ANTEROSUPERIOR MEDIASTINUM.
Where is THYMUS derivative?	THird pharyngeal pouch (ENDODERM) wheres Thymid Lymphocytes are of MESODERMAL ORIGIN.
What are the Thymus parts ?	Cortex ( Immature T cells ) - Medulla ( Pale & Mature T cells & HASSAL CORPUSCLES - Containing Epithelial reticular cells.
Is there a Thymus in neonates?	Sail shaped Thymus on CxR.
What if an ABSENT THYMIC SHADOW in a newborn?	SCID - DiGeorge Syndrome.
What is a Thymoma	Neoplasm of thymus.
What diseases are associated with a Thymoma?	MYASTHENIA GRAVIS - SUPERIOR VENA CAVA SYNDROME - PURE RED APLASIA - GOOD SYNDROME.
What components are part of INNATE IMMUNITY?	Neutrophils - Macrophages - Monocytes - Dendritic cells - NKs - Complement - Physical epithelial barriers - Secreted enzymes.
What components are part of ADAPTATIVE IMMUNITY?	T cells - B cells & Circulating ABs.
What mechanism are part of INNATE IMMUNITY?	Germline encoded.
What mechanism are part of ADAPTATIVE IMMUNITY?	Variation through V(D)J RECOMBINATION during Lymphocyte development.
How is the resistance of INNATE IMMUNITY?	Resistance persist throught generation - Does NOT change within an organism's lifetime
How is the resistance of ADAPTATIVE IMMUNITY?	Microbial resistance NOT heritable.
How is the response to pathogens in INNATE IMMUNITY?	Non Specitic - RAPIDLY (minuts - hours) - NO MEMORY.
How is the response to pathogens in ADAPTATIVE IMMUNITY?	Highly Specific - OVER LONG PERIODS - Memory response is faster and more robust.
Which are the secreted proteins in INNATE IMMUNITY?	LYSOZYME - Complement - C Reactive Protein (CRP) Defensins.
Which are the secreted proteins in ADAPTIVE IMMUNITY?	Immunoglobulins.
What are the key features in Pathogen Recognition?	TOLL LIKE Receptors - Recognize Pathogen - Associated Molecular Patterns (PAMPs) and lead activation of NF- kappaB. (PAMPs = LPS (gram negative bacteria - Flagellin - Nucleic acids)
Which gene encondes for MHC?	HLA genes.
What is MHC function?	Present antigen fragmnts to T cells and bind T cell receptors (TCRs) .
Which are the MHC I Locis?	HLA - A / HLA - B / HLA - C / 1 Letter.
Which are the MHC II Locis?	HLA - DP / HLA - DQ / HLA - DR / 2 Letters.
Where does the MCH I binds to ?	TCRs & CD8
Where does the MCH II binds to ?	TCRs & CD4
What is the MCH I structure?	1 LONG chain & 1 SHORT chain.
What is the MCH II structure?	2 EQUAL Lenght chain (2 alpha, 2 beta)
Where is the MCH I expressed?	ALL NUCLEATED CELLS, APCs, Plateles (Except RBCs)
Where is the MCH II expressed?	APCs.
What is MCH I function?	Present ENDOGENOUS antigens (VIRAL or CYTOSOLIC proteins) to CD8+ Cytotoxic T CELLs.
What is MCH II function?	Present EXOGENOUS antigens (BACTERIAL) to CD4+ herper T cells.
What is the ANTIGEN LOADING for MHC I ?	ANTIGEN PEPTIDES - loaded onto MHC I in RER after delivery via TAP (Trasporter associated with antigen processing)
What is the ANTIGEN LOADING for MHC II ?	ANTIGEN loaded following release of INVARIAN CHAIN in a ACIDIFIED ENDOSOME.
Associated proteins with MHC I ?	Betta 2 - Microglobulins.
Associated proteins with MHC II?	Invariant chain.
What disease is associated with HLA subtype A3 ?	HEMOCHROMATOSIS - HA3mochromatosis.
What disease is associated with HLA subtype B8?	ADDISON disease - MYasthenia gravis - GRAves disease // Don´t Be late(8) - Dr. ADDISON, or else you'll send MY patient to the GRAVE.
What disease is associated with HLA subtype B27?	Psoriatic arthritis - Ankylosing spondylitis, IBD - associated arthriris - Reactive arthritis. // PAIR = Also Known as SERONEGATIVE Arthropathies.
What disease is associated with HLA subtype C ?	Psoriasis.
What disease is associated with HLA subtype DQ8/DQ2?	Celiac disease / I ate (8) too (2) mucho glutten ar Diary Queen
What disease is associated with HLA subtype DR2 ?	MULTIPLE sclerosis, HAY fever, SLE, GoodPASTURE syndrome // "Multiple hay pastures are Dirty (DR2)"
What disease is associated with HLA subtype DR3 ?	DM Type I - SLE - Graves disease - Hashimoto thyroiditis - Addison disease.
What disease is associated with HLA subtype DR4 ?	Rheumatoid arthritis - DM type I - Addison disease.
What disease is associated with HLA subtype DR5 ?	Hashimoto Thyroiditis.
What is a natural killer¡	A lymphocyte member of INNATE IMMUNE System
How is the mechanism of action of a NK cell?	Use PERFORIN & GRANZYMES to induce APOPTOSIS of virally infcted cells and tumor cells. - Also kiss via antibodydependent cell mediated citotoxicity. (CD16 binds to FC region of bound IgG activating the NK cell.
What elements enhanced tha actuvity of a NK:	IL -2 / IL - 12 // IFN-alpha / and IFN - beta.
What us the major function of B Cells?	Humoral Immunity // Bcell recognize antigen - Undergoes hypermutation to optimize Ag specificity - Procude Ab - Defferentiate into PLASMA cells to secrete Igs. MANTAIN MEMORY
What us the major function of T Cells?	Cell mediated Immunity // DELAYED CELL MEDIATED HYPERSENSITIVITY. (Type IV) // ACUTE & CHRONIC cellular organ reaction.
What us the major function of T CD4 + Cells?	CD4 + (Helper) - Help B cells make Ab and produce CYTOKINEs to recruit PHAGOCYTES and activate other LEUKOCYTES.
What us the major function of T CD8 + Cells?	CD8 + (Cytotoxic) - Directly kill VIRUS infected cells.
Which IL RECEPTOR is present in cells to survive and hace memory ?	IL - 7
What is POSITIVE selection in T cell differentiation?	T cells expressiong TCRs capable of binding SELF-MHC on cortical epithelial cells survive. Takes place in THYMIC CORTEX.
What is NEGATIVE selection in T cell differentiation?	T cells expressiong TCRs with HIGH affinity for SELF ANTIGENS undergo APOPTOSIS or become REGULATOY T CELLS . Takes place in THYMIC MEDULLA.
What is responsable for the Tissue - Restricted - SELF Ag ?	Action of Autoimmune regulator (AIRE)
What disease is associated with AIRE deficiency?	AUTOIMMUNE POLYENDOCRINE SYNDROME - 1
How many subtypes of T CD8+ cells there are ?	Four / /Th1 - Th2 - Th12 - Treg
What is SECRETED by Th1 cells ?	IFN - gamma / IL - 2
What is Th1 cell function ?	Activate MACROPHAGES & Cytotoxic T cells to kill PHAGOCYTOSED MICROBES.
What induces Th1 cell function?	INF gamma / IL - 12
What INHIBITS Th1 cell funcition.	IL -4 & IL- 10 ( from Th2 cell)
What diseases are related with Th 1 immunodeficiency?	Mendelian Suceptibily to Mycobacterial disease.
What is SECRETED by Th2 cells ?	IL - 4 - 5 - 6 - 10 - 13
What is Th2 cell function ?	Activate EOSINOPHILS & promote IgE PRODUCTION for PARASITE DEFENSE.
What induces Th2 cell function?	IL - 2 - 4.
What INHIBITS Th2 cell funcition.	INF gamma (From Th 1 )
What is SECRETED by Th17 cells ?	IL 17 - 21 - 22
What is Th17 cell function ?	Immunity against EXTRACELLULAR MICROBES, induction of NEUTROPHILIC Inflammation.
What induces Th17 cell function?	TGF Betta - IL 1 - 6
What INHIBITS Th1 cell funcition.	INF gamma - IL 14
What diseases are related with Th 17 immunodeficiency?	Hyper IgE syndrome.
What is SECRETED by Treg cells ?	TGF Betta - IL 10 - 35
What is Treg cell function ?	PREVENTS AUTOIMMUNITY - by maintaining tolerance to SELF AG. Is identified by CD3 - CD4 - CD25 & FOXP3 expression.
What induces Treg cell function?	TGF Betta - IL 2
What INHIBITS Treg cell funcition.	IL 6
What diseases are related with Treg immunodeficiency?	Immunodysregulation polyendocrinopathy enteropathy X-linked (or IPEX) syndrome
Which are the features associated with these desease?	Genetic defiviency of FOXP3 - Autoimmunity // Enteropathy - Endocrinopathy - Nail destroy - Dermatitis - DIABETES in MALE INFANTS /Association/
What is macrophage lymphocyte interaction?	Th1 cells secrete IFN - Gamma which ++ the ability of monocytes and machropagues to kill microbes - This is also enhanced by interacion of T cells with CD40 in macrophages.
What functions have in general Cytotoxic T cells	Kill VIRUS infected - NEOPLASTIC - DONOR GRAFT cells by induciong APOPTOSIS.
Which are the two types od memory on B cells ?	Central memory ( 25 years - Live in lymphoid tissue) Effector memory (Around body - Respond as in primary immune response.
Hoy many signals are required for T & B cell activation ?	Two
T cell activation process?	APC samplesAg, processes it and migrates to the draining lymphonode // SIGNAL 1 (Ag is presented on MHC II and recognized by a TCR of CD4 +, Endogenous or cross presented Ag is presented on MHC I to CD8 + cells. // PROLIFERATION and survival (SIGNAL 2) Costimulatore interaction thanks to B7 - CD80/60 & cd27 interaction // Th cells activates and produces cytokines
B cell activation process?	Th cell activation. // CD40 receptor on Th cell CD40 L. Th cells secrete cytokines that determine Ig CLASS SWITCHING of B cells.
Ab structure ?	FAB containing VARIABLE / HYPERVARIABLE regions - Consist of a LIGHT & HEAVY chains.
What is FAB	Fragment antigen binding. It DETERMINES IDIOTYPE - only 1 antigenitc specificity expressed por B cells
What is OPSONIZATION - NEUTRALIZACION - COMPLEMENT ACTIVATION	Opsonization : Ab promotes phagocytois // Neutralizacion : Ab prevents bacterial asherence // COMLEMENT ACTIVATION: Ab activates complement enhanci oponiacion an grey.
What is a Immunoglobulin Isotype.?	Immunoglobulin. Exist in monomers (all of them).Meture Naive B cells prior to activation express IgM & IgD. They mature and differenciate in germinal center// This is stimulated by CD40L & CYTOKYNES.
IgG characteristics?	1. Main AB y SECUNDARY reponse to an AG - 2. Most abundant isotype 3. Fixes complement 4. Opsonizes bacteria 5. Neutralizes bacterial TOXINS & VIRUSES.
Does IgG crosses the PLACENTA?	YES - Provides infants with PASSIVE IMMUNITY that starts to WANE 6 MONTHS of age.
How many types of IgGs there are?	IgG1 - IgG2 - IgG3 - IgG4.
IgA Charateristics?	1. Prevents attachment of BACTERIA & VIRUS to MUCOUS MEMBRANES. 2. Does not fix complement. 3. MONOMER in circulation DIMER when secreted. 4. MOST PRODUCED AB overall (20%=*) , lower serum concentrations. 5. Transcytosis to cross epithelial cells.
Where does IgA is produced?	1. GI Track by Peyer patches. Protects against GUT infections. 2. Tears 3. Saliva 4. Mucus 5. Breast milk.
IgM Characteristics?	Produced in the PRIMARY response to an AG. 2. Fixes complement 3. MONOMER in B cells & PENTAMER when secreted. 4. 4% of all Igs. Made without T cell help.
IgD Characteristics?	UNCLEAR function. On B cells surface.
IgE Characteristics?	1. Binds MAST cells & BASOPHILS. 2. Immediate (Type I Hypersensitivity) 3. Realise inflammatory mediators such as HISTAMINE. 4. Immunity to PARASITES, activate EOSINOPHILS. 5. Lowest concentration in serum.
What is a THYMUS - INDEPENDENT AG	AG lacking a PEPTIDE component. Cannot be presente by MHC to T CELLS.
What is a THYMUS - DEPENDENT AG	AG containing a PROTEIN component. Producess CLASS SWITCHING AND IMMUNOLOGIC MEMORY ocurs as a result of direct contact of B cell with Thelper cell.
What is Complement ?	System of Hepatically synthesized plasma proteins that play a role in INNATE IMMUNITY ands INFLAMMATION.
What is the Membrane Attack Complex (MAC) ?	it is a part of the COMPLEMENT that defedns against GRAM NEGATIVE BACTERIAS.
How many pathways there are to activate the COMPLEMENT?	3. 1. CLASSIC (IgG or IgM mediated) // 2. ALTERNATIVE (Microbe surface molecules) // 3. LECTIN (Mannose or other sugars on MICROBE surface).
What is C3b function?	OPSONIZATION. C3b binds to lipopolysaccharides on BACTERIA // Also helps CLEAR IMMUNE COMPLEXES
What are C3a - C4a - C5a Function?	Anaphylaxis.
What is C5 a Function?	Neutrophil chemotaxis.
What is C5b - C6 - C7- C8 - C9 function?	Cytolysis by MAC.
Which are the Opsonins?	C3b - IgG are the PRIMARY opsonins in BACTERIAL DEFENSE = Enhance phagocytosis.
Which are the Inhibitors?	DAF (Decay - accelerating factor) Aka CD55 & C1 esterase inhibitor (C1 depends on Ca+2 L Ca L C1) - Help preventing COMPLEMENT activation on SELF CELLS (eg. RBCs)
Early complement deficiecies (C1 - C4)	H: Risk of SEVERE - recurrent PYOGENIC SINUS & RESPIRATORY tract infections. H: Risk of SLE - Chronic renal disease.
Terminal complement deficiencies (C5 - C9)	H: Susceptibility to RECURRENT NEISSERIA BACTEREMIA.
C1 Esterasa inhibitor deficiency	HEREDIRATY ANGIOEDEMA (Unregulated activation of KALLIKREIN = H: BRADYKININ.
What is decreased in C1 Esterase Inhibitor deficiency?	C4 levels.
What is GROUP of drugs are contraindicated in C1 Esterase deficiency ?	ACE Inhibitors
What causes Paroxysmal Nocturnal Hemoglobinuria?	Defect in PIGA gene. // Causes a Complement Mediated INTRAVASCULAR HEMOLYSIS = L: Haptoglobin, dark urine.
What is the physiologic explanation of PNH?	Preventing in formation of GLYCOSYLPHOSPHATIDYLINOSITOL (GPI) anchors for complement inhibitors such DAF / CD55 and membrane inhibitors of reactive lysis (MIRL/CD50)
What etiology has PNH?	Inherited: Mostly Autosomal RECESSIVE // Adquired: LUPUS.
What Cytokines are secreted by Macrophages?	Interleukin - 1 // Interleukin - 6 // Tumor necrosis factor alpha // Interleukin - 8 // Interleukin - 12
Interleukin - 1 characteristics?	Fever // Activates ENDOTHELIUM to express ADHESION MOLECULES // Induces chemokine secretion to recruit WBC. Aka = Osteoclast-activating factor.
Interleukin - 6 characteristics?	Fever // Production of ACUTE PHASE PROTEINS
Tumor necrosis factor alpha characteristics ?	Activates ENDOTHELIUM, Causes WBC recruitment, Venous leak // Causes: CACHEXIA in MALIGNANCY / Maintains GRANULOMAS in TB
Interleukin - 8 characteristics?	MAJOR CHEMOTACTIC factor for NEUTROPHILS
Interleukin - 12 characteristics?	DIFFERENTIATION of T cells into TH1 cells - ACTIVATES NK Cells.
What Cytokines are secreted by All T cells?	Interleukin - 2 / Interleukin - 3
Interleukin - 2 characteristics?	+ Growth of HELPER - CYTOTOXIC - Regulatory T cells & NK cells
Interleukin - 3 characteristics?	Growth & Differentiation of BONE BARROW STEM CELLS. Functions like GM - CSF.
What Cytokines are secreted by All Th1 cells?	Interferon - gamma
Interferon - gamma characteristics? (4)	By NK cells & T cells in RESPONSE TO IL 12(macrophages) or AG // + Macro to kill phacogytosed pathogens. INHIBITS DIFFERENTIATION OF TH2 CELLS. // Activates NK to kill VIRUS infected cells. Increases MHC expression and AG presentation to the cell.
What Cytokines are secreted by All Th2 cells?	Interleukin - 4 // Interleukin - 5 // Interleukin - 10
Interleukin - 4 characteristics? (3)	Differentiation of T cells into TH2 cells // GROWTH of B cells - Class switching to IgE and IgG.
Interleukin - 5 characteristics? (3)	Growth & Differentiation of B cells & EOSINOPHILS / Class switching to IgA
Interleukin - 10 characteristics?	ATTENUATES inflammatory response. DECREASES expresion of MHC class II and TH1 cytokines. // INHIBITS activates macro & dendritic cells. SECRETED BY T reg cells.
What cytokines ATTENUATE the immune response?	IL -10 & TGF betta.
What cytokines mediate FEVER & SEPSIS?	IL - 1 / IL - 6 / TNF a.
Mnemotecnia “Hot T - BONE - stEAK”	IL 1 - Hot (fever) // IL - 2 +T cells // IL - 3 + BONE marrow // IL - 4 + IgE // IL - 5 + IgA // IL - 6 aKute phase protein production.
What is the RESPIRATORY BURST?	Aka OXIDATIVE BURST. An important vía in IMMUNE RESPONSE, realease Reactive Oxygen Species (ROS).
What does the OXIDATIVE BURST includes?	Activation of the phagocyte NADPH OXIDASE COMPLEX which utilizes O2 as a substrate. Release ROS // NADPH plays a role in both creation and neutralization of ROS. // It also produces an K influx with releases LYSOSOMAL ENZYMES //
What gives sputum its color?	Myeloperoxidase
What disease is related with NADPH oxidase	Chronic Granulomatous Disease
CGD characteristics?	NADPH Oxidase deficiency // Phagocytes utilize H202 generated by organism and converted it on ROS. // HIGH risk for CATALASE POSITIVE SPECIES ( Neutralizing their own H2O2 leaving phagocytes without ROS for fighting infections)
Examples of catalase + species?	S. Aureus - Aspergillus.
What is special about P. Aeruginosa?	It generates ROS to kill competing pathogens.
What is Lactoferrin?	Protein found in SECRETORY FLUIDS and NEUTROPHILS that INHIBITS microbial growth via IRON CHELATION.
Which are the interferons ?	IFN-a // INF-b // INF-g
Interferons characteristics?	INNATE host defense. INTERFERE with RNA & DNA viruses. // DOWNregulate protein synthesis to resist potential viral replication // UPREGULATING MHC expression to facilitate RECOGNITION (Antitumor immunity).
Use of Interferons?	Chronic HBV // HCV // Kaposi sarcoma // Hairy cell leukemia // Condyloma acuminatum // Renal cell carcinoma // Malignant melanoma // Mutiple sclerosis // Chronic granulomatous disease.
Adverse effects of interferons	Flu like // Depression // Neutropenia // Myopathy // Interferon induces AUTOIMMUNITY.
What cell surface proteins are present in T cells?	TCR / CD3 / CD28 (Binds B7 on APC)
What cell surface proteins are present in T HELPER cells?	CD4 - CD40L - CXCR4/CCD5 (Co receptos for HIV)
What cell surface proteins are present in CYTOTOXIC T cells?	CD8
What cell surface proteins are present in Reg T cells?	CD4 - CD25
What cell surface proteins are present in B cells?	Ig (for Ag binding) // CD19 - CD20 - CD21 (Receptor for Epstein - Bar) - CD40 // MHC II - B7.
What cell surface proteins are present in Macrophages?	CD14 (Receptor for PAMPs ) CD40 // CCR5 // MHC II // B7 // Fc & C3b receptors (Enhanced phagocytosis)
What cell surface proteins are present in NK cells?	CD16 (Binds Fc of IgG) CD56 (suggestive marker for NK)
What cell surface proteins are present in Hematopoietic stem cells?	CD34
What is anergy?	State during which a cell cannot become activated by exposure to its Ag.
What of the mean of acquisition on passive immunity?	Receiving preformed AB.
What is the mean of acquisition on active immunity?	Exposure of foreign AG.
How is the Passive immunity onset?	Rapid
How is the Active immunity onset?	Slow
What is the Passive immunity duration?	Short span of AB ( Half life 3 WEEKS )
What is the Active immunity duration?	Long - lasting protection (memory)
Examples of Passive immunity ?	IgA in breast milk // Maternal IgG // Antitoxin // Humainzed monoclonal AB.
Which VACCINES are passive?	To Be Healed Very Rapidly before Dying Tetanus Toxin // Botulinum // HBV // Varicella // Rabies // Dipththeria.
Which VACCINES can be COMBINED with passive & active immunity?	Hepatitis B // Rabies exposure.
Examples of Active immunity ?	Natural infection // Vaccines // Toxoid.
What is a Live attenuated vaccine ?	The bug loses pathogenicity but induces CELLULAR & HUMORAL response.
What are PROs & CONs of a Live - Attenuated vaccine ?	PRO: Strong - Lifelong immunity. CONS: Contraindicated in PREGNANCY & IMMUNODEFICIENCY.
Which vaccines are Live - Attenuated?	Attention Teachers! Please Vaccinate Small Beautiful Young Infants with MMR Regularly Adenovirus (Non attenuated given to military recruits) Typhoid (Oral) Polio (Sabin) Varicella // Smallpox // BCG // Yellow fever // Influenza (Intranasal) MMR // Rotavirus.
What about Varicella & MMR in HIV patients ?	Can be given is CD4 count > 200 cells/mm3.
What is a Killed or inactivated vaccine ?	Pathogen is inactivated. Maintaining EPITOPE structure on surface. Induces HUMORAL response.
What are PROs & CONs of a Killed vaccine ?	PRO: Safer CONS: Weaker immune response // Booster shots required.
Which vaccines are Killed?	RIP AlwayTs Rabies // Influenza (Injection) Polio (Salk) Hepatitis A / Typhoid (Vi polysaccharide, IM)
What is a Subunit vaccine?	Includes ONLY AG that best stimulate Immune System.
What are PROs & CONs of a Subunit vaccine ?	PRO: Lower chance of adverse reactions // CONs: Expensive // Weaker immune response.
Which vaccines are Subunit vaccines?	HBV (ag: HBsAg) HPV (Types 6 - 11 - 16 & 18) // Acellular pertussis (aP) // Neisseria meningitidis // Streptococcus Pneumoniae // Haemophilus influenza type B.
What is a Toxoid vaccine?	Denatured bacteria toxin with INTACT receptor binding site. Stimulate immune system to make AB without causing disease-
What are PROs & CONs of a Toxoid vaccine ?	PRO: Protect agains bacterial toxins. // CONs: Antitoxin levels decrease with time, may require a booster.
Which vaccines are Toxoid vaccines?	Clostidium tetani / Corynebacterium diphtheriae.
How many types of Hypersensitivity reactions there are?	Four / ABCD: Anaphylactic and Atopic (Type I) // antiBody - mediated (Type II) // immune Complex (Type III) // Delayed (Cell mediated Type IV)
Which types are AB mediated?	Type I - II - III.
What are Type I Hypersensitivity Characteristics ?	ANAPHYLACTIC & ATOPIC // Two phases: IMMEDIATE (minutes) & LATE (hours)
What happen in the IMMEDIATE phase?	AG crosskins with PREFORMED IgE on PRESENSITIZED mast cells = Immediate degranulation = HISTAMINE (vasoactive) & TRYPTASE (mast cell activation) release.
What happen in the LATE phase?	Chemokines attract inflammatory cells & other mediators (Leukotrienes) from mast cells cause INFLAMMATION & TISSUE DAMAGE.
How do you test Type I Hypersensitivity?	Skin or blood test ELISA for Allergen specific IgE.
What are examples of Type I Hypersensitivity?	ANAPHYLACIS - ALLERGIC ASTHMA.
What are Type II Hypersensitivity Characteristics ?	AB binds to CELL SURFACE AG = Cellular destruction - Inflammation - Cellular dysfunction
How is Cellular destruction produced?	(Cells is opsonized by AB leading to either phagocytosis and or complement activation or NK cell killing)
Exaples of Cellular destruction in Hype Type II?	Autoimmune - Hemolytic Anemia // Immune thrombocytopenia // Transfusion reactions // Hemolytic disease of the newborn.
How is Inflammation produced?	( Complement activation & FC receptor mediated inflammation)
Exaples of inflammation in Hype Type II ?	Goodpasture syndrome // Rheumatic Fever // Hyperacute transplant rejection.
How is Cellular dysfunction produced?	(Abnormal blockade or activation of Downstream process)
Exaples of Cellular dysfunction in Hype Type II ?	Myasthenia gravis - Graves disease - Pemphigus vulgaris.
How do you test for Hype Type II?	DIRECT COOMBS TEST (Detects AB attached directly to the RBC surface) INDIRECT COOMS TEST (Detects presence of unbound AB in serum.
What are Type III Hypersensitivity characteristics?	IMMUNE COPLEX ( AG - AB ) Mostly with IgG. They activate COMPLEMENT = neutrophils attraction - Lysosomal ez. (Type III: Ag - Ab - Complement)
Examples of Hype Type III?	SLE // Polyarteritis nodosa / Poststreptococcal glomerulonephritos / Serum sickess / Arthus reaction.
What is the Serum sickness disease?	AB to foreign proteins are produced 1-2 weeks later / Ab - Ag compleces form and deposit in tissues / Complement activation / Inflamation & tissue damage.
What are Serum sickness sympthoms?	Fever - Urticaria - Arthralgia - proteinurina - Lymphadenopathy 1 - 2 weekd after Ag exposure. It is also associated with some drugs (Haptes eg. Penicillin) and infections (eg. Hep B)
What is the Arthus reaction?	Local subacute immune complex mediated hypersensitivity reaction. Intradermal injection of Ag into presensitized individual to immune complex formation in the skin - EDEMA - NECROSIS - COMPLEMENT ACTIVATION.
What are Type III Hypersensitivity characteristics?	CELL MEDIATED - Direct cell cytotoxicity & Inflammatory reaction. DOES NOT INVOLVE AB. 4T's = T cells / Transplant rejection / TB skin test / Touching (Contact dermatitis)
How is Direct cell cytotoxicity produced?	CD8 + Cytotoxic T cells kill TARGETED cells.
How is Inflammatory reaction produced?	Effector CD4 + T cells recognize Ag & release inflammation inducing cytokines.
Examples of Type IV Hypersensitivity reaction?	Contac dermatitis (Poison ivy, nickel allergy ) - Graft vs host disease.
How do you test for Hype Type IV?	PPD for TB infection / Patch test for concact dermatitis / Candida skin test for T cell immune function.
How is the Type I hypersensitivity produced in Blood transfusion?	Allergic/Anaphylactic // Reaction agains plasma proteins in transfused blood // Within minutes to 2-3 hours.
What are the Symptoms of a Type I Hypers in BT?	Urticaria - Pruritus - Fever - Wheezing - Hypotension - Respiratory arrest - Shock.
What about IgA deficient individuals?	MUST recieve blood products without IgA.
How is the Type II hypersensitivity produced in Blood transfusion?	Acute hemolytic transfusion reaction // INTRAVASCULAR Hemolysis (ABO blood group incompatibility) or EXTRAVASCULAR hemolysis (Host AB reaction agains foreing AG on donor RBSs) Within 1 hour.
What are the Symptoms of a Type II Hypers in BT?	Fever - Hypotension - Tachypnea - Tachycardia - Flak pain - Hemoglobinuria (Intravascular Hemolysis ) Jaundice (Extravascular)
How is Febrile NON hemolytic transfusion reaction produced?	Two mechanisms 1. Induced by cytokines created and accumulate during the storage of blood products OR 2. Associated with type II hypersensitivity reaction with Host AB directed agains DONOR HLA & WBCs. Within 1-6 hours.
What are Symptoms of a Febrile NON hemolytic transfusion reaction?	Fever - Headaches - Chills - Flushing // PREVENTED BY LEUKOREDUCTION OF BLOOD PRODUCTS.
How is Transfusion - related acute llung injury produced?	Donor anti - leukocyte AB agains recipient NEUTROPHILS & PULMONARY ENDOTHELIAL CELLS. Within 6 hours.
What are Transfusion - related acute llung injury symptoms ?	Respiratory distress & Noncardiogenic Pulmonary edema.
Anti - ACh receptor	Myasthenia Gravis.
Anti - Presynaptic voltafe gated calcium channel.	Lambert Eaton Myasthenic Syndrome.
Anti - Betta 2 glycoprotein I	Antiphospholipid syndrome
Antinuclear (ANA)	NON specific, often associated with SLE.
Anti - cardiolipin, Lupus anticoagulant	SLE - Antiphospholipid syndrome
Anti - dsDNA - Anti smith	SLE
Anti - Histone	Drug induced Lupus.
Anti - 1 RNP (Ribonucleoprotein)	Mixed connective tissue disease
Rheumatoid factor (IgM AB agains IgG Fc region), Anti - CCP (more specific)	Rheumatoid arthritis.
Anti - Ro/SSA, Anti - La/SSB	Sjögren Syndrome.
Anti - Scl - 70 ( Anti DNA topoisomerase I)	Scleroderma (diffuse)
Anticentromere	Limited scleroderma (CREST Syndrome)
Antisynthetase (eg. anty Jo-1), Anti - SRP, Antihelicase (Anti MI - 2)	Polymyositis - Dermatomyositis.
Antimitochondrial	Primary biliary cholangitis.
Anti - smooth muscle	Autoimmune hepatitis type I
MPC - ANCA / p - ANCA	Microscopi polyangitis - Eosinophilic granulomatosis with polyangiitis (Churg Strauss Syndrome) Ulcerative Colitis.
PR3 - ANCA / C - ANCA	Granulomatosis with polyangitis (Wegener)
Anti - phospholipase A2 receptor	Primary membranous nephropathy.
Anti - Hemidesmosome	Bullous pemphigoid
Anti - desmoglein (Anti - desmosome)	Pemphigus vulgaris.
Anti - microsomal / Anti thyroglobulin / Anti - thyroid peroxidase	Hashimoto Thyroiditis.
Anti - TSH receptor	Graves Disease
IgA - anti - endomysial / Anti - tissue transglutaminase / IgA & IgG deaminated gliadin peptic	Celiac disease
Anti - Glutamic acid decarboxylase - Islet cell cytoplasmic AB.	Type I DM.
Antiparietal cell - Anti - intrinsic factor	Pernicious anemia.
Anti - Glomerular basement membrane	Goodpasture syndrome.
X LINKED AGAMMAGLOBULINEMIA features?	BRUTON disease // X - Linked recessive // Defect in BTK gene (Tyrosine kinase gene) // NO B cell maturation //
What is the presentation of a Patient with BRUTON disease?	Recurrent BACTERIAL & ENTEROVIRAL infections after 6 MONTHS ( When maternal IgG decreases) // Acute & Chronic pharyngitis / Sinusitis / Otitis media / Enteroviruses (Polio / Coxsackie viruses // T cell immunity is intact
What are the Blood findings of a BRUTON disease patient?	ABSENT B cells IN PERIPHERAL BLOOD / Low levels of all Igs // Absent - scanty lymph nodes and tonsils ( 1 follicles and germinal centers absents . LIVE VACCINES ARE CONTRAINDICATED.
SELECTIVE IgA DEFICIENCY features?	1/600 Europeans // MOST COMMON PRIMARY IMMUNOGLOBULIN IMMUNODEFICIENCY //
Selective IgA deficiency presentation?	Major Asymptomatic / Airway & GI tract infections / Autoimmune disease / Atopy / Anaphylaxis to IgA - containing products // HIGH rick GASTRIC & COLON CA // High susceptibility to GIARDIASIS. (Lots of sinus & lung infections)
What is the diagnosis for selective IgA deficiency ?	Dx: Low IgA with NORMAL or INCREASED IgE // NORMAL IgG & IgM levels //
COMMON VARIABLE IMMUNODEFICIENCY features ?	Defect in B cell differentiation / Unknown cause // After age 2, H: risk of Autoimmune disease / Bronchiectasis / Lymphoma / Sinopulmonary infections
Common variable immunodeficiency features?	Low: Plasma cells / Low Immunoglobulins.
What is PRIMARY IMMUNOGLOBULIN M Deficiency?	L: IgM other normal / L: Free floating IgM Ab.
Primary immunoglobulin M deficiency features ?	Can be asymptomathic or SEVERE (Sinusitis - Skin . Diarrhea) // ENCAPSULATED BACTERIA (Strep Pneumoniae / Haemophilus influenza type B) Asthma - Atopia.
What is THYMIC APLASIA	Aka: DiGeorge Syndrome. 22q11 MICRODELETION - Failure to DEVELOP 3rd and 4rd PHARYNGEAL POUCHES ( TBX1 gene) - Absent thymus & parathyroids.
TRIAD in DiGeorge syndrome?	Thymic & Parathyroid aplasia + Cardiac defects (Tetralogy of Fallot - Truncus arteriosus).
TRIAD in VELOCARDIOFACIAL syndrome?	Palate - Facial - Cardiac defects .. (+ Schizophrenia)
Thymic aplasia presentation ?	CATCH - 22 "Cardiac defects (Conotruncal abnormalities: Tetralogy of Fallot, Truncus arteriosus) Abnormal facies, Thymic hypoplasia (T cell deficiency = Reccurrent VIRAL & FUNGAL & PROTOZOOAL infections) Cleft palate, Hypocalcemia 2 to Parathyroid aplasia = Tetani
Which are the signs for Hypocalcemia?	CHVOSTEK & TRUSSEU (Chvostek - espasmo facial, especialmente de la comisura labial al percutir el nervio facial por delante de la oreja - Trousseau - espasmo muy doloroso del carpo al aumentar la presión del manguito de tensiÃ³n arterial por encima de las cifras sistó³licas durante 3 minutos)
Thymic aplasia findings?	L: T cells / L: PTH - L: Ca +2 // Thymic Shadow absent on CxRx
What is IL - 12 RECEPTOR DEFICIENCY ?	A. RECESSIVE. Decrease in Th1 response.
IL - 12 R. deficiency features?	DISSEMINATED MYCOBACTERIAL & FUNGAL infections. May present afted BCG vaccine administrarion
IL - 12 R. deficiency findings?	L: IFN - gamma.
What is AUTOSOMAL DOMINANT HYPER IgE SYNDROME ?	a.k.a. JOB Syndrome. Deficiency of Th17 cells - STAT3 MUTATION - Imparied recruitment of neutrophils. (IFN gamma - impaired PMNN chemyotaxis)
A. Dominant Hyper IgE syndrome features?	"The ABCDEF's to get a Job" // Abscesses (Staphylococcal) - Baby teeth - Coarse facies (Broad nose - Prominent forehead - Deep set eyes - Doughy skin) - Dermatologyc problems (eczema) - H: IgE - bone Fractures
A. Dominant Hyper IgE syndrome findings?	H: IgE & Eosinophils.
What is CHRONIC MUCOCUTANEOUS CANDIDIASIS?	T cell dysfunction - IMPAIRED CELL MEDIATED IMMUNITY AGAINST CANDIDA Sp. Classic form caused by defects in AIRE.
Chronic mucocutaneous candidiasis features ?	NONINVASIVE Candida albicans infections of SKIN& MUCOUS membranes.
Chronic mucocutaneous candidiasis findings?	ABSENT: In vitro & Cutaneous T cell proliferation in response to Candida AGs.
What is SEVERE COMBINED IMMUNODEFICIENCY ?	7 different genes deficiency // Several types: IL -2R gamma chain (MOST COMMON X - RECESSIVE) // ADA deficiency (A. RECESSIVE)
Severe combined immunodeficiency PRESENTATION?	Faliure to thrive - Chronic diarrhea - Thrush . Recurrent VIRAL - BACTERIAL - FUNGAL - PROTOZOAL infection. CONTRAINDICATED: LIVE VACCINES / Give Antimibrobial prophylaxis ans IVIG - BONE MARROW TRANSPLANT CURATIVE (No concern for rejection).
Severe combined immunodeficiency findings?	L: T cell receptor excision circles (TRECs) // ABSENT THYMIC SHADOW / GERMINAL CENTERS & T CELLS /
What is ATAXIA TELANGIECTASIA?	A. RECESSIVE // Defects in ATM gene / Chromosee 11 - Failure to detect DNA damage.
What is Ataxia telangiectasia TRIAD?	ATAXIA - Cerebellar defects / ANGIOMAS - Telangiectasia / IgA deficiency. + HH: Sensitivity to RADIATION. Aspiration pneumonia.
Ataxia telangiectasia findings?	H: AFP after 8 months of age. / L: IgA - IgG - IgE. / Lymphopenia, Cerebellar aptophy // H: RISK OF LYMPHOMA AND LEUKEMIA (ACUTE)
What is Hyper IgM syndrome?	Several etiologies // 1. MOST COMMON X. RECESSIVE = NO CD40L on Th cells (Class swithching defect) 2. A. RECESSIVE - NO CD40 3. NEMO (Recessive mutation in Ez for class switching.
Hyper IgM syndrome presentarion?	SEVERE PYOGENIC INFECTIONS early in life - OPPORTUNISTIC infection with Pneumocystis - Cryptosporidium - CMV & ENCAPSULATED BACTERIA. Dx: Flow Cytometry.
What are the Hyper IgM syndrome findings ?	Normal or H: IgM // L: IgAGE. Failure to make GERMINAL CENTERS. Treat: Infusion of Igs - TMP - SMX - Bone marrow in some cases.
What is WISKOTT - ALDRICH SYNDROME?	X. RECESSIVE. Type 1. Mutation in WAS gene - Leukocytes & platelets unable to reorganize actin cytoskeleton = DEFECTIVE AG PRESENTATION Type 2. Mutation in WIPF1 gene.
Wiskott Aldrich Syndrome presentation?	WAITER: Wiskott Aldrich - Thrombocytopenia - Eczema IN trunk - Recurren pyogenic infections H RISK of autoimmune diseae & malignancy (Leukemia & Lymphoma)
Which microorganisms can affect W-A patients?	ENCAPSULATED: S. pneumoniae / H. Influenza / N. Meningitidis. FUNGI: P. Jirovecii / C. Albicans. VIRUSES: Molluscum contagiosum / Varicella Zoster / CMV.
W - A findings?	L to normal IgG - IgM // H: IgE & IgE. NO IgM against capsular polysaccharide bacteria. FEWER & SMALLED PTL.
W - A Dx & Treatment?	Dx: 1. Symptoms / 2. Peripheral smear & Flow cytometry 3. Gene sequencing // Treat: ATB - IV Igs / PLT transfussion / Surgery - Splenectomy - Immunosupressants.
What is LEUKOCYTE ADHESION DEFICIENCY? (Type 1)	A. RECESSIVE. Defect in LFA - 1 integrin CD18 protein on PHAGOCYTES. Impaired migration & chemotaxis. Type 2 (Absence of SIALYL LEWIS X)
Leukocyte adhesion deficiency presentation?	Recurrent skin and mucosal bacterial & fungal infections, ABSENT PUS, IMPAIRED WOUND HEALING ( > 30 days ) delayed separation of umbilical cord. Dx: Flow cytometry
Leukocyte adhesion deficiency findings?	H: Neutrophils in blood - Absence of N at INFECTION SITES. Treat: Hematopoietic Stem Cell Transplant.
What is CHÃ‰DIAK HIGASHI SYNDROME?	A. RECESSIVE. Defect in Lysosomal Trafficking regulator gene (LYSY) Microtubule dysfunction in phagosome- lysosome fusion. (Can't get EZ into Lysosomes.
ChÃ©diak Higashi Syndrome presentation?	PLAIN: Progressive neurodegeneration, Lymphohistiocytosis, Albinism (partial), recurrent pyogenic Infections, peripheral Neuropathy (atazia seizzures)
ChÃ©diak Higashi Syndrome findings?	GIANT granules in Glanulocytes & platelets // Pancytopenia // Mild cuagulation defects.
What is CHRONIC GRANULOMATOUS DISEASE?	X LINKED. Defect in NADPH oxidase : L: Reactive Oxigen Species L Respiratory burst in PMN - N.
Chronic Granulomatous disease presentation?	H: Susceptibility to CATALASE + ORGANISMS // - "Cats have been places"
Catalase + Microorganisms	S. Aureus - E. Coli - Klebsiella spp Aspergillus spp - Candida spp - Burkholderia - Nocardia - Pasteurella - Listeria - Serratia.
Chronic Granulomatous disease findings?	Abnormal DIHYDRORHODAMINE tes (Flow cytometry) L: Green fluorescence. ( Negative Nitroblue tetrazolium Dye reduction test (Obsolete) Fails to turn blue. TREAT: Phrofilaxic TMP SMX - ITRACONAZOLE - IFN Gamma - HEMATOPOIETIC STEM CELL TRANSPLANT
X LINKED IMMUNODEFICIENCIES?	WACH ( Wiskott - A (Brutton disease) - Chronig granulomatous disease - Hyper IgM Syndrome.
What happen when bacteria attacks in a T CELL DEFICIENCY?	Sepsis
What bacterias cause recurrent infections in a B CELL DEFICIENCY?	Encapsulated: "Please SHINE my SKiS" Pseudomona Au / S. Pneumoniae / H. Influenza type B / Neisseria meningitidis / E. Coli / Salmonella / Klebsiella Pneumoniae / Group B Streptococcus.
What bacterias cause recurrent infections in a GRANULOCYTES DEFICIENCY?	"Some Bacteria Produce No Serious granules" Staphylococcus / Burkholderia cepacia / Pseudomona aeruginosa / Nocardia / Serratia.
What bacterias cause recurrent infections in a COMPLEMENT DEFICIENCY?	Encapsulated species with EARLY complement deficincies // NEISSERIA with late (C5 - C9)
What viruses cause recurrent infections in a T CELL DEFICIENCY?	CMV - EBV - JC virus - VZV // Chronic infection with RESPIRATORY / GI VIRUSES
What viruses cause recurrent infections in a B CELL DEFICIENCY?	Enteroviral ENCEPHALITIS / POLIOVIRUS ( CONTRAINDICATED LIVE VACCINES)
What viruses cause recurrent infections in a GRANULOCYTES DEFICIENCY?	NONE
What viruses cause recurrent infections in a COMPLEMENT DEFICIENCY?	NONE
What FUNGI / PARASITES cause recurrent infections in a T CELL DEFICIENCY?	Candida (Local) PCP - Cryptococcus.
What FUNGI / PARASITES cause recurrent infections in a B CELL DEFICIENCY?	GI Giardiasis (No IgA)
What FUNGI / PARASITES cause recurrent infections in a GRANULOCYTES DEFICIENCY?	Candida (Systemic) Aspergillus - Muco
What FUNGI / PARASITES cause recurrent infections in a COMPLEMENT DEFICIENCY?	NONE.
What is HYPERACUTE transplant rejection?	O: Minutes / Pre - existing recipient AB react with donor AG (TYPE II hypersensitivity reation) Activates complement.
Hyperacute transplant rejection features?	Widespread THROMBOSIS OF GRAFT vessels = ISCHEMIA / NECROSIS = GRAFT MUST BE REMOVED.
What is ACUTE transplant rejection?	O: Weeks to months / CELLULAR: CD8+ &/or CD4+ T cells ACTIVATED against donor MHCs (TYPE IV hypersensitivity reation. - HUMORAL: Similar yo hyperacute, except AB develop after transplant.
ACUTE transplant rejection features?	VASCULITIS of graft vesselts with dense interstitial lymphocytic cellular infiltrate. T: PREVENT / REVERSE with IMMUNOSUPPRESSANTS.
What is CHRONIC transplant rejection?	O: Months to years /CD4 + T cells respond yo recipient APCs presenting donor peptides - Including allognic MHC. Both cellular and humural component (Type II & IV hypersensitivity reactions)
Chronic transplant rejection features?	Recipient T cells react and secrete Cytokines = Proliferation of vascular smooth muscle, parenchymal atrophy, interstitial fibrosis. Domitated by Arteriosclerosis. / Organ Specific EXAMPLES: BRONCHIOLITIS OBLITERANS / ACCELERATED ATHEROSCLEROSIS / CHRONIC GRAFT NEPHROPATHO / VANISHING BILE DUCT SYNDROME (Liver)
What is GRAFT VS HOST DISEASE?	O: Varies / Grafted immunocompetent T cells profiferate in the Immunocompromised host and REJECTs HOST CELLS with "foreing" proteins = SEVERE ORGAN DYSFUNCTION (TYPE IV hypersensitivity reaction)
Conditions that are neccesary to produce GRAFT vs HOST disease?	Graft must CONTAIN IMMUNE CELLS (Bone marroe / Umbilical cord) // Host immune system must be SUPPRESED // Host must be immunological different to the donor. < 3 months (ACUTE - Skin) > 3 months (CHRONIC)
GRAFT VS HOST disease features?	Maculopapular RAHS / Jaundice / Diarrhea / Hepatosplenomegaly / (Bone marrow & Liver transplants) POTENTIALLY BENEFICAL IN BONE MARROW TRANSPLANT for leukemia // Irradiate blood products priortransfusion for immunocomprimised patiend to PREVENT GVHD. Dx: Tx biopsy Treat: Corticoids.
What are ImmunosuppressantsÂ	Block lymphocyte activation & proliferation / REDUCE ACUTE TRANSPLANT REJECTION // Chronic suppression: H RISK for INFECTION & MALIGNANCY.
What is the MOA of CYCLOSPORINE ?	BLOCK T CELL ACTIVATION / Prevents IL-2 trascription/ Calcineurin inhibitor binds cyclophilin.Â
What is the INDICATIONs of CYCLOSPIRINE?	Psoriasis - Rheumatoid arthritis.
What is the TOXICITY of CYCLOSPIRINE?	NEPHROTOXIXITY - HTA - Hypertension - Hyperlipidemia - Neurotoxicity - Gingival Hyperplasia - Hirsutism.
What is the MOA of TACROLIMUS (FK596) ?	BLOCK T CELL ACTIVATION / Prevents IL-2 trascription/ Calcineurin inhibitor binds FK506 binding protein.
What is the INDICATIONs of TACROLIMUS?	-
What is the TOXICITY of TACROLIMUS?	Cyclosporine like (NEPHROTOXICITY) - H: Risk of DM & NEUROTOXICITY - NO: Gingival hyperplasia or Hirsutism.
What is the MOA of SIROLIMUS (RAPAMYCIN) ?	BLOKS T CELLS ACTIVATION & B CELL DIFFERENTIATION by preventing reponse to IL-2 / mTOR inhibitor, binds FKBP
What is the INDICATIONs of SIROLIMUS (RAPAMYCIN)?Â	KYDNEY transplant REJECTION PROPHYLAXIS
What is the TOXICITY of SIROLIMUS (RAPAMYCIN)?	"PanSirtopenia" / Insulin resistance - NOT nephrotoxic. SYNERGISTIC WITH CYCLOSPORINE.
What is the MOA of BASILIXIMAB ?	BLOCKs IL - 2R / Monoclonal Antibody.
What is the INDICATIONs of BASILIXIMAB?	KYDNEY transplant REJECTION PROPHYLAXIS
What is the TOXICITY of BASILIXIMAB?	Edema - Hypertension - Tremor.
What is the MOA of AZATHIOPRINE ?	INHIBITS LYMPHOCYTE PROLIFERATION by blocking NT synthesis. Antimetabolite precursor of 6 - MERCAPTOPURINE (Degraded by Xanthine Oxidase - Toxicity INCREASE by ALLOPURINOL.
What is the INDICATIONs of AZATHIOPRINE ?	Rheumatoid Arthritis - Chrohn diseae - Glomerulonephritis - Other Autoimmune conditions
What is the TOXICITY of AZATHIOPRINE ?	Pancytopenia
What is the MOA of MYCOPHENOLATE MOFETIL ?	INHIBITS reversibly IMP dehydrogenase - PREVENTING PURINE SYNTHESIS OF B & T CELLS
What is the INDICATIONs of MYCOPHENOLATE MOFETIL ?	LUPUS NEPHRITIS.
What is the TOXICITY of MYCOPHENOLATE MOFETIL ?	GI upset - Pancytopenia - Hypertension - Hyperglycemia - LESS NEPHROTOXIC & NEUROTOXIC. // Associated with CMV infection.
What is the MOA of GLUCOCORTICOIDS ?	SUPPRESS BITH B & T CELL FUNCTION by decrease transcription of many cytokines - INDUCE T CELL APOPTOSIS. Inhibits NF - kB
What is the INDICATIONs of GLUCOCORTICOIDS ?	Many Autoimmune & inflammatory disorders - Adrenal insufficiency - Asthma - CLL - Non-hodking lymphoma.
What is the TOXICITY of GLUCOCORTICOIDS ?	CUSHING SYNDROME - OSTEOPOROSIS - HYPERGLYCEMIA - DM - Amenorrhea - Adrenocortical atrophy - Atrophy - Peptic ulcer - Psychosis - Cataracts - AVASCULAR NECROSIS (femoral head). ADRENAL INSUFFICIENCY may develop if DRUG is STOPPED abruptly after chronic use.
What cytokines are used for BONE MARROW STIMULATION?	Erythropoietin - Colony stimulating factor - Thrombopoietin.
Erythropoietin like factors?	Epoietin alfa (EPO analog)
Clinical uses of Erythropoietin like factors?	Anemias (Especially in renal faliure
Wich are Colony Stimulating factors	Filgastrim (G - CSF) Sargramostim (GM CSF)
Clinical uses of Colony Stimulating factors?	Leukopenia - Recovery or Granulocyte and Monocyte counts.
Wich are the Thrombopoietin like factors?	Romiplostim (TPO analog) Eltrombopag (TOP receptor agonist)
Clinical uses of Thrombopoietin like factors?	Autoimmune thrombocytopenia - Platelet Stimulator.
What cytokines are used as IMMUNOTHERAPY?	Interleukin - 2 // Interferon
Wich are the Interleukin . 2 like factors?	Aldesleukin
Clinical uses of Interleukin - 2 like factors?	Renal cell carcinoma - Metastatic melanoma.
Wich are the Interferon ike factors?	INF - a // INF - b // INF - g
Clinical uses of Interleukin - 2 like factors?	A: Chronic hepatitis C & B - Renal cell carcinoma // B: Multiple Sclerosis // G: Chronic Granulomatous disease.
Therapeutic antibodies used in cancer therapy?	Alemtuzumab / Bevacizumad / Rituximab / Trastuzumab.
What is the targed for ALEMTUZUMAB?	CD52
What is alemtuzumab used for?	CLL / MS
What is the targed for BEVACIZYMAB?	VEGF
What is bevacizymab used for?	Colorectal CA - Renal cell carcinoma - Non-small cell Lung cancer. // Also for neovascular age - related macular degeneration - Proliferative diabetic retinopathy - Macular edema.
What is the targed for RITUXIMAB?	CD20
What is rituximab used for?	B CELL NON HODGKING lymphoma - CLL - Rheumatoid arthritis - ITP - MS // Risk of PLM in patients with JCA virus.
What is the targed for TRASTUZUMAB?	HER 2
What is rituximab used for?	Breast cancer - Gastric Cancer.
Therapeutic antibodies used in autoimmune disease therapy?	Adalimumab, Infliximab / Eculizumab / Natalizumab / Ustekinumab
What is the targed for ADALIMUMAB, INFLIXIMAB?	Solible TNF -a
What is adalimumab, ingliximab used for?	IBD - RA - Ankylosing spondylitis, Psoriasis. // ETANERCEPT IS A DECOY TNF - a RECEPTOR and NOT a MONOCLONAL AB.
What is the targed for ECULIZUMAB?	Complement protein C5
What is Eculizumab used for?	Paroxysmal Nocturnal Hemoglobinuria.
What is the targed for NATALIZUMAB ?	Alpha 4 - integrin.
What is Natalizumab used for?	MS - Chrohn disease // RISK of PML in patients with JC virus.
What is the targed for USTEKINUMAB?	IL - 12 / IL 23
What is rituximab used for?	Psoriasis - Psoriatic arthritis.
What is ABCIXIMAB used for?	Antiplatelet agent for prevention for ISCHEMIC complication in patients UNDERGOING PERCUTANEOUS CORONARY INTERVETION. / Unestable Angina / TARGET Platelet glycoproteins IIB/IIIA
What is DENOSUMAB used for?	Osteoporosis - Inhibits osteoclast maturation / Target RANKL.
What is OMALIZUMAB used for?	Refractory Allergic Asthma / Prevents IgE binding to FcEri / Target IgE.
What is PALIVIZUMAB used for?	RVS prophylaxis for high - risk infants / Target RVS F protein.
Aspirin MOA?	Blocks synthesis of Tromboxane A2 "COX - 1 & COX - 2"
Which are ADP R Inhibitors ?	CLOPIDOGREL - PRASUGREL - TICLOPIDINE (Can cause Thrombotic Thrombocytopenic Purpura.

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