gefigupo's version from 2015-06-09 00:59


Question Answer
Necrosis leadsInflammation
Apoptosis leadsNo inflammation
Acute Inflammation composed ofNeutrophils(multilobed) & Edema
Acute InflammationInnate Immunity
Which macrophage recognizes LPS in GN bacteriaCD 14
Phosphlipase A2 releasesArachnoid Acid
Arachnoid Acid works on what 2 pathways?Cyclooxygenase & 5-lipooxygenase
Cyclooxygenase producesProstaglandins(Vasodilation)
PGE2Fever & pain
5-Lipoxygenase producesLeukotrienes(vasoconstriction, bronchospasm)
LTB4Attracts and activates neutrophils
Classical Path wayC1 binds to IgG OR IgM
Alternative PathwayMicrobial products activate complement
Mannose binding lecthin pathwayBinds mannose on microorganisms and activates complement
C3BOpsonin for phagocytosis
C5AAttract neutrophils
C3a & C5aTrigger mast cell degranulation
MACLyses microbes by creating holes in cellmembrane
Reasons for Delayed wound healingInfection, Vit-C Hydroxylation, Copper(Lysyl oxidase), zinc deficiency, foreign body, ischemia, diabetes, malnutrition
Hageman factor plays a role inDIC
Hageman factor activatesCoagulation and fibrinolytic system, complement, kinin system(vasodilation,pain,vascular permeability)
FeverIL-1 -> Increase Cox activity in perivascular cells of hypothalamus
P-Selectin released from?Weibel Palade bodies -> vWillabrand & P-selectin
E-Selectin released from?TNF & IL-1
Th1 madeup ofIL-2 & IFN-Y
Th2 madeup ofIL-4,IL-5, IL-10
Granuloma hallmark featureEpitheloid Histiocytes (macrophages with abundant pink cytoplasm)
Non caseating GranulomaLack central necrosis (Crohn, Cat scratch, Sarcoidosis, Reaction to foreign material, Beryllium)
Caseating GranulomaExhibit Central Necrosis (TB, Fungal)
KeloidExcess type 3 collagen
02 -> 02-Nadph oxidase
02- -> H202Superoxide Dismutase
h202 -> HOCLMyeloperoxidase
Leukocyte Adhesion deficiencyDefect of Integrins(CD18) -> Delayed separation of umblical cord, Neutrophilia, Recurrent bacterial infection with no pus formation
Chediak HigashiProtein Trafficking defect(railroad) impaired phagolysome formation -> Albinism, Neutropenia, Giant granules in leukocytes, Recurrent pyogenic infections, Peripheral Neuropathy
Wiskott-AldrichTIE -> Thrombocytopenia, Infections, Eczema due to WASP gene mutation
C5-C9 DeficiencyNisseria Infections
C1 inhibitor deficiencyHerediatry angioedema, edema especially in periorbital area and mucosal
Myeloperoxidase DeficiencyDefective conversion of H202 to HOCL -> NBT test normal
Chronic Granulamtous DiseasePoor o2 killing due to NADPH oxidase deficiency -> Granuloma formation with Catalase+ organims(S.Aureus, P.Cepacia, S.Marcerans, Nocardia, Aspergillus)
Chronic Granulamtous Disease testNormal if it turns blue because NADPH OXIDASE can convert to 02 -> 02-
CGD Test normal but lack HOCLMyeloperoxidase deficiency because need this enzyme to make HOCL -> pRESENTS WITH CANDIDA INFECTIONS
DigeorgeFailure of 3rd & 4th pharyngeal pouches due to 22q11 microdeletion -> Tcell deficiency(Lack of thymus) Hypocalcemia(Lack of parathyroid) Heart & vessel abnormalities
SCIDDefective Humoral(Bacteria) & Cell mediated(Viral) due to adenosine deaminase deficiency, Cytokine receptor defects, MHC class II deficiency
SCID ContraindicationLive vaccine
X-linked agammaglobulinemiaLack of b cell maturation leading to lack of plasma cells to make immunoglobulin. Recurrent bacterial, enterovirus, giardia infections after 6 months of life.
CVIDLow immunoglobulin leading to bacterial, enterovirus, giardia and with HIGHER INCIDENCE of autoimmune & lymphoma
IgA deficiencyMost common deficiency with IgA lacking. Increased incidence of mucosal infections
Hyper IgM deficiencyElevated IgM due to mutated CD40 ligand or receptor leading to low IgG, IgE, IgA with mucosal infections
SLEType2&3 Hypersensitivity reactionwith antibodies affecting multiple organs. Symptoms - (Fever & Weightloss) (Malar Rash upon sunlight exposure, Arthritis, Pleuritis, Pericarditis)
SLE most common reason of deathRenaldamage ->Diffuse Proliferative Glomerulonephritis
SLE heart symptomsLibeman sack endocarditis -> Both sides of valve affected with no signs of bacteria in blood
Drug Induced LupusHIP - Hydralazine, Isoniazid, Procainamide & Quinidine
Antiphopholipid SyndromeAntibodies(Anticardiolipin-false positive for syphils) agianst proteins bound to phospholipids and falsely elevated PTT lab studies leading to Deep Vein/Placental/Hepatic vein - Thrombosis
SjogrenAutoimmune destruction parotid and lacrimal glands leading to lymphocyte mediated damage -> Type4 Hypersensitivity with other autoimmune conditions like Rheumatoid Arthritis
Sjogren b cell lymphoma presentationUnilateral enlargement of parotid late in disease
SclerodermaAutoimmune damage with activation of fibroblasts and deposition of collagen -> Esophagus most commonly affected(Dysphagia) and anti-topisomerase
CREST Syndrome Localized SclerodermaCalcinosis/anti-Centromere, Raynauds Phenomenon, Esophageal Dismotility, Sclerodactyly, Telangiectasis of skin
ADAMTS13Job is to cleave vWF multimers in smaller monomers for degradation

Neutophil Activation

Question Answer Column 3
Step1MarginationVasodilation -> Slows blood flow in post capillary venules -> Cell Marginate from center to periphery
Step2RollingSelectin Speed bumps help slow down neutrophils -> BIND TO Sialyal Lewis X on WBC
Step3AdhesionCell adhesion molecules upregulated by TNF & iL1 BIND TO Integrins on WBC upregulated by C5a & LTB4 -> adhesion to cell wall
Step4Transmigration & ChemotaxisLeukocytes transmigrate across endothelium -> Neutrophils are attracted by bacterial products IL-8,C5a, LTB4
Step5PhagocytosisConsumption of pathogens -> Internalized and merged with lysosomes to form phagolysosomes
Step6Destruction of phagocytosed materialO2 dependent killing by making HOCL by oxidiative burst
Step7ResolutionNuetrophils undergo apoptosis


Question Answer
Primary HomeostasisQuantitive or Qualitative
Primary Homeostasis SymptomsEpistaxis, Hemoptysis, GI bleeding, Hematuria, Intracranial Bleeding
Quantitative Bleeding SymptomPetechiae
Idiopathic ThrombocytopeniaAutoimmune production of IgG against platelet antigens(GpIIb/IIIa), Spleen makes and destroys platelets -> Thrombocytopenia
ITP HistoryViral or Immunization history acute and self limiting
ITP labs↓Platelets, - PT/PTT, ↑Megakaryocytes
ITP txCorticosteroids or splenectomy(Refractorycases)
Microangiopathic Hemolytic AnemiaPathologic formation of platelet microthrombi in small vessels
Microangiopathic Hemolytic Anemia causesTTP(↓Adams TS13) & HUS(E.Coli 0157:h7)
Microangiopathic Hemolytic Anemia
Question Answer
HUSSkin mucosal bleeding, Microangiopathic Hemolytic Anemia, Fever, Renal Insufficiency(HUS), CNS Abnormalities(TTP)
Microangiopathic Hemolytic Anemia Labs↓BT(LOW Platelets), - PT/PTT, ↑Megakaryocytes, Shistocytes
Microangiopathic Hemolytic Anemia TxPlasmapheresis, Corticosteriods
Bernard SoulierGenetic GP1B deficiency - Platelet adhesion problem
Bernard Soulier blood smearEnlarged Platelets(Big suckers)
Glanzmann thrombastheniagIIb/IIIa deficiency platelet aggregation is impaired

Secondary Hemoastasis

Question Answer
Main problem in secondary HemostasisDeficiency of Coagulation factors
Main symptoms in secondary HemostasisDeep tissue bleeding into muscles and joints / Rebleeding after surgical procedures
PTTHeparin - 12,11,9,8
PTWarfarin - 5,2,1,7
Hemophilia AVIII Deficiency / X linked recessive affecting Males
Hemophilia A Labs↑PTT, -PT, -Platelets, -BT
Hemophilia BIX deficiency, ↑PTT, -PT, -Platelets, -BT
Coagulation factor inhibitorAntibody agianst coagulation factor, Anti-FVIII
Coagulation factor InhibitorMixing normal plasma with patient plasma doest not correct the issue unlike Hemophilias
vWFCommon inherited coagulation disorder
vWF labs↑BT, ↑PTT, -PT, Abnormal Ristocetin Test
vWF TXDesmopressin leads to release of vWF from Weibel Palade bodies from endothelial cells
Vit KLeads to deficiency of coagulation factors, follow liver failure by using PT
HITPlatelet destruction after heparin therapy
DICBleeding from IV sites due to pathologic activation of platelets
DIC Secondary toObsteric Coagulation, Sepsis, Adenocarcinoma, AML, Rattle snake bite
DIC Labs↓platelets, ↓fibrinogen, ↑PT/PTT, Elevated D dimer
d-DimerElevated during a break down of thrombus and is waste product
Radical ProstectomyRelease urokinase leading to activation of plasmin
Lines of ZahnDifferentiates a thrombus clot after or before death


Question Answer
Disruption of blood flowImmobilization, Cardiac wall dysfunction, Aneurysm
Endothelial cell damageAtherosclerosis, Vasculitis, High levels of Homocysteine(Vit b12 or folate deficiency OR Cystathione Beta Synthase)
Hypercoaguable stateProtein C or S Deficiency(usually inactivate factors V & VIII), Factor V Leiden, Prothrombin20210, Oral Contraceptives(estrogen increases production of coagulation factors)-> Stroke