ACEM Primary Exam (Written) - Pathology - AnkiDeckLib

Hierarchically tagged cloze deletion flashcards for the ACEM primary exam. The backs of the cards contain explanations from either the Pocket Companion to Robbins & Cotran, or a set of study notes to put the question in context. The notes were given to me by a friend and we don't know who the original author is. Some topics are perhaps covered in too much detail. These were intended to be used for the written part of the exam rather than the viva. Hope someone finds them useful!

Sample Data

Text	Mediators of Immediate Hypersensitivity The {{c1::delayed::initial / delayed}} response is driven by lipid mediators and cytokines produced by activated mast cells
Extra	An initial rapid response (5 to 30 minutes) is characterized by vasodilation, increased vascular permeability, bronchial smooth muscle contraction, and glandular secretions. This is driven by preformed mediators stored in secretory vacuoles and typically resolves within 60 minutes: Biogenic amines (e.g., histamine): Bronchial smooth muscle contraction, increased vascular permeability and dilation, and increased mucous secretion Enzymes contained in granule matrix (e.g., chymase, tryptase): Generate kinins and activated complement by cleaving precursor proteins Proteoglycans (e.g., heparin) A second (delayed) phase, with onset 2 to 24 hours after initial allergen exposure is characterized by inflammatory cell infiltrates and tissue damage (especially epithelium). It can persist for days and is driven by lipid mediators and cytokines produced by the activated mast cells: Lipid mediators are produced from precursors released from mast cell membranes by phospholipase A2 Leukotriene B4: Highly chemotactic for neutrophils, monocytes, and eosinophils Leukotrienes C4, D4, and E4: Thousand-fold more potent than histamine for increasing vascular permeability and bronchial smooth muscle contraction Prostaglandin D2: Intense bronchospasm and mucous secretion Platelet-activating factor (PAF): Platelet aggregation, histamine release, bronchoconstriction, vasodilation, and increased vascular permeability; chemotactic for neutrophils and eosinophils and can cause activation with degranulation Cytokine mediators recruit and activate inflammatory cells; these include tumor necrosis factor (TNF), IL-1, and chemokines. IL- 4 released from mast cells amplifies the TH2 response. The consequences of mast cell activation are schematized in Figure 6.15
Tags	Primaries::Pathology::Diseases_of_the_Immune_System::Hypersensitivity

Text	Vitamin C (Ascorbic Acid) Supraphysiologic doses of vitamin C {{c1::do not protect::protect / do not protect}} against the common cold
Extra	Vitamin C (Ascorbic Acid) Vitamin C (ascorbic acid) is present in many foods and is abundant in fruits and vegetables, so that all but the most restricted diets provide adequate amounts. Vitamin C ExcessSupraphysiologic doses of vitamin C do not protect against the common cold but do have a mild antihistamine effect; likewise there is no efficacy in cancer prevention. Bioavailability of vitamin C is limited by intrinsic instability, modest intestinal absorption, and rapid urinary excretion. Toxicities of overdosing include possible iron overload (vitamin C increases elemental iron uptake), hemolytic anemia in the setting of glucose-6-phosphate dehydrogenase deficiency, and calcium oxalate kidney stones.
Tags	Primaries::Pathology::Environmental_and_Nutritional_Diseases::Nutritional_Diseases

Text	Defects in Lymphocyte Activation and Function In isolated IgA deficiency, {{c1::mucosal}} immunity is most affected.
Extra	Isolated Immunoglobulin A Deficiency Isolated IgA deficiency is a common immunodeficiency (in the United States, 1 in 600 people of European descent) with virtually absent serum and secretory IgA (also occasionally IgG2 and IgG4 subclasses). It can be familial or acquired after toxoplasmosis, measles, or other viral infection. The basic defect is failure of IgA- positive B cells to mature; immature forms are present in normal numbers. Features include the following: Mucosal immunity is most affected. Although usually asymptomatic, patients can have recurrent sinopulmonary and GI infections. Increased incidence of respiratory tract allergies and autoimmune diseases (SLE, rheumatoid arthritis). Patients can have antibodies directed against IgA, and transfusion of IgA-containing blood products can induce anaphylaxis. X-Linked Lymphoproliferative Syndrome X-linked lymphoproliferative syndrome is characterized by the inability to clear EBV, leading to fulminant mononucleosis, as well as EBV-associated B-cell tumors. Eighty percent of cases are caused by mutations in an adaptor molecule (SLAM-associated protein [SAP]) that interacts with cell surface receptors that activate T, B, and NK cells. SAP defects lead to poor T- and NK-cell activation, as well as inadequate follicular helper T-cell activation; the latter results in meager germinal center formation and poor production of high-affinity antibodies.
Tags	Primaries::Pathology::Diseases_of_the_Immune_System::Immunodeficiency_Syndromes