Presentations

granulocytes that release chemicals to promote inflammation

granulocytes that are cytotoxic killers that primarily target parasites

phagocytic granulocytes that ingest and kill bacteria

Antigen presenting cells that ingest pathogens and activate helper T-cells

Antigen specific cells that have not come into contact with their antigen

Activated B-lymphocytes that have been in contact with their antigen, and produce specific antibodies

cells that have been in contact with their antigen, and are in circulation to fight secondary exposure

lymphocytes that release cytokines to help activate B-lymphocytes

lymphocytes that kill self cells carrying foreign antigens by inducing apoptosis

lymphocytes that target abnormal self cells and induce apoptosis

Inhibits vitamin K epoxide reductase

promotes endogenous anti-thrombin activity

Direct thrombin inhibitor

Factor Xa inhibitor

• Derivative of Rapamycin
• Immunosuppresent for organ transplants
• Acts on T and B cells by binding FKBP, which forms immunosuppressive complex inhibiting mTOR activity (mammalian target of rapamycin)

Binding mTOR inhibits cell proliferation/synthesis

Extends glycogen chains (a-1,4-glycosidic bonds)

breaks glycogen chains (a-1,4-glycosidic linkages)

transfers 7 linked glucose residues to the next chain (a-1,6-glycosidic linkage)

transfers 3 residues to another chain (a-1,6-glycosidic chain)

deficiency in glycogen synthase

• most common: 
• deficiency in glucose-6-phosphatase or G6P transporter

alpha-1,4-glycosidase deficiency in heart+ lysosomes

inherited: build up of glycogen due to glycogen debranching enzyme deficiency

buildup of glycogen due to glycogen branching enzyme deficiency

Deficiency of myophosphorylase (cant break glycogen in muscle)

deficiency in liver glycogen phosphorylase (leads to liver enlargement)

Deficiency in phosphofructokinase in muscles-> inability to use glycogen leads to muscle breakdown for energy.

Clozapine, Dapsone, Aminopyrine

• Direct or immune mediated toxicities
• Treatment based on neutrophil recovery.

symptoms: headache, drowsiness, fingernail pigmentation change

• Arsenite (3+): binds GSH, inhibits pyruvate dehydrogenase
• Arsenate (5+): binds where phosphate usually binds. inhibits glycolysis

Can be treated with dermercaptusuccinic acid (DMSA)