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Basophils
granulocytes that release chemicals to promote inflammation
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Eosinophils
granulocytes that are cytotoxic killers that primarily target parasites
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Neutrophils
phagocytic granulocytes that ingest and kill bacteria
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Monocytes/Macrophages
Antigen presenting cells that ingest pathogens and activate helper T-cells
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B-lymphocytes
Antigen specific cells that have not come into contact with their antigen
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Plasma cells
Activated B-lymphocytes that have been in contact with their antigen, and produce specific antibodies
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Memory B-cells
cells that have been in contact with their antigen, and are in circulation to fight secondary exposure
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Helper T cells
lymphocytes that release cytokines to help activate B-lymphocytes
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Cytotoxic T-cells
lymphocytes that kill self cells carrying foreign antigens by inducing apoptosis
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Natural Killer cells
lymphocytes that target abnormal self cells and induce apoptosis
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Warfarin
Inhibits vitamin K epoxide reductase
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Heparin
promotes endogenous anti-thrombin activity
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Dabigatran
Direct thrombin inhibitor
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Apixaban
Factor Xa inhibitor
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Sirolimus
- 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
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Glycogen synthase
Extends glycogen chains (a-1,4-glycosidic bonds)
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Glycogen phosphorylase
breaks glycogen chains (a-1,4-glycosidic linkages)
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Glycogen branching enzyme
transfers 7 linked glucose residues to the next chain (a-1,6-glycosidic linkage)
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Glycogen debranching enzyme
transfers 3 residues to another chain (a-1,6-glycosidic chain)
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Type 0 GSD
deficiency in glycogen synthase
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Type 1 GSD
- most common:
- deficiency in glucose-6-phosphatase or G6P transporter
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Type 2 GSD
alpha-1,4-glycosidase deficiency in heart+ lysosomes
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Type 3 GSD
inherited: build up of glycogen due to glycogen debranching enzyme deficiency
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Type 4 GSD
buildup of glycogen due to glycogen branching enzyme deficiency
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GSD Type 5
Deficiency of myophosphorylase (cant break glycogen in muscle)
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GSD type 6
deficiency in liver glycogen phosphorylase (leads to liver enlargement)
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GSD type 7
Deficiency in phosphofructokinase in muscles-> inability to use glycogen leads to muscle breakdown for energy.
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Name 3 of the most common drugs that induce agranulocytosis
Clozapine, Dapsone, Aminopyrine
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Agranulyctosis
- Direct or immune mediated toxicities
- Treatment based on neutrophil recovery.
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Arsenate poisoning
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)
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