Febrile Neutropenia Flashcards

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1
Q

Febrile Neutropenia

A

Chapter 89 CCM 3rd edition

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2
Q

What are the three primary mechanisms of neutropenia?

A

increased neutrophil use, decreased bone marrow production and immune-mediated destruction

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3
Q

what are the three ways neutrophils kill pathogens?

A

degranulate to release destructive peptides and proteases into the extracellular matrix or into an intracytoplasmic phagosome containing ingested pathogens

reactive oxygen species generator (NADPH oxidase complex) on the membrane of a phagosome or on the outer cell membrane, which produces an oxidative burst when activated by microorganisms.

form neutrophil extracellular traps (NETs). During this process, deoxyribonucleic acid, histones, and other nuclear material combine with destructive peptides and proteases from intracytoplasmic granules and are expelled from the cell into the extracellular space. This web of cytotoxic material ensnares and kills pathogens while also containing the destructive molecules to prevent damage to regional tissues.

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4
Q

What happens to neutrophils during NETosis

A

anuclear neutrophils continue to live and retain their normal behavior, moving through tissues and phagocytizing microbes

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5
Q

what is the most important cytokine responsible for neutrophil production?

A

granulocyte colony-stimulating factor (G-CSF)

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6
Q

What diseases may effect bone marrow production of granulocytes

A

parvo, FIV, FELV, anaplasma, ehrlichia

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7
Q

What drugs are most commonly associated with neutropenia?

A

Chemotherapy agents, estrogen

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8
Q

What is myelophthisis?

A

BM infiltration with neoplastic cells or collagen

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9
Q

What is dysgranulopoiesis?

A

Normal numbers of progenitor cells they are just non-functional

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10
Q

When should neutropenic patients have abs ?

A

If bellow 0.75 or if they have a fever

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11
Q

What ab is beneficial in patients with febrile neutropenia

A

base on culture but a broad spectrum beta lactam

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12
Q

Why should recombinant human G-CSF not be used?

A

Bc dogs can develop antibodies to their own G-CSF and become chronically neutropenic

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