Clin Path Flashcards

1
Q

Methemoglobinemia

A

-Diminution of the oxygen-carrying capacity of circulating hemoglobin occurs due to the conversion of some or all of the four iron species from the reduced ferrous (Fe2+) state to the oxidized ferric (Fe3+) state
-Unable to bind and transport oxygen

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2
Q

How do neutrophils become activated?

A

-Move from circulation into the tissues by attaching first loosely and then tightly to receptors on activated endothelial cells.
-Once adhered, they move between or through endothelial cells and pericytes into the interstitial space.
-Become activated when PRRs bind to PAMPs or DAMPs

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3
Q

How do neutrophils kill pathogens?

A

1) degranulate to release destructive peptides and proteases into the extracellular matrix or into an intracytoplasmic phagosome containing ingested pathogens
2) Assemble reactive oxygen species generator (NADPH oxidase complex) on the membrane of a phagosome or on the outer cell membrane
3) Neutrophils form NETs

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4
Q

NETs

A

-neutrophil extracellular traps
-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
-forms a web of cytotoxic material that ensnares and kills pathogens while also containing the destructive molecules to prevent damage to regional tissues.

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5
Q

What cytokine is most responsible for maintaining neutrophil homeostasis?

A

-granulocyte colony-stimulating factor (G-CSF)
-produced by bone marrow stromal cells, macrophages, monocytes, endothelial cells, fibroblasts

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6
Q

Neutrophil production

A

-Produced by progenitor cells in the bone marrow
-in bone marrow, they mature into segmented neutrophils
-bone marrow houses a large reserve pool of mature neutrophils
-Under stimulation of growth factors and cytokines (G-CSF, granulocyte-macrophage CSF, TNF alpha, TNF beta, complement 5a -> neutrophils are released from bone marrow

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7
Q

Neutrophil pools

A

1) circulating pool- neutrophils travel rapidly to through the center of larger vessels along with RBCs, sampled on CBC
2) marginated pool- neutrophils move slowly along the endothelium of smaller vessels and capillaries and tend to stagnate in postcapillary venules

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8
Q

Febrile neutropenia develops by:

A

1) increased use of neutrophils
2) decreased egress of bone marrow
3) immune-mediated destruction

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9
Q

Causes of bone marrow hypoplasia

A

-infectious diseases
-exposure to drugs and toxins
-radiation
-myelophthisis
-cyclic hematopoiesis (gray Collie syndrome)

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10
Q

Ineffective granulopoiesis

A

-presence of adequate granulocyte precursors in the bone marrow coupled with peripheral neutropenia
-due to maturational arrest of the neutrophil cell line or retention and/or destruction of mature neutrophils in the bone marrow
-FeLV, FIV, myelodysplasia, lithium administration in cats, acute myeloid leukemia, trapped neutrophil syndrome (Border Collies)

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11
Q

Drugs that cause neutropenia

A

-anti-infective agents
-antiepileptics
-cochicine
-captopril
-methimazole
-phenylbutazone
-chemotherapy agents
-estrogen analogs

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12
Q

Myelopthisis

A

failure of bone marrow to continue normal hematopoiesis because of decimation by infiltrating abnormal tissue (neoplastic cells, collagen (myelofibrosis), osteoid, diffuse intramedullary inflammation (fungal osteomyelitits))

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13
Q

Canine cyclic hematopoiesis

A

-Autosomal recessive genetic disorder
-AKA gray Collie syndrome
-severe neutropenia every 10-14 days

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14
Q
A
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15
Q

Platelet life span

A

5-7 days

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16
Q

Platelet production

A

Thrombopoesis

Mediated by hormone thrombopoietin that is synthesized in the liver

17
Q

3 stages of platelet activity

A

Primary hemostasis

1) adhesion occurs when damaged endothelial cells expose collagen that binds to platelets. Damage endothelium release vWF and binds to platelets.

2) activation occurs when there is interaction with the platelet and the collagen and BWF complexes which activate the platelet and cause granule release

3) aggregation occurs when integrin in cooperation with VWF released from the platelets leads to aggregation by bridging multiple activated platelets to form a platelet plug

18
Q

Platelet granules

A

Alpha granules are the most abundant secretary granules in platelets

Release during platelet activation

Please a roll in adhesion between platelets and other cells, inflammation, and coagulation

19
Q

Platelet plasma membrane

A

Made up of phospholipids including phosphatidylcholine (PC), phosphatodylserine (PS), phosphatidylethanolamine (PW), sphingolipid sphingomyelin (SM)

PS is negatively charged

PS and PE are inner membrane, PC and SM are outer membrane

20
Q

Platelet membrane enzymes

A

Flippase- moves phospholipids inwards

Floppase- moves phospholipids outwards

Scramblase- moves PS from the inner to the outer leaflet of the plasma membrane once platelet is activated

Activity of scramblaze is regulated by calcium release from the dense granules

21
Q

Scott Syndrome

A

Reduced pro-coagulant activity due to decreased activity of transmembrane phospholipid scramblase.

Predisposed in German shepherds

Bleeding occurs because platelets are unable to adhere to damaged endothelium

22
Q

Platelet function testing

A

BMBT

Platelet function analyzers

Platelet aggregometry

23
Q

Viscoelastic coagulation assay

A

Global assessment of clot formation kinetics and strength in which platelet function plays a pivotal role.

TEG, ROTEM, VCM

24
Q

DOGiBAT Score

A

Grades ITP

Comprises site-specific grades of nine different anatomical sites

0- none
1- mild
2- severe