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49 Cards in this Set

  • Front
  • Back
Neutrophil Function
Circulation-> margination-> diapedesis-> chemotaxis-> adherence-> phaygocytosis-> (phagosome)-> lysis or apoptosis
receptors that recognize carbohydrate moieties

one on blood vessel wall and one on PMN for reciprocal recog.
L-selectin and E-selectin
L: leukocyte selctin

E: endothelial selectin (also P)
chemotactic factors for PMNs
1. Proteins: complement (C3a, C5a), thrombin, kallikrein

2. Leukotrienes: LTA4, LTE4

3. peptides: N-formyl-methionyl-oligopeptide
neutrophils bind bavcteria through

antibody bridge (Fc-receptor-Ab)
complement bridge (CR1-C3b)
PMN: phagocytosis
engulfing-> phagosome-> attracts lysosome-> merge-> phagolysosome
PMN: Killing of bacteria
Proteases: primary granules: myeloperoxidase, elastase AND secondary granules: lactoferrin, etc.

oxidative burst
oxidative burst
Hexose shunt-> NADPH oxidase-> superoxide and H2O2-> oxygen radicals-> kill bacteria in lysozome
myeloperoxidase deficiency
no problem

unless w/ diabetes: poor circulation-> ^infection-> can have problems
inhibitors of oxygen radicals and proteases
to minimize collateral damage

oxygen radicals: superoxide-> H2O2-> (catalase)-> water & Oxygen
H2O2-> (glutathione)-> water

proteases in oxy radical inhibition
neutralized by

alpha1-antitrypsin, alpha2-macroglobulin, elafin, secretory leukoprotease inhibitor
there to protect body from digesting own tissues
made in liver, 2 alleles:
MM: normal
MZ: mild deficiency
ZZ: uncontrolled protease activity
alpha1-antitrypsin deficiency
MZ: cigarette smoke inactivates alpha1-antitr.-> collateral damage-> fibrous tissue in lungs-> can't expand-> barrel chest

emphysema and liver disease
alpha1-antitryp. deficiency diagnosis and treatment
liver disease in ZZ children-> hepatic coma (can't clear toxins)

isoelectrc focusing

finish alter

small %

inefficient in phagocytosis
Kuppfer cells:liver sinuses
Osteoclasts: bone
Microglia: brain (HIV haven, MS)
Alveolar macrophage: lung (Silica dust-> mesotheliomas)
Dendritic cell: in L-Node for antigen processing
Vit B12

-> ^Homocysteine
-> ^MM CoA
-> v Folate
Folate deficiency
megaloblastic anemia

big RBCs, oval shaped

anemia, no neurological probs
Iron: char and defic
xferrin(blood)-> ferritin in cytoplasm for "storage iron"

deficiency-> microcytic hypochromic anemia
red cell indices
MCV: avg. vol of RBC (90 fL)

MCH: Hb in each RBC (30pg)

MCHC: %RBC mass that's Hb (35%)

PCV: 50%
Classical aplastic anemia
-loss of CD34 cells
-50% idiopathic
-dry bone tap
-marrow xplant needed
-maybe autoimmune?
Megaloblastic anemia: fxn prob, marrow char, RBC morpho, causes
v DNA synthesis
hyperplastic, megaloblastic
macrocytic RBCs
Causes: v Cobalamin, v folate
Hypochromic anemia: fxn prob, marrow char, RBC morpho, causes
v HB synthesis
hyperplastic, deficient Hbzation
microcytic, hypochromic
causes: Fe deficiency, chronic disease, THALASSEMIAS
cobalamin deficiency
neurological probs

megaloblastic anemia
2Ί or physiologic: hypoxia-> EPO-> RBCs released early

Vera: hypersensitivity to EPO (bleed them)
stem cell prolif->
^white blood cells, block of lymphoid cell creation

philadelphia chromosome: abl-bcr (9-22)

marrow xplant
acute myelogenous leukemia

^committed stem cells

no chronic phase, need chemo-> marrow xplant
Howell Jolly Bodies
when orthochromatic e-blasts don't get rid of all nucleus

-> trapped in spleen, destroyed

no spleen-> see lots
1 day in circ before -> mature RBC

cytoplasmic RNA stains w/supravital dye

.5 to 2%

^ w/ bleeding or hemolysis
v w/ aplastic anemias & other v production issues
how RBCs are forced into central, fast stream in large BV

in small BV-> umbrella shape
RBC cytoskeleton components
spectrin: most abundant, α & β chains

interlinked by actin, ankyrin & band 4.1, and band 3
RBC destruction
b/c they can't un-bend

extra (spleen) and intravascularly (blood stream)
extravascular hemolysis
engulfed by Mphages in liver and spleen

globin chains and Fe stripped-> bilirubin-> liver-> excreted
intravascular destruction of RBC
10% of RBCs

Haptoglobin binds Hb-> hepatic parenchyma

Hemopexin binds heme-> catabolized by liver cells
Hereditary Spherocytosis
spectrin defect-> obese, rigid RBCs

use osmotic fragility test

treatment: splenectomy (b/c gettin caught in narrow spleen passages)
G-6-(P) DH deficiency
no NADPH to protect RBCs from H2O2


look for Heinz bodies (denatured Hb precipitates)
Different Hbs
adult: HbA: alpha2beta2
embryonic: Gower-1: E2zeta2
fetal: alpha2gamma2
HbA2: alpha2delta2 (3% adult)
Hb Barts: gamma4: v alpha, ^O2 affinity
HbH: beta4: = Barts, but unstable
α Thalassemia minor
deletion of α genes

hypochromic, microcytic anemia
Hemoglobin H disease
deletion of 3 α genes

embryonic Hb ok, but-> fetal Hb-> Hb Barts (γ4: useless)-> adult-> HbH (RBC w/ precipitates)

microcytic hypochromic anemia, hemolysis
hydrops fetalis
no alpha globin-> fatal in utero
beta Thalassemias
minor: pretty OK
major: homozygote, server anemia, w/ loss of HbF-> ^erythropoesis-> chipmunk face, etc.
sickle cell anemia
Hb S, polymerizes

-> hemolysis, blockage

Hb AS-> trait (carrier)
early block: neuro and mental symptoms
late: dermatological sensitivity
bilobed nucleus

participate in opsonization

parasites: hydrolytic enzymes
basophils, mast cells
in skin and mucosa

histamine, serotonin, L-trienes, etc.

IgE (aillergEEEE!) receptors
neutrophil: margination
epinephrine & corticosteroids cause demargination

IL-1 & TNF-α attract PMNs from BM to circ.-> L-selectin (leukocyte) on PMN binds BV and E-selectin (endothel.) binds PMN surface
neutrophil: diapedesis and chemotaxis
ICAM-1 w/ E-selectin-> spreading-> makes openings betw. cells-> diapedesis

chemotactic factors (C3a, C5a, clotting factors, etc.)
Neutrphil: phagocytosis
tethers Igs (@ Fab) to PMN (@Fc receptor)= opsonization

bactericidal agents released into phagolysosome
Neutrophil probs
Chronic Granulamatous Disease (CGD): can't generate oxygen species to kill b/c no NADPH oxidase

Use NBT test to see if cells make H2O2, etc.