Physiology - Blood Cells - Chandy

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Neutrophil Function

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Circulation-> margination-> diapedesis-> chemotaxis-> adherence-> phaygocytosis-> (phagosome)-> lysis or apoptosis

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selectins

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receptors that recognize carbohydrate moieties

one on blood vessel wall and one on PMN for reciprocal recog.

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L-selectin and E-selectin

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L: leukocyte selctin

E: endothelial selectin (also P)

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chemotactic factors for PMNs

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1. Proteins: complement (C3a, C5a), thrombin, kallikrein

2. Leukotrienes: LTA4, LTE4

3. peptides: N-formyl-methionyl-oligopeptide

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opsonization

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neutrophils bind bavcteria through

antibody bridge (Fc-receptor-Ab)
and
complement bridge (CR1-C3b)

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PMN: phagocytosis

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engulfing-> phagosome-> attracts lysosome-> merge-> phagolysosome

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PMN: Killing of bacteria

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Proteases: primary granules: myeloperoxidase, elastase AND secondary granules: lactoferrin, etc.

oxidative burst

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oxidative burst

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Hexose shunt-> NADPH oxidase-> superoxide and H2O2-> oxygen radicals-> kill bacteria in lysozome

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myeloperoxidase deficiency

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no problem

unless w/ diabetes: poor circulation-> ^infection-> can have problems

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inhibitors of oxygen radicals and proteases

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to minimize collateral damage

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

proteases:

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proteases in oxy radical inhibition

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neutralized by

alpha1-antitrypsin, alpha2-macroglobulin, elafin, secretory leukoprotease inhibitor

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Alpha1-antitrypsin

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there to protect body from digesting own tissues
made in liver, 2 alleles:
MM: normal
MZ: mild deficiency
ZZ: uncontrolled protease activity

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alpha1-antitrypsin deficiency

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MZ: cigarette smoke inactivates alpha1-antitr.-> collateral damage-> fibrous tissue in lungs-> can't expand-> barrel chest

emphysema and liver disease

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alpha1-antitryp. deficiency diagnosis and treatment

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liver disease in ZZ children-> hepatic coma (can't clear toxins)

isoelectrc focusing

finish alter

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monocytes

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short-lived

small %

inefficient in phagocytosis

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macrophages

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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

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Vit B12

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=cobalamin

-> ^Homocysteine
-> ^MM CoA
-> v Folate

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Folate deficiency

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megaloblastic anemia

big RBCs, oval shaped

anemia, no neurological probs

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Iron: char and defic

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xferrin(blood)-> ferritin in cytoplasm for "storage iron"

deficiency-> microcytic hypochromic anemia

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red cell indices

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MCV: avg. vol of RBC (90 fL)

MCH: Hb in each RBC (30pg)

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

PCV: 50%

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Classical aplastic anemia

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-loss of CD34 cells
-50% idiopathic
-dry bone tap
-marrow xplant needed
-maybe autoimmune?

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Megaloblastic anemia: fxn prob, marrow char, RBC morpho, causes

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v DNA synthesis
hyperplastic, megaloblastic
macrocytic RBCs
Causes: v Cobalamin, v folate

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Hypochromic anemia: fxn prob, marrow char, RBC morpho, causes

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v HB synthesis
hyperplastic, deficient Hbzation
microcytic, hypochromic
causes: Fe deficiency, chronic disease, THALASSEMIAS

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cobalamin deficiency

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neurological probs

megaloblastic anemia

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polycythemias

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

Vera: hypersensitivity to EPO (bleed them)

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CML

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stem cell prolif->
^white blood cells, block of lymphoid cell creation

philadelphia chromosome: abl-bcr (9-22)

marrow xplant

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AML

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acute myelogenous leukemia

^committed stem cells

no chronic phase, need chemo-> marrow xplant

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Howell Jolly Bodies

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when orthochromatic e-blasts don't get rid of all nucleus

-> trapped in spleen, destroyed

no spleen-> see lots

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reticulocytes

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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

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Rouleaux

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how RBCs are forced into central, fast stream in large BV

in small BV-> umbrella shape

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RBC cytoskeleton components

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spectrin: most abundant, α & β chains

interlinked by actin, ankyrin & band 4.1, and band 3

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RBC destruction

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b/c they can't un-bend

extra (spleen) and intravascularly (blood stream)

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extravascular hemolysis

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engulfed by Mphages in liver and spleen

globin chains and Fe stripped-> bilirubin-> liver-> excreted

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intravascular destruction of RBC

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10% of RBCs

Haptoglobin binds Hb-> hepatic parenchyma

Hemopexin binds heme-> catabolized by liver cells

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Hereditary Spherocytosis

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spectrin defect-> obese, rigid RBCs

use osmotic fragility test

treatment: splenectomy (b/c gettin caught in narrow spleen passages)

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G-6-(P) DH deficiency

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no NADPH to protect RBCs from H2O2

x-linked

look for Heinz bodies (denatured Hb precipitates)

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Different Hbs

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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

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α Thalassemia minor

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deletion of α genes

hypochromic, microcytic anemia

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Hemoglobin H disease

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deletion of 3 α genes

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

microcytic hypochromic anemia, hemolysis

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hydrops fetalis

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no alpha globin-> fatal in utero

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beta Thalassemias

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minor: pretty OK
major: homozygote, server anemia, w/ loss of HbF-> ^erythropoesis-> chipmunk face, etc.

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sickle cell anemia

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Hb S, polymerizes

-> hemolysis, blockage

Hb AS-> trait (carrier)

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porphyrias

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early block: neuro and mental symptoms
AIP
late: dermatological sensitivity
PCT

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eosinophils

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bilobed nucleus

participate in opsonization

parasites: hydrolytic enzymes

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basophils, mast cells

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in skin and mucosa

histamine, serotonin, L-trienes, etc.

IgE (aillergEEEE!) receptors

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neutrophil: margination

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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

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neutrophil: diapedesis and chemotaxis

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ICAM-1 w/ E-selectin-> spreading-> makes openings betw. cells-> diapedesis

chemotactic factors (C3a, C5a, clotting factors, etc.)

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Neutrphil: phagocytosis

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tethers Igs (@ Fab) to PMN (@Fc receptor)= opsonization

bactericidal agents released into phagolysosome

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Neutrophil probs

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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.