Gen Path: Rr Inflammation

Front 1

5 Latin terms of Acute Inflammation:

Back 1

1) Rubor (Histamine, vasodilation arterioles)

2) Calor (Histamine, vasodilation arterioles)

3) Tumor (vasopermeability of venules)

4) Dolor (Bradykinin, Pain)

5) Functia Laesa

Front 2

Rubor and Calor

Back 2

1) Redness -due to vasodilation of ARTERIOLES.

***Histamine is KING of vasodilators, and dilates arterioles***

2) Hot - due to histamine, heat given off due to vasodilation ARTERIOLES(e.g warm skin in endotoxic shock or septic shock instead of cold skin)

Front 3

Tumor and Dolor

Back 3

1) Swelling (raised structure), is histamine mediated but this time it inc VASOPERMEABILITY of VENULES. (producing an exudate and swelling of tissue)

***Inc Vasopermeability occurs at venule level not at arteriole level because venules are thinner and so histamine contracts the endothelial cells of venules***

2) Pain - due to Bradykinin and PGE2 (Bradykinin is a part of the kininogen system; between Hageman's Factor 12 and Plasma thromboplastin Antecedant 11)

***when you activate the intrinsic pathway of Coagulation you automatically activate the Kininogen system, thus factor 12 activates factor 11 and the kininogen system, the en product of which is Bradykinin***

Front 4

What degrades Bradykinin? What is a complication of using Ace-inhibitors?

Back 4

-Degradation of Bradykinin is by ACE (angiotensin converting enzyme)

Complication:
-Angioedema (swelling of tissues)

**ACE inhibitors inhibit the metabolism of bradykinin which inc the vascular permeability leading to Angioedema**

**bradykinin produces cough also**

Front 5

What are the steps of Acute inflammation?

Back 5

Includes Margination, rolling, adhesion and transmigration

Chemotaxis

Phagocytosis via opsonization.

Front 6

What cells are the Important cells in Acute inflammation?

Back 6

Neutrophils

Front 7

How do neutrophils get through the basement membrane?

Back 7

Neutrophils have type 4 collagenase b/c basement membrane is composed of type 4 collagen (drill a hole through BM, usually the venules)

***Cancer cells have adhesion molecules usually against laminin in the BM, also have type 4 collagenase (thats how they metastasize)

Front 8

Explain Neutrophil chemotaxis after Diapedesis (transmigration)?

Back 8

Directed chemotaxis by molecules such as C5a, LTB4(which are also involved in making adhesion molecules for neutrophils) and IL-8.

*binding of these chemotactic factors causes release of Ca which inc neutrophil motility*

Front 9

What are the two Opsonins involved in preparation for bacteria to get destroyed by Neutrophils?

Back 9

IgG, C3b and other proteins (c-reactive protein)

Front 10

Name a disease with Opsonization defect?

Back 10

Bruton's Agammaglobulinemia

-x linked recessive Dx where all the Igs are missing. Produces hypogamma-globinemia.

**most common cause of death in these pts is due to infection because neutrophils cannot phagocytose foreign material if not opsonized**

Front 11

What is I-cell Dx?

Back 11

**Defect in the Post-translational modification of lysosomal enzymes in the Golgi**


-Mannose residues on newly synthesized lysosomal enzymes cannot be phosphorylated (def of phosphotransferase) therefore the enzymes are not marked w/ phosphorus and thus the Lysosomes are empty.

*unmarked enzymes are emptied by the golgi into the extracellular space, undigested substrates accumulate as large inclusion in the cytosol, showing INCLUSION bodies under the microscope*

Front 12

Neutrophils use what 2 Intracellular Microbial Killing mechanisms?

Back 12

1) O2 dependant Myeloperoxidase system (MPO system)

2). O2 independant system

Front 13

**O2 dependant Myeloperoxidase system mechanism

Back 13

Mechanism:

-Molecular O2 is converted by NADPH oxidase (membranes of neutrophils and monocytes, NOT macrophages) to superoxide.

***where is most NADPH formed? Pentose phosphate shunt*** (enzyme responsible is Glucose6PO4 dehydrogenase, which converts g6p into p-phosphogluconate, generating NADPH and GLUTATHIONE, neutralizing factor for FRs)

-NADPH converts O2 into a FR, superoxide (has an unpaired e- in its outer orbit which gives off energy called Resp. burst)

-Superoxide is neutralized by SOD into Peroxide (neutralized by glutathione peroxidase).

-MPO combines peroxide (H2O2) with chlorine (Cl-) to form hypochlorous FRs (HOCL) [BLEACH]


*most potent BACTERICIDAL mechanism*

Front 14

How is Resp burst measured?

Back 14

1) radiation detectors

2) Nitroblue Tetrazolium (NBT dye test)- if superoxide and resp burst is present it will cause a color change (bluish)

**NBT is used to find out if you have Chronic Granulomatous Dx from childhood**

Front 15

What is the reservoir cell for AIDS in CNS?

what is reservoir cell outside the CNS?

Back 15

-Microglial cells (which are macrophages in the CNS)

-Dendritic cells, macrophages found in the Lymph nodes.

Front 16

Why is that Infection is the MC thing that precipitates Hemolysis in G6PD def?

Back 16

-Because you don't have NADPH (G6PD makes NADPH in the Pentose Phosphate Shunt) which means you have NO functioning O2 dependant MPO thus you are susceptible to infection, which will set off the hemolysis of RBCs.

Front 17

What are the characteristics of Chronic Granulomatous Dx of childhood?

What can they kill and what can't they kill?

Back 17

X-linked recessive Dx

-deficiency of NADPH oxidase, thus are missing Resp burst.

No Superoxide or Peroxide.

Has MPO and Cl

**Kids are missing NADPH oxidase thus don't make Peroxide**

**KILL - Strept (doesn't have catalase, so making peroxide adds to the MPO system thus child can make bleach and kill Strept)

**CAN'T Kill - Staph (coagulase +ive but also Catalase +ive, will neutralize peroxide and thus will kill the child)

Front 18

characteristics of Myleoperoxidase Deficiency?

Back 18

Autosomal recessive

HAVE- peroxide, superoxide and Cl, resp. burst **normal NBT dye test**

can't kill bacteria because of def of MPO due to which you can't make Bleach.

Front 19

Give an EX of Adhesion molecule or Beta 2 Integrin Defect?

Back 19

Delayed separation of Umbilical cord

***Selectin or Cd11a:Cd18 def***

Front 20

Characteristics of Serotonin and its Fxns?

Back 20

Tryptophan makes it, it is a neurotransmitter

**depression in deficiency of Serotonin and dec NE**

FXN= vasodilator and inc vascular permeability.

Front 21

Complement system: anaphylatoxins - C3a, C5a fxns

Back 21

Stimulate mast cells to release Histamine.

**they play a role in shock**

Front 22

Characteristics of Nitric Oxide

Back 22

-Mainly made in endothelial cells
-Potent vasodilator.

**used in treatment of Pulmonary Hypertension**

plays BIG role in Septic Shock.

Front 23

IL-1

Back 23

Associated with fever, is a pyrogen and stimulates the hypothalamus to make prostaglandins, which stimulate your thermoregulatory center to produce fever

Front 24

Corticosteroids (general)

Back 24

FXN = Inhibits phospholipase A2 = you don't release arachidonic acid from phospholipids (thus you don't make PGs or leukotrienes) and Decreases adhesion molecule synthesis.

**Supreme anti-inflammatory agent because it blocks both PGs and Lts**

Linoleic acid (Omega 6 fatty acid) make arachidonic acid

Linolenic (Omega 3) protects heart and blocks platelet aggregation.

Front 25

Zileutin Mechanism?

Back 25

Blocks 5-Lipoxygenase

**blocks LTs (C4, D4, E4 receptors) because they are Very potent bronchoconstrictors**

Front 26

Aspirin blocks what?

Back 26

Cyclooxygenase Pathway irreversibly in Platelets.

Front 27

PGI2

Back 27

-derives from endothelial cells

aka prostacyclin synthase

FXN = vasodilator and inhibits platelet aggregation (opposite of Thromboxane A2)

Front 28

Thromboxane A2

Back 28

-made in the platelet

FXN = vasoconstrictor, bronchoconstrictor and promotes platelet aggregation (opposite of PGI2)

Front 29

What drug blocks Thromboxane synthase and is used in doing stress testing in Coronary Artery Dx?

Back 29

Dipyrramidal blocks Thromboxane A2 Synthase.

Front 30

PG-E2

PG-F2

Back 30

E2- Vasodilator in Kidney, Patent Ductus Arteriosus, mucous barrier in the stomach,

F2- dysmenorrhia, inc uterine contractility, abortifactant.

Front 31

Effects of Corticosteroids on cells? Mechanism?

Back 31

1) Decreases adhesion molecule synthesis (along with other steroids like epinephrine and NE)

***Dec adhesion molecules synthesis will lead to INC neutrophils on CBC***

2) destroy B-cells b/c they are lymphocytotoxic.

3) Dec Lymphocyte and Eosinophil counts **used in Type 1 Hypersensitivity**

MECH: dec WBC's (B-cells and T-cells) via apoptosis.

**in other words corticosteroids are the signal to activate Caspases(play a major role in cell apoptosis) to kill the cell**

Front 32

What happens to the Neutrophil, lymphocyte and eosinophil count in Addison's Dx?

Back 32

b/c pts do not have Cortisol

-Neutrophil ct Dec
-Eosinophil ct Inc

Front 33

What is the mechanism by which a person in MI has a CBC ct of 18,000 or more?

Back 33

-Most of them are Neutrophil

Mech:

**Epi dec adhesion molecule synthesis and Neutrophil ct goes up**

Front 34

***Look over Electron Microscopy of:

Back 34

Type II pneumocytes, Monocytes, macrophages, lymphocyte (T cells, 60% of peripheral blood lymphocytes and B cells, 20%)

**Helper T cell CD4 ratio to Suppressor T cell CD8 is 2:1**

Plasma cell- has RER (look like a thumbprint) and ribosomes on it make proteins (like Ig's) *cytoplasm is always sky blue, are derived from B-cells and located in the Germinal Follicle of the B-cell*

Granulocytes:
1) Eosinophil (red color similar to RBCs, only inflammatory cell that have crystals in granules)

**charcot-leiden crystals (look like spearheads) in sputum of asthmatic patient which are degenerated Eosinophils in the sputum**

2) Basophils- have purplish granules

Front 35

What is the mechanism for killing Invasive Helminths? Mech?

Back 35

-Type II Hypersensitivity (major basic protein is involved)

Mech:
-Eosinophils have IgE receptors.
-Hook into IgE antibodies (bind to Helminths)
-release the chemicals (major basic protein)
-Destroys the helminth

Front 36

Effector cells of Type II Hypersensitivity? Fxn of the effector cell in Type I Hypersensitivity?

Back 36

Eosinophils (Type II, invasive Helminths)

Type I = b/c they have histaminase and arysulfatase (neutralize leukotrienes), the fxn of Eosinophils in type I is to knock off some of the chemical mediators produced in the rxn.

Front 37

Effector cells of Type I Hypersensitivity? Mech?

Back 37

Mast Cells (release histamine, Eosinophil chemotactic factor)

Mech:

Front 38

***Cluster Designations:***

1) Helper T cell

2) Cytotoxic T cell

3) Marker for AG recognition site for all T cells is?

4) Marker for Histiocytes (including Langerhan's cells) is?

5) Marker for MC leukemia in children is (Positive B-cell leukemia)?

6) Reid Steinberg cell?

7) What does EBV hook onto and where are they found?

8) Burkett's Lymphoma is what cell lymphoma?

Back 38

1) CD4

2) CD8

3) CD3

4) CD1

5) CD10 (C-ALL Antigen)

6) CD 15 and 30

7) CD21, which is found only on B-cells.

8). B-cell lymphoma

Front 39

Who is responsible for FEVER?

Back 39

**IL-1(most of the time) and PG-E2**

Fever is good because it Rt shifts the ODC, so
(more O2 in infected tissues --> O2 dependant MPO)

Front 40

What are the types of Acute Inflammation?

Back 40

1) Purulent (suppurative) inflammation

2) Fibrinous inflammation

3) Serous inflammation

4) Pseudomembranous inflammation

Front 41

Purulent (suppurative) inflammation

MCC of skin abscess?

Back 41

there is localized proliferation of pus forming organisms

**S. aureus MCC of a skin abscess, b/c it has coagulase which cleaves fibrinogen into fibrin and traps bacteria and neutrophils**

EX = Post Partum woman, with pus coming out of lactiferous duct or Bone of child with sepsis, metaphysis of bone there was a yellowish area, it was an abscess this is Osteomyelitis, organism = S. aureus (if the child had Sickle cell Dx then organism = Salmonella)

**in the bone example, why metaphysis of bone? b/c most of the blood supply goes there, so the Mechanism of Spread in Osteomyelitis is Hematogenous**

Front 42

Fibrinous Inflammation definition and Exs

Back 42

Due to INC vessel permeability, with deposition of fibrin rich Exudate. (often occurs on the SEROSAL lining of the pericardium, peritoneum or pleura)

**"bread and butter" Pericarditis**
**Lupus = MC heart lesion in lupus (friction rub)**

**seen in first week of MI, and 6 weeks after in Dressler's syndrome (a post MI syndrome characterized by pleuritic chest pain, pericarditis, fever and leukocytosis)**

**Coxsackie infections**

Front 43

Serous Inflammation definition and Exs

Back 43

Characterized by Thin watery Exudate (b/c there is insufficient amount of fibrinogen to produce fibrin)

EX

1) Blisters from Burns

**MC organism to infect in 3rd degree burns is Pseudomonas and the color of Pus is Green due to pyocyanin**

2) Viral pleuritis

Front 44

Pseudomembranous Inflammation def and Exs

Back 44

Bacterial toxin-induced damage of the Mucosal lining which produces a shaggy membrane of necrotic tissue (pseudomembrane)

EX = 2 organisms that produce analagous pseudomembranes.
1) C. Diphtheria
2) Clostridium Difficile

**Corynebacterium Diptheriae(gram +ive), which makes an exotoxin, messing up the ribosylation of proteins via Elongation Factor 2 (EF2), the toxin damages the mucosa and submucosa producing a pseudomembrane**

[The bacteria don't invade, but produce a toxin that invades]

(toxin measured in stool to get the diagnosis)

Front 45

Steps in wound healing by Primary intention?

Back 45

1) Fibrin clot (hematoma develops), neutrophils are the first to respond.

2) Basal cell layer on both sides of cut, proliferate and go underneath the clot to seal it (after 48 hrs), and macrophages emigrate to the wound.

3) Granulation tissue begins to form (day 3), macrophages replace neutrophils, deposition of type 3 collagen (but does not bridge the incision site yet)

4) Granulation tissue formation peaks, and collage bridges the incision site (days 4-6)

5) by week 2 collagen compresses blood vessels in fibrous tissue (reduced bld flow, tensile strength is 10%)

6) By 1 month, Collagenase remodeling of the wound occurs (replacement of Type 3 by type 1 collagen, with the help of Zinc (cofactor for collagenase), which inc tensile strength)

**Deficiency of Zinc = poor wound healing**

-max tensile strength ~3 months (80%)

Front 46

What is Fibronectin and its Fxn?

Back 46

Proteoglycan involved in healing of a wound.

**is an adhesion agent and a chemotactic agent that invites fibroblasts etc to help in the healing process.

Front 47

Exs of Poor wound healing

Back 47

Ehlers Danlos- defect in collagen due to synthese or breaking it down.

Marfans - defects in fibrillin.

Scurvy- defect in hydroxylation of 2 a.a (lysine and proline), hydroxylation is imp b/c it promotes cross-bridges in collagen leading to inc strength (enzyme = Lysyl oxygenase, cofactor = Cu, both are responsible for forming crossbridges)

**in scurvy you have weak abnormal collagen b/c of no crossbridging, thus poor wound healing, hemorrhages and hemarthrosis(bleeding into jt spaces)**

Front 48

MCC of impaired wound healing?

Back 48

Infections

**Staph. aureus is the MC pathogen**

-inc in nosocomial and community acquired MRSA infections (Vancomycin as Tx for nosocomial infs, TMP-SMX for Tx of Community acquired infs)

Front 49

Keloid (hypertropic scar)?

Back 49

-excessive type 3 collagen, due to fibroblasts.

-causes tumor looking lesions, esp in blacks

Ex 3rd degree burns also (know the relationship btw Squamous Cell Carcinoma and scar tissue in 3rd degree burns)

Ex Chronically draining sinus tract in the skin, tried putting antibiotics on it, didn't work! what is it? Squamous cell Carcinoma.

**Squamous Cell Carcinoma is very common in settings of scars related to 3rd degree burns and also from Chronically draining sinus tracts(such as Chronic Osteomyelitis)**

b/c at the orifice of the draining sinus tract there is a lot of Hyperplasia of the epithelium and it predisposes to cancer****

Front 50

Acute VS Chronic Inflammation

*Main Ig of acute and chronic
*Isotype switching

Back 50

AI- IgM then 10 days or so IgG (IgG only activates complement cascade till C3), IgM IMP b/c you need a lot of complement components (C3a, C5a, C3b etc). IgM is the most potent activator of the complement system (b/c it has 10 Ag recognition sites, its a pentamer) and it will activate the whole of complement cascade (C1-C9).

IS(10days to 2 wks)-same plasma cell that was making IgM, splices out the Mu heavy chain (defines specificity of the Ig) and splices in gamma heavy chain, so now the same Plasma cell makes IgG.


CHRONIC:
-very brief phase of IgM (hrs) b4 it goes to IgG, IgG is the MAIN Ig of Chronic inflammation.

Front 51

What types of inflammatory cells act in the Acute inflammation:

1) Key cells in AI

2) Cells in Allergic Acute Rxn

3) Acute Viral infections

Back 51

1) Neutrophils

2) Eosinophils
**you won't see mast cells b/c they're in tissues**

3) Lymphocytes

Front 52

What types of Inflammatory cells act in Chronic inflammation:

Back 52

-Monocytes and macrophages are key.

*more plasma cells and more lymphocytes in tissue. NO PUS/ EXUDATE*

Front 53

Exudate (Pus)

Back 53

Inc vessel permeability leads to emigration of Neutrophils into interstitial tissue, the protein rich fluid (> 3 gms of protein/dL) and cell rich fluid is called an Exudate.

***Produces the tumor of Acute Inflammation***

Front 54

Ex of Type 4 hypersensitivity rxn in Chronic Inflammation

Back 54

Ex *Granuloma* = caseous necrosis in someone with TB.

Feature = roundish, pink with multinucleated Giant cells.

Pathogenesis = type 4 Hypersensitivity Rxn (delayed Hypersensitivity)

**CD8 cells are main cells in type 4 HPS Rxn (no Ab's involved), they kill neoplastic, virally infected cells*** (Poison Ivy is another Ex of Hypersensitivity Type 4)

****Key cells in delayed Hypersensitivity Rxn = macrophages****

Front 55

Process of a Tuberculous Infection?
(Granulomas and type 4 hypersensitivity Rxn)

Back 55

1) Alveolar Macrophage phagocytise it, goes all over the body (Lymphohematogenous spread)

2) Meanwhile the Macrophage is processing the Ag.

3) After weeks they present Ag to Th1-cells (eventually become memory T-cells) by their class II MHC sites.

4) Th1-cells release cytokines (Gamma IFN, and Macrophage inhibitory factor are involved in Granulomas)

5) Gamma IFN activates the macrophage to kill the TB (cryptococcus, histoplasmosis etc)

**Gamma interferon is a key Trigger**

-Since TB (and systemic fungi) have a lot of lipid in their cell wall, killing them produces release of these lipids and causes Caseous Necrosis.

**Epitheliod cells = Activated Macrophages (by Gamma IFN), so when they Die they fuse together and form Multi-nucleated Giant cells***

Front 56

What substance do macrophages release to present Ag to Th-cells?

Back 56

IL-12 = involved in activating the memory of Subset 1 Th-cells (Th1-cells)

- thus the Subset 1 of Th-cells becomes the memory T-cell.

Front 57

Mechanism of "+" PPD (purified protein derivative)?

Effects of Age on response? what about Aids or immunodeficiency ?

Back 57

1) injected into the skin.

2) the macrophage of the skin is Langerhan's cell, which have Birbeck granules *that look like tennis rackets on EM. (Langerhan's cells = histiocyte, marker= CD1)

2) presentation of Ag to Th1-cell (memory T-cells) through MHC class II Ag site.

3) recognition by Th-cell which releases cytokines producing an inflammatory rxn with INDURATION called the "+" PPD.

*Older pts dono't host a very good Type 4 hypersensitivity rxn (they have less response to "+" PPD)- therefore you do a double test on them*

***Aids pts may not get a rxn (they don't have enough Th-cells) and will NOT get a granuloma in tissue***

"+" PPD Normal (low incidence areas) > 15mm
(high incidence areas) > 10mm
Aids pts ~5mm as "+"

Front 58

Reactions to Injury of permanent tissue:

1). HEART

2). KIDNEY
2a) What part of the kidney is most susceptible to Ischemia?
2b) what parts of the nephron are most susceptible to tissue hypoxia?

Back 58

-Formation of Scar tissue

-Scar tissue doesn't contract, more damage to free wall of left ventricle will lead to dec ejection fraction (SV/EDV) b/c fibrous tissue doesn't contract.

2). Kidney has the same response to injury as heart.

A)***Medulla is most susceptible to Ischemia***

B)Most susceptible areas in the nephron to hypoxia are:
B1) Straight portion of the Proximal Tubule (most susceptable) b/c most of the oxidative metabolism is located in that (w/ brush borders etc)

Fxn = This is where the reabsorption of sodium and reclaiming of Bicarbonate, and more occurs.

B2) Medullary segment of the Thick Ascending limb of the Loop of Henry (second most susceptible to hypoxia)

Fxn = Impermeable to water, this is where the NA/K-2Cl cotransport pump is -- which is where Lasix and loop diuretics block.

Front 59

Na/K-2Cl cotransport pump generates free water, explain the concept and differences between Obligate and Free water produced by the medullary segment of the Thick ascending limb of the Loop of Henle?

Back 59

2 types of water in Urine: Obligate H2O and Free H2O

OBLIGATE H2O = water that is obligated to go out with every Na/K/Cl (that water is about 20ml/ion, for every ion there is 20ml of H2O that goes out)

FREE H2O [ADH reabsorbs or gets rid of free H2O; ADH doesn't work at the Na/K-2Cl] = is generated when you take away the water from Na/K/Cl via the Na/K-2Cl pump (which used to be obligate H2O)

*So if there is an ion of each Na/K-2Cl there is 80ml(20x4 =80ml) of obligate H2O for each secreted out, but the reverse where the same are reabsorbed by Na/K-2Cl cotransport pump, it generates Free H2O ~80ml.

**this is the pump that loop diuretics and lasix block**

Front 60

What is the repair cell of the Lung?

Back 60

Type II Pneumocyte (it can even repair or replace Type I cells)

**Also they make surfactant**

Front 61

what is the repair cell of the CNS?

Back 61

Astrocyte

**Since it is a Stable cell, it can proliferate, it is NOT a neuron**

**when it proliferates it can produces inc in its protoplasmic processes called Gliosis (which is a rxn to injury in the brain, due to astrocyte proliferation)
-just like fibroblasts laying down collagen type 3 in the wound

Front 62

What is mechanism of repair in the PNS?

Back 62

Wallarian Degeneration is the mech of axonal regeneration.

**PNS has Schwann cells while CNS has Oligodendrocytes (both of whom make myelin)**

Tumor of Schwann cell = Schwannoma.

Whats another name for that if it involves CN VIII it is called Acoustic Neuroma.

What genetic Dx that is Autosomal Dominant has an association with Acoustic neuroma? Neurofibromatosis Type II.

Front 63

ESR

What are RBC's called when they stick together stacked like coins?

What causes RBC's to clump?

Back 63

A). putting whole bld into cylinder and see how many mm/hr it settles, the higher the density or weight therefore they'll settle quicker and therefore Inc ESR.

B) Roulouex formation

-when aggregated together = Inc ESR (the cause of this is Inc IgG and fibrinogen, which includes every acute and chronic inflammation)

C) IgM = b/c there is a neg charge which normally keeps RBCs from sticking together. IgM is a lot bigger and offsets negative charges that repel RBCs.

**Cold Agglutinins are associated with IgM Abs, leading to agglutination (thus in cold weather you can get Reynaud's phenomenon) causing Ischemia***

**Cryoglobulins - Ig's that congeal (coagulate esp by cooling) in cold weather and show the same symptoms (lips, nose, ears, toes, fingers turn blue)**

****High association of Hep C with Cryoglobulins****

*Multiple Myeloma = Inc ESR due to Inc IgG*

***Waldenstroms Macroglobinemia (lymphoplasmacytic lymphoma) = See in IgM (thus Inc ESR)

Front 64

If pt has Acute Apendicitis and you get CBC what do you want to look for?

Back 64

1) Absolute neutrophilic leukocytosis (meaning inc of neutrophils in peripheral blood)

2) look for toxic granulation

3) A LEFT shift (def. = greater than 10% band neutrophils aka stabs, or 1 metamyelocyte or myelocyte)

**Left to right in maturation from Myeloblast to Segmented Neutrophil, but a left shift is going to more immature neutrophils***

***Toxic granulation ensures that there is enough Myeloperoxidase (found in the azurophilic granules which are lysosomes of the Neutrophils) to work the potent Bactericidal O2 dependant MPO system***