INFLAMMATION Skin: LANGHERHAN’S CELL EPITHELIUM – invading

- 1st response of the tissue (phagocyte) microorganism, would release

- If one phase is absent, Brain: SCHWANN CELL toxins (GRAM + / EXOTOXIN)
inflammation won’t take place Nervous: MICROGLIA
Lungs: DUST CELL ENDOTOXIN / GRAM- - not
Cardinal signs: Liver: KUPFFER CELL released by cell wall, surface of
Calor cell as expressed by
Rubor MESANGIAL CELL – considered but LIPOPOLYSACCHARIDE
Dolor
Tumor NEUTROPHIL – physiologic Organs are lined by
Function laesa immune surveillance MESOEPITHELIUM

EPITHELIUM – 1st lining of defense
of the body
STRATIFIED – lining epithelium of
skin
2 types of oral mucosa:
MASTICATORY –
keratinized (stratum corneum is
nucleated)
NON MASTICATORY – non
keratinized (non nucleated)
PARAKERATINIZED – intact nucleus
but pyknotic
Oral mucosa: LANGERHAN’S CELL
& NEUTROPHIL
MYELINEATION – myelin sheath –
node of ranvier (gap) – neurons –
dendrites & axons
C3a – LANGERHAN’S CELL
(macrophage) & NEUTROPHIL
C5b6789 / LYSIS – invading cells
C3a C4a C5a – activation of mast
cell & basophil = RELEASING
HISTAMINE & HEPARIN > induces
vasodilation >
CELL WALL/PEPTIDOGLYCAN
Gram – thinner
Gram + thicker
EPTIHELIAL CELLS & FIBROBLASTS
– if stress would produce or
release CYTOKINE
2 most important cells: will
activate & produce receptor
(INTERCELLULAR ADHESION
MOLECULE 1 & INTEGRINS)
IL-1
TNF-α / TUMOR NECROSIS
FACTOR

ORTHOKERATINIZED – normal If blood vessel dilates it increases 2 groups of WBC / LEUKOCYTES:

ANTIGEN – foreign molecule, it
has a strong propensity
ANTIBODY – 1st activation of
antigen
ANTIGEN-ANTIBODY COMPLEX
3 most important fragments:
C3a
C5b6789
C4a
C5a
C3a – OPSONIZATION – process of
activating phagocytes to produce
phagocytosis
Two immediate phagocytes:
MACROPHAGE
permeability GRANULOCYTES
NEUTROPHIL – bacteria, 70%
If doesn’t dilate it won’t go out EOSINOPHIL – parasite, 1-0%
BASOPHIL – histamine for
PLASMA – by zymogen vasodilation, 0.5%
SERUM – without zymogen AGRANULOCYTES –
monocyte in cell circulation into
FIBRINOGEN – walls of macrophage
permeability LYMPHOCYTE
o T-cell
MAST CELL – organ CYTOTOXIC / CD8
HELPER / CD4
BASOPHIL – in circulation SUPRESSOR/REGULATORY / CD25
– regulates the function of CD4 &
COAGULATION CASCADE CD8
Plastic is permeable. - If very low, there’s no
regulation
- When foreign body is
eliminated
o B-cell – plasma cell
CYTOKINE > NEUTROPHIL >
HEMOTAXIS > DIAPEDESIS
RBC / ERYTHROCYTE
PLATELET / THROMBOCYTE
MONOCYTE – 2nd line defense
Antigen presenting cells:
MACROPHAGE
DENDRITIC CELLS – most
important
2 types of complex:
o MAJOR
HISTOCOMPATIBILITY COMPLEX I /
MHC I – activates cytoxic cells >
PERFORIN (creates perforation)
o MAJOR
HISTOCOMPATIBILITY COMPLEX /
MHC II – helper tcells (helps
cytotoxic cells) that would release:
IL-2, 3,4,5,6
GRANULOCYTE
MONOCYTE
COLONY
STIMULATING FACTOR
= PPHSC (PLUROPOTENTIAL
HEMATOPOIETIC STEM CELL)
INTERFERRON GAMMA – causes +
feedback mechanism for MHC II
Bcells
IL-2 – lymphokines which come
out lymphocytes
- Signals helper tcells to
induce + feedback mechanism
GRAM – FEEDBACK MECHANISM –
HPG/O would stop producing GH
GRAM + FEEDBACK MECHANISM –
continue
IL-3 – activation of pluropotential
hematopoietic stem cell or PPHSC
- Precursor cell, signals
bone marrow
IL-4 5 6 – initiates differentiation
of Bcells to plasma cells
- Because plasma cell is
responsible for antibodies or
immunoglobulins
Bone marrow is the house of
PPHSC.
5 (Ig) immunoglobulins that is
secreted by plasma cells:
IgG – most predominant, can cross
placental barrier
IgA - secretion
IgM - start
IgE – allergy (allergic
rxn/hypersensitivity)
IgD – unknown fxn
Inflammation would stop if there’s
an acute
SELECTION
PROTECTION
= prevents further recruitment of
macrophage & neutrophil
If M&D die leads to PUS
RESOLVIN – activates remaining
macrophages
AUTOIMMUNE DISEASES – attacks
the body CD4 & CD8. It becomes
hyperactive coz no stopping them
HIV
Target cell: CD4
HIV I – predominant worldwide
HIV II – endemic
VIRUS – living things, carried
around by the blood stream
- Replicates until
predominates
COAGULATION CASCADE
WOUND HEALING/HEMOSTASIS
HEMOSTATIS – state of balance
- How the body performs in
order to maintain in desirable
body environment
HOMEOSTASIS – prevents further
circulation of blood
4 processes of hemostasis:
TRANSIENT/TEMPORARY
VASOCONSTRICTION
– Sympathetic autonomic nervous
system
Physiologically:
SOMATIC
AUTONOMIC – to temporary
constricts blood vessel
Parasympathetic
Sympathetic
Enteric
PLATELET ACTIVATION
TUNICA INTIMA
TUNICA MEDIA/MUSCULARIS
TUNICA ADVENTITIA/EXTERNA –
well invested, collagen type I
THROMBOXANE-A2 – adhere a
platelet, prostaglandin
- Signal to other platelet
VON WILLEBRAND FACTOR – if cut
thrombocyte
PLATELET AGGREGATION –
process
PRIMARY PLATELET PLUG – result
COAGULATION CASCADE

IN VIVO/EXTRINSIC
3 / TISSUE FACTOR / TISSUE
THROMBOPLASTIN (first
activation)
7 / STABLE FACTOR /
PROCONVERTIN
7a
10 / STUART PROWER FACTOR + 4
/ CALCIUM + 5 / PROACCELERIN /
LABILE FACTOR
= PROTHROMBIN ACTIVATOR
2 / PROTHROMBIN
2a / THROMBIN
1 / FIBRINOGEN
1a
13 / FIBRIN STABILISING FACTOR
IN VITRO/INTRINSIC “glass”
12 / HEGMAN FACTOR +
HMW / HIGH MOLECULAR
WEIGHT / FITZGERALD FACTOR +
PK / PREKALLIKREIN / PLEKKER
11 / TISSUE THROMBOPLASTIN /
ANTIHEMOPHILIA C
11a
9 / CHRISTMAS FACTOR /
ANTIHEMOPHILIA D + (work
together with factor 8)
8 / ANTIHEMOPHILIA A
10 / STUART PROWER FACTOR
Duration:
PROTHROMBIN TIME 12s
CLOTTING TIME 6-10s
BLEEDING TIME – 1-6s von
willebrand disease (most common
disease, if BT is increased)
Classic hemophilia – if clotting
time is increased
FACTORS 9 10 7 2 (1972) – vit k
dependent factor
FIBRINOLYSIS – dissolution
of clot
THROMBUS - attached in the
blood vessel; blood clot that forms
in a vein
EMBOLUS – circulating, lodge on
the blood vessels, travels through
the blood vessels
VASCULAR STASIS
VARICOSE VEINS
HEMORRHOIDS
THROMBOEMBOLISM
TISSUE PLASMINOGEN ACTIVATOR
– enzyme that plasminogen
converted to plasmin (to prevent
thromboembolism)
ANTICOAGULANTS: factors why
we aren’t suffering from
thromboembolism..
- Smoothness of blood
vessel
- Presence of glycocalyx
- THROMBOMODULIN –
produces protein C
- Heparin of mast cell