Path Exam 1

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Russell Bodies: Round accumulations of proteins within ER
Xanthomas: Tumor-like masses form on skin and tendons

- usually associated with hypercholesterolinemia
Fatty change (steatosis): *Intracellular* - accumulation of TIGs within parenchymal cells

- usually reversible

Causes: chronic alcoholism, chronic hypoxia, diabetes mellitus, protein malnutrition

pg. 31
Fatty infiltration: *Extracellular - accumulation of lipids within the stromal CT

- does not affect the function of the organ (unlike fatty change)

- reversible

- CT is converted into lipocytes

- Heart (RV) and pancreas
Coagulative Necrosis: Tissue appears pale and firm

- cell detail is lost but the cell outline can be recognized!

Hypoxia or ischemia --> decrease of ATP & increase Ca2+ ==> irreversible mito dysfunction

Heart, kidney, adrenal gland
Liquefactive necrosis: Soft area due to the action of hydrolytic enzymes

- lysosomes release hydrolases in the case of *bacterial infections or abscesses*

- brain
Caseous Necrosis: Soft and white resembling cottage cheese

*Associated with granulomatous inflammation (TB!)**

- Lung
Fat Necrosis: Necrosis of adipose tissue - chalky white patches overlyiung yellow fat

- basophilic calcium salts

- enzymes released from injured acinar cells and ducts --> destruction of fat cell membranes and split TIG esters present with in the fat cells --> released FA combine with calcium to form calcium soaps~

- pancreas
Fibrinoid Necrosis: Seen in cases of vasculitis and hypertension

- deposition of fibrin in the damaged necrotic walls of blood vessels

*blood vessels
Gangrenous Necrosis: Tissue that has lots its blood supply, can be ..

coagulative necrosis (dry gangrene)

OR

liquefactive necrosis (wet gangrene)
Hypoplasis: incomplete or partial growth of an organ
Agenesis: (Aplasia)

complete failure of growth of an organ
Dysplasia: disorderly growth and maturation of cells

- usually seen in epithelial lining
cardinal signs of inflammation: heat
redness
swelling
pain
loss of function
lipofuscin: "aging pigment"

- accumulation of lysosomes as cell ages

*light brown to yellow-brown, intracytoplasmic granules
Hemosiderin: yellow-brown granular pigment derived from iron in the heme portion of hemoglobin

- When excess Fe, ferritin (intracellcular storage form) aggregate to form hemosiderin

*found in mononuclear phagocytes, may be found in hepatocytes*
Bilirubin: dervived from the non-iron-containing porphyrin ring of the heme portion of hemoglobin

- major pigment of bile

- hyperbilirubinemia leads to jaundice
anthracosis: condition of inhaled carbon or coal dust
pneumoconiosis: general term for condition associated with any inhaled dust
Active hyperemia: increased blood flow due to arteriolar dilation

- lasts 1 to 2 hours

*mediated by histamine and NO*
Vascular events in inflammation: - initial transient arteriolar constriction

- arteriolar dilation*

- passive venous congestion

- transudation of fluid into tissue

- progressive increase in vascular permeability*

- exudation of fluid into tissue (includes fibrin)
Functions of fibrin in inflammation: *acute*

blood clotting

isolation/confinement of inflammatory agent

chemotactic for neutrophils

scaffold for healing (migration of endothelial cells, fibroblasts)
Serous inflammation: *acute*

exudate is composed of watery, serum-like fluid

- fluid comes from plasma

(ie. blister)
Fibrinous Inflammation: *acute*

- results with more sever evascular leakage than serous

- soluble fibrinogen --> insoluble fibrin

**characteristic pattern of acute inflammation in body cavities.. peritoneum, pericardium, etc*
Suppurative or purulent inflammation: *acute*

pus - composed of necrotic cellular debris and neutrophils

*associated with pyogenic bacteria like: staph & strep!!
Abscess: discrete accumulation of pus
Nonsuppurative Inflammation: *chronic*

Eudate is an even mix of mononuclear inflammatory cells
Granulmoatous Inflammation: *chronic*

macrophages predominate in the exudate
Fibrinous vs fibrous: Fibrinous - early phases of inflammation

Fibrous - late phases of inflammation
"left shift": elevated number of *immature* neutrophils in peripheral blood

.. happens when there is a high demand needed
Neutrophilia: elevated # of mature neutrophils in peripheral blood

- common in bacterial infections
Lymphocytosis: elevated # of lymphocytes in peripheral blood

- common in viral infections
Vasoactive Amines: Histamine - granules in mast cells, arteriolar dilation, increased vascular permeability

Serotonin - from platelets, vasoconstriction, increased vascular permeability

Platelet-activation factor (PAF) - from membrane phospholipids, proinflammatory and procoaculatory effects
Acute Phase Proteins: exhibit marked changes in plasma concentration as a result of an inflammatory response

increase in concentration (+) = C-reactive protein, fibrinogen, serum amyloid A

*associated with clinical signs such as fever, malaise, loss of appetite, and changes in heart rate and BP*
1 of 4 plasma-derived protease cascades... Coagulation cascade: Produces fibrin and thrombin (cleaves fibrinogen --> fibrin)
1 of 4 plasma-derived protease cascades... Fibrinolysis system: Fibrinolysis BY plasmin ON fibrin to sustain exudation of leukocytes and chemical mediators to the tissue site of inflammation
1 of 4 plasma-derived protease cascades... Complement Cascade: Cleavage of C3 --> C3b and C3a(anaphylaxtoxin)...

C3a: increases vascular permeability and smooth muscle contraction - triggers release of histamine

C3b: opsonin that enhances phagocytosis by phagocytes

C5a: chemotaxin that attracts and activates leukocytes

C5bC6C7C8C9 - membrane attack complex that lysis the cell
1 of 4 plasma-derived protease cascades... Kinin system: bradykinin causes vasodilation or vasoconstriction
- increased vascular permeability
- is a mediator of the pain response of ACUTE inflammation
Cyclooxygenase pathway: Cell membrane phospholipids --> Arachidonic acid:

- COX1
- COX2
- Thomboxane A2
- Prosacycline (PGI2)
Thromboxane A2: produced primarily by platelets

pro-coagulatory effects (vasoconctriction, platelet aggregation)
Prostacyclin (PGI2): produced primarily by endothelial cells

anti-coaculatory effects (vasodilation, inhibit platelet aggregation)
Prostaglandins: ***Also part of the cyclooxygenase pathway**

vasoconstriction/dilation

increased vascular permeability

pain (PGE2)
Lipoxygenase pathway: Lipoxins

5-HETE

Leukotrien B4 (LTB4)

LTC4, LTD4, LTE4
Lipoxins: secreted by platelets

*anti-inflammatory - inhibit leukocyte chemotaxis and adhesion to endothelial cells
Leukotrien B4 (LTB4): potent mediator of neutrophil and monocyte/macrophage chemotaxis and activation
LTC4, LTD4, LTE4: vasoconstriction, increased vascular permeability, leukocyte chemotaxis

bronchospasm (bronchial smooth muscle contraction) - more potent than histamine!

** important in asthma**
Glucocorticoids: down-regulate expression of genes encoding for COX-2 and PLA2

Up-regulate genes encoding for lipocortin, which inhibits release of arachidonic acid from membrane phospholipids
Nitric Oxide: produced by endothelial cells!

- vasodilation

- decreases platelet aggregation and adhesion

- slows leukocyte recruitment

**can cause damage to host cells via lipid peroxidation
**can cause damage to pathogenic microbes by combining with O2- or OH radical
Master Cytokines: IL-1: produced by activated macrophages

IL-6

Tumor Necrosis Factor (TNF-alpha)
Major effects of bacterial endotoxin: - LPS activates macrophages --> attracts and activates other leukocytes

- direct injury to microvasculature --> increased vascular permeability

- activates neutrophils --> increase release of toxic oxygen free radicals --> widespread vasodilation (spetic shock)

- can directly activate complement cascade
Granulation Tissue: highly vascular, immature fibrous connective tissue
..often edematous because of the leakiness of new blood vessels

- the most mature tissue is at the base of the defect, or at the periphery of the area of healing
Hyaluronic acid: abundant in the inflammatory phase

- makes the healing issue rather fluid and allows cell movement through the matrix
Healing by 1st intention: - closed wound healing

- wounds with minimal tissue loss and limited cell death

-wound edges can be apposed (a sutured surgical incision)

- rapid repair

- small scar
Healing by 2nd intention: Open wound healing

- wounds with significant tissue loss (wound edges cannot be apposed)

- less rapid healing because large volume of exudate must be removed & signifcant fibroblast and endothelial cell proliferation required

- larger scar than 1st
Dehiscence: the breakdown and rupture of a closed wound
keloids: scar tissue grows beyond the boundaries of the original wound

*predispositin in some african-americans
"exuberant" granulation tissue: excessive granulation tissue which prtrudes above the skin surface, and impedes re-epithelialization

- must be removed by cautery or surgery
Desmoids: "aggressive fibromatoses"

- excessive proliferation of fibroblasts and ECM which may recur even after surgical ecision
- borders on neoplasia

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Number of cards 58

Created By alstoner