Ch.2-4: Inflammation Flashcards by Dhesseny Buenafe

ongoing, balanced

cell injury

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allows recovery

reversible

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apoptosis/necrosis

irreversible

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Etiology of cell injury include

Physical (mechanical, thermal, electric)
Radioactive
Chemical (substances, drugs, lead, mercury)
Biologic (viruses, bacteria, parasites)
Nutritional imbalance (deficits & excesses)

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Cell injury mechanisms/ direct&indirect: MAIN

free radicals formation
hypoxia and atp depletion
intra-cellular calcium accumulation

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Cell injury mechanisms/ direct&indirect: OUTCOMES:

Reversible (cell injury recovery)
Swelling & Fatty changes
Irreversible (death)
Apoptosis & Necrosis

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What are the Stresses that endanger norm structure & function cause adaptive cell change for function & survival?

overwhelming stress
ineffective adaptation
maladaptive change
death

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Adaptive cell response is necessary for

normal cell function

determine cell differentiation charactheristics

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cell are able to adapt to increase work demands or threats to survival by changing their size, number and form

adaptation

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decrease in cell size

atrophy

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increase in cell size

hypertrophy

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increase in the number of cells

hyperplasia

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reversible change in which an adult cell is replaced with another adult cell (chronic smoker)

metaplasia

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deranged cell growth, changes vary, change is size, shape, and how they are organized (pap smear)

dysplasia

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Refers to cell death in an organ or tissue that is still part of a living person. Differs from apoptosis.

necrosis

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Path of cell dissolution include

liquefaction
coagulation
infarction

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discharge of content

liquefaction

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form of coagulation, soft cheese

caseous necrosis

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denature of enzymes

coagulation

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artery and body becomes occluded

infarction

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mass of tissue - necroses, results from infection . clostridium

gas gangrene

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A form of necrosis or programmed cell death.
A highly selective process that eliminates injured and aged cells, controlling tissue regeneration.Thought to be responsible for several normal physiologic processes, including programmed destruction of cells during embryonic development, hormone dependent involution of tissues, death of immune cells, cell death by T cells, and cell death in proliferating cell populations.

apoptosis

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death receptor dependent

extrinsic pathway

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death receptor independent

intrinsic pathway

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execution phase of extrinsic and intrinsic pathways begins by prolitic enzymes called

caseaspaces

the reaction of vascularized tissues to cell injury or death. It is characterized by the elaboration of inflammatory mediators and the movement of fluid an d leukocytes from the vascular system into the extravascular tissues.

inflammation

Common causes of inflammation

burns, chemical irritants, frostbite, toxins, infection by pathogens, physical injury, hypersensitive immune reactions, ionizing radiation, foreign bodies, stress, and trauma.

Acute inflammation: | Vascular response

increased blood flow vascular permeability leakage of protein-rich fluid into the extravascular tissues

Acute inflammation: | Cellular Response

changes in endothelial cell lining | movement of phagocytes to injury

Cellular Response: | Delivery and activation of leukocytes STEPS:

Adhesion and margination Transmigration Chemotaxis Activation and phagocytosis

CARDINAL SIGNS OF INFLAMMATION:

``` rubor (redness) swelling heat pain loss of function/ alteration in function ```

persistent (weeks to years) condition, recurrent Etiologies: persistent infection, viruses, bacteria, fungi, parasites, injured tissue, chronic/ autoimmune disease, obesity Manifestations: mononucleosis, angiogenesis, fibrosis, DNA damage (cancer risk)

chronic inflammation

Acute inflammation

vascular change, edema, neutrophils cardinal signs/ systemic manifestation exudate production tissue repair

Chronic inflammation

monocytes predominant, angiogenesis/ fibrosis follow acute inflammation insidious onset, asymptomatic to tissue damage aimed at treating persistence

vasoactive/ first mediators to be released

histamine and seretonin

broad inflammatory effects, enhance serotonin releases, enhanced leukocyte adhesion, and stimulate the production of prostaglandin

platelet-activating factor

regulate/ amplify inflammatory process

nitric oxide, and oxygen derived free radicals

anti-inflammatory effect on cell membrane- fish

omega 3 polyunsaturated fatty acids

mediate inflammation

cytokines/ chemokines

clear, watery fluid

serous

bloody meshwork

fibrinous

necrotic cells enmeshed in fibroprulent exudate

membranes

yellow/greenish, contains pus which is composed of degraded WBCs, proteins, and tissue debris

purulent

red leakage of red blood cells from capillaries

sanguineous

pink (combo of serous and sanguineous)

sero- sanguineous

Systemic manifestation of inflammation include:

fever leukocytosis lethargy/fatigue

Increases set point of hypothalamic thermoregulation center | To promote pathogen-hostile environment

fever

Increased leukocyte count to 15K-20K To efficiently fight inflammation/infection Release pyrogenic (fever-making) mediators

leukocytosis

Metabolism change from energy-making to heat-making | To maintain fever-induced pathogen-hostile environ

lethargy/fatigue

Types of fever: | return to normal after 24 hours

intermittent fever

Types of fever: | temp above normal, very little variation

sustained fever

Types of fever: | does not return to the normal level

remittent fever

Types of fever: | recurrent, last for days between each episode

relapsing fever

LAB TEST: | ESR

erythrocyte sedenmation measures the rate RBC settle normal: M-15 F-20 increase in ESR (rise in fibrinogen/ RBC stack)

LAB TEST: | CRP

C-reactive protein normal: less than 1.0 rise acute infection

Acetaminophen

antipyretic, analgesic | NOT INFLAMMATORY

Acetylsalicylic acid (ASA)

antipyretic, analgesis, anti-inflammatory (NSAID)

Tissue type: (continuously-dividing) Readily regenerate if stem cell pool preserved (skin)

labile

Tissue type: (restricted dividing) Capable of regeneration if proper stimuli (kidney)

stable

Tissue type: (non-dividing) Incapable of regeneration, fibrous scar switch (nerves)

fixed

Local and systemic factors of wound healing:

``` blood flow, and O2 delivery Infection, wound separation, forcing bodies nutrition inflammation aging ```

sutured surgical incision

primary intention

larger wounds (greater loss of tissue & contamination

secondary intenion

Healing phases include:

inflammatory (prepares for healing) proliferative maturation/remodeling