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MSK > Inflammation/Healing > Flashcards

Inflammation/Healing Flashcards

Acute + Chronic + Wound Healing

1
Q

Acute Inflammation

Acute Inflammation

A

Rapid & Exudate
Eliminate/prevent/remove necrotic tissue from spreading
Results: Complete resolution, chronic inflammation, fibrosis/scarring

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2
Q

Acute Inflammation

Hallmarks

A

Red (rubor)
Heat (calor)
Swelling (Tumor)
Pain (Dolor)
Loss of Function (funcitonal lasse)

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3
Q

Acute Inflammation

Cellular infiltrates in inflammation

A

PMN/PMNLs (neutrophil) and cause apoptosis + macrophages enter

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4
Q

Acute Inflammation

Steps

A

Vasodilation (redness/warmth) and permeability (inflammation), macrophages (phagocytosis)

Diapedesis is PMS migrating across to where they need to go and cheokines push them to the site, they activate pain followed macrophages

Short life for neutrophils, macrophages clean it up so the dead neutrophils do not cause pus to form

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5
Q

Acute Inflammation

Serous Inflammation

A

Copius Effusion from plasma/mesothelial cells –> seperation of layers (blister)

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6
Q

Acute Inflammation

Fibrinous inflammation

A

Meshwork of fibrin (pink strands) exuded out of the blood

Examples: fibrinous pericarditis/emningitis, can be broken down by fibrinolysis

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7
Q

Acute Inflammation

Purulent Inflammation

A

Localized vicous exudate - pus, dying neutrophils

Results: Complete Resolution/abcess (pus), sinus, fistula (w/liquefactive necrosis)

Microscope: Capillary walls congested –> yellow exudate

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8
Q

Acute Inflammation

Vasoactive Amines

A

Vasodilation/vascular permeability
Mast cell - histamine
Platlet - histamine/serotonin

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9
Q

Acute Inflammation

Complement

A

Mast Cell stimulation, chemotaxis

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10
Q

Acute Inflammation

Kinins

A

Vascular permeability, pain, smooth muscle contraction (vasodilation)
Kallikren: attract neutrophils

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11
Q

Acute Inflammation

APP

A

Made by liver released in blood

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12
Q

Acute Inflammation

Coagulation Factors

A

Clot pathways to activate kinins

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13
Q

Chronic Inflammation

Fibrinous and Fibrous Inflammation

A

Fibrinous and fibrous inflammation from fibrin deposition fibromas  chronic fibrous inflammation (fibroblast surrounding collagen fibers in dense connective tissue)

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14
Q

Chronic Inflammation

Granulomatous Inflammation

A

Granulomatous Inflammation is the collection of cells that can’t eliminate: multinucleated cells, activated macrophages, lymphocytes

Microscope: pale nuclei, pink cytoplasm, palisading

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15
Q

Chronic Inflammation

Transudate vs. Exudate

A

Transudate is clear, low protein, low cell content/ low gravity caused by starling forces

Exudate opaque, high protein, high protein count, high gravity caused by damage to endothelial wall

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16
Q

Chronic Inflammation

Acute vs. Chronic Pneumonia

A

Acute Bronchopneumonia is acute bacterial infection of terminal bronchioles extending into alveoli, leads to outpouring of PMNs and red blood cells  pus created  macrophages eat up  exudate removed

Chronic Pneumonia is inflammation w/I alveoli and distal bronchioles is inflammatory exudates that fill alveoli and may be transformed into nodules (no necrosis + neutrophil infiltration) and is secondary to injury via drugs

17
Q

Chronic Inflammation

Acute vs. Chronic Bronchitis

A

Acute Bronchitis: viral infection, desquamated cells, infiltrates in bronchial mucosa, predominantly neutrophilic

Chronic Bronchitis: Inflammatory swelling and mucous production, never healed from acute (>3 mnths), ↑ size of mucus-secreting gland, goblet cells, , squamous epithelial cell, mononuclear consist of lymph and plasma cells

18
Q

Chronic Inflammation

SIRS + Sepsis

A

SIRS (massive release of cytokines in blood, HPA axis, high RR/HR, acute phase response)  +Infection = SEPSIS  + EOD = Severe Sepsis  + Hemodynamic instability = Septic Shock

19
Q

Chronic Inflammation

Labatory Markers

A

Acute phase proteins (APPs) – trigger release of cytokines (alpha 1, 6),

C reactive proteins increases 100-1000x,

procalcitonin commonly used for if a patient responds to antibiotics,

ESR tells if a blood sample has how many RBCs and relies on fibrinogen which if there is a lot of it can mask the RBCs,

high fibrinogen will mask the RBCs if it comes down quicker it is being masked and is an inflammatory response.

CBC will have high or low leukocytes, high bands (bandemia), leukemoid reaction is increase in WBC count that limits leukemia, leukopenia=neutropenia

Left shift – increase in immature form of neutrophils

20
Q

Wound Healing

Define Regeneration vs Repair

A

Regeneration (same replacement), Repair (fibrous scar tissue replacement)

21
Q

Wound Healing

Describe the basic elements of regeneration and repair (Liable, Stable, Permanent Cells)

A

a. Liable Cells are continuous exfoliation and replacement (lining of the uterus)
b. Stable Cells regenerate when prompted (parenchymal cells – liver, kidney, pancreas)
c. Permanent Cells are least likely to regenerate/lost their ability to divide (neurons, cardiomyocytes, no CNS, no PNS)
d. Complete resolution can occur with stable/liable cells whereas with permanent cells leads to scarring.

22
Q

Wound Healing

Indicate factors that favor resolution versus repair; note exceptions

A

Factors favoring complete resolution include proteolytic digestion and respobrtion of exudates & absence of necrosis. Exceptions include the accumulation of exudate in large volumes

23
Q

Wound Healing

Recognize the contribution of granulation tissue to wound healing

A

a. WOUND HEALING

b. Specialized tissue of repair that is highly vascularized/leaky/lacking epithelial coverage, angiogenesis (new capillary buds)  contains glycosaminoglycans/collagen fibers/myofibroblasts, appearance wet and exudate

24
Q

Wound Healing

Compare primary and secondary union

A

Primary Union is the first intention, few cells die, scab forms quickly (small cut, surgical incision)

Secondary Union is second intention, intense inflammatory rxn, necrosis (MI, inflammatory ulceration, abscess formation)

25
Q

Wound Healing

List the phases of cutaneous wound healing and events in each stage

A

Homeostasis (vasoconstriction, release of clotting factors, platelet plug, thrombus)  Inflammation (ROS , neutrophil, macrophages release)  Proliferative (“filling the covered wound” – angiogenesis, fibroblasts  Remodeling-Maturation (collagen, scar tissue formation)

26
Q

Wound Healing

Distinguish among the different forms of an ulcer

A

Infection can cause abnormal wound healing causing ulcer

Non-healing wounds will become chronic due to multiple factors

Pressure – immobile, pressure on bony area

Diabetic foot - damage to sensory, autonomic, and motor nerves

Venous – hydrostatic pressure increase, slow capillary blood flow

Arterial insufficiency – reduced blood flow to affected limb

27
Q

Wound Healing

Identify and describe aberrant responses to wound healing, including dehiscence, keloids, incisional hernias, contracture, adhesions, and fistula

A

Aberrant response
Deficient scar formation

Dehiscence – splitting open of a wound

Evisceration – dehiscence with exterior exposure of organs

Incisional hernias – big area without external appearance

Keloids – scars beyond the borders of the injured site

Contracture – exaggeration of normal contraction

Adhesions – fibrous bands between tissues, commonly caused by surgery, becomes fibrinous tissue they will not break down but can cause strangulation of an intestine

Fistula – abnormal passage between two organs, typically via arterial/vein formation that previously did not exist

Bone spur – osteophytes, osteoarthritis can be caused by wear and tear damage

28
Q

Wound Healing

Define: Organization, Granulation, Scarring, Abrasion, Laceration, Puncture, Erosion/ulcer, infarct, infarction

A

Organization – intermediate of healing and repair

Granulation – vascularized wound repair

Scarring – repair with fibrous tissue replacement

Abrasion – surface damage

Laceration – jagged wound

Puncture – wound that forces debris/bacterium in

Erosion/ulcer – craters on tissue surfaces

Infarct – localized dead tissue

Infarction – ischemic necrosis

MSK (22 decks)

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