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Patho > Module 5 - Infalmmation > Flashcards

Module 5 - Infalmmation Flashcards

1
Q

The inflammation process is… meaning that inflammation is responsive to…

A

responsible for localizing and eliminating any foreign substances,
meaning that inflammation is responsive to infections, allergies, or tissue injuries

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2
Q

The first line of defense in the body is…

A

bodily fluids, skin, and mucous membranes
Non-specific defense

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3
Q

The second line of defense in the body is…

A

the inflammatory process and phagocytosis
Non-specific defense

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4
Q

The third line of defense in the body is…

A

specific defense mechanisms

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5
Q

Phagocytosis

A

neutrophils and macrophages engulf and destroy foreign matter, pathogens, and cellular debris

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6
Q

Steps in the inflammation process

A
  1. Capillary and tissue cells are injured causing the release of bradykinin
  2. Bradykinin stimulates sensory nerve impulses that cause pain
  3. Pain causes mast cells and basophils to release histamine
  4. Bradykinin and histamine the lead capillaries to dilate, increasing blood flow and capillary permeability to the area
  5. Bacteria then enters the tissue causing neutrophils and monocytes to travel to the site of injury
  6. The neutrophils destroy the bacteria through phagocytosis with the help of their hydrolytic enzyme of their lysosomes
  7. Monocytes that mature into macrophages level the bloodstream and quickly become phagocytic microbes to help neutrophils.
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7
Q

The complement system is…

A

a series of enzymes releasing and following pathways to control inflammation and destroy pathogens.
This process promotes phagocytosis, increases vascular permeability, initiates chemotaxis, and cellular lysis

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8
Q

Platelet activation causes

A

prostaglandin (PG) formation,
Some of the subtypes of (PG)in turn prevents platelet and neutrophils from clustering
PG also initiates pain and febrile(fever) response

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9
Q

Thromboxane (one PG) is

A

a potent vasoconstrictor as well as platelet-aggregating agent. Initially thromboxane produces brief vasoconstriction and paleness at the injury site, creating a clot
-The effects of thromboxane are short-lived, so the area becomes red as a result of vasodilation (after vasoconstriction from thromboxane) and histamine release (from mast cells and basophils).

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10
Q

Leukotrienes form the slow-reacting substance of anaphylaxis (SRS-A)
causing

A

smooth muscle constriction of the bronchi - leads airways to narrow and increase capillary permeability and airway edema

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11
Q

Exudate contains

A

fluid and leukocytes that more from the circulation to the site of injury

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11
Q

Injury response - Vascular

A

-the local arterioles briefly undergo transient vasoconstriction to prevent the release of erythrocytes from bleeding that occurs
-then histamine and other chemicals are released that cause vasodilation
- capillaries then increase permeability and cause fluid to move from capillaries to tissue spaces
-serous fluid (containing plasma protein - mainly albumin) then becomes inflammatory exudate
-this process causes redness, heat, and swelling at the site of the injury and surrounding tissue

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12
Q

Injury Response - Cellular

A

-neutrophils and monocytes move from circulation to the site of injury due to chemotaxis (movement of a motile cell or organism, or part of one, in a direction corresponding to a gradient of increasing or decreasing concentration of a particular substance)
-Platelets move to the site of injury to promote clotting
-Neutrophils show up first (within 6-12 hours). They participate in phagocytosis to rid the area of bacteria, foreign material, and damaged cells. (neutrophils only live 24-48 hours so they start to build up at the site of injury)
-The mix of dead neutrophils, digested bacteria, and other cell debris accumulates as a creamy substance, known as pus.
-monocytes/macrophages are the second to arrive (3/7 days after onset inflammation)
-macrophages assist with phagocytosis, so the area is clean before it heals
-lymphocytes arrive last

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12
Q

Histamine - Chemical mediator

A

Found in granules of basophils, mast cells, and platelets
Causes;
Vasodilation
Increased capillary permeability
Serous fluid accumulation

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12
Q

Serotonin - chemical mediator

A

Found in platelets, mast cells, and enterochromaffin (a type of neuroendocrine cell found in the gastric glands that aid in the production of gastric acid), cells of the gastrointestinal tract
causes;
Vasodilation
Increased capillary permeability
Stimulates smooth muscle contraction

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12
Q

Kinins (brandykinins) - Chemical Mediator

A

Comes from precursor factor kininogen due to hagman factory (VII) activation from the clotting system
Causes;
Vasodilation
Increased capillary permeability
Stimulates smooth muscle contraction

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12
Q

Complement Components (C3a, C4a, C5a) - chamical mediator

A

Anaphylatoxin fragments that are produced as part of the activation of the complement system
Causes;
Stimulates the release of histamine and chemotaxis

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13
Q

Prostaglandins (PGs) and Leukotrienes (LTs) - chemical mediators

A

-Synthesized by arachidonic acid (is a precursor in the biosynthesis of prostaglandin)
-Proinflammatory
causes;
Prostaglandins cause vasodilation
Leukotrienes cause chemotaxis

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14
Q

Cytokines

A

-secreted by WMCs
-over 100 cytokines in the body
-some cytokines are beneficial to the body
-classified into interleukins, interferons, and tumor necrosis factor
Causes;
Proinflammatory mediators
Promotes b-cell production
Activates t-cells and macrophages

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15
Q

Acute inflammatory response

A

lasts 8-10 days and stops when pathogen/foreign substances are gone

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16
Q

Fluid that accumulates at the site of inflammation is drained by

A

Lymph vessels

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17
Q

Fever occurs due to…

A

cytokines release from neutrophils and macrophages

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18
Q

Leukocytosis

A

Increases WBC formation
Produces more immature neutrophils
WBC coin is >11,000 mL^3 in adults

19
Q

Plasma Protein Synthesis

A

Used as a pro- and anti- inflammatory
Contains coagulation components
Contains complement proteins

20
Q

Chronic Inflammation

A

(lasts over a few weeks) can be caused by unresolved acute inflammation, an infection, antigen, or foreign substance in the area.

21
Q

Granulomas formation

A

Granulomas form when macrophages differentiate into large epithelioid cells that clean up cellular debris and other small particles. Other macrophages become multinucleated giant cells that consume very large particles—larger than can be consumed by a single macrophage. These macrophages form the center of the granuloma and are surrounded by a wall of lymphocytes. The granuloma is frequently surrounded by fibrous deposits of collagen and may become cartilaginous or possibly calcified by deposits of calcium carbonate and calcium phosphate. Examples of pathogens that form granulomas include the Listeria sp., Brucella sp., fungi such as histoplasmosis and coccidioidomycosis, and parasites like leishmaniasis, schistosomiasis, and toxoplasmosis

22
Q

Local clinical Manifestation of acute inflammation - rubor

A

Redness
Hyperemia (excessive blood near the surface as a result of inflammatory response causes vasodilation and thus redness at the skin’s surface)

23
Q

Local clinical Manifestation of acute inflammation - heat

A

Metabolism is increased at the site of inflammation

24
Q

Local clinical Manifestation of acute inflammation- pain

A

pH changes
Increases fluid from exudate causes pressure
Nerve stimulation from histamine and prostaglandins

25
Q

Local clinical Manifestation of acute inflammation - swelling

A

Exudate accumulation
Fluid shifts into the interstitial spaces from increased capillary permeability

26
Q

Local clinical Manifestation of acute inflammation - loss of function

A

Swelling
Pain

27
Q

Local clinical Manifestation of acute inflammation- Exudates

A

Varies

28
Q

Serous Exudate

A

Drainage is water. It occurs due to mild inflammation and contains very few plasma proteins or leukocytes. The fluid in a blister

29
Q

Serosanguinous exudate

A

Drainage is pinkish-yellow due to an accumulation of red blood cells and serous drainage. This is commonly found in surgical drains post-operatively

30
Q

Fibrinous Exudate

A

The drainage is thick and clotted and occurs with more severe or advanced inflammation. An example is a person with pneumonia. Their lungs will be filled with fibrinous exudate

31
Q

Purulent Exudate

A

The drainage consists of pus and occurs if too many leukocytes accumulate. Purulent exudate is a characteristic of walled-off lesions (cysts or abscesses)

32
Q

Hemorrhagic Exudate

A

Drainage is bloody and is filled with erythrocytes. An example is a hematoma

33
Q

Catarrhal Exudate

A

Drainage is of mucus consistency and is clear in color. An example is a runny nose from an upper respiratory infection

34
Q

Systemic Manifestation of Inflammation- fever

A

Can be severe if caused by a microorganism
Occurs due to the release of pyrogens (fever-producing substances), white blood cells, or macrophages
Can inhibit pathogen proliferation
Pyrogens cause the hypothalamus to increase cell metabolism

35
Q

Systemic Manifestation of Inflammation - leukocytosis with left shift

A

Immature neutrophils are producing in large numbers in response to a pathogen
WBC>11,000/mL^3

36
Q

Systemic Manifestation of Inflammation - malaise

A

occurs due to an overwhelming inflammatory response
Achiness and low energy

37
Q

Systemic Manifestation of Inflammation - anorexia and nausea

A

Results from increased pathogens in the system as well as cellular debris

38
Q

Systemic Manifestation of Inflammation - tachycardia

A

Stems from fluid shifts from the vascular compartment to the interstitial spaces, causing decreased circulating fluid volume
Heart works harder to pump less volume

39
Q

Systemic Manifestation of Inflammation - tachypnea

A

Chemical mediators being release affect respiratory rate
Fever increases metabolism and increases respiratory rate

40
Q

Potential complication

A

Joint inflammation can impair mobility
Infection can occur in inflamed tissues
Lung inflammation limits expansion and decreases oxygen and gas exchange
Inflamed tissue increases the ability for microorganisms to enter when the skin or mucosa is damaged and the blood supply is impaired. Some microbes escape phagocytosis and the inflammatory exudate is an excellent medium for microorganisms to reproduce and colonize the inflamed area
Inflammation from musculoskeletal injuries such as sprains, tendinitis, or fractures can lead to muscle spasms
A spasm can place extra pressure on the nerves and increase pain

41
Q

RICE

A

Rest, Ice, Compression and immobilization, Elevation

42
Q

Rest

A

Aids body to use nutrients and O2 for the healing process
Repair process is facilitated due to fibrin and collagen forming across the wound

43
Q

Ice

A

First 24 is the application of ice only to decrease swelling, pain, and promote vasoconstriction
After 48 hours, alternate between heat and ice

44
Q

Compression and immobilization

A

Compression prevents edema formation due to fluid shifts
Stops bleeding
Support injured joints
Assess capillary refill to ensure compression isn’t too tight

45
Q

Elevation

A

Decrease edema
Decrease pain
May be contraindicated in patients with peripheral arterial disease

46
Q

Aspirin (Acetylsalicylic Acid)

A

Side effects- Gastrointestinal bleeding
Increased bleeding time
Other uses-Antiplatelet
Prevention of cardiac events
Antipyretic
Other info - N/A

47
Q

Acetaminophen (tylenol)

A

Side effects- Hepatotoxicity
Other uses-
-Antipyretic
-Analgesic
Other info - NA

48
Q

Non-steroid anti-inflammatory (NSAID)
Ibuprofen (motrin)
Naproxen (aleve, Anaprox)
Diclofenac (Voltaren)

A

Side effects-
Gastrointestinal bleeding
Increases bleeding time
Other uses- none
Other info - NA

49
Q

Glucocorticoids
Deltasone (prednisone)
Dexamethasone (decadron)
Methylprednisolone (solumedrol)

A

Side effects-
Hyperglycemia
Delayed wound healing
Water retention
Weight gain
Increased appetite
Suppresses the immune response
Other uses-
Prevention of organ transplant rejection
Autoimmune disease treatment
Other info -
Cautious use in patients with diabetes mellitus due to hyper-glycemic effects
Decreases capillary permeability
Enhances epinephrine and norepinephrine effects
Decreases number of leukocytes to area

50
Q

Cox-2 Inhibitors
Celecoxib (celebrex)
Valdecoxib (bextra)

A

Side effects-
Cardiac events
Gastrointestinal bleeding
Other uses-
Arthritic Pain
Other info -
Some drugs in this class have been taken off the market due to cardiovascular side effects

Patho (19 decks)

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