EXAM 1 Flashcards

1
Q

Inflammation can be ___ or ____

A

acute or chronic

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2
Q

What are the 3 stages of acute inflammation?

A
  • vascular permeability
  • cellular chemotaxis
  • systemic responses
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3
Q

exudate

A

the fluid that leaves capillaries and is a protein rich filtrate of blood that contains WBC

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4
Q

transudate

A

fluid that contains little protein and is mainly watery filtrate of blood

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5
Q

abscess

A

a localized, walled off collection of purulent exudate within tissue

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6
Q

effusion

A

any accommodation of fluid in a body cavity

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7
Q

What are the 5 cardinal signs of inflammation?

A
  • rubor (redness)
  • tumor (swelling)
  • calor (heat)
  • dolor (pain)
  • loss of function (function laesa)
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8
Q

What are cytokines?

A

Small proteins that are crucial in controlling
other immune system cells. They signal the immune system to do its job – modulate and
control it.

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9
Q

What are systemic effects of cytokines and what are labs to measure them?

A

stimulate the liver to release acute phase proteins – C REACTIVE
PROTEIN and FIBRINOGEN

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10
Q

What is considered normal WBC count?

A

4000-10000

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11
Q

What WBC count would be considered leukocytosis?

A

greater than 11000

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12
Q

What WBC count would be considered leukopenia?

A

below 2500

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13
Q

What % of our WBS are neutrophils?

A

55-70%

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14
Q

What is a shift to the left?

A
  • indicates an increase in newly formed neutrophils
  • indicates an acute inflammatory process is occurring
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15
Q

What happens during vascular permeability?

A
  • histamine, serotonin, and bradykinin dilate vessels
  • fluid, WBCs, and platelets travel to injury
  • toxins are diluted
  • WBCs phagocytize (eat) foreign matter and debris
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16
Q

What happens during cellular chemotaxis?

A
  • chemical signals attract platelets and WBCs
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17
Q

What happens during margination?

A
  • WBCs line up along the endothelium and release inflammatory mediators (cytokines, CRP, and fibrinogen)
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18
Q

Where are WBCs made?

A

bone marrow

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19
Q

macrophages

A

-help stimulate the immediate inflammatory responses and antibody mediated and cell mediated immunity. PHAGOCYTOSIS is their main job.

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20
Q

eosinophils

A

limit inflammatory reactions – so their number will increase during allergic reactions

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21
Q

lymphocytes

A
  • NK cells, B cells, T cells
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22
Q

What happens during the systemic response phase of acute inflammation?

A
  • wide spread vasodilation
  • fever
  • lymphadenopathy
  • poor appetite
  • sleepiness
  • lethargy
  • anemia
  • weight loss
  • histamine release
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23
Q

What are the 3 outcomes of inflammation?

A
  1. complete resolution
  2. healing by connective tissue
  3. chronic, persistent inflammation
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24
Q

What is the best case scenario regarding inflammation

A

complete resolution

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25
Q

How does chronic inflammation differ from acute inflammation?

A
  • predominance of monocytes, lymphocytes, and macrophages
  • granuloma formation
  • macrophages aggregate and are transformed into epithelial like cells
  • continual secretion of cytokines damages healthy tissues stimulating further inflammation
  • T and B lymphocytes amplify and perpetuate inflammatory signals
  • autoimmune disorders
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26
Q

What are the 4 components of wound healing?

A
  1. hemostasis (limit blood loss)
  2. inflammation
  3. proliferation, granulation tissue formation, angiogenesis (new blood supply), and epithelialization
  4. wound contraction and remodeling (new growth)
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27
Q

What are some factors that affect wound healing?

A
  • NUTRITION (NEED PROTEIN, CARBS, FATS)
  • blood flow and O2 delivery
  • immune strength
  • infection
  • foreign bodies (wound won’t heal or it will try to heal around it)
  • mechanical factors
  • AGE
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28
Q

What kind of wounds have a lot of tension?

A

abdominal wounds

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29
Q

wound dehiscence

A

wound opens up (surgical)
- cover with normal saline

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30
Q

wound evisceration

A

wound opens up and organs start to come out
- PT NEEDS TO GET TO OR

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31
Q

contracture

A
  • a condition of shortening and hardening of muscles, tendons, or other tissue, often leading to deformity and rigidity of joints
  • skin looks like a cup
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32
Q

fistula

A

organ or tissue connecting to another organ or tissue

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33
Q

What does immunocompetence require?

A
  • inflammatory response
  • cell mediated immunity
  • antibody immunity
34
Q

What are antigens?

A

proteins able to stimulate an immune response

35
Q

Is the innate immune system specific or nonspecific?

A

nonspecific (meaning it protects you in general)

36
Q

Is adaptive immune system specific or nonspecific?

A

specific (meaning you ACQUIRE it from somewhere)
- MEMORY RESPONSE

37
Q

What type of cells are associated with adaptive immunity?

A
  • B cells (antibody mediated)
  • T cells (cell mediated)
38
Q

Key points for antibody mediated immunity

A
  • sensitization of b cells
  • antibody production and release
  • sustained immunity
  • B cells make an antibody to fight the antigen
39
Q

key points for cell mediated immunity

A
  • no memory
  • cytokines
  • t cells fight the battle themselves
40
Q

Helper T cells

A
  • show antigen B cells
  • self vs. non self recognition
41
Q

suppressor T cells

A

regulate or suppress a overreaction of immune system

42
Q

cytotoxic t cells

A

cells that kill other cells

43
Q

Natural active immunity

A
  • longest lasting
  • in the natural world you came in contact with the antigen
  • your body actively made antibodies
44
Q

Artificial active immunity

A
  • vaccines, boosters
  • you artificially get the antigen
  • body still actively makes the antibody
  • not as long lasting but you can re up it (second booster dose etc)
45
Q

Natural passive immunity

A
  • mom to baby
  • mom’s body made the antibodies and passes them to child
  • temporary antibodies
  • gotten through placenta, breastmilk
  • when the antibody dies, baby can’t make more
46
Q

artificial passive immunity

A
  • artificially got antibody
  • immunoglobulin infusion
  • gives antibodies to ppl that are very sick
  • only lasts the life of the antibody
47
Q

anergy panel

A

taking blood to look for antibodies
- positive anergy = you are making antibodies
- negative = immunocompromised

48
Q

antibody screening and titer

A

screening= looking for something specific
titer= how much you have

49
Q

allergy testing

A
  • skin test to see what a pt is allergic to
  • want a negative result
50
Q

acronym to remember hypersensitivity

A

ACID
- Type 1: anaphylaxis (immediate/allergies)
- Type 2: cytotoxic
- Type 3: immune complex
- Type 4: delayed hypersensitivity

51
Q

What happens during type 1 hypersensitivity

A
  • hives
  • nasal drainage
  • bronchial asthma
  • inflamed intestinal tract
52
Q

what is anaphylaxis

A

inflammatory response so large the airway closes

53
Q

signs of type 2 hypersensitivity

A
  • high temp
  • may itch
  • BP changes
  • HR changes
54
Q

What is happening during type 2 hypersensitivity

A
  • IGs attack antigens on cell surface
  • antibody mediated cell lysis results
  • ex. blood transfusion reaction
55
Q

what is happening during type 3 hypersensitivity

A
  • antigen-antibody complex deposited in tissues
  • tissue damage results
  • can be systemic (lupus) or localized (RA)
  • results in constant inflammatory response
56
Q

What is happening during type 4 hypersensitivity

A
  • T CELL MEDIATED
  • previous exposure to antigen primes the T cells
  • T cell attack does not occur until days after initial exposure
    ex. poison ivy, transplant rejection
57
Q

What is occuring when you have an autoimmune disorder

A
  • the body is fighting itself
  • the cells do not know the difference between themselves and another cell
58
Q

key things about SYSTEMIC lupus erythematosus

A
  • autoimmune
  • likes kidneys and connective tissue
  • chronic
  • progressive
59
Q

how is lupus diagnosed

A

by eliminating everything else

60
Q

How is lupus treated

A
  • corticosteroids (immunosuppressants)
  • NSAIDs
  • DMARDs
61
Q

what is the first sign of a lupus exacerbation

A

fever

62
Q

what are things to monitor/look out for with lupus

A
  • cardiac health
  • weight and food intake
  • new infections
63
Q

What is RA?

A

chronic joint inflammation

64
Q

What does RA look like

A

symmetrical, tender, bilateral, swollen joints

65
Q

What is the treatment goal of RA

A

stop progression with corticosteroids

66
Q

hydrostatic pressure

A
  • PUSHING pressure
  • pushes fluid from bloodstream to cells
67
Q

osmotic/oncotic pressure

A
  • created by solutes (mostly albumin)
  • PULLS fluid back from cells into bloodstream
    ALWAYS HIGHER THAN HYDROSTATIC
68
Q

tonicity

A

how many particles are in fluid

69
Q

hypotonic solution

A

fewer particles (more water) than blood

70
Q

isotonic solution

A

same tonicity as blood

71
Q

hypertonic solution

A

more particles (less water) than blood

72
Q

What starts the RAAS system

A

kidneys want more blood because they are not perfusing

73
Q

Sequence of RAAS

A

low circulation or low bp —> sensed by kidneys —> kidneys secrete RENIN which stimulates the liver —> liver secretes angiotensinogen —> converted to angiotensin 1 in lungs —> then to angiotensin 2 —> which then stimulates adrenal glands to release ALDOSTERONE —> aldosterone increase sodium and water REABSORPTION into bloodstream and causes potassium secretion into urine

74
Q

what is the net effect of RAAS

A
  • increases blood volume
  • increases bp
75
Q

edema

A

excess of fluid in the ISF and ICF compartments

76
Q

effusion

A

any fluid that accumulates in body cavities normally free of fluid

77
Q

what are signs/symptoms of fluid volume overload

A
  • lower extremity edema
  • effusion
  • high BP
78
Q

what is another name for fluid volume deficit

A

hypovolemia

79
Q

signs/symptoms of hypovolemia

A
  • thirst
  • dry mouth
  • tachycardia
  • hypotension
  • headache
  • dry skin
  • poor skin turgor
  • decreased urination
80
Q

what is the gold standard of assessing fluid balance

A

daily weight

81
Q

other ways to assess fluid balance

A
  • 24 hr I&O
  • vital signs: HR, BP, hypotension
  • assess mucous membranes and skin turgor
  • urine output
  • edema