EXAM 1 Flashcards
(81 cards)
1
Q
Inflammation can be ___ or ____
A
acute or chronic
2
Q
What are the 3 stages of acute inflammation?
A
- vascular permeability
- cellular chemotaxis
- systemic responses
3
Q
exudate
A
the fluid that leaves capillaries and is a protein rich filtrate of blood that contains WBC
4
Q
transudate
A
fluid that contains little protein and is mainly watery filtrate of blood
5
Q
abscess
A
a localized, walled off collection of purulent exudate within tissue
6
Q
effusion
A
any accommodation of fluid in a body cavity
7
Q
What are the 5 cardinal signs of inflammation?
A
- rubor (redness)
- tumor (swelling)
- calor (heat)
- dolor (pain)
- loss of function (function laesa)
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.
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
10
Q
What is considered normal WBC count?
A
4000-10000
11
Q
What WBC count would be considered leukocytosis?
A
greater than 11000
12
Q
What WBC count would be considered leukopenia?
A
below 2500
13
Q
What % of our WBS are neutrophils?
A
55-70%
14
Q
What is a shift to the left?
A
- indicates an increase in newly formed neutrophils
- indicates an acute inflammatory process is occurring
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
16
Q
What happens during cellular chemotaxis?
A
- chemical signals attract platelets and WBCs
17
Q
What happens during margination?
A
- WBCs line up along the endothelium and release inflammatory mediators (cytokines, CRP, and fibrinogen)
18
Q
Where are WBCs made?
A
bone marrow
19
Q
macrophages
A
-help stimulate the immediate inflammatory responses and antibody mediated and cell mediated immunity. PHAGOCYTOSIS is their main job.
20
Q
eosinophils
A
limit inflammatory reactions – so their number will increase during allergic reactions
21
Q
lymphocytes
A
- NK cells, B cells, T cells
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
23
Q
What are the 3 outcomes of inflammation?
A
- complete resolution
- healing by connective tissue
- chronic, persistent inflammation
24
Q
What is the best case scenario regarding inflammation
A
complete resolution
25
How does chronic inflammation differ from acute inflammation?
- 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
26
What are the 4 components of wound healing?
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)
27
What are some factors that affect wound healing?
- 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
28
What kind of wounds have a lot of tension?
abdominal wounds
29
wound dehiscence
wound opens up (surgical)
- cover with normal saline
30
wound evisceration
wound opens up and organs start to come out
- PT NEEDS TO GET TO OR
31
contracture
- 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
32
fistula
organ or tissue connecting to another organ or tissue
33
What does immunocompetence require?
- inflammatory response
- cell mediated immunity
- antibody immunity
34
What are antigens?
proteins able to stimulate an immune response
35
Is the innate immune system specific or nonspecific?
nonspecific (meaning it protects you in general)
36
Is adaptive immune system specific or nonspecific?
specific (meaning you ACQUIRE it from somewhere)
- MEMORY RESPONSE
37
What type of cells are associated with adaptive immunity?
- B cells (antibody mediated)
- T cells (cell mediated)
38
Key points for antibody mediated immunity
- sensitization of b cells
- antibody production and release
- sustained immunity
- B cells make an antibody to fight the antigen
39
key points for cell mediated immunity
- no memory
- cytokines
- t cells fight the battle themselves
40
Helper T cells
- show antigen B cells
- self vs. non self recognition
41
suppressor T cells
regulate or suppress a overreaction of immune system
42
cytotoxic t cells
cells that kill other cells
43
Natural active immunity
- longest lasting
- in the natural world you came in contact with the antigen
- your body actively made antibodies
44
Artificial active immunity
- 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
Natural passive immunity
- 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
artificial passive immunity
- artificially got antibody
- immunoglobulin infusion
- gives antibodies to ppl that are very sick
- only lasts the life of the antibody
47
anergy panel
taking blood to look for antibodies
- positive anergy = you are making antibodies
- negative = immunocompromised
48
antibody screening and titer
screening= looking for something specific
titer= how much you have
49
allergy testing
- skin test to see what a pt is allergic to
- want a negative result
50
acronym to remember hypersensitivity
ACID
- Type 1: anaphylaxis (immediate/allergies)
- Type 2: cytotoxic
- Type 3: immune complex
- Type 4: delayed hypersensitivity
51
What happens during type 1 hypersensitivity
- hives
- nasal drainage
- bronchial asthma
- inflamed intestinal tract
52
what is anaphylaxis
inflammatory response so large the airway closes
53
signs of type 2 hypersensitivity
- high temp
- may itch
- BP changes
- HR changes
54
What is happening during type 2 hypersensitivity
- IGs attack antigens on cell surface
- antibody mediated cell lysis results
- ex. blood transfusion reaction
55
what is happening during type 3 hypersensitivity
- antigen-antibody complex deposited in tissues
- tissue damage results
- can be systemic (lupus) or localized (RA)
- results in constant inflammatory response
56
What is happening during type 4 hypersensitivity
- 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
What is occuring when you have an autoimmune disorder
- the body is fighting itself
- the cells do not know the difference between themselves and another cell
58
key things about SYSTEMIC lupus erythematosus
- autoimmune
- likes kidneys and connective tissue
- chronic
- progressive
59
how is lupus diagnosed
by eliminating everything else
60
How is lupus treated
- corticosteroids (immunosuppressants)
- NSAIDs
- DMARDs
61
what is the first sign of a lupus exacerbation
fever
62
what are things to monitor/look out for with lupus
- cardiac health
- weight and food intake
- new infections
63
What is RA?
chronic joint inflammation
64
What does RA look like
symmetrical, tender, bilateral, swollen joints
65
What is the treatment goal of RA
stop progression with corticosteroids
66
hydrostatic pressure
- PUSHING pressure
- pushes fluid from bloodstream to cells
67
osmotic/oncotic pressure
- created by solutes (mostly albumin)
- PULLS fluid back from cells into bloodstream
ALWAYS HIGHER THAN HYDROSTATIC
68
tonicity
how many particles are in fluid
69
hypotonic solution
fewer particles (more water) than blood
70
isotonic solution
same tonicity as blood
71
hypertonic solution
more particles (less water) than blood
72
What starts the RAAS system
kidneys want more blood because they are not perfusing
73
Sequence of RAAS
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
what is the net effect of RAAS
- increases blood volume
- increases bp
75
edema
excess of fluid in the ISF and ICF compartments
76
effusion
any fluid that accumulates in body cavities normally free of fluid
77
what are signs/symptoms of fluid volume overload
- lower extremity edema
- effusion
- high BP
78
what is another name for fluid volume deficit
hypovolemia
79
signs/symptoms of hypovolemia
- thirst
- dry mouth
- tachycardia
- hypotension
- headache
- dry skin
- poor skin turgor
- decreased urination
80
what is the gold standard of assessing fluid balance
daily weight
81
other ways to assess fluid balance
- 24 hr I&O
- vital signs: HR, BP, hypotension
- assess mucous membranes and skin turgor
- urine output
- edema
