EXAM 1 Flashcards
Inflammation can be ___ or ____
acute or chronic
What are the 3 stages of acute inflammation?
- vascular permeability
- cellular chemotaxis
- systemic responses
exudate
the fluid that leaves capillaries and is a protein rich filtrate of blood that contains WBC
transudate
fluid that contains little protein and is mainly watery filtrate of blood
abscess
a localized, walled off collection of purulent exudate within tissue
effusion
any accommodation of fluid in a body cavity
What are the 5 cardinal signs of inflammation?
- rubor (redness)
- tumor (swelling)
- calor (heat)
- dolor (pain)
- loss of function (function laesa)
What are cytokines?
Small proteins that are crucial in controlling
other immune system cells. They signal the immune system to do its job – modulate and
control it.
What are systemic effects of cytokines and what are labs to measure them?
stimulate the liver to release acute phase proteins – C REACTIVE
PROTEIN and FIBRINOGEN
What is considered normal WBC count?
4000-10000
What WBC count would be considered leukocytosis?
greater than 11000
What WBC count would be considered leukopenia?
below 2500
What % of our WBS are neutrophils?
55-70%
What is a shift to the left?
- indicates an increase in newly formed neutrophils
- indicates an acute inflammatory process is occurring
What happens during vascular permeability?
- histamine, serotonin, and bradykinin dilate vessels
- fluid, WBCs, and platelets travel to injury
- toxins are diluted
- WBCs phagocytize (eat) foreign matter and debris
What happens during cellular chemotaxis?
- chemical signals attract platelets and WBCs
What happens during margination?
- WBCs line up along the endothelium and release inflammatory mediators (cytokines, CRP, and fibrinogen)
Where are WBCs made?
bone marrow
macrophages
-help stimulate the immediate inflammatory responses and antibody mediated and cell mediated immunity. PHAGOCYTOSIS is their main job.
eosinophils
limit inflammatory reactions – so their number will increase during allergic reactions
lymphocytes
- NK cells, B cells, T cells
What happens during the systemic response phase of acute inflammation?
- wide spread vasodilation
- fever
- lymphadenopathy
- poor appetite
- sleepiness
- lethargy
- anemia
- weight loss
- histamine release
What are the 3 outcomes of inflammation?
- complete resolution
- healing by connective tissue
- chronic, persistent inflammation
What is the best case scenario regarding inflammation
complete resolution
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
What are the 4 components of wound healing?
- hemostasis (limit blood loss)
- inflammation
- proliferation, granulation tissue formation, angiogenesis (new blood supply), and epithelialization
- wound contraction and remodeling (new growth)
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
What kind of wounds have a lot of tension?
abdominal wounds
wound dehiscence
wound opens up (surgical)
- cover with normal saline
wound evisceration
wound opens up and organs start to come out
- PT NEEDS TO GET TO OR
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
fistula
organ or tissue connecting to another organ or tissue
What does immunocompetence require?
- inflammatory response
- cell mediated immunity
- antibody immunity
What are antigens?
proteins able to stimulate an immune response
Is the innate immune system specific or nonspecific?
nonspecific (meaning it protects you in general)
Is adaptive immune system specific or nonspecific?
specific (meaning you ACQUIRE it from somewhere)
- MEMORY RESPONSE
What type of cells are associated with adaptive immunity?
- B cells (antibody mediated)
- T cells (cell mediated)
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
key points for cell mediated immunity
- no memory
- cytokines
- t cells fight the battle themselves
Helper T cells
- show antigen B cells
- self vs. non self recognition
suppressor T cells
regulate or suppress a overreaction of immune system
cytotoxic t cells
cells that kill other cells
Natural active immunity
- longest lasting
- in the natural world you came in contact with the antigen
- your body actively made antibodies
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)
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
artificial passive immunity
- artificially got antibody
- immunoglobulin infusion
- gives antibodies to ppl that are very sick
- only lasts the life of the antibody
anergy panel
taking blood to look for antibodies
- positive anergy = you are making antibodies
- negative = immunocompromised
antibody screening and titer
screening= looking for something specific
titer= how much you have
allergy testing
- skin test to see what a pt is allergic to
- want a negative result
acronym to remember hypersensitivity
ACID
- Type 1: anaphylaxis (immediate/allergies)
- Type 2: cytotoxic
- Type 3: immune complex
- Type 4: delayed hypersensitivity
What happens during type 1 hypersensitivity
- hives
- nasal drainage
- bronchial asthma
- inflamed intestinal tract
what is anaphylaxis
inflammatory response so large the airway closes
signs of type 2 hypersensitivity
- high temp
- may itch
- BP changes
- HR changes
What is happening during type 2 hypersensitivity
- IGs attack antigens on cell surface
- antibody mediated cell lysis results
- ex. blood transfusion reaction
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
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
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
key things about SYSTEMIC lupus erythematosus
- autoimmune
- likes kidneys and connective tissue
- chronic
- progressive
how is lupus diagnosed
by eliminating everything else
How is lupus treated
- corticosteroids (immunosuppressants)
- NSAIDs
- DMARDs
what is the first sign of a lupus exacerbation
fever
what are things to monitor/look out for with lupus
- cardiac health
- weight and food intake
- new infections
What is RA?
chronic joint inflammation
What does RA look like
symmetrical, tender, bilateral, swollen joints
What is the treatment goal of RA
stop progression with corticosteroids
hydrostatic pressure
- PUSHING pressure
- pushes fluid from bloodstream to cells
osmotic/oncotic pressure
- created by solutes (mostly albumin)
- PULLS fluid back from cells into bloodstream
ALWAYS HIGHER THAN HYDROSTATIC
tonicity
how many particles are in fluid
hypotonic solution
fewer particles (more water) than blood
isotonic solution
same tonicity as blood
hypertonic solution
more particles (less water) than blood
What starts the RAAS system
kidneys want more blood because they are not perfusing
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
what is the net effect of RAAS
- increases blood volume
- increases bp
edema
excess of fluid in the ISF and ICF compartments
effusion
any fluid that accumulates in body cavities normally free of fluid
what are signs/symptoms of fluid volume overload
- lower extremity edema
- effusion
- high BP
what is another name for fluid volume deficit
hypovolemia
signs/symptoms of hypovolemia
- thirst
- dry mouth
- tachycardia
- hypotension
- headache
- dry skin
- poor skin turgor
- decreased urination
what is the gold standard of assessing fluid balance
daily weight
other ways to assess fluid balance
- 24 hr I&O
- vital signs: HR, BP, hypotension
- assess mucous membranes and skin turgor
- urine output
- edema
