Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
inflammation
pathophysiology NUR 304
| Question | Answer |
|---|---|
| What is inflammation? | the body's response to injury |
| What does the immune system mediate? | inflammatory response |
| What is the purpose of inflammatory response? | contain and destroy antigen with macrophages and lymphocytes, prevent further damage to the tissue by diluting toxins released by antigen, prevent spread of infection by it off, and heal the injury |
| What is always present with infection? | inflammation |
| Is infection always present with inflammation? | no |
| Define acute inflammation | resolves when the invader is eradicated, it is a rapid response to injury, enhances healing, and self limiting |
| What triggers acute inflammation? | infection, toxins, physical injury, surgery, cancer, chemicals, tissue necrosis, foreign bodies, and immune reactions |
| Define chronic inflammation | persistent inflammation, reaction persists > 2 weeks, inhibits healing, causes continual cellular damage leading to organ dysfunction, elevated lymphocytes, macrophages, and monocytes, may be a gradual independent process |
| What is another name for white blood cells? | leukocytes |
| How are leukocytes measured? | with a complete blood count |
| How do you know the specific type of leukocytes? | with a complete blood count test and a differential test |
| What are the different kinds of WBCs? | neutrophils, monocytes, lymphocytes, basophils, and eosinophils |
| Define neutophils | the most common types of leukocyte, the "first responders", they are released within the first 24-48 hours, responds to bacteria, there are two types: bands/stabs and segs |
| Define bands/stabs | immature neutrophils that are released when segs run out |
| Define segs | mature neutophil |
| Define basophils | responds to allergic reactions and autoimmune exacerbations |
| Define monocytes | released 48 hours after injury, longer life span, and differentiate into macrophages and dendritic cells aka the "pac-man" because they consume the invader |
| Define eosinophils | responds to parasites, allergic reactions, and chronic disease exacerbations |
| Define lymphocytes | immune system cells that are elevated in response to a virus |
| What are the types of lymphocytes? | T cells, B cells, and NK cells |
| Define T cell lymphocytes | helper T cells: produces cytokines cytotoxic T cells: recognize antigens the body has previously had and release enzymes to destroy it |
| Define cytokines | a protein that affects the immune system |
| Define NK cells | natural killer cells, aka humoral immunity that kills tumor cells and virus infected cells without prior exposure, activated cell apoptosis |
| Define phagocytosis | When WBCs travel to site of injury, they surround and consume the foreign invaders which produces additional fluid surrounding the tissue (purulent exudate and transudate) |
| What is purulent exudate? | aka pus, fluid that is rich in proteins from WBCs, microbial organisms and cellular debris, occurs in infected wounds, has a creamy color and possible odor |
| What is transudate? | watery fluid with little WBCs proteins present, occurs with non-infected injuries like blisters |
| What are the cardinal signs of inflammation? | erythema, edema, loss of function, pain, heat |
| What are the stages of inflammation? | vascular permeability, cellular chemotaxis, and system responses |
| Explain vascular permeability stage of inflammation | where mediators dilate blood vessels and increase permeability, permets WBCs, fluids, & platelets to site of injury, increased vasodilation of arterioles leads to flow of fluid to injury site, increased fluid to dilute toxins, and area becomes swollen |
| Explain cellular chemotaxis stage of inflammation | a chemical signal from microbes, endothelial cells, & WBCs attracting platelets & other WBCs to the site of injury, margination happens; WBCs surround the injury & releases mediators, cytokines amplifies or deactivates the reaction, and then increases WBC |
| Explain systemic response of inflammation | doesnt always occur, but w/ bad injuries, histamine releases which is stimed by the injury & other mediators, vasoconstriction, & increased permeability occurs, prostaglandins from WBCs stim hypothalamus to reset core temp (fever), & lymph nodes enlarge |
| What are some widespread symptoms of the body's inflammatory response to injury? | fever, pain, lymphadenopathy, anorexia, fatigue, lethargy, anemia, and weightloss |
| What are the outcomes of acute inflammation? | complete resolution, healing by connective tissue replacement (scar tissue)(can happen internally too), and the progression of tissue response to chronic inflammation |
| What are some diseases that can have evidence of chronic inflammation? | chronic exposure of injuries, chronic inflammatory conditions like asthma, autoimmune disorders, microorganisms like tuberculosis, syphilis, and other viruses, bacteria, parasites, or fungus |
| Define granuloma | area where macrophages have aggregated and transformed into epithelioid cells (large pocket of scar tissue) |
| What are some common causes of inflammation? | trauma, burns, electrical injury, chemical injury, radiation damage, infection, allergic response, and foreign bodies |
| What is a CBC without differential lab? | a lab test that tracts WBCs, RBCs, and platelets, the differential is necessary to identify probable cause |
| What is a C-reactive protein lab? | a lab test that is a marker for inflammation, if the results are elevated, then it indicates a non-specific inflammatory response |
| What erythrocyte sedimentation rate (ESR) lab? | a lab test that measures how quickly erythrocytes (RBCs) settle at the bottom of a test tube. normally RBCs settle slowly. a faster than normal rate may indicate inflammation in the body |
| What do antibody lab tests identify? | various antibodies that indicate inflammation and various disease processes |
| Define rheumatoid arthritis (RA) | a chronic, systematic, and progressive autoimmune disorder in which the synovium of joints deteriorate BILATERALLY |
| What is the cause of RA? | unknown, but multifactorial with strong genetic predispositions |
| What is RA characterized by? | inflammation |
| What are the three processes of RA? | neutrophils & other cells in the synovial fluid are activated, inflammatory cytokines induce enzymatic breakdown of cartilage & bone, t-cells convert synovium to a thick abnormal layer of pannus |
| Define pannus | granulation tissue |
| What are some symptoms seen with the gradual onset of RA? | usually the S/S are vague or not apparent, and not many diagnoses are made at this stage inflammation, fever, fatigue, weakness, anorexia, weight loss, general aching, & STIFFNESS IN THE MORNING |
| What are some symptoms seen as RA progresses? | inflamed joints, pain, tenderness, stiffness, decreased ROM, warmth, redness, edema, and BOGGY AND SPONGY JOINTS ON PALPATION |
| What are some symptoms seen in the late stages of RA? | joint deformities, ulnar deviation of the fingers, swan neck deformity, boutonniere deformity, rheumatoid nodules in elbows, hands, forearms, and toes |
| Define swan neck deformity | deformity of the proximal interphalangeal joint |
| Define boutonniere deformity | deformity caused by an extension of the distal interphalangeal joint |
| What symptoms of RA seen outside of the joints? | vasculitis, pericarditis, and splenomegaly |
| How is RA diagnosed? | a presence of autoantibodies: anti citrullinated peptide antibody (ACPA) or rheumatoid factor (RF) |
| Is there a cure for RA? | no |
| How is RA treated? | early treatment with disease modifying antirheumatic drugs |
| Define cirrhosis | irreversible inflammatory fibrotic liver disease |
| What is the pathophysiology of cirrhosis? | liver cells are replaced w/fibrous tissue leading to inadequate liver function, portal vein is shunted from liver (portal htn), regeneration process is disrupted, liver takes on a cobbly appearance, liver becomes larger or smaller & hard to palpate |
| What is the disease progression of cirrhosis? | healthy liver -> fatty liver -> liver fibrosis -> cirrhosis |
| What are some causes of cirrhosis? | alcohol abuse, obesity with metabolic syndrome, viral & parasitic infection , biliary cirrhosis, hep A,B, & C, nonalcoholic steatohepatitis (NASH) fatty liver disease, autoimmune disorders, HF, cystic fibrosis, A1AT deficiency, metabolic disorders |
| Define biliary cirrhosis | blocked bile ducts; from gallstones. not reversible, but stops progression |
| What are some CM of cirrhosis? | fatigue, easy bruising & bleeding, esophageal varices, jaundice, pruritus, lethargy, dyspnea, asterixis, nausea, loss of appetite, weight loss, edema in lower extremities, spider nevi, red palms, confusion, slurred speech, ascites, caput medusa |
| Define esophageal varices | enlarged veins in the esophagus |
| Defune asterixis | muscle tremors causing downward flap of hand when arm is extended |
| Define spider nevi | spider like blood vessels on the skin |
| Define ascites | fluid accumulation on the abdomen |
| Define caput medusa | blue veins on the abdomen from increased pressure |
| How do we diagnose cirrhosis? | liver biopsy, low vitamin K, elevated ammonia levels, ultrasound, elevated prothrombin time, hypoalbuminemia, transient elastography (firbo-scan) |
| How do we treat cirrhosis? | no cure, look towards prevention, lifestyle changes, watch meds ingested, hepatitis vaccines, LOW NA+ DIET FOR FLUID RETENTION, treat encephalopathy from raised ammonia level, paracentesis to remove excess fluid |
| What is the gold standard disease confirmation for cirrhosis? | liver biopsy |
Created by:
keiondraharden
Popular Nursing sets