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Med Surg Exam 2
| Question | Answer |
|---|---|
| What is pain?! | Most universal/personal symptom. No one person experience pain like any other. |
| What are some types of pain? | Chronic, Acute, Neuropathic, Persistent, and Breakthrough. |
| What are some pain characteristics? | •cutaneous •somatic •visceral •neuropathic |
| Cutaneous | (superficial skin/tissues): “tender/sharp/itchy” that last short hours to days. (Sunburn/Minor Scrapes) |
| Somatic | (deeper tissue/joint/bones): “dull/achy/cramping/sore/stabbing” that can be short or very long. |
| Visceral | (hollow organ pain): “cramping/achy/dull/pressure” that can be short or long. (Myocardial pain/appendicitis) |
| Neuropathic | (peripheral/central nervous system): “numbness/tingling/shooting/burning/pins and needles” that lasts months to years. (Diabetic neuropathy/carpal tunnel) |
| What is acute pain? | Short duration (Hours/Weeks). Sudden/Immediate Onset (Tissue Injury/Damage). Responds to common pain management. Able to predict the outcome as it progresses/heals. |
| What is chronic pain? | Long duration. (Months/Years). Affects ADL’s (work/sleep/eat/social). Inconsistent response to common and other pain management strategies. Inconsistent it comes/goes over time. |
| Name of the pain scale? | 0-10, Wong Baker (Children/Impaired Adults), Descriptive Scale, Visual Scale |
| What is osteoarthritis? | Affects weight-bearing joints. (Knees/Hips/Feet/Spine/Hands) Unilateral (One Sided) *Patients hands may have Bouchard/Herden's nodes.* |
| Factors for osteoarthritis? | age/female sex/obesity/occupation (repetitive motion like carpentry) |
| Diagnosis of osteoarthritis? | based on clinical manifestations or radiograph. Patients 45 or older. |
| Clinical manifestations of osteoarthritis? | progressive pain over time/decreased range of motion/tenderness to touch over joint/bony and soft tissue swelling/deformity. |
| Treatment for osteoarthritis? | pharmacological/non-pharmacological therapies. Nonpharmacological Therapy is weight loss, heat/cold compresses, PT/OT, assistive devices for ADL’s. |
| Pharmacological treatment for osteoarthritis? | Tylenol/NSAIDS/Opioid Analgesics/Corticosteroids. |
| NSAID warnings? | may cause increased risk of MI, stroke, renal insufficiency. GI adverse effect such as bleeding, ulceration, and perforation. Contraindicated in patients with renal failure. |
| What to monitor for corticosteroids? | Monitor the glucose level as this medication can temporarily increase the blood glucose. Use this in conjunction with oral medications. |
| What to monitor for Tylenol? | Monitor for hepatic toxicity. (Especially with Alcoholics). |
| What to monitor for Nonacetylated Salicylate? | use as alternative to NSAID/monitor for ototoxicity. |
| What to monitor for Opioid Analgesics? | Use for moderate/severe pain. Monitor for nausea/constipation/confusion/drowsiness and respiratory depression. *Potential for addiction* |
| What is Rheumatoid Arthritis? | Autoimmune Inflammatory Disease. Affects freely moving joints like wrist/ankles/knees. Bilateral (Both Sided) |
| Labs for rheumatoid arthritis? | CRP/ESR, Hg, Albumin, Platelet, ALT/AST |
| Clinical manifestations for rheumatoid arthritis? | joint pain/swelling. Morning stiffness/fatigue. Inflammation of synovial membrane. (Synovitis) Patient’s fingers will have swan-neck deformity/ulnar deviation. |
| Diagnosis for rheumatoid arthritis? | Laboratory/radiograph/ultrasound. Treatment is pharmacological (Analgesics/NSAIDS/glucocorticoids)/non-pharmacological therapies (ROM, PT/OT) |
| Methotrexate Warning? | monitor for hepatic toxicology, take folic acid to prevent oral ulcers, renal insufficiency can have low dose. |
| What Is Lupus? | Chronic Inflammatory Disease that affect any organ system. Triggers are pregnancy/sunlight/illness/major surgery. |
| Diagnosis for lupus? | Clinical Manifestations (skin rash/oral ulcers/thinning hair/joint tenderness/renal urine protein. |
| Clinical manifestations of lupus? | Skin: Malar or “Butterfly Rash” on face/alopecia/photosensitivity/oral or nasal ulcers. Renal: nephritis/hematuria/proteinuria. Neuro: Stroke/Seizures/Neuropathy/Psychosis. Cardio: pericarditis/increased CVD/endocarditis. |
| Treatment for lupus? | Nonpharmacological (avoid sun, well-balanced diet, frequent rest periods, regular sleep/exercise.) Pharmacological (Antimalarial like hydroxychloroquine) |
| Diagnostic for Lupus? | Radiograph/Ultrasound/Echocardiogram/Tomography/MRI |
| What is gout? | Disease where crystals are deposited into joints/bone/soft tissue. Chronic Tophaceous Gout: repeated attack of years leading to production of uric acid in joint. 80% of patients present with first attack to LE metatarsophalangeal joint (toe). |
| Treatment for gout? | Nonpharmacological (weight management/splinting of affected joint. Pharmacological (NSAIDS/ glucorticosteroids). *Although Aspirin is an NSAID, it should be avoided because it can/will produce more uric acid.* |
| Labs for gout? | Serum Uric Acid Level |
| Meds for gout? | analgesics/anti- inflammatory/glucorticoid |
| What is Fibromyalgia? | Chronic pain disorder of soft connective tissues. Common between women 20-55. Commonly found in patients with RA and Lupus. |
| Diagnosis for fibromyalgia? | History/Physical Assessment |
| Treatment for fibromyalgia? | Nonpharmacological (PT/minimizing stress/exercise/adequate sleep.) Pharmacological (Serotonin/Norepinephrine. Opioids). |
| Meds for fibromyalgia? | Nonsteroidal anti- inflammatory/anti-depressants/anti- seizures |
| What is innate (natural) immunity? | Provides the first/second lines of defense. |
| What is adaptive (acquired) immunity? | Natural exposure (infection/maternal antibodies/vaccines) |
| What is Inflammatory Response? | Second Line (inflammatory response that occur due to tissue damage such as a break in the skin) Inflammation is to prevent/limit infection. |
| What is Primary Immune Dysfunction? | Occurs with individuals that are born with deficient immune system. (Intrinsic) is inborn, congenital/genetic cause. Primary immunodeficiencies result in defective T/B lymphocytes. B cells produce humoral immune response, which is antibody response. |
| What is DiGeorge’s Syndrome? | “CATCH” Cardiac Abnormality, Abnormal Face, Thyme Aplasia, Cleft Palate, Hypocalcemia- hypoparathyroidism |
| What is Secondary Immune Dysfunction? | Acquired Immune Deficiency occurs when damage is cause by extrinsic/external environment. Example: HIV, Irradiation, Malnutrition, Chemo |
| What is Type 1 Hypersensitivity (Immediate)? | Rapid/immediate allergic reaction. (Allergic Rhinitis/Hay Fever) Runny nose/sneezing.) |
| Patho of type 1 hypersensitivity? | primarily immunoglobulin (E) *Anaphylaxis is most severe form of Type 1 hypersensitivity* For anaphylaxis monitor respiratory/skin reactions. |
| Diagnosis for type 1 hypersensitivity? | WBC, Eosinophils, Skin Test |
| Type 2 Hypersensitivity (Cytotoxic) | Three subtypes. |
| Sub-1: Complement and Antibody Medicated Cell Destruction Hypersensitivity | (cytotoxic/antibody dependent) Function not working (susceptible to autoimmune disease) Antibodies are (immunoglobulin M/G) |
| Sub-2: Complement and Antibody-Medicated Inflammation | Causes inflammation not destruction. ‘Goodpasture’s Syndrome” which is an autoimmune disease triggered when immune system attacks goodpastures antigen in the glomerular membrane. |
| Sub-3: Antibody-Mediated Cellular Dysfunction | Antibodies bind to cell-surface. Example: Myasthenia Gravis where the autoantibodies bind to acetylcholine receptors. Decreased neuromuscular function/weakness. |
| Type 3 Hypersensitivity (Immune Complex) | Immune Complex-Mediated Reactions Formation of antigen-antibody complexes (RA, Lupus, Serum Sickness) Serum Sickness: develops 7-12 days after exposure, occurs when body mistakes protein for antiserum. |
| Type 4 Hypersensitivity (Delayed) | Example: Poison Ivy, TB Test, Latex Allery. |
| Where are T-cells formed? | Formed in Bone Marrow/Mature in Thymus. |
| What do T cells (cellular) do? | “Adaptive/Cellular Mediated Response” -Eliminate cells infected by pathogens and continue to activate the inflammatory response against infection. |
| Where are B-Cells (Humoral) formed? | Formed/Mature in bone marrow. |
| What do B cells do? | “Adaptive/Humoral Mediated Response” Subset of lymphocytes that mature in bone marrow/produce antibodies or immunoglobulins. |
| Types of transmission? | Contact, airborne, vehicle, and vector. |
| Contact transmission? | occur when person/object comes in contact with pathogen |
| Airborne transmission? | Occur when pathogen are carried through air |
| Vehicle transmission? | Indirect mode of transmission, occurs when disease-carrying agent touches body/ingested |
| Vector transmission? | Indirect transmission, occurs when organism (bug) bites/infects person. |
| What is MRSA | “ Methicillin-Resistant Staphylococcus Aureus” Gram+ Found in environment/people. Easily transferred to skin/other body areas. Resistant to antibiotics. Minor Skin Infections: pimples/abcesses/impetigo Serious: PNA/skin and soft tissue |
| Meds for MRSA | IV vanco |
| Precautions for MRSA? | Contact precautions. |
| What is Vancomycin-Resistant Enterococci (VRE)? | Bacteria that live in GI tract/female peri tract. Resistant to antimicrobial agents/emergence of vancomycin-resistant-s. Aureus. |
| What is CDIFF? | Increased ABT usage. Gram+ spore forming anaerobic bacillus, transmitted oral-fecal route. Lives month on surfaces. Oral-fecal Route. |
| Type of precaution for CDIFF? | Contact precautions. |
| HIV | Several stages (acute infection/death.) STD, usually contract through IV drug use. |
| Stage 1 HIV? | CD4+ are at least 500 cells (No AIDS) |
| Stage 2 HIV? | CD4+ are at least 200-499 (No Aids) |
| Stage 3 HIV? | CD4+ less 200 (AIDS) |
| Progression of HIV? | Viral Transmission to Acute Viral Infection (1-2 week) to Seroconversion to Asymptomatic Chronic Infection (3-10 year) to Symptomatic/AIDS to Death. |
| Clinical manifestations of HIV? | S/S are fever, cough, weakness, night sweats, enlarge lymph nodes, cough. |
| AIDS | *Kaposi Sarcoma* CD4+ continues to fall and immune system is not able to fight infection. Most die from opportunistic infections. *Pneumocystis pneumonia, Mycobacterium avium complex* |
| WHO’S GOING TO PASS THIS EXAM | MEEEE!!😍 |
Created by:
rosuna
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