Final Exam
Quiz yourself by thinking what should be in
each of the black spaces below before clicking
on it to display the answer.
Help!
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| Primary Prevention | - Health promotion, risk asst and management, and disease prevention
ex: exercise, nutrition, immunizations, wear seat belt
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| Secondary Prevention | -Behaviors that promote early detection of disease
ex: mammogram, dental exam, physical, eye or ear exam
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| Tertiary Prevention | - Activities related to rehabilitation after disease is diagnosed
ex: Breast reconstruction after mastectomy, rehab
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| Tumor | A mass or swelling
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| Neoplasm | Abnormal mass, no useful purpose
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| Benign neoplasm | -Harmless growth
-no spreading
-Can put pressure on surrounding organs
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| Malignant Neoplasm | -Harmful mass
-Can spread to organs and adjacent tissue
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| Cancer | -Ability to proliferate cells is altered
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| Adenocarcinoma | -Glandular tissue
-Ex: Breast, lung, thyroid, and pancreas
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| Carcinogens | -Tobacco,asbestos,coal tar,soot (lung)
-Smoked,salty,pickled food (oral,stom)
-Fumes,alcoholism(stom,colon)
-Benzene,ethylene oxide (leukemia)
-Prolonged UV rays (melanoma, basal cell)
-Alcohol (liver)
-Viruses(stom,bladder, liver,lymphoma)
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| 4 Causative Agents | -Radiation
-Chemicals
-Viruses (HPV, Hep B & C, H.Pylori)
-Physical Agents
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| Cell Cycle Phases | -G0-At rest from cell division, longest phase
-G1-RNA synthesis, variable phase,happens different amount of time in cells
-S-DNA synthesis,High number = poor prognosis
- G2-Prep for mitosis, make more RNA, short phase
- M-cell division,mitosis
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| Malignant Cell Characteristics | -Loss of control of Mitosis
-Decrease Specialization
-Decrease cell boundary respect
-Almost immortal
-Irreversibility
-Altered cell structure
-Transplantability
-Ability to create protective structures to support own survival
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| Neoplasm, Tissue of Origin | -Fibroma - benign fibrous tissue often in uterus, can grow to the size of a 9 mo pregnancy
-Lipoma-benign fat tumors
-Leiomyoma-benign tumor of smooth muscle
-Sarcoma-malignant tumor of connective tissue,cartilage,bone
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| TNM staging of tumors | T-graded 0-4, primary tumor size
N-graded 0-3, regional lymph nodes
M-graded 0-3, metastasis
-Angiogenesis - ability of tumor cells to secrete substance that stimulates blood vessel growth
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| Radiation Therapy | -60% of pts
-Targets rapidly multiplying cells but kills other cells within it's
path
-Primary tx = cure
-Adjuvant
-Palliative
-Goal - control tumor growth size
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| How Radiation Works | -Cell radiosensitivity
-Damages DNA, cell can't reproduce
-Damages all cells w/in field (normal cells can repair themselves)
-Not dependent on cell cycle
-O2 free radicals are formed -interact with surrounding tissue causing cell damage
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| Nursing Interventions:Radiation Therapy | -Keep skin dry
-Use warm/cool water,mild soap only
-Ink marks
-Avoid powder,lotions,deodorant on radiated skin
-Avoid clothing friction
-Use electric razor only
-Protect from sun exposure,and chlorinated pool
-Control D if pelvic radiation
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| Side effects of Radiation | -Skin reaction - mild redness to 3rd degree skin reaction
-Fatigue
-Site specific:mucositis, xerostomia,esophagitis,dysphagia, alopecia,bone marrow suppression
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| Chemotherapy | -IV
-Cure,control,or palliation
-Use when: disease is widespread, not localized, risk of hidden disease is high, tumor can't be resected d/t location or size, tumor is resistant to radiation therapy
-Adjuvant chemo
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| How Chemo Works | -Diff drugs target diff cell phases
-Generally need more than one exposure to effect death of all cancer cells
-Drugs used in comb0,or w/ radiation
-Classification according to effect on cell cycle some are cell-cycle specific, some not
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| Nursing Care during Chemotherapy | -Alopecia
-GI effects
-Anorexia
-Stomatitis
-Pain
-Mylelosupression
-All effects are related to rapidly reproducing cell destruction
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| Pain | -From tumor pressure or V
-From extravasation of chemo (apply ice immediately, stop IV fluid, leave needle in, aspirate any drug)
-Antihistamine - antidote
-Liberal analgesics - If the patient says they have pain, they have pain
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| Neutropenia | -Seen 7-14 days after chemo
-Increased potential for infection
-Protective isolation - limit visitors
-Steroids used for tx add to infection potential - inhibit immune system
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| Nursing Interventions and Neutropenia | - Good hand washing
-Frequent oral care
-Don't share eating utensils
-Fevers - treated as emergency
-Avoid ppl w/ infections
-Avoid animal feces
-Avoid fresh flowers
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| Anemia | -Blood loss
-Altered hemoglobin
-Altered hematocrit
-fatigue,dizziness,dyspnea, tachycardia
-Blood transfusion, packed red cells
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| Thrombocytopenia Interventions | -Shave w/electric razor
-Prevent dry cracked skin
-Good oral care
-Avoid C,enemas,rectal temps
-Pressure on bleeding for 10 min
-Avoid IM,SQ
-Watch for tarry stools,blood in urine
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| Thrombocytopenia Interventions | -Watch for petechia
-Watch for change in LOC,early sign of intracranial bleeding
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| Phases of Wound Healing | -Vascular Response (immediate)
-Inflammation
-Proliferation or Resolution
-Maturation or Reconstruction
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| Vascular Response | -Immediate after an injury
-Constriction - w/in seconds after you are injured,to control bleeding,reduce bacterial entry
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| Vascular Response:Clotting | -Platelets: stick together to control bleeding initially
-Fibrin: cause clot to form
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| Vascular Response: Capillary Dilation | -15 minutes after injury
-Allow plasma to flow into area and dilute any toxins that may be present
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| Inflammation Phase | -Begins the moment of the injury
-May extend 4-6 days
-Limits the effect of pathogens
-Fibrinogen
-WBCs (neutrophils begin phagocytosis, macrophages mature monocytes, eosinophils/basophils
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| Bacterial Infection | -Leukocytosis: > 10,000
-Neutrophils - 1st line of defense
-Segs respond immediately
-Bands also respond (major infection)
-Total lymphocytes maybe normal range
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| Primary Intention | -Use of stitches or sutures to close
-Little scarring
-Low infection
-Usually occurs through collagen synthesis
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| Secondary Intention | -Wound left open to heal
-Longer (inflammation, proliferation,maturation)
-Ex: Pressure Ulcer
-May need skin or muscle flap
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| Tertiary Intention | -Infections
-Wound left open
-Ex: wound dehiscence (wound that has burst open)
-Contaminated, high risk of infection
-Promote healing from inside out
-Wound vacs
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| Intrinsic Factors | -Infection:Prolong inflammation process
-Foreign Body
-Inadequate blood supply(CVD,less fibroblast,need good arterial flow for healing)
-SMOKING-vasoconstriction, decrease 02,increase CO
-Neuropathy-Can't feel area around injury, inadeaquate bf to are
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| Extrinsic Factors | -Malnutrition (protein, vit C, carbs)
-Diabetes - suppress immune system and healing
-Steroids - impair all phases of healing
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| Medical Management | -Control edema (Rest Ice Compression Elevation)
-Reduce inflammation
-Monitor systemic responses (temp-only give antipyretics for fevers over 101*, HR - increase, BP-increase, WBC-increase)
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| Incisions | -Assess ever 8h
-Heal in 3-5 days
-Asepsis
-Don't clean unless ordered
-Monitor for drainage
-Don't apply pressure
-Sutures/staples removed in 7d to 2wks
-Glue
-Drainage devices
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| Non-Opiod Analgesics | -Aspirin: not with viral infections at any age
-Salicylate salts: fewer gastric side effects
-Acetaminophen: action not known
-NSAIDS: +bone pain
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| Opiod Analgesics | -Morphine
-Codeine
-Oxycodeine
-Hydromorphone
-Meperidine
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| Adverse effects of Opiods | -Respiratory Depression
-C
-N/V
-Hypotension
-Skin effects
-Urinary retention
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| Fluid Compartments | -60% body weight composed of water in an adults - decreases with age
-Two Compartments:Intracellular-66%
Extracellular - 33%
-Interstitial Fluid (b/w cells)
-Vascular compartment (blood in veins and arteries and lymph in the lymphatic system)
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| What regulates fluid balance? | -Thirst Mechanism:Decrease w/age, regulated by menstrual cycle and aldosterone
-Kidney:From adrenal glands, promotes Na retention, water goes to ECF
-Aldosterone: causes more Na to be released
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| -Atrial natriuetic peptide/brain natriuetic peptide:from post pit., prevents diuresis&urination
-ADH:Water Regulation-alcohol inhibits ADH secretion,so nephrons in kidneys to become less permeable to water=more water leaving body could be dehydration
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| Hemodilution | -Hemodilution(Fluid overload) and dehydration affect hematocrit level in opposite directions
-Critical Values: >55% dehydration
< 35% fluid overload
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| Sodium | -Major component of ECF
-Regulation:Intake (dietary, meds)/Output, Kidneys, Hormones (Directly - aldosterone, Indirectly - ADH,BNP)
-Hyponatremia: <135 fluid overload
-Hypernatremia:>145 dehydration
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| Blood Urea Nitrogen | -Measures end-product of protein metabolism
-Regulated by: Kidneys and liver, diet-protein intake, hydration status, drugs
-Blood level - increases with age
-Elevates with dehydration and renal failure
-Creatinine: Directly reflects kidney function
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| Dehydration | -Hypovolemic "dry"
-Fluid loss (blood,sweat,urinate, vomit, D, wound drainage, nasal gastric tubes, burns)
-Shift of fluid b/w compartments
-ECF deficit for ICF deficit
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| Dehydration: Levels of Severity | -Mild: Loss of 1-2 L or 2% of body wt
-Moderate: Loss of 3-5 L or 5% of body wt
-Severe: Loss of 5-10 L or 8% body wt
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| Third Spacing | -Excess fluid in the body leaves the vascular space (blood vessels); occurs very frequently after surgery
-Gets into the tissues
-Causes swelling (edema): extremities, sacrum, peri-orbital areas
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| Fluid Volume Deficit: Subjective | -Complaints of Dizziness, feeling confused, weakness, constipation
-Caused by low BP, not enough fluid, not enough O2 or changes in Na
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| Fluid Volume Deficit: Objective | -Weight Loss**(Most accurate mst of fluid balance=accuracy of weights,1kg of weight=1 L of fluid
-Changes in vs
-Dry mucous membranes
-Changes in skin turgor
-Flattened veins
-Confusion
-I-Na,osmolality,hematocrit,BUN
-I-urine specific gravity
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| Fluid Intake | -Normal = 1500 - 2000 mL daily
-800 mL from food
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| Complications of Fluid Volume Deficit | -Cardiac Output: alteration or decreased
-Urinary Output: decreased
-Impaired mucous membranes
-Risk for injury
-Cognitive impairment
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| Output | -Should be at least 30 mL of urine per hour
-240 mL per 24h
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| Isotonic Solutions | -Normal saline (0.9%) or Lactated Rings
-Amounts of electrolytes and water are close to plasma level
-Caution: LR can alter acid-base balance, don't use in alkalotic state, don't use for liver failure
-Considered volume expander
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| Hypotonic Solutions | -5% Dextrose in water (D5W, 45% normal saline
-Used for flood losses sever intracellular dehydration
-Pushes fluid back into cells
-Fluid, no electrolytes (Dextrose is metabolized and water is left; electrolyte status can become diluted)
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| Hypertonic Solution | -D5 0.45 NACL, D5 0.22 NS, D5 0.9 NS
-Adds both water and electrolytes
-Extra solutes pull fluid from ICF back into ECF
-Good for postoperative swelling
-Food for pts with mild to moderate fluid overload
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| Hypervolemia | -Excess fluid volume
-R/T to pts in ability to control: fluid volume shift to ECF or ICF either in the vascular space, b/w cells or in cells, increased intake, decreased output, and some diseases (CHF, kidney failure, pit disease)
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| Hypervolemia AEB | -Edema
-Pulmonary congestion (hear crackles)
-Changes in vs (BP increase)
-Changes in neck veins (NVD)
-Neurologic changes (confusion d/t brain swelling)
-Decreased osmolality,hematocrit,NA and BUN
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| Hypervolemia: Diagnostic Findings | -Plasma: below 75
-Chest x ray
-Sodium: < 135
-BUN: < 8
-Hematocrit: <45
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| Cause of 3rd spacing | -Surgery
-Heart Failure (ventricles aren't able to pump or push fluid into system and so it backs up into body/lungs)
-Kidney failure - fluid can't get out
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| Hyponatremia | -Low sodium
-Very common in elderly
-Plasma volume <135
- Excessive Na loss through fluid losses such as GI losses, 3rd spacing, burns
-Not enough aldosterone from adrenal glands (addison's)
-Kidney disease
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| Hyponatremia: Assessment | -No symptoms if moderately low
-N/V/D, cramping
-Crackles (rales in lungs)
-With critically low values cause lethargy,weakness, hallucinations, seizures, and coma possibly death, hypotension
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| Hypernatremia: Assessment | -Confusion
-N/V
-Restless, agitated
-Seizures
-Coma
-Respiratory paralysis
-death
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| Nursing Interventions: Hyponatremia | -Fluid Restriction <1500 per 24 h
-High Na foods
-IV (slow) replacement
-Medication: inhibit ADH
-Monitor Na levels
-Treat N w/ anti-emetics
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| Hypernatremia | -Sodium retention or fluid losses will raise the serum sodium level (lots of urine output, D, burns)
-Excessive aldosterone secretion
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| Nursing Interventions: Hypernatremia | -Fluid replacement (IV or oral)
-Encourage fluids
-Low Na foods
-IV (slow) replacement: Hypotonic (D5W, 0.45 NS)
-Meds: Diuretics
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| Potassium | -Major ICF
-Maintains acid-base balance in the body
-Very important in regulating membrane potentials in neuromuscular tissue and the heart
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| Hypokalemia | -Low dietary intake
-GI losses, sweat
-other electrolyte imbalances
-Renal disease
-Medications: Diuretics, steroids, insulin
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| Hypokalemia: Symptoms | -Fatigue, Decreased Reflexes, paresthesia, irritability to seizures an coma
-Fibrillation, ECG changes, decrease musc contraction
-Muscle weakness and cramps
-Anorexia and N
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| Hypokalemia: Interventions | -Monitor Cardiac precautions
-K+ supplements (take with food)
-IV - 10-20 mEq in 50-100 ml fluid over 1h max rate, never push meds, must be diluted on IV pump device, not gravity
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| Hyperkalemia | -Greater concerns the higher it is
-Associated with: renal failure, cellular injury, IV infusions
-Cellular changes - Decrease cell excitability: neural, cardiac, muscle
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| Hyperkalemia: Assessment Findings | -Cardiac: HR faster,extra beats,tall peaked T wave, P wave almost nonexistent, QRS widened
-Gastric: N/V,anorexia,D
-Muscular irritability, twitching
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| Hyperkalemia: Interventions | -Dietary restriction
-Increase urine output: Diuretics
-Hydration
-Meds
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| Hypocalcemia | -Reciprocal with Phosphorous
-Associated with: Inadequate diet(Ca, Vit D), Decrease parathyroid hormone, pancreatitis,GI malabsorption,
meds,cancer
-Cellular changes: increased cell excitability (cardiac, muscle)
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| Hypocalcemia: Assessment | -Parathesis:numbess, tingling hands, feet, lips
-Emotional lability
-VS changes
-Chvostek's sign (tap cheek of facial nerve, see twtiching)
-Trousseau sign (use BP cuff and see hand, fingers twitching)
-Low albumin levels
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| Hypocalcemia: Interventions | -Increase intake: Ca, Vit D
-IV replacement: Ca chloride, Ca gluconate
-Patient safety: fall risk, bleeding risk, cardiac arrhythmias
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| Hypercalcemia | -Associated with: Cancer with metastasis, hyperparathyroidism, thiazide diuretic therapy, excessive intake, prolonged immobilization, metabolic acidosis
-Cellular changes: decrease cell excitability (cardiac, muscular); production of renal stones
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| Hypercalcemia: Assessment | -N/V
-Anorexia
-Lethargy
-Muscle Weakness
-Kidney stones or hx of kidney stones
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| Hypercalcemia: Interventions | -Identify pt at risk
-Dietary restrictions foods high in Ca
-Hydration with diuresis (IV normal saline with lasix)
-Meds
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| Magnesium | -Major ICF cation
-Most is in soft tissue,bone, muscle with only 1% in blood
-Important for cardiac electrical function
-Low Mg can contribute to low K+ and low Ca++
-Treat low Mg++ before treating K+ and Ca++
-Mg is used to treat toxemia in pregnan
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| Hypermagnesemia | -Most cases are caused by renal failure
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| Hypomagnesemia | -Associated w/ low K and low Ca
-Inadequate food intake
-IV nutrition/fluids
-ETOH abuse
-Malabsorption syndromes
-Low Mg++=Trousseau and Chvostek signs
-Low Mg + Low K Increases risk for cardiac electrical problems (ventricular arrhythmias)
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| Carbohydrates | -Mono,Di: milk,cane sugar,beet sugar,fruits
-Polysaccharides:grains,legumes, root veggies
-Are converted to glc, excess converted to glycogen or fat
-Recommended daily intake = 125-175g, most should be complex carb (poly) like milk, whole grains
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| Protein:Complete | -Eggs, Milk Products, Meat
-Meet body's AA needs for tissue growth
-Building blocks of protein - AA
-Recommended daily intake: 56g men, 45g women
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| Vitamin A | -Found in fish oil (Salmon,walleye) egg yolks,animal liver,fortified milk,margarine
-Orange veg and fruits
-Needed for vision, skin, repro, cell membrane structure
-Deficit - night blindness
-Excess - dry lips, bone pain, hair loss
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| Vitamin D | -Formed by action of sun on skin
-Necessary for blood Ca stability, clotting, bone formation, neuromuscular function
-Deficit - has to do with how much Ca gets used, joint pain
-Excess - calcification of soft tissues
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| Vitamin E | -Veg oil,margarine,whole grains,dark green veg; additive product (oil, margarine)
-Antioxidant - prevent oxidation of vit A&C necessary for cell membrane integrity
-Deficit-lipid absorption problems
-Excess - liver/kidney failure
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| Vitamin K | -Synthesized by coliform bacteria in large intestine
-Green leafy veg,cabbage, cauliflower, pork
-Essential for formation of clotting protein
-Deficit - bruising
-Excess - hemolytic anemia (cells lysed), jaundice in babies (CBD block)
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| Vitamin C | -Citrus fruit,potatoes,tomatoes,grn leafy veg
-Help form connective tissue, conversion of cholesterol to bile salt
-Antioxidant and vasoconstrictor (watch pts w/HTN)
-Deficit-dry mouth,hair loss, itching
-Excess-GI upset
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| Anuria | -Urine output <100 ml/24
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| Oliguria | -< 30 - 50 ml per hour or 100-400 ml/24h
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| Polyuria | -Unusually large amounts of urine output
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| Frequency | -Voiding more often then every 2 hours
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| Urgency | -Strong sudden urge to void
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| Dysuria | - Burning on urination
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| Nocturia | -> need to urinate at night
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| Hesitancy | -Difficulty starting a stream of urine
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| Residual | -Urine left in the bladder after voiding
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| Retention | -The amount of urine left in the bladder
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| Cystitis | -UTI
-Most common type
-Prevalence 8x higher in women
-Increases during hospitalization
-Wipe from front to back
-More common with increased sexual activity, poorly fitting diaphragms, tight clothing, wet bathing suites, indwelling catheters
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| UTI Causative Organisms | -E Coli (80%)
-Klebsiella
-Enterobacter and proteus
-Chlamydia trachomatis
-Trichomonas vaginalis
-Neisseria gonorrhea
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| UTI signs and symptoms | -Burning
-Frequency
-Urgency
-Cloudy urine
-Inability to void
-Malaise
-Mental status changes - in elderly might be first sign
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| UTI Medical Management | -Inhibit bacterial growth (antibiotic)
-Meds (can affect bc)
-Diet Modification (avoid high caffeine, spicy foods)
-Increase fluid intake (3-4L/d)
-Prevent complications
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| Urosepsis | -Gram-Negative bacteremia originating in the gu tract
-Can lead to septic shock and death without aggressive, immediate tx
-Elderly,Indwelling cath,Untreated UTI
-Ecoli most common cause
-Chemo
Observe for:I temp,change in mental status,Low bp
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| IC Symptoms and Damage | -Bladder tenderness
-Urinary urgency
-Frequency (60+/day)
-Nocturia
-Dyspareunia - painful intercourse
-Variable manifestations
Damage: ulcerations and hemorrhages in bladder wall
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| Bladder Cancer | -Most frequent neoplasm of urinary tract
-Strong correlation with smoking
-Industrial exposure
-Chronic cystitis
-Pelvic Radiation
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| Bladder Cancer Manifestations | -Painless hematuria (85% of all cases) Typically first sign; Amt not significant to stage of disease
-Initially intermittent bleeding
-Obstruction
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| Urinary Calculi | -Commonly called stones
-Causes: urinary stasis, supersaturation of urine
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| Types of stones | -Calcium - 90% (phosphate or oxidase)
-Oxalate (soy bean based products)
-Struvite (bacteria)
-Uric acid (GOUT)
-Cystine (autosomal recessive disorder)
-Xanthaene (rare)
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| Urinary Calculi Symptoms and Dx | -Sharp sudden onset of pain
-Infection
-N/V
-KUB
-IVP
-Cystoscopy
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| Urinary Retention | -Inability of bladder to empty: post void residual >100ml, detrusor failure in women, enlarged prostate in men
-Manifestation of another pathologic condition
-Causes: sensory input to/from bladder, muscle tension/anxiety, neurologic conditions
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| Urinary Incontinence | -4 Major types
-Stress-force of exertion(laugh, preg,sneeze,radiation,overwt)
-Detrusor over activity-urge incontinence (spontaneous bladder contract:parkinson,alzheimer,stroke)
-Overflow-frequency,constant dribble,wk musc,block,tumor
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| -Functional:d/t physical, psychosocial of pharmacologic causes unrelated to urinary system (dementia,pharm,arthritis)
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| Neurogenic Bladder | -Bladder dysfunctions caused by lesions of CNS/PNS
-Uninhibited-constant urine flow
-Sensory-bladder can't sense fullness
-Motor-no contraction
-Autonomous-can't start flow
-Reflex-no sensation but bladder contracts
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| Hydronephrosis | -Distention of the renal pelvis caused by obstruction of normal urine flow
-Tx:relieve obstruction&prevent infection
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| Nephrotic vs Nephritic | -Nephrotic: leaking protein, failure of glomerular basement wall
-Nephritic: usually see hematuria or blood in urine
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| Acute Renal Failure | -Abrupt loss of Kidney function (days to weeks, can be life threatening)
-GFR decrease, serum creatinine and BUN increase
-Urine output Decrease
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| Non-oliguric | -Excrete as much as 2000 ml/24h with increase in GFR, BUN, and Creatinine
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| Classifications | -Pre-renal: decrease bf to kidney (cardiac issues)
-Intra-renal: structures w/in kdineys-trauma, infection
-Post-renal: obstruction in urinary tract-BPH, tumors
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| Nursing Asst:Pre-Renal | -Tachycardia
-Hypotension
-Dry mucous membranes
-Flat neck veins
-Coma
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| Nursing Asst:Intra-renal | -Hypovolemia
-Vomiting
-Diarrhea
-Cool
-Lethargy
-Confusion
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|
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| Chronic Kidney Disease | -Kidney damage for 3 months as defined by structural or functional abnormalities with or without decreased GFR or a GFR of 60ml/min/1.73m2 or less, with or without kidney damage
🗑
|
||||
| Cause of CKD | -Diabetes (40%)
-HTN
-Inflammation
-Heredity
-Chronic Infection
-Obstruction
-Accidents
🗑
|
||||
| Stage 1: CKD | -Normal or decreased GFR
-Structural or functional abnormality of kidney markers of kidney disease
-May have normal BP
-No serum lab abnormalities
-No symptoms
Action:Dx,Tx,slow progression, tx comorbidities, CVD risk reduction
🗑
|
||||
| Stage 2: CKD | -GFR 60-89
-Generally asymptomatic
-HTN usually develop
-Lab abnormalities may or may not be present
-Action: estimate progression
🗑
|
||||
| Stage 3: CKD | -GFR 30-59
-Lab abnormalities may be present indicating anemia, bone disease and disorder of Ca and Phosphorus
-Usually asymptomatic
-HTN usually present
-Action: evaluate and treat complications
🗑
|
||||
| Stage 4: CKD | -GFR 15-29
-Symptoms: mild fatigue, anorexia, edema, impaired memory
-HTN
-Diabetes
-Action: prepare for renal replacement therapy
🗑
|
||||
| Stage 5: CKD | -GFR <15
-Symptoms increase: malaise, wt loss/gain, trouble sleeping, anorexia,N/V, musc cramp, cognitive decline
-Metallic taste from build up
-Action: Renal replacement therapy
🗑
|
||||
| Diabetes | -Disorder of metabolism-the way our bodies use digested food for energy
-Chronic,sytemic disease characterized by either a deficiency of insulin or decreased ability of the body to use insulin
-Pancreas is responsible for insulin levels
🗑
|
||||
| Alpha Cells | -Produce glucagon
-Stimulate breakdown of glycogen in liver (glycogenolysis)
-Stimulated formation of carb in liver
-Stimulate breakdown of lipids
-Secretion is regulated by blood sugar
-Secretion is regulated by blood sugar levels
🗑
|
||||
| Beta Cells | -Secrete insulin-helps glucose to move across the cell membrane, decrease blood glucose levels
-Secretion is regulated by blood glucose level
-Synthesize and secrete insulin
🗑
|
||||
| Delta Cells | -Produces somatostatin-inhibits the production of glucagon and insulin
-Balances alpha and beta cell funtion
-Acts as mediator
🗑
|
||||
| Classification of DM | -Type 1, Insulin dependent DM, juvenile onset
-Type 2, Non insulin dependent DM, adult onset
-Disease of pancreas or genetic disease
-Gestational DM-during pregnancy
🗑
|
||||
| Type 1 | -Autoimmune disease
-Often leads to absolute insulin dependency
-Affects 10% of ppl with DM
-Develops most often in children and young adults
-Strongly inherited
-Immune system fights beta cells
🗑
|
||||
| Type 2 | -Most common
-usually diagnosed after 40 but seen in younger and younger ppl
-Associated with older age, obesity,family Hx, previous gestational dm,physical inactivity, certain ethnic populations
🗑
|
||||
| Risk Factors Type 1 | -Genetic Predisposition
-Exposure to environmental factors (viruses, smoked products, nitrates)
-No known health promotion activity to prevent but regular exercise and balanced diet may limit the complications
🗑
|
||||
| Risk Factors Type 2 | -Hx of DM in parents of siblings
-Obesity
-Physical inactivity
-HTN
-Women with gestational diabetes hx
-Race/ethnicity
🗑
|
||||
| Decreased Glucose Utilization | -Skeletal, cardiac, fat cells don't need insulin
-Ingested glc can't be transported into cells, plasma level rise
-Liver can't store glc as glycogen w/out adequate insulin
-Blood glc level rise
-Glc appears in urine
-Dehydration appears-osmotic diu
🗑
|
||||
| Increased Fat Mobilization | -Muscle cry for glc so fat stores broken down
-Ketones fomred as byproduct and produce hydrogen ions-measure in urine and smelled on breath
-Lipid breakdown increase lipid level - lead to arteriosclerosis
🗑
|
||||
| Increased Protein Utilization | -AA converted to glc in liver, further elevate glc level
-Insulin needed to build protein
-Type 1 often appear emaciated d/t constant protein breakdown
🗑
|
||||
| Symptoms of DM | -Cardinal: POLYURIA,POLYDYPSIA, POLYPHAGIA
-Weight loss (type 1)
-Blurred vision
-Pruitis,vaginitis
-Weakness,fatigue,dizziness
-Asymptomatic (type 2)
-Slow healing wounds, dark patches
🗑
|
||||
| Diagnosis of DM | -Symptoms + postload glc > or = 200
-Fasting glc > or = 126
-2 hr post GTT > = 200
-Glycosylated Hemoglobin not used for dx
-FBS 110-126
🗑
|
||||
| Normal | -FBS: < 100
-Glucose Tolerance: < 140
🗑
|
||||
| Hypoglycemia | -Etiology: insulin od, omitting meals, vomiting, over exercise without carbs, alcohol intake
-Normal feedback loop is dirupted
🗑
|
||||
| Hypoglycemic symptoms | -Early signs (adrenergic: increaseing epinepherine, shaky, irritable, tachycardia, hunger, pale, paresthesias
-Later signs (neuroglycopenic): lack of glc avail to brain, Ha, slurred speech, blurred vision, confusion, lethargy, coma, sz, death
🗑
|
||||
| Tx of Hypoglycemia | -Depends more on symptoms than blood glucose levels
-Start with 10-15g of CHO (4oz OF, 6oz regular soda, 8oz 2% milk, 4tsp sugar)
-20-30g of CHO (double above, glucagon, 1mg subq or IM)
-50% dextrose IV (glucagon IM or IV)
🗑
|
||||
| Chronic Complications | -Eyes,heart,kidneys,brain, Macrovascular (larger vessels)
-CAD,crebrovascular disease,HTN,peripheral vascular disease
-Occur years before symptoms of DM even appear
🗑
|
||||
| Microvascular complications | -Retinopathy
-Nephropathy
-Damage to smaller blood vessels
-No symptoms early
-Late symptoms-swelling, proteinuria, renal failure
-Checking urine protein is important
🗑
|
||||
| Neuropathic Complications | -Most common problem
-Numbness,tingling,pain
🗑
|
||||
| Musculoskeletal System | -Movement/Positioning
-Provides:support,protection, movable frame,storage for Ca and other ions (I movement of Ca stimulate osteoclasts to break down bone and release Ca 1)stimulate osteoclasts 2)reabsorb bone 3) new bone-osteoblasts
-Bone marrow fx
🗑
|
||||
| Bone Marrow Function | -Osteoblasts - bone forming in bone matrix
-Osteocytes - bone matrix, mature osteoblasts
-Osteoclasts - remove old, damaged bones-growth and repair
🗑
|
||||
| Stages of Bone Healing | 1) Hematoma or inflammatory (1-3d)
2) Fibrocartilage formation (3d - 2wk)
3) Callus formation (2-6wk)
4) Ossification (3-24wk)
5)Consolidation and remodeling (6wk - 1y)
🗑
|
||||
| Osteoarthritis: Definition | -Painful, degenerative joint disease that often involves the hips, knees, neck, lower back or the small joints of the hands
🗑
|
||||
| Osteoarthritis | -Oldest and most common
-Not just associated with aging
-Cartilage deterioration, joint destruction
-Chronic, incurable
-Affects weight bearing joints
-Obesity major risk factor
🗑
|
||||
| OA Assessment: Subjective | -Pain and stiffness that increases with activity and decreases with rest
-Pain worse at the end of the day
-Pain relieved by rest
-Mild tenderness in joint areas
-Joints lock give way when going down stairs
-Symptoms:worsening pain,limit of movement
🗑
|
||||
| OA Assessment: Objective | -Crepitus/grating noise
-Deficient ROM
-Joint enlargement
-Heberden's nodules DIP
-Bouchard's nodules PIP
🗑
|
||||
| Phamacotherapy for OA | -Acetaminophen:DRUG OF CHOICE
-NSAID:Motrin
-Capsacin cream
-Steroid injections-cortisone, decrease pain,many SE
-Hyaluronan injections-allows for smooth musc. movement: >synovial fluid production
-COX-2 drugs:celebrex
-Supplements
🗑
|
||||
| Osteoporosis | -Systemic skeletal disorder that compromises bone strength&I risk of bone fracture
-2 components of bone strength: density and quality
-Risk factors:women-small body,underwt,older,hx of OP)
-Med Mngt: prevent loss of bone mass & bone resorption
🗑
|
||||
| Risk Factors: Major | -Hx of fractures as an adult
-Hx of fragility or low trauma fractures 1st degree relative
-Low body wt (<128)
-Cigarette smoking**
-Steroids use for > 3 months
🗑
|
||||
| Paget's Disease | -Tibia,lower spine,pelvis,head
-Viral infection can begin process
-Rare under 40
-Can be asymptomatic
🗑
|
||||
| Osteomalacia | -Inadequate vit D
-Decalcification and softening bones, Asian and women more prone, vegan-similar to rickets in children
-CM: fatigue, malaise,bone pain, muscle weakness
-Daily vit d replacement, ensure adequate ca and phosphorus intake
🗑
|
||||
| Gout and Gouty Arthritis | -Uric acid lab levels
-Metabolic acid of purine- mostly in big toe
-Develop in stages
-NSAIDS, allopurinal prevent flareups
-Primary: inherited, more common in men
-Secondary: acquired with renal disorders
🗑
|
||||
| Rhabdomylosis | -Can see as side effect from statins: rare occasion
-Trauma – break down of muscle fibers, Electrical burns,Ischemic conditions,Prolonged immobilization
-I creatine kinase (CK) – 5X normal value, Hyperkalemia ,HBG and myoglobin in urine
🗑
|
||||
| Fracture Classification | -Closed – deformity but no opening, skin in tact
-Open: Grade I–wound w < 1 cm, minimal contamination - lacteration
Grade II – greater than 1, moderate contamination
Grade III – greater than 6-8 cm with extensive damage and high contamination
🗑
|
||||
| Closed Reduction | -Manual traction applied to move fx fragments&align bone
-Should be performed as soon after injury as possible, wait until swelling goes down to fix it
-Immobilization device must be applied right after Xray confirms bone alignment (i.e.cast)
🗑
|
||||
| Open Reduction and Internal Fixation | -Sx
-Surgeon realigns fx
-Tx of choice for compound fx’s
-Femoral and joint fx’s are treated with ORIF
-Maintains immobilization and prevents deformity
-Screws, plates, pins, wires or nails are used to maintain the alignment
🗑
|
||||
| External Fixation | -Immobilization
-Support
-Maintain position
-Common sites:face,jaw, extremities,pelvis,ribs,fingers and toes
-Around the clock medication
🗑
|
||||
| Traction | -Use since prehistoric times!!
-Application of a pulling force to an injured part or extremity while counteraction pulls in opposite direction
hands (manual traction)
-Weights (more common)
-Not as prevalent today
🗑
|
||||
| Nursing Implications: Traction | -Never interrupt the wts of skeletal traction
-Skin traction,remove wts only w intermittent skin traction
-Dont wedge foot or place it flush with foot board of bed
-Maintain line of pull/dont knot ropes
-Wt should hang freely at all times
🗑
|
||||
| Synthetic/Fiberglass Cast | usually dries within 30 min
Cooler and more lightweight
Generates heat while drying
Tell the patient he/she will feel heat under cast during this time
OK to use a cool blow dryers
🗑
|
||||
| Plaster Cast | Plaster-may take 1-2 days to dry completely
when dry the cast is odorless
DO NOT cover with blanket or towel while drying!
DO NOT use a blow dryer at this time!
WHY? – can burn patient and can crack cast
🗑
|
||||
| Cast Application | Pad over bony prominences w/o wrinkles
while cast wet support the cast with open,flat palm of hand at all times-avoid using fingertips
avoid rapid cast drying wexcessive heat
use pillows to elevate
keep edges smooth
turn q2h,Turn toward unaffected li
🗑
|
||||
| Cast Care | Provide/teach correct skin,cast care
bathe only accessible skin
apply lotion only to exposed skin, skin under cast use alcohol-will dry
inspect for loose plaster
avoid using powder in cast
inspect padding
Do not insert any foreign object under cast!
🗑
|
||||
| Delegation | LPNS can gather information, provide educational materials but not evaluate learning and perform most interventions. They do not plan care
Nursing assistants CAN measure and gather data; they CANNOT assess, teach, evaluate or plan care.
🗑
|
||||
| Compartment Syndrome | -Asst,Prevention is the key
-Monitor NV status of injured limb
unrelieved,increase in pain in affected limb
Pain w passive stretch of toes or fingers
mottled skin
excessive swelling
poor cap refill
paresthesia
inability to move toes or fingers
🗑
|
||||
| Compartment Syndrome: Late Symptoms | pallor
dim,absent pulses
cold skin
-Arterial occlusion from swelling of soft tissues 2nd to bone trauma
Assess peripheral nerve function q1h for 1st 24 hours
-poor venous return results in edema which impedes arterial flow and nerve impulse
🗑
|
||||
| Fat Embolism | Most often seen with femur fx
Pathophysiology:
fat globules enter the vascular space and become emboli
eventually travel to the lung
pulmonary embolus can cause death
Fat embolisms usually occur 12-36 hrs. post injury
🗑
|
||||
| Classic Signs of Fat Embolism | tachypnea> 30/min
sudden onset of chest pain or dyspnea
restlessness, apprehension, anxiety
confusion
**impending doom
elev temp >103
inc pulse rate >140
petechial skin rash of neck, conjunctiva, axilla, or chest
🗑
|
||||
| Hemorrhage/Hematoma Formation | Bleeding or Hemorrhage due to trauma
monitor for s/s of shock/hemorrhage
> pulse or < BP
UO = <30cc/hr
restless, agitated, change in mental status
> RR
< peripheral pulses
cool, pale or cyanotic skin
thirst
🗑
|
||||
| Lower GI problems: Inflammatory Disorders | -Can be in any portion of the bowel
-Clostridium Dificile (large dose of antibiotics, on antibiotics >7d, contagious and pt in isolation, MUST wash hands)
-Gastroenteritis-inflammation of stomach and small bowel-pain&D (can have N&V,fever,anorexia)
🗑
|
||||
| Appendicitis: Symptoms | -Appendix ruptures=no pain but peritonitis develop
-DON'T do enema w/appendicitis= rupture
-Acute ab pain,comes in waves
-Feeling of pressure to pass gas
-Pain starts in epigastrium, localizes to RLQ
-Guarding of ab by drawing up legs
-Tx=appendecto
🗑
|
||||
| Nursing Issues with Appendicitis | -Never give enema or laxative
-Never apply ab heat
-Assess for rebound tenderness= when push down=no pain, but when let go have pain
-Assess for pain that abruptly changes and ab becomes rigid or board like-rupture
-
🗑
|
||||
| Pathophys of Peritonitis | -Systemic effects
-Inflammatory process shunts blood to site diverting it from other organs
-Peristalsis stops, fluid&air in bowel I ab pressure
-O2 needs are I by inflammation
-Ventilation D d/t pain&ab pressure
🗑
|
||||
| Symptoms of Peritonitis | -Diffuse/localized pain
-Rebound tenderness
-Severe rigidity
-Distention
-Anorexia, N, V
-D or absent bowel sounds
-Fever
-Can cause severe systemic problems
🗑
|
||||
| Clinical Manifestations of Crohn's and UC | -Ab pain
-D,V
-Fluid imbalances
-Wt loss
-Fever in acute phase-flare-up
-Hemorrhoids-varicose veins of rectal area
-Perianal abscess w/ crohn's
🗑
|
||||
| Ulcerative Colitis | -Predominant symptom-rectal bleeding
-20 or more stools per day
-Colicky pain in LLQ
-Can have severe dehydration w/ D K
-Symptoms worse with stress, poor diet, laxatives or antibiotics
🗑
|
||||
| Irritable Bowel Syndrome (IBS) | -Dysfunction in bowel motility:D alternate with C
-Seen in middle age, very common
-Risk factors:diet high in fat, gas producing food, lactose, carbonated bev, caffeine, alcohol, smokers, high stress
🗑
|
||||
| Pathophys of IBS | -Alternating D/C
-Hypersensitivity of bowel wall to distension,alter peristalsis
-Crampy pain in LQ
-Hypersecretion of bowel mucous
-Flatus,N,anorexia
-Relief of pain w/defecation
-Fiber,fruit,alcohol,caffeine,fatigue irritate sx
-Connection to ser
🗑
|
||||
| Symptoms of Colon Cancer | -Rectal Bleeding**
-Change in bowel habits, shape of stool
-Ab pain
-Wt loss
-Anorexia
-Anemia
🗑
|
||||
| Candidiasis-Moniliasis | -Thrush
-Candida-albicans-yeast like fungus
-Immunosupression,DM,ATB/Steroid Rx, tube feeding
-Secondary inf
-Pt on chemo
🗑
|
||||
| Nursing Care of oral Disorders | -Best to use warm saline
-Avoid anything alcohol based (mouth wash)
-Analgesia 30-45 min b/f meals
-Small, frequent feedings
🗑
|
||||
| Esophageal Disorders: Dysphagia | -Difficulty swallowing
-Clinical manifestation of an esophageal disorder
-Obstructive cause:tumors, congenital defects,hiatal hernia
-Motility Cause:DM,parkinson's, stroke
🗑
|
||||
| Symptoms of GERD | -Heartburn,dysphagia,salty secretions in mouth (water brash)
-Pain described as burning that moves up and down
-If severe,spasm may radiate to neck,back,jaw, an mimic a cardiac episode: treat w/nitro
-Pain relieved by fluids or antacids
🗑
|
||||
| Medications for GERD | -Antacids: 1h ac or 2-3h pc, relief 10-30m,neutralize gastric acid,sooth mucosal lining
-H2: 1h b/f or after antacids BID,taper to prn,inhibit histamine in parietal cells
-PPI:tx failure,30ac daily,completely control acid secretion
🗑
|
||||
| -Antiemetic Cholinergic: increases LES pressure, increases gastric emptying, 30-60 ac
🗑
|
|||||
| Radiography | -Ab flat plate: simple xray (tumors,gas patterns,fluid collection)
-Upper GI:barium swallow (stool white)(esophagus,stomach,duodenum,jejunum, NPO after midnight, scheduled AFTER other ab tests)
-Lower GI:barium enema (sigmoid colon,rectum)
🗑
|
||||
| -CT scan:npo after bfast, masses, inflammation, abscesses
🗑
|
|||||
| Chronic Gastritis | -> 6mo
-Type A (autoimmune):fundus of stomach,loss of parietal cells
-Type B (most common):H pylori,peptic ulcer disease, gastric sx
-Complications:blding,pernicious anemia, gastric cancer
-PPI changed this, not so much bleeding
🗑
|
||||
| Peptic Ulcer Disease | -Seen in all parts of upper GI
-90% b/c of H pylori
-Helivax vaccine
-Aspirin,NSAIDS breakdown gastric lining allow acids to damage mucosa
-Stress stimulates vagus nerve, I acid production, I gastric motility
-Stress ulcers occurs in critically ill
🗑
|
||||
| Aggressive v Defensive Factors | Aggressive (acid)
-stomach acid
-H pylori - if hubby has it, wife prob does too
-smoking
-alcohol
Defensive
-mucous
-adequate bf to stomach lining
-balanced diet
🗑
|
||||
| Symptoms of GI ulcer | -Acute pain-burning,gnawing,cramping
-Gastric: food causes pain,V relieves pain
-Duodenal ulcer:pain on empty stomach, food eases pain
-N,V most freq in gastric
-Blding if ulcer erodes thru bld vessel
🗑
|
||||
| How to check for Tactile fremitus | -Place hands on chest while patient says 99
-Increased vibrations=fluid in lungs
-Decreased vibrations=air in lungs, obstruction (pneumothorax), emphysema
🗑
|
||||
| Resonance | -Hyper resonance- normal only in chronic obstructive disease, children, and very thin pts
-Dull-abnormal,mass/tumor,pneumonia
-Flat-over bony prominence
-Tympanic-air in peripheral space (pneumothorax)
🗑
|
||||
| Auscultation | -Vesicular-peripheral
-Bronchial-meniculum
-BV-1st,2nd ic space b/w scapula and where trachea divides
🗑
|
||||
| Adventitious breath sounds | -Crackles/Rales:popping,sudden opening sounds when alveoli are fluid filled, doesn't clear with cough, inspiration/expiration, can come and go
-Rhonchi:air pass through airway narrowed w/fluid, snoring,clears w/cough,expiration ex:bad cold
🗑
|
||||
| -Wheezes:high pitched musical sounds caused by bronchoconstriction, can be heard w/out stethoscope, foreign bodies, fluid can cause
-Pleural Friction Rubs: grating sound, pleuritis, inflammation of pleura
🗑
|
|||||
| Definitions | -Eupnea-breathing is normal
-Tachypnea-breathing is fast
-Dyspnea-trouble breathing
-Exertional dyspnea-when i lift things, lose my breath
-Orthopnea-can't breathe lying flat
-Parozysmal nocturnal dyspnea-sat up in bed and couldn't catch breath
🗑
|
||||
| -Hypoxia-low oxygen
-Hypoxemia-low oxygen in blood
-Anoxia-no oxygen in bld or tissues
-Hemoptysis-coughing up blood
-Atelectasis-collapse of alveoli in lower lobes
🗑
|
|||||
| Normal drive to breathe | -Brain gets the signal that there is a high CO2 level
-Arterial blood levels
🗑
|
||||
| pH | -Normal serum pH = 7.35 - 7.45
- < 7.35 = acidosis
- > 7.45 = alkalosis
🗑
|
||||
| Obtaining Arterial Blood Gases | -Draw bld from artery to measure O2, CO2,pH, bicarb, base excess
-Also measure electrolytes
-Usually draw from radial artery
-Done by MD,PA,NP,RT,RN
🗑
|
||||
| -Sample must be collected in a syringe with agent to prevent O2 metabolism which would falsely lower the reading&placed on ice in a syringe
-Allen test (pg 180)
-ABG test = painful
-Hold pressure at site for 5 min after drawing blood
🗑
|
|||||
| ABGs: Normal Levels | -PaO2 (80-100mmHg)
-PaCO2 (35-45 mmHg) reflects acid base balance
-pH (7.35 - 7.45)
-Bicarbonate (22-26 meq/L) represents acid-base balance
-Base Excess - -1 to +1
🗑
|
||||
| Important Concepts: ABGs | -If blood pH < 7.35 = acidotic or has acidosis
-If blood pH > 7.45 = alkalotic or has alkalosis
-If CO2 > 45 = hypercarbic AND acidotic
-If CO2 < 35 = hypocarbic AND alkalotic
🗑
|
||||
| -O2=91,CO2=50,pH=7.33,HCO3=24 -O2=87,CO2=33,pH=7.48,HCO3=22 | -Respiratory Acidosis
-Respiratory Alkalosis
🗑
|
||||
| CT | -More sophisticated multidimensional images than xray
-Radioactive dye is given
-Assess for iodine allergies
-NEED TO KNOW CREATININE IF DYE IS GIVEN
-Can use CT scan for interventions like biopsies
🗑
|
||||
| Bronchoscopy | -Scope inserted into airway for:examination,tissue specimen,removal of foreign bodies,suctioning of thick secretions,remove lesions
-Pre:NPO 6h,sedation,sore throat-numbed and affects swallowing
-Post:monitor vs,suction,assess swallowing-check gag refle
🗑
|
||||
| Thoracentesis | -MD insert cath into lung,drain fluid/air,fluid can be checked for inf,cancer cells,insert med
-Pre:painful,sit up and lean over table,topical anesthetic,10-15min
-Post:xray-check for pneumothorax,turn to unaffected side,monitor vs&subq crepitus
🗑
|
||||
| Pulse Oximetry | -SaO2
-Non-invasive and continuous
-Measure amt of hemoglobin saturated w/oxygen through fractionated light
-Normal = 92-100
-Problems: affected by motion, poor circ, cold
🗑
|
||||
| Asthma Asst | -Dyspnea,chest pain, feel anixous, can't stop coughing
-Objective: nasal flaring,cyanosis,use of acc musc,wheeze, tachypnea/cardia, pursed lip breathing,cough-night time
🗑
|
||||
| Classification of Asthma Severity | 1)Mild intermittent:sx<2xwk,brief exacerbations;no prob w/lung fx
2)Mild Persistent:sx>2xwk but < 1time/d;exacerbation may affect activity
3)Moderate Persistent:daily sx w/daily use of inhaler;exacerbation affect activity
🗑
|
||||
| 4)Severe Persistent:continual sx;limited physical activity, freq exacerbations
🗑
|
|||||
| Medications for Asthma | -Beta2:Bronchiolators,oral
-Short,long acting
-SE:tremor,nervousness, HTN,tachycardia,oral candidiasis (rinse mouth)
-Albuterol,Proventil,Theophylline
-Most pts start out on short-acting and progress to long-acting or oral as disease progresses
🗑
|
||||
| -Inhales Steroids (corticosteroids)
-Inhaled, oral (sicker pt)
-Reduced inflamm
-D mucous production
-Make receptors more receptive to beta agonists
-SE:thrush,dysphonia
-rinse mouth
-Use spacer to reduce SE
-Beta2 combined with steroid
🗑
|
|||||
| -Oral Steroids
-More prone to inf d/t immuno-suppression
-Bone loss d/t dimineralization
-I BS b/c cortisol
-Fluid retention d/t aldosterone
-Stomach ulcers d/t affects protective layer of stom
-Suppression of growth in kids
🗑
|
|||||
| Oral Steroids
-Give smallest dose in am b/c of hormone levels
-Used as disease progresses or if there are exacerbations
-Tapered slowly so that inherent adrenal function returns
🗑
|
|||||
| -Leukitriene Modifiers
-Tremendous benefit (good drug,less SE)
-Reduce bronchoconstriction, inflamm, mucous production
-Singulair
🗑
|
|||||
| Medication Management for Long term Control | 1)Mild Intermittent:short act bronchodilator prn
2)Mild Persistent:low dose inhaled steroids daily
3)Moderate Persistent: low-med dose inhaled steroids daily, long acting beta 2 daily
4)High dose inhaled steroids daily,long acting beta2 daily
🗑
|
||||
| COPD | -Emphysema,Chronic Bronchitis
-Chronic airflow limitation*
-Can include bronchial edema, decreased elastic recoil
-Risk factors: smoking,chronic resp inf, environment
🗑
|
||||
| Chronic Bronchitis | -I mucous produc(I goblet cells, I mucous glands)
-Impaired cililary func
-Thick mucous cause air trap/alveolar collapse
-I risk inf
-Retain CO2
-Hypoxemic
-Polycythemic:high rbc,hgb b/c pt have chronic low O2,body thinks need more,make more rbc
🗑
|
||||
| Chronic Bronchitis: Signs and Symptoms | -Productive cough
-Decreased exercise tolerance
-Wheezing
-SOB
-Copious sputum
-Freq pul inf
-Chronic hypoxemia
-Chronic I Co2
-High hgb
-Finger nail clubbing
🗑
|
||||
| Emphysema | -Aleolar wall destroyed d/t conn tissue destruction
-Deficiency in alpha1 antitrypsin
-I dead space in lungs-non functioning lung tissue
-I work of breathing
-Co2 retention is less of problem
🗑
|
||||
| Emphysema: Signs and Symptoms | -Progressive dyspnea on exertion, progress to dyspnea @rest
-Barrel chest
-Hyperresonance
-Clubbing of fingers
-Wt loss
-High Co2
-High hgb
-Rt heart failure
-Hypoxemia
🗑
|
||||
| Complications of COPD | -Inf
-Collapsed lung
-Worsens @night
-More likely to go into resp failure and need ventilator after acute illness
-May need home O2
🗑
|
||||
| Medications for COPD | -Bronchodilators
-Steroids, oral and inhaled
-OXYGEN IN LOW DOSES: Low flow (1-3L/min); Low flow venturi mask; Nasal cannula (1-3L)
🗑
|
||||
| Pulmonary Emboli | -Occlusion of portion of blood vessel in pul vascular system
-Can be lethal depending on size
-Mortality rate,50,000 unchanged in over 20y
-Silent Pulmonary emboli
-High risk:major surgeries,long plane rides, sit for a long time, vascular disorders
🗑
|
||||
| Pulmonary Emboli: Causes | -Thrombosis related (80%)
-Prolonged bed rest
-Obesity
-Long operations
-Long plane flights
-Afib
-Rt side hrt failure
-CHF
-Pelvix fx or large bone
🗑
|
||||
| Virchow's Triad: What you need to create an emboli | -Blood stasis: pooling
-Blood coagulation alterations: coagulation disorders
-Vessel wall abnormalities: atherosclerosis, DM
🗑
|
||||
| Diagnostic findings of Pulmonary Emboli | -Some have no symptoms
-Dyspnea (81%)
-Sudden pleuritic pain
-Tachycardia,tachypnea
-ECG changes
🗑
|
||||
| Asst Findings Pulmonary Emboli | -Dyspnea
-Apprehension
-Diaphoresis
-Syncope
-Chest pain
-Rales
-Fixed splitting of S2
-Murmur
-Cyanosis
-Fever
-Shock
-Cough, hemopysis
🗑
|
||||
| **Serum lab tests that represent clotting** | -PT (prothrombin time), extrinsic pathway: normal = 11-13sec
-INR (international radio), extrinsic pathway: normal: 0.8-1.2 (used more often than PT)
-PTT (partial thromboplastin time),intrinsic pathway: normal=21-35 sec
🗑
|
||||
| Anticoagulation Therapy for PE | -Heparin Drip (blocks promthrobin-thrombin)
-I PTT to 2-2.5 times normal (>70)
-WON'T dissolve clot, prevent others from devloping
-Bld draws q4h until established level
-Only give IV, coumadin for home
🗑
|
||||
| Anticoagulation Therapy for PE | -Coumadin
-Oral, depresses clotting factors
-Begin 3-5 days before d/c heparin
-PT 2x normal (>26 sec)
-Most often we follow INR and keep it in 2-3
-Continue therapy for approx 6 months
🗑
|
||||
| Arteries | -3 Layers: Intima (single layer of endothelial cells,elastic membrane); Media (near vessel lumen receive O2/nutrients by direct diffusion in small arteries;vasa vasorum in larger arteries); Adventia (conn tissue,nerve fibers,vasa vasorum)
🗑
|
||||
| Three types of Arteries | -Large Elastic
-Medium Muscular (HTN)
-Small (within tissues and organs)
🗑
|
||||
| Arterioles | -Principle point of resistance to blood flow
-Sharp decrease in pressure and velocity
-Changes from pulsatile to stead flow
🗑
|
||||
| Veins | -Larger diameters
-Larger lumina
-Thinner less organized walls
-High volume,low pressure (go back to heart)
-Reverse flow is prevented by venous valves in the extremities
-Valve damage = varicose veins
🗑
|
||||
| Blood Flow | -Flow = pressure gradient/resistance
-Pressure = arterial pressure
-Flow = CO
-Resistance = total peripheral resistance (depends on: size of vessel,fluid viscosity, length of vessel)
🗑
|
||||
| Regulation of Body Fluid Volume | -When sodium and water levels increase the total blood volume is increased
-Disease that change kidney function alter BP:vasoconstriction= high peripheral vasc resistance; systolic = < 70, kidneys not getting O2
🗑
|
||||
| Renin-Angiotensin-Aldosterone | -ADH now released d/t increased osmolaritiy, begins to reabsorb water to try to decrease serum omolarity
-Increased reabsorption of water increases blood volume, increase venous return, which can increase stroke volume, thus increasing CO and bp
🗑
|
||||
| Blood Pressure | -Reflects left ventricular function
-Systolic reading represents force of ventricular contraction
-Diastolic reading indicates vascular resistance (afterload)
-Pulse pressure-difference b/w systolic and diastolic, normal = 40 mmhg
🗑
|
||||
| Stages of Hypertension | -Normal 120/80
-Pre:120-139/80-89, No meds,need lifestyle mod
-Stage 1:>140-159/90-99,Thiazides,consider ACEI,ARB,BB,CCB;<130/80 pts w/DM or CKD
-Stage 2:>160/>100, two drug combo, thiazide +ACEI,ARB,BB,CCB
🗑
|
||||
| Preload | -Blood coming back to heart
-Venous return that builds during diastole
-Ventricles stretch just before contraction
-Hypovolemia = increased preload
🗑
|
||||
| Afterload | -Increase in high bp, vasoconstriction
-Resistance that the heart must overcome to achieve ejection
-HTN- increase the word load of the heart
🗑
|
||||
| Types of HTN | -Primary (essential): no renal disease or tumor, just have HTN
-Secondary: b/c of something else
-Isolated systolic: get horrible news, nervous
-Resistant (malignant): can be lethal, cardiac or brain insult
🗑
|
||||
| Smoking | -Smoking affects blood vessels in 2 ways
-Endothelial damage (carbon and tar): fat,cholesterol,lipids can sneak into inner layer and build up plaque
-Vasoconstriction (nicotine)
🗑
|
||||
| Pharmacotherapy: Diuretics | -Thiazide:first line
-Loop diuretics (K+ wasting) Lasix
-Potassium sparing: (>K+) aldactone,midamor
🗑
|
||||
| Pharmacotherapy: Beta-Blockers | -D HR,contractility,afterload,CO,renin secretion
-<effectiveness in AA,elderly
-Contraindicated in asthma
-ED in men
-Caution in DM
-Reduce O2 (know hr,bp before admin)
-olols
🗑
|
||||
| Pharmacotherapy: Calcium Channel Blockers | -Cause smooth musc relax,vasodilation block calcium to influx musc
->effect in AA when w/thiazide
-D L ventricular wall stress by D afterload
-Diltiazem,il,pine
🗑
|
||||
| Pharmacotherapy: ACE inhibitors | -Inhibits ACE so block PRODUCTION of angiotensin II
-More effective in caucasian than aa
-Better for diabetes, slow progression of nephropathy
-Useful for asthmatics,hf,pvd
-Can cause dry cough,1st dose htn,hyperkalemia,renal failure,angioedema
-pril
🗑
|
||||
| Pharmacotherapy: Angiotensin II receptor blockers (ARB) "sartans" | -Block the ACTION of angiotensin II by blocking receptors
-DON'T cause hyperkalemia,cough or angioedema
-SE: low incidence of dizziness
🗑
|
||||
| What symptoms would your patient complain of if they had reduced/blocked arterial flow? | -Angina
-SOB
-Fatigue
-Heart burn
-Tightness
-Tingling
-Numbness
-In the leg: poor pulse, cold
🗑
|
||||
| Arterial Assessment | -Weak/Absent pulses
-Dependent rubor
-Pallor with elevation
-Hypertrophied toenails
-Tissue atrophy
-Ulcers
-Gangrene
-Absence of hair
-Parasthesia
-Tingling
-Numbness
🗑
|
||||
| Intermittent Claudication | -Most important manifestation of chronic arterial occlusive disease
-Pain that occurs when a muscle is forced to contract w/out adequate bld supply
-Any musc claudicate,but is more common in lower
-Reproducible pain
🗑
|
||||
| -Aortic-iliac disorders:pain in thighs,buttocks,hips
-Femoral-popliteal:calf
-Popliteal-tibial:leg and food
🗑
|
|||||
| Arterial Ulcers | -Arterial occlusion
-Intermittent claudication with > pain at rest
-Decreased/absent pulse
-Pale color
-Cool temp
-Skin:thin,shiny,hair loss
-Ulcers on feet,toes,heels
-Gangrene may develop
🗑
|
||||
| Amputation: Post op | -Elevate stump to reduce edema
-Wrap stump to reduce edema
-Immobilize knee in BKA
-Trapeze to assist in moving, developing upper body strength
-Phantom Limb sensation:normal for up to 2 years after surgery
🗑
|
||||
| Abdominal Aortic Aneurysm (AAA) | -Most common in men 40-70
-Large diameter and stress on area>susceptibility to rupture
-Most are asymptomatic
-Pt may c/o pulsating mass,back or groin pain
-Mottling of extrem
-Often,incidental finding on x-ray,ct,ultrasound
-Operable if >/5cm
🗑
|
||||
| AAA surgical repair | -Major surgery
-Recommended for >6cm or 4-6cm good surgical risk
-Incision for xiphoid process to symphysis pubis
🗑
|
||||
| AAA: Post op | -Risk for hemorrhage/fluid vol deficit
-Monitor vs
-Monitor UO (30-50ml/hr)
-Monitor abdominal girth
-Maintain Hgb > 8
-Monitor for hypovolemia
🗑
|
||||
| Hemostasis and Clot Formation | -Damaged blood vessels have several events that occur to prevent excessive blood loss
-3 stages: Vascular Spasm (vessel clamps down) Platelet plug formation (1st to site-make sticky plug) Coagulation
🗑
|
||||
| Parenteral Anticoagulants (SC/IV) | -Heparin sodium:wt based,can be reversed by protamine (1mg protamine per 100 units hep), monitor PTT,platelet,hematocrit
-Low molecular wt SC heparin:longer half life,need less lab monitor,lovenox, fragmin, therapeutic w/in 30min
🗑
|
||||
| Lovenox (enoxaparin sodium) | -Current recommended dosage is 1mg/kg SC every 12h
-New tx protocols: 1.5mg/kg qd for acute DVT w/concurrent warfarin sodium therapy; w/average LOS of 1.1d; continue at outpatient
🗑
|
||||
| Oral: Coumadin | -Reversible w/Vit K (not immediate)
-Dosage based on INR: should be in 2-3 range, 2.5-3.5 for prosthetic mechanical heart valve
-Don't use PT to determine dosage
-Affect extrinsic clotting
-Monitor PT/INR
-Has a half life of 0.5-3d
🗑
|
||||
| -Watch for bleeding: Overt (frank-nose bleed) Covert (tarry stools,blood in urine, NG drainage)
-Inform medical specialists if an invasive test is planned
-Green leafy veg can counteract effect
-Caffeine counteracts effect
-Many drug and herb reaction
🗑
|
|||||
| Antiplatelet Agents | -Inhibit platelet aggregation, usually by inhibiting synthesis of thromboxane A2
-Arterial thrombi: primarily platelet aggregates, antiplatelet agent used
-Venous thrombi: primarily fibrin and RBC, so anticoagulant drug used
🗑
|
||||
| Deep Vein Thrombosis | -Age>40
-Sx>30 min
-Venous stasis
-Heart attack/disease
-Pregnancy
-Trauma
-ERT/Oral contraceptives
-Malignancy
-Obesity
-Family hx
-Dehydration
-Long plane flights
🗑
|
||||
| DVT: Clinical Manifestations | -50% are asymptomatic
-Unilateral swelling distal to site
-Pain
-Redness,warmth of leg
-Low grade fever
-First sign may be PE
-Homan's sign:doesn't always mean DVT
🗑
|
||||
| Nursing Management DVT | -Elevate legs
-Compression stocks
-DON'T MASSAGE LEGS
-DON'T USE EPC IN AFFECTED LEG
-Monitor anticoagulation: bleeding,bruising,flank pain
-Monitor for PE: acute/lethal complication of DVT,SOB,maintain airway,chest pain,hemoptysis
🗑
|
||||
| Varicose Veins | -Permanently distended veins from loss of valve competence:congenital, trauma/obstruction to valves
-Not necessarily from prolonged standing
-C/O aching,heaviness,itching, swelling
-Early Rx:compression hose
🗑
|
||||
| Venous Ulcers | -Venous Occlusion
-Pain is aching
-Normal pulses
-Brown pigmentation over time
-Normal temp
-Marked edema
-Ulcers medial side of legs
-NO gangrene
🗑
|
||||
| Lymphadema | -Accumulation of lymphatic fluid in interstitial spaces:cause: swelling, usually arms&legs; surgical removal of lymph nodes or damage
-Can be bilateral,unilateral
-C/O of dullness or heaviness in limb, not necessarily pain
🗑
|
||||
| What if the pump (heart) is Ineffective? | -Decreased bf to organs and tissues
-Decreased O2 delivery
-Impaired waste removal
-Kidney function impaired 1st b/c require high bf
-All organs will fail eventually
🗑
|
||||
| Functional Diseases | -Corornary Artery Disease: impaired bf to pump b/c arteries that supply myocardium are partially occluded d/t atherosclerosis
-Heart Failure: pump is damaged so CO of blood is decreased
🗑
|
||||
| Heart Failure | -RHF is caused by LHF usually
-Pump failure could be a result of CAD because fluid backs up into lungs
-COPD can cause RHF as well
🗑
|
||||
| Electrophysiology Problems | -CAD: circ to myocardium and electrical system is impaired; impedes musc function and creates alterations in rhytm (v fib)
-HF: ineffective pump and altered anatomy can cause changes
🗑
|
||||
| Terms | -Contractility: pump part of the heart
-Conduction: electrical system in heart
-Cannot have one part function without the other
🗑
|
||||
| Cardiac Output | -Amount of bld ejected by the L ventricle in 1 min
-HR x SV
-Normal=4-8 L/min
-Measurement: swan-ganz cath in hosp or during cardiac procedures
🗑
|
||||
| Cardiac Index | -CO x body surface area
-2.5 - 4L/min
-Individualized measurement
-Watch in people who have had heart surgery
🗑
|
||||
| Preload | -Forced used to stretch cardiac musc
->EDV causes>preload > venous return
-Affected by: fiber length,stretch,vol, wall stress
-Frank-Starling law:> stretch = > force of contraction
🗑
|
||||
| Measuring preload | -BP
-Hydration status
-Cap refil
-JVD
-Lung sounds
-Weight
🗑
|
||||
| Afterload | -SV is inversely related
-Initial resistance that must be overcome by the ventricles to develop force and contract to open semilunar valves, push bld
-Resistance: L=systemic vasc
R=pulmonary vascular
🗑
|
||||
| Swan Ganz Catheter | -Special IV that goes into heart and measures: central venous pressure, pulmonary artery pressure, cardiac output
🗑
|
||||
| Measuring Afterload | -Blood pressure
-As blood pressure goes up, resistance goes up
-As resistance increases, so does the workload on the heart
🗑
|
||||
| Cardiac Symptoms | -Chest pain (angina)
-Palpitations (heart pounding, sob, ventricular arrhythmias)
-Tachcardia
🗑
|
||||
| Respiratory Symptoms | -Cyanosis
-Dyspnea
🗑
|
||||
| Related Symptoms | -Fatigue
-Syncope
-Weight gain
-Irritability
🗑
|
||||
| Heart Sounds | -S1 closure of mitral and tricupid, happens with onset of systole
-S2-closure of pulmonary and aortic, end of systole
-S3-normal in children
-S4-Atrial kick, HF,ventricles stiff
-Pericardial friction rub-fluid
-Murmurs-blowing sounds
🗑
|
||||
| Exercise Stress Tests | -Treadmill-with or without dye, non invasive
-Women can pass but have disease
-Balanced ischedmia in heart will show normal
-Dipyridamole Thallium-hold caffeine 24h, NPO, hold theophylline,aminophylline
🗑
|
||||
| Cardiac Cath | -Invasive
-Pre: NPO, iodine allergy, bleeding time, kidney function
-Post: bedrest for femoral for 6h, asses insertion site and check pulses distal q1hx6h, force fluids
🗑
|
||||
| Cardiac Enzymes | -Triponin I- only there is there is heart damage done
🗑
|
||||
| Cholesterol Levels | -HDL (healthy): >40, >60 ppl with CHD
-LDL (lousy): <160 w/0-1rf, <130 w/2+rf, <100 w/ CHD
-Triglycerides: <150
🗑
|
||||
| Cholesterol Management | -Overall goal = maintain total cholesterol <200
-LDL contributes the most in development of CAD
-Statin Drugs: Lipitor and Crestor (reduce LDL,triglyceride, Increase HDL); Adverse effects: musc weakness, liver toxicity
🗑
|
||||
| Obesity and Diabetes | -BMI: normal = 19-25, BMI = 25-30 (overweight), BMI = 30 (obesity)
-Diabetics: Keep fasting blood sugar <112
-HbA1c: <7%
🗑
|
||||
| Contributing Risk Factors | -Stress
-Homocysteine levels
-Elevated C-reactive protein
-Menopause
-Bacterial contamination
🗑
|
||||
| Pathophys of CAD: Atherogenesis | -Phase 1: <30y, clinically silent Type I,II,III lesions
-Phase 2:may be clinically silent, STABLE ANGINA, vulnerable plaque; Type IV, Va lesions
-Phase 3:Disruption of lesion w/thrombus,ACS,TypeVI lesion
🗑
|
||||
| -Phase 4:>degree of occulsion, ACS
-Phase 5:thrombus over disrupted lesion calcifies, crhonic angina and sometiem collateral circ, Type Vb-c
🗑
|
|||||
| Coronary Arteries:Left | -Divides into: left anterior descending which supplies anterior myocardium
-Circumflex-supples post wall, bld to av (10%) node and SA (45% of pop) node
🗑
|
||||
| Coronary Arteries: Right | -Supplies: blood to inferior and right side of heart
-blood to AV node (90%) and blood to SA node (55%)
🗑
|
||||
| Angina Pectoris | -clinical syndrome characterized by discomfort in chest,jaw,shoulder,back or arm
-transient
-d/t lack of o2 to cardiac cells
-caused by atherosclerosis
-doesn't mean you're having heart attack
-bld supply<bld demand
🗑
|
||||
| Stable Angina | -Pain/discomfort triggered by predictable degree of exertion/emotion
-stable pattern of symptom
-Pain/discomfort relieved by: nitroglycerin or rest
🗑
|
||||
| Unstable Angina | -Triggered by unpredictable exertion or emotion
-May occur at night
-I in freq,quality,severity, duration
-Medical Emergency:call 911
-Nitro may not relieve pain, nor rest
-Has progressed and could mean pt is having MI
🗑
|
||||
| Variant Angina | -Prinzmetal's
-Similar to classic angina; last longer
-Caused by arterial spasm,not blockage
-Usually occurs b/w midnight and 8am
-Occurs at rest w/out precipitating factor
🗑
|
||||
| Other Angina | -Nocturnal-occurs during REM
-Intractable-nothing you do makes it go away
-Postinfarction-after a heart attack still having ischemia
🗑
|
||||
| Assessment of Angina | -Characteristics:dyspnea,pallor,sweating, faintness,palpitations,dizziness,GI
-Aggravation: activity
-Relieving factors: nitro, rest, time
🗑
|
||||
| Diagnostic Tests for Angina | -EKG
-Stress test
-Cardiac Cath
-Echocardiogram
🗑
|
||||
| Treatment of Angina | -Relieve discomfort (MONA)
-Restore bf
-Prevent further attacks
-Pharmacotherapy:Nitro most common; beta blockers (reduce O2 demand), Aspirin (prevent platelet aggregation)
🗑
|
||||
| Nitro | -Anticipate side effects: headaches,orthostatic hypotension
-Monitor BP
-Remove transdermal patches at night
-Rotate sites
🗑
|
||||
| Other meds for Angina | -Morphine Sulfate: 2-6mg IV until pain relieved, decrease pain and workload on heart
-CCB: vasodilator, open coronary arteries
-Antiplatelet meds: aspirin,plavix, decrease stickiness of platelets
-Lipid-lowering agents
🗑
|
||||
| Emergency Treatment for AMI | -First 24h greatest risk for sudden death
-ER-door to needle time (thrombolytic therapy w/in 30min or angioplasty w/in 1h)
-4 Ds: door, data, decision, drug
🗑
|
||||
| AMI Pathophys | -3 zones of infarction: Infarct and necrosis; pneumbra (hypoxic); ischemia (reversible)
-Most common sites: Anterior (LAD), Posterior (RCA, L circ), Inferior (RCA)
🗑
|
||||
| All Suspected patients get MONA | -Morphine
-O2
-Nitro
-Aspirin
🗑
|
||||
| Myocardial Infarction | -Lack of O2 to cardiac cells beyond the occlusion in a coronary artery d/t blockage or spasm in artery
-Causes cell death
-Cell death = tissue death
-Tissue death = organ death
-Main cause of death=arrhythmias
-Longer the ischemia=greater cell dea
🗑
|
||||
| When do coronary arteries receive blood? Most common site for AMI? Time of day are AMIs most likely to occur? | -Diastole
-Anterior Wall
-In the morning
🗑
|
||||
| Medical Treatment for MI | -Diagnose type of MI
-Reduce pain
-Monitor cardiac rhythm
-Improve perfusion
-Primary angioplasty
-Stenting
-CABG
🗑
|
||||
| Thrombolytic Agents | -Dissolve the clot (urokinase,streptokinase)
-ABSOLUTELY contraindicated for hemorrhagic stroke, intracranial tumors, active internal bleeding
-RELATIVELY contraindicated with recent trauma, current use of anticoagulants,recent surgery, pregnancy
🗑
|
||||
| Complications Post MI | -Arrhythmias
-Cardiogenic Shock (fluid overload)
-CHF
-Pulmonary edema
-Pulmonary embolism
-Recurrent MI
-Pericarditis
-Renal failure
-Anxiety and Fear
🗑
|
||||
| Alteration in Comfort | -Pain means myocardial tissue death, PRIORITY!
-Limit visitors unless patient requests
-Calm environment
-Administer morphine
-Verbalize relief of pain w/in 15-20 mins
🗑
|
||||
| Normal Wave Form | -Depolarization= contract
-Repolarization = relax
🗑
|
||||
| Dysrhythmias vs Arrhythmias | -Most like to cause death in 1st 24h
-Continuous ECG monitoring
-Heart tones
-Monitor for ECG changes
-Give anti-dysrhythmics
-Monitor K+
🗑
|
||||
| Blood Brain Barrier | -Essential barrier to provide the best environment for the neurons (keeps parasites, bacteria out)
-Certain substances can not enter, or enter very slowly – many medications are not able to pass this barrier
-Water, glucose, oxygen go through quickly
🗑
|
||||
| Level of Consciousness | -Glasgow Coma Scale 1-15 (used for unconscious states) – below 9 is some level of coma: Best Eye Opening, Best Motor Response, Best Verbal Response
🗑
|
||||
| Neuro Checks | -Will depend on level of injury
-LOC (orientation X4) The most important indicator of neurologic function**
🗑
|
||||
| Cranial Nerves Testing | I-Olfactory–smell
II-Optic–visual acuity, periph vision,eye position
III-Occulomotor,IV-trochlear,VI-abducens – shape,size of pupils,nystagmus(lateral shaking of pupil),reaction to light & accommodation
V-Trigeminal-face sensation,chewing,jaw musc
🗑
|
||||
| VII-Facial–taste,expression,corneal reflex
VIII-Acoustic – whisper test, watch tick
IX-Glossopharyngeal – gag, say ah
X-Vagus – check voice for hoarseness, swallow reflex
🗑
|
|||||
| XI-Spinal accessory – shrug shoulders, turn head, move head against resistance
XII-Hypoglossal – deviation of tongue, asymmetry
🗑
|
|||||
| Motor Assessment | Muscle strength 5 point scale
0/5= contraction, movement absent
1/5= trace of contraction
2/5= movement with gravity only
3/5= movement against gravity
4/5= full ROM but with some weakness
5/5= Full ROM, normal strength
🗑
|
||||
| Gait Disturbances | Ataxic – staggering (drunk)
Dystonic – irregular, poor direction, like ataxic but weirder
Dystrophic – broad based – waddling
Equine – high steps (like a show horse) – help maintain balance
Festinating – on toes fast pace
🗑
|
||||
| Hemiplegic – one arm and leg swing wide with each step
Parkinsonian, short shuffling, leaning forward, dangerous gait, look at the floor, feet close together
🗑
|
|||||
| Scissor steps- slow, short steps, with legs crossing
Steppage – foot and toes high, foot slaps down (similar to equine)
🗑
|
|||||
| Sensory Assessment Terms | -Stereognosis-ability to feelfamiliar object wout looking
-Absence=astereognosis
-Graphesthesia-ability to recognize a written symbol
-Extinction-simultaneous stimulation
2-point stimulation- ability to differentiate 2 pin pricks from 1
🗑
|
||||
| Abnormal Sensations | Paresthesia- distorted sensation
Light touch feels like burning pain
Dysesthesia – localized, irritating sensation
Prickly, crawling
Hypoesthesia- reduced sensation
Hyperesthesia- abnormal excessive sensation
🗑
|
||||
| Response to Painful Stimulation | Localization- push away source of pain
Flexion withdrawal- move purpose
Decorticate
Flex withdrawal-moves wout purpose, grimacing
Abn Flex-adduct,internally rotate wrists,arms,extend legs
Abn Extend- extend,pronate,extend legs,arch back
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| Superficial Reflexes | Corneal- touch cornea
Pharyngeal- touch posterior pharynx with cotton tip applicator
Abdominal- stroke skin at umbilicus
Anal- stroke perianal region
Plantar- stroke sole of foot
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| Deep Tendon Reflex | Causes the muscle to stretch
Bicep jerk
Tricep jerk
Brachioradial jerk
Knee jerk
Ankle jerk
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| Abnormal Reflexes | Babinski
Snout- tap around mouth, pursing
Rooting- stroke side of face, mouth opens & head turns toward stim.
Sucking- touch lips, lips tongue and jaw move forward
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| Coma | Sustained unconsciousness
No response to verbal stimuli
Varying response to painful stimuli
No voluntary movement
Often altered respirations
Often altered pupil response
No blinking
**Consciousness = wakefullness,
aware of self/surounding
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| Causes of Coma | -Lesion putpressure on brain stem,esp RAS
Gunshot,Auto accident,blding in head,tumor
Sx generally unilateral
-Metabolic disorders affect brain supply of glc or O2
Hypoxia,blood loss,ischemia from cardiac condition,DM
Sx usually bilateral
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| CVA | Neurovascular deficit resulting in decreased blood flow to brain
Ischemic
Thrombus
Embolus
Hemorrhagic
Neurologic deficit
Determined by area or brain injured
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| Risk Factors for CVA | Hypertension
DM
Sickle Cell Anemia
Substance Abuse
Atherosclerosis
Obesity
Oral contraceptives
Anything that can change the lumen of a blood vessel
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| Thrombic CVA | Thrombus forms at bifurcation
Carotid, vertebral, basilar arteries
Cause is atherosclerosis- platelets get stuck in small lumen
Occur rapidly and progress slowly
Swelling in brain
Often occur during sleep
Lacunar CVA with DM
Collateral circulation
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| Embolic CVA | Thrombus mobilizes and occludes flow
Usually in middle cerebral artery or carotids
Generally more deficits – no time for collateral circulation to form
Source of clot
Carotids- plaque
Left ventricle – artial fibrillation
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| Hemorrhagic CVA | Aneurysm
Trauma- head injury
Hypertension
Rapid onset, rapid progression
Most fatal prognosis
Often see seizures – blood irritation
Avoid increasing bleeding
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| Transient Ischemic Attack | Temporary neurologic symptoms caused by short term hypoxia
Autoregulation fails
Return to full function possible
Serves as warning of possible CVA
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| Deficits of CVA | Hemiparesis, contralateral- weakness
Hemiplegia, contralateral- paralysis
Aphasia
Receptive
Expressive
Global
Dysarthria- often called dysphasia
Dysphagia- not dysphasia
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| Apraxia- can’t make purposeful movements
Vision changes
Homonymous Hemianopsia
Visual loss in same half of each visual field
Horner’s Syndrome
Eye paralysis, ptosis, constricted pupil, no tearing
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| Agnosia- can’t recognize familiar objects through senses
Unilateral neglect
Behavior changes
Incontinence
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| Right CVA | Confusion, usually pleasant
Impulsive
Poor judgment
Distracted
Left sided paresis or paralysis
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| Left CVA | Usually alert
Aphasia, more severe mobility issues
Easily frustrated
Emotional, crying
Right sided paresis or paralysis
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| Epilepsy | Recurrent episodes of one or more:
Loss of consciousness
Convulsive movements
Sensory phenomena
Behavior abnormalities
Caused by any process that disrupts the nerve cell membrane causing hyperexcitability
Drugs, head injury, tumors
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| Focal (Partial, Simple) Seizures | Most common
Abnormal discharge from 1 specific part of brain
Often begin in upper extremity&moves to entire side of body–Jacksonian march
Somatosensory affects certain sense
Tingling, seeing flashing lights, strange taste, strange smell, slurred speec
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| Complex Partial Seizure | Often called temporal lobe seizure
Automatisms- purposeless, repetitive activities while in a dream-like state
Often seen as psychotic behavior
Last 2-3 minutes, some up to 15
Patient is unaware of activity during seizure and is drowsy postictal
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| Generalized Seizures | What distinguishes generalized seizures from partial seizures is that there is always a loss of consciousness in generalized seizures
Tonic-clonic or absence
Various manifestations exist, but both hemispheres are generally involved
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| Absence Seizures | Usually in children age 4-puberty
Vacant stare, unaware of environment, unresponsive, rarely fall (not in a conscious state)
Lasts 5-30 seconds, 100 X per day
Interferes with learning, postictal confusion
Trigger, ↓ blood sugar, photic stimulation
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| Myoclonic Seizure (generalized) | Involves sudden uncontrollable jerking movements of a single muscle group or near muscle groups
Loss of consciousness and confusion postictally
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| Tonic-Clonic Seizures | Sudden loc
Tonic-body stiff,fall,cry,eyes open,pupils fixed,apnea (15-60 sec)
Clonic-rhythmic jerk,incontinent,bit tongue/lip,excess saliva,hyperventilation (2-5 min)
Post ictal-stupor/coma up to 1h quiet breathing,confusion,tired,deep sleep.
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| Trigger for Seizures | Hunger(↓ BS)
Fatigue, lack of sleep- cell excitability
Hyperventilation- CO2
Sensory stimuli – strobe light, loud sounds, certain music
Certain odors
Emotional stress
Fever, ETOH, injury, menstruation
Will be different for each patient
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| Nursing Interventions | Protection- padded rails, bed in low position at all times
Airway maintenance- tongue blades not used unless inserted before the tonic clonic phase
Roll on side if possible, loosen clothing around neck
Do not restrain
Reorient after seizure
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| Anti-seizure meds | Phenobarbital (10-25 day onset)
Therapeutic blood level 10-40
PO, IV
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| Dilantin (5-10 day onset)
Therapeutic blood level 10-20
PO, IV, (IM causes tissue breakdown)
Precipitates in dextrose solutions
Gingival hyperplasia, rash, blood dyscrasias, slurred speech, ataxiaMuscle pain, fever, rash
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| Status Epilepticus | Medical Emergency!
Seizures in succession or continuous seizures for 30 minutes or longer
Caused by sudden withdrawal of meds
Glucose and oxygen to brain becomes inadequate- permanent brain injury
Treat with IV anti seizure meds or Valium
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| Trigeminal Neuralgia | Intermittent episodes of intense pain in face
Entrapped trigeminal nerve, compression, tumor
Triggered by touch, cold, talking, chewing, brushing teeth
No diagnostic test
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| Treatment of Trigeminal Neuralgia | -Tegretal -to decrease the irritability of the nerve cells (neurons)
Anti spasmotics- Baclofen- to ↓ muscle spasms in face
Nerve blocks and peripheral neurectomy help to alter the perception of the pain- can affect facial movement
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| Bell's Palsy | Affects motor portion of the facial nerve (5th cranial nerve)
Unilateral paralysis of the muscles of expression – can’t show teeth, smile, raise eyebrows
Symptoms generally improve in a few weeks
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| Carpal Tunnel Syndrome | Entrapment of medial nerve
Sensory/motor changes in thumb, index, middle finger, & radial aspect of ring finger
Associated with gout, pregnancy, hypothyroidism, and repetitive use of hands and wrists
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| Testing | Tinel’s sign- tingling in hands,fingers when wrist tapped
Phalen’s test- numbness,tingling when wrist forcefully flexed for 20-30 sec
Wrist compression test-30 sec of pressure over the flexor retinaculum
EMG can also be done to definitively diagnose
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| Parkinson's Disease | Chronic, progressive
Caused by loss of dopamine
Cardinal symptoms
Resting tremors (pill-rolling)
Rigidity
Bradykinesia- slow, shuffling gait
Flexed posture – trunk, neck, limbs
Freezing movements (akinesia)
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| Nursing Assessment | Stooped posture,loss of balance, little facial expression,Shuffling,propulsive gait, leaning forward
Speech
Monotone,drooling,aphasia
Eating- dysphagia
Handwriting
Progressive micrographia
Hand tremors- pill-rolling (resting)
Restlessness- pacing
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| Huntington's Disease | Degenerative, genetically transmitted
Abnormal movement- chorea
Begin subtly and become dramatic
Intellectual decline
Emotional disturbances
Progressive, fatal from respiratory complications
No known treatment
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| Multiple Sclerosis | Chronic, progressive, demyelinating
Onset age 20-40, in cold climates
Immune disorder?
As myelin degenerates, plaque forms causing inflammation, edema, scarring
Nerve impulse does not conduct appropriately
Exacerbations & remissions are classic
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| Symptoms of MS | Vary widely
Weakness/paresthesia in 1 extremity
Vision changes/loss
Incoordination
cerebellar involvement
Bowel/bladder dysfunction
spinal cord involvement (constipation)
Fatigue
Memory loss, confusion
Characterized by relapsing-remitting
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| Guillain-Barré Syndrome (GBS) | Inflammatory, unknown cause
Degeneration of myelin on peripheral nerves
Often preceded by URI, or GI infection
Cytomegalovirus, Epstein-Barr, Campylobacter jejuni are thought to be causes
Associated with HIV
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| Symptoms of GBS | Initial phase
Ascending weakness,evolve over h/d
Plateau phase-no progression of sx
Loss of deep tendon reflexes
Paresthesia
Resp musc weakness
Recovery phase-6 mo.-2y
Remyelination in descending pattern
Not always complete recovery of motor/senso
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| Myasthenia Gravis | Autoimmune disease
Loss of acetylcholine receptors in postsynaptic neurons of neuromuscular junction
Cause unknown
Young women > men
Older men > women
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|
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| Symptoms of MG | Increasing weakness with muscle use
Ptosis, diplopia most common
Dysphagia, nasal speech
Weak peripheral muscles
Respiratory depression
Tensilon test- definitive diagnosis
Atropine as antidote
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| Pathophys of MG | ACH- neurotransmitter needed for proper muscle function
Antibodies occupy the ach receptor sites
Cholinesterase (acetylcholinesterase) stops the action of ach.
Cholinesterase inhibitors are drugs that prevent the breakdown of ach.
-No cure
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| Complications of MG | Myesthenic Crisis
Insufficient med (sudden stop)
Treat w/cholinesterase inhibitor
Possible mechanical ventilation
Extreme musc weakness
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|
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| Cholinergic Crisis
Over med
Abd cramping,excessive lung secretions, severe musc weakness
Possible mechanical ventilation
Treat w/Atropine
🗑
|
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