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Adult Health
Exam 3
| Question | Answer |
|---|---|
| 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) |
| Lower GI problems: Gastroenteritis | -Caused by food-borne bacteria -Pts strain to have a bowel movement -Expect them to resolve in 1-5 days |
| Appendicitis | -Causes: stone occludes the lumen of the appendix -Bowel swelling,adhesions, kink -Bacterial Infection |
| 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 - |
| Peritonitis | -Double-layered membrane lining walls&organs of ab cavity;filled w/1500ml fluid;lots of nerve endings in peritoneum -Inflammation from perforated colon,fistula, contamination during bowel sx, ruptured bile duc -Agents: ecoli,klebsiella, pseudomonas |
| 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 |
| Diagnosing Peritonitis | -Ab flat plate-air in peritoneum, dilated bowel loops -I WBC -Fever -Shallow respirations to try not to move which I pain -N,V |
| Tx for Peritonitis | -Laparotomy to correct perforation -Abscess-surgical draining (PJP drains, systemic antibiotics not helpful) -Incision may be left open to heal by tertiary intention |
| Inflammatory Bowel Disease | -Types: Crohn's disease, Ulcerative colitis -Chronic, recurrent (each leaves colon more scarred and less able to absorb nutrients) -Young adults (15-30) -No known cure, tx-symptomatic |
| Crohn's Disease | -Involve any part of GI,usually terminal ileum/LI -Involves all layers of GI mucosa -Lesions in several segments at same time -Granular lesion on mucosa -Fissues penetrate bowel wall -Fistuals connect bowel to other structures |
| Ulcerative Colitis | -Crypt abscess,secrete purulent discharge-necrotic -Involves mucosa&submucosa only -Starts in rectum -Inf cause further inflamm -Perforation of ulcer lead to peritonitis -Lead to colon cancer -Contiguous portions of bowel -Remissions/exacerbatio |
| 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 |
| Crohn's Nutrition Problems | -Less intestinal absorptive surface -Malabsorption of protein, carb, fat, vit -Metabolic needs increase d/t inf and inflam - body work harder -Immune system affected-poor nutrition=D resistance to inf, D wound healing |
| 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 |
| Tx of Crohn's and UC | -Surgical removal of:damaged colon, fistulas, obstruction d/t inflam -UC: total removal of LI w/ permanent ileostomy -Antibiotics/steroids short term -TPN -Exacerbations w/remissions are common |
| Ostomy | -Stoma should be pink; if cyanotic, pale, dusky notify surgeon immediately -NPO until bowel activity returns |
| Applying Stoma Pouch | -Stoll is irritating to ab skin -Pouch should fit snuggly around stoma, to minimize skin exposure to stool |
| Teaching for Pt with Stoma | -Enteric Coated pills-look in stool -Assess skin w/ each pouch change -May not be able to tolerate some foods-if D or pain eliminate the foods -Need to chew food more completely -High fiber can cause C/obstruction |
| 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 |
| GI Cancer | -Generally in large intestine or rectum -R/t low residue, high fat, highly refined food intake -Genetic link,hereditary -Polyps are a precursor, usually removed |
| Symptoms of Colon Cancer | -Rectal Bleeding** -Change in bowel habits, shape of stool -Ab pain -Wt loss -Anorexia -Anemia |
| Tx of Colon Cancer | -Surgical removal -Prognosis depends on: depth of penetration, grade of tumor, lymph nodes involved, margins of removed tumor -Radiation, Chemo |
| Diverticulitis vs. Diverticulosis | -Inflammation of an out pouching or herniation of the intestinal mucosa through the muscular coat of the LI, usually sigmoid -Common with obesity -Pain is most likely symptom |
| Intestinal Obstruction | -Most in SI -Can be partial or complete -Caused by adhesions, hernia, cancer, intussusception, lack of blood supply, twisting of colon -V and pain most likely symptoms |
| Oral Disease | -Tooth decay and Peridontal disease (plague and tobacco use, enamel missing w/pts who force vomit) -Most common cause of tooth loss -Best tx=prevention |
| Musocitis/Stomatitis | -Inflam of oral cavity soft tissue -Systemic/Traumatic -Can be braces,mouth breathers,chem trauma, harsh hygiene products, foods |
| Primary and Secondary | -Herpex simplex(viral)local (common,can lay dormant and then erupt,stress,can tx with sovrix) -Vincent's Angina(bacterial) entire mouth pain,choking sensation, fever, loss of app, lymph node involvement in head and neck) -Secondary-opportunistic inf |
| Candidiasis-Moniliasis | -Thrush -Candida-albicans-yeast like fungus -Immunosupression,DM,ATB/Steroid Rx, tube feeding -Secondary inf -Pt on chemo |
| Oral Tumors | -Occupy space and cause pressure on adjacent structures -Functional and cosmetic problems |
| Leukoplakia | -Cause-chronic irritation (smoking), ill fitting dentures, excessive alcohol,HIV, marijuana, poor nutrition -Looks like canker sore, whiter and waxier -Precancerous -Generally sx removed -More common in men (30-40) -Doesn't usually hurt |
| 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 |
| Esophageal Disorders: Regurgitation | -Incompetent lower esophageal sphincter -Overtime acid burns esophagus and leads to scarring and leads to strictures |
| Esophageal Disorders: Dyspepsia | -Gastric vs cardiac (right coronary artery which feeds right side of heart which is close to diaphragm and can show signs similar to GERD |
| Esophageal Disorders:Achalasia | -Incomplete relaxation of LES -Cause: motor disorder, unknown, < motility of lower 2/3 of esophagus -Can lead to: dysphagia, emesis, progression in freq -Semi-fowlers position: don't lie down after eating a meal, head of bed up -Obsesity-prone to thi |
| Gastroesophageal Reflux Disease | -GERD -Backward flow of GI contents into esophagus -Stomach acid irritates lining -Caused by relaxed LES -Associated w/obesity,pregnancy, smoking, caffeine/chocolate, and ETOH intake |
| 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 |
| Lifestyle Changes: GERD | -Small meals,more freq -Drink fluids to help food pass -Eat slowly,drinking b/w bites -Avoid hot,spicy,fatty foods, alcohol,choc,citrus juice to D acid production -HOB 6-8in, not with pillows,use blocks -Lose wt -Upright 3h after meals |
| 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 |
| Medications for GERD | -Antiemetic Cholinergic: increases LES pressure, increases gastric emptying, 30-60 ac |
| Hiatal Hernia | -Part of stomach protrudes through diaphragm into thoracic cavity -Type I: sliding, upper stomach& gastroesophageal junction displaced upward into thoracic, most common -Type II: rolling, gastroesophageal junction stays below diaphragm |
| Esophageal Cancer | 1)Squamous cell: alcohol use, smoking,HPV 2)Adenocarcinoma:barrett's esophagus, obesity, ingestion of smoked meats, vit a/c deficiency, pain w/swallowing, general pain -Symptoms:progressive dysphagia,odynophagia,pain |
| Enternal Nutrition Therapy | -NG tube: easy to dislodge,throat irritation -G or J tube (long term,sx) out of sight, feeding more elemental b/c stomach digestion is bypassed -PEG:most common permanent long term feeding, non surgical outpt, check if pt has deviated septum |
| Methods of Tube Feeding | -Bolus: 300-500ml several times a day, 60 ml increments 10-15 min or gravity bag over 30-60 min -Continuous: 24h feeding w/a pump, can still eat, better tolerated, HOB up at all times |
| Enteral Feeding Potential Problems | -Aspiration especially with NG tubes -Vomiting up NG tube -Pain after PEG placement (few days) -Irritation or infection at skin site -Nasal irritation from NG |
| Blood Tests | -Serum protein:intravascular oncotic pressure (swelling of tissue) -Lymphocyte count:part of immune system,measure of nutritional state -Nitrogen:catabolism v anabolism -Stool analysis: culture and lipid content |
| 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) |
| Radiography | -CT scan:npo after bfast, masses, inflammation, abscesses |
| Ultrasound | -Non-invasive, need conducting gel -Sound waves that bounce back to wand -Visualizes tumors, adipose tissue,abscesses, hematomas -Not good for bone visualization -NPO for 8-12 h-gas interferes -Pelvic ultrasound-force fluids to get a full bladder |
| Endoscopy | -Direct visualization of GI mucosa, NPO -Useful for GI bleed, esophageal injury, inflammatory bowel, gall bladder disease -Sedation given IV, throat spray anesthesia |
| Upper Endoscopy Procedure | -Procedure consent required -NPO 8-12h, check pt for loose teeth/dentures -Left lateral sims position-prevent aspiration -Scope through mouth -Check gag reflex before re instituting oral intake! -Throat discomfort rare |
| Gastric Analysis | -Obtained through endoscopy or by inserting NG for 1h -Hpylori-gastric ulcer -malignant cells -HCL and pepsin levels-ulcer,carcinoma,pernicious anemia -Esophageal manometry-motor function |
| Clinical Manifestations of GI dysfunction | -Pain -Anorexia -N,V -Bleeding -D -Belching and flatulence -Indigestion |
| GI tubes | -Purpose for insertion 1)decompression: get rid of air (short) 2)lavage: rinse out (short) 3)gastric analysis 4)tube feedings |
| Acute Gastritis | -Inflammation of gastric mucosa d/t breakdown in mucus lining -Incidence I w/age -At risk-heavy smokers,drinkers -Aspirin,NSAIDS at risk -Severe N,V,ab tenderness, epigastric burning, aching, bleeding,D -NPO until symptoms ease,then slowly increase |
| 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 |
| Complications after Surgery | -Sx only if meds don't work -Ulcer at incision site in stomach -Hemorrhage -GERD -Absorption problems leading to nutritional problems (I intrinsic, I GI emptying) -Dumping syndrome -Pyloric Obstruction |
| TPN | -Special IV solution designed to support the nutritional needs of clients who do not have a functioning GI -Solution is indiv to the nutritional needs of the pt and is managed by dietician -Regular blood tests monitor changing nutritional needs |
| When to use TPN | -When a pt can't be fed orally or by tube feeding -usually used for pt who need long term nutritional support, when GI access is not possible -No functioning gut -Rarely a short term tx |
| What is in TPN | -Carbs-50-70% glucose solution -Fat emulsion-10-30% daily caloric intake -AA -Electrolytes -Minerals -Vit -Trace elements -Bld tests daily to monitor levels -Cannot give ANYTHING through same tubing |
| How is TPN supplied | -3000 ml bag with all nutrients added to infuse for 24 hours -Lipid can be added to large bag or given separately -Home:TPN often smaller bags and lipids are added to solution |
| Vascular access for TPN | -Central venous access required so blood volume can mix with solution and dilute it -Subclavian line, PICC, port-a-cath -Peripheral veins become inflamed by high concentration of TPN and collapse or become phlebotic |
| 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 |
| How to check symmetric chest expansion | -Place hands on post chest, thumbs facing each other -Have pt take deep breath -Movement should be symmetrical |
| 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 |
| Adventitious breath sounds | -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 |
| Definitions | -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 |
| Respiratory Diagnostic Tests | -Pulmonary Function Tests:spirometry tests to measure vital capacity, tidal vol,etc -Arterial blood gas -Ventilation-perfusion scan -Chest xray -CT scan -MRI -Pulmonary angiography -Pulse ox |
| pH | -Normal serum pH = 7.35 - 7.45 - < 7.35 = acidosis - > 7.45 = alkalosis |
| Lungs | -Volatile acids are acids that can be converted to gases -During respiration lungs exhale large quantities of potential acid-CO2 |
| Kidneys | -Acids that can't be converted to gases must be eliminated in the urine -Fixed acids are excreted through the kidneys by the regulation of bicarbonate, which is a base |
| Regulation of Acid-Base | -If any disease process,meds affect pH. the kidneys or lungs will COMPENSATE for the alteration -Lungs will blow off or retain acid by regulating CO2 -Kidneys will eliminate or retain acid by regulation of HC03 - |
| 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 |
| Obtaining Arterial Blood Gases | -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 |
| -pH = 7.55 -pH = 7.23 -CO2 = 55 -CO2 = 33 | -Alkalotic -Acidotic -Resp acidosis -Resp alkalosis |
| -PaO2 (oxygen) = 66 -CO2 = 51 -pH = 7.32 | -hypoxic -hypercarbic -acidotic |
| -CO2 > 45 -CO2 < 35 -Bicarb > 26 -Bicarb < 22 | -Respiratory-could cause increase acid -Respiratory-could cause increase base -Metabolic-more base -Metabolic-more acid |
| -O2=91,CO2=50,pH=7.33,HCO3=24 -O2=87,CO2=33,pH=7.48,HCO3=22 | -Respiratory Acidosis -Respiratory Alkalosis |
| More ABGs | -pH out of range just a little wont affect pt much -As pH gets higher&higher or lower&lower,expect that cellular death is occurring,pH must be corrected -High CO2=acidosis -Low CO2=alkalosis -High HCO3=alkalosis -Low HCO3=acidosis |
| 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 |
| MRI | -Uses magnetic fields rather than radiation to create pics -More detailed than CT -No metal -No dye needed most of the time -Claustrophobia |
| 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 | -Lower -REVERSIBLE bronchiole spasms -exposure to allergens/irritants/triggers -IgE initiates inflam process -Chronic Inflam process:histamine, bradykinins,prostaglandins released cause inflam; edema secretion,fluid accum;mucous, airway restriction |
| 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 |
| Diagnostic tests: Asthma | -Pulmonary function tests - most important to determine degree of dysfunction -Pulse ox -ABGs -Chest xray |
| 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 |
| Classification of Asthma Severity | 4)Severe Persistent:continual sx;limited physical activity, freq exacerbations |
| Medical Goals: Asthma | -Reverse airway spasm -Prevent complications -Maintain effective gas exchange -Control inflammation -Emergency control begin with beta 2 antag -Anticholinergics block parasymp and relax smooth musc -Steroids reduce inflamm |
| Asthma:Medical and Nursing Goals | -Prevent acute attacks (can cause irreversible damage) -Maintain normal activity levels -Maintain normal lung function -Minimal use of drugs -Reduce side effects of meds -Client satisfaction |
| 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 |
| Medications for Asthma | -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 |
| Medications for Asthma | -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 |
| Medications for Asthma | -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 |
| Types of Emphysema | 1)Centrilobular/Centriacina:most common, damage in bronchioloes&UL, smokers 2)Panloular/panacinar:affect bronchioles&alveoli, affect LL,smokers,AAT deficiency, lung base of smokers w/centriacinar form |
| Types of Emphysema | 3)Parasetptal/Panacinar:alveoli in LL,alphatrypsin1 deficiency, prone to pneumothorax, will spontaneously just blow a hole in outer layer of lung |
| 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 |
| Why right sided heart failure? | -Can occur with both bronchitis and emphysema -Due to high bld pressure in lungs -Causes increased workload on rt side of heart which feeds bld to lungs -aka cor pulmonale |
| 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) |
| Hx of Asthma and COPD | -More prone to respiratory inf -May need to by on O2 longer -More focused on asst on lungs/puml status -harder to get off mechanical vent -Lungs are first organ to fail in shock, at greater risk for mortality |
| 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 |
| Pulmonary Emboli: Origination and Composition | -Air Embolus: IV infusions, uterine douches, sx tx of head/neck, neurosurgery, open heart sx, chest trauma -Fat embolus:long bone fx, soft tissue damage, ovary&stom cancer, pancreatitis, renal transplant,cardiopul bypass, burns |
| Pulmonary Emboli | -Lower lobes are more frequently affected:high velocity of blood flow -Ventilation-Perfusion Mismatch: altered gas exchange (shunting of oxygenated blood) |
| Medical Consequences of Pulmonary Emboli | -VQ mismatch: increase alveolar dead space -Pneumoconstriction (blood vessels constrict): increase airway resistance, hypoxia, hypoxemia, humoral agents released, loss of surfactant |
| 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 |
| Diagnostic Tests Pulmonary Emboli | -X-ray:rule out other dx -EKG:R ventricular strain,change in ST segment,arrhythmia -ABGs:D PO2&PCO2 -V/Q:distribution of ventilation, pulmonary vasculature,should be =distribution -Pul Angiogram: most effective but tendency for more complications |
| REMEMBER | -If you suspect PE, your first concern is always the pts airway! -When pt survive a PE, they will need to be anticoagulated |
| **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 |
| Management of Client with Pulmonary Emboli | -Fibrinolytic Therapy -Used if hemodynamically ustable -Lysis clot to restore right sided heart failure -Little impact on national mortality rate -Most common drugs: streptokinase, urokinase |
| Medical Management of Pulmonary Emboli | -Venal cava interruption: umbrella filter, greenfield filter -Pulmonary embolectomy -Position: semi-fowlers -Cough/deep breathe -Morphine |
| Vascular System | -Vast network of vessels -Delivers nutrients to tissues -Removes metabolic wastes -Blood flow is delivered proportionate to metabolic needs -Systemic and Pulmonary circulation |
| Primary Nursing Diagnosis | -Alteration in Tissue perfussion |
| 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 |
| Vascular System | -Arteries-arterioles-cap-venules-veins-hrt-arteries -Hydrostatic force-energy when hrt contract forces bld out of hrt along vasc path -Bld flow/hydrostatic force D as gets further from hrt -Vol of bld flow from arteries to cap determines bp |
| 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) |
| Blood Viscosity | -Polycythemia = I viscosity -Anemia - D viscosity -Aspirin,Coumadin,Heparin = D viscosity |
| Blood Pressure control Systems | -Arterial baroreceptor and chemoreceptor system -Regulation of body fluid volume -Renin-angiotensin system -Vascular autoregulation |
| Baroreceptor Chemoreceptor Control | -Baroreceptor: in aorta in carotid sinuses, send to medulla - arterioles; sensitive to O2,CO2, and pH = affect BP |
| Hormonal Response | -Long term adaptive mechanisms -Renin-angiotensin-aldosterone system activated by renal system -Bradykinins and histamine can cause vasodilation, I cap wall permeability -Serotonin, prostaglandins can have vasoconstrive/vasodilation effects |
| 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 system | -Retention of Sodium by kidney -Water retention by kidney -Salt appetite, drink will increase bp |
| 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 |
| Vascular auto regulation | -Endothelial cells produce nitric oxide (dilate arterioles) -Tissue regulation (local-except brain and heart) -Neural control (sympathetic activity <tissue circ > brain and heart circ) |
| 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 |
| Taking an accurate blood pressure | -Be aware of mastectomy,fistulas,stents -Best indicator of arterial perfusion -Arm @hrt level -Proper cuff size -Both arms;supine,sit&stand 1st time -Document position -Repeat in arm w/highest rding -Assess for anxiety -Rest 5 min b/w each |
| Hypertension | -Silent Killer -Prevalence:eldery,AA,<educated&socioeconomic -ACS #1 consequence -ASHD,CVA,PVD,AA,nephropathy |
| 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 |
| Primary HTN | -Multifactoral with no identifiable cause -Persistent,progressive,>peripheral artery resistance -Severity depends on: # of risk factors, rf length of time, comorbid conditions |
| Secondary HTN | -Identifiable cause -Chronic renal disease (renal artery stenosis) -Adrenal tumors (pheochromocytoma) -Increased aldosterone -Acute stress -Pituitary tumors |
| Risk Factors for HTN | Non-modifiable: genetics,age,gender,ethnicity, family hx -Modifiable:diabetes,stress,obesity,nutrition (high Na diet, low Ca,K,Mg), substance abuse |
| 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 |
| Aterial Disorders | -Ateriosclerosis -Atherosclerosis -Arterial disorders -Arterial Ulcers -Aneurysms -No/wk pulse, cool, blue |
| Arteriosclerosis | -Generic term -Thickening,loss of elasticity, and calcification of arterial walls -Occurs with aging -Most often associated w/htn and DM -Hardening of the arteries |
| Atherosclerosis | -Peripheral art occlusive disease -Chronic complex inflam -Occludes elastic/muscular art -Yellowish plaques of choles,lipids,&cellular debris collect in inner walls of art -Vessels become thick,fibrotic,calcified,lumen narrows -D circ to organs/tis |
| Unstable or Vulnerable Plaques | -Most dangerous hidden in walls of art, undetected until sudden rupture -Thin fibrous caps,inflam -Tx for traditional plaque blockages are the same -Rare have s/s,missed on caths&stress tests, detected by intracoronary ultrasound |
| Atherosclerosis | -Most common at bifurcations -Major cause: of CAD,angina,MI,CVA,abdominal aneurysms,PVD -Risk factors:age,hereditary,smoking,diabetes,HTN, hyperlipidemia, obesity,menopause |
| 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 |
| Non-Invasive Vascular Studies | -Doppler ultrasound studies -Flow velocity testing -X-rays -Exercise testing -CT scans and MRI -Lab work |
| Invasive Vascular Studies | -Intravascular ultrasound studies -Intracoronary ultrasound studies -Angiography -Arteriography:looks specifically at arterial blood flow |
| Recommended Behavioral Changes | -Stop smoking -Exercise -Lipid control -HTN and DM control -Avoid sitting standing for too long -Avoid restrictive clothing, stockings or crossing legs -Inspect feet daily -Elevate legs may cause more pain, may need to LOWER legs to improve bf |
| Interventional and Surgical Therapies | -Interventional:balloon angioplasty,artherectomy, intravascular stenting -Surgical:Endarectomy (remove plaque from arteries) Bypass Grafting (put in completely new artery) |
| Peripheral Arterial Disorders | -Arteries deliver oxygenated blood to extremities -If blood flow is impaired: collateral circ develops, anaerobic metabolism = acidosis, cellular death, loss of tissue/extremity |
| 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 |
| Intermittent Claudication | -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 | -Oldest surgery known to man -Tx for:gangrene,severe inf,injuries, cancers,limb threatening disease, rest pain |
| 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 |
| Aneurysms | -Permanent localized dilation of an artery -Develop gradually -Most commonly caused by atherosclerosis and compounded by HTN -Can occur in any artery but has worst prognosis in brain,thoracic and abdominal aorta |
| 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 |
| Clot formation | -Thrombus:platelets encounter damaged or diseased areas on walls of blood vessels or heart&attached clot forms -Embolus:thrombus that breaks loose&travels through the circ system -Both can cause death if they block bld supply to essential organs |
| Anticoagulant Therapy | -Prophylactic action, act by preventing:fibrin deposits,extension of thrombus, thromboembolic complications -Prevention of intravascular thrombosis by decreasing blood coaguability -No effect on clots that have already formed |
| 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 |
| Coumadin | -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 |
| Antiplatelet Medications | -Aspirin,Plavix,Persantine,Ticlid, Glycoprotein ihibitors (emergency), Pletal |
| Aspirin | -Inhibits a COX enzyme, decrease thromboxane A2 mediated platelet aggregation -Average dose=81-325 mg po daily -Average cost=$10 for 100 pills -No labs to monitor |
| Plavix | -Inhibits ADP receptor site on platelet, prevent ADP-mediated platelet aggregation -75mg po daily -Decrease risk of second stroke or MI -Take daily with aspirin -Does not require routine lab monitoring |
| Venous and Lymphatic Disorders | -Thrombophlebitis -DVT -Venous ulcers -Varicosities -Lymphedema -Swelling,redness,still have pulse |
| Thromboplebitis | -Cause:thrombus,inflammation on superficial or deep veins -Superficial:easy to dx,post IV or caustic IV infusion -DVT:blood clot in deep veins, 1/3 pt after sx, women>men |
| 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 |
| Deep Vein Thrombosis | -Virchow's Triad: Venous stasis, hypercoagulability, trauma to venous wall |
| 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 |
| Post Op Prevention of DVT | -Reduce venous stasis -Passive/active ROM -EPC (bedrest > 24h) -Compression stockings -Elevate foot of bed -Change position often -Reduce hypercoagulability: low dose anticoagulation |
| DVT Medical Management | -Dx:Venous duplex scanning -Anticoagulation:prevent clot extension,development of new thrombi -Heparin:monitor APTT (20-36 sec), IV continuous fusion,4h half life,monitor blding,reverse with protamine,maintain APTT 1.5-2.5x normal (60sec) |
| Coumadin | -Monitor INR -Keep INR 2-3.5 -Take 24-48 hr to take effect -Start w/heparin and add coumadin and when INR is 2-3 then heparin is d/c -Taken for 6 mo after resolution of clot -Antidote is vit K |
| Fibrinolytics | -Clot busters -TPA,Streptokinase -Infused into vascular system to dissolve a clot |
| 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 |
| Varicose Veins | -Sclerotherapy-cosmetic, contraindicated before sx -Vein ligation,stripping |
| 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 |
| Lymphadema Treatment | -No cure -Compression stockings on limbs -Pneumatic pumps -Elevation -Keep moving |
| FOOT CARE | KNOW THIS: PAGE 1313 |
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