Finals For Adult Health2

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sudden onset, insidious occult bleeding can also be major problems. severity of bleeding depends on whetere the origin is venous, capillary or arterial. bright red blood has not been in contact with stomach acids. "coffee ground" vomitus reveals that blood and other contents have been in teh stomach for some time.Melena (black, tarry stools) indicate slow bleeding from upper GI. most common causes: drug induced, esophague (esophgeal varices, esophagitis, malory weiss tears), gastric cancer, hemorrhagic gastritis,, PUD, stress ulcer, blood dyscrasias, leukemia, aplastic anemia, renal failure. Clinical manifestations: N/V, blood stools, vomiting bright red blood

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upper GI bleed etiology and clincial manifestations

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coagulate or thrombose the bleeding artery and then reduce the necessity for sugery. use thermal (heat) probe,(etc.) surgical therapy: indicated when bleeding continues regardless of therapy provided and know teh location of the bleed. Drug therapy: during acute phase decrease HCl acid secretions and neutralize HCl acid. injection therapy wtih abosulte alcohol or epinephrine is effective for acute hemostasis. vasopressin tehrapy is used to treat variceal bleeding-vasoconstriction. it is used to treat upper GI bleeding in those who do not respond to other therapies.

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collaborative care upper Gi bleed

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assess: LOC, vitals, appearance of neck veins, skni color and cap refill, check for distention, guarding, and peristalsis in the abdomen.
Acute interventions: start and infusion and maintain IV line for fluid and blood replacement, acurate I&Os-urine checked hourly. avoid beets and mouthwash, hemodynamic monitoring provides an accurate adn quick assessment of blood flow and pressure wtih the cardiovascular system. montior for blood in stools, Hgb & Hct. every 4-6hrs. if actively bleeding, BUN and creatnine, oral feedings of clear liquids or milk.

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Uper GI bleed

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occur in any portion of the stomach, most commonly in teh less curvature in close proximity to antral junction; mortality rate high than for duodenal ulcers in people >50, found in individuals with lower socioeconomic class or unskilled workers, H.pylori in 50-70% of patients, drugs that induce: asprin, corticosteroid, NSAIDS, and reserpine.
clinical man.: not rich in pain sensory, lack of pain, pain high in the epigastria adn occurs spontaneously about 1-2 hours after meals-burning or gaseous-can occur if stomach is empty or when food injested.pain usually occurs 2-4hrs. after meals. relieved by antacids alone or in combination with H2R block and sometimes by foods that neutralize and dilute HCl acid.

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gastric ulcer

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Clinical man: when pain occurs-burning or crampliketendecny to occur continuously for a frew weeks or months and then disappear and reappear later. account for 80% peptic ulcers, (35-45yrs), develpment associated with high HCl acid secretion. high risk for development from these diseases: COPD, cirrhosis of liver, chronic pancreatitis, hyperparathyroidism, chronic renal failure, alcohol injestion adn heavy msoking habits, H.pylori in 90%-plays heavy role.

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duodenal ulcers

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most common complication of peptic ulcer disease. It develops from erosion of the granulation tissue found at the base of the ulcer during healing or from erosion of the ulcer through a major blood vessel. Duodenal ulcers account for a greater percentage of upper GI bleeding episodes than gastric ulcers.

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hemorrhage

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considered most lethal complication of PUD, commonly seen in penetrating duodenal uclers,perforated gastric ulcers most often located on less curvature of stomach,gastric ulcers mortality rate is higher even though dodenal ulcers perforate more.characterized by sudden and dramatic onset, patietn experience sudden, severe upper abdominal pain that quickly spreads through out the abdomen

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perforation

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in early phase gastric emptying is normal to near normal.patient may show signs of swelling in upper abdomen indicating dilation of teh stomach, loud peristalsis can be heard, adn visible peristaltic waves are often observed passing across abdomen from left to right.

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gastric outlet obstruction

Front 9

Conservative therapy:
Adequate rest
Bland diets (six small meals a day)
Cessation of smoking
Drug therapy
H2R blockers
PPI
Antibiotics for H. pylori
Antacids
Anticholinergics
Cytoprotective drugs
Stress reduction

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collaborative care for gastric and duodenal ulcers

Front 10

Acute exacerbation without complications:
NPO
NG suction
Adequate rest
Cessation of smoking
IV PI
Antacids
Anticholinergics
Sedatives

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collaborative care for gastric and duodenal ulcers

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Acute exacerbation with complications (hemorrhage, perforation, obstruction)
NPO
NG suction
Bed rest
IV fluid replacement (LR solution)
Blood transfusion
Stomach lavage (possible)
Surgical therapy
Perforation-simple closure with omentum graft
Gastric outlet obstruction-pyloroplasty and vagotomy
Ulcer removal/reduction
Billroth I and II
Vagotomy and pyloroplasty

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collaborative care for gastric and duodenal ulcers

Front 12

heartburn most common symptom-burning, tigh sensation, can follow ingestion of food or drugs taht decrease LES pressure or are directly irritating to esophageal mucosa. relieved by milk or alkaline substances or water. small frequent meals advised. no milk at bedtime, chocolate, peppermint, coffee, tea, OJ, tomato based products, drug therapy starts with antacids and OTC H2R blockers adn increased to H2R blockers (pepcid) and finally PPIs (prilosec). surgical therapy necessary if conservative therapy fails-nissen fundoplication, toupet fundoplication

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GERD

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produce quick but short lived relief of heartburn. They act by neutralizing HCl. They should be taken 1-3 hours after meals and at bedtime. OTC antacids with or without alginic acid may be useful in patients with mild, intermittent heartburn. The alginic acid reacts with sodium bicarb. And forms a viscous solution that floats tot eh surface of the gastric contents and coast the esophagus, acting as a mechanical barrier to reflux.

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antacids

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Cimetidine): inhibits histamine at H2 receptor site in the gastric parietal cells, which inhibits gastric acid secretion. Used for short term duodenal and gastric ulcer treatment and maintenance; management of GERD. SE: confusion, headache, anxiety, diarrhea
AR: paralytic ileus, jaundice, agranulocytosis, thrombocytopenia, Neutropenia, aplastic anemia, increase in PT, exfoliative dermatitis, convulsions, dysrhythmias

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H2 antagonists

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suppresses gastric secretion by inhibiting hydrogen/potassium ATPase enzyme system in gastric parietal cell; characterized as gastric acid pump inhibitor, since it blocks final step of acid production. SE: diarrhea, headache, dizziness, asthenia, abdominal pain, vomiting, constipation, flatulence, acid regurgitation, rash, back pain, upper respiratory infections
AR: proteinuria, hematuria, pancytopenia, thrombocytopenia, Neutropenia, leukocytosis

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PPIs (prilosec)

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associated with hyperosmolar composition postsurgical, stomach can no longer control amt. of gastric chyme entering small intestine, large bolus of hypertonic fluid enters inetestine. pt. get instruction sof rset, small dry feedings daily, low in carbs and restricted in refined sugars, contain mod. amts of protein and fat. fluid taken between meals, rest for 30 min. after each meal in recumbent position.

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Dumping syndrome

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is the presence of a chronic productive cough for 3 months in each of 2 successive years in a patient in whom other causes a chronic cough have been excluded, extensive production of mucus in the bronchi accompanied by a recurrent cough that persists for at least 3 months of the year during at least 2 successive years. Pathologic changes in the lung consist of hyperplasia of mucous secreting glands in the trachea and bronchi, increase in goblet cells, disappearance of cilia, chronic inflammatory changes and narrowing of small airways and altered function of alveolar macrophages, leading to increased bronchial infections. Chronic inflammation is the primary pathologic mechanism involvedin causing the changes characteristic of chronic bronchitis, the inflammatory response causes vasodilation, congestion, and mucosal edema. Hypoxemia and hypercapnia develop more frequently. Clinical manifestations include: bluish red color results from polycythemia and cyanosis. Frequent productive cough during most winter months, it is often exacerbated by cold, and irritants. Bronchospasms can occur at the end of paroxysms

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Chronic bronchitis

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hyperinflation of alveoli, destruction of alveolar capillary walls, narrowed otrtuous small airways, loss of lung elasticity. abnormal permanent enlargement of airspaces distal to terminal bronchioles with destruction of their walls without obvious fibrosis. respiratory bonchioles enlarged and walls destroyed, bronchioles become confluent. elastin and collagen destroyed. no pull or traction on walls of broncioles, clinical man: early symptoms of dyspnea-> becomes progressively worse, minimal cough prsent, no sputum, alveoli become over distended, increasing amts of air trapping

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emphysema

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irritating effect of the smoke causes hyperplasia of cells, resulting in increased production of mucus, hyperplasia reduces airway diameter adn icnreases difficulty in clearning secretions; reduces ciliary activity may lose actual ciliated cells.

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smoking

Front 20

Usually administered to treat hypoxemia cause by respiratory disorders such as COPD, cor pulmonale, pneumonia, telecasts, lung cancer, and pulmonary emboli, cardiovascular disorders such as MI, arrhythmias, angina pectoris, and cardiogenic shock, and CNS disorders such as overdose of narcotics, head injury and disordered sleep.
Complications: combustion, CO2 narcosis, O2 toxicity, infection, absorption atelectasis

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O2 delivery

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CXR:emphysema: hyperinflation, flat diaphragm, small or normal heart, widened intercostal margins. Chronic bronchitis: cardiac enlargement, noraml or flattened diaphragm, evidence of chronic inflammation, congested lung fields)ABGS:emphsema: near normal,mild decrease PaO2, noraml or decreased PaCO2, chornic bronchtis: decreased PaO2, increased PaCO2

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diagnostics emphysema chronic bronchitis

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Breathing retraining, postural drainage, effective coughing, chest physiotherapy, percussion, flutter mucus clearance device, aerosol nebulization therapy

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airway clearance COPD

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pH< 7.35 PaCO2> 45 HCO3:Normal

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respiratory acidosis

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pH: >7.45 PaCO2 <35 HCO3: normal

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respiratory alkalosis

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Pursed lip breathing: prolongs exhalation and prevents collapse and air trapping
Daiphragmatic breathing: focuses on using diaphragm to breathe instead of accessory muscles to achieve maximum inhalation and slow respiratory rate.

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COPD breathing

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impaired gas exchange related to alveolar hypoventilation as manifested by headache on awakening, PaCO2>45mmHg and abnormal for patient’s baseline, PaO2<60mmHg, or SaO2 <90% at rest
rapid shallow breathing, inability to speak, prolong expiratory phase; puresed-lip breathing, wheezing, rhonchi, crackles, use of accessory muscles, tachycardia, arrhythmias, right sided S3 (cor pulmonale), ascites, increased anteroposterior diameter (barrel chest), abnormal ABGS.

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COPD

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B2 adrenergic agonist, bronchodilator given by Nebulizer, oral tabs.
Selectively stimulates beta 2 receptors, relaxes smooth muscle producing bronchodilator
SE: tachycardia, nervousness, N/V, hypokalemia, hypotension, bronchospasm

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albuterol

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anticholinergic- bronchodilator given by Neb or MDI
Inhibits interaction of acetylcholine at receptor sites on bronchial smooth muscle
SE: palpitations, anxiety, N/V, cough, bronchospasm

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ipatropium

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decreases inflammation by inhibiting mast cells, macrophages, and leukotrienes. Antinflammatory and vasoconstrictor properties. It’s role is to decrease the inflammation and decrease congestion related to allergies; has immunosuppressive effects. Decreases edema in bronchial airways

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flucticasone

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(IV)-decreases inflammation by the suppression of migration of polymorph nuclear leukocytes. It’s role is to decrease edema in bronchial airways, decrease mucus secretion; has inflammatory and immunosuppressive effects. Because it is IV, it produces systemic effects taking away from the therapeutic actions.

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methylprednisone

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it’s action is to decrease inflammation and capillary permeability, oral corticosteroids are indicated for treatment of acute asthma

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prednisone (oral)

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are used to decrease inflammation in order to make breathing easier

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corticosteroid

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enlargement of the right ventricle and secondary to diseases of lung, thorax, and pulmonary circulation.; it follows preexisting condition of pulmonary HTN
dyspnea, chronic productive cough, wheezy respirations, substernal pain, and fatigue. can be triggered by an acute respiratory tract infection and if heart failure accompanies may have peripheral edema, weight gain, distended neck veins, bounding pulses, and an enlarged liver.
Low O2 is used to correct hypoxemia and decrease the vasoconstriction in chronic states of respiratory disorders. Diuretics and low sodium diet will help decrease the plasma volume and load on the heart. If the problem is obstructive bronchodilator therapy is used.

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Cor Pulmonale

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The major risk factors include: until recently rheumatic heart disease was the most common cause of infective endocarditis. Currently the main contributing factors include: aging, IV drug abuse and increased survival rate of children with congenital heart disease. Predisposing conditions for the development of infective endocarditis: rhumatic heart disease, aortic valve leaflet abnormalities, mitral valve prolapse with murmur, cyanotic congential heart disease, proshtetic valves, degenerative valvular lesions, prior endocarditis, marfan syndrome, asymmetric septal hypertrophy, idiopathic hypertrophy sub aortic stenosis, IV illicit drug use, nosocomial bacteremia, IV devices
Tx: of streptococcal endocarditis- IV or IM Rocephin; IV/IM ceftriaxone + gentamicin; IV/IM ceftriaxone followed by oral amoxicillin

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infective endocarditis

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hallmark finding is pericardial fruction rub; ECG findings are KEY diagnostic clues and evolve over a period of hours to days

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diagnostic Marker pericarditis

Front 36

the speed of fluid accumulation effects the severity of the clinical manifestations, patients are often confused, agitated and restless, they have tachycardia and tachyon with a low output state, the neck veins usually makedly distended because of jugular vein pressure elevation, and significant pulsus paridoxus (an inspiratory drop in systolic b/p greater than 10mm HG) present.

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Cardiac Tamponade

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an inspiratory drop in systolic blood pressure greater than 10mm Hg results because the normal inspiratory decline in systolic b/p of less than 10mm Hg is exaggerate in cardiac tamponade.
It is measured by making a during quiet breathing with stable rhythm, establish systolic B/P, inflate b/p cuff until no sounds are heard on expiration, and note the pressure, deflate cuff slowly until systolic sounds are heard on expiration, and note the pressure; deflate cuff until systolic pressure sounds are heard throughout the respiratory cycle, not the pressure; determine the difference between the measurements taken this will equal the

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pulsus paradoxis

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history of:valvular, congenital, or syuphilitic cardiac disease (including valve repair or replacement); previous endocarditis, childbirth, staphylococcal or streptococcal infections, nosocomial bacteremia

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infective endocarditis

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past history of recent B-hemolytic streptococcal infection, previous rheumatic fever or rheumatic heart disease

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rheumatic heart disease

Front 40

dyspnea, hemoptysis; fatigue, palpitations, loud, accentuated S1; opening snap, low pitched, rumbling diastolic murmur

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mitral valve stenosis

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palpitations, dyspnea, chest pain, activity intolerance, syncope, mobile midsystolic no ejection click and a late or holosystolic murmur

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mitral valve prolapse

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angina pectoris, syncope, heart failure, normal or soft S1, prominent S4, crescendo-decrescendo murmur

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aortic stenosis

Front 43

more durable and last longer than biologic tissue valvues but have an increased risk of throb embolism, which necessitates the use of long term anticoagulant therapy. Considered for a younger patient because it is more durable and lasts longer but it is not indicated for women of childbearing age because of the need of anticoagulant therapy.

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mechanical valve

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offer the patient freedom from anticoagulant therapy as a result of low thrombogenicity. However, their durability is limited by the tendency for early calcificiation, tissue degeneration, and stiffening of the leaflets. Used for patients who can not take anticoagulant therapy (women of childbearing age)

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biologic valve

Front 45

inhibits the sodium potassium ATPase, which makes more calcium available for contractile proteins, resulting in increased cardiac output; increases force of contraction (+isotropic effect), decreases heart rate (chronotropic effect); decreases AV conduction speed.

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digoxin

Front 46

cause vasodilation by acting directly on the smooth muscle of the vessel wall. Their effects primarily involve increasing venous capacitance, dilating the pulmonary vasculature, and improving arterial compliance. Therefore the major homodynamic effect of nitrates is to decrease preload. Nitrates are particularly beneficial in the management of myocardial ischemia related to CHF because they promote vasodilation of the coronary areteries. One specific deterrent to the use of nitrates in CHF is nitrate tolerance. Nitrates are contraindicated in stenosis because they reduce preload which is necessary to free stiffened valves so they can open. It can cause really low blood pressure

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nitrates

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Atelectasis is considered a ventilation mismatch because it involves alveolar collapse resulting in pain

COPD is considered a ventilation mismatch because it involves increased secretions being present in the airways.

Pulmonary embolus affects the perfusion portion of the V/Q mismatch. The embolus limits blood flow but has no effect on airflow to the alveoli again causing V/Q mismatch.

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ventilation perfusion

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Early signs: tachycardia and mild hypertension, dyspnea, tachycardia, prolonged expiration, intercostal muscle retraction, use of accessory muscles in respiration, decreased SpO2, decreased respiratory rate or increased rapid rate with shallow respirations decreased tidal volume, decreased minute ventilation

Late signs: cyanosis, parodoxic chest movement with respiratory cycle (abdomen and chest move in opposite manner), coma arrhythmias, hypotension, tremor seizures

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acute respiratory failure

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disorders that compromise lung ventilation and CO2 removal including drug overdoses with CNS depressants, neuro diseases, trauma or diseases involving the spinal cord and its role in lung ventilation. Brain stem infarction, cervical cord injury, phrenic nerve injury, amyotrophic lateral sclerosis (ALS), Guillian-Barre, muscular dystrophy, multiple sclerosis, poliomyelitis, myasthenia gravis

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hypercapnic failure

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disorders that interfere with oxygen transfer into the blood including: pneumonia, pulmonary emboli, and alveolar injury related to inhalation of toxic gases, low cardiac output

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hypoxemic respiratory failure

Front 51

dyspnea, tachypnea, prolonged expiration, intercostal muscle retraction, use of accessory muscles in respiration, paradoxic chest/abdominal wall movement with respiratory cycle, cyanosis, agitation, disorientation, delirium, restless, combative behavior, confusion, decreased LOC, coma, tachycardia, hypertension, skin cool, clammy and diaphroetic, arrhythmias, hypotension, fatigue, unable to speak without pausing to breathe

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hypoxemia

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dypsnea, decreased respiratory rate, oir increased respiratory rate with shallow respirations, decreased tidal volume, decreased minute ventilation, morning headache, disorientation, somnolence, coma (late), arrhythmias, HTN, tachycardia, bounding pulse, muscle weakness, decreased deep tendon reflexes, tremor, seizures (late), pursed lip breathing, use of tripod position.

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hypercapnia

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At the time of the initial injury and for several hours to one or two days afterward, the patient may not experience respiratory symptoms or the patient may exhibit only dyspnea, tachypnea, cough and restlessness. Chest auscultation may be normal or reveale fine, scattered crackles, ABGs usually indicate mild hypoxemia and respiratory alkalosis caused by hyperventilation. The chest x ray may be normal or exhibit evident of minimal scattered interstitial infiltrates

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ARDS

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a sudden and progressive form of acute respiratory failure in which the alveolar capillary membrane becomes damaged and more permeable to intravascular fluid. The alveoli fill with fluid, resulting in severe dyspnea, hypoxemia, refractory to supplemental oxygen, reduced lung compliance and diffuse pulmonary infiltrates.

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ARDS

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used during mechanical ventilation to compensate for loss of glottic function caused by the endotracheal tube. Levels typically range from 10-20cm H20 for patients with ARDS. This level allows for the collapsed alveoli to be reopened and the FIO2 to return to a level of 60%.
complications:can cause compromise venous return to the right side of the heart, decreasing preload, cardiac output, and blood pressure. It can also cause hyperinflation of the alveoli, compression of the pulmonary capillary bed, a reduction in blood return to the left side fo the heart and a dramatic reduction in blood pressure. It in itself can cause volu-pressure trauma and barotraumas

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PEEP therapy

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indicated primarily for those who have a chronic illness, such as lung and heart disease and diabetes mellitus. Individuals recovering from a severe illness, individuals 65+ years and individuals in long term care facilities. There is significance dut to rate of drug resistant S. pneumoniae infection increasing. Pneumococcal vaccine is good for a lifetime; however, those that are immunosuppressed run the risk for fatal consequences of the infection should be revaccinated every 5 years

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pneumococcal vaccine

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presents with frequent waking at night, insomnia, excessive daytime sleepiness, and witnessed apneic episodes. Other symptoms include loud snoring, morning headaches (from hypercapnia), personality changes, and irritability. Paitent will describe effects of chronic sleep loss (ie inability to concentrate, impaired memory, etc)

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sleep apnea

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Latent TB occurs when an individual becomes infected with TB but does not become acutely ill. Drug therapy can be used to prevent infection from developing into a clinical disease. In latent TB, there is a significant reaction to tuberculin skin test, negative bacteriologic studies, no x-ray findings compatible with TB, no clinical evidence of TB. An active case would manifest in x-ray and clinical findings as well as with the tuberculin test.

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interpretation of positive PPD

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patients are more likely to have a false-negative if they were infected with TB many years ago and persons with an active current infeciton. False positives may occur in people such as healthcare workers or those who have decreased response to allergens which often warrant them to have a second PPD test, the response may be accelerated and misinterpreted as positive

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false positive; false negative PPD

Front 60

Respiratory isolation is used in hospitals via a negative pressure isolation room that offers 6 or more exchanges per hour. UV radiation of the air in the upper part of the room is another option. HEPA masks are used to filter particles but must be molded to tightly fit the face

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prevent transmission of TB

Front 61

caused by Myobacterium tuberculosis and kills more people than any other infectious disease. It is spread via airborne droplets from speaking and sneezing, making it difficult to avoid. It cannot be spread by hands or objects. During the activation of the immune system response, the bacteria can easily spread to lymph nodes, causing further problems.

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TB

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In the case of latent TB infection, INH is the drug of choice, and should be continuously used for 6-9 months, and longer in patients with HIV. In the case of an active TB disease, the drugs of choice are INH, Rifamate, Pyrazinimide, Streptomycin, and Myambutol. What is important to remember is that often four of these drugs will be given aggressively to reduce the risk of drug resistant TB. This is also done for 6-9 months.

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Drug therapy TB

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Early symptoms include persistent cough with sputum, local or unilateral chest pain, dyspnea, and an asculatory wheeze. Later symptoms sometimes show and include anorexia, fatigue, hoarse voice and dysphagia

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lung cancer

Front 64

Flail chest from multiple rib fractures, causing instability of the chest wall. The chest wall cannot provide the bony structure necessary to maintain ventilation. The chest will suck in on inhalation, and protrude out during exhalation. It can usually be seen on visual examination of the patient. Tension pneumothorax shows rapid accumulation of air in the pleural space causing severely high pressure which results in tension of the heart. Air can enter but not escape . It is an emergency in which the patient is likely to die from hypoxemia, so a large-bore needle must be inserted into the chest to release trapped air. Pleural effusion is shows fluid in the pleural space, and is not a disease itself but an indication of other disease, such as infection.

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flail chest, tension pneumothorax, PE

Front 65

Priorities include monitoring chest drainage, monitoring respirations, administer oxygen, help client to change positions regularly, and promote ambulation. Also assess for anxiety and pain control, giving pain medications as necessary.

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patient care post pneumonectomy

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An EIA is done to detect serum antibodies that bind to HIB antigens on test plates. Blood samples that are negative on this tesat are reported as negative. Posstest counseling should include an assessment of risk behaviors, if recent risks are found encourage retesting at 3 weeks, 6 weeks and 3 months. If the blood is EIA positive, the test is repeated. If the blood is repeatedly EIA positive, a more specific confirming test such as the Western Blot test is done, or IFA is done. WB testing uses purified HIV antigens electrophosresed on gels. These are incubated with serum samples. If antibody in the serum is present, it can be detected. IFA is used to identify HIV in infected cells. Blood that is reactive in the first three steps is reported as HIV antibody positive. If the results are indeterminant, the following steps are taken: if in-depth risk assessment revealst hat the individual does not have a history of high risk activities, reassure the patient that he or she is extremely unikely to be infected with HIV and suggest retesting in 3 months.if in depth risk assessment reveals the individual to have a high risk history repeat antibody test at 1, 2, and 6 months; discuss harm reduction measures to protect partners from infection, consider tests for HIV antigen detection

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method for testing for HIV

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Development of HIV specific antibodies (seroconversion) are the most useful screening tests for HIV are those that detect HIV specific antibodies. The major problem with these tests is tha tthere is a median delay of 2 months after infection before antibodies can be detected. This creates a window period during which an infected individual will not test HIV antibody positive

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seroconversion and how this relates to interpretation of tests for HIV.

Front 68

Safe sexual activities eliminate the risk of exposure to HIV in semen and vaginal secretions. Abstaining from all sexual activity is the most effective way to accomplish this goal but there are safe options for those who cannot or do not wish to obstain. Outercourse limiting sexual behavior to activities in which the mouth, penis, vagina or rectum does not come in contact with a partner’s mouth, penis, vagina or rectum is safe because there is no contact with blood, semen, or vaginal secretions. Outercourse includes massage, masturbation, mutual masturbation, telephone sex, and other activities that meet the no contact requirements. Insertive sex between partners who are not infected with HIV are not at risk of being infected with HIV is considered safe sex. Riskrediucing sexual activities decrease the risk of contact with HIV through the use of barriers. To reduce the risk of HIV by illicit drug use the basic rules are as follows: do not use drugs, if you use drugs do not share equipment and do not have sexual intercourse when under the influence of any drug that impaires decision making ability. To reduce the risk of perinatal transmission the best way to prevent it is to prevent HIV infection in women.

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risk factors for HIV

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Women who are already infected with HIV should be asked about reproductive desires( if no kids need to have birth control), if HIV infected pregnant women are treated with zidovudine (ZDV, AZT, Retrovir) the rate of perinatal transmission is decreased. This treatment has minimal side effects for the baby. Combination ART as appropiate for the mother’s HIV infection can further decrease the risk of perinatal transmission to less than 2%. The current standard of care is that all women who are pregnant or contemplating pregnancy should be counseled about HIV infection, informed of their choices, routinely offered access to voluntary HIV antibody testing and if infected, provided with optimal ART as desired. Decreased risk of infection from occupational exposure to HIV is small but real. Employers are required to protect workers from exposure to blood and other potentially infectious materials. post exposure prophylaxis with combination ART basedon the type of exposure volume of the exposure, and the status of the source patient has been shown to significantly decrease the risk of infection

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risk factors and education for HIV

Front 70

development of HIV specific antibodies is frequently accompanied by a flulike syndrome of fever, swollen lymph glands, sore throat, headache, malaise, nausea, muscle and joint pain. Generally occurs 1-3 weeks after the initial infection and last from 1-2 weeks. During this time the level of HIV in the blood is noted and CD4+T cell counts fall temporarily but quickly return to baseline. In some people neuralgic complications, such as aseptic meningitis, peripheral neuropathy, facial palsy, or Guillain Barre syndrome have developed

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acute HIV infection

Front 71

the median interval between untreated HIV infection and a diagnosis of AIDS is about 10 years. During this time CD4+ T lymphocyte counts remain above 500 cells/ul ( normal or slightly decreased). And the viral load in the blood will be low. This phase has been referred to as asymptomatic disease but fatigue, headache, low grade fever, night sweats, persistent general lymphadenopathy (PGL), and other symptoms often occur.

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early chronic HIV infection

Front 72

when the CD4+T cell count drops to 200-500 cells/ul, the viral load rises and HIV advances to a more active stage. Symptoms seen in earlier phases tend to become worse, causing persistent fever, frequent drenching night sweats, chronic diarrhea, recurrent headaches, and fatigue severe enough ot interrupt normal routines. Other problems that may occur at this time include localized infections, lymphadenopathy, and nervous system manifestations. The most common infection associated with this phase of HIV disease is oropharyngeal candidiasis or thrush. Other infections include shingles, persistent vaginal candidial infections, outbreaks of oral or genital herpes, bacterial infections and Kaposi’s sarcoma, Oral hairy leukoplakia, an Epstein barre virus infection that causes painless white raised lesions on the lateral aspect of the tongue can also occur. Oral lesions may provide the earliest indication of HIV infection. Oral hairy leukoplakia is also an indicator of disease progression

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intermediate chronic HIV infection

Front 73

CD4+T cells fall below 200 cells/ul. Development of opportunistic infections: candidiasis of bronchi, trachea, lungs, or esophagus, pneumocystitis carinii pneumonia, disseminated or extra pulmonary histoplasmosis. Cytomegalovirus disease other than liver, spleen, or nodes; CMV retinitis (with loss of vision); herpes simplex with chronic ulcers or bronchitis, pneumonitis, or esophagi is; progressive multimodal leukoencephalopathy; extra pulmonary Cryptococcosis. Disseminated or extra pulmonary coccidioidomycocis, toxoplasmosis of the brain, chronic intestinal isosporiasis, chronic intestinal cryptosporidiosis, mycobacterium tuberculosis, recurrent salmonella septicemia. Development of opportunistic cancers; invasive cervical cancer, Kaposi’s sarcoma, burkitt’s lymphoma, or primary lymphoma of the brain. Wasting syndrome occurs, dementia develops. (fungal, viral, protozoal, bacterial infections)

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late chronic infection (AIDS)

Front 74

To treat respiratory system opportunistic diseases: bactrim (pneumocystis carinii pneumonia), NebuPent(PCP), cleocin (PCP), neutrexin, fungizone, diflucan,-PCP
INH, Myambutol, Rifampin, Pyrazinamide,- mycobacterium tuberculosis
Streptomycin amphotericin B, Diflucan, Sporanox,- Coccidioides immitis
cancer chemotherapy , alpha interferon, radiation-Kaposi’s sarcoma
Acyclovir, Famvir, Valtresx, Foscavir-Herpes simplex type 1 and 2
Acyclovir, Famvir, Valtrex, Foscavir- Varicella Zoster virus
Cancer chemotherapy, alpha interferon, radiation of lesions, liquid nitrogen, cry therapy for skin lesion- Kaposi’s sarcoma
Erythromycin, doxycycline- bacillary angiomatosis
Cytovene, Focsani, visited, valcyte, vitrisert-cytomegalovirus retinitis
Antidiarrheals, humatin, zithromax,mepron, sandostatin-cryptosporidium muris
Cytovene, Focsani, visitide-cytomegalovirus

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characteristics and treatment for opportunistic diseases associated with AIDS

Front 75

All infants born to mothers with HIV will be positive on the HIV antibody test because maternal antibodies cross the placental barrier. These antibodies remain present for up to 18 months. For that reason early detection of HIV infection in infants depends on testinf ro HIV antigen through the use of HIV DNA polymerase chain reaction. HIV RNA PCR or viral culture. These tests can definitively diagnose HIV in infected infants by 4 weeks of age. HIV infected pregnant women are treated with ZDV, AZT,Retrovir, the rate of perinatal trasmission is decreased. Combination ART as appropriate for the mother’s HIV infectoin can further decrease the risk of perinatal trasmission to less than 2%. The current standards of care is that all women who are considering pregnancy or are pregnant be screened and counseled about HIV infection

Back 75

transmission of HIV from mother to child and education and treatment

Front 76

The goal of drug therapy in HIV infection are to decrease HIV RNA levels to less than 50 copies/ul, maintain or raise CD4+ T cells counts to greater than 200 cells/ul, delay the development of HIV related symptoms, including a wide range of opportunistic diseases. A variety of drug therapies are available to help patients meet their goals. Resistance can occur very rapidly when a patient misses a dose or delay does of their drugs. For this reason strict adherence to treatmetn protocols is extremely important. In general drugs used to treat HIV are antiretroviral drugs that work on various points in the HIV replication cycle. Current approved drugs include 3 gropus that inhibit the ability of HIV to make a DNA copy early in replication, one gropu that inhibit’s the ability of the virus to reproduce in the late stages or replication and one gropu that prevents entry of HIV into the cell. Initiation of therapy is used for symptomatic AIDS, severe symptoms), asymptomatic, AIDS with a CD4+T cell count of <200, asymptomatic with CD4 count of 200-350, asymptomatic with CD4 count <350 and plasma count >30,000 or 55,000(RT-PCR)-some experts recommend initiating therapy, asymptomatic CD4 cell count < 350 with plasma HIV RNA <30,000 9bDNA or <50,000RT-PCR)-many experts would defer therapy and observe.

Back 76

principles of drug therapy for HIV, indications for initiation of therapy, and relevant patient teaching

Front 77

combine with reverse transcriptase enzyme to block the process needed to convert HIV RNA into HIV DNA

Back 77

Nonnucleoside reverse transcriptase inhibitors (NNRTIs)-

Front 78

insert a bit of protein into the developing HIV DNA chain, blocking further development of the chain and leaving the production of the new strand of reverse transcriptase.

Back 78

Nucleoside reverse transcriptase inhibitors (NRTIs)-

Front 79

inhibit the action of reverse transcriptase

Back 79

Nucleotide reverse transcriptase inhibitors

Front 80

prevent the protease enzyme from cutting HIV proteins into the proper lengths needed to allow viable virions to assemble and bud out from the cell membrane

Back 80

Protease inhibitors (PIs)-

Front 81

prevent binding of HIV cells, thus preventing entry of HIV into healthy cells

Back 81

Fusion inhibitors (entry inhibitors)-

Front 82

-(TMP-SMX), dapsone, diapsone with pyrimethamine + folic acid aerosolized pentamidine, atovaquone

Back 82

PCP

Front 83

INH + pyridoxine

Back 83

Mycobacterium Tuberculosis

Front 84

trimethoprim-sulfamethoxazole, dapsone with pyrimethamine + folic acid

Back 84

Toxoplasmosis

Front 85

Biaxin, zithromax, mycobutin

Back 85

Mycobacterium avium complex (MAC):

Front 86

varicella zoster immune globulin administered within 96 hours after an exposure, preferably within 48 hrs.

Back 86

Varicella zoster virus

Front 87

pneumococcal vaccine

Back 87

Pneumococcal pneumonia

Front 88

whole or split virus influenza vaccine

Back 88

influenza virus

Front 89

hepatitis B vaccine series; screen and vaccinate those who show no evidence of previous HBV infection

Back 89

hepatitis B virus

Front 90

hepatitis A vaccine series; screen and vaccinate those without evidence of previous HAV infection

Back 90

hepatitis A virus

Front 91

Drug that is used to prevent or cure a disease caused by a virus, by interfering with the ability of the virus to multiply in number or spread from cell to cell.

Back 91

antiviral drugs

Front 92

Treatment and medication for infection by retroviruses—tumor-producing viruses that contain RNA and reverse transcriptase—primarily HIV. Different antiretroviral drugs act at various stages of the HIV life cycle.

Back 92

anitretroviral drugs

Front 93

Treatment must be directed toward shock management and high-dose hydrocortisone replacement. Large volumes of 0.9% saline solution and 5% dextrose are administered to reverse hypotension and electrolyte imbalances until blood pressure returns to normal.
Vital signs and signs of fluid volume deficit and electrolyte imbalance should be assessed every 30 minutes to 4 hours for the first 24 hours depending on the patient’s instability. In addition daily weights, diligent corticosteroid administration, protection against exposure to infection and complete assistance with daily hygiene should be practiced. The patient should be protected from noise, light, and environmental temperature extremes

Back 93

care priorities for Addison's disease

Front 94

Clinical manifestations do not tend to be evident until 90% of the adrenal cortex is destroyed, the disease is often advanced before it is diagnosed. The manifestations have a very slow (insidious) onset and include progressive weakness, fatigue, weight loss and anorexia as primary features. Skin hyper pigmentation, a striking feature, is seen primarily in sunexposed areas of the body at pressure points over joints, and increases, especially palmar creases. It is most likely due to increased secretion of B-isotropic (which contains melanocytestimulating hormone (MSH) or ACTH. These tropic hormones are increased because of decreased negative feedback and subsequent low corticosteroid levels. Other frequent manifestations include: hypotension, hyponatremia, hyperkalemia, nausea and vomiting and diarrhea

Back 94

clinical manifestations Addison's disease

Front 95

Hypokalemia may develop, predisposition to peptic ulcer disease, skeletal muscle atrophy and weakness occurs, mood and behavior changes may be observed, glucose intolerance predisposes to diabetes mellitus, fat from extremities is redistributed to trunk and face, hypocalcaemia related to anti-vitamin D effect may occur, healing is delayed, at increased risk for wound dehisance, susceptibility to infection is increased, infection develops more rapidly and spreads more widely, suppression of pituitary ACTH synthesis occurs, corticosteroid deficiency is likely if hormones are withdrawn abruptly, increased blood pressure occurs because of excess blood volume and potentiation of vasoconstrictor effects, hypertension predisposes to heart failure, protein depletion decreases bone formation, density, and strength, predisposes to pathologic fractures, especially compression fractures of the vertebrae (osteoporosis)

Back 95

patient teaching needs for a person on corticosteroid replacement therapy or long-term corticosteroid therapy

Front 96

Past medical history: pituitary tumor (cushing’s syndrome), adrenal, pancreatic or pulmonary neoplasms, GI bleeding, frequent infections
Medicational use of corticosteroids
Malaise, weight gain, anorexia, polyuria, prolonged wound healing, easy bruising, weakness, fatigue, insomnia, poor sleep quality, headache, back, joint, bone, and rib pain; poor concentration and memory, negative feelings regarding changes in personal appearance, amenorrhea, impotence, decreased libido, anxiety, mood disturbancees, emotional lability, psychosis,
Objective: truncal obesity, supraclavicular fat pads, buffalo hump, moon facies, plethora; hirsutism of body and face, thinning of head hair, thin friable skin; acne, petechiae, purpura; hyperpigmentation; purplish red striae on breast, buttocks, and abdomen, edema of lower extremities, HTN, muscle wasting, thin extremities, awkward gait, gynecomastia, testicular atrophy, enlarged clitoris, hypokalemia, hyperglycemia, dyslipidemia, lyumphocytopenia, eosinopenia, increased plasma cortical, high, low or normal ACTH levels; abnormal dexamethasone suppression test; increase urine free cortical, 17-ketosteroids; glycosuria, hypercalciuria, osteoporosis on x-ray

Back 96

Cushing's syndrome

Front 97

If the underlying cause is a pituitary adenoma, the standard treatment is surgical removal of the pituitary tumor using the transsphenoidal approach. Adrenalectomy is indicated for cushing syndrome caused by adrenal tumors or hyperplasia, occasionally, bilateral adrenalectomy is necessary. An open surgical adrenalectomy is the treatment of choice for adrenal cancer. The goal of drug therapy is the inhibition of adrenal peripheral metabolism of cortical, and decreases plasma and urine corticosteroid levels. This drug essentially results in medical adrenalectomy. If cushing syndrome has developed during the course of prolonged administration of corticosteroids one or more of the following alternatives may be tried: gradual discontinuance of corticosteroid therapy, reduction fo the corticosteroid dose, conversion to an alternate day regimen, gradual tapering of the corticosteroids is necessary to avoid potentially life threatening adrenal insufficiency. An alternate day regimen is one in which twice the daily dosage of shorter acting corticosteroid is given every other morning to minimize hypothalamic pituitary adrenal suppression, growth suppression and altered appearance.
Nursing management should include monitoring of vital signs, daily weight, glucose, possible infection (especially pain, loss of function, and purulent drainage, because other signs and symptoms of inflammation such as fever and redness may be minimal or absent, and sign and symptoms of abnormal thromboembolic phenomena, such as sudden chest pain, dyspnea or tachypnea.

Back 97

nursing management priorities in person with Cushing’s disease

Front 98

Changes in appearance such as centripetal obesity, multiple bruises, hirsutism in women, and gynecomastia in men can be distressing. The patient may feel unattractive repulsive or unwanted. The patient must be reassured that physical changes and much of the emotional lability will resolve when hormone levels return to normal.

Back 98

body image and cushing's disease

Front 99

Individuals have enlargment of the hands and feet, the fingertips develop a tufted or clubbed like appearance , the enlargement of the bones and cartilage may cause symptoms that range from mild joint pain to deforming, crippling arthritis, changes in physicall appearance occur with thickening and enlargement of bony and soft tissue on the face and head. Enlargement of the mandible, enlargement of soft tissue around the eyes, nose and mouth results in a coarsening of facial features, enlargement of the tongue in speech difficulties and the voice deepens as a result of hypertrophy of the vocal cords. Sleep apnea, skin becomes thick leathery and oily, may experience peripheral neuropathy and proximal muscle weakness. The patient may exhibit manifestations of diabetes mellitus such as polydipsia and polyuria, cardiovascular disease may manifest as HTN, angina pectoris, and congestive heart failure. The enlarged pituitary tumor gland can exert pressure on surrounding structures within the brain, leading to visual disturbances and headaches.

Back 99

assessment findings in acromegaly

Front 100

Patient should be instructed to avoid valsalva maneuver, vigorous coughing, sneezing to prevent cerebrospinal fluid leakage from the point at which the sella turcica was entered. The head of the bed should be elevated at 30 degrees at all times, monitoring neurologic status, including papillary response, should be done in order to detect neurologic complications, any clear nasal drainage should be sent to the laboratory to be tested fro glucose. Complaints of persistent and severe generalized or suborbital headache may indicated CSF leakage into the sinuses. Mild analgesia is given for headaches, mouth cares should be performed every 4 hours to keep the surgical area clean and free of debris and to promote patient comfort, tooth brushing should be avoided for at least 10 days to prevent disrupting the suture line and avoid discomfort

Back 100

post-op care (including activities to avoid) of the person following transsphenoidal hypophysectomy.

Front 101

is an autoimmune disase of unknown etiology marked by diffuse thyroid enlargement and excessive thyroid hormone secretion. Precipitating factors such as insufficient iodine supply, infections, and stressful life events may interact with genetic factors that control the immune response and metabolic abnormalities to cause Grave’s Disease. The patient develops antibodies to the TSH receptor. The antibodies attach to the receptors and stimulate the thyroid gland to release T3 or T4 or both. The excessive release of thyroid hormone leads to clinical manifestations of thyrotoxicosis.
Clinical manifestations: palpitation of the thyroid gland reveals a goiter, auscultation of the thyroid gland may reveal bruits, ophthalmopathy-abnormal eye appearance or function. Exophthalmos-classic sign-protrusion of the eyeballs from the orbits. In noninflitrative ophthalmopathy the upper lids are usually retracted and elevated with the sclera visible above the iris. When the eyelids do not close completely, the exposed corneal surfaces become dry and irritated. Serious consequences such as corneal ulcers and eventual loss of vision can occur

Back 101

Grave's Disease

Front 102

increased thirst, increased urination, excertion of large quantities of urine with a low specific urine gravity and urine osmolality, serum osmolality is elevated as a result of hypernatremia due to pure water loss in the kidney., patient’s try to compensate for loss of water by drinking more water.

Back 102

Diabetes Insipidous

Front 103

excess ADH increases distal tubule and collecting duct permeability and reabsorption of water in to the circulation, extra cellular fluid volume expands, plamsa osmolality declines the glomerular filtration rate increases, and sodium levels decline, hyponatremia causes muscle cramps and weakness. Patient will experience low urinary output and increased body weight. As serum sodium levels fall manifestations become more severe and include vomiting, abdominal cramps, muscle twitching, and seizures, as plasma osmolality and serum sodium levels continue to decline cerebral edema may occur, leading to lethargy, anorexia, confusion, headache, seizures, and coma.

Back 103

SIADH

Front 104

preexisting goiter, recent infection or trauma, immigration from iodine deficient area, autoimmune disease, use of thyroid hormone, positive family history of thyroid or autoimmune disorders, insufficient iodine intake, weight loss, increased appetite, thirst; nausea, diarrhea, polyuria; sweating, dyspnea on exertion; palpitations, muscle weakness, fatigue, insomnia, chest pain, nervousness, heat intolerance; pruritus, decreased libido, impotence, gynecomastia, amenorrhea in women, emotional lability, irritability, restlessness, personality changes, delirium
Objective:
Agitaiton, rapid speech and body movements, hyperthermia, enlarged or nodular thyroid gland, exophtalmos, eyelid retraction; infrequent blinking, warm, daiphoretic, velvety skin, thin, loose nails, fine silky hair and hair loss, palmar erythematic, clubbing, white pigmentaiton of skin, diffuse edema of legs and feet, tachypnea, tachycardia, bounding pulses, systolic murmurs, arrhythmias, hypertension, increased bowel sounds, hepatosplenomegaly, hyperreflexia, diplopia, fine tremors of hands, tongue, eyelids; stupor, coma, muscle wasting, menstrual irregularities, infertility, impotence, gynecomastia in men

Back 104

Hyperthyroidism:

Front 105

weight gain, fatigue, mental changes, slowed, slurred speech, cold intolerance, skin changes such as increased dryness or thickening, constipation and dyspnea, bradycardia, distended abdomen, dry, thick ,cold skin; thick brittle nails, paresthesias, and muscular aches and pains

Back 105

hypothyroidism

Front 106

the overall goal is to block the adverse effects of the thyroid hormones and to stop their oversecretion.three primary treatment options are ant thyroid medications, radioactive iodine and subttoal thyroidectomy, treatmetn of choice in no pregnant adults is radioactive iodine.the choice of treatment is influenced by the patient’s age, severity of the disorder, complicating features, and patient’s preference. Drug therapy includes: anithyroid drugs: (PTU, Tapazole), Iodine, beta adrenergic blockers (propranolol), radation therapies (radioactive iodine), surgical therapy (subtotal thyroidectomy), Nutritional therapy (high calorie diet, high protein diet, frequent meals)

Back 106

hyperthyroidism

Front 107

overall treatment is restoration fo euthyroid state as safely and rapidly as possible with hormone replacement therapy. A low calorie diet is indicated to promote weight loss. Levothyroxine (synthroid) is the drug of choice to treat hypothyroidism, in the young and healthy the maintenance replacement can be started at once. The increased oxygen demand can cause angina and cardiac arrhythmias, any chest pain should be reported immediately and and ECG and serum cardiac enzyme test must be performed. In the patient with side effects the dose is increased at 1-4 week intervals. Lifelong therapy is required.

Back 107

hypothyroidism

Front 108

Hyperthyroidism can occur (toxic syndrome from hypothyroidism), thyroid replacement therapy is lifelong, there is a need for a comfortable, warm environment because of intolerance to cold, soap should be used sparingly and lotion applied to skin to prevent skin breakdown, caution should be taken when taking sedatives if they must be used use the lowest dose possible. Famly members should closely monitor mental status, level of conciousness and respirations, patient should take a gradual increase in activity and exercise, increased fiber in diet, use of stool softners, and maintenance of a regular bowel elimination, use of enemas should be avoided. Contact a health provider if develop signs of overdose-orthopnea, dyspnea, rapid pulse, palpitations, nervousness, or insomnia

Back 108

precautions for the patient starting thyroid replacement hormones including implications for patient instructions and possible complications

Front 109

Assess for increased nerve excitability and sustained muscle contraction that is referred to as tetany-clinical signs of tetany include: Trousseau’s sign and Chvostek’s sign, trousseau’s sign refers to carpal spasms induced by inflating a blood pressure cuff on the arm, the blood pressure cuff is inflated above the systolic pressure, carpal spasms become evident within 3 minutes if hypocalemia is present. Chvostek’s sign is contraction of facial muscles in response to a tap over the facial nerve in front of the ear. And it also indicates hypocalcaemia with latent tentany. Other symptoms of tetany include: laryngeal stridor, dysphagia, and numbness and tingling around the mouth in the extremities. Hypocalcaemia results in decreased cardiac contractility and ECG change.

Back 109

Recognize assessment findings associated with low serum calcium.

Front 110

(anthithyroid drug): the first line anithyroid drug used in treatment of hyperthyroidism, these drugs inhibit the synthesis of thyroid hormones. PUT also blocks peripheral conversion of T4 to T3. Although it is considerable individual variation, improvement usually begins in 1-2 weeks after the initiation of therapy. Major disadvantage of these drugs are patients noncompliance and a high rate of recurrence of hyperthyroidism when the drugs are discontinued.

Back 110

PTU

Front 111

inhibits synthesis of thyroid hormone

Back 111

Methimazole

Front 112

useful in conjunction with other ant thyroid drugs in the preparation of thyrotoxic crisis. The admission of iodine in large doses rapidly inhibits synthesis of T3 and T4 and blocks the release of these hormones into circulation. It also decreases the vascularity of the thyroid gland, making surgery safer and earsier. The maximum effect of iodine is usually seen within 1-2 weeks. Long term iodine therapy is not effective in controlling hyperthyroidism. Iodine is available in the form of saturated solution of potassium and Lugol’s solution.

Back 112

Iodine

Front 113

used for symptomatic relief of thyrotoxicosis that results from increased B-adrenergic receptor stimulation caused by excess thyroid hormones. Propranolol (inderal) the most frequently used B-blocker is usually administered with other antithyroid agents and rapidly provides symptomatic relief. Atenolol is the preferred B-blocker for use in hyperthyroid patient with asthma or heart disease

Back 113

B-adrenergic blockers

Front 114

radioactive iodine therapy is the treatment of choice for most nonpregnant adults. RAI damages or destroys thyroid tissue thus limiting thyroid hormone secretion. Radioactive iodine has a delayed response and maximum effects may not be seen in 2-3 months.

Back 114

I-131

Front 115

If too much tissue is taken the gland will not regenerate after surgery and hypothyroidism will result. Complications include: hypothyroidism, damage to or inadvertent removal of the parathyroid glands causing hypoparathyroidism and hypocalcaemia, hemorrhage, injury to the recurrent or superior laryngeal nerve, thyrotoxic crisis, and infection. Trach set should be set up incase of need to intubate because of airway obstruction, laryngeal stridor may often occur during inspiration and expiration as a result of tetany, to treat tetany calcium salts such as calcium gluconate and calcium chloride should be readily available for IV administration 1. Assess patient every 2hrs for sign of hemorhhage or tracheal compression, 2)place the patient into semi fowlers position and support the patient’s head with pillows, avoid flexion of neck, and any tension on the suture lines. 3) monitor vitals 4)control postoperative pain by giving meds.

Back 115

stridor may often occur during inspiration and expiration as a result of tetany, to treat tetany calcium salts such as calcium gluconate and calcium chloride should be readily available for IV administration

Front 116

Risk for hemorrhage is increased, large amounts of hormones may be released into circulation from surgery, producing marked fluctuations in the metabolic processes affected by these hormones. Postoperatively blood pressure, fluid balance, and electrolyte levels tend to be unstable because of the hormone fluctuations. High doses of corticosteroids are administered intravenously during surgery and for several days afterwards. HTN may develop, any rapid or significant changes in BP, respirations, or HR should be reported, the critical period for circulatory instability ranges from 24-48hrs after surgery, IV corticosteroids are given and the dose and rate of flow are adjusted to the patients clinical manifestations. Oral doses are given as tolerated. IV line may be kept in place after IV corticosteroids are withdrawn to keep a line open for quick administrations of corticosteroids or vasopressors. Morning urine levels of cortical are measured to evaluate the effectiveness of the surgery. If cortocosteroid dosage is tapered too rapidly after surgery adrenal insufficiency may develop-vomiting, increased weakness, dehydration, and hypotension indicate hypcorticosolism. Meticulous care should occur when changing dressings and during any other procedures that necessitate access to body cavities.

Back 116

post-operative nursing considerations for the person having an adrenalectomy

Front 117

Pheochromocytoma is a rare condition characterized by a tumor of the adrenal gland that produces excessive catecholamines (epinephrine, norepinephrine). Pheochromocytoma can occur at any age and in either gender but it is found most commonly in young to middle aged adults-in most cases effective adults the tumor is benign, encapsulated, unilateral, and solitary. The secretion of excessive catecholamines results in severe hypotension.

Clinical manifestations: the most striking clinical feature of pheochromocytoma include episodic hypertension, accompanied by the classic triad of severe, pounding headache, tachycardia, and profuse sweating. Attacks of episodic HTN are due to sympathetic nervous system stimulation and are often accompanied by anxiety and palpitations. Attacks can be provoked by meications including antihypertensive, opioids, radiologic contrast media and tryciclic antidepressants

Back 117

pheochromocytoma and identify clinical manifestations

Front 118

a syndrome by decreased tissue perfusion and impaired cellular metabolism. This results in imbalance between the supply of and demand of oxygen and nutrients

Back 118

shock

Front 119

is defined as cardiogenic and hypovolemic shock

Back 119

low blood flow shock

Front 120

is septic and anaphylactic and Neurogenic shock.

Back 120

maldistribution shock

Front 121

occurs when either systolic or diastolic dysfunction of the myocardium results in compromised cardiac output. The hearts inability to pump the blood forward is classified as systolic dysfunction-it primarily effects the left ventricle. When systolic dysfunction effects the right side of the heart blood flow through the pulmonary circulation is compromised. Precipitating causes of systolic dysfunction include myocardial infarction, cardiomyopathies, severe systemic or pulmonary HTN. Dyastolic dysfunction is an impaired ability of the right or left ventricle to fill during diastole. Decreased filling of the ventricles will result in decreased stroke volume.
Cardiogenic shock occurs when a primary ventricular ischemia, structural problems or arrhythmias lead to systolic dysfunction: ineffective forward movement of blood leading to decreased stroke volume which leads to decreased CO and decreased cellular oxygen supply resulting in decreased tissue perfusion and impaired cellular metabolism. Or it results from diastolic dysfunction: ineffective filling causing increased pulmonary pressures which lead to pulmonary edema and decreased oxygenation resulting in decreased cellular oxygen supply, decreased tissue perfusion and decreased cell metabolism

Back 121

cardiogenic shock

Front 122

Clinical manifestations: (early): tachycardia, hypotension, narrowed pulse pressures, an increase in systemic vascular resistance (SVR) increases the workload of the heart thus increasing the myocardial oxygen consumption. The heart’s inability to pump blood forward will result in low cardiac index. On examination the patient will be tachypneic, and pulmonary congestion will be evident by the presence of crackles. The homodynamic profile will demonstrate an increase in the pulmonary artery wedge pressure (PAWP) and pulmonary vascular resistance. Sings of peripheral hypoperfusion (cyanosis, cool and clammy skin, pallor, decreased cap refill time), decreased renal blood flow will result in sodium and water retention and decreased urine output, anxiety and delirium may develop as cerebral perfusion is impaired

Back 122

cardiogenic shock

Front 123

occurs when there is a loss of intravascular fluid volume. In hypovolemic shock the volume is inadequate to fill the vascular space. Absolute hypovolemic results when fluid is lost through hemorrhage, GI loss , fistula drainage, diabetes insipidus or diuresis. In relative hypovolemic fluid volume moves out of the vascular space into extra vascular space (interstitial, and intracavitary space-3rd spacing). In hypovolemic shock the vascular compartment remains unchanged while the volume of blood or plasma decreases. Decreased venous return to the heart, decreased preload, decreased stroke volume, decreased CO occurs

Back 123

hypovolemic shock

Front 124

Clinical manifestations: decreased: preload, stroke volume, capillary refill time, tachyon leads to bradypnea, decreased urine output, pallor, cool and clammy skin, anxiety, confusion, agitation, absent bowel sounds. Decreased hematocrit, increased lactate, increased urine specific gravity, changes in electrolyte

Back 124

hypovolemic shock

Front 125

homodynamic phenomenon that occurs after a spinal cord injury at the fifth thoracic vertebra or above. The injury results in a massive vasodilation without compensation as a consequence of the loss of SNS vasoconstrictor tone. This massive vasodilation leads to a pooling of blood in the blood vessels, the most important clinical manifestations are hypotension (from the massive vasodilation) and bradycardia the unopposed activation of the parasympathetic nervous system leads to bradycardia. The patient in Neurogenic shock also characteristically has hypothalamic dysfunction, which may result in temperature dysregulation. The patient will often have poikilothermia (taking on the temp of the environment) which combined with massive vasodilation, promotes heat loss, often resulting in hypothermia. With poikilothermia, the skin could be cool or warm depending on the ambient temp. in either case the skin is usually dry. Initially the skin may be warm due to the massive dilation without compensation. As the heat dissipates the skin loses heat and the patient is at risk for hypothermia. Onset of Neurogenic shock can begin a soon as 30 minutes after the injury, and may last from days to weeks following spinal cord injury

Back 125

neurogenic shock

Front 126

inhibits synthesis of thyroid hormone

Back 126

Methimazole

Front 127

useful in conjunction with other ant thyroid drugs in the preparation of thyrotoxic crisis. The admission of iodine in large doses rapidly inhibits synthesis of T3 and T4 and blocks the release of these hormones into circulation. It also decreases the vascularity of the thyroid gland, making surgery safer and earsier. The maximum effect of iodine is usually seen within 1-2 weeks. Long term iodine therapy is not effective in controlling hyperthyroidism. Iodine is available in the form of saturated solution of potassium and Lugol’s solution.

Back 127

Iodine

Front 128

used for symptomatic relief of thyrotoxicosis that results from increased B-adrenergic receptor stimulation caused by excess thyroid hormones. Propranolol (inderal) the most frequently used B-blocker is usually administered with other antithyroid agents and rapidly provides symptomatic relief. Atenolol is the preferred B-blocker for use in hyperthyroid patient with asthma or heart disease

Back 128

B-adrenergic blockers

Front 129

therapy is the treatment of choice for most nonpregnant adults. damages or destroys thyroid tissue thus limiting thyroid hormone secretion. Radioactive iodine has a delayed response and maximum effects may not be seen in 2-3 months.

Back 129

I-131

Front 130

If too much tissue is taken the gland will not regenerate after surgery and hypothyroidism will result. Complications include: hypothyroidism, damage to or inadvertent removal of the parathyroid glands causing hypoparathyroidism and hypocalcaemia, hemorrhage, injury to the recurrent or superior laryngeal nerve, thyrotoxic crisis, and infection. Trach set should be set up incase of need to intubate because of airway obstruction, laryngeal stridor may often occur during inspiration and expiration as a result of tetany, to treat tetany calcium salts such as calcium gluconate and calcium chloride should be readily available for IV administration 1. Assess patient every 2hrs for sign of hemorhhage or tracheal compression, 2)place the patient into semi fowlers position and support the patient’s head with pillows, avoid flexion of neck, and any tension on the suture lines. 3) monitor vitals 4)control postoperative pain by giving meds.

Back 130

stridor may often occur during inspiration and expiration as a result of tetany, to treat tetany calcium salts such as calcium gluconate and calcium chloride should be readily available for IV administration

Front 131

Risk for hemorrhage is increased, large amounts of hormones may be released into circulation from surgery, producing marked fluctuations in the metabolic processes affected by these hormones. Postoperatively blood pressure, fluid balance, and electrolyte levels tend to be unstable because of the hormone fluctuations. High doses of corticosteroids are administered intravenously during surgery and for several days afterwards. HTN may develop, any rapid or significant changes in BP, respirations, or HR should be reported, the critical period for circulatory instability ranges from 24-48hrs after surgery, IV corticosteroids are given and the dose and rate of flow are adjusted to the patients clinical manifestations. Oral doses are given as tolerated. IV line may be kept in place after IV corticosteroids are withdrawn to keep a line open for quick administrations of corticosteroids or vasopressors. Morning urine levels of cortical are measured to evaluate the effectiveness of the surgery. If cortocosteroid dosage is tapered too rapidly after surgery adrenal insufficiency may develop-vomiting, increased weakness, dehydration, and hypotension indicate hypcorticosolism. Meticulous care should occur when changing dressings and during any other procedures that necessitate access to body cavities.

Back 131

post-operative nursing considerations for the person having an adrenalectomy

Front 132

Pheochromocytoma is a rare condition characterized by a tumor of the adrenal gland that produces excessive catecholamines (epinephrine, norepinephrine). Pheochromocytoma can occur at any age and in either gender but it is found most commonly in young to middle aged adults-in most cases effective adults the tumor is benign, encapsulated, unilateral, and solitary. The secretion of excessive catecholamines results in severe hypotension.

Clinical manifestations: the most striking clinical feature of pheochromocytoma include episodic hypertension, accompanied by the classic triad of severe, pounding headache, tachycardia, and profuse sweating. Attacks of episodic HTN are due to sympathetic nervous system stimulation and are often accompanied by anxiety and palpitations. Attacks can be provoked by meications including antihypertensive, opioids, radiologic contrast media and tryciclic antidepressants

Back 132

pheochromocytoma and identify clinical manifestations

Front 133

a syndrome by decreased tissue perfusion and impaired cellular metabolism. This results in imbalance between the supply of and demand of oxygen and nutrients

Back 133

shock

Front 134

is defined as cardiogenic and hypovolemic shock

Back 134

low blood flow shock

Front 135

is septic and anaphylactic and Neurogenic shock.

Back 135

maldistribution shock

Front 136

occurs when either systolic or diastolic dysfunction of the myocardium results in compromised cardiac output. The hearts inability to pump the blood forward is classified as systolic dysfunction-it primarily effects the left ventricle. When systolic dysfunction effects the right side of the heart blood flow through the pulmonary circulation is compromised. Precipitating causes of systolic dysfunction include myocardial infarction, cardiomyopathies, severe systemic or pulmonary HTN. Dyastolic dysfunction is an impaired ability of the right or left ventricle to fill during diastole. Decreased filling of the ventricles will result in decreased stroke volume.
Cardiogenic shock occurs when a primary ventricular ischemia, structural problems or arrhythmias lead to systolic dysfunction: ineffective forward movement of blood leading to decreased stroke volume which leads to decreased CO and decreased cellular oxygen supply resulting in decreased tissue perfusion and impaired cellular metabolism. Or it results from diastolic dysfunction: ineffective filling causing increased pulmonary pressures which lead to pulmonary edema and decreased oxygenation resulting in decreased cellular oxygen supply, decreased tissue perfusion and decreased cell metabolism

Back 136

cardiogenic shock

Front 137

Clinical manifestations: (early): tachycardia, hypotension, narrowed pulse pressures, an increase in systemic vascular resistance (SVR) increases the workload of the heart thus increasing the myocardial oxygen consumption. The heart’s inability to pump blood forward will result in low cardiac index. On examination the patient will be tachypneic, and pulmonary congestion will be evident by the presence of crackles. The homodynamic profile will demonstrate an increase in the pulmonary artery wedge pressure (PAWP) and pulmonary vascular resistance. Sings of peripheral hypoperfusion (cyanosis, cool and clammy skin, pallor, decreased cap refill time), decreased renal blood flow will result in sodium and water retention and decreased urine output, anxiety and delirium may develop as cerebral perfusion is impaired

Back 137

cardiogenic shock

Front 138

occurs when there is a loss of intravascular fluid volume. In hypovolemic shock the volume is inadequate to fill the vascular space. Absolute hypovolemic results when fluid is lost through hemorrhage, GI loss , fistula drainage, diabetes insipidus or diuresis. In relative hypovolemic fluid volume moves out of the vascular space into extra vascular space (interstitial, and intracavitary space-3rd spacing). In hypovolemic shock the vascular compartment remains unchanged while the volume of blood or plasma decreases. Decreased venous return to the heart, decreased preload, decreased stroke volume, decreased CO occurs

Back 138

hypovolemic shock

Front 139

Clinical manifestations: decreased: preload, stroke volume, capillary refill time, tachyon leads to bradypnea, decreased urine output, pallor, cool and clammy skin, anxiety, confusion, agitation, absent bowel sounds. Decreased hematocrit, increased lactate, increased urine specific gravity, changes in electrolyte

Back 139

hypovolemic shock

Front 140

homodynamic phenomenon that occurs after a spinal cord injury at the fifth thoracic vertebra or above. The injury results in a massive vasodilation without compensation as a consequence of the loss of SNS vasoconstrictor tone. This massive vasodilation leads to a pooling of blood in the blood vessels, the most important clinical manifestations are hypotension (from the massive vasodilation) and bradycardia the unopposed activation of the parasympathetic nervous system leads to bradycardia. The patient in Neurogenic shock also characteristically has hypothalamic dysfunction, which may result in temperature dysregulation. The patient will often have poikilothermia (taking on the temp of the environment) which combined with massive vasodilation, promotes heat loss, often resulting in hypothermia. With poikilothermia, the skin could be cool or warm depending on the ambient temp. in either case the skin is usually dry. Initially the skin may be warm due to the massive dilation without compensation. As the heat dissipates the skin loses heat and the patient is at risk for hypothermia. Onset of Neurogenic shock can begin a soon as 30 minutes after the injury, and may last from days to weeks following spinal cord injury

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neurogenic shock

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Clinical manifestations: increased/decreased temp, dysfunction related to level of injury, decrease skin perfusion, cool or warm dry skin, flaccid paralysis below the level of the lesion, loss of reflex activity, bowel and bladder function.

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neurogenic shock

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is an acute and life-threatening hypersensitivity (allergic) reaction to a sensitizing substance, it is an immediate reaction that causes massive vasodilation, release of vocative mediators, and an increase in capillary permeability. As capillary permeability increases, fluid leaks from the vascular space into the interstitial space. Anaphylactic shock can lead to respiratory distress, as a result of laryngeal edema or severe bronchospasm, and circulatory failure, as a result of massive vasodilation. The patient experience a sudden onset of symptoms, including hypotension, chest pain, swelling of the lips and tongue, wheezing, and stridor, skin changes include flushing, pruritus, uritcaria, and angioedema. In addition the patient may feel an impending sense of doom an become very anxious and confused. A patient can develop a severe allergic reaction possibly leading to anaphylactic shock, after contact, inhalation, ingestion, or injection of an antigen (allergen ) to which the person has previously been sens

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anaphylactic shock

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is the presence of sepsis with hypotension despite fluid resuscitation along with the presence of tissue perfusion abnormalities. Sepsis progressing to septic shock is the leading cause of death in no coronary intensive care units, with mortality rates as high as 40-60%. The primary organisms that cause septic shock are gram negative and gram positive bacteria. In septic shock there is an increase in coagulation and inflammation and a decrease in fibrinolysis. The release of platelet activating factor results in the formation of micro thrombi and obstruction of the microvasculature. In addition to the cardiovascular dysfunction that accompanies sepsis, respiratory failure is common. The patient will initially hyperventilate as a compensatory mechanism, resulting in respiratory alkalosis. Once the patient can no longer compensate, respiratory acidosis will develop. Other clinical signs of septic shock include decreased urine output, alteration in neurologic status, and GI dysfunction, such a GI bleeding and paralytic ileus

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septic shock

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The process of infection by bacteria or fungi can result in systemic signs and symptoms that are variously described. In rough order of severity, these are bacteremia or fungemia; septicemia; sepsis, severe sepsis or sepsis syndrome; septic shock; refractory septic shock; multiple organ dysfunction syndrome, and death.
The condition develops as a response to certain microbial molecules which trigger the production and release of cellular mediators, such as tumor necrosis factors (TNF); these act to stimulate immune response. Besides TNFα, other cytokines involved in the development of septic shock include interleukin-1β, and interferon γ

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septic shock

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1. Early stage: oliguria, sudden fever (over 101 F [38.3° C]), chills, nausea, vomiting, diarrhea, and prostration.
2. Late stage: restlessness, apprehension, irritability, thirst from decreased cerebral tissue perfusion, tachycardia, and tachypnea. Hypotension, altered level of consciousness, and hyperventilation may be the only signs among infants and elderly people.
Hypothermia and anuria are common late signs. Complications of septic shock include disseminated intravascular coagulation (DIC), renal failure, heart failure, GI ulcers, and abnormal hepatic function

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signs and symptoms of septic shock

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Successful management of the patient in shock includes: indentificatio of patients at risk for the development of shock, integration fo the patient’s history, physical examination, and clinical findings to establish a diagnosis. Interventions to control or eliminate the causes of the decreased perfusion, protection of target and distal organs from dysfunction. Provisions of multisystem support care. General management strategies for patient in shock begins with ensuring patent airway, once the airway is established, either with a natural airway or end tracheal tube, oxygen delivery must be optimized. Mechanical ventilation may be needed to support the delivery of oxygen to maintain an arterial oxygen sat of 90% or greater. Except for cardiogenic shock, all other classifications of shock involve decreased circulating blood volume. The cornerstone of therapy for septic, hypovolemic, Neurogenic, and anaphylactic shock is volume expansion with the administration of the appropriate fluid. Before beginning fluid resuscitation, two large-bore IV catheters must be inserted, preferably into the antecubital veins. Both crystalloids (normal saline) and colloids have a role in fluid resuscitation. Lactated ringers solution should be used cautiously in all shock situations because the failing liver cannot convert lactate to bicarbonate, thus increasing the serum lactate levels.

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collaborative therapy shock

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Drug therapy: the primary goal of drug therapy for shock is the correction of decreased tissue perfusion, medications used to improve perfusion in shock are administered intravenously via an infusion pump and often via a central venous line.

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drug therapy for shock

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dobutamine (dobutrex), dopamine (intropin), epinephrine (adrenalin), norepinephrine (levophed), nitroglycerin (tridil), Sodium Nitroprusside (Nipride)
Improve O2 delivery by decreased demand, reestablish blood flow with thrombolytics, angioplasty, emergency revascularization, increase O2 supply by providing supplemental O2.
Drug therapy: dilate coronary arteries (nitrates), improve contractility (inotropes), reduce preload (nitrates, morphine, diuretics, ACE inhibitors) reduce after load (ACE inhibitors, phosphodiesterase inhibiors, B-adrenergic agonists, vasodilators), reduce heart rate (B-adrenergic blockers, calcium channel blockers,) reduce contractility (B-adrenergic blockers, contraindicated with low ejection fraction) correct arrhythmias, circulatory assist devices: IABP, VAD

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cardiogenic shock

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optimize oxygenation, correct the cause (stop bleeding, GI losses) volume replacement (blood/blood products, crystalloids, calloids), rapid fluid replacement with two large bore (14-16 gauge) peripheral Ivs, use warm fluids, endpoints of resuscitation: CVP 15mmHg, PAWP 10-12mm Hg CI, >3L/min/m2, blood lactate <4mmol/L, base deficit -3 to +3 mmol/L

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hypovolemic shock

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optimize oxygen delivery by increase supply/decrease demand, fluid resusciation, optimize cardiac output: volume, vasopressors, vasopressors and inotropes (dobutamine) vasopressors (increase BP, dopamine, norepinephrine, phenylephrine), correct acidosis, obtain culture before antibiotics, antacids as ordered.

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septic shock

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treat according to cause, minimize spinal cord trauma with stabilization, careful administration of fluids, drug therapy: dopamine for hypotension and bardycardia, administration of phenylephrine or nor epinephrine to increase SVR, monitor for hypothermia

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neurogenic shock

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prevention via avoidance of known allergies, premedication with history of prior sensitivity (contrast media), identify and remove offending cause, maintain patient airway, intubation/mechanical ventilation, drug therapy: epinephrine subcutaneous, IV, nebulized, bronchodilators: nebulized, IV, antihistamines, corticosteroids (if hypotension persists), fluid resuscitation with colloids

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anaphylactic shock

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may not be clinically apparent; the patient will have no outward signs of decreased tissue perfusion despite the fact that the body begins to respond to the imbalance of oxygen supply and demand at the cellular level, metabolism changes from aerobic to anaerobic as a result lactic acid which is harmful to cells begins to accumulate as a waste product. The lactic acid must be removed by the blood and broken down by the liver. This process also requires oxygen which is unavailable at the cellular level in shock.

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inital stage of shock

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the next stage of shock; in this stage the body activates several compensatory mechanisms in an attempt to overcome the increasing consequences of anaerobic metabolism and to maintain homeostasis. There are neural, hormonal, and biochemical compensatory mechanisms. The patient’s clinical presentation begins to reflect the body’s responses to the imbalance in oxygen supply and demand.

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compensatory stage of shock

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begins as compensatory mechanisms fail. In this stage aggressive interventions are necessary to prevent the development of MODS. The hallmarks of this stage of shock are decreased cellular perfusion and altered capillary permeability, the altered capillary permeability allows leakage of fluids and portein out of the vascular space into the surrounding interstitial space. In addition to the decrease in circulating volume there is an increase in systemic interstitial edema. Fluid leakage from the vascular space affects the solid organs (liver, spleen, GI tract, lungs) as well as the peripheral tissues.

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progressive stage of shock

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the final stage of shock it results in decreased perfusion from peripheral vasoconstriction and decreased cardiac output exacerbate anaerobic metabolism. The accumulation of lactic acid contributes to an increased capillary permeability and dilation of the capillaries. Increased capillary permeability allows fluid and plasma proteins to leave the vascular space and move to the interstitial space. Blood pools in the capillary beds secondary to the constricted venules and dilated arterioles. The loss of intravascular volume worsens hypotension and tachycardia and decreases coronary blood flow. Decreased coronary blood flow leads to worsening myocardial depression and a further decline in CO. cerebral blood flow cannot be maintained and cerebral ischemia results. The patient in this stage of shock will demonstrate profound hypotension and hypoxemia. The failure of the liver, lungs and kidnesy’s will result in accumulation of waste products, such as lactate, urea, ammonia, and carbon dioxide. The failure of one organ system will have an effect on several other systems. Recovery is unlikely.

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recovery stage of shock

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mimic the SNS activity. The drug activity is mediated through their binding to alpha adrenergic or b-adrenergic receptors. Many of the sympathomimetic drugs cause peripheral vasoconstriction and are referred to as vasopressin drugs (epinephrine, norephinephrine) at high doses these drugs have the potential to cause severe peripheral vasoconstriction. The increased SVR increases the workload of the heart and can be detrimental to a patient in cardiogenic shock by causing further myocardial damage. Use of vasopressin drugs is generally reserved for patients who have been unresponsive to other therapies. Adequate volume replacement must be administered before the use of any vasopressin because peripheral vasoconstrictor effects in patients with low blood volume will cause further reduction in tissue perfusion. The goals of vasopressor therapy is to maintain a MAP of at least 60 mmHg. The nurse must continuously montior end-organ perfusion to ensure that he BP is providing adequate perfusion

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Sympathomimetic drugs and their role in shock
-vasopressors

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some patients in shock show evidence of excessive vasoconstriction and poor tissue profusion in spite of volume replacement and normal or even high systemic BP. This is especially true of patients with cardiogenic shock. Although generalized sympathetic vasoconstriction is a useful compensatory mechanism for maintaining systemic pressure,e excessive constriction can reduce tissue blood flow and increase the workload of the heart. The rationale for using vasodilator therapy for a patient in shock is to break the deleterious cycle in which widespread vasoconstriction causes a decrease in CO and BP, resulting in further sympathetic-induced vasoconstriction. The vasodilator most often used for the patient in cardiogenic shock is nitroglycerin, vasodilation may be enhanced with nitropresside (Nipride) in noncardiogenic shock.

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vasodilator drugs adn their role in shock

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a systemic inflammatory response to a variety of insults, including infection, ischemia, infarct and injury. characterized by a generalized inflammation in organs remote from the initial insult. Normally the inflammatory process is contained within a confined environment. A systemic inflammatory response can be triggered by many things including: burns, crash injuries, surgical procedures, abscess formation, intraabdominal, extremities, ischemic or necrotic tissue: pancreatitis, vascular disease, MI, microbial invasion: bacteria, viruses, fungi, parasites.

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Systemic Inflamatory response syndrome (SIRS)

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mulitple organ dysfunction syndrome is the failure of more than one organ system in an acutely ill patient such as homeostasis cannot be maintained without the intervention. results from SIRS. can develop as a result of primary injury (primary MODS) or a secondary injury (Secondary MODS).

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MODS

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occurs wearly and results from a well defined illness or injury (pulmonary contusion, inhalation injury, aspiration).

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primary MODS

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results from uncontrolled systemic inflammation with resultant organ dysfunction. It develops latently, often after many insults

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secondary MODS

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Collaborative care focuses on prevention and treatment of infection, maintenance of tissue oxygenation, nutritional and metabolic support, and appropriate support of individual failing organs. Appropriate cultures should be sent and broad-spectrum antibiotics started. Early aggressive surgery is recommended for removal of necrotic tissue that provide a culture medium for microogranisms. Aggressive pulmonary management including early ambulation, can reduce risk of infection. Strict aseptic technique when it comes to intra-arterial lines, endotracheal tubes, urinary catheters, IV lines to prevent infection. Interventions that decrease O2 demand and increase O2 delivery are essential. Sedation, mechanical ventilation, analgesia, paralysis, and rest may decrease oxygen demand and should be considered. Oxygen delivery may be increased by maintaining normal levels of Hgb, and PaO2, using PEEP, increasing preload or myocardial contractility to enhance CO, or reducing after load to increase CO. the goal for nutrition therapy is to preserve organ funciton. Providing adequate nurtion decreases morbidity and mortality; the use of enteral route is preferable to potential nutrition and may limit translocation of gut bacteria. Support of failing organs is a primary goal of therapy

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nursing and collaborative management of MODS

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erythematic, blanching on pressure, pain and mild swelling no vesicles or blisters (although after 24hr skin may blister and peel) looks like sunburn

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superficial burns

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fluid filled vessicles that are red, shiny, wet (if vesciles have ruptured); severe pain caused by nerve injury; mild to moderate edema

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partial thickness burns

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dry, waxy, white, lethary, or hard skin, visible thrombosed vessels, insensitivity to pain and pressure because of nerve destruction, possible involvement of muscles, tendons and bones

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full thickness burns

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The greatest initial threat to a patient with a major burn is hypovolemic shock. It is caused by a massive shift of fluid out of blood vessels as a result of increased capillary permeability. As the capillary walls become more permeable, water, sodium, and later plasma proteins (especially albumin) move into interstitial spaces and other surrounding tissues. The colloidal osmotic pressure decreases with progressive loss of protein form the vascular space. This results in more fluid shifting out of the vascular space into the interstitial spaces (fluid accumulation in the interstitial is termed second spacing). Fluid also moves to areas that normally have minimal to no fluid-3rd spacing. Examples of 3rd spacing include exudate and blister formation. The net result fluid shift is intravascular volume depletion. Edma, decreased BP, increased pulse, and other manifestions of hypovolemic shock are clinically detectable signs. If not corrected these events could lead to irreversible shock and death.

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pathophys of burns

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Clinical manifestations: blisters filled with fluid and protein may occur in partial thickness burns. Fluid is not acutally lost from the body as much as it is sequestered to the interstitial spaces and third spaces. Extreme edema. Signs of adynamic ileus, absent bowel sounds as a response to trauma and potassium shifts. Shivering may occur b/c of heat loss, anxiety and pain. Difficulty recalling the sequence of events, unconciousness or altered mental status usually hnot a result fo the burn. Most common reason is hypoxia associated with smoke inhalation,head trauma, or excessive amounts of sedatives or pain meds

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clinical manifestations of burns

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cardiovascular complications: arrhythmias and hypovolemic shock. Circulation in the extremities may be impaired b/c of circumferential burns and subsequent edema formation. Occlusion of blood supply, causing ischemia, paesthesias, necrosis, and eventually gangrene. Microcirculation is impaired because of damage to skin structures-sludging

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complications of burns

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Respiratory: smoke inhalation; upper airway burns that acuse edema foration and obstruction of the airway. Inhalation injury, upper airway distress may occur with or without smoke inhalation, and airway injury at either level in absence of burn injury to the skin.

Urinary system: acute tubular necrosis because of hypovolemic state blood flow to the kidneys is decreased causing renal ischemia. If this continues acute renal failure can occur.

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complications of burns

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Emergent phase: assess fluid needs, begin IV fluid replacement, insert indwelling urinary catheter, montior urine output, start hydrotherapy or cleansing, debride as necessary, assess extent and depth of burns, initiate topical antibiotic therapy, administer tetanus toxoid or tentus antitoxin, assess and manage pain and anxiety

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collaborative care of burns

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Acute phase: fluid therapy-replace fluids depending on individual patient needs, assess wound daily, observe for complications, continue hydrotherapy, cleansing, continue debridement if necessary, continue assessing for and treating pain and anxiety, provide homografts, provide autografts, care for donor site, provide adequate diet to support wound healing, begin PT for maintenance and rehabilitation of movement.

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acute phase of collaborative care of burns

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An NG is inserted and connected to low intermittent suction for decompression. When bowel sounds return at 48-72 hrs after injury oral intake can be initiated beginning with clear liquids and progressing to a diet high in protein and calories. Massive catabolism can occur and is characterized by protein breakdown and increased gluconeogenesis. Calorie needs are often in the 5000 kcal per day range,. Failure to supply adequate calories and protein leads to malnutrition and delayed healing. Calorie containing liquids are given to drink instead of water.

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nutritional therapy needs of the burn patient.

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Collaborative care focuses on prevention and treatment of infection, maintenance of tissue oxygenation, nutritional and metabolic support, and appropriate support of individual failing organs. Appropriate cultures should be sent and broad-spectrum antibiotics started. Early aggressive surgery is recommended for removal of necrotic tissue that provide a culture medium for microogranisms. Aggressive pulmonary management including early ambulation, can reduce risk of infection. Strict aseptic technique when it comes to intra-arterial lines, endotracheal tubes, urinary catheters, IV lines to prevent infection. Interventions that decrease O2 demand and increase O2 delivery are essential. Sedation, mechanical ventilation, analgesia, paralysis, and rest may decrease oxygen demand and should be considered. Oxygen delivery may be increased by maintaining normal levels of Hgb, and PaO2, using PEEP, increasing preload or myocardial contractility to enhance CO, or reducing after load to increase CO. the goal for nutrition therapy is to preserve organ funciton. Providing adequate nurtion decreases morbidity and mortality; the use of enteral route is preferable to potential nutrition and may limit translocation of gut bacteria. Support of failing organs is a primary goal of therapy.

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nursing and collaborative management of MODS

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erythematic, blanching on pressure, pain and mild swelling no vesicles or blisters (although after 24hr skin may blister and peel) looks like sunburn

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superficial burns

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fluid filled vessicles that are red, shiny, wet (if vesciles have ruptured); severe pain caused by nerve injury; mild to moderate edema.

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partial thickness burns

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dry, waxy, white, lethary, or hard skin, visible thrombosed vessels, insensitivity to pain and pressure because of nerve destruction, possible involvement of muscles, tendons and bones

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full thickness burns

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The greatest initial threat to a patient with a major burn is hypovolemic shock. It is caused by a massive shift of fluid out of blood vessels as a result of increased capillary permeability. As the capillary walls become more permeable, water, sodium, and later plasma proteins (especially albumin) move into interstitial spaces and other surrounding tissues. The colloidal osmotic pressure decreases with progressive loss of protein form the vascular space. This results in more fluid shifting out of the vascular space into the interstitial spaces (fluid accumulation in the interstitial is termed second spacing). Fluid also moves to areas that normally have minimal to no fluid-3rd spacing. Examples of 3rd spacing include exudate and blister formation. The net result fluid shift is intravascular volume depletion. Edma, decreased BP, increased pulse, and other manifestions of hypovolemic shock are clinically detectable signs. If not corrected these events could lead to irreversible shock and death.

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pathophys of burns

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Clinical manifestations: blisters filled with fluid and protein may occur in partial thickness burns. Fluid is not acutally lost from the body as much as it is sequestered to the interstitial spaces and third spaces. Extreme edema. Signs of adynamic ileus, absent bowel sounds as a response to trauma and potassium shifts. Shivering may occur b/c of heat loss, anxiety and pain. Difficulty recalling the sequence of events, unconciousness or altered mental status usually hnot a result fo the burn. Most common reason is hypoxia associated with smoke inhalation,head trauma, or excessive amounts of sedatives or pain

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burns

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Encouraging patient to ventilate feelings of anger, hostility, and frustration can be a useful strategy. These interventions can help the nurse cope with interventions that cause pain. Order a dosage for a range opioid (morphine sulfate 5-10mg IV) every 1-3 hours for pain. Second intervention involves the use of several drugs in combination such as morphine with haloperidol (haldol). Ativan, Valium, Versed, the effect of Versed is a short term amnesia, so it is given 15-20 min before a dressing change- it lasts 30-60 minutes after it is administered. Buprenex is another durg that is useful to treat pain; it is an opioid antagonist so it cannot be used in combination with other opioid analgesics.- it may work well for the patient who does not obtain pain relief with high dose opioids. Use of relaxation tapes, visualization, guided imagery biofeedback, and meditation. PCAs are also used.

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interventions that the nurse may use in the management of pain in the burn patient.

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it is performed to remove unsightly flabby folds of adipose tissue. The patient who whoses lumpectomy does so simply for cosmetic reasons. There is no evidence of regeneration of adipose tissue occurs at the surgical sigths. However; it must be emphasized to the patient that surgical removal does not prevent obesity from recurring, especially if lifetime eating habits remain the same. The dangerous effects of anesthesia and poor wound healing should be indicated

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Lipectomy

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suction assisted lumpectomy. The current use is for cosmetic purposes and not for weight reduction; this intervention helps improve facial appearance or body contours. A good candidate for this surgery is one who has achieved weight reduction but who has excess fat under the chin, along the jaw line, in the nasolabial folds, over the abdomen, around the waist and upper thighs. A long hollow stainless steel cannula is inserted through a small incision over the fatty tissue to be suctioned. The purpose is to improve body appearance and self concept

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Liposuction

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most frequently used procedure to produce weight loss in obese people. The approach leads to physical restriction of food intake. The stomach is partitioned into a small upper portion along the lesser curvature of the stomach; this pouch drastically limits capacity. In addition the stoma opening to the rest of the stomach is banded to delay emptying of solid food from the proximal pouch. Problems associated with gastric restriction include intractable vomiting from too rapid intake, distention of wall of proximal pouch, rupture of the staple line, and erosion of the band in the stomach.

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virtical banded gastroplasty

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the Roux-en Y surgical procedure is the most commonly used procedure gastric bypass surgery. In this procedure stomach size is decreased with a gastric pouch anastomosis emptying directly into the jejunum. Variations of this procedure include: stapling the stomach without transection to create a small, gastric pouch. Creating an upper and lower gastric pouch and total disconnecting the pouches and creating an upper gastric pouch an completely removing the lower pouch. Complications include dumping syndrome.

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gastric bypass

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All patients admitted for surgical therapy have an NG tube placed during surgery and attached to low suction after surgery. The patient should know that oral nutrition will be impossible for a few days after the surgery and that IV fluids will be the main source of intake. Early ambulation is essential for the obese patient. It is important that the patient know that it is usually necessary to get out of bed soon after surgery and with increasing frequency there after usually 3-4 times each day. Elastic stockings, elastic compression stockings or elastic wraps will be used and that active and passive ROM exercises will be performed throughout daily care. Low dose heparin is often ordered. Pain meds if given IM must be given with an extra long needle to get into the muscle. Keep the head of the bed elevated at 30 degrees to help ventilatory efforts. Position changes and ROM are instituted immediately after surgery and carried out every 1-2 hrs. encourage and assist with turn, cough deep breathe; frequent mouth and nose care will be needed. Abdominal wounds require frequent observation for amount and type of drainage, condition of sutures, and signs of infection.skin should be cared for several times a day; make sure NG tube is patent; vomiting occurs frequently with gastric surgery. Clear liquids are given orally when tolerance is established.

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nursing management related to surgical therapy for obesity