Exam 2 Study Doc PDF

The pathology of chronic obstructive pulmonary disease is chronic bronchitis related to smoking and repeated airway infections. Is also emphysema related to smoking and chronic exposure to irritants. Clinical manifestations of COPD are leaning forward with hands on knees and tachypenia, respiratory...

The pathology of chronic obstructive pulmonary disease is chronic bronchitis related to smoking and repeated airway infections. Is also emphysema related to smoking and chronic exposure to irritants. Clinical manifestations of COPD are leaning forward with hands on knees and tachypenia, respiratory acidosis with a low pH high CO2 and decreased O2, barrel chest, small and thin with emphysema, overweight and coughing with mucus for chronic bronchitis the mucus will be mucopurulent. The treatments and interventions are monitor for polycythemia excess blood cells to compensate for lack of oxygen to tissues. Rest and elevate the head of the bed take vital signs with a pulse ox give bronco dilators and mucolytics do cough, deep breathe exercises and pulmonary secretion and removal methods.  The pathology for acute bronchitis is viral or non-viral smoke inhalation, allergic reaction, airway, becoming inflamed and narrow, swelling and mucus production, decreased ciliary function. Clinical manifestations are cough with recent onset. Symptoms are mild and self limiting sore throat, postnasal, drip, and fever. For treatment monitor symptoms encourage rest nutrition and fluids typically self limiting they may need bronchodilators. Abnormal breathing patterns are Cheyne Stokes This has a regular cycle of breathing, where the rate and depth of breathing increase then decrease until apnea occurs apnea may lengthen. Biots has a period of normal breathing, followed by apnea and is irregular think overdose breathing. Obesity and obstructive sleep apnea the pathology is a body mass index of over 30 which causes decreased Avola ventilation leading to hypoxemia polycythemia and cor pulmonale. Cor pulmonale also known as pulmonary heart disease causes the right side of the heart to overwork and enlarge leading to right sided heart failure. Manifestations of obstructive sleep apnea are loud snoring with no breathing for 10 seconds or longer. Interventions are low fowlers maximizes, diaphragmatic chest expansion, and decreases hypoventilation. They may be placed on CPAP or BiPAP and educated on weight loss.  Ankylosing spondylitis pathology is more common in males in their twenties to 30s. The cause is unknown. There is transient acute arthritis of the peripheral joints and chronic inflammation at the site of the ligamentous insertion to the spine or sacral iliac joints. The respiratory system is affected by limited chest expansion and the formation of pulmonary fibrosis in the upper lobes. The clinical manifestation is low to mid back pain and stiffness. There is no cure you can only treat the symptoms. This can be diagnosed by a pulmonary function, tests, and chest x-rays. Plural effusion pathology is a collection of fluid or pus in the plural cavity. The clinical manifestations are absent breath sounds shortness of breath and pleauritic pain. If there is less than 300 mL of fluid, it can be asymptomatic. Treatments is thoracentesis To do this, he must position the patient so there is easy access to the effusion. Educate the patient on using arms to splint the chest for pain.  Pneumonia's pathology is an infection that inflames the alveoli. It can be mycoplasma from atypical bacteria, legionnaires from air mist, anaerobic from aspiration, opportunistic from fungal aspergillus in old homes and jiroveci. it can be bacterial viral community hospital acquired or atypical also. High risks are the elderly multiple comorbidities and on antibiotics or immunosuppressed. Clinical manifestations are bronchial breath sounds fever, chills, cough, and headache. Treatments are sputum cultures the mouth out and then spit.  Hypersensitivity pneumonitis risk factors are restrictive, occupational disease, and predominantly seen in non-smokers.  Tension pneumothorax pathology is trauma induced from penetrating or non-penetrating injury, central line, placements, thoracentesis, lung, biopsy, and ventilators. It may also result from the buildup of air under pressure in plural space. Enter plural space during inhalation, but cannot escape during expiration so the lung collapses and the ribs spring outwards. Clinical manifestations are tracheal shift to the left shortness of breath dyspnea severe tachycardia, and hypotension. This is an emergency and requires thoracentesis and chest tube. Tuberculosis pathology is mycobacterium is inhaled and enters the lungs. Alveolar macrophages ingest the bacteria, and T cells/ macrophages surround the bacteria creating a granuloma Ghon Tuberclenodule can become necrotic and has lymph components. Risks are immunosuppressed HIV and tight living quarters. Reactivation can occur when Ghon Tuberclenodule can form in lymph nodes they released the Mycobacterium. The disease can stay latent for several years. Clinical manifestations are diaphoresis- soaking the sheets. Treatment is medications such as isoniazid taken with rifampin, pyrazinamide and ethambutol (b6) daily for 8 weeks. After that isoniazid will be taken with rifampin for 7 months. They will need liver panels monthly as it is rough on the liver ALT and AST. They will need to avoid tuna, aged cheese, red wine, soy sauce, and yeast.  For PA02 greater than 70mmHg is normal. Safe is 45 to 70 dangerous is below 40. A big drop means decrease oxygen and ventilation, this is very dangerous, especially if it happens at rest. The pathology of hemophilia is an X linked recessive disorder with deficient factor, eight and factor nine creates an abnormal sequence of intrinsic pathway coagulation to form a fibrin clot, resulting in bleeding. Clinical manifestations are easy, bruising, and spontaneous bleeding. Treatments are Tylenol for pain. aPPT normal is around 30 to 40 but hemophilia would have a higher number like 80-ish. Pathology of Von Willebrand disease is an autosomal dominant disorder that affects factor eight von Willebrand factor (plasma protein) and platelet dysfunction. This disease occurs in both males and females and leads to the absence of platelet adhesion at injury site. Clinical manifestations are mucosal and G.I. bleeding and excessive bleeding after surgery. Labs such as activated partial thromboplastin (aPTT), PT, hemoglobin and platelets must be monitored. Immune thrombocytopenia Purpura (ITP) pathology is autoimmune with inflammation of small vessels, causing infiltration of supportive tissue. It can also be abnormal blood vessels due to medication such as warfarin or allergies. Clinical manifestations are bruising heavy menses,petechia, risk for bleeding membranes including G.I. and pulmonary. Interventions are labs platelets less than 30,000. Education about bleeding risk, including meds and activities. The patient can learn to live a productive functioning life with low platelets.  Thrombocytopenia is decreased platelets less than 150,000. At less than 100,000 symptoms occur at less than 50,000 petechia starts, less than 20,000 bleeding starts. This is related to chemotherapy. Bone marrow issues can cause a drop in platelet counts because this is the blood cell factory. Bone marrow cancers would be a situation that would cause a delay in making platelets, dropping the platelet levels in the body. Deep vein thrombosis is a thrombosis in the leg. Clinical manifestations are Adema tenderness and inflammation. Treatment and interventions are pain is relieved by elevating the leg applying moist heat, acetaminophen, and continuing anticoagulant and avoiding exercise. If there is too much heparin, give protamine sulfate to reverse. Complications are pulmonary embolism you should monitor for shortness of breath. Reynards pathology is affects on local nerve function. This is extreme vasal construction.  Risks are immuno deficiency, trauma woman, smoking, cold temperatures, and emotional stress. Manifestations are cyanosis fingers and toes with pain and numbing. Interventions are stop smoking and avoid cold temperatures. Buerger's pathology is a very rare inflammatory condition that affects small and medium-size arteries and veins of the upper and lower extremities producing varying degrees of obstruction. This is associated with smokers. Clinical manifestations are decreased arterial flow leading to cold, no hair, absent pulses, and ulcers. You should monitor for decreased pulses and there is a potential need for amputation. Venus insufficiencies and obstructions pathology is related to heart disease and the valves are incompetent. Clinical manifestations are red beefy tissue opening on the inside medial part of the ankle, pain that decreases with ambulation and elevation. Venous stasis ulcers with warm, tough, thickened skin, areas of dark, pigmentation, aching, cramping, and edema. If an obstruction occurs so will edema increased hydrostatic, capillary pressure and deep vein thrombus. Treatment and interventions are education on walking to relieve pain using compression stockings while in bed to elevate legs above the heart do not cross legs, exercise, and ambulate throughout the day with recommended 24 times a day to keep the extremities protected, clean and dry.  Barcos veins pathology are impaired Venus return caused by standing increased pressure and pulling. At risk for increased capillary, pressure and edema. Clinical manifestations are aching, heavy discomfort, and darkened raised tortuous veins. Venus ulcers may develop. Treatment and interventions are pain, relief for varicose veins, elevate legs above the heart.   Peripheral vascular disease, pathology wounds, cause insufficient blood flow to tissues. Clinical manifestations are deep circular black ulcers on the great toe with painful, dry, gangrene around proximal joint spaces with no edema. Chronic arterial obstructions pathology is related to arthrosclerosis making it difficult to allow oxygen to get to tissues. The clinical manifestations are intermittent claudication with activity, absent pulses, and ulcer on toe. Treatment and interventions rest, avoid crossing legs and angioplasty. Atherosclerosis /arteriosclerosis risk factors are males patients with hyper, lipidemia, diabetics, and smokers. They are at risk for ischemic strokes, retinal, injuries, renal, impairments, angina, and heart failure. These patients must have education such as testing the water temperature before getting in the bath, to avoid hot waters and heating pads on the extremity, they can use them on the abdomen for reflex vasodilation. Keep the extremities protected and warm no cold temperatures. Walk and exercise until pain then rest. Keep legs in a neutral position leg dangling head of bed up maybe reclined or with feet resting on floor. No crossing legs, tight clothing or socks. Hypertension causes are unknown many risk factors that are modifiable and non-modifiable. Modifiable risk factors are physical activity and decreasing blood glucose. Secondary hypertension is high blood pressure that occurs secondary to another cause. It can be a symptomatic. Treatment or lifestyle modification such as decreasing smoking and alcohol drinking less than one to two times a day exercising three times a week or up to 150 minutes a week. Recommend 30 minutes five times a week. Restricting sodium to less than 2 g a day and potassium intake should be 3500 to 5000 mg a day. -- Diet, which is fruits, vegetables, low-fat dairy, decreased saturated, fats, and total fats with healthy grains. Maintain a BMI of 18.5 to 24.9.  Hypertensive emergencies are a diastolic that is equal or greater than 120 or a systolic that is equal or greater than 180. End organ damage equals hypertensive emergency. Risk factors are African-American males. Smoking deteriorates the lining of vessels and creates thrombus, increases LDL and triglycerides and decreases myocardial oxygen and increases vasospasms. Orthostatic hypotension is a response to position change. There is a drop in systolic blood pressure of over 20 or decrease in diastolic blood pressure of 10 or more in three minutes of standing. Think about the patient lying flat, then standing blood rushes and pools in the legs and we need that blood evenly distributed so that our heart continues to pump oxygenated blood. Body increase blood pressure by increasing cardiac output, basal constriction, peripheral vessels, so blood becomes evenly distributed.  With bradycardia, we will be concerned with hypoxia with a fib. We will be concerned with myocardial hypertrophy. Also a pulse that is decreased in the radial compared with the apical may be a fib. ST elevation we are concerned with myocardial blockage, occlusion, and pericarditis. Review the EKG strips in the study guide. If a patient has an ICD placed, and now you hear, muffled heart sounds suspect, cardiac tamponade.  Becks Triad is hypotension, muffled heart tones, and jugular vein distention. This means there is cardiac tamponade.  In circulatory hypoxia, there is decreased cardiac output that may be from an obstruction in an artery or vein.  Mitral valve regurgitation is a loud pan systolic, high-pitched blowing radiating to the axilla. Mitral valve stenosis pathology is complication right ventricle hypertrophy due to backflow from stenosis, which will cause the decreased function. If there is a backflow then there will be venous pulmonary hypertension and a fib. Clinical manifestations are pulmonary congestion, Ing difficulty breathing, especially with exertion chest pain, fatigue, hemoptysis, dizziness, but maybe asymptomatic. With backflow, there will be difficult breathing on exertion due to pulmonary venous hypertension. Look up treatments.  The pathology of aortic stenosis is the aortic cusp has calcified creating a narrowing in the valve. Clinical manifestations are diminished, cardiac output, syncope, fatigue, tiredness, low systolic, blood pressure angina with faint pulses. There can be a crescendo decrescendo murmur in S4. Look up treatments and interventions. Rheumatic heart disease causes damage to connective tissue in the heart which leads to inflammation and swelling and erosion, which then leads to our platelets and vibrant clumping up and collecting in the valve leaflets just like when there is an injury to a vessel, they will try to patch it up.  The pathology of pericarditis is if it is chronic, there is a dysfunction, and the sack is destroyed, and the outside of the heart will adhere to the surrounding mediastinal structure. Clinical manifestations are radiating pain, fever, malaise, extreme exercise, intolerance, weakness, fatigue, systemic venus congestion. Treatment is pain, relief upright in a chair leaning forward.  The pathology of left sided heart failure is right ventricular issues and failure to pump the blood to the lungs, and then the left side of the heart increase pulmonary pressure and Adema with blood in the lungs and the heart must work hard to get to the body, there will be decreased peripheral circulation back to the heart. If there is no blood to pump there is a failure. With right sided cor pulmonale increase resistance to pulmonary arterial flow due to obstructive/restrictive lung issues which leads to compensatory right ventricular hypertrophy, which can lead to right sided heart failure. Clinical manifestations of left sided heart failure are backflow, causing difficult deep breathing on exertion, orthopnea, coughing paroxysmal nocturnal dyspnea, cyanosis, and basilar crackles. With left sided heart failure forward flow. The manifestations are fatigue oliguria increased heart rate, paint, pulses, restlessness, confusion, and anxiety. In general shortness of breath with exertion, like walking upstairs and needing to stop halfway and increase blood pressure to compensate for decreased oxygen in myocardial tissue. Right sided signs and symptoms are lower extremity edema, jugular vein, distention, hepatomegaly society, splenomegaly increased heart rate, fatigue, and oligoria. Treatments are monitor for fluid overload, strict intake and outtake. Education is to call the PCP with worsening swelling, shortness of breath with activity or rest gaining more than 5 pounds in a week and gaining more than 2 pounds in a day. The pathology of myocardial infarction/ angina is insufficient, blood flow, causing decreased oxygen in the myocardial tissue. Clinical manifestations are angina, which is chest pain and shortness of breath. This can be predictable with physical activity as there is increased demand for oxygen, and the vessels may have plaque buildup which narrows the vessels and decreases oxygen supply and atypical signs and symptoms, back pain, fatigue, and weakness. Treatment and interventions are to take vitals, then get a chest x-ray, EKG and supply oxygen nitroglycerin aspirin, and morphine. if patient comes in with chest pain but normalizes after 24 hours with normal CK isoenzyme, you should evaluate for another cause of the chest pain that is not an MI. age related concerns are a late diastolic suggestive of S for gallop. another is increased systolic blood pressure, ventricle wall, thickening, decreased detention of heart failure. You should look for shortness of breath and weakness, decreased renal function diuretics not working then creating distention. With tube feedings, you should assess the placement of the tube every 4 hours. The head of bed should be elevated to 45° if possible change meds from pill form to liquid form and use water flushes. For a blood donation, you must weigh at least 50 kg have a temperature less than 99.6 have a systolic blood pressure between 80 to 180 with a diastolic blood pressure of 50 to 100 and your hemoglobin must be at least 12.5 a 17-year-old with parental consent can donate. Atropine should be given to a patient with a low heart rate, dizziness, and nausea. Valsartan is an angiotensin receptor blocker it decreased blood pressure by vasodilation which decreases cardiac workload and helps prevent heart failure symptoms. You need to be monitoring kidney function with this medication. Propranolol is a beta blocker that decreases contractility and vasodilation. Avoid this medication with asthma. Nifedipine is a calcium channel blocker given with aortic valve disease and angina due to vascular vasodilation Diltiazem is a calcium channel blocker that acts mainly on the heart with cardiac contractility to reduce oxygen demand. Isoniazid refer to TB