MS Nursing Lecture

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discussion for the nurses' review regards the medical surgical problems in relation to the nursing practice

rsm, md

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MS Nursing Lecture

  1. 1. Dr. Ronald Sanchez – Magbitang <ul><li>EDUCATIONAL ATTAINMENT </li></ul><ul><li>NEHS </li></ul><ul><li>UST – B.S. Biology (Pre-Med) </li></ul><ul><li>SLU – Doctor of Medicine </li></ul><ul><li>(“Meritus”) </li></ul><ul><li>TRAININGS </li></ul><ul><li>Dr. PJGMRMC – Internal Medicine </li></ul><ul><li>Children's Medical Center – Hematology </li></ul><ul><li>RITM – 1 st In-Country Training in HIV AIDS </li></ul><ul><li>PCP Symposium and Conventions </li></ul><ul><li>PHA Conventions </li></ul><ul><li>PRESENT POSITION </li></ul><ul><li>Chief of Hospital </li></ul><ul><li>Gov. Eduardo L. Joson Memorial Hospital </li></ul><ul><li>Daan Sarile, Cabanatuan City </li></ul>
  2. 2. PRE - TEST <ul><li>Primary symptom complained by patients with myocardial infarction … </li></ul><ul><li>Normal BP is below… mmHg </li></ul><ul><li>Aneurysm is due to the weakness of the blood vessel walls of veins… True or False? </li></ul><ul><li>The different cardiac valves are…. The AV and semilunar valves </li></ul><ul><li>The normal physiologic pacemaker of the heart is the… </li></ul><ul><li>The heart has two sides, with 2 chambers left and right… True or False? </li></ul><ul><li>Different categories of stroke according to time course, are… </li></ul><ul><li>Endocrine system functions is primarily controlled by this gland </li></ul><ul><li>Atrophy of the brain is noted in Alzheimer’s… True or False? </li></ul><ul><li>TNM classification is used in what type of ailments? </li></ul>
  3. 3. PRE - TEST <ul><li>ECG means… </li></ul><ul><li>EEG means… </li></ul><ul><li>EMG means… </li></ul><ul><li>CT scan means… </li></ul><ul><li>MRI means… </li></ul><ul><li>PET means… </li></ul><ul><li>LP means… </li></ul><ul><li>CSF means… </li></ul><ul><li>FEV means… </li></ul><ul><li>RIND and TIA means… </li></ul>
  4. 5. Medical – Surgical Nursing <ul><li>CARDIOVASCULAR </li></ul><ul><li>Myocardial Infarction </li></ul><ul><li>Cardiac Anomalies </li></ul><ul><li>Valvular Heart Disease </li></ul><ul><li>Cardiac Conduction Problems </li></ul><ul><li>Hypertension </li></ul><ul><li>Aneurysm </li></ul><ul><li>DVT </li></ul><ul><li>Neurology </li></ul><ul><li>Cerebro-vascular Accident </li></ul><ul><li>Myasthenia Gravis </li></ul><ul><li>Multiple Sclerosis </li></ul><ul><li>Guillain Barre Syndrome </li></ul><ul><li>Parkinson’s Disease </li></ul><ul><li>Alzheimer’s Disease </li></ul><ul><li>Huntington’s Chorea </li></ul><ul><li>RESPIRATORY </li></ul><ul><li>Bronchial Asthma </li></ul><ul><li>COPD – Bronchitis & Emphysema </li></ul><ul><li>Pneumonia </li></ul><ul><li>ENDOCRINE </li></ul><ul><li>Cushing’s Disease </li></ul><ul><li>Hypothyroidism / Hyperthyroidism </li></ul><ul><li>Diabetes Insipidus </li></ul><ul><li>Diabetes Mellitus </li></ul><ul><li>Grave’s Disease </li></ul>0NCOLOGY EENT Meniere’s Disease Glaucoma Cataract INTEGUMENTARY / SKIN / DERMATOLOGY GASTROENTEROLOGY Liver Cirrhosis RENAL / NEPHROLOGY Renal Failure – Acute, Chronic, ESRD Dialysis – Peritoneal, Hemodialysis GENITO-URINARY / UROLOGY MUSCULOSKELETAL Arthritis HEMATOLOGY Leukemia
  5. 6. THE HEART
  6. 7. How the Heart Works <ul><li>The heart has two sides, separated by an inner wall called the septum . The right side of the heart pumps blood to the lungs to pick up oxygen. Then, oxygen-rich blood returns from the lungs to the left side of the heart, and the left side pumps it to the body. </li></ul><ul><li>The heart has four chambers and four valves , and it is connected to various blood vessels. Veins are the blood vessels that carry blood from the body to the heart, while arteries are the vessels that carry blood away from the heart to the body. </li></ul>
  7. 8. <ul><li>Heart Chambers </li></ul><ul><li>The heart has four chambers or &quot;rooms&quot;—two on the left side of the heart and two on the right. </li></ul><ul><li>The atria (AY-tree-uh) are the two upper chambers that collect blood as it comes into the heart. </li></ul><ul><li>The ventricles are the two lower chambers that pump blood out of the heart to the lungs or other parts of the body </li></ul>
  8. 9. <ul><li>Heart Valves </li></ul><ul><li>Four valves control the flow of blood from the atria to the ventricles and from the ventricles into the two large arteries connected to the heart. </li></ul><ul><li>The four valves are: </li></ul><ul><li>The tricuspid (tri-CUSS-pid) valve is in the right side of the heart, between the right atrium and the right ventricle. </li></ul><ul><li>The pulmonary valve is in the right side of the heart, between the right ventricle and the entrance to the pulmonary artery that carries blood to the lungs. </li></ul><ul><li>The mitral (MI-trul) valve is in the left side of the heart, between the left atrium and the left ventricle. </li></ul><ul><li>The aortic (ay-OR-tik) valve is in the left side of the heart, between the left ventricle and the entrance to the aorta, the artery that carries blood to the body. </li></ul><ul><li>Valves are like doors that open and close. They open to allow blood to flow through to the next chamber or to one of the arteries, and then they shut to keep blood from flowing backwards. </li></ul><ul><li>When your heart's valves open and close, they make the familiar &quot;lub-DUB&quot; or &quot;lub-DUPP&quot; sounds that your doctor can hear by using a stethoscope. </li></ul><ul><li>The first sound is made by the tricuspid and mitral valves closing at the beginning of systole (SIS-toe-lee). Systole is when the heart contracts, or squeezes, and pumps blood out of the heart. </li></ul><ul><li>The second sound is made by the aortic and pulmonary valves closing at the beginning of diastole (di-AS-toe-lee). Diastole is when the heart relaxes and fills with blood. </li></ul>
  9. 10. <ul><li>Arteries </li></ul><ul><li>The arteries are the major blood vessels connected to your heart. </li></ul><ul><li>The pulmonary artery carries blood pumped from the right side of the heart to the lungs to pick up a fresh supply of oxygen. </li></ul><ul><li>The aorta is the main artery that carries oxygen-rich blood pumped from the left side of the heart out to the body. </li></ul><ul><li>The coronary arteries are the other important arteries attached to the heart. They carry oxygen-rich blood to the heart muscle, which must have its own blood supply to function. </li></ul><ul><li>Veins </li></ul><ul><li>The veins are major blood vessels connected to your heart. </li></ul><ul><li>The pulmonary veins carry oxygen-rich blood from the lungs to the left side of the heart so the blood can be pumped out to the body. </li></ul><ul><li>The vena cava is a large vein that carries oxygen-poor blood from the body back to the heart. </li></ul>
  10. 12. MYOCARDIAL INFARCTION Myocardial Infarction – refers to the process by which the myocardial/ cardiac tissue is destroyed in the region of the heart that are deprived of an adequate blood supply (reduced coronary artery blood flow) Causes/Etiologies: - narrowing or complete occlusion of coronary artery - decreased coronary blood flow - increased demand for oxygen Myocardial Infarction maybe defined by the location of the injury to the heart muscle or by the point in time in the process of infarction
  11. 13. <ul><li>Risk factors for atherosclerosis are generally risk factors for myocardial infarction: </li></ul><ul><ul><li>older age </li></ul></ul><ul><ul><li>male gender[ citation needed ] </li></ul></ul><ul><ul><li>cigarette smoking </li></ul></ul><ul><ul><li>hypercholesterolemia (more accurately hyperlipoproteinemia , especially high low density lipoprotein and low high density lipoprotein ) </li></ul></ul><ul><ul><li>diabetes (with or without insulin resistance ) </li></ul></ul><ul><ul><li>high blood pressure </li></ul></ul><ul><ul><li>Obesity (defined by a body mass index of more than 30 kg/m2, or alternatively by waist circumference or waist-hip ratio ). </li></ul></ul><ul><li>Many of these risk factors are modifiable, so many heart attacks can be prevented by maintaining a healthier lifestyle. Physical activity, for example, is associated with a lower risk profile. Non-modifiable risk factors include age, gender, and family history of an early heart attack (before the age of 60), which is thought of as reflecting a genetic predisposition </li></ul><ul><li>Socioeconomic factors such as a shorter education and lower income (particularly in women), and living with a partner may also contribute to the risk of MI. To understand epidemiological study results, it's important to note that many factors associated with MI mediate their risk via other factors. For example, the effect of education is partially based on its effect on income and marital status </li></ul><ul><li>Women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking. </li></ul>
  12. 14. Clinical Manifestation <ul><li>Chest pain – may radiate to the jaw, neck, shoulders, and arm (usually left) </li></ul><ul><li>Pain may be accompanied by cool skin, pallor, clammy diaphoresis, tachycardia, and tachypnea </li></ul><ul><li>Patients with DM may not experience severe pain! (because of the neuropathy that accompanies DM can interfere with neuroreceptors, dulling the pain) </li></ul>
  13. 16. Assessment and Diagnostic Methods <ul><li>Patient History </li></ul><ul><li>ECG – within 10 minutes of pain onset or arrival at the ER </li></ul><ul><li>Serial Serum enzymes and isoenzymes (Creatinine Kinase and isoenzymes), myoglobin, and troponin </li></ul>
  14. 17. <ul><li>WHO criteria have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied: </li></ul><ul><ul><li>Clinical history of ischaemic type chest pain lasting for more than 20 minutes </li></ul></ul><ul><ul><li>Changes in serial ECG tracings </li></ul></ul><ul><ul><li>Rise and fall of serum cardiac enzymes (biomarkers) such as creatine kinase , troponin I, and lactate dehydrogenase isozymes specific for the heart. </li></ul></ul><ul><li>The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers. [25] According to the new guidelines, a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI. </li></ul>
  15. 18. Right Coronary Artery (RCA) I, aVL II, III, aVF, V 1 , V 4 R, V 5 R, V 6 R Right ventricular (Usually associated with Inferior) Posterior Descending (PDA) (branch of the RCA or Circumflex (LCX) ) V 1 ,V 2 ,V 3 , V 4 V 7 , V 8 , V 9 Posterior (Usually associated with Inferior or Lateral but can be isolated) Circumflex (LCX) or Obtuse Marginal II, III, aVF I, aVL, V 5 , V 6 Lateral Right Coronary Artery (RCA) or Circumflex (LCX) I, aVL II, III, aVF Inferior Left main coronary artery (LCA) II, III, aVF V 1 ,V 2 ,V 3 , V 4 , V 5 , V 6 , I, aVL Extensive anterior (Sometimes called Anteroseptal with Lateral extension) Left Anterior Descending (LAD) , Circumflex (LCX) , or Obtuse Marginal II, III, aVF V 3 , V 4 , V 5 , V 6 , I, aVL Anterolateral Left Anterior Descending (LAD) None V 1 , V 2 , V 3 , V 4 Anteroseptal Left Anterior Descending (LAD) None V 3 , V 4 Anterior Left Anterior Descending (LAD) None V 1 , V 2 Septal Suspected Culprit Artery Leads Showing Reciprocal ST Segment Depression Leads Showing ST Segment Elevation Wall Affected
  16. 22. Electrocardiogram <ul><li>The primary purpose of the electrocardiogram is to detect ischemia or acute coronary injury in broad, symptomatic emergency department populatons. </li></ul><ul><li>However, the standard 12 lead ECG has several limitations. An ECG represents a brief sample in time. Because unstable ischemic syndromes have rapidly changing supply versus demand characteristics, a single ECG may not accurately represent the entire picture. </li></ul><ul><li>It is therefore desirable to obtain serial 12 lead ECGs , particularly if the first ECG is obtained during a pain-free episode. Alternatively, many emergency departments and chest pain centers use computers capable of continuous ST segment monitoring. It should also be appreciated that the standard 12 lead ECG does not directly examine the right ventricle , and does a relatively poor job of examining the posterior basal and lateral walls of the left ventricle . </li></ul><ul><li>In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG . This can be offset or even eliminated by the use of non-standard ECG leads like the right-sided ECG lead V4R and posterior leads V7, V8, and V9. In spite of these limitations, the 12 lead ECG stands at the center of risk stratification for the patient with suspected acute myocardial infarction. Mistakes in interpretation are relatively common, and the failure to identify high risk features has a negative effect on the quality of patient care </li></ul>
  17. 23. <ul><li>The 12 lead ECG is used to classify patients into one of three groups: </li></ul><ul><li>those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with thrombolytics or primary PCI ), </li></ul><ul><li>those with ST segment depression or T wave inversion (suspicious for ischemia), and </li></ul><ul><li>those with a so-called non-diagnostic or normal ECG. </li></ul>
  18. 24. Right Coronary Artery (RCA) I, aVL II, III, aVF, V 1 , V 4 R, V 5 R, V 6 R Right ventricular (Usually associated with Inferior) Posterior Descending (PDA) (branch of the RCA or Circumflex (LCX) ) V 1 ,V 2 ,V 3 , V 4 V 7 , V 8 , V 9 Posterior (Usually associated with Inferior or Lateral but can be isolated) Circumflex (LCX) or Obtuse Marginal II, III, aVF I, aVL, V 5 , V 6 Lateral Right Coronary Artery (RCA) or Circumflex (LCX) I, aVL II, III, aVF Inferior Left main coronary artery (LCA) II, III, aVF V 1 ,V 2 ,V 3 , V 4 , V 5 , V 6 , I, aVL Extensive anterior (Sometimes called Anteroseptal with Lateral extension) Left Anterior Descending (LAD) , Circumflex (LCX) , or Obtuse Marginal II, III, aVF V 3 , V 4 , V 5 , V 6 , I, aVL Anterolateral Left Anterior Descending (LAD) None V 1 , V 2 , V 3 , V 4 Anteroseptal Left Anterior Descending (LAD) None V 3 , V 4 Anterior Left Anterior Descending (LAD) None V 1 , V 2 Septal Suspected Culprit Artery Leads Showing Reciprocal ST Segment Depression Leads Showing ST Segment Elevation Wall Affected
  19. 25. Management <ul><li>MEDICAL MANAGEMENT: </li></ul><ul><li>Goal – to minimize myocardial damage, preserve myocardial function, and prevent complications (lethal dysrythmias and cardiogenic shock) </li></ul><ul><ul><li>Oxygen administration </li></ul></ul><ul><ul><li>Emergency PTCA </li></ul></ul><ul><ul><li>Coronary artery bypass or minimally invasive direct coronary artery bypass (MIDCAB) </li></ul></ul><ul><li>PHARMACOLOGIC THERAPY: </li></ul><ul><ul><li>Nitrates (nitroglycerine) </li></ul></ul><ul><ul><li>Anticoagulants (heparin) </li></ul></ul><ul><ul><li>Analgesics (Morphine) </li></ul></ul><ul><ul><li>ACE inhibitors </li></ul></ul><ul><ul><li>Beta blockers </li></ul></ul><ul><ul><li>Thrombolytics </li></ul></ul>
  20. 26. <ul><li>Complications may occur immediately following the heart attack (in the acute phase), or may need time to develop (a chronic problem). After an infarction, an obvious complication is a second infarction, which may occur in the domain of another atherosclerotic coronary artery, or in the same zone if there are any live cells left in the infarct. </li></ul><ul><li>Congestive heart failure </li></ul><ul><ul><li>A myocardial infarction may compromise the function of the heart as a pump for the circulation , a state called heart failure . There are different types of heart failure; left- or right-sided (or bilateral) heart failure may occur depending on the affected part of the heart, and it is a low-output type of failure. If one of the heart valves is affected, this may cause dysfunction, such as mitral regurgitation in the case of left-sided MI. </li></ul></ul><ul><li>Myocardial rupture </li></ul><ul><ul><li>Myocardial rupture is most common three to five days after myocardial infarction, commonly of small degree, but may occur one day to three weeks later, in as many as 10% of all MIs.[ citation needed ] This may occur in the free walls of the ventricles, the septum between them, the papillary muscles , or less commonly the atria . Rupture occurs because of increased pressure against the weakened walls of the heart chambers due to heart muscle that cannot pump blood out effectively. The weakness may also lead to ventricular aneurysm , a localized dilation or ballooning of the heart chamber. </li></ul></ul><ul><ul><li>Risk factors for myocardial rupture include completion of infarction (no revascularization performed), female sex, advanced age, and a lack of a previous history of myocardial infarction.[ citation needed ] The shear stress between the infarcted segment and the surrounding normal myocardium (which may be hypercontractile in the post-infarction period) makes it a nidus for rupture.[ citation needed ] </li></ul></ul><ul><ul><li>Rupture is usually a catastrophic event that may result a life-threatening process known as cardiac tamponade , in which blood accumulates within the pericardium or heart sac, and compresses the heart to the point where it cannot pump effectively. Rupture of the intraventricular septum (the muscle separating the left and right ventricles) causes a ventricular septal defect with shunting of blood through the defect from the left side of the heart to the right side of the heart. Rupture of the papillary muscle may also lead to acute mitral regurgitation and subsequent pulmonary edema and possibly even cardiogenic shock . </li></ul></ul>
  21. 27. <ul><li>Life-threatening arrhythmia </li></ul><ul><ul><li>A 12 lead electrocardiogram showing ventricular tachycardia. </li></ul></ul><ul><ul><li>Since the electrical characteristics of the infarcted tissue change (see pathophysiology section ), arrhythmias are a frequent complication. The re-entry phenomenon may cause too fast heart rates ( ventricular tachycardia and even ventricular fibrillation ), and ischemia in the electrical conduction system of the heart may cause a complete heart block (when the impulse from the sinoatrial node , the normal cardiac pacemaker, doesn't reach the heart chambers any more). </li></ul></ul><ul><li>Pericarditis </li></ul><ul><ul><li>As a reaction to the damage of the heart muscle, inflammatory cells are attracted. The inflammation may reach out and affect the heart sac. This is called pericarditis . In Dressler's syndrome , this occurs several weeks after the initial event. </li></ul></ul><ul><li>Cardiogenic shock </li></ul><ul><ul><li>A complication that may occur in the acute setting soon after a myocardial infarction or in the weeks following it is cardiogenic shock . Cardiogenic shock is defined as a hemodynamic state in which the heart cannot produce enough of a cardiac output to supply an adequate amout of oxygenated blood to the tissues of the body. </li></ul></ul><ul><li>While the data on performing interventions on individuals with cardiogenic shock is sparse, trial data suggests a long-term mortality benefit in undergoing revascularization if the individual is less than 75 years old and if the onset of the acute myocardial infarction is less than 36 hours and the onset of cardiogenic shock is less than 18 hours. [86] If the patient with cardiogenic shock is not going to be revascularized, aggressive hemodynamic support is warranted, with insertion of an intra-aortic balloon pump if not contraindicated. [86] </li></ul>
  22. 28. Valvular heart disease <ul><li>Valvular heart disease is any disease process involving one or more valves of the heart . </li></ul><ul><li>The valves in the right side of the heart are the tricuspid valve and the pulmonic valve . </li></ul><ul><li>The valves in the left side of the heart are the mitral valve and the aortic valve . </li></ul>
  23. 29. <ul><li>Each valve may be too narrow ( stenosis ) or too wide or loose, causing regurgitation . There are different types of valvular heart disease: </li></ul><ul><ul><ul><li>Aortic insufficiency </li></ul></ul></ul><ul><ul><ul><li>Aortic valve stenosis </li></ul></ul></ul><ul><ul><ul><li>Endocarditis </li></ul></ul></ul><ul><ul><ul><li>Heart valve dysplasia </li></ul></ul></ul><ul><ul><ul><li>Libman-Sacks endocarditis </li></ul></ul></ul><ul><ul><ul><li>Loeffler endocarditis </li></ul></ul></ul><ul><ul><ul><li>Mitral regurgitation </li></ul></ul></ul><ul><ul><ul><li>Mitral stenosis </li></ul></ul></ul><ul><ul><ul><li>Mitral valve prolapse </li></ul></ul></ul><ul><ul><ul><li>Pulmonary valve stenosis </li></ul></ul></ul><ul><ul><ul><li>Tricuspid insufficiency </li></ul></ul></ul><ul><ul><ul><li>Tricuspid valve stenosis </li></ul></ul></ul>
  24. 30. The Heart with TETRALOGY OF FALLOT <ul><li>In Tetralogy of Fallot , there are four specific defects in the heart: </li></ul><ul><li>Pulmonary valve stenosis is a narrowing of the pulmonary valve and the area below the valve. This narrowing slows the flow of blood from the right side of the heart to the lungs. The heart must pump harder to push blood through the smaller opening to the lungs where the blood picks up oxygen. </li></ul><ul><li>Ventricular septal defect (VSD) is a hole in the wall that separates the lower chambers (ventricles) of the heart. </li></ul><ul><li>Overriding aorta is a defect in the position of the large artery (aorta) that takes oxygen-rich blood to the body. In a normal heart, the aorta attaches to the left lower chamber of the heart (ventricle). In tetralogy of Fallot, the aorta sits between the left and right ventricles, over the VSD. This causes mixing of oxygen-rich blood and oxygen-poor blood. </li></ul><ul><li>Right ventricular hypertrophy is the thickening of the right lower chamber of the heart (ventricle). Unlike other muscles in your body, when the heart thickens, it does not work well. The heart has to pump harder to move blood through the narrowed pulmonary valve and the area below it. </li></ul>
  25. 31. The Heart with TETRALOGY OF FALLOT <ul><li>Pulmonary Valve stenosis; 2. VSD; 3. Overriding of the Aorta; 4.RVH </li></ul>
  26. 32. <ul><li>These defects can cause: </li></ul><ul><ul><li>Less blood flow to the lungs. </li></ul></ul><ul><ul><li>Mixing of oxygen-rich (red) and oxygen-poor (blue) blood inside the heart. </li></ul></ul><ul><ul><li>Low levels of oxygen in the blood. </li></ul></ul><ul><ul><li>When oxygen levels are low, the baby's skin, fingertips, or lips have a bluish tint. This condition is called cyanosis (SY-uh-NO-sis). An infant with cyanosis is sometimes called a &quot;blue baby.&quot; </li></ul></ul><ul><ul><li>Each year in the United States, about 3,000 babies are born with tetralogy of Fallot. It is the congenital heart defect that causes the most cases of cyanosis. </li></ul></ul><ul><ul><li>Every infant or child with tetralogy of Fallot needs surgery, usually within the first year of life. Because of advances in surgery and treatment, many children born with tetralogy of Fallot have successful surgery and live to adulthood. </li></ul></ul>
  27. 33. CARDIAC CONDUCTION SYSTEM
  28. 34. <ul><li>In the normal human heart each heart beat originates in the Sinoatrial node (SA node) , which is the heart's normal pacemaker. </li></ul><ul><li>The SA node is located in the upper- posterior wall of the right atrium and initiates a depolarization wave at regular intervals to bring about contraction of the heart. </li></ul><ul><li>Normally, the SA node generates an electrical impulse which travels through the right and left atrial muscles producing electrical changes which is represented on the electrocardiogram (ECG) by the P-wave . </li></ul><ul><li>The electrical impulse then travels through the atrioventricular node (AV Node), which conducts electricity at a slower speed. </li></ul><ul><li>This will create a pause ( PR interval ) before the ventricles are stimulated. This pause is helpful since it allows blood to be emptied into the ventricles from the atria prior to ventricular contraction to push blood out into the body. </li></ul><ul><li>The QRS complex (in the ECG) represents ventricular contraction. </li></ul><ul><li>This is followed by the T-wave which corresponds to the electrical changes in the ventricles as they relax and the whole process is repeated. </li></ul>
  29. 35. <ul><li>The discharge rate of the SA node determines the heart rate, which is the number of times the heart beats per minute. </li></ul><ul><li>At rest, the heart beats about 70 times a minute. However, the sinus rhythm maintains a rate of 60-100 beats per minute, which is the normal range of the pacing rate. </li></ul><ul><li>A rhythm originating in the heart's SA node with a rate slower than 50 beats per minute is called Sinus Bradycardia . </li></ul><ul><li>Sinus tachycardia occurs when the sinus rhythm is faster than 100 beats per minute and results from increased automaticity of the SA node. </li></ul><ul><li>The heart rate is slowed during sleep and accelerated by emotion, exercise, fever and other stimuli. </li></ul>
  30. 36. Approximate normal conduction velocity at each part of the pathway is summarized below: 0.5 m/s Ventricular Tissue 1-4 m/s Purkinje Fibers 2 m/s Bundle Branches 2 m/s His Bundle 0.05 m/s AV Node 1 m/s Atrial Tissue Conduction velocity Location
  31. 39. ANEURYSM, AORTIC <ul><li>Aneurysm is a localized sac or dilatation of an artery formed at a weak point in the vessel wall </li></ul><ul><li>Most common cause: </li></ul><ul><ul><li>Atherosclerosis </li></ul></ul><ul><ul><li>Other causes: arterial wall trauma, infection (pyogenic, or syphilitic), and congenital defects of the arterial wall </li></ul></ul><ul><li>Most common forms: </li></ul><ul><ul><li>Saccular anerysm – one side of the vessel only </li></ul></ul><ul><ul><li>Fusiform aneurysm– involve dilatation of the entire arterial segment </li></ul></ul><ul><ul><li>Mycotic aneurysm – small anerysm due to local infections </li></ul></ul><ul><ul><li>Aortic aneurysm </li></ul></ul><ul><ul><li>Thorasic </li></ul></ul><ul><ul><li>Abdominal </li></ul></ul><ul><ul><li>Dissecting </li></ul></ul><ul><li>Men are affected more than women </li></ul><ul><li>Rupture can lead to hemorrhage and death </li></ul>
  32. 40. <ul><li>THORASIC AORCTIC ANEURYSM </li></ul><ul><li>Occur most frequent in men between ages 40 and 70 years </li></ul><ul><li>Thoracic area is the most common site for dissecting aneurysm </li></ul><ul><li>About one-third of patients die from rupture </li></ul><ul><li>ABDOMINAL ANEURYSM </li></ul><ul><li>Most common among whites between ages 60 and 90 years </li></ul><ul><li>Most common below the renal arteries </li></ul><ul><li>40% have symptoms </li></ul><ul><li>Risk factors: genetic predisposition, smoking, hypertension </li></ul><ul><li>DISSECTING ANEURYSM </li></ul><ul><li>Caused by rupture in the intimal layer, by blood dissecting the vessel layers </li></ul><ul><li>Associated with poorly controlled hypertension </li></ul><ul><li>3x more common in men between ages 50 and 70 years </li></ul>
  33. 41. Clinical Manifestations <ul><li>Variable symptoms </li></ul><ul><li>Depend on how rapid the aneurysm dilates </li></ul><ul><li>Affects the sorrounding intrathoracic structures </li></ul><ul><li>Thoracic aortic aneurysm: boring pain; dyspnea, cough, or stridor; hoarseness, weak voice, aphonia; dysphagia; dilated superficial veins on chest, neck, or arms; edematous areas on chest wall; cyanosis; unequal pupils </li></ul><ul><li>Abdominal aortic aneurysm: “heart beating”; “blue-toe syndrome” (occlusion of digital vessels); severe back or abdominal pain (sign of impending rupture) </li></ul><ul><li>Dissecting aneurysm: sudden onset of severe, persistent “tearing” or “ripping” pain over the interior chect or back, extending to the shoulders, epigastric area, or abdomen; pallor, sweating, and tachycardia; elevated BP or markedly different from one arm to the other; and death usually caused by external rupture of the hematoma </li></ul>
  34. 42. Assessment and Diagnostic Methods <ul><li>Chest radiograph </li></ul><ul><li>Angiogram </li></ul><ul><li>Transesophageal echocardiography </li></ul><ul><li>MRI </li></ul><ul><li>Ultasonography or CT scan – determine size, length, location of aneurysm </li></ul><ul><li>Systolic bruit – heard on auscultation over the pulsating mass of the abdominal aortic aneurysm at the middle and upper abdomen </li></ul>
  35. 43. Management – Medical / Surgical <ul><li>Medical or Surgical treatment depends on the type of aneurysm </li></ul><ul><li>Poor prognosis for ruptured aneurysm and surgery is performed immediately </li></ul><ul><li>Medical Measures: </li></ul><ul><ul><li>Strict control of BP and reduction in pulsatile flow </li></ul></ul><ul><ul><li>Systolic pressure maintained at 100 to 120 mmHg (i.e. Nitroprusside ) </li></ul></ul><ul><ul><li>Pulsatile flow reduction with reduce cardiac contractility (i.e. Propranolol ) </li></ul></ul><ul><li>Surgical Management: </li></ul><ul><ul><li>Goal: Removal of the aneurysm and restoration of vascular continuity with graft (resection and bypass graft or endovascular grafting – the treatment of choice for abdominal aortic aneurysm larger than 5cm (2 inches) in diameter or enlarging </li></ul></ul><ul><li>Intensive monitoring in the Critical Care Unit is required </li></ul>
  36. 44. ANEURYSM, INTRACRANIAL <ul><li>Intracranial (cerebral) aneurysm – dilatation of the walls of the cerebral artery as a result of weakness in the arterial wall </li></ul><ul><li>Causes: </li></ul><ul><ul><li>Unknown </li></ul></ul><ul><ul><li>Maybe due to atherosclerosis, congenital defects of the arterial walls, hypertensive vascular disease, head trauma, or advancing age </li></ul></ul><ul><li>Commonly affects the internal carotid, anterior or posterior cerebral, anterior or posterior communicating, and middle cerebral arteries </li></ul><ul><li>Symptoms are produced when the aneurysm enlarges and presses on the nearby cranial nerves or brain tissue, or ruptures, causing Subarachnoid hemorrhage. </li></ul><ul><li>Prognosis depends on the age and neurologic condition of patient, associated diseases, and extent and location of the aneurysm </li></ul>
  37. 45. Clinical Manifestations <ul><li>With rupture: </li></ul><ul><ul><li>Sudden unusually severe headache </li></ul></ul><ul><ul><li>Loss of consciousness </li></ul></ul><ul><ul><li>Pain and rigidity of the back of the neck and spine </li></ul></ul><ul><ul><li>Visual disturbances (visual loss, diplopia, ptosis) </li></ul></ul><ul><ul><li>Tinnitus, dizziness, and hemiparesis </li></ul></ul><ul><li>If the aneurysm leaks and forms clot: </li></ul><ul><ul><li>Show little neurologic deficit, or severe bleeding , resulting in cerebral damage followed rapidly by coma and death. </li></ul></ul>
  38. 46. Assessment and Diagnostic Methods <ul><li>CT scan </li></ul><ul><li>Cerebral angiography </li></ul><ul><li>Lumbar puncture </li></ul><ul><li>Hunt – Hess Classification of Clinical Grades – guide for diagnosing the severity of Subarachnoid hemorrhage after an aneurysm bleeds </li></ul>
  39. 47. Medical Management <ul><li>Allow the brain to recover from the initial bleeding </li></ul><ul><li>Prevent or minimize the risk of rebleeding </li></ul><ul><li>Prevent or treat other complications : rebleeding, cerebral vasospasm, acute hydrocephalus, and seizures </li></ul><ul><li>Provide bed rest with sedation to prevent agitation and stress </li></ul><ul><li>Maintain cerebral blood flow and oxygenation ; maintain hemoglobin and hematocrit levels and adequate hydration. Avoid blood presure extremes (Hypertension or Hypotension) </li></ul><ul><li>Manage vasospasm with calcium-channel blockers (i.e. Nimodipine, Verapamil, and Nifedipine ). Endovascular technique may also be used </li></ul><ul><li>Arterial bypass or medical treatment to prevent rebleeding </li></ul><ul><li>Manage increased intracranial pressure (ICP) by draining cerebrospinal fluid (CSF) via LP or ventricular catheter drainage </li></ul><ul><li>Administer Mannitol to reduce ICP, and monitor for signs of dehydration and rebound elevation of ICP </li></ul><ul><li>Administer fibrinolytic agents to delay or prevent dissolution of the clot if surgery is delayed or contraindicated </li></ul>
  40. 50. <ul><li>Stroke is the third leading cause of death in America and the No. 1 cause of adult disability. </li></ul><ul><li>80% of strokes are preventable </li></ul><ul><li>YOU CAN PREVENT STROKE ! </li></ul>Cerebro-Vascular Accident
  41. 51. What is Stroke ? <ul><li>A stroke or &quot;brain attack&quot; occurs when a blood clot blocks an artery (a blood vessel that carries blood from the heart to the body) or a blood vessel (a tube through which the blood moves through the body) breaks, interrupting blood flow to an area of the brain.  </li></ul><ul><li>When either of these things happen, brain cells begin to die and brain damage occurs. </li></ul>
  42. 52. <ul><li>When brain cells die during a stroke, abilities controlled by that area of the brain are lost. </li></ul><ul><li>These abilities include speech, movement and memory. </li></ul><ul><li>How a stroke patient is affected depends on where the stroke occurs in the brain and how much the brain is damaged. </li></ul><ul><li>For example, someone who has a small stroke may experience only minor problems such as weakness of an arm or leg. </li></ul><ul><li>People who have larger strokes may be paralyzed on one side or lose their ability to speak. </li></ul><ul><li>Some people recover completely from strokes, but more than 2/3 of survivors will have some type of disability. </li></ul>
  43. 53. <ul><li>Stroke as the primary neurologic problem in the US and in the world </li></ul><ul><ul><li>15% Hemorrhagic </li></ul></ul><ul><ul><li>85% Ischemic/Nonhemorrhagic </li></ul></ul><ul><li>Stroke categories according to cause: </li></ul><ul><ul><li>Thrombosis 20% </li></ul></ul><ul><ul><li>Small penetrating thrombosis 25% </li></ul></ul><ul><ul><li>Cardiogenic embolic stroke, cryptogenic (unknown cause) 25% </li></ul></ul><ul><ul><li>Others ( cocaine use, coagulopathies, migraine, spontaneous dissection of the carotid or vetebral arteries 5% </li></ul></ul><ul><li>Stroke classified according to the time course: </li></ul><ul><ul><li>Transient ischemic attack (TIA) </li></ul></ul><ul><ul><li>Reversible ischemic neurologic deficit (RIND) </li></ul></ul><ul><ul><li>Stroke in evolution </li></ul></ul><ul><ul><li>Completed stroke </li></ul></ul>
  44. 54. Risk Factors <ul><li>Hemorrhragic strokes: arteriovenous malformations (AVM’s), aneurysm ruptures, certain drugs, uncontrolled hypertension, hemangioblastomas, and trauma </li></ul><ul><li>Ischemic strokes: cardiovascular disease (cerebral embolism may originate in the heart) and dysrhythmia (atrial fibrillation); risk factors for CAD; vasospasm, migraines, and coagulopathies (high hematocrit) </li></ul><ul><li>General cerebral ischemia maybe caused by excessive or prolonged drop in BP </li></ul><ul><li>Drug abuse (cocaine), particularly in adolescents and young adults </li></ul><ul><li>Alcohol consumption may also be a risk factor </li></ul>
  45. 55. Clinical Manifestations <ul><li>General signs and symptoms: </li></ul><ul><ul><li>Numbness or weakness of the face, arm, or leg </li></ul></ul><ul><ul><li>Confusion or change in mental status </li></ul></ul><ul><ul><li>Trouble speaking or understanding speech </li></ul></ul><ul><ul><li>Visual disturbances </li></ul></ul><ul><ul><li>Loss of balance </li></ul></ul><ul><ul><li>Dizziness </li></ul></ul><ul><ul><li>Difficulty in walking </li></ul></ul><ul><ul><li>Sudden severe headache </li></ul></ul>
  46. 56. <ul><li>MOTOR LOSS </li></ul><ul><ul><li>Hemiplegia, hemiparesis </li></ul></ul><ul><ul><li>Flaccid paralysis and loss of or decrease in deep tendon reflexes (initial) and increased muscle tone (spasticity after 48 hrs) </li></ul></ul><ul><li>COMMUNICATION LOSS </li></ul><ul><ul><li>Dysarthria (difficulty in speaking) </li></ul></ul><ul><ul><li>Dysphasia or aphasia (defective or loss of speech) </li></ul></ul><ul><ul><li>Apraxia (inability to perform a prviously learned action) </li></ul></ul><ul><li>PERCEPTUAL DISTURBANCES AND SENSORY LOSS </li></ul><ul><ul><li>Visual perceptual dysfunctions (homonymous hemianopia – loss half of the visual field) </li></ul></ul><ul><ul><li>Disturbances in visuospatial relationship – left hemispheric damage </li></ul></ul><ul><ul><li>Sensory losses: impair touch or severe loss of propioception, difficulty in interrupting visual, tactile, and auditory stimuli </li></ul></ul><ul><li>IMPAIRED CIGNITIVE AND PSYCHOLOGICAL EFFECTS </li></ul><ul><ul><li>Impaired learning capacity, memory, or other higher cortical intellectual functions common in frontal lobe damage – limited attention span, difficulties in comprehension, forgetfullness, and lack of motivation </li></ul></ul><ul><ul><li>Depression, other psychological problems: emotional lability, hostility, frustration, resentment, and lack of cooperation </li></ul></ul><ul><li>BLADDER DYSFUNCTION </li></ul><ul><ul><li>Transient urinary incontinence </li></ul></ul><ul><ul><li>Persistent urinary incontinence or urinary retention </li></ul></ul><ul><ul><li>Continuing bladder and bowel incontinence </li></ul></ul>
  47. 57. Assessment and Diagnostic Methods <ul><li>Complete Physical and Neurologic Examination </li></ul><ul><li>Non-contrast CT or MRI scan </li></ul><ul><li>Transthoracic or transesophageal echocardiogram </li></ul><ul><li>Carotid ultrasonography </li></ul><ul><li>Cerebral angiography </li></ul><ul><li>Transcranial Doppler flow studies </li></ul><ul><li>Electrocardiography </li></ul><ul><li>Prevention </li></ul><ul><li>Help patient alter risk factors for stroke </li></ul><ul><li>Prepare and support patient through carotid endarterectomy </li></ul><ul><li>Administer anticoagulant agents as ordered </li></ul>
  48. 58. Medical Management <ul><li>Recombinant tissue plasminogen activator (t-pA), unless contraindicated; monitor for bleeding </li></ul><ul><li>Management of increased ICP: osmotic diuretics, maintain PaCO 2 at 30 – 35 mmHg, avoid hypoxia, elevate head of bed, pulmonary toilet with supllemental oxygen, airway patency </li></ul><ul><li>Intubation with an ET to establish patent airway, if necessary </li></ul><ul><li>Maintain cardiac output at 4 – 8 L/min </li></ul><ul><li>Anticoagulation therapy </li></ul><ul><li>Carotid endarterectomy (for managing TIA, and small stroke) </li></ul><ul><li>Management of Complications </li></ul><ul><li>Cerebral hypoxia: administer supplemental oxygen, maintain hemoglobin and hematocrit at acceptable levels </li></ul><ul><li>Decreased cerebral blood flow and extension of the area of injury: adequate hydration, avoid hypertension or hypotension </li></ul>
  49. 59. MYASTHENIA GRAVIS <ul><li>An autoimmune disorder affecting the myoneural junction </li></ul><ul><li>Antibodies or autobodies are directed at the neurotransmitter (acetylcholine) receptor on the motor end plate – disrupt the transmission of transmission of voluntary muscles of the body </li></ul><ul><li>Excessive weakness and fatigability occurs </li></ul><ul><li>Affects women between ages 20 and 40 years </li></ul><ul><li>Affects men older than 40 years </li></ul>
  50. 60. Clinical Manifestations <ul><li>Purely a motor disorder, with no effect on sensation or coordination, extreme muscular weakness and easy fatigability, which worsen after effort and are relieved by rest </li></ul><ul><li>Symptoms vary according to the muscles affected: </li></ul><ul><li>early symptoms: diplopia and ptosis </li></ul><ul><li>Sleepy masklike expression because facial muscles are affected </li></ul><ul><li>Dysphonia (voice inpairment), with nasal sound or difficulty in articulation </li></ul><ul><li>Problems with chewing and swallowing, which can present danger of choking and aspiration </li></ul><ul><li>Weakness of arm and hand muscles, less commonly leg muscles </li></ul><ul><li>Progressive weakness of diaphragm and intercoastal muscles, which may produce respiratory distress (acute emergency) </li></ul>
  51. 61. Assessment and Diagnostic Evaluation <ul><li>Presumptive diagnosis based on history and PE – patient presents with ocular, bulbar symptoms or fluctuating weakness will need a diagnostic workup for MG </li></ul><ul><li>Injection of Endrophonium (Tensilon) – confirms the diagnosis (improve muscle strength represent a positive test) </li></ul><ul><li>MRI – enlarged thymus gland </li></ul><ul><li>Serum analysis for acetylcholine receptor and EMG to measure electrical potential of muscle cells </li></ul>
  52. 62. Complications <ul><li>Myasthenia Crisis </li></ul><ul><ul><li>Result of under medication or no cholinergic medication </li></ul></ul><ul><ul><li>Result from progression of the disease, emotional upset, systemic infections, medications, surgery, or trauma </li></ul></ul><ul><ul><li>Manifested as sudden onset of acute respiratory distress and inability to swallow or speak </li></ul></ul><ul><li>Cholinergic Crisis </li></ul><ul><ul><li>Caused by overmedication with cholinergic or anti-cholinesterase drugs </li></ul></ul><ul><ul><li>Produce muscle weakness and the respiratory depression of myasthenia crisis and gastrointestinal symptoms (nausea, vomiting, diarrhea), sweating, increased salivation, and bradycardia </li></ul></ul>
  53. 63. Management <ul><li>Directed at improving function through the administration of anticholinesterase medications and by reducing and removing circulating antibodies </li></ul><ul><li>Anticholinesterase medication – increases muscle response to nerve impulses and improves strength (effects within an hour after administration) </li></ul><ul><ul><li>Pyridostigmine bromide (Mestinon) </li></ul></ul><ul><ul><li>Neostigmine bromide (Prostigmin) </li></ul></ul><ul><li>Immunosuppressive Therapy – reduce the production of antireceptor antibody or removal directly by plasma exchange </li></ul><ul><ul><li>Corticosteroids </li></ul></ul><ul><ul><li>Plasma exchange (Plasmapheresis) </li></ul></ul><ul><ul><li>Thymectomy </li></ul></ul><ul><li>Managed on an out-patient basis unless hospitalization is required for managing symptoms or complications </li></ul>
  54. 64. MULTIPLE SCLEROSIS <ul><li>A chronic, degenerative, progressive disease of the CNS </li></ul><ul><li>Characterized by small patches of demyelination in the brain and SC </li></ul><ul><li>Demyelination – destruction of the myelin sheath results in impaired transmission of nerve impulses </li></ul><ul><li>Unknown cause, but defective immune response probably plays a major role </li></ul><ul><li>Sensitized T-cells inhabit the CNS and facilitate the infiltration of other agents that damage the immune system </li></ul><ul><ul><li>Cause the inflammation that destroys myelin and oligodendroglial cells that produce the myelin in CNS </li></ul></ul><ul><ul><li>Plaques of sclerotic tissue </li></ul></ul><ul><ul><li>Demyelination interrupts the flow of nerve impulses </li></ul></ul><ul><li>More common in Northern temperate zones, one of the most disabling neurologic diseases of young adults (20 to 40 years old) </li></ul><ul><li>Affects more women than men </li></ul>
  55. 65. <ul><li>DISEASE COURSE </li></ul><ul><li>Relapsing-remitting course – with complete recovery between relapses </li></ul><ul><li>Chronic progressive course – with progressive decline in function and potential development of quadriparesis, cognitive dysfunction, visual loss, and brain-stem syndrome </li></ul><ul><li>Benign course with normal life span – very mild symptoms, do not seek treatment </li></ul>
  56. 66. Clinical Manifestations <ul><li>Signs and symptoms reflect the location of lesion/s (plaque) </li></ul><ul><li>Primary symptoms: fatigue, weakness, numbness, difficulty in coordination, and loss of balance </li></ul><ul><li>Visual disturbances: blurring of vision, patchy blindness (scotoma), or total blindness </li></ul><ul><li>Spastic weakness of the extremities and loss of abdominal reflexes, ataxia, and tremors </li></ul><ul><li>Sensory dysfunction </li></ul><ul><li>Cognitive and psychosocial problems; emotional lability and euphoria </li></ul><ul><li>Bladder, bowel, and sexual problems possible </li></ul>
  57. 67. Assessment and Diagnostic Methods <ul><li>Magnetic Resonance Imaging (MRI) – primary diagnostic tool to visualize small plaques, evaluate course and effect of treatment </li></ul><ul><li>Electrophoresis study of the spinal fluid; abnormal IgG appears in the CSF in 95% of patients </li></ul><ul><li>Neuropsychological testing – assess cognitive impairment </li></ul><ul><li>Sexual history – identify changes in sexual function </li></ul>
  58. 68. Medical Management <ul><li>NO CURE !!! </li></ul><ul><li>Goal of treatment: to delay the progression of the disease, manage chronic symptoms, and treat acute exacerbations </li></ul><ul><li>Management strategies target the various motor and sensory symptoms and effects of immobility that can occur </li></ul><ul><li>Radiation therapy – to induce immunosuppression </li></ul>
  59. 69. Pharmacologic Therapy <ul><li>“ ABC” drugs: Interferon-beta-1a (Avonex) and beta-1b (Betaseron) and Glatiramer acetate (Copaxone) – for relapsing-remitting MS </li></ul><ul><li>Mitoxantrone (Novantrone) – anti-neoplastic recently approved for secondary progressive MS </li></ul><ul><li>Immunotherapeutic medications ( Azathioprine, Interferon, Cyclophosphamide ) – to modulate the immune response and reduce progression and frequency and severity of exacerbations </li></ul><ul><li>Corticosteroids and ACTH – anti-inflammatory agents and to improve nerve conduction </li></ul><ul><li>Amantadine (Symmetrel), pemoline (Cylert), or fluoxetine (Prozac) – to treat fatigue </li></ul><ul><li>Beta-adrenergic blockers ( Inderal ), anti-seizure agents ( Neurontin ), and benzodiazepines ( Klonopin ) – to treat ataxia </li></ul><ul><li>Beclofen – for spasticity </li></ul><ul><li>Anti-cholinergic, alpha-adrenergic blockers, or anti-spasmodic agents – to treat bowel dysfunctions </li></ul><ul><li>Ascorbic acid – to acidify the urine </li></ul><ul><li>Antibiotics when appropriate </li></ul><ul><li>Non-Pharmacologic: self-catheterization, assessment of UTI </li></ul>
  60. 70. GUILLAIN-BARRE SYNDROME <ul><li>Also known as POLYRADICULONEURITIS </li></ul><ul><li>Acute, rapid, segmental demyelination of nerves, causing an ascending weakness </li></ul><ul><li>Usually preceded by an infection (GI or respiratory) 2 – 3 weeks before the onset of symptoms </li></ul><ul><li>May occur after vaccination, pregnancy, or surgery </li></ul><ul><li>PATHOPHYSIOLOGY: </li></ul><ul><li>Results from an autoimmune reaction that attacks the myelin sheath of the peripheral, spinal, and cranial nerves </li></ul><ul><li>Schwann cell is spared in GBS – allowing remyelination in the recovery phase of the disease </li></ul>
  61. 71. Clinical Manifestations <ul><li>Classic clinical features: areflexia and ascending weakness </li></ul><ul><li>Does NOT affect the cognitive functions or level of consciousness </li></ul><ul><li>Initial neurologic symptoms: muscle weakness of the legs, progress to upper extremities, trunk and facial muscles; hyporeflexia and weakness may be followed by complete paralysis, including paralysis of the diaphragm and intercostal muscles, resulting in respiratory failure </li></ul><ul><li>Cranial nerves are frequently affected, leading to paralysis of the ocular, facial, and oropharyngeal muscle, causing difficulty in talking, chewing, and swallowing </li></ul><ul><li>Autonomic dysfunction frequently occurs in the form of overactivity or underactivity of the sympathetic or parasympathetic NS – manifested as disturbance in heart rate, rhythm (tachy- or bradycardia), blood pressure changes (hypertension or orthostatic hypotension), and other vasomotor disturbances </li></ul><ul><li>Severe, persistent pain in the back and calves </li></ul><ul><li>Loss of positional sense and diminished or absent tendon reflexes </li></ul><ul><li>Sensory changes manifested as paresthesias (tingling and numbness) </li></ul><ul><li>Most patients make a FULL RECOVERY after several months to a year; about 10% have residual disability </li></ul>
  62. 72. Assessment and Diagnostic Findings <ul><li>Clinical presentation – upward progression of weakness, history of recent viral infection, and results of laboratory and diagnostic studies – *key for diagnosis </li></ul><ul><li>Spinal fluid (CSF) – increased protein concentration with normal cell count </li></ul><ul><li>Electrophysiologic studies – marked slowing of nerve conduction velocity </li></ul><ul><li>Pulmonary function tests: check impending respiratory failure – vital capacity and negative inspiratory force changes </li></ul>
  63. 73. Medical Management <ul><li>Medical emergency !!! Manage in ICU </li></ul><ul><li>Mechanical ventilation in 25% of patients </li></ul><ul><li>Plasmapheresis (Plasma exchange) or IV immunoglobulins – to limit deterioration and demyelination </li></ul><ul><li>Continuous ECG monitoring – cardiac dysrhythmias and labile autonomic complications </li></ul><ul><li>Alpha-adrenegic blockers to treat hypertension </li></ul><ul><li>Increased IVF for hypotension </li></ul><ul><li>Atropine – for bradycardia </li></ul><ul><li>Anti-coagulants and thigh-high elastic compression stockings or sequential compression boots – to prevent thrombosis and pulmonary emboli secondary to immobility </li></ul>
  64. 74. ALZHEIMER’S DISEASES <ul><li>HISTORY OF ALZHEIMER’S </li></ul><ul><li>Alzheimer’s was first categorized by Emil Kraepelin , a German psychiatrist, who realized the symptoms and Alois Alzheimer who observed the characteristics of this disorder. </li></ul><ul><li>Alzheimer was also a German psychiatrist and neuropathologist and &quot;co-discovered&quot; Alzheimer’s disease with Kraepelin in 1906. </li></ul><ul><li>Alzheimer worked in Kraepelin’s laboratory and was awarded the name of the disorder by Kraepelin who attached importance to finding the neuropathological basis for psychiatric disorders. </li></ul><ul><li>For most of history, Alzheimer’s was diagnosed in individuals aged 45-65 as they developed symptoms of dementia ( presenile dementia , to be exact). The term &quot;Alzheimer’s&quot; began to be used in patients demonstrating symptoms of this form of dementia in later age groups as well as they began to develop the symptoms of their younger counterparts. </li></ul>
  65. 75. <ul><li>Alzheimer’s disease is a form of a mental disorder known as &quot;dementia&quot;. </li></ul><ul><li>Dementia is a brain disorder that seriously hampers the brain’s ability to process rational or normal thought and inhibits the daily activities of its sufferers because of this. </li></ul><ul><li>Alzheimer’s disease, therefore, affects the part of the brain that is responsible for thought, memory, and language. </li></ul>
  66. 76. Clinical Manifestations <ul><li>Forgetfulness and subtle memory loss – with progression of disease patient gets lost in a familiar environment or repeats the same story </li></ul><ul><li>Social and behavior pattern remain intact </li></ul><ul><li>Abstract thinking disappears </li></ul><ul><li>Inappropriate impulsive behavior </li></ul><ul><li>Personality changes: depressed, suspicious, paranoid, hostile, and combative </li></ul><ul><li>Speaking skills deteriorate to nonsense syllables; agitation and increased physical activity </li></ul><ul><li>Voracious appetite due to high activity level to dysphagia with progression of disease </li></ul><ul><li>Eventually patients requires help with ALL aspects of daily living </li></ul><ul><li>Terminal stage may last for months </li></ul>
  67. 77. <ul><li>There are several observable brain pattern changes that occur with Alzheimer’s disease . </li></ul><ul><li>An anomalous protein called &quot;amyloid beta&quot; deposits itself outside of nerve cells in the form of &quot;amyloids&quot; or various types of protein fragments. </li></ul><ul><li>Also known as &quot;diffuse plaques&quot;, these protein fragments form the core of more organized pieces that are known as &quot;senile plaques&quot; and effectively gather other proteins along the way to form a fairly large portion of proteins that accumulate in the blood vessels in the brain. </li></ul><ul><li>This accumulation of proteins in the blood vessels builds up and forms in the structure of filaments that diffuse atrophy and contribute to loss of neurons. </li></ul><ul><li>Atrophy is simply known as the wasting away of a part of the body, so the brain is effectively wasting away from the mass of proteins in the cerebral cortex portion and affects various regions of the brain, gradually eating away at valuable memory portions and other areas. </li></ul>
  68. 78. <ul><li>Both Alzheimer's and Parkinson's disease affect nearly half a million people each year with their ..... </li></ul><ul><li>Alzheimer’s disease then arrives from the reduced levels of basic brain chemicals , namely serotonin, somatostatin, norepinephrine, and acetylcholine .The levels of glutamate in the brain are elevated. </li></ul><ul><li>There are many theories as to where the disease originates; some believe it is caused be the reduction of acetylcholine and hold that by replacing the level of acetylcholine, the effects of Alzheimer’s disease could be lessened. This reasoning, however, has not led to a cure even though most of the early medications for Alzheimer’s disease were based on this hypothesis. </li></ul>
  69. 79. Assessment and Diagnostic Methods <ul><li>THE DIAGNOSIS, which is one of exclusion, IS CONFIRMED BY AUTOPSY </li></ul><ul><li>Health history and physical findings and results of functional abilities assessments (i.e. Functional Independence Measure [FIM], Mini-Mental Status Examination ) </li></ul><ul><li>EEG </li></ul><ul><li>CT scan </li></ul><ul><li>MRI </li></ul><ul><li>Blood and CSF examinations </li></ul>
  70. 80. PARKINSON’S DISEASE <ul><li>A slowly progressive degenerative neurologic disorder affecting the brain center that are responsible for control and regulation of movement </li></ul><ul><li>Parkinson’s disease is a debilitating, neurological disorder that can prevent people from performing simple, daily activities. </li></ul><ul><li>But new therapies are available that can control tremors associated with Parkinson’s disease, and help people achieve a better quality of life. </li></ul><ul><li>In order to receive the very best treatment, it is essential that patients and their caregivers stay abreast of the latest developments in Parkinson’s disease therapy research. </li></ul>
  71. 81. <ul><li>The causes of Parkinson's disease--a progressive disorder of the nervous system--are still a mystery to modern medicine. But years of research have led to a better understanding of how the disease works, and how to slow down the steady loss of muscle control that patients suffer. </li></ul><ul><li>Stores of the neurotansmitter DOPAMINE are lost in the substantia nigra and the corpus striatum of a degenerative process – imbalance between acetylcholine and dopamine affecting voluntary movements </li></ul><ul><li>Medications for Parkinson's disease can be effective, but they sometimes wear off too soon. Discover what's being done to allow patients to get longer responses to their treatment. </li></ul>
  72. 82. Clinical Manifestations <ul><li>3 CARDINAL SIGNS: </li></ul><ul><ul><li>Tremor </li></ul></ul><ul><ul><li>Rigidity </li></ul></ul><ul><ul><li>Bradykinesia </li></ul></ul><ul><li>Impaired movement: bradykinesia includes difficulty in initiating, maintaining, and performing motor activities; muscle stiffness or rigidity </li></ul><ul><li>Resting tremors: slow, unilateral turning of the forearm and hand and a pill-rolling motion of the thumb against the fingers, tremors at rest anf increasing with concentration and anxiety </li></ul><ul><li>Muscle weakness </li></ul><ul><li>Hypokinesia (abnormally diminished movement), gait disturbances, flexed posture, postural instability </li></ul>
  73. 83. <ul><li>OTHER CHARACTERISTICS: </li></ul><ul><li>Micrographia (shrinking, slow handwriting) as dexterity declines </li></ul><ul><li>Dysphonia </li></ul><ul><li>Masklike facial expression </li></ul><ul><li>Loss of postural reflexes – patients stands with head bent forward and walks with propulsive gait (shuffling gait); difficulty pivoting and loss of balance, results in risk for falls </li></ul><ul><li>Depression and psychiatric manifestations (personality changes, psychosis, dementia, and confusion) </li></ul><ul><li>Sleep disorders, uncontrolled sweating, orthostatic hypotension, gastric and urinary retention, and constipation </li></ul>
  74. 84. Assessment and Diagnostic Methods <ul><li>Patient’s history and presence of two of the three cardinal manifestations </li></ul><ul><li>Positron emission tomography (PET) scanning </li></ul><ul><li>Neurologic examination and response to pharmacologic management </li></ul>
  75. 85. Medical Management <ul><li>Goal of treatment: to control symptoms and maintain functional independence; no approach prevents disease progression </li></ul><ul><li>PHARMACOLOGIC THERAPY: </li></ul><ul><li>Levodopa therapy (converts to dopamine) – most effective to relieve symptoms, in combination with carbidopa (Sinemet) which prevents the levodopa breakdown </li></ul><ul><li>Budipine – non dopaminergic, anti-parkinson that reduces akinesia, rigidity, and tremor </li></ul><ul><li>Anti-histamine to allay tremors </li></ul><ul><li>Dopamine agonist (Pergolide [Permax], bromocriptine mesylate [Parlodel], ropinirole, and pramipexole) – used to delay the initiation of cardidopa and levodopa </li></ul><ul><li>Anti-cholinergic theray – to control tremors and rigidity </li></ul><ul><li>Amantadine HCl (Symmetrel) – anti-viral used to reduce rigidity, tremor, and bradykinesia </li></ul><ul><li>Monoamine oxidase inhibitors (MAOI’s) – inhibit dopamine breakdown </li></ul><ul><li>Anti-depressants </li></ul><ul><li>Trials of cathecol-O-methyltransferase (COMT) inhibitors </li></ul>
  76. 86. Surgical Management <ul><li>Surgery to destroy a part of the thalamus – stereotactic thalamotomy and pallidotomy to interrupt nerve pathways and alleviate tremor or rigidity </li></ul><ul><li>Transplantation of neural cells from fetal tissue of human or animal source to reestablish normal dopamine release </li></ul><ul><li>Deep brain stimulation with pacemaker-like brain implants shows promise but is waiting for FDA approval </li></ul>
  77. 87. HUNTINGTON’S CHOREA <ul><li>Huntington’s disease is a chronic, hereditary disease of the nervous system that results in progressive involuntary choreiform (dance-like) movements and dementia </li></ul><ul><li>Glutamine abnormally collects in certain brain cell nuclei, causing cell death </li></ul><ul><li>Affects men and women of all races </li></ul><ul><li>Transmitted as an autosomal dominant genetic disorder – 50% chance of inheriting from a parent with Huntington’s </li></ul><ul><li>Onset usually occurs between 35 and 45 years of age </li></ul>
  78. 88. Clinical Manifestations <ul><li>Most prominent clinical features: abnormal involuntary movements (chorea), intellectual decline, and emotional disturbances </li></ul><ul><li>Constant writhing, twisting, and uncontrollable movements of the entire body occurs as the disease progresss </li></ul><ul><li>Facial movements produce ticks and grimaces; speech becomes slurred, hesitant, often explosive, and then eventually unintelligible </li></ul><ul><li>Chewing and swallowing are difficult, and aspiration and choking are dangers </li></ul><ul><li>Gait becomes disorganized, and ambulation is eventually impossible; patient eventually confined to a wheelchair </li></ul><ul><li>Bowel and bladder control is lost </li></ul><ul><li>Progressive intellectual impairment occurs with eventual dementia </li></ul><ul><li>Uncontrollable emotional changes occur but become less acute as the disease progresses. Patient maybe nervous, irritable, or impatient; uncontrollable anger; profound often suicidal depression; apathy; or euphoria at the early stage of the disease </li></ul><ul><li>Hallucinations, delusions, and paranoid thinking may precede appearance of disjointed movements </li></ul><ul><li>Patient die in 10-15 years from heart failure, pneumonia, or infection or as a result of fall or choking </li></ul>
  79. 89. Assessment and Diagnostic Methods <ul><li>Diagnosis is made on the basis of clinical presentation, positive family history, and exclusion of other causes </li></ul><ul><li>Imaging studies: CT scan, MRI – may show atrophy of the striatum </li></ul><ul><li>A genetic marker for Huntington’s disease has been located – offers hope of cure oe even specific determination of onset </li></ul>
  80. 90. Medical Management <ul><li>NO TREATMENT STOPS OR REVERSES THE PROCESS </li></ul><ul><li>Palliative care is given </li></ul><ul><li>Patients’ needs and abilities are the focus of treatment </li></ul><ul><li>Medications – to improve chorea and temporarily decrease rigidity in some patients: phenothiazines (Haloperidol), butyrophenones, and thioxanthenes to block the dopamine receptors; anti-parkinsonism therapy (L-dopa) </li></ul><ul><li>Motor signs are continually assessed and evaluated – “akathisia” (motor restlessness) in overmedicated patient is dangerous and should be reported </li></ul><ul><li>Psychotherapy aimed at allaying anxiety and reducing stress may be beneficial; anti-depressants are given for depression or suicidal ideation </li></ul>
  81. 92. <ul><li>PRE – TEST </li></ul><ul><li>Gas exchange is a function of what system? </li></ul><ul><li>Prominent feature/s of bronchial asthma… of COPD…? </li></ul><ul><li>Status asthmaticus ? </li></ul><ul><li>Bronchodilators </li></ul><ul><li>Pneumococcal vaccination </li></ul><ul><li>Integumentary system ? </li></ul><ul><li>“ Kraissl line” – line of greatest tension? </li></ul><ul><li>Endocrine glands, functions, hormone/s produced? </li></ul><ul><li>Diabetes Mellitus ? </li></ul><ul><li>Causes of blindness ? </li></ul>
  82. 93. <ul><li>PRE – TEST </li></ul><ul><li>11. Liver functions </li></ul><ul><li>12. Immunization/s schedule </li></ul><ul><li>13. Blood test/s to assess renal function </li></ul><ul><li>14. Difference/s between ARF, CRF, and ESRD </li></ul><ul><li>15. Dialysis </li></ul><ul><li>16. Forms/ types of arthritides </li></ul><ul><li>17. Bone marrow and blood functions </li></ul><ul><li>18. Leukemia </li></ul><ul><li>19. Anemia </li></ul><ul><li>20. Cancer – TNM classifications </li></ul>
  83. 96. THE RESPIRATORY SYSTEM
  84. 97. How the Lungs Work <ul><li>The lungs provide a very large surface area (the size of a football field ) for the exchange of oxygen and carbon dioxide between the body and the environment. </li></ul><ul><li>A slice of normal lung looks like a pink sponge filled with tiny bubbles or holes ( alveoli ) . These bubbles, surrounded by a fine network of tiny blood vessels, give the lungs a large surface to exchange oxygen (into the blood where it is carried throughout the body) and carbon dioxide (out of the blood). This process is called gas exchange . Healthy lungs do this very well. </li></ul><ul><li>Here is how normal breathing works: </li></ul><ul><li>You breathe in air through your nose and mouth The air travels down through your windpipe ( trachea ) then through large and small tubes in your lungs called bronchial (BRON-kee-ul) tubes </li></ul><ul><li>The larger tubes are bronchi (BRONK-eye), and the smaller tubes are bronchioles (BRON-kee-oles) </li></ul><ul><li>The word &quot;airways&quot; is used to refer to the various tubes or passages that air must travel through from the nose and mouth into the lungs. The airways in your lungs look something like an upside-down tree with many branches. </li></ul>
  85. 98. <ul><li>At the ends of the small bronchial tubes, there are groups of tiny air sacs called alveoli (al-VEE-uhl-EYE). The air sacs have very thin walls, and small blood vessels called capillaries run in the walls. </li></ul><ul><li>Oxygen passes from the air sacs into the blood in these small blood vessels. At the same time, carbon dioxide passes from the blood into the air sacs. Carbon dioxide , a normal byproduct of the body's metabolism, must be removed. </li></ul><ul><li>The airways and air sacs in the lung are normally elastic —that is, they try to spring back to their original shape after being stretched or filled with air, just the way a new rubber band or balloon would </li></ul><ul><li>This elastic quality helps retain the normal structure of the lung and helps to move the air quickly in and out </li></ul>
  86. 99. <ul><li>In Bronchial Asthma , there is hypersensitivity of the “airways” causing reactive bronchoconstriction that leads to feeling of shortness or difficulty in breathing </li></ul><ul><li>In COPD , much of the elastic quality is gone , and the airways and air sacs no longer bounce back to their original shape </li></ul><ul><li>This means that the airways collapse, like a floppy hose, and the air sacs tend to stay inflated. The floppy airways obstruct the airflow out of the lungs, leading to an abnormal increase in the lungs' size </li></ul><ul><li>In addition, the airways may become inflamed and thickened, and mucus-producing cells produce more mucus , further contributing to the difficulty of getting air out of the lungs. </li></ul>
  87. 100. Bronchial Asthma Asthma is a chronic disease that affects your airways. The airways are the tubes that carry air in and out of your lungs. If you have asthma, the inside walls of your airways are inflamed (swollen) The inflammation makes the airways very sensitive, and they tend to react strongly to things that you are allergic to or find irritating . When the airways react, they get narrower , and less air flows through to your lung tissue. This causes symptoms like wheezing (a whistling sound when you breathe), coughing, chest tightness , and trouble breathing , especially at night and in the early morning.
  88. 101. <ul><li>Asthma cannot be cured , but most people with asthma can control it so that they have few and infrequent symptoms and can live active lives. </li></ul><ul><li>When your asthma symptoms become worse than usual, it is called an asthma episode or attack . </li></ul><ul><li>During an asthma attack , muscles around the airways tighten up, making the airways narrower so less air flows through . Inflammation increases , and the airways become more swollen and even narrower. Cells in the airways may also make more mucus than usual. This extra mucus also narrows the airways. These changes make it harder to breathe. </li></ul>
  89. 102. <ul><li>Asthma attacks are not all the same—some are worse than others. In a severe asthma attack, the airways can close so much that not enough oxygen gets to vital organs. This condition is a medical emergency. People can die from severe asthma attacks . </li></ul><ul><li>So, if you have asthma, you should see your doctor regularly . You will need to learn what things cause your asthma symptoms and how to avoid them. Your doctor will also prescribe medicines to keep your asthma under control. </li></ul><ul><li>Taking care of your asthma is an important part of your life. Controlling it means working closely with your doctor to learn what to do, staying away from things that bother your airways, taking medicines as directed by your doctor, and monitoring your asthma so that you can respond quickly to signs of an attack. By controlling your asthma every day, you can prevent serious symptoms and take part in all activities. </li></ul><ul><li>If your asthma is not well controlled , you are likely to have symptoms that can make you miss school or work and keep you from doing things you enjoy. Asthma is one of the leading causes of children missing school. </li></ul>
  90. 103. <ul><li>Asthma can begin at any age; but most common chronic disease of childhood </li></ul><ul><li>Risk factors for asthma: </li></ul><ul><ul><li>Allergy – strongest factor </li></ul></ul><ul><ul><li>Chronic exposure to airway irritants or allergens (grass, weed pollens, mold, dust, dust mites, animal dander, fumes, perfumes, irritating strong odors, etc.) </li></ul></ul><ul><li>Common triggers for asthma: </li></ul><ul><ul><li>Airway irritants (pollutants, cold, heat, strong odors, smoke, perfumes) </li></ul></ul><ul><ul><li>Exertion </li></ul></ul><ul><ul><li>Stress </li></ul></ul><ul><ul><li>Sinusitis </li></ul></ul><ul><ul><li>Esophageal reflux </li></ul></ul>
  91. 104. Clinical Manifestations <ul><li>Cough (with or without mucus production), dyspnea, and wheezing (initially on expiration then eventually during inspiration) </li></ul><ul><li>Attacks frequently occurs at night or in the early morning </li></ul><ul><li>Frequently preceded by increasing symptoms over days, but may begin abruptly </li></ul><ul><li>Chest tightness and dyspnea occurs </li></ul><ul><li>Expiration requires effort and become prolonged </li></ul><ul><li>Central cyanosis due to severe hypoxia </li></ul><ul><li>Other symptoms: diaphoresis, tachycardia, and widened pulse pressure </li></ul><ul><li>Status asthmaticus </li></ul><ul><li>Eczema, urticaria, and temporary edema are allergic reaction </li></ul>
  92. 105. Assessment and Diagnostic Methods <ul><li>Family environment, and occupational history is essential </li></ul><ul><li>During acute episodes, sputum and blood test, pulse oximetry, arterial blood gases (ABG’s), and hypocapnia and respiratory alkalosis and pulmonary function (FEV and FVC decreased) tests are performed </li></ul>
  93. 106. Medical Management <ul><li>PHARMACOLOGIC THERAPY: </li></ul><ul><ul><li>2 classes of medications – long-acting control and quick-relief (short-acting) – as well as combinations </li></ul></ul><ul><ul><li>Leukotriene modifiers inhibitors/ antileukotrienes block receptors to revert bronchoconstrictors </li></ul></ul><ul><ul><li>Beta-adrenergic agonists </li></ul></ul><ul><ul><li>Methylxanthines </li></ul></ul><ul><ul><li>Anti-cholinergics </li></ul></ul><ul><ul><li>Corticosteroids: MDI </li></ul></ul><ul><ul><li>Mast cell inhibitors </li></ul></ul>
  94. 107. What Is COPD? <ul><li>Chronic obstructive pulmonary disease (COPD) is a lung disease in which the lungs are damaged , making it hard to breathe. In COPD, the airways—the tubes that carry air in and out of your lungs—are partly obstructed , making it difficult to get air in and out. </li></ul><ul><li>Cigarette smoking is the most common cause of COPD. Most people with COPD are smokers or former smokers. Breathing in other kinds of lung irritants, like pollution, dust, or chemicals, over a long period of time may also cause or contribute to COPD. </li></ul><ul><li>The airways branch out like an upside-down tree, and at the end of each branch are many small, balloon-like air sacs. In healthy people, each airway is clear and open. The air sacs are small and dainty, and both the airways and air sacs are elastic and springy. When you breathe in, each air sac fills up with air like a small balloon; when you breathe out, the balloon deflates and the air goes out. </li></ul>
  95. 108. The septum or partitions/ divisions between alveoli (abnormal increase in lung’s size) are destroyed in Chronic Obstructive Pulmonary Disease with increase mucus (phlegm)
  96. 109. <ul><li>In COPD, the airways and air sacs lose their shape and become floppy. Less air gets in and less air goes out because: </li></ul><ul><ul><ul><li>The airways and air sacs lose their elasticity (like an old rubber band). </li></ul></ul></ul><ul><ul><ul><li>The walls between many of the air sacs are destroyed. </li></ul></ul></ul><ul><ul><ul><li>The walls of the airways become thick and inflamed (swollen). </li></ul></ul></ul><ul><ul><ul><li>Cells in the airways make more mucus (sputum) than usual, which tends to clog the airways. </li></ul></ul></ul>
  97. 110. <ul><li>COPD develops slowly, and it may be many years before you notice symptoms like feeling short of breath. Most of the time, COPD is diagnosed in middle-aged or older people. </li></ul><ul><li>COPD is a major cause of death and illness, and it is the fourth leading cause of death in the United States and throughout the world. </li></ul><ul><li>There is no cure for COPD . The damage to your airways and lungs cannot be reversed, but there are things you can do to feel better and slow the damage. </li></ul><ul><li>COPD is not contagious—you cannot catch it from someone else. </li></ul>
  98. 111. Clinical Manifestations <ul><li>Characterized by dyspnea, cough, and increased work of breathing as well as dyspnea on mild exertion, advancing to dyspnea at rest </li></ul><ul><li>Weight loss is common </li></ul><ul><li>Symptoms are specific to the disease </li></ul><ul><li>Changes in ventilation-perfusion ratios </li></ul>
  99. 112. Medical Management <ul><li>COPD - Bronchitis ? </li></ul><ul><li>Emphysema ? </li></ul><ul><li>Bronchodilators </li></ul><ul><li>Oxygen therapy – nighttime oxygen </li></ul><ul><li>Varied treatments specific to disease </li></ul>
  100. 113. PNEUMONIA <ul><li>Pneumonia is an inflammation of the lung parenchyma commonly caused by microbial agents </li></ul><ul><li>Categorized as: bacterial; typical; atypical; anaerobic/cavitary; or opportunistic </li></ul><ul><li>Classified as: </li></ul><ul><ul><li>Communiy-acquired pneumonia </li></ul></ul><ul><ul><li>Hospital-acquired pneumonia </li></ul></ul><ul><ul><li>Pneumonia in the immunocompromised host </li></ul></ul><ul><ul><li>Aspiration pneumonia </li></ul></ul><ul><li>At risk for pneumonia often have chronic underlying disorders, severe acute illness, a suppressed immune system from disease or medications, immobility, and other factors that interfere with normal lung protective function </li></ul>
  101. 114. Pathophysiology <ul><li>Inflammatory reaction in the alveoli – producing an exudates that partially occludes the bronchi or alveoli </li></ul><ul><li>Bronchospasm occur in patients with reactive airway disease that interferes with gas exchange </li></ul><ul><li>Bronchopneumonia – most common form, is distributed in a patchy fashion extending from the bronchi to the surrounding lung parenchyma </li></ul><ul><li>Lobar pneumonia – if a substantial part of one lobe or more lobes is involved </li></ul>
  102. 115. Microbial Causes of Pneumonia <ul><li>Pseudomonas aeruginosa </li></ul><ul><li>Klebsiella sp. </li></ul><ul><li>Staphylococcus aureus </li></ul><ul><li>Haemphilus influenzae </li></ul><ul><li>Staphylococcus pneumoniae </li></ul><ul><li>Enteric Gram – negative bacilli </li></ul><ul><li>Fungi </li></ul><ul><li>Viruses (most common in children) </li></ul>
  103. 116. Clinical Manifestations <ul><li>Depending on the causative agents and the patient’s disease: </li></ul><ul><ul><li>Sudden chills, rapidly rising fever (38.5 o C to 40.5 o C) and profuse sweating </li></ul></ul><ul><ul><li>Pleuritic chest pain, aggravated by respiration and coughing </li></ul></ul><ul><ul><li>Severely ill patient with marked tachypnea (25 – 45 breaths/min) and dyspnea; orthopnea when not propped up </li></ul></ul><ul><ul><li>Pulse rapid and bounding; may increase 10 beats/min of temp elevation ( o C) * </li></ul></ul><ul><ul><li>Relative bradycardia (suggest viral infection or Mycoplasma or Legionella sp. Infection ** </li></ul></ul><ul><ul><li>Purulent sputum, rusty blood-tinged, viscous, or green </li></ul></ul><ul><li>Other signs: fever, crackles, and signs of lobar consolidation; initial upper respiratory tract symptoms (nasal congestion, sore throat) </li></ul><ul><li>Severe pneumonia: flushed cheeks; lips and nail beds demonstrate central cyanosis </li></ul>
  104. 117. Assessment and Diagnostic Methods <ul><li>Primarily history </li></ul><ul><li>Physical examination: cardio-pulmonary findings </li></ul><ul><li>Chest radiographs (PA, AP-Lat, Lordotic views) </li></ul><ul><li>Blood C/S </li></ul><ul><li>Sputum Gram stain, C/S </li></ul>
  105. 118. Medical Management <ul><li>Antibiotics – based on the gram stain results and antibiotic guidelines. Combination therapy maybe used </li></ul><ul><li>Supportive treatment includes: hydration, antipyretics, antihistamines, or nasal decongestants </li></ul><ul><li>Bed rest is recommended </li></ul><ul><li>Oxygen therapy is given for hypoxemia </li></ul><ul><li>Respiratory support: ET intubation, high inspiratory oxygen concentrations, and mechanical ventilation </li></ul><ul><li>Treatment of atelectasis, pleural effusion, shoch, respiratory failure, or superinfection, if needed </li></ul><ul><li>For groups at high risk for community-acquired pneumonia – Pneumococcal vaccination * </li></ul>
  106. 119. Adult Immunization Schedule Vaccine is usually given once to individuals > 65 years of age. A repeat dose may be given 5 years later for those at higher risk. Immunization is also recommended for younger people with chronic medical problems, such as heart disease, diabetes, renal failure, and sickle cell anemia, and for those who work or live with high-risk persons. Streptococcus pneumoniae (polysaccharide) Vaccine is administered yearly to individuals > 55 years of age; to younger people with chronic medical problems, such as heart disease and diabetes; and to those who work or live with high-risk persons Influenza 2 doses are given to individuals > 13 years of age who have not had chickenpox. The 2 nd dose is given 1 -2 months after the 1 st Varicella A 3-dose schedule applies for individuals who have not received an initial immunization series in childhood. The 2 nd dose is given 1 month after the 1 st and the 3 rd dose 6 months after the 2 nd . Boosters are given every 10 years Tetanus/Diptheria toxoids, absorbed 1 dose is given to adults born in 1957 or later and not previouslt immunized. A second dose may be required in some work or school settings Measles/Mumps/Rubella 3 doses are given, with the 2 nd dose 1 month after the 1 st , and 3 rd dose 5 months after the 2 nd Hepatitis B 2 doses are recommended for long-term protection, with the 2 nd dose 6 – 12 months after the first Hepatitis A Timing of Immunization Vaccine
  107. 121. INTEGUMENTARY SYSTEM (THE SKIN) <ul><li>The skin or cutis covers the entire outer surface of the body </li></ul><ul><li>Consists of two layers which differ in function, histological appearance and their embryological origin </li></ul><ul><ul><li>The outer layer or epidermis is formed by an epithelium and is of ectodermal origin </li></ul></ul><ul><ul><li>The underlying thicker layer, the dermis , consists of connective tissue and develops from the mesoderm </li></ul></ul><ul><ul><li>Beneath the two layers we find a subcutaneous layer of loose connective tissue or hypodermis , which binds the skin to underlying structures </li></ul></ul><ul><li>Hair, nails and sweat and sebaceous glands are of epithelial origin and collectively called the appendages of the skin . </li></ul>
  108. 124. <ul><li>The red and yellow hues of the skin are due to haemoglobin in the red blood cells, which pass through the capillaries beneath the epidermis, and carotene , which accumulates in fat cells found in the dermis and hypodermis. </li></ul><ul><li>Melanocytes </li></ul><ul><ul><li>The brown colour component is due to melanin , which is produced in the skin itself in cells called melanocytes </li></ul></ul><ul><ul><li>Melanin is located in membrane-bound organelles called melanosomes </li></ul></ul>
  109. 125. <ul><li>Langerhans Cells – are another cell type found within the epidermis </li></ul><ul><ul><li>Morphologically they are not unlike melanocytes, but functionally they are more closely related to macrophages. They are important in immune reactions of the epidermis </li></ul></ul><ul><li>T-lymphocytes – are like Langerhans cells, a group of cells functioning in the immune system </li></ul><ul><ul><li>Some of them will be present in the epidermis. </li></ul></ul><ul><ul><li>Together with Langerhans cells they are sometimes referred to as SALT , i.e. skin-associated lymphoid tissue. </li></ul></ul>
  110. 126. <ul><li>The Dermis </li></ul><ul><li>The dermis is the thick layer of connective tissue to which the epidermis is attached. Its deepest part continues into the subcutaneous tissue without a sharply defined boundary. Its thickness is for this reason difficult to determine but 1-2 mm is a good estimate for &quot;average&quot; skin. The dermis may be divided into two sublayers (again without a sharp boundary): </li></ul><ul><ul><li>The papillary layer consists of loose, comparatively cell-rich connective tissue, which fills the hollows at the deep surface ( dermal papillae ) of the epidermis. Capillaries are frequent. Collagen fibres appear finer than in the reticular layer. </li></ul></ul><ul><ul><li>The reticular layer appears denser and contains fewer cells. Thick collagen fibres (5-10 µm) often aggregate into bundles (up to 100 µm thick). The fibres form an interlacing network, although their predominant direction is parallel to the surface of the skin. A preferred orientation of the collagen fibres is not visible in the sections, but the main orientation of the fibres differs in skin from different parts of the body </li></ul></ul><ul><ul><li>Usually, their main orientation will follow the &quot; lines of greatest tension &quot; in the skin ( Kraissl lines ). This is of some surgical importance since incisions parallel to these lines will heal faster and with less formation of scar tissue. </li></ul></ul>
  111. 127. Appendages of the Skin <ul><li>Hair </li></ul><ul><ul><li>A characteristic feature of the human skin is the apparent lack of hair ( pili ) on most of the body surface. This is actually not quite true. Most of the skin is haired although the hair in most areas is short, fine and only lightly pigmented. This type of hair is called vellus hair . </li></ul></ul><ul><ul><li>Truly hairless are only the palms of hands and soles of feet, the distal phalanges and sides of fingers and toes and parts of the external genitalia. </li></ul></ul>
  112. 128. <ul><li>Sebaceous glands </li></ul><ul><ul><li>It empty their secretory product into the upper parts of the hair follicles. They are therefore found in parts of the skin where hair is present. The hair follicle and its associated sebaceous gland form a pilosebaceous unit . </li></ul></ul><ul><ul><li>Sebaceous glands are also found in some of the areas where no hair is present, for example, lips, oral surfaces of the cheeks and external genitalia. </li></ul></ul>
  113. 129. <ul><li>Sweat Glands </li></ul><ul><li>Two types of sweat glands are present in humans. They are distinguished by their secretory mechanism into merocrine (~eccrine) sweat glands and apocrine sweat glands </li></ul><ul><ul><li>Merocrine sweat glands are the only glands of the skin with a clearly defined biological function. </li></ul></ul><ul><ul><li>The excretory ducts of merocrine sweat glands empty directly onto the surface of the skin </li></ul></ul><ul><ul><li>Apocrine sweat glands occur in, for example, the axilla. They are stimulated by sexual hormones and are not fully developed or functional before puberty. Apocrine sweat is a milky, proteinaceous and odourless secretion. The odour is a result of bacterial decomposition and is, at least in mammals other than humans, of importance for sexual attraction </li></ul></ul><ul><ul><li>The excretory duct of apocrine sweat glands does not open directly onto the surface of the skin. Instead, the excretory duct empties the sweat into the upper part of the hair follicle . Apocrine sweat glands are therefore part of the pilosebaceous unit. </li></ul></ul>
  114. 132. ENDOCRINE GLANDS <ul><li>Glands are small but powerful organs that are located throughout the body. They control very important body functions by releasing hormones. </li></ul><ul><li>Pituitary Gland </li></ul><ul><li>Hypothalmus </li></ul><ul><li>Thymus </li></ul><ul><li>Pineal Gland </li></ul><ul><li>Testes </li></ul><ul><li>Ovaries </li></ul><ul><li>Thyroid </li></ul><ul><li>Adrenal Glands </li></ul><ul><li>Parathyroid </li></ul><ul><li>Pancreas </li></ul>
  115. 133. <ul><li>The pituitary gland is sometimes called the &quot;master gland&quot; because of its great influence on the other body organs. Its function is complex and important for overall well-being. </li></ul><ul><li>The pituitary gland is divided into two parts, front (anterior) and back (posterior). </li></ul>PITUITARY GLAND
  116. 134. <ul><li>The anterior pituitary produces several hormones: </li></ul><ul><ul><li>Prolactin or PRL - PRL stimulates milk production from a woman's breasts after childbirth and can affect sex hormone levels from the ovaries in women and the testes in men. </li></ul></ul><ul><ul><li>Growth hormone or GH - GH stimulates growth in childhood and is important for maintaining a healthy body composition. In adults it is also important for maintaining muscle mass and bone mass. It can affect fat distribution in the body. (For more information go to the Growth section on this site) </li></ul></ul><ul><ul><li>Adrenocorticotropin or ACTH - ACTH stimulates production of cortisol by the adrenal glands. Cortisol, a so-called &quot;stress hormone,&quot; is vital to survival. It helps maintain blood pressure and blood glucose levels. </li></ul></ul><ul><ul><li>Thyroid-stimulating hormone or TSH - TSH stimulates the thyroid gland to make thyroid hormones, which, in turn, control (regulate) the body's metabolism, energy, growth and development, and nervous system activity. </li></ul></ul><ul><ul><li>Luteinizing hormone or LH - LH regulates testosterone in men and estrogen in women. </li></ul></ul><ul><ul><li>Follicle-stimulating hormone or FSH - FSH promotes sperm production in men and stimulates the ovaries to release eggs (ovulate) in women. LH and FSH work together to allow normal function of the ovaries or testes. </li></ul></ul>
  117. 135. <ul><li>The posterior pituitary produces two hormones: </li></ul><ul><ul><li>Oxytocin - Oxytocin causes milk letdown in nursing mothers and contractions during childbirth. </li></ul></ul><ul><ul><li>Antidiuretic hormone or ADH - ADH, also called vasopressin, is stored in the back part of the pituitary gland and regulates water balance. If this hormone is not secreted properly, this can lead to problems of sodium (salt) and water balance, and could also affect the kidneys so that they do not work as well. </li></ul></ul><ul><li>In response to over- or underproduction of pituitary hormones, the target glands affected by these hormones can produce too many or too few hormones of their own. </li></ul><ul><li> For example, too much growth hormone can cause gigantism, or excessive growth, while too little GH may cause dwarfism, or very short stature. </li></ul>
  118. 136. DIABETES INSIPIDUS <ul><li>A disorder of the posterior lobe of the pituitary gland due to the deficiency of anti-diuretic hormone (ADH) or vasopressin </li></ul><ul><li>Characterized by: </li></ul><ul><ul><li>Polydypsia </li></ul></ul><ul><ul><li>Polyuria </li></ul></ul><ul><li>Maybe: secondary to head trauma, brain tumor, surgical ablation or irradiation; nephrogenic; or primary </li></ul>
  119. 137. Clinical Manifestations <ul><li>POLYURIA </li></ul><ul><ul><li>Enormous daily output or very dilute urine (sp gr 1.001 – 1.005); abrupt onset </li></ul></ul><ul><li>POLYDIPSIA </li></ul><ul><ul><li>Intense thirst, drinking 2 to 20 liters of fluid per day with special craving for cold water </li></ul></ul><ul><li>Polyuria continues even without fluid replacement </li></ul><ul><li>Assessment and Diagnostic Findings </li></ul><ul><li>Fluid deprivation test – unable to increase the urine specific gravity </li></ul><ul><li>Specific gravity, serum osmolality, and serum sodium level may be obtaines </li></ul>
  120. 138. Medical Management <ul><li>Objective of the therapy are to ensure adequate fluid replacement , to replace vasopressin , and to search for and correct the underlying intracranial pathology </li></ul><ul><li>Nephrogenic type: thiazide diuretics, mild salt depletion, and prostaglandins inhibitors (Ibuprofen, Indomethacin, and ASA) </li></ul><ul><li>Vasopressin/ADH replacement: </li></ul><ul><ul><li>Desmopressin – intranasally </li></ul></ul><ul><ul><li>Lypressin </li></ul></ul><ul><ul><li>IM ADH every 24 to 96 hours </li></ul></ul><ul><li>Fluid Conservation: </li></ul><ul><ul><li>Clofibrate – OHA but with antidiuretic effect </li></ul></ul><ul><ul><li>Chlorpropamide – OHA that potentiates action of vasopressin </li></ul></ul><ul><ul><li>Thiazide diuretics </li></ul></ul>
  121. 139. HYPOTHALAMUS <ul><li>The hypothalamus is part of the brain that lies just above the pituitary gland. </li></ul><ul><li>It releases hormones that start and stop the release of pituitary hormones . </li></ul><ul><li>The hypothalamus controls hormone production in the pituitary gland through several &quot;releasing&quot; hormones . </li></ul><ul><li>Some of these are </li></ul><ul><ul><li>growth hormone-releasing hormone, or GHRH (controls GH release) </li></ul></ul><ul><ul><li>thyrotropin-releasing hormone, or TRH (controls TSH release) </li></ul></ul><ul><ul><li>corticoptropin-releasing hormone, or CRH (controls ACTH release) </li></ul></ul><ul><ul><li>Gonadotropin-releasing hormone, or GnRH (controls LH & FSH release) </li></ul></ul><ul><ul><li>Follicle-stimulating hormone, or FSH (for normal puberty) </li></ul></ul><ul><ul><li>Gonadotropin-releasing hormone (GnRH) tells the pituitary gland to make luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which are important for normal puberty. </li></ul></ul>
  122. 140. THYMUS <ul><li>The thymus is a gland needed early in life for normal immune function. </li></ul><ul><li>It is very large just after a child is born and weighs its greatest when a child reaches puberty. Then its tissue is replaced by fat. </li></ul><ul><li>The thymus gland secretes hormones called humoral factors . </li></ul><ul><ul><li>These hormones help to develop the lymphoid system, which is a system throughout the body that help it to reach a mature immune response in cells to protect them from invading bodies, like bacteria. </li></ul></ul>
  123. 141. PINEAL GLAND <ul><li>Scientists are still learning how the pineal gland works. </li></ul><ul><li>They have found one hormone so far that is produced by this gland: melatonin . </li></ul><ul><ul><li>Melatonin may stop the action of (inhibit) the hormones that produce gonadotropin, which causes the ovaries and testes to develop and function. </li></ul></ul><ul><ul><li>It may also help to control sleep patterns. </li></ul></ul>
  124. 142. TESTES <ul><li>Males have twin reproductive glands, called testes, that produce the hormone testosterone . </li></ul><ul><ul><li>Testosterone helps a boy develop and then maintain his sexual traits . </li></ul></ul><ul><ul><li>During puberty, testosterone helps to bring about the physical changes that turn a boy into an adult male, such as growth of the penis and testes, growth of facial and pubic hair, deepening of the voice, increase in muscle mass and strength, and increase in height. </li></ul></ul><ul><ul><li>Throughout adult life, testosterone helps maintain sex drive, sperm production, male hair patterns, muscle mass, and bone mass </li></ul></ul><ul><li>Testicular cancer, which is the most common form of cancer for males between ages 15 and 35, may need to be treated by surgical removal of one or both testicles. </li></ul><ul><li>The resulting decrease or absence of testosterone may cause decreased sexual drive, impotence, altered body image, and other symptoms. </li></ul>
  125. 143. OVARIES <ul><li>The two most important hormones of a woman's twin reproductive glands, the ovaries, are estrogen and progesterone. </li></ul><ul><li>These hormones are responsible for developing and maintaining female sexual traits , as well as maintaining a pregnancy. </li></ul><ul><li>Along with the pituitary gonadotropins (FH and LSH), they also control the menstrual cycle . </li></ul><ul><li>The ovaries also produce inhibin , a protein that curbs (inhibits) the release of follicle-stimulating hormone from the anterior pituitary and helps control egg development. </li></ul><ul><li>The most common change in the ovarian hormones is caused by the start of menopause , part of the normal aging process. </li></ul><ul><ul><li>It also can occur when ovaries are removed surgically. </li></ul></ul><ul><ul><li>Loss of ovarian function means loss of estrogen , which can lead to hot flashes, thinning vaginal tissue, lack of menstrual periods, mood changes and bone loss, or osteoporosis. </li></ul></ul><ul><li>A condition called polycystic ovary syndrome (PCOS) is caused by overproduction of male hormones in females. </li></ul><ul><li>PCOS can affect menstrual cycles, fertility, and hormone levels, as well as cause acne, facial hair growth, and male pattern balding. </li></ul>
  126. 144. THYROID GLAND <ul><li>The thyroid is a small gland inside the neck, located in front of your breathing airway (trachea) and below your Adam's apple. </li></ul><ul><li>The thyroid hormones control your metabolism </li></ul><ul><li>The body's ability to break down food and store it as energy and the ability to break down food into waste products with a release of energy in the process. </li></ul><ul><li>The thyroid produces two hormones, </li></ul><ul><ul><li>T3 (called tri-iodothyronine) </li></ul></ul><ul><ul><li>T4 (called thyroxine). </li></ul></ul>
  127. 145. <ul><li>Thyroid disorders result from too little or too much thyroid hormone. </li></ul><ul><li>Symptoms of hypothyroidism (too little hormone) include: </li></ul><ul><ul><li>decreased energy, slow heart rate, dry skin, constipation, and feeling cold all the time. </li></ul></ul><ul><ul><li>In children, hypothyroidism most commonly leads to slowed growth. Infants born with hypothyroidism can have delayed development and mental retardation if not treated. </li></ul></ul><ul><ul><li>In adults, this disorder often causes weight gain. An enlarged thyroid, or goiter, may develop. </li></ul></ul><ul><li>Hyperthyroidism (too much hormone) may result in </li></ul><ul><ul><li>exophthalmic goiter, or Grave's disease </li></ul></ul><ul><ul><li>Symptoms include: </li></ul></ul><ul><ul><ul><li>anxiety, fast heart rate, diarrhea, and weight loss. </li></ul></ul></ul><ul><ul><ul><li>An enlarged thyroid gland (goiter) and swelling behind the eyes that causes the eyes to push forward, or bulge out, are common. </li></ul></ul></ul>
  128. 146. Medical Management <ul><li>Treatment is directed toward regulating the thyroid activity (normal metabolic state) for symptomatic relief and removing the cause of complications: </li></ul><ul><ul><li>Irradiation – 131 I or 123 I for destructive effects on gland </li></ul></ul><ul><ul><li>Pharmacotherapy – Levothyroxine for hypothyroid, and anti-thyroid (propylthiouracil [PTU] and methimazole [Tapazole]) for hypothyroid patients </li></ul></ul><ul><ul><li>Surgery </li></ul></ul>
  129. 147. PARATHYROID GLAND <ul><li>Located behind the thyroid gland are four tiny parathyroid glands. </li></ul><ul><li>These make hormones that help control calcium and phosphorous levels in the body. </li></ul><ul><li>The parathyroid glands are necessary for proper bone development. </li></ul><ul><li>In response to too little calcium in the diet, the parathyroid glands make parathyroid hormone, or PTH , that takes calcium from bones so that it will be available in the blood for nerve conduction and muscle contraction </li></ul><ul><li>If the parathyroids are removed during a thyroid operation, low blood calcium will result in symptoms such as irregular heartbeat, muscle spasms, tingling in the hands and feet, and possibly difficulty breathing. </li></ul><ul><li>A tumor or chronic illness can cause too much secretion of PTH and lead to bone pain, kidney stones, increased urination, muscle weakness, and fatigue. </li></ul>
  130. 148. ADRENAL GLANDS <ul><li>Each adrenal gland is actually two endocrine organs. </li></ul><ul><ul><li>The outer portion is called the adrenal cortex. </li></ul></ul><ul><ul><li>The inner portion is called the adrenal medulla. </li></ul></ul><ul><li>The hormones of the adrenal cortex are essential for life. </li></ul><ul><li>The hormones of the adrenal medulla are not. </li></ul>
  131. 149. <ul><li>The adrenal cortex produces glucocorticoids (such as cortisol ) that help the body control blood sugar, increase the burning of protein and fat, and respond to stressors like fever, major illness, and injury. </li></ul><ul><li>The mineralcorticoids (such as aldosterone) control blood volume and help to regulate blood pressure by acting on the kidneys to help them hold onto enough sodium and water. </li></ul><ul><li>The adrenal cortex also produces some sex hormones, which are important for some secondary sex characteristics in both men and women. </li></ul>
  132. 150. <ul><li>Two important disorders caused by problems with the adrenal cortex are: </li></ul><ul><ul><li>Cushing's syndrome (too much cortisol) </li></ul></ul><ul><ul><li>Addison's disease (too little cortisol). </li></ul></ul><ul><li>The adrenal medulla produces </li></ul><ul><ul><li>Epinephrine (adrenaline), which is secreted by nerve endings and increases the heart rate, opens airways to improve oxygen intake, and increases blood flow to muscles, usually when a person is scared, excited, or under stress </li></ul></ul><ul><ul><li>Norepinephrine also is made by the adrenal medulla, but this hormone is more related to maintaining normal activities as opposed to emergency reactions. </li></ul></ul><ul><ul><li>Too much norepinephrine can cause high blood pressure. </li></ul></ul>
  133. 151. CUSHING’S SYNDROME <ul><li>Result from excessive adrenocortical activity , from excessive administration of ACTH or from hyperplasia of the adrenal cortex </li></ul><ul><li>Caused by several mechanism – tumor of the pituitary glands or an ectopic malignancy that produces ACTH </li></ul><ul><li>The normal feedback mechanism that control the function of the adrenal cortex become ineffective, resulting in the oversecretion of glucocorticoids, androgens, and mineralocorticoid </li></ul><ul><li>Occurs 5X more often in women ages 20 to 40 years than in men </li></ul>
  134. 152. Clinical Manifestations <ul><li>Arrested growth, weight gain and obesity, musculoskeletal changes, and glucose intolerance </li></ul><ul><li>Classic features: central-type obesity, with fatty “buffalo hump” in the neck and supraclavicular areas, a heavy trunk, and relatively thin extremities, skin is thin, fragile, easily traumatized, with ecchymoses and striae </li></ul><ul><li>Weakness and lassitude </li></ul><ul><li>Retention of sodium and water </li></ul><ul><li>“ moon-faced” appearance, oiliness of skin and acne </li></ul><ul><li>Slow healing of minor cuts and bruises – susceptibility to infection </li></ul><ul><li>Hyperglycemia or overt diabetes </li></ul><ul><li>Virilization in females (due to excess androgens) </li></ul><ul><li>Mood and mental activity changes </li></ul><ul><li>Visual disturbances in case secondary to pituitaty tumor </li></ul>
  135. 153. Assessment and Diagnostic Methods <ul><li>Plasma and urinary cortisol measurements </li></ul><ul><li>24-hour urine collection for free cortisol level </li></ul><ul><li>Dexamethasone suppression test </li></ul><ul><li>CT scan or MRI or ultrasound may localized adrenal tissue and detect adrenal tumors </li></ul>
  136. 154. Medical Management <ul><li>Treatment is directed at the pituitary gland because most cases are due to pituitary tumors rather than tumors of the adrenal cortex ( transsphenoidal hypophysectomy ) </li></ul><ul><li>Surgical removal of tumor </li></ul><ul><li>Radiation of the pituitary gland </li></ul><ul><li>Adrenalectomy </li></ul><ul><li>Post-op replacement therapy with hyydrocortisone </li></ul><ul><li>Lifetime replacement of adenal cortex hormones for post-bilateral adrenalectomy </li></ul><ul><li>Adrenal enzyme inhibitors (metyrapone or mitotane) </li></ul><ul><li>Drug dose tapering if disease is due to exogenous corticosteroids </li></ul>
  137. 155. PANCREAS <ul><li>The pancreas is a large gland behind your stomach that helps the body to maintain healthy blood sugar (glucose) levels </li></ul><ul><li>The pancreas secretes insulin , a hormone that helps glucose move from the blood into the cells where it is used for energy </li></ul><ul><li>The pancreas also secrete

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