Makalah Modul G Kel 16

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HUMAN FUNCTION MODULE B SCENARIO PROBLEM BASED LEARNING
PRESENTED BY: GROUP 16th
FACULTY OF MEDICINE AIRLANGGA UNIVERSITY
HUMAN FUNCTION MODULE 16th Group
3rd SEMESTER 2010 HUMAN FUNCTION MODULE B SCENARIO PROBLEM BASED LEARNING
Scenario Creator Esti Hindariati, dr., Sp.JP(K)
16th Group Members

Leader : Dini Nur Aini Members: Muhammad Achdiar R Filipus Michael Yofrido Togar Erkasan Sitorus Christopher Njotokusgito Karin Dhia Fahmita Wirawan Indra P. Rizal Constantino Susilo Shaleh Muhammad D Agnes Candra Pradhita 010911152 010911154 010911155 010911157 010911158 010911169 010911170 010911171 010911172 010911163
Tutor : Prof. Dr. H Margono Al Imam Sjahrir Sp. S(K) dr. Sri Purwaningsih
CONTENTS
Cover ......................................................................................................................1 Scenario Creator....................................................................................................2 Group Members ....................................................................................................3 Contents .................................................................................................................4 Instructional Objectives .......................................................................................5 Chapter I : 1st Tutorial ..........................................................................................6 1.1 Scenario.............................................................................................................6 1.2 Main Problem ........................................................................................6 1.3 Keywords ..............................................................................................6 1.4 Additional Information..........................................................................7 1.5 Early Hypothesis ...................................................................................7 1.6 Early Mind Mapping .............................................................................8 1.7 Learning Issue 1.....................................................................................9 Chapter II : 2nd Tutorial .....................................................................................10 2.1 Methods and Steps to Find the Information.........................................10 2.2 The Answer of Learning Issue 1..........................................................10 2.3 Learning Issue II .................................................................................28 Chapter III : 3rd Tutorial ....................................................................................29 3.1 The Answer of Learning Issue 1I.........................................................29 3.2 Analysis ...............................................................................................47 3.3 Final Hypothesis .................................................................................50 3.4 Final Mind Mapping............................................................................51 3.5 Group Opinion.....................................................................................53 3.6 Obstacles..............................................................................................54 References ............................................................................................................55 EBL & Critical Appraisal ..................................................................................59 Appendix (Journal Appraisal) ...........................................................................66 Journal ................................................................................................................73
SEVENTH MODULE HUMAN FUNCTION MODULE PROBLEM BASED LEARNING

INSTRUCTIONAL OBJECTIVES
After completing this module, student in Third Semester of Medical Faculty of Airlangga University is expected to be able to explain health problem through the comprehension of normal physiology of body and its patophysiology.
CHAPTER I FIRST TUTORIAL

1.1 Scenario 1.2. Main Problem Mr. M (40 years old) comes with a complaint shortness of breath. Perceived breathlessness since 2 days before entering the hospital at the time patient is in the office
Shortness of breath since 2 days before entering the hospital 1.3 Key Words
1.3.1. 40 years old 1.3.2. Office 1.3.3. Male
1.4 Additional Information 1.4.1. Mr. M is a heavy smoker 1.4.2. Shortness of increasingly intense, palpitations, cold sweat, breath sounds 1.4.3. Coughing, white phlegm, and a few days experiencing abdominal pain 1.4.4. During one year Mr. M often complaining shortness of breath when doing physically activity 1.4.5. Blood pressure is 150/100 mmHg, pulse 100/minute regular, respiratory rate 28/minute, bodys temperature 37.3 C 1.4.6. Mr. M is a private employee 1.4.7. The Jugular Vein Pressure (JVP) is high 1.4.8. Thorax: Ictus ICS 5 is 2 cm lateral from left midclavicular 1.4.9. Pulmo: Wet ronchi in lungs 1.4.10. Abdomen: Hepar is 2 cm from articulatio costae
1.5 Early Hypothesis
Liver disorder Renal disorder Hyperthyroidism Anemia
1.6 Early Mind Mapping
FINANCIAL CONDITION
Mr. M Patophysiology Definition
Dyspnea
Symptoms Causes Kinds
Smoking
Pulmonary Disturbances
Heart disturbances
Others
Mechanism Wet Ronchi White Sputum
JVP
Hepatomegaly
1.7 Learning Issue 1
1.7.1. 1.7.2 1.7.3 1.7.4 1.7.5 1.7.6 1.7.7
How is the physiology of dyspnea? What are the symptoms and causes of shortness of breath? What is the bad effect of smoking? How is the location of organs in the human body? How is the normal condition of liver? What is heart failure? What is hypertension?
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CHAPTER II SECOND TUTORIAL

2.1 METHODS AND STEPS TO FIND THE INFORMATION To get the information we need, we use some sources, such as: 1. Text Books We used text books from library, our relatives books. We also bought some books to get more information. 2. Internet We got information from internet in the form of scientific journals and articles. By typing the keywords in the search engine, we got much information both in English and in Indonesian. Sources in English are cited directly into this report but sources in Indonesian are translated into English first.
2.2 THE ANSWERS OF LEARNING ISSUES I
2.2.1
How is the physiology of dyspnea?
Dyspnea is frequently associated with conditions in which respiratory drive is increased or the respiratory system is subject to a mechanical load. These conditions are characterized by a sensation of air hunger or increased effort or work of breathing. Some disorders are associated with the stimulation of irritant receptors in the lungs; patients with these disorders may describe their discomfort by phrases such as breath stops, chest tightness, and constriction. In addition to these qualitative factors, the intensity of dyspnea may be modified by the relative match between the respiratory motor command or signal originating in
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the central nervous system and afferent feedback arising from various receptors in the respiratory system (Manning, et al.1995). Dyspnea causation is multifactorial, but certain researches indicate that the combination of increased ventilatory demand and abnormal dynamic ventilator mechanics is likely important. For smokers who experience persistent and apparently disproportionate dyspnea (with reference to FEV1), cardiopulmonary exercise testing is useful in uncovering the severity and mechanisms of this symptom, on an individual basis (Ofir et al., 2008). 2.2.2 Symptoms: 1. At the start of symptoms similar to chronic bronchitis 2. Panting accompanied by a sound like a whistle 3. Chest shaped like a barrel, neck muscles stood out, patient to bend 4. Lips look blue 5. Weight loss due to decreased appetite 6. Chronic cough Causes: 1. Chronic bronchitis related to smoking 2. Sucking smoke / dust 3. Effect of age 2.2.3 What is the bad effect of smoking? What are the symptoms and causes of shortness of breath?
Smoking is one of the bad habits humans have done. It really becomes a serious matter across the world. Many countries have made some policies to manage cigarette use. Despite of that, smoking still becomes a threat for human
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being because many smokers cant afford to leave their smoking habits though they know what is the dangerous of smoking.
Smoking brings a great impact in our health. Many diseases occur because of smoking habit directly or indirectly. Not just the smokers, smoking can also hurt people around the smokers. The dangerous effect of smoking caused by the chemical matters spread whenever cigarette is burned. There are many kinds of chemical matters included in cigarette, but the most dangerous ones are nicotine and CO. CO gas produced by 1 cigarette is 3-6 % and CO gas can be inhaled by everyone, both the smokers and all people around them. The smokers only inhale one third of the CO. The side stream of the gas still outside. CO gas can bind to Hemoglobin (Hb) in red blood cells easier than the binding of Oxygen (O2) . So, whenever there is cigarettes smoke, not only the O2 rate reduced but also red blood cells are lack of oxygen because the Hb prefers CO to O2. Body cells compensate the lack of oxygen by spasm or lesser diameter of vessels. If the spasm goes too long, the vessels can be injured easily by the atherosclerosis. The narrowing of blood vessels can be happened everywhere inside our body, e.g. in the brain, heart, lungs, kidneys, on foot, in line hybrid, or in the placenta in pregnant women. (Kusmana,2009) Nicotine contained in cigarette smoke is between 0.5 - 3 ng, and all of it is absorbed, so in the blood fluid or plasma, the amount is between 40-50 ng / ml. The effect of nicotine causes the stimulation of hormones cathecolamine (adrenaline) which spur heart and blood pressure. The heart was not given the opportunity of rest and blood pressure will further elevate, resulting incidence of hypertension. Another effect is the stimulated platelets grouping (blood clotting cells), platelets will clot and eventually will clog the blood vessels that are narrow due to smoke containing CO derived from cigarettes. (Kusmana,2009) In smokers, cigarette smoke can damage blood vessel walls. Then the nicotine contained in cigarette smoke stimulates adrenal hormone which
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consequently would alter the metabolism of fat which will decrease HDL levels. Adrenaline also causes the stimulation of the heart and constricts blood vessels (spasm). Besides, the adrenaline will cause platelet grouping. So, all the narrowing process will occur. In the end, cigarette smoke that seems simple it can be a cause of coronary heart disease. (Kusmana,2009) Similarly, stress factors that greatly affect the adrenaline, causing the process of coronary heart disease occur as cigarette smoke. Someone who is stressed and then took refuge with smoking is actually the same as multiplying the coronary heart disease process in itself. (Kusmana,2009) About 90% of patients with arteritis obliterans at level III and IV will generally also suffer heart disease. Because the process of narrowing of the coronary arteries that supply heart muscle, the need of blood supply arise (ischemia). When you do physical activity or stress, the need of blood supply increase, giving feeling chest pain (angina pectoris). Severe narrowing or blockage of one or more coronary artery ended with the death of tissue (myocardial infarction, heart attack). Complications of myocardial infarction including cardiac arrhythmia (irregular heart rhythm) and / or the heart stops suddenly. Severe ischemia can cause the heart muscle loses its ability to pump (heart failure) that resulted in the collection of fluid in peripheral tissues (swelling / edema feet) as well as accumulation of fluid in the lungs (pulmonary edema). (Kusmana,2009) People who smoke more than 20 cigarettes per day had 6-fold risk of myocardial infarction exposed compared with nonsmokers. Cardiovascular disease is the leading cause of death in industrialized countries, which is about 30% of all deaths due to heart disease linked with the result of smoking. (Kusmana,2009) Respiratory tract consists of the membrane which overgrown with cilia (hairs) that send the breath-borne dust and then secreted with a cough reflex. Smoking paralyzes cilia function. In large airways, mucous cells enlarge (hyperthropy) and mucous glands multiply (hyperplasia) that resulted in narrowing of the airways. (Irawan,2009).
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Smoking habits eventually change the form of airway tissue and cleaning functions vanish, the tract swell and narrow or clog. Someone who shows symptoms of severe cough for at least 3 months in each year for 2 years, can be diagnosed as chronic bronchitis. It occurs in about half of smokers over 40 years. The weakened bronchial collapse so that air cant be distributed and alveoli (bubble breath) widened causing pulmonary emphysema. Complications from bronchitis and emphysema are the deaths that occurred 4-25 times higher in smokers compared with nonsmokers. (Kusmana,2009) Smokers life expectancy level is reduced in accordance with: (Kusmana,2009) 1. Number of years smoking 2. The number of cigarettes consumed per day 3. Tar and nicotine level 4. The depth of cigarettes inhalation 5. The range to the filter used
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2.2.4
How is the location of organs in the human body?
In the image on the left show the organs contained in the thoracic, which consists of heart, lung, esophagus, etc. On the right shows the organs in the abdomen where the kidney and spleen covered by the stomach and intestines.
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2.2.5
How is the normal condition of liver?
Liver is the largest gland in the human body. Liver in humans is located on the top of the abdominal cave, below the diaphragm, on both sides of the quadrant, which are mostly found on the right. The upper surface is in contact below the diaphragm, located below the surface of contact on the abdominal organs. Liver were fixed in close by intra-abdominal pressure and wrapped by peritoneum except in areas adjacent to the posterior-superior and inferior with v.cava direct contact with the diaphragm. Parts that are not covered by the peritoneum is called bare area. There is peritoneal reflection from the anterior abdominal wall, diaphragm and abdominal organs to the liver in the form of ligaments. Various kinds of the ligament: 1. Ligamentum falciformis: Connecting the liver into the wall ant. abdomen lies between the umbilicus and diaphragm. 2. Ligamentum teres hepatis: Round ligament: Represents the bottom of the Lig. falciformis; are remnants v.umbilicalis who had been settled. 3. Gastrohepatica ligament and ligamentum hepatoduodenalis: It is part of the lesser sac who range from minor gastric and duodenal curvatura beside liver. 4. Coronaria ligament Anterior: A reflection of peritoneum extending from the diaphragm to the liver. 5. Triangularis ligament : A fusion of the anterior and posterior coronaria ligament and the lateral edge of the left and right of the liver. Anatomically, the liver organ located on the right hipochondrium and epigastrium, and widen to the left hipochondrium. The liver is surrounded by the cavum thorax and even normal people can not be palpated. Surface of the right lobe interchangeable reached between the ribs 4 / 5 just below aerola mammary. Lig falciformis divides the liver topographically not anatomically become a large right lobe and left lobe.
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Hepatomegaly is swelling of the liver beyond its normal size. If both the liver and spleen are enlarged, it is called hepatosplenomegaly. (David C. Dugdale, 2009) The liver edge is normally palpable in children and thin adults and some patients may have a palpable right lobe of the liver.(Gurvinder Rull, 2009) The edge of the liver is normally thin and firm, and it cannot be felt with the finger tips below the edge of the ribs, except when you take a deep breath. It may be considered enlarged if a health care provider can feel it in this area.(David C. Dugdale, 2009) Hepatomegaly may be confirmed by palpation, percussion, or radiologic tests. It may be mistaken for displacement of the liver by the diaphragm, in a respiratory disorder; by an abdominal tumor; by a spinal deformity such as kyphosis; by the gallbladder; or by fecal material or a tumor in the colon. (Springhouse, 2007) The best way to assess size is by percussion - a normal sized liver can appear enlarged if displaced downwards by lung disorders. An enlarged liver expands down and across towards the left iliac fossa. To avoid missing a really
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big liver, always begin liver palpation in the LIF and work back towards the right upper quadrant. (Gurvinder Rull, 2009) This sign may stem from diverse pathophysiologic mechanisms, including dilated hepatic sinusoids (in heart failure), persistently high venous pressure leading to liver congestion (in chronic constrictive pericarditis), dysfunction and engorgement of hepatocytes (in hepatitis), fatty infiltration of parenchymal cells causing fibrous tissue (in cirrhosis), distention of liver cells with glycogen (in diabetes), and infiltration of amyloid (in amyloidosis).(Springhouse, 2007) Medical Causes The liver is involved in many bodily functions and is affected by a variety of conditions, many of which result in hepatomegaly. Causes of hepatomegaly may include: Alcohol use Alkohol menggunakan :

Congestive heart failure Hepatitis B Hereditary fructose intolerance Leukemia Niemann-Pick disease Reye syndrome Sclerosing cholangitis
* Glycogen storage disease * Hepatocellular carcinoma * Infectious mononucleosis * Neuroblastoma * Primary biliary cirrhosis * Sarcoidosis
Hemolytic-uremic syndrome (HUS) * Hepatitis A
Steatosis (fat in the liver from metabolic problems such as diabetes, obesity, and high triglycerides) Tumor metastases Congestive blood flow in the liver causes hepatomegaly. Suprahepatic
(David C. Dugdale, 2009) obstruction from congestive heart failure, restrictive pericardial disease, hepatic vein thrombosis (Budd-Chiari), or suprahepatic vascular webs are examples. Veno-occlusive disease causes hepatomegaly by obstructing intrahepatic blood flow. This problem occurs mainly in bone marrow transplant patients. (Ann Wolf and Joel E.Levine, 2000)
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Hepatomegaly Relationship With Cardiac Abnormalities Heart Failure Heart failure produces hepatomegaly along with jugular vein distention, cyanosis, nocturia, dependent edema of the legs and sacrum, steady weight gain, confusion and, possibly, nausea, vomiting, abdominal discomfort, and anorexia due to visceral edema. Ascites is a late sign. Massive right-sided heart failure may cause anasarca, oliguria, severe weakness, and anxiety. If left-sided heart failure precedes right-sided heart failure, the patient exhibits dyspnea, orthopnea, paroxysmal nocturnal dyspnea, tachypnea, arrhythmias, tachycardia, and fatigue. (Springhouse, 2007) Incidence and pathophysiology Abnormal liver enzymes and liver function in congestive, right sided heart failure has long been recognized (13,17) and occurs quite frequently in acute and chronic failure This is thought to be due to direct centrizonal compression (18). It is less recognized that left-sided failure also leads to impairment of hepatic function due to a low-flow state (1-3,6,8). The mechanism is due to the fact that the liver gets a fixed amount of cardiac output (13); the decrease in flow is compensated for by an increase in oxygen extraction leading to anoxic necrosis in the centrizonal area. This is supported by a comparison of liver biopsies with and without centrizonal necrosis in patients with CHF; necrosis was only seen when also either marked venous congestion and/or hypoxemia existed (6). Of note is that even minor impairments of left ventricular function can lead to marked liver enzyme abnormalities (2,15); similarly, in known CHF, an episode of hypotension can be elicited in only 45 % (6). In chronic congestion, LFT's are abnormal dependent on the reduction in CO 1. Manifestations: Range from laboratory abnormalities over a presentation undistinguishable from acute hepatitis to fulminant failure (3,14). The latter
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can lag behind the acute episode by 1 - 3 days (3); the latter authors found in their review of the literature a mortality of 69 % (11/16). Birgens et al. claim that hypotension of > 24 h is required for shock liver to develop (1); this is clearly not true - in up to 50 % of patients with hypoxic hepatitis no shock is observed (19). Hepatomegaly, often tender, in 95 - 99 % in right-sided failure, splenomegaly in 12 - 25 %; ascites 7 - 64 % (4). In CT mottled appearance of contrast, similar to Budd-Chiari (12). 2. Laboratory: In right-sided heart failure hyperbilirubinemia rarely exceeds 50 mmoles/l and the transaminases are moderately elevated; occasionally isolated elevation of cholestatic enzymes. Vitamin-K refractory hypoprothrombinemia. In left-sided failure much more marked elevation of serum bilirubin (3) and of transaminases (3,5,9); typically, transaminase values tend to return very rapidly towards normal when the CHF is treated (5,14). According to the histologic lesion, ABT is reversibly decreased during the acute episode (7,16). 3. Pathology: In right sided heart failure central necrosis, condensation of reticulin stroma. If of longer duration reverse lobulation and "cirrhose cardiaque" (4). In left sided failure disappearance of centrizonal hepatocytes with replacement by RBC's. No fibrosis (1). In both conditions, notable absence of inflammatory cells. In an autopsy review, midzonal necrosis was found to be typical of congestive failure, in particular when associated with episodes of hypotension occurring in 1.8 % of all autopsies in in 8 % of patients with centrizonal necrosis (3). In a review of 140 post-mortem specimens (figure 3),cardiac fibrosis was quite frequent but frank cirrhosis only observed once (11). 2.2.6 What is heart failure?
Heart failure or heart trouble is the clinical syndrome (a collection of signs and symptoms) characterized by shortness of breath (dispneu) and fatigue (fatigue), either at rest or during activity) caused by structural abnormalities or
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cardiac function, which impairs the ability of the ventricles (heart chambers) to fill and bleed into the circulation. Congestive heart failure is a clinical syndrome characterized by abnormalities of left ventricular function and abnormal neurohormonal regulation, accompanied by intolerance of physical working capacity of fluid retention, and shortened lifetime. The cause of reversible heart failure include: arrhythmia (eg atrial fibrillation), pulmonary embolism (PE), malignant or accelerated hypertension, thyroid disease (hypothyroidism or hyperthyroidism), valvular heart disease, unstable angina, high output failure, failure kidney problems caused by treatment (medication-induced problems), intake (intake), high salt, and severe anemia. According to Cowie MR, Dar O (2008), the causes of heart failure can be classified into six main categories: 1. The failure associated with myocardial abnormalities, can be caused by loss of myocytes (myocardial infarction), uncoordinated contractions (left bundle branch block), reduced contractility (cardiomyopathy). 2. The failure associated with the overload (hypertension). 3. The failure associated with valve abnormalities. 4. Failure is caused by abnormalities in heart rhythm (tachycardia). 5. Failure is caused by abnormalities perikard or effusion (tamponade). 6. Abnormalities Congenital heart. Predisposition factor and factor triggers Predisposition Factor Which is a predisposing factor to heart failure include: hypertension, coronary artery disease, cardiomyopathy, enyakit blood vessels, congenital heart disease, mitral stenosis, and pericardial disease. Factor Triggers Which is a trigger of heart failure include: increased intake (intake), salt, noncompliance to undergo anti congestive heart failure, acute myocardial infak, hypertension, acute arrhythmia, infection, fever, pulmonary embolism, anemia, thyrotoxicosis, pregnancy, and infective endocarditis.
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Pathophysiology Impaired contractility of left ventricular myocardium is decreased in heart failure would disrupt the ability of ventricular emptying, so that the residual ventricular volume is increased due to reduced stroke volume by left ventricular injected. With the increase in EDV (End Diastolic Volume), then there is also increased LVEDP (Left ventricle End Diastolic Pressure), which is the degree of improvement depends on the flexibility of the ventricles. Therefore, during diastole the atria and ventricles are directly related, then the increase in LVEDP will increase LAP (Left Atrium Pressure), so that the capillary pressure and pulmonary veins will also increase. If the hydrostatic pressure in the pulmonary capillary pressure exceeds onkotik vascular, then it will happen transudation of fluid into the interstitial and when the liquid seeps into the alveoli, pulmonary edema occurs. Improvement of chronic pulmonary venous pressure may increase pulmonary artery pressure called pulmonary hypertension, pulmonary hypertension, which increases the resistance to right ventricular ejection. If the process that occurs in left heart also occur in right heart, systemic congestion will eventually happen and edema. According to Laksono S (2009), there are several pathophysiological mechanisms of heart failure: 1. Neurohormonal mechanisms Arrangements (sympathetic involving nervous neurohormonal system activation adrenergic will nervous system of increase levels
norepinephrine), renin-angiotensin system, oxidative stress (elevated levels of ROS / reactive oxygen species), arginine vasopressin (increasing), natriuretic peptides, endothelin, neuropeptide Y, urotensin II , nitric oxide, bradykinin, AM (increasing), and apelin (downhill). 2. Remodeling of left ventricle Progressive left ventricular remodeling is directly related to the deteriorating ability of the ventricles in the future. 3. Biologic changes in cardiac myocytes
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Hypertrophy of cardiac myocytes occurs, contraction-excitation of complex changes, changes in infarction, necrosis, apoptosis, autofagi. 4. Changes in left ventricular structure This change makes the heart swell, changing the heart becomes more spherical shape lead to ventricular require more energy, resulting in increased left ventricular dilatation, reduced cardiac output, and increased hemodynamic overloading. Clinical Manifestation Clinical manifestations of right heart failure (decompensatio dextra), among others: JVP increases, dilated right heart border (there is RVH and epigastric pulsation), liver enlargement (hepatomegaly), enlarged spleen (splenomegaly), fluid in the abdominal cavity (ascites), swelling (edema ) in the limbs. While the clinical manifestations of left heart failure (decompensatio the left) are: shortness of breath (dispneu, orthopneu, paroxismal nocturnal dispneu), dilated left heart border (there LVH), Cheyne Stokes breathing, bluish (cyanosis), Right Bundle Branch (RBB), and S3 sounds (Gallop). Enforcement Diagnosis Diagnosis of heart failure based on history, physical examination, ECG, thorax images, ekokardigrafi-doppler and catheterization. Functional Classification of The New York Heart Association (NYHA), generally used to express the relationship between awitan symptoms and degrees of physical exercise: Class I : Class II : Class III: Class IV: no symptoms on daily activities, symptoms will occur in more severe activities of daily activities. symptoms arise in their daily activities. symptoms occur at lighter activity of daily activities. symptoms occur at rest.
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Framingham criteria can also be used to diagnose congestive heart failure. Major criteria: 1. 2. 3. 4. 5. 6. 7. 8. 1. 2. 3. 4. 5. 6. 7. Paroxismal Nocturnal Dispneu Distention of neck veins Ronkhi lung Kardiomegali Acute pulmonary edema Gallop S3 Jugular venous pressure elevation Reflux hepatojugular Extremity edema Cough at night Dispneu de effort Hepatomegaly Pleural effusion Tachycardia Decrease in vital capacity a third of the normal
Minor criteria:
Criteria for major or minor Weight loss> 4.5 kg in 5 days after therapy Diagnosis of 2 major criteria or 1 major criteria and 1 minor criteria must exist at the same time. 2.2.7 What is hypertension?
Sheps (1999) said that: when the complex system that regulates the blood pressure doesnt work as its supposed to, too much pressure can develop within the arteries. Increased pressure n your arteries that continues on a persistent basis is called high blood pressure. The medical term for the condition is hypertension, meaning high tension in your arteries. Hypertension doesnt mean nervous tension, as many people
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often believe. You can be a calm, relaxed person and still have high blood pressure. The blood pressure is considered high if the systolic pressure is consistently 140 mm Hg or higher, the diastolic pressure consistently 90 mm Hg or higher, or both. Symptoms High blood pressure is often called the silent killer because it doesnt produce any signs or symptoms to warn you that you have a problem. People often think that headaches, dizziness or nosebleeds are common warning signs of high blood pressure. Its true that a few people with early-stage high blood pressure have a dull ache in the back of their head when they wake in the morning. Or, perhaps they have a few more nosebleeds than normal. But generally, most people dont experience any signs or symptoms. Risk factors Certain genetic traits or lifestyle habits play an important role in the development of essential high blood pressure. Generally, the more of these risk factors you have, the greater the odds that youll have high blood pressure during your lifetime. Most risk factors we can control, others we cant. Unmodifiable risk factor There are four major risk factors for high blood pressure that we cant control Race. High blood pressure occurs almost two times more frequently in blacks of African-American descent than in whites. The highest rates of high blood pressure in the United States are among blacks living in the southeastern states. Age. Your risk for high blood pressure increases with your age. Although high blood pressure can occur at any age, its most often detected in people age 35 or older. Among Americans age 65 or older, more than half have high blood pressure
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Family history. High blood pressure tends to run in families. If one of your parents has high blood pressure you have about a 25 percent chance of developing it during the lifetime. If both of our mother and father have high blood pressure, we have a 60 percent chance of acquiring the disease. Sex. Among young and middle-aged adults, men are more likely to have high blood pressure than women. Later on, the reverse is true. After about age 50, when most women are beyond menopause, high blood pressure becomes more common in women than in men. Modeifiable risk factor There are risk factors for high blood pressure that we can control Obesity. Being overweight increases the risk for development of high blood pressure for several reasons. The more body mass we have, the more blood we need to supply oxygen and nutrients to our tissues. That means the volume of blood being circulated through our blood vessels is increased, creating extra force on our artery walls. Excess weight also can increase our heart heart rate and the level of insulin in our blood. Increased insulin causes our body to retain sodium and water. In addition, some people who are overweight fllow a diet thats too high in fat, especially saturated and trans fats. These fats promote the accumulation of fatty deposits (plaque) in our arteries, causing narrowing of our arteries. Our diet contains too much fat if more than 30 percent of our total daily calories come from fat Inactivity. Lack of physical activity increases our risk for high blood pressure by increasing our risk for becoming overweight. People who are inactive also tend to have higher heart rates and their heart muscle has to work harder with each contractions. The harder and more often our heart has to pump, the greater the force being exerted on our arteries. Tobacco use. The chemicals in tobacco can damage the lining of our artery walls, making them more prone to the accumulation of plaque.
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Nicotine in tobacco also makes our heart work harder by temporarily constricting our blood vessels and increasing our heart rate and blood pressure. These effects occur because of increased hormone production during tobacco use, including increased levels of the hormone epinephrine (adrenaline). In addition, carbon monoxide in cigarette smoke replaces oxygen in our blood. This can increase blood pressure by forcing our hart to work harder to supply adequate oxygen to our bodys organs and tissues. Sodium sensitivity. Our body needs a certain amount of the mineral sodium to maintain the chemistry that occurs within our cells. A common source of sodium is table salt (sodium chloride), which is composed of about 40 percent sodum and 60 percent chloride. However, some peoples bodies are more sensitive to the presence of sodium in their blood than others. People who are sodium-sensitives retain sodium more easily, leading to fluid retention and increased blood pressure. If were among this group, excessive sodium in our diet can increases our chances for having high blood pressure. Low potassium. Potassium is a mineral that helps balance the amount of sodium in cell fluids. It gets rid of excess sodium in our cells by way of our kidneys, which filter out the sodium to be excreted in our urine. If our diet doesnt include enough potassium, or our body isnt able to retain a proper amount, too much sodium can accumulate, tincreasing our risk for development of high blood pressure. Excessive alcohol. People who have three or more drinks a day have a greater incidence of high blood pressure than people who dont drink alcohol or who have less than three drinks daily. Excessive alcohol use contributes to about 8 percent of all cases of high blood pressure Stress. Stress doesnt cause persistent high blood pressure. But high levels of stress can lead to a temporary, but dramatic, increase in blood blood pressure. If these temporary episodes occur often enough, over time they
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can damage our blood vessels, heart and kidneys in the same manner as persistent high blood pressure Stress also can promote high blood pressure by causing us to develop unhealthful habits known to increase our risk for the disease. Some people bothered by stress turn to smoking, alcohol, or food (usually fatty or salty foods) to relieve their stress.
2.3 LEARNING ISSUES II 2.3.1 2.3.2 2.3.3 2.3.4 2.3.5 2.3.6 2.3.7 What are indicated by Jugular Venous Pressure? What is a wet rhonchi, and what is the indication of rhonchi? What causes hypoxia? What does white-phlegm-cough indicate? What causes it? What is the definition of Chronic Obstructive Pulmonary Disease (COPD)? What is the correlation between abdominal pain and dyspnea? What are liver disorders? explain it?
2.3.8 There are many diseases that have dyspnea symptom, mention and
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CHAPTER III THIRD TUTORIAL

3.1 THE ANSWERS OF LEARNING ISSUES II
3.1.1 What are indicated by jugular venous pressure? The jugular venous pressure (JVP) can yield valuable information about cardiac function (especially of the right ventricle) and pulmonary function and is an important component of the assessment of volume status. The JVP is most commonly elevated with a raised venous pressure due to cardiac failure or hypervolaemia. Causes of a raised JVP: 1. Heart failure 2. Constrictive pericarditis (JVP increases on inspiration called Kussmaul's sign) 3. Cardiac tamponade 4. Fluid overload e.g. renal disease 5. Superior vena cava obstruction (no pulsation) Kussmauls Sign This is a rise in the JVP seen with inspiration. It is the opposite of what is seen in normal people and this reflects the inability of the heart to compensate for a modest increase in venous return. This sign is classically seen in constrictive pericarditis in association with a raised JVP. This condition was originally described in tuberculous pericarditis and is rarely seen. Kussmauls sign is also seen in right ventricular infarction, right heart failure, tricuspid stenosis, and restrictive cardiomyopathy. It is not seen in acute cardiac tamponade- although it may be seen if tamponade occurs with a degree of constricive pericardiditis.
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3.1.2 What is a wet rhonchi, and what is the indication of rhonchi? Rhonchi are additional sound generated by the lung that is not audible at normal lung, this sound arising from the existence of secret in the airways, narrowing of the airway lumen and the opening of acinus / alveolar collapse earlier. There are 2 kinds of rhonchi that is wet with sound disjointed and dry rhonchi with uninterrupted sound. Rhonchi wet rough like the sound of a large air bubble that burst, respiratory sounds great when supplied with various secret. Rhonchi wet is like the sound of tiny bubbles that burst, heard when the secret in the small and medium breathing airway, usually in bronchiectasis and bronchopneumonia. Fine moist rhonchi not have the nature bubbles again, sounding like the friction of hair, usually in early pneumonia. 3.1.3 What causes hypoxia?
The following is a descriptive classification of the causes of hypoxia: 1. Inadequate oxygenation of the blood in the lungs because of extrinsic reasons a. Deficiency of oxygen in the atmosphere b. Hypoventilation (neuromuscular disorders) 2. Pulmonary disease a. Hypoventilation caused by increased airway resistance or decreased pulmonary compliance b. Abnormal alveolar ventilation-perfusion ratio (including either increased physiologic dead space or increased physiologic shunt) c. Diminished respiratory membrane diffusion 3. Venous-to-arterial shunts (right-to-left cardiac shunts) 4. Inadequate oxygen transport to the tissues by the blood a. Anemia or abnormal hemoglobin b. General circulatory deficiency
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c. Localized circulatory deficiency (peripheral, cerebral, coronary vessels) d. Tissue edema 5. Inadequate tissue capability of using oxygen a. Poisoning of cellular oxidation enzymes b. Diminished cellular metabolic capacity for using oxygen, because of toxicity, vitamin deficiency, or other factors This classification of the types of hypoxia is mainly self-evident from the discussions earlier in the chapter. Only one of the types of hypoxia in the classification needs further elaboration: this is the hypoxia caused by inadequate capability of the bodys tissue cells to use oxygen (Guyton, 2006). Inadequate Tissue Capability to Use Oxygen The classic cause of inability of the tissues to use oxygen is cyanide poisoning, in which the action of the enzyme cytochrome oxidase is completely blocked by the cyanideto such an extent that the tissues simply cannot use oxygen even when plenty is available.Also, deficiencies of some of the tissue cellular oxidative enzymes or of other elements in the tissue oxidative system can lead to this type of hypoxia. A special example occurs in the disease beriberi, in which several important steps in tissue utilization of oxygen and formation of carbon dioxide are compromised because of vitamin B deficiency (Guyton, 2006). Effects of Hypoxia on the Body Hypoxia, if severe enough, can cause death of cells throughout the body, but in less severe degrees it causes principally (1) depressed mental activity, sometimes culminating in coma, and (2) reduced work capacity of the muscles (Guyton, 2006). Oxygen Therapy in Different Types of Hypoxia Oxygen can be administered by (1) placing the patients head in a tent that contains air fortified with oxygen, (2) allowing the patient to breathe either pure oxygen or high concentrations of oxygen from a mask, or (3) administering
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oxygen through an intranasal tube. Recalling the basic physiologic principles of the different types of hypoxia, one can readily decide when oxygen therapy will be of value and, if so, how valuable. In atmospheric hypoxia, oxygen therapy can completely correct the depressed oxygen level in the inspired gases and, therefore, provide 100 per cent effective therapy. In hypoventilation hypoxia, a person breathing 100 per cent oxygen can move five times as much oxygen into the alveoli with each breath as when breathing normal air. Therefore, here again oxygen therapy can be extremely beneficial. (However, this provides no benefit for the excess blood carbon dioxide also caused by the hypoventilation.). In hypoxia caused by impaired alveolar membrane diffusion, essentially the same result occurs as in hypoventilation hypoxia, because oxygen therapy can increase the Po2 in the lung alveoli from the normal value of about 100 mm Hg to as high as 600 mm Hg. This raises the oxygen pressure gradient for diffusion of oxygen from the alveoli to the blood from the normal value of 60 mm Hg to as high as 560 mm Hg, an increase of more than 800 per cent.This highly beneficial effect of oxygen therapy in diffusion hypoxia is demonstrated in Figure 428, which shows that the pulmonary blood in this patient with pulmonary edema picks up oxygen three to four times as rapidly as would occur with no therapy. In hypoxia caused by anemia, abnormal hemoglobin transport of oxygen, circulatory deficiency, or physiologic shunt, oxygen therapy is of much less value because normal oxygen is already available in the alveoli. The problem instead is that one or more of the mechanisms for transporting oxygen from the lungs to the tissues is deficient. Even so, a small amount of extra oxygen, between 7 and 30 per cent, can be transported in the dissolved state in the blood when alveolar oxygen is increased to maximum even though the amount transported by the hemoglobin is hardly altered.This small amount of extra oxygen may be the difference between life and death. In the different types of hypoxia caused by inadequate tissue use of oxygen, there is abnormality neither of oxygen pickup by the lungs nor of transport to the tissues. Instead, the tissue metabolic enzyme system is simply incapable of using the oxygen that is delivered. Therefore, oxygen therapy is of hardly any measurable benefit (Guyton, 2006).
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Cyanosis The cyanosis and its term means cause is
blueness of the skin, excessive amounts of deoxygenated hemoglobin in the skin blood especially capillaries. deoxygenated hemoglobin has an intense dark blue-purple color that is transmitted through the skin. In general, definite cyanosis appears whenever the arterial blood contains more than 5 grams of deoxygenated hemoglobin in each 100 milliliters of blood.A person with anemia almost never becomes cyanotic because there is not enough hemoglobin for 5 grams to be deoxygenated in 100 milliliters of arterial blood. Conversely, in a person with excess red blood cells, as occurs in polycythemia vera, the great excess of available hemoglobin that can become deoxygenated leads frequently to cyanosis, even under otherwise normal conditions (Guyton, 2006). 3.1.4 What does white-phlegm-cough indicate? What causes it? in vessels, the This
Coughing is a protective mechanism of the respiratory tract while trying to remove foreign objects or excessive mucus production. Coughing up phlegm mucus that clog the respiratory tract infection. If the infection causes a cough, it will be reflected on the color of mucus which vomited. Here, white sputum is not showed that patients had no respiratory bacterial infection. This occurs because
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the smoke can be deadly to cilia movement, so the mucous will accumulate, and expelled through coughing. 3.1.5 What is the definition of Chronic Obstructive Pulmonary Disease (COPD)? Chronic Obstructive Pulmonary Disease (COPD)
COPD is a chronic lung disease characterized by airflow resistance in the airways progressive nature nonreversible or partially reversible. COPD comprises chronic bronchitis and emphysema or a combination of both. (Departemen Kesehatan RI, 2007) - Chronic bronchitis Abnormalities of the airways characterized by chronic cough with phlegm at least 3 months of the year, at least two consecutive years - also, not caused by other diseases. - Emphysema An anatomical abnormalities of the lung that is characterized by a widening of the air cavity of the distal terminal bronchioles, accompanied by damage to the walls of the alveoli. Risk factors: 1. Smoking habits 2. History of exposure to air pollution in the environment and the workplace 3. Hyperactivity of the bronchus 4. History of recurrent lower respiratory tract infections 5. Deficiency antitrypsin alpha - 1, generally rare in Indonesia In chronic bronchitis there is enlargement of bronchial mucous glands, goblet cell metaplasia, inflammation, respiratory smooth muscle hypertrophy and distortion due to fibrosis. Emphysema is characterized by a widening of the air
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cavity of the distal terminal bronchioles, accompanied by damage to the walls of the alveoli. In the science of anatomy, divided into three types Emphysema: - Sentro acinar emphysema, starting from the respiratory bronchioles and extends to the periphery, especially on the top of the lung is often a result of a long smoking habit - Emphysema acinar pan (pan lobuler), equally involving all the alveoli, particularly at the lower lung - Distal acinar emphysema (the septal), more attacking in the distal airways, alveolar ducts and saccus. This process is localized at or near the pleural septa Airway obstruction in COPD is irreversible and occurs because of structural changes in small airways, which are: inflammation, fibrosis, goblet cell metaplation, and smooth muscle hypertrophy are major cause airway obstruction. Clinical features: a. Anamnesis - History of smoking or ex-smokers with or without symptoms of respiratory problems - History of significant exposure to irritant substances in the workplace - History emphysema disease on families - There is a predisposing factor in the infant / child, eg low birth weight (LBW), recurrent respiratory infections, environmental tobacco smoke and air pollution - Recurrent cough with or without sputum - Shortness with or without wheezing sound b. Physical examination Early COPD is generally not found any abnormality Inspection - Pursed - lips breathing (mouth closed half-forward) - Barrel chest (diameter Antero - posterior and transverse comparable) - The use of auxiliary breathing muscles
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- Muscle hypertrophy respirator - Widening between the ribs - When right heart failure has occurred looks pulse jugular vein in the neck and leg edema - Appearances pink puffer or a blue bloater Palpation In emphysema fremitus weakened, broke ribs widened Percussion In hipersonor emphysema and heart boundaries shrinking, where the lower diaphragm, liver driven down Auscultation - Normal vesicular breath sounds, or weakened - There were rhonchi and / or wheezing during normal breathing or forced expiratory - Expiratory lengthwise - The sound of distant heart sounds Pink puffer The picture is typical of emphysema, patients with thin, reddish skin and respiratory pursed lips breathing Blue bloater Typical picture of chronic bronchitis, cyanosis obese patients, there is edema of the legs and rhonchi wet in the basal lung, central and peripheral cyanosis Pursed - lips breathing It is the attitude of someone who is breathing with the mouth that extends and expiratory. This attitude occurs as the body's mechanism for the release of
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CO2 retention which occurs as the bodys mechanism for the release of CO2 retention which occurs in chronic respiratory failure. 3.1.6 What is the correlation between abdominal pain and dyspnea?
Abdominal pain is pain that is felt in the abdomen. The abdomen is an anatomical area that is bounded by the lower margin of the ribs and diaphragm above, the pelvic bone (pubic ramus) below, and the flanks on each side. (U.S. National Library of Medicine, 2010) Although abdominal pain can arise from the tissues of the abdominal wall that surround the abdominal cavity (such as the skin and abdominal wall muscles), the term abdominal pain generally is used to describe pain originating from organs within the abdominal cavity. Organs of the abdomen include the stomach, small intestine, colon, liver, gallbladder, spleen, and pancreas. Dyspnea is a sign of serious disease of the airway, lungs, or heart. The onset of dyspnea should not be ignored but is essential to seek medical attention. The word dyspnea comes the Greek "dys-", difficulty + "pnoia", breathing = difficulty breathing. Dyspnea is the American spelling and dyspnoea is the British (mis)spelling. (MedicineNet, 2010) Evaluation of the complaint is complicated by the fact that in many circumstances shortness of breath is a normal consequence of exertion. Furthermore, perception of shortness of breath varies considerably among individuals at the same level of fitness and work and even in the same individual performing comparable work at different times. In disease states, perception of dyspnea can vary greatly among individuals. Consequently, assessment of the subjective sensation of dyspnea must balance the concepts of physiologic work and ventilatory demand with the individuals perception of breathlessness. (The Snowdrift Pulmonary Foundation, 2000) Abdominal pain can arise from any of the structures within the abdomen or the abdominal wall. In addition, pain messages originating in the chest, back, or pelvis can sometimes be perceived as coming from the abdomen. For example, patients with heart attacks, pneumonia, or myocardial infaction sometimes
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complain of upper abdominal pain rather than chest pain. There are many reasons why you may have pain in your abdomen. People often worry about appendicitis, gallstones, ulcers, infections and pregnancy problems. Doctors also worry about these, as well as many other conditions. Abdominal pain may not come from the abdomen. Some surprising causes include heart attacks and pneumonias, conditions in the pelvis or groin, some skin rashes like shingles, and problems with stomach muscles like a strain. (State Government of Victoria, 2010) 3.1.7 What are liver disorders?
Liver disorder applies to many diseases and disorders that cause the liver to function improperly or cease functioning. Abnormal results of liver function tests often suggest liver disease. (U.S. National Library of Medicine, 2010) Several kinds of liver disorders: Wilson's Disease Wilson's disease is a rare inherited disorder. If both parents carry an abnormal gene for Wilson's disease, there is a 25% chance in each pregnancy that the child will have the disorder. Wilson's disease causes the body to take in and keep too much copper. The copper deposits in the liver, brain, kidneys, and the eyes. The deposits of copper cause tissue damage, death of the tissues, and scarring, which causes the affected organs to stop working correctly. Symptoms * Abnormal posture of arms and legs * Difficulty walking (ataxia) * Loss of IQ points (occasionally) * Splenomegaly * Difficulty moving arms and legs, stiffness * Emotional or behavioral changes * Vomiting blood * Tremors of the arms or hands * Enlargement of the abdomen (abdominal distention) *Uncontrollable, slow or decreased movement and expressions of the face
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* Yellow skin (jaundice) or yellow color of the white of the eye (icterus)
Biliary Atresia Biliary atresia is a blockage in the tubes (ducts) that carry a liquid called bile from the liver to the gallbladder. The condition is congenital, which means it is present from birth. Symptoms * Jaundice, dark urine * Floating stools * Pale or clay-colored stools * Slow or no weight gain Cirrhosis Cirrhosis is scarring of the liver and poor liver function as a result of chronic liver disease. Symptoms * Abdominal indigestion or pain men * Nausea and vomiting * Pale or clay-colored stools * Nosebleeds or bleeding gums * Small, red spider-like blood vessels on the skin * Swelling or fluid buildup of the legs (edema) and in the abdomen (ascites) * Vomiting blood or blood in stools * Weakness * Weight loss * Yellow color in the skin, mucus membranes, or eyes (jaundice) Hepatitis A Hepatitis A is inflammation (irritation and swelling) of the liver caused by the hepatitis A virus. * Confusion or problems thinking * Impotence, loss of interest in sex, and breast development (gynecomastia) in * Enlarged spleen * Foul-smelling stools * Slow growth
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Symptoms * Dark urine * Itching * Low-grade fever * Pale or clay-colored stools Hepatitis B Hepatitis B is inflammation (irritation and swelling) of the liver due to the hepatitis B virus (HBV). Symptoms * Appetite loss * Low-grade fever * Nausea and vomiting * Fatigue * Muscle and joint aches * Yellow skin and dark urine due to jaundice * Fatigue * Loss of appetite * Nausea and vomiting * Yellow skin (jaundice)
People with chronic hepatitis may have no symptoms, even though gradual liver damage may be occurring. They may have some or all of the symptoms of acute hepatitis. Hepatitis C Hepatitis C is a viral disease that leads to swelling (inflammation) of the liver. Symptoms * Abdominal pain (right upper abdomen) * Bleeding varices (dilated veins in the esophagus) * Fatigue * Jaundice * Low-grade fever * Pale or clay-colored stools * Ascites * Dark urine * Generalized itching * Loss of appetite * Nausea * Vomiting
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Hemochromatosis Hemochromatosis is a disorder that results in too much iron being absorbed from the gastrointestinal tract. Symptoms * Abdominal pain * Joint pain * Loss of body hair * Weight loss * Fatigue * Lack of energy * Loss of sexual desire * Weakness * Generalized darkening of skin color (often referred to as bronzing)
A physical examination shows liver and spleen swelling, and skin color changes. Blood tests may help make the diagnosis. Tests may include: * Serum ferritin (high) Other tests may include: * Blood sugar (glucose) level * Alpha fetoprotein * Echocardiogram to examine the heart's function * Electrocardiogram (ECG) to look at the electrical activity of the heart * Imaging tests such as CT scans, MRI, and ultrasound * Liver function tests The condition may be confirmed and treated with a liver biopsy or phlebotomy, a procedure that removes blood to lower the amount of iron in the body. Autoimmune hepatitis Autoimmune hepatitis is inflammation of the liver that occurs when immune cells mistake the liver's normal cells for harmful invaders and attack them. Symptoms * Abdominal distention * Fatigue * Dark urine * Generalized itching * Serum iron (high) * Percentage of transferrin saturation (high)
* General discomfort, uneasiness, or ill feeling (malaise)
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* Loss of appetite * Pale or clay-colored stools
* Nausea and vomiting
Other symptoms that may occur with this disease include absence of menstruation (amenorrhea). Primary biliary cirrhosis Primary biliary cirrhosis is irritation and swelling (inflammation) of the bile ducts of the liver, which blocks the flow of bile. This obstruction damages liver cells and leads to scarring called cirrhosis. Symptoms More than half of patients have no symptoms at the time of diagnosis. Symptoms usually come on gradually and may include: * Abdominal pain * Fatigue * Fatty stools * Jaundice Hepatocellular carcinoma Hepatocellular carcinoma is cancer of the liver. Symptoms * Abdominal pain or tenderness, especially in the upper-right part * Easy bruising or bleeding * Yellow skin or eyes (jaundice) Physical examination may show an enlarged, tender liver. Tests include: * Abdominal CT scan * Liver biopsy * Liver scan whether tumors are developing. * Abdominal ultrasound * Liver enzymes (liver function tests) * Serum alpha fetoprotein * Enlarged abdomen * Enlarged liver * Fatty deposits under the skin * Itching * Soft yellow spots on the eyelid
Some high-risk patients may get periodic blood tests and ultrasounds to see
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Reye syndrome Reye syndrome is sudden (acute) brain damage (encephalopathy) and liver function problems of unknown cause. The syndrome has occurred with the use of aspirin to treat chickenpox or the flu in children. However, it has become very uncommon since aspirin is no longer recommended for routine use in children. Reye syndrome often begins with vomiting, which lasts for many hours. The vomiting is quickly followed by irritable and aggressive behavior. As the condition gets worse, the child may be unable to stay awake and alert. Other symptoms of Reye syndrome: * Confusion * Loss of consciousness or coma * Nausea and vomiting * Lethargy * Mental changes * Seizures
* Unusual placement of arms and legs (decerebrate posture) -- the arms are extended straight and turned toward the body, the legs are held straight, and the toes are pointed downward Other symptoms that can occur with this disorder include: * Double vision * Speech difficulties * Hearing loss * Weakness in the arms or legs * Muscle function loss or paralysis of the arms or legs
Comparing the learning issue data we have and the patients additional data in the scenario, we conclude that Mr. M are not experiencing liver disorders.
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3.1.8
There are many diseases that have dyspnea symptom, mention and explain it?
There are anamneses characteristic of dyspnea patient that are caused by spesific disease (Suharto,2010) Lung Disease 1. Asthma In anamnesis found three main symptoms: tightness, wheezing (breath sounds) and cough. In the family history found there were other family members who suffer from asthma. Recurrence of dyspnea is usually due to physical exercise, infection or stress. 2. Chronic bronchitis Found a history of cough with sputum for at least 3 months in 2 consecutive years, without any other disease. Wheezing and shortness can also be occurred because of inhaling irritant material or acute respiratory tract infection. Usually found smoking history. 3. Emphysema Patients generally have asthma, chronic bronchitis, or smoking history. Patients usually complain of dyspnea when running activities. 4. Pneumonia The patient complained of cough, chills and fever.Sputum are purulent and found chest pain. 5. Pneumothorax Dyspnea occurred suddenly, preceded by chest pain, after activities that cause increased pressure intratoraks. For example: cough, straining. Patients appear cyanotic. Chest pain, when encountered usually spread to the neck. 6. Pulmonary embolism Occur suddenly, usually patients lying in bed for a long time in hospital, found a history of anti-pregnant drug use and found haemoptysis.
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Heart Disease 1. Congestive heart disease There are basic disease and the factors of precipitation, partly because: Myocardial infarction, ischemic heart disease, with or without Hypertension disease with a sudden increase in high blood pressure Eat lots of salt, excessive physical labor or economic crisis Heart rhythm disturbances (arrhythmias), which sooner or later Cardiomiopathy caused by rheumatic fever, viral infection Valvular heart disease, because of endocarditis, fibrosis chest pain
calcification / normal In patients found dyspnea, Orthopnea (dyspnea that occurs when the patient lying down), feeling weak, tired, there may be disturbances of consciousness, insomnia, impaired memory and found PND 2. Pulmonary Edema Pulmonary Edema is a form of severe congestive heart disease, Anamnesis represents like-bad heart symptomps. The patient is severely ill, sweating. Looked nervous, scared to death. Foamy sputum containing blood. 3. Cardiac Asthma (Paroxysmal Nocturnal dyspnea) Tightness, wheezing sound, especially at night. There are factors that increase pulmonary vascular precipitation congestion, such as eating too much salt, working too hard. Hematologic 1. Anemia Often without a complaint, if it happens slowly and does not in the severee degree. Anemia is suddenly occurred due to production can not offset the bleeding or hemolysis. Anemia which is fast, not offset, make the patient complained of tightness, palpitations, especially when performing exercise.
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There will be symptoms of heart failure if heart is disturbed. There are dizziness, headache, tinnitus or vertigo. 2. Poisoning carbonmonoxida Patients exposed to car exhaust gas leaks or other machine, and there are no ventilation. Symptoms depend on the concentration and duration of exposure carbonmonoxide. Low levels will cause a decrease in their power, which increases levels will cause headaches, nausea, vomiting, lethargy, heart disturbances, unconsciousness and death. Metabolic Diseases 1. Diabetic ketoacidosis Diagnosis is easy when the patient is known to have diabetes. Usually found frequent urination, disorders of consciousness or coma. The patient may be anorexia, nausea vomiting. There are other complications of diabetes, such as dilatation, stomach, brain edema, electrolyte abnormalities, myocardial infarction, infection, respiratoty distress syndrome. 2. Other Acidosis Acute acidosis: without symptoms, fatigue, stupor, coma Chronic acidosis: weakness, fatigue Lactic acidosis: disturbance of consciousness Aspirin overdose: vertigo, tinnitus, hearing loss, nausea, vomiting, hyperventilation Neurological disease Brain lesions are found in congestive heart disease, brain trauma, brain hemorrhage, chronic hypoxia or be in the altitude. There are found Cheyne Stokes, alternating apnea or hyperpnea breathing patterns , that amplitude changes gradually.
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3.2 ANALYSIS
Mr M complained of shortness of breath every time he has to work a little heavy. From the results of anamnesis data showed that Mr M is a heavy smoker and already 20 years have high blood pressure. High blood pressure is one of the main causes of the problems that suffered by the Mr M. High blood pressure and suffering chronically may result in compensation in the left ventricle in removing the cardiac output with higher pressure. As a form of compensation is the left ventricular enlargement of mr Ms heart. This can be proven by thorax X-ray and ECG master M which results :
5,13
Tip blunt of the lungs
7,73
showed cardiomegaly with a cardio-thorax ratio (CTR) = 0.66 (it called cardiomegaly if CTR> 0.5). From the ECG, obtained clock wise direction of the transition zone (between v4 - v5) and old anteroseptal myocardial infarction.
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This chronically process takes time, so sooner the left ventricle could no longer make compensation to pump blood on high pressure. Thats why there will be happened the left cordis decompesation or left heart failure on Mr Ms heart. The occurrence of left heart decompensation has resulted in congestion of blood flow from the left atrium into the left ventricle. Thus, the left intraatrial pressure will increase because blood which supplied to the ventricle is not been pumped maximally around the body by the left ventricle. As a result, therere disturbed peripheral perfusion of Mr M body. It is shown from Mr M akral which is cold and sweaty. The high pressure in the left atrium is become the beginning of the problem of respiration and pulmonary ventilation of him. The high pressure in the left atrium will lead to the encouragement and congestion of the flow of v. Pulmonary. The blood which cannot get into the left atrium will be pushed back/backflow to the lungs, resulting in higher pulmonary capillary hydrostatic pressure. The high hydrostatic pressure will make plasma extravasation from pulmonary capillaries to alveolar tissue, which is known as pulmonary edema. This edema can be seen in the thorax X-ray of Mr M above. Shown in Mr m lung image that theres sinus costophrenicus blunt of the edge of the lung (butterfly-like appearence) because of fluid accumulating in the basal lung when Mr. M stands. This process also lasts for years and as long as that process happens, transudation of fluid in the lungs will be more and more then fills the pulmonary alveo-capillary, which initially narrow (which is useful for air diffusion respiration) to be thicker. That will disrupt the process of diffusion of O 2 into the pulmonary capillary . Those that happens above is a clinical manifestation of the main complaints of patients, that namely shortness of breath. Permeation of fluid in the lungs also gives rise to the sound of ronchi wet in the basal lung. Ronchi sound is also found on physical examination of Mr M. The characteristic of the Mr Ms shortness of braeth is Orthopnea, which is depending on patients body position. This is proven by the results of anamnesis which said that Mr. M usually sleeps with 4 pillows. Because the more horizontal body position, the more alveoli are flooded with fluid. So, the high pillow used the master M indicates the
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shortness of time the body in a horizontal position or we can say when mr M are sleeping in flat position. Chronic high blood pressure suffered by Mr. M also affects the kidneys. Mentioned by Guyton that glomerular hypertension can stretch and cause the glomerulus obliteration. This will reduce glomerular kidneys work in reabsorpting substances in the body metabolites. This statement is strenghten by the results of laboratory examination of Mr M with serum creatinine. Mr M is obtained had serum creatinine 1.8 mg / dL. This value is higher than normal rate for adult males, ie 0.6 to 1.2 mg / dL. Then, if Mr M develops the left cordis decompesation, how can the pressure v. Jugular Mr M increases ? Physiologically, a person who has left heart failure and pulmonary edema, it will eventually lead to the congestion in pulmonary artery because lung is already filled by fluid. This will improve the works of right ventricle to pump harder. This process is also similar to what had happened in the left ventricle, because of pumping harder, sooner the right ventricular decompensation will happen. Because of cordis decompsation occurs in the right ventricle, therere congestion in the systemic veins. This is the basis cause of hepatomegaly and the increased jugular venous pressure. Abdominal pain that Mr M felt are the result of stretching of the capsula glison of the liver because of the livers size increased. The existence of white sputum when Mr M coughing solely caused by cigarettes smoked. Cigarette smoke is an irritant to the airway and the lung itself. Cigarettes also can paralyze the respiratory cilia motility. Irritants that attach to the respiratory tract could stimulate the release of histamine leading of secretions from goblet cells, then the airways will be bronchoconstricted. This will add the difficulty in breathing of Mr M. These secretions of histamine in normal person would be removed or moved upwards until it reach the larynx and then into the esophagus and the secret will moved out by coughing. But in heavy smokers who had reduced cilias motility, will suffer excessive cough reflex with white sputum. This white sputum signifies no infection from pathogenic bacteria.
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3.3 FINAL HYPOTHESIS
Mr. M is experiencing left cordis decompensation (left heart failure) with left ventricle hypertrophy earlier since Mr. M suffers chronic hypertension. Then Mr. M also undergo right cordis decompensation due to the resistance from pulmonal edema caused by the left cordis decompensation
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3.4 FINAL MIND MAPPING CASE MAPPING Mr. M with his dyspnea Anamnesis: Dyspnea and orthopnea Use 4 pillow at sleep 20 years has hypertension Heavy smoker Family sick history (-) Cold sweat Cough with white phlegm Abdominal pain Urinate and defecation normal Smoking
vital sign examination:
Examination Abdomen : Hepar 2cm from arch costae Lien normal Ascites (-) Thorax : Ictus cordis ICS 5, 2cm lateral from midclavicle line Margin of cor widen
Not obese Pulse : 100/min; regular RR : 28/min; irregular Temp: 37,3oC Blood pressure : 150/100 mmHg High jugular vein pressure Extremities : Edema (-)
Wet ronchi in lung Murmur Thrill (-)
Dyspnea
Hypertensio n Heart disorder
Wet sweat
Labs analysis : Creatinin serum 1,8 mg/dL Rontgen: CTR = 0,66 Rontgen: Edema polmunal ECG : chronic infark myocard
Chronic left decompensatio cordis
Edema pulmonal Right decompensatio cordis

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GENERAL MAPPING
Heavy smoking for years

Bronchoconstriction and inmotility cilia in tracheabronchus
Chronic Hypertension
Dyspnea
Hypertrophy of left ventrikel
Cough with white phlegm
Left Heart Failure
Congestion in pulmonal arteries High Pressure in Right Atrium

Back Flow to systemic veins
Congestion in left atrium and pulmonal veins
Back Flow to lung
Edema Pulmonal Increase the Jugular Venous Pressure Wet Ronchi Sound Hepatomegaly Anamnesis results Physics and laboratory examinations Patophysiology
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Main complaint 3.5 GROUP OPINION
Based on analysis we made, our group thinks that Mr. M should be given treatment for cure his problem. The treatment for Mr.M focuses on treating the disorder causing heart failure, making lifestyle changes, and treating with drugs or with surgery or other interventions. These are the example drugs for treat heart failure: Angiotensin Beta-blockers Vasodilators Aldosterone receptor blockers Diuretics
Oxygen can also be given for mr.M. Other drugs such as nitroglycerin given intravenously or under the tongue can produce rapid, dramatic improvement. Morphine can relieve the anxiety that usually accompanies acute pulmonary edema. It also decreases the rate of breathing, slows the heart rate, dilates blood vessels, so can reduces the amount of work the heart. Surgical like reconstruction surgery or even transplantation may be an option if the heart failure is worsening and if the drug therapy hasnt responded. Mr.M also must change lifestyle. Smoking habit should be stopped. Excess salt in the diet can cause fluid retention, which counteracts drugs given to increase the excretion of water, so mr.M should limit his intake of table salt and salty foods and his use of salt in cooking. Mr. M is also should follow an exercise program as described by a doctor. From all of those treatments, we hope Mr. M could feel better and have a longer and healthy life.
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3.6 OBSTACLES
1. We are lack to ask more completely about patient examination so its hard for us in making decision of analysis and final mind-map. 2. Difficult for gathering the members of our group because of our bustle.
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References
Manning, et al., 1995, Pathophysiology of Dyspnea, The NEW ENGLAND JOURNAL of MEDICINE. (Online), Vol. 333, No. 23. Available at: http://www.nejm.org/doi/pdf/10.1056/NEJM199512073332307 (Accessed on October 4th 2010) Ofir, et al. 2007, Mechanisms of Dyspnea during Cycle Exercise in Symptomatic Patients with GOLD Stage I Chronic Obstructive Pulmonary Disease. AMERICAN JOURNAL OF Respiratory and Critical Care Medicine. (Online), 4th 2010) Dokter Online, 2010, Emfisema/Sesak Nafas. Available at: Vol. 177. Available at: http://ajrccm.atsjournals.org/cgi/reprint/177/6/622. (Accessed on October
http://ezcobar.com/dokter-online/dokter15/index.php? option=com_content&view=article&id=147:emfisema-sesaknafas&catid=47:paru&Itemid=64 (Accessed on October 5th 2010) Irawan, Dimas Sondang. 2009. Pengaruh Kebiasaan Merokok Terhadap Daya Tahan Jantung Paru.Program Studi Diploma Iv Fisioterapi Fakultas Ilmu Kesehatan Universitas Muhammadiyah Surakarta. Kusmana Dede, Prof. Dr.dr. SpJP. 2009. Rokok dan Kesehatan Jantung. Available at : http://www.pjnhk.go.id/content/view/2212/31/. (Accessed on October 4th 2010) Frank H. Netter, MD., 2006, Atlas of Human Anatomy, 4th Edition. Philadephia: W.B. Saunders Jacob L Heller., 2009, Abdominal Organ. (Accessed on October 14th 2010) Reichen, Jurg., 1992, THE LIVER IN CONGESTIVE HEART FAILURE [Online] (Update August 31st 2006) Available
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at: http://www.ikp.unibe.ch/lab2/heartfailure.htm (Accessed on October 5th 2010) Daugdale, David, C., 2009, Hepatomegaly. [Online](Update 2 May 2009) Available http://www.nlm.nih.gov/medlineplus/ency/article/003275.htm on October 5th 2010) Rull, Gurvinder, 2009, Hepatomegaly. [Online] (Update 5 Jul 2009) Available at: http://translate.google.co.id/translate?hl=id&langpair=en| id&u=http://www.patient.co.uk/doctor/Hepatomegaly.htm (Accessed on October 5th 2010) Springhouse, 2007, Hepatomegaly: Excerpt from Signs & Symptoms: A 2-in-1 Reference for Nurses. [Online] (Update 14 May 2010) Available at: http://translate.google.co.id/translate?hl=id&langpair=en| id&u=http://www.wrongdiagnosis.com/h/hepatitis/book-diseases-14a.htm (Accessed on October 5th 2010) Ann and Joel.2000. Hepatomegaly in Neonatus and Children (Pediatrics in Review. 2000;21:303-310. doi:10.1542/pir.21-9-303). Available at http://pedsinreview.aappublications.org/cgi/content/full/21/9/303 (Accessed on October 5th 2010) Ulfa, M. 2009. Penatalaksaan Serosis Hepatis Berdasarkan Evidance Based Nursing 2010) Anurogo, Dito, 2010, Misteri Gagal Jantung. Available at: http://netsains.com/2009/08/misteri-gagal-jantung, (Accessed on October 6th 2010) Sheps, Sheldon G.,1999, Mayo Clinic On High Blood Pressure. 1st ed. United States of America: Kensington Publishing Corporation Nair B Kichu ed., 2008. Adult Physical Examination: The jugular venous pressure. Available at: http://physicalexamination.org/?q=node/35 (Accessed on October 8th 2010) (EBN). Available at : www.stikesmataram.ac.id/data/books/Sirosis_hepatis.doc (Accessed on October 5th at: (Accessed
58
Rull
Gurvinder,
2009,
Jugular
Venous
Return.
EMIS.
Available
at:
http://www.patient.co.uk/doctor/Jugular-Venous-Pressure.htm on October 8th 2010)
(Accessed
Nair B Kichu ed., 2008, Adult Physical Examination: The jugular venous pressure. Available at: http://physicalexamination.org/?q=node/35 (Accessed on October 8th 2010) Handojo, Farida. February 9th 2010, Anamnesa dan Pemeriksaan Fisik. (Accessed on October 9th 2010) Guyton, Arthur and John E. Hall. 2006. Textbook of Medical Physiology 11th edition. Philadelphia: Elsevier Begany, Timothy, 2000, Sputum Color Is The Key to Treating Acute COPD Exacerbations. October 11th 2010) Departemen Kesehatan RI, 2007, Pedoman Pengobatan Dasar di Puskesmas. Available at: http://www.depkes.go.id/downloads/doen2008/puskesmas_2007.pdf (Accessed on October 11th 2010) U.S. National Library of Medicine, 2010. Abdominal Pain. Department of Health and Human Services. Available at: (Accessed College of at: http://www.nlm.nih.gov/medlineplus/ency/article/003120.htm on October 13th 2010) Schiller Lawrence R., 2010, Abdominal Pain. Available American Gastroenterology. 2010) State Government of Victoria, 2009, Abdominal Pain. State Government of Victoria. Available at: http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Abdominal _pain_in_adults (Accessed on October 13th 2010) Available at: www.pulmonaryreviews.com/aug00/pr_aug00_sputum.html (Accessed on
http://www.acg.gi.org/patients/gihealth/aps.asp (Accessed on October 13th
59
The Snowdrift Pulmonary Foundation, 2000, Dyspnea sensation of breathlessness cardiopulmonary disease. The Snowdrift Pulmonary Foundation. Available at: http://www.nlhep.org/books/pul_Pre/dyspnea.html (Accessed on October 13th 2010) U.S. National Library of Medicine, 2010. Liver Disorders. Department of Health and Human Services. Available at: (Accessed http://www.nlm.nih.gov/medlineplus/ency/article/000205.htm on October 13th 2010) Suharto. 2010. Anamnesis Sesak. Pedoman Keterampilan Medik Semester 3 Edisi ke-7 2010, edited by Rehatta, M. , Hasan, H. Fakultas Kedokteran Universitas Airlangga
CRITICAL APPRAISAL EBL and Critical Apraissal For Answering Question Searching Method Information Type Validity Foundation Result Importance Foundation Result
60
Applicability Foundation Result
LEARNING ISSUES 1
http://www.nej m.org/doi/pdf/1 0.1056/NEJM19 9512073332307 (Accessed on October 4th 2010) http://ajrccm.atsj ournals.org/cgi/r eprint/177/6/622 (Accessed on October 4th 2010) http://ezcobar.co m/dokteronline/dokter15/ index.php? option=com_co ntent&view=arti cle&id=147:emf isema-sesaknafas&catid=47: paru&Itemid=64 (Accessed on October 5th 2010)
Internet Browsing
Digital
Journal
Yes
Content of information
Yes
Is it applicable?
Yes
Internet Browsing
PDF
Journal
Yes
Yes
Is it applicable?
Yes
Internet Browsing
Digital
Idea
No
Yes
Is it applicable?
Yes
61 Pengaruh Kebiasaan Merokok Terhadap Daya Tahan Jantung Paru http://www.pjnh k.go.id/content/v iew/2212/31/. (Accessed on October 4th 2010) Atlas of Human Anatomy, 4th Edition Abdominal Organ http://www.ikp. unibe.ch/lab2/he artfailure.htm (Accessed on October 5th 2010) http://www.nlm. nih.gov/medline plus/ency/article /003275.htm (Accessed on October 5th 2010) http://translate.g
Using Textbook
Text
Textbook
Yes
Yes
Is it applicable?
Yes
Internet Browsing
Digital
Idea
Yes
Yes
Is it applicable?
Yes
4 4
Using Textbook Using Textbook Internet Browsing
Text Text
Textbook Textbook
Yes Yes
Content of information Content of information Content of information
Yes Yes
Is it applicable? Is it applicable? Is it applicable?
Yes Yes
Digital
Article
Yes
Yes
Yes
Internet Browsing
Digital
Article
Yes
Yes
Is it applicable?
Yes
Internet
Digital
Idea
No
Content of
Yes
Is it
Yes
62 oogle.co.id/trans late? hl=id&langpair= en| id&u=http://ww w.patient.co.uk/ doctor/Hepatom egaly.htm (Accessed on October 5th 2010) http://translate.g oogle.co.id/trans late? hl=id&langpair= en| id&u=http://ww w.wrongdiagnos is.com/h/hepatiti s/book-diseases14a.htm (Accessed on October 5th 2010)
Browsing
information
applicable?
Internet Browsing
Digital
Idea
No
Yes
Is it applicable?
Yes
63
http://pedsinrevi ew.aappublicati ons.org/cgi/cont ent/full/21/9/303 (Accessed on October 5th 2010)
Internet Browsing
Digital
Article
Yes
Yes
Is it applicable?
Yes
www.stikesmataram.ac.id/dat a/books/Sirosis_ hepatis.doc (Accessed on October 5th 2010) http://netsains.c om/2009/08/mis teri-gagaljantung, (Accessed on October 6th 2010) Mayo Clinic On High Blood Pressure. 1st ed.
Internet Browsing
Digital
Article
Yes
Yes
Is it applicable?
Yes
Internet Browsing
Digital
Idea
No
Yes
Is it applicable?
Yes
Using Textbook
Textbook
Article
Yes
Yes
Is it applicable?
Yes
LEARNING ISSUES 2
64
http://physicalex amination.org/? q=node/35 (Accessed on October 8th 2010)
Internet Browsing
Digital
Article
Yes
Yes
Is it applicable?
Yes
http://www.patie nt.co.uk/doctor/J ugular-VenousPressure.htm (Accessed on October 8th 2010) http://physicalex amination.org/? q=node/35 (Accessed on October 8th 2010) Anamnesa dan Pemeriksaan Fisik Textbook of Medical Physiology 11th edition
Internet Browsing
Digital
Idea
No
Yes
Is it applicable?
Yes
Internet Browsing
Digital
Idea
No
Yes
Is it applicable?
Yes
Using Textbook Using Textbook
Text
Textbook
Yes
Content of information Content of information
Yes
Is it applicable? Is it applicable?
Yes
Text
Textbook
Yes
Yes
Yes
65
www.pulmonary reviews.com/au g00/pr_aug00_s putum.html (Accessed on October 11th 2010)
Internet Browsing
Digital
Article
Yes
Yes
Is it applicable?
Yes
http://www.depk es.go.id/downlo ads/doen2008/p uskesmas_2007. pdf (Accessed on October 11th 2010) http://www.nlm. nih.gov/medline plus/ency/article /003120.htm (Accessed on October 13th 2010) http://www.acg. gi.org/patients/g ihealth/aps.asp (Accessed on October 13th
Internet Browsing
PDF
Article
Yes
Yes
Is it applicable?
Yes
Internet Browsing
Digital
Article
Yes
Yes
Is it applicable?
Yes
Internet Browsing
Digital
Article
Yes
Yes
Is it applicable?
Yes
66 2010) http://www.bette rhealth.vic.gov.a u/bhcv2/bhcartic les.nsf/pages/Ab dominal_pain_in _adults (Accessed on October 13th 2010) http://www.nlhe p.org/books/pul _Pre/dyspnea.ht ml (Accessed on October 13th 2010) http://www.nlm. nih.gov/medline plus/ency/article /000205.htm (Accessed on October 13th 2010) Pedoman Keterampilan Medik Semester 3 Edisi ke-7 2010
Internet Browsing
Digital
Article
Yes
Yes
Is it applicable?
Yes
Internet Browsing
Digital
Article
Yes
Yes
Is it applicable?
Yes
Internet Browsing
Digital
Article
Yes
Yes
Is it applicable?
Yes
Using Textbook
Text
Report
Yes
Yes
Is it applicable?
Yes
67
68 SCIENTIFIC PAPER APPRAISAL
Appendix
Group : Title : 16th group Mechanisms of Dyspnea during Cycle Exercise in Symptomatic Patients with GOLD Stage I Chronic Obstructive Pulmonary Disease
1. PAPER COMPLETION : Item Title Abstract and or Summary Introduction, Background Method Result Discussion Acknowledgement Reference Existence (with page) Yes (page 622) Yes (page 622-623) Yes (page 622-623) Yes (page 623) Yes (page 623-627) Yes (page 627-628) No Yes (page 628-629)
Conclusion : the format is not complete
2. RESEARCH VALIDITY Objective: To examine ventilatory constraints during exercise in symptomatic smokers with GOLD (Global Initiative for Chronic Obstructive Lung Disease) stage I chronic
69 obstructive lung disease (COPD) so as to uncover potential mechanisms of dyspnea and exercise curtailment. Method: Cross-sectional Study Item Design Hierarchy of Evidence Sample Items found (with page) Cross-sectional study (Page 623) 5 We studied 21 symptomatic
patients with GOLD stage I COPD (postbronchodilator FEV1 > 80% predicted and FEV1/FVC , 0.7) (12) who were referred to the COPD Centre at our institution. In addition, 21 healthy subjects normal (FEV1 age-and were > baseline 80% sex-matched with spirometry predicted, included
FEV1/FVC > 0.7) and absence of any health problems, including cardiovascular, neuromuscular, musculoskeletal, or respiratory diseases that could contribute to breathlessness Sample Size or exercise limitation. (Page 623) A sample size of 16 was used to provide the power (80%) to detect a significant difference in dyspnea intensity (Borg scale) measured at a standardized work rate during incremental cycle exercise based on a relevant
70 difference in Borg ratings of 61, an SD of 1 for Borg ratings changes found at our laboratory, Eligibility Criteria alpha= 0.05 (Page 623) We studied 21 symptomatic patients with GOLD stage I COPD (postbronchodilator FEV1 > 80% predicted and FEV1/FVC , 0.7) (12) who were referred to the COPD Centre at our institution. In addition, 21 healthy subjects normal (FEV1 age-and were > baseline 80% sex-matched with spirometry predicted, included
FEV1/FVC > 0.7) and absence of any health problems, including cardiovascular, neuromuscular, musculoskeletal, or respiratory diseases that could contribute to breathlessness Exclusion Criteria or exercise limitation. (Page 623) Patients were excluded if they had (1) other unstable medical conditions that could cause or contribute to breathlessness (i.e., metabolic, other cardiovascular, that or other respiratory diseases) or (2) disorders could interfere with exercise testing, such as neuromuscular diseases
71 or Sampling Frame Collecting Data Method musculoskeletal problems.
(Page 623) Total Sampling Routine spirometry, constant-
volume body plethysmography, singlebreath diffusing capacity (DLCO), and maximum inspiratory and expiratory mouth pressures (PImax and PEmax, measured at FRC and TLC, respectively) were performed in accordance with recommended techniques (1620) using an automated pulmonary function testing system (6200 Autobox DL CA). and Closing Vmax229d; Yorba volumes Linda, were SensorMedics,
measured using the single-breath nitrogen test as modified by Anthonisen and colleagues (21). Measurements were repeated 30 minutes post-bronchodilator (400 mg salbutamol) in all patients with mild COPD and in 10 healthy subjects. Measurements were standardized as percentages of predicted normal values (22 28); predicted normal values for inspiratory capacity (IC) were calculated
as
predicted
TLC
72 minus predicted FRC. (Page 623) In patients with COPD compared with control subjects, peak oxygen consumption and power output were significantly reduced by more than 20% and dyspnea ratings (P,0.05). were higher for a the givenwork rate and ventilation Comparedwith control group, the COPD group had evidence of extensive small airway increased requirements during dysfunction with exercise, ventilatory
Measurement and or assessment
likely on the basis of greater ventilation/perfusion abnormalities. Changes in endexpiratory lung volume during exercise were greater in COPD than in health (0.54 6 0.34 vs. 0.06 6 0.32 L, respectively; P , 0.05) and breathing pattern was correspondingly more shallow and rapid. Across expressed groups, as a dyspnea intensity increased as ventilation percentage of capacity increased (P , 0.0005) and as inspiratory reserve volume decreased (P , Instrument 0.0005). (Page 622) Group responses at different time
73 points and/or intensities during exercise were compared using t tests with appropriate Bonferroni adjustments comparisons. frequency compared exact contributors COPD multiple Randomization Intervention Analysis Method (Page 623) Statistical Method (Page 623) were test. to statistics using for multiple Dyspnea and
descriptors were analyzed as the Fishers Physiologic exertional by
dyspnea intensity in subjects with determined regression analysis.
Coherence between design and objective: coherent Coherence between measurement and instrument used: coherent Conclusion: valid (ONLY BASED FROM TWO CONCLUSIONS ABOVE) 3. IMPORTANCE CI P : : There is no CI. <0.05
If this research were done repeatedly (100x), <5 researches will show the same result as the previous result (by chance). Conclusion : Because there is no CI, the importance cant be measured
74

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1

HUMAN FUNCTION MODULE B SCENARIO PROBLEM BASED LEARNING

PRESENTED BY: GROUP 16th

FACULTY OF MEDICINE AIRLANGGA UNIVERSITY

HUMAN FUNCTION MODULE 16th Group

Scenario Creator Esti Hindariati, dr., Sp.JP(K)

HUMAN FUNCTION MODULE 16th Group

16th Group Members

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

SEVENTH MODULE HUMAN FUNCTION MODULE PROBLEM BASED LEARNING

HUMAN FUNCTION MODULE 16th Group

CHAPTER I FIRST TUTORIAL

1.3.1. 40 years old 1.3.2. Office 1.3.3. Male

HUMAN FUNCTION MODULE 16th Group

1.5 Early Hypothesis

Liver disorder Renal disorder Hyperthyroidism Anemia

HUMAN FUNCTION MODULE 16th Group

1.6 Early Mind Mapping

Mr. M Patophysiology Definition

Mechanism Wet Ronchi White Sputum

HUMAN FUNCTION MODULE 16th Group

1.7 Learning Issue 1

1.7.1. 1.7.2 1.7.3 1.7.4 1.7.5 1.7.6 1.7.7

HUMAN FUNCTION MODULE 16th Group

CHAPTER II SECOND TUTORIAL

2.2 THE ANSWERS OF LEARNING ISSUES I

How is the physiology of dyspnea?

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

How is the location of organs in the human body?

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

How is the normal condition of liver?

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

Hemolytic-uremic syndrome (HUS) * Hepatitis A

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

CHAPTER III THIRD TUTORIAL

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

Cyanosis The cyanosis and its term means cause is

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group

HUMAN FUNCTION MODULE 16th Group