Makalah Modul g Kel 16

1

HUMAN FUNCTION MODULE

B SCENARIO

PROBLEM BASED LEARNING

PRESENTED BY:

GROUP 16th

FACULTY OF MEDICINE

AIRLANGGA UNIVERSITY

3rd SEMESTER – 2010


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B SCENARIO


Scenario Creator

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


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16th Group Members

Leader :

Dini Nur Aini 010911163

Members:

Muhammad Achdiar R 010911152

Filipus Michael Yofrido 010911154

Togar Erkasan Sitorus 010911155

Christopher Njotokusgito 010911157

Karin Dhia Fahmita 010911158

Wirawan Indra P. 010911169

Rizal Constantino Susilo 010911170

Shaleh Muhammad D 010911171

Agnes Candra Pradhita 010911172

Tutor :

Prof. Dr. H Margono Al Imam Sjahrir Sp. S(K)

dr. Sri Purwaningsih


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CONTENTS

Cover ..................................................................................................................................1

Scenario Creator................................................................................................................2

Group Members ................................................................................................................3

Contents .............................................................................................................................4

Instructional Objectives ...................................................................................................5

Chapter I : 1st Tutorial .....................................................................................................6

1.1 Scenario..............................................................................................................61.2 Main Problem ....................................................................................................61.3 Keywords ..........................................................................................................61.4 Additional Information......................................................................................71.5 Early Hypothesis ...............................................................................................71.6 Early Mind Mapping .........................................................................................81.7 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


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INSTRUCTIONAL OBJECTIVES

5

SEVENTH MODULE



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.


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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

1.1 Scenario

1.3 Key Words

1.2. Main Problem

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CHAPTER I

FIRST TUTORIAL

Shortness of breath since 2 days before entering the hospital

1.3.1. 40 years old

1.3.2. Office

1.3.3. Male


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1.5 Early Hypothesis

1.4 Additional Information

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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, body’s temperature 37.3 ºC

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

Liver disorder

Renal disorder

Hyperthyroidism

Anemia


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1.6 Early Mind Mapping

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FINANCIALCONDITION

Causes

Smoking

Mechanism

Heart disturbancesPulmonaryDisturbances

Others

JVP ↑

Wet Ronchi White Sputum

Hepatomegaly

Dyspnea

KindsSymptoms

Patophysiology Definition

Mr. M

1.7 Learning Issue 1

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1.7.1. How is the physiology of dyspnea?

1.7.2 What are the symptoms and causes of shortness of breath?

1.7.3 What is the bad effect of smoking?

1.7.4 How is the location of organs in the human body?

1.7.5 How is the normal condition of liver?

1.7.6 What is heart failure?

1.7.7 What is hypertension?


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2.1 METHODS AND STEPS TO FIND THE INFORMATION

2.2 THE ANSWERS OF LEARNING ISSUES I

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CHAPTER II

SECOND TUTORIAL

To get the information we need, we use some sources, such as:

1. Text Books

We used text books from library, our relative’s 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.

2.2.1 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 What are the symptoms and causes of shortness of breath?

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?

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 can’t 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 cigarette’s 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 can’t 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)

Smoker’s 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?


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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 * Glycogen storage disease

Hemolytic-uremic syndrome (HUS) * Hepatitis A

Hepatitis B * Hepatocellular carcinoma

Hereditary fructose intolerance * Infectious mononucleosis

Leukemia * Neuroblastoma

Niemann-Pick disease * Primary biliary cirrhosis

Reye syndrome * Sarcoidosis

Sclerosing cholangitis

Steatosis (fat in the liver from metabolic problems such as diabetes,

obesity, and high triglycerides)

Tumor metastases

(David C. Dugdale, 2009)

Congestive blood flow in the liver causes hepatomegaly. Suprahepatic

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, non-

compliance 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 involving neurohormonal adrenergic nervous system

(sympathetic nervous system activation will increase levels of

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 : no symptoms on daily activities, symptoms will occur in more

severe activities of daily activities.

Class II : symptoms arise in their daily activities.

Class III: symptoms occur at lighter activity of daily activities.

Class IV: symptoms occur at rest.


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Framingham criteria can also be used to diagnose congestive heart failure.

Major criteria:

1. Paroxismal Nocturnal Dispneu

2. Distention of neck veins

3. Ronkhi lung

4. Kardiomegali

5. Acute pulmonary edema

6. Gallop S3

7. Jugular venous pressure elevation

8. Reflux hepatojugular

Minor criteria:

1. Extremity edema

2. Cough at night

3. Dispneu de effort

4. Hepatomegaly

5. Pleural effusion

6. Tachycardia

7. Decrease in vital capacity a third of the normal

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 doesn’t work as it’s 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 doesn’t 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 doesn’t

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. It’s 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 don’t 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 you’ll have high blood pressure during

your lifetime. Most risk factors we can control, others we can’t.

Unmodifiable risk factor

There are four major risk factors for high blood pressure that we can’t

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, it’s 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 that’s 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 body’s 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 people’s 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 we’re 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 doesn’t include enough potassium, or our body isn’t 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 don’t 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 doesn’t 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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2.3 LEARNING ISSUES II

29

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.

2.3.1 What are indicated by Jugular Venous Pressure?

2.3.2 What is a wet rhonchi, and what is the indication of rhonchi?

2.3.3 What causes hypoxia?

2.3.4 What does white-phlegm-cough indicate? What causes it?

2.3.5 What is the definition of Chronic Obstructive Pulmonary Disease

(COPD)?

2.3.6 What is the correlation between abdominal pain and dyspnea?

2.3.7 What are liver disorders?

2.3.8 There are many diseases that have dyspnea symptom, mention and

explain it?


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3.1 THE ANSWERS OF LEARNING ISSUES II

30

CHAPTER III

THIRD TUTORIAL

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)

Kussmaul’s 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 body’s 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 cyanide—to 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 patient’s 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 42–8, 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 term

cyanosis means

blueness of the skin,

and its cause is

excessive amounts of

deoxygenated

hemoglobin in the skin

blood vessels,

especially in the

capillaries. This

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?

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 body’s 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 individual’s 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 moving arms and legs,

stiffness

* Difficulty walking (ataxia) * Emotional or behavioral changes

* Enlargement of the abdomen (abdominal distention)

* Loss of IQ points (occasionally) * Vomiting blood

*Uncontrollable, slow or decreased movement and expressions of the face

* Splenomegaly * Tremors of the arms or hands


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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 * Enlarged spleen

* Floating stools * Foul-smelling stools

* Pale or clay-colored stools * Slow growth

* 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 * Confusion or problems thinking

* Impotence, loss of interest in sex, and breast development (gynecomastia) in

men

* Nausea and vomiting * Nosebleeds or bleeding gums

* Pale or clay-colored stools * 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.


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Symptoms

* Dark urine * Fatigue

* Itching * Loss of appetite

* Low-grade fever * Nausea and vomiting

* Pale or clay-colored stools * Yellow skin (jaundice)

Hepatitis B

Hepatitis B is inflammation (irritation and swelling) of the liver due to the

hepatitis B virus (HBV).

Symptoms

* Appetite loss * Fatigue

* Low-grade fever * Muscle and joint aches

* Nausea and vomiting * Yellow skin and dark urine due to 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) * Ascites

* Bleeding varices (dilated veins in the esophagus) * Dark urine

* Fatigue * Generalized itching

* Jaundice * Loss of appetite

* Low-grade fever * Nausea

* Pale or clay-colored stools * 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 * Fatigue

* Generalized darkening of skin color (often referred to as bronzing)

* Joint pain * Lack of energy

* Loss of body hair * Loss of sexual desire

* Weight loss * Weakness

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) * Serum iron (high)

* Percentage of transferrin saturation (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 * Dark urine

* Fatigue * Generalized itching

* General discomfort, uneasiness, or ill feeling (malaise)


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* Loss of appetite * Nausea and vomiting

* Pale or clay-colored stools

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 * Enlarged liver

* Fatigue * Fatty deposits under the skin

* Fatty stools * Itching

* Jaundice * Soft yellow spots on the eyelid

Hepatocellular carcinoma

Hepatocellular carcinoma is cancer of the liver.

Symptoms

* Abdominal pain or tenderness, especially in the upper-right part

* Easy bruising or bleeding * Enlarged abdomen

* Yellow skin or eyes (jaundice)

Physical examination may show an enlarged, tender liver.

Tests include:

* Abdominal CT scan * Abdominal ultrasound

* Liver biopsy * Liver enzymes (liver function tests)

* Liver scan * Serum alpha fetoprotein

Some high-risk patients may get periodic blood tests and ultrasounds to see

whether tumors are developing.


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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 * Lethargy

* Loss of consciousness or coma * Mental changes

* Nausea and vomiting * 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 * Hearing loss

* Muscle function loss or paralysis of the arms or legs

* Speech difficulties * Weakness in the arms or legs

Comparing the learning issue data we have and the patient’s 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 chest pain

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 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.

There will be symptoms of heart failure if heart is disturbed. There are

dizziness, headache, tinnitus or vertigo.


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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

48

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 M’s

heart. This can be proven by thorax X-ray and ECG master M which results :

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.

This chronically process takes time, so sooner the left ventricle could no

longer make compensation to pump blood on high pressure. That’s why there will

be happened the left cordis decompesation or left heart failure on Mr M’s


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7,73

Tip blunt of the lungs

49

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, there’re

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 there’s 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 M’s shortness of braeth is Orthopnea, which is depending on patient’s 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

shortness of time the body in a horizontal position or we can say when mr M are

sleeping in flat position.


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50

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 kidney’s 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, there’re 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 liver’s 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 cilia’s 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

51

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

52

CASE MAPPING


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Chronic left decompensatio cordisLab’s analysis :

Creatinin serum 1,8 mg/dL

Rontgen: CTR = 0,66

Rontgen: Edema polmunal

ECG : chronic infark myocard

Thorax :Ictus cordis ICS 5,

2cm lateral from midclavicle line

Margin of cor widen

Wet ronchi in lung

Murmur

Thrill (-)

Extremities :Edema (-)

Wet sweat

Smoking

DyspneaHypertensio

n

Heart disorder

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

vital sign examination:Not obese

Pulse : 100/min; regular

RR : 28/min; irregular

Temp: 37,3oC

Blood pressure : 150/100 mmHg

High jugular vein pressure

Abdomen :Hepar 2cm from arch costae

Lien normal

Ascites (-)

Edema pulmonal

Right decompensatio cordis

Mr. M with his dyspnea

Examination

53

GENERAL MAPPING

Anamnesis results

Physics and laboratory examinations

Patophysiology

Main complaint


16th Group

Chronic Hypertension

Heavy smoking for years

Hypertrophy of left ventrikel

Left Heart Failure

Congestion in left atrium and pulmonal veins

Back Flow to lung

Edema Pulmonal

Dyspnea

Bronchoconstriction and inmotility cilia in trachea-bronchus

Congestion in pulmonal arteries

High Pressure in Right Atrium

Back Flow to systemic veins

Increase the Jugular Venous Pressure

Hepatomegaly

Wet Ronchi Sound

Cough with white phlegm

3.5 GROUP OPINION

54

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 hasn’t 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

55

1. We are lack to ask more completely about patient examination so it’s

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.


16th Group

56

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), Vol. 177. Available at:

http://ajrccm.atsjournals.org/cgi/reprint/177/6/622. (Accessed on October

4th 2010)

Dokter Online, 2010, Emfisema/Sesak Nafas. Available at:

http://ezcobar.com/dokter-online/dokter15/index.php?

option=com_content&view=article&id=147:emfisema-sesak-

nafas&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


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

at: http://www.ikp.unibe.ch/lab2/heartfailure.htm (Accessed on October 5th

2010)


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http://www.ikp.unibe.ch/lab2/heartfailure.htm

http://www.pjnhk.go.id/content/view/2212/31/

http://ezcobar.com/dokter-online/dokter15/index.php?option=com_content&view=article&id=147:emfisema-sesak-nafas&catid=47:paru&Itemid=64



http://ajrccm.atsjournals.org/cgi/reprint/177/6/622

http://www.nejm.org/doi/pdf/10.1056/NEJM199512073332307

57

Daugdale, David, C., 2009, Hepatomegaly. [Online](Update 2 May 2009)

Available at:

http://www.nlm.nih.gov/medlineplus/ency/article/003275.htm (Accessed


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


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 (EBN). Available at :

www.stikes-mataram.ac.id/data/books/ Sirosis _ hepatis .doc (Accessed on

October 5th 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



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http://physicalexamination.org/?q=node/35

http://netsains.com/2009/08/misteri-gagal-jantung

http://www.stikes-mataram.ac.id/data/books/Sirosis_hepatis.doc


http://translate.google.co.id/translate?hl=id&langpair=en%7Cid&u=http://www.wrongdiagnosis.com/h/hepatitis/book-diseases-14a.htm


http://translate.google.co.id/translate?hl=id&langpair=en%7Cid&u=http://www.patient.co.uk/doctor/Hepatomegaly.htm


http://www.nlm.nih.gov/medlineplus/ency/article/003275.htm

58

Rull Gurvinder, 2009, Jugular Venous Return. EMIS. Available at:

http://www.patient.co.uk/doctor/Jugular-Venous-Pressure.htm (Accessed


Nair B Kichu ed., 2008, Adult Physical Examination: The jugular venous

pressure. Available at: http://physicalexamination.org/?q=node/35


Handojo, Farida. February 9th 2010, Anamnesa dan Pemeriksaan Fisik. (Accessed


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. Available at:

www.pulmonaryreviews.com/aug00/pr_aug00_sputum.html (Accessed on

October 11th 2010)

Departemen Kesehatan RI, 2007, Pedoman Pengobatan Dasar di Puskesmas.

Available at:

http://www.depkes.go.id/downloads/doen2008/puskesmas_2007.pdf


U.S. National Library of Medicine, 2010. Abdominal Pain. Department of Health

and Human Services. Available at:



Schiller Lawrence R., 2010, Abdominal Pain. American College of

Gastroenterology. Available at:

http://www.acg.gi.org/patients/gihealth/aps.asp (Accessed on October 13th

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)


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http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Abdominal_pain_in_adults


http://www.acg.gi.org/patients/gihealth/aps.asp



http://www.pulmonaryreviews.com/aug00/pr_aug00_sputum.html


http://www.patient.co.uk/doctor/Jugular-Venous-Pressure.htm

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


U.S. National Library of Medicine, 2010. Liver Disorders. Department of Health

and Human Services. Available at:



Suharto. 2010. Anamnesis Sesak. Pedoman Keterampilan Medik Semester 3 Edisi

ke-7 2010, edited by Rehatta, M. , Hasan, H. Fakultas Kedokteran

Universitas Airlangga


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http://www.nlhep.org/books/pul_Pre/dyspnea.html

60

EBL and Critical Apraissal

For AnsweringQuestion

Searching Method

Information Type

Validity Importance ApplicabilityFoundation Result Foundation Result Foundation Result

LEARNING ISSUES 1 http://www.nejm.org/doi/pdf/10.1056/NEJM199512073332307 (Accessed on October 4th 2010)

1Internet

BrowsingDigital Journal Yes

Content of information

YesIs it

applicable?Yes

http://ajrccm.atsjournals.org/cgi/reprint/177/6/622 (Accessed on October 4th 2010)

1Internet

BrowsingPDF Journal Yes


YesIs it

applicable?Yes


2 Internet Browsing

Digital Idea No Content of information

Yes Is it applicable?

Yes


16th Group

CRITICAL APPRAISAL










61

(Accessed on October 5th

2010)

Pengaruh Kebiasaan Merokok Terhadap Daya Tahan Jantung Paru

3Using

TextbookText Textbook Yes


YesIs it

applicable?Yes

http://www.pjnhk.go.id/content/view/2212/31/. (Accessed on October 4th 2010)

3Internet

BrowsingDigital Idea Yes


YesIs it

applicable?Yes

Atlas of Human Anatomy, 4th Edition

4Using



YesIs it

applicable?Yes

Abdominal Organ

4Using



YesIs it

applicable?Yes

http://www.ikp.unibe.ch/lab2/heartfailure.htm (Accessed on October 5th 2010)

5Internet

BrowsingDigital Article Yes


YesIs it

applicable?Yes


16th Group







62

http://www.nlm.nih.gov/medlineplus/ency/article/003275.htm (Accessed on October 5th 2010)

5Internet



YesIs it

applicable?Yes

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)

5Internet

BrowsingDigital Idea No


YesIs it

applicable?Yes

http://translate.google.co.id/translate?hl=id&langpair=en|id&u=http://www.wrongdiagnosis.com/h/hepatitis/book-diseases-14a.htm

5 Internet Browsing



Yes


16th Group










63

(Accessed on October 5th

2010)

http://pedsinreview.aappublications.org/cgi/content/full/21/9/303 (Accessed on October 5th

2010)

5Internet



YesIs it

applicable?Yes

www.stikes-mataram.ac.id/data/books/Sirosis _ hepatis .d oc (Accessed on October 5th 2010)

5Internet



YesIs it

applicable?Yes

http://netsains.com/2009/08/misteri-gagal-jantung, (Accessed on October 6th 2010)

6Internet



YesIs it

applicable?Yes


16th Group










64

Mayo Clinic On High Blood Pressure. 1st ed.

7Using

TextbookTextbook Article Yes


YesIs it

applicable?Yes

LEARNING ISSUES 2

http://physicalexamination.org/?q=node/35 (Accessed on October 8th 2010)

1Internet



YesIs it

applicable?Yes

http://www.patient.co.uk/doctor/Jugular-Venous-Pressure.htm (Accessed on October 8th 2010)

1Internet



YesIs it

applicable?Yes

http://physicalexamination.org/?q=node/35 (Accessed on

1 Internet Browsing



Yes


16th Group










65

October 8th 2010)Anamnesa dan Pemeriksaan Fisik

2Using



YesIs it

applicable?Yes

Textbook of Medical Physiology 11th edition

3Using



YesIs it

applicable?Yes

www.pulmonaryreviews.com/aug00/pr_aug00_sputum.html (Accessed on October 11th

2010)

4Internet



YesIs it

applicable?Yes

http://www.depkes.go.id/downloads/doen2008/puskesmas_2007.pdf (Accessed on October 11th 2010)

5Internet

BrowsingPDF Article Yes


YesIs it

applicable?Yes

http://www.nlm.nih.gov/medlineplus/

6Internet



YesIs it

applicable?Yes


16th Group









66

ency/article/003120.htm (Accessed on October 13th

2010)

http://www.acg.gi.org/patients/gihealth/aps.asp (Accessed on October 13th

2010)

6Internet



YesIs it

applicable?Yes

http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Abdominal_pain_in_adults (Accessed on October 13th

2010)

6Internet



YesIs it

applicable?Yes

http://www.nlhep.org/books/pul_Pre/dyspnea.html (Accessed on October 13th

2010)

6Internet



YesIs it

applicable?Yes

http:// 7 Internet Digital Article Yes Content of Yes Is it Yes


16th Group













67

www.nlm.nih.gov/medlineplus/ency/article/000205.htm (Accessed on October 13th

2010)

Browsing information applicable?

Pedoman Keterampilan Medik Semester 3 Edisi ke-7 2010

8Using

TextbookText Report Yes


YesIs it

applicable?Yes


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68

SCIENTIFIC PAPER APPRAISAL

Appendix

Group : 16th group

Title : Mechanisms of Dyspnea during Cycle Exercise in Symptomatic Patients with

GOLD Stage I Chronic Obstructive Pulmonary Disease

1. PAPER COMPLETION :

Item Existence (with page)

Title Yes (page 622)

Abstract and or Summary Yes (page 622-623)

Introduction, Background Yes (page 622-623)

Method Yes (page 623)

Result Yes (page 623-627)

Discussion Yes (page 627-628)

Acknowledgement No

Reference Yes (page 628-629)

Conclusion : the format is not complete


16th Group

69

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

obstructive lung disease (COPD) so as to uncover potential mechanisms of

dyspnea and exercise curtailment.

Method: Cross-sectional Study

Item Items found (with page)

Design Cross-sectional study (Page 623)

Hierarchy of Evidence 5

Sample 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 age-and sex-matched

subjects were included with

normal baseline spirometry

(FEV1 > 80% predicted,

FEV1/FVC > 0.7) and absence of

any health problems, including

cardiovascular, neuromuscular,

musculoskeletal, or respiratory

diseases that could contribute to

breathlessness or exercise

limitation. (Page 623)

Sample Size A sample size of 16 was used to


16th Group

70

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

difference in Borg ratings of 61,

an SD of 1 for Borg ratings

changes found at our laboratory,

alpha= 0.05 (Page 623)

Eligibility Criteria 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 age-and sex-matched

subjects were included with

normal baseline spirometry

(FEV1 > 80% predicted,

FEV1/FVC > 0.7) and absence of

any health problems, including

cardiovascular, neuromuscular,

musculoskeletal, or respiratory

diseases that could contribute to

breathlessness or exercise

limitation. (Page 623)

Exclusion Criteria Patients were excluded if they

had (1) other unstable medical


16th Group

71

conditions that could cause or

contribute to breathlessness (i.e.,

metabolic, cardiovascular, or

other respiratory diseases) or (2)

other disorders that could

interfere with exercise testing,

such as neuromuscular diseases

or musculoskeletal problems.

(Page 623)

Sampling Frame Total Sampling

Collecting Data Method 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 (16–20) using an

automated pulmonary function

testing system (6200 Autobox

DL and Vmax229d;

SensorMedics, Yorba Linda,

CA). Closing volumes were

measured using the single-breath

nitrogen test as modified by

Anthonisen and colleagues (21).

Measurements were repeated 30

minutes post-bronchodilator (400


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72

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

minus predicted FRC. (Page

623)

Measurement and or assessment In patients with COPD compared

with control subjects, peak

oxygen consumption and power

output were significantly reduced

by more than 20% and dyspnea

ratings were higher for a

givenwork rate and ventilation

(P,0.05). Comparedwith the

control group, the COPD group

had evidence of extensive small

airway dysfunction with

increased ventilatory

requirements during exercise,

likely on the basis of greater

ventilation/perfusion

abnormalities. Changes in end-

expiratory 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 ,


16th Group

73

0.05) and breathing pattern was

correspondingly more shallow

and rapid. Across groups,

dyspnea intensity increased as

ventilation expressed as a

percentage of capacity increased

(P , 0.0005) and as inspiratory

reserve volume decreased (P ,

0.0005). (Page 622)

Instrument Group responses at different time

points and/or intensities during

exercise were compared using t

tests with appropriate Bonferroni

adjustments for multiple

comparisons. Dyspnea

descriptors were analyzed as

frequency statistics and

compared using the Fisher’s

exact test. Physiologic

contributors to exertional

dyspnea intensity in subjects with

COPD were determined by

multiple regression analysis.

(Page 623)

Randomization -

Intervention -

Analysis Method Statistical Method (Page 623)

Coherence between design and objective: coherent


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74

Coherence between measurement and instrument used: coherent

Conclusion: valid (ONLY BASED FROM TWO CONCLUSIONS ABOVE)

3. IMPORTANCE

CI : There is no CI.

P : <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 can’t be measured


16th Group

Documents

Makalah Modul g Kel 16