SGD 7 LBM 6 MODUL RESPIRASI STEP 1 : Ptosis : palpebra cannot open Miosis : condition when diameter of pupil is smaller less than 2 mm Facial anhidrosis : condition where the body cannot product sweat Horner’s syndrome : the combination of clinical manifestation ptosis,miosis,facial anhidrosis Puffy face : swelling of the face Opaque : white appearance in radiograph STEP 2 : 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21.
Pathogenesis? Why can he suffering cough with phlegm? Why does he have shortness of breath? Why the man appearance puffy face? Why the PA found thoracic radiograph define opaque mass? Find the picture Why the result of PE facial anhidrosis,ptosis,miosis? Why does he have fever? Why he has hoarse voice? Why does he decrease his apetite? Why he coughing up blood? Etiology ? What are the risk factor? Clinical manifestation? Classification? DD of opaque mass in lung? What are the Therapy? Supportive examination? The complication? Stage of lung malignancy? Diagnosis examination to evaluate lung malignancy How is the prognosis of lung malignancy
STEP 3 : 1. Pathogenesis? Local tumor growth : presented haemoptisis,wheezing,stridor,abses,atelektasis Invasion / obstruction on nearby structure of lung : pancoast syndrome (shoulder pain) Growth of tumor in regional lymphnode and spread occurs to lymphatic spread until brains,bone,adrenal.if regional tumor spread into thorax that include tracheal obstruction dyspnea,oesophageal compression with dysphagia symptom,etc
Growth in places metastases after hematogeneus spread : ex paraneoplastic syndrome occur as a result of peptide hormon secretion by tumor due tu immunology cross reaction between antigen of tumor tissue and antigen of normal tissue
2. Why can he suffering cough with phlegm? Caused by growth of abnormal cell give a pressure to nerves cough in bronchus. Lung tumor occur in epithel bronchus give pressure to capillary until its rupture. Normal physiology because of iritation of mucous bronchus Cilia heal hypertrophy of mucous cell hypersecret of goblet cell cough with phlegm 3. Why does he have shortness of breath? There are iritation of mucous bronchus obstruction in respyratory tract cannot breathing easily Pleural effusion : fluid in pleural cavity limiting the capacity of lung
4. Why the man appearance puffy face? Derivat symptom secondary metastasis,give preassure to VCS blood cannot regulate to lower part of body edem/puffy face Syndrome result of invasion VCS and caused headache,congestive,swelling 5. Why the PA found thoracic radiograph define opaque mass? Caused by Infiltrat in the lung Opaque : mass or infiltrat Lucent : air in lung Find the picture! 6. Why the result of Physical Examination facial anhidrosis,ptosis,miosis? Ptosis : tumor press the symphatic nerve nerve become paralysis.this nerve have relation with m.levator palpebra the muscle cannot contraction palpebra cannot opened Miosis : Facial anhidrosis : the otonom nerves (control the sweat) was damaged destruction of sweat gland Horner’s syndrom Have a relation with ganglion thoracocervical 7. Why does he have fever? He cannot produce sweat in body heat cannot release from body 8. Why he has hoarse voice? Cause of the nervus laryngeus reccurens have compresed by mass 9. Why does he decrease his apetite?
Apetite controlled by hipothalamus especially nucleus ventromedial has central of satiety,lateral nucleus is central of starve.the body adaptation with molecul HIFA (hypoxi inducible factor 1A) induction of leptin loss apetite Related with nutrition of tumor.tumor need 5x glucose than normal body.ex : esophageal compressiondysphagia symptom,related to decreasing apetite
10. Why he coughing up blood? Tumor can metastasis to respiratory tract press the vascular vascular rupture coughing blood 11. Etiology ? idiopatik inhalation of uranium,chromade and arcent polution decreasing of immunity genetic factor lung disease asbestos (industrial material) expossure 12. What are the risk factor? Hard smoker more than 20 cigar per day Pollution : lung carcinogen (asbestos,arcent,nikel,chromade,zinc,uranium,etc) Scaring of the lung as result of Previous lung disease : undergo malignant transformation like pulmonary TB,chronic bronchitis,etc Genetic factor : mutation of gen, mutation of lung structure Men are high risk factore Passive smoker in women Work or live in bad environment Low consumption of beta carotene,selenium and vitamin A 13. Clinical manifestation? Shoulder pain spread into neck and head Cough with plegm Anoreksia Haemoptysis Secondary symptom: hoarse VCS syndrome : edem in face,dilatation vein in neck and upper arm Chest pain Difficulty to swallow Fever Weight loss Horner’s syndrome
14. Classification? 2 mayor categories : 1. Small cell lung cancer (SCLC) : aggressive and often occur in smokers.rapidly growing and roughly 60 percent of patient have wide spread metastatic disease at time of diagnosis .can be called oatcell CA shape like wheat.therapy using chemotherapy. 2. Non small cell lung cancer (NSCLC) : clinical behavior of NSCLC is more variable and depends on histologic type but 40 percent of patient have metastatic outside of chest at the time of diagnosis .therapy using surgery Based on biologic similarity of treatment and prognosis classificated into 4 : 1. Bronchialveolar carcinoma : spread trans bronchial,the surface of alveolar full of tumor and it can disturb the diffusion system 2. Squamos cell : derived from bronchial epithel and there is ceratinization process 3. Large cell : ususally rises as a large mass in peripheral 4. Adenocarcinoma : most frequently occur in non-smoker 15. DD opaque mass in lung? 16. What are the Therapy? SCLC : chemotherapy NSCLC : surgery Supportive treatment : controll the diet,consumtion vitamin and mineral Treatment symptomatic : morfin,petidine analgetic Treatment for cancer : surgery,radiotherapy,chemotherapy,combination 17. Supportive examination?
Sumber : Aplikasi Klinis Patofisiologi – Valentina L. Brashers 18. The complication?
STEP 4 :
CLINICAL MANIFESTATION
LUNG CANCER
THERAPY
PROGNOSIS
RISK FACTOR
ETIOLOGY
SUPPORTIVE EXAMINATION
PATOGENESIS
DD
COMPLICATION
CLASSIFICATION
STEP 7 1. Pathogenesis? Sebab-sebab keganasan tumor masih belum jelas, tetapi virus, faktor lingkungan, faktor hormonal dan faktor genetik semuanya berkaitan dengan resiko terjadinya tumor. Permulaan terjadinya tumor dimulai dengan adanya zat yang bersifat intiation yang merangasang permulaan terjadinya perubahan sel. Diperlukan perangsangan yang lama dan berkesinambungan untuk memicu timbulnya penyakit tumor. Initiati agen biasanya bisa berupa unsur kimia, fisik atau biologis yang berkemampuan bereaksi langsung dan merubah struktur dasar dari komponen genetik ( DNA ). Keadaan selanjutnya diakibatkan keterpaparan yang lama ditandai dengan berkembangnya neoplasma dengan terbentuknya tumor, hal ini berlangsung lama mingguan sampai tahunan. Kanker paru bervariasi sesuai tipe sel daerah asal dan kecepatan pertumbuhan. Empat tipe sel primer pada kanker paru adalah karsinoma epidermoid ( sel skuamosa ), Karsinoma sel kecil ( sel oat ), karsinoma sel besar ( tak terdeferensiasi ) dan adenokarsinoma. Sel skuamosa dan karsinoma sel kecil umumnya terbentuk di jalan napas utama bronkial. Karsinoma sel besar dan adenokarsinoma umumnya tumbuh dicabang bronkus perifer dan alveoli. Karsinoma sel besar dan karsinoma sel oat tumbuh sangat cepat sehigga mempunyai progrosis buruk. Sedangkan pada sel skuamosa dan adenokar. Paru merupakan organ yang elastis, berbentuk kerucut dan letaknya di dalam rongga dada atau toraksinoma prognosis baik karena pertumbuhan sel ini lambat. ( Zerich 150105′ weblog ) 2. Why can he suffering cough with phlegm? 3. Why does he have shortness of breath? Difficulty in breathing (also known as shortness of breath, breathlessness, or dyspnea) is caused by various mechanisms related to different problems in the body. In one’s lifetime, one may experience rare episodes of shortness of breath as part of high levels of activity like exhaustive exertion, or during environmental conditions such as high altitude or very warm or cold temperatures. Other than these extreme conditions, shortness of breath is commonly a sign of a medical problem.
Recent infections, such as bronchitis or pneumonia, or prolonged (chronic) infections, such as tuberculosis or chronic bronchitis. Shortness of breath may be accompanied by discolored phlegm and/or fever. Asthma, chronic obstructive lung disease (COPD), and emphysema: The airways are narrowed with increased resistance to exhaling air from the lung, resulting in air entrapment in the lung. Shortness of breath may be accompanied by wheezing. With asthma, there is usually an allergy history, whereas with COPD or emphysema, there is usually a smoking history. Lung cancer and other tumors: Shortness of breath is commonly accompanied by unintentional appetite and weight loss. There is usually a long history of heavy smoking. Scarring and damage of lung tissue by toxins (such as asbestosis) or by systemic illnesses (such as rheumatoid arthritis). There is usually a known history of these systemic illnesses or occupational exposures.
Clot in the lung circulation (pulmonary embolus): Breathlessness is usually sudden and associated with rapid breathing and may be accompanied by chest pain. People with blood clots in the legs or pelvis (deep vein thrombosis, or DVT), debilitating medical conditions, immobility, or inherited tendency of forming clots may be prone to this condition (for more information about pulmonary embolism, see the Cardiology Patient Page by Goldhaber and Morrisson. Pulmonary embolism and deep vein thrombosis. Circulation. 2002;106:1436–1438). Diseases of the lung sac (pleura): If the pleura thickens, becomes scarred, or gets filled with fluid or blood because of infection (pleurisy), cancer, or toxins (asbestosis), or if it becomes filled with air (called pneumothorax) because of trauma, it will hinder expansion of the lung, resulting in shortness of breath. Diseases of the diaphragm and/or chest wall: The diaphragm is the muscle that expands the lung. It may become paralyzed after chest surgery. Obesity and spine or chest wall deformities also can produce difficulty in breathing. http://circ.ahajournals.org/content/108/2/e11.full 4. Why the man appearance puffy face? Puffy Face Swollen or puffy face may be normal if you develop it occasionally or once in a blue moon (requiring no medical work-up) however, if you are experiencing frequent episodes of facial puffiness, you should seek immediate medical intervention as it may be a sign of a grave underlying pathology that must be corrected. You should also observe if your family members or siblings had/ have a history of facial puffiness after waking up in the morning. Symptoms of Puffy Face Knowing associated symptoms of puffy face are helpful in diagnosing the primary etiological event that has led to the development of puffy face. The associated symptoms of facial puffiness respond very well to lifestyle modification and home remedies to restore the natural healthy look on your face. 1. Mild Symptoms Mild symptoms that are associated with puffy face includes pain, redness of entire face or localized redness at or around eyes, nose or upper/ lower face. In addition, facial puffiness may also be associated with hives, rashes, bumps or localized lesions. Other mild symptoms include low grade or high grade fever, nausea and sneezing. 2. Severe Symptoms Severe symptoms that are associated with facial puffiness warrant emergent medical attention to prevent life threatening consequences. These symptoms include swelling of throat that may lead to difficulty with swallowing or breathing, swelling of tongue that increases the risk of sudden death due to angioedema and obstruction of respiratory passageways, swelling of nostrils and other vital structures that are associated with breathing. Causes of Puffy Face There are a number of causes that may present as puffy face. Few popular ones are listed as under: 1. Dehydration One of the most common causes of facial puffiness is dehydration. In situations when the total body intake of water is low, the kidneys conserve water by increasing the absorption of water that is stored in soft tissues. Moderate dehydration leads to puffiness of face in addition to swelling of feet and hands. The puffiness of face due to dehydration responds very well to water intake. 2. Dietary Factor Certain foods and nutrients significantly increase the risk of developing temporary puffy face. This includes fatty foods or beverages that dehydrate your body like coffee and tea. In addition to
dehydration, deficiency of vitamin C also presents with puffy face and responds to supplemental vitamin C and water- melon juice. If you consume alcohol in moderate amounts, cutting down intake also helps tremendously. 3. Kidney Diseases Kidney diseases (or renal failure) may also present with puffy face but in vast majority of cases, the swelling is more pronounced in the peri-orbital region, hands and feet. Speak to your healthcare provider if you are also experiencing urinary symptoms that points to a renal pathology. 4. Hypothyroidism Hormonal disorders are yet another common cause of puffy face due to alteration in the normal metabolic pathways. In addition to puffy face, you will also have other symptoms of hypothyroidism like weight gain, constipation, dryness of skin and changes in the rhythm of heart. 5. Cushing's Syndrome Cushing’s syndrome is marked by high cortisol levels that alter normal vascular metabolism and leads to a round moon-shaped puffy due to deposition of fat. It may be a result of endogenous hyper-secretion of cortisol or exogenous intake of steroids to relieve chronic inflammatory conditions like arthritis, asthma or other similar ailments. 6. Other Causes Other uncommon conditions that may also present with puffy face includes obesity, insect bite, allergic reaction to drugs or certain foods, angioedema, abscess or infection of tooth, sinuses or associated structures of head and neck region, nephritic or nephrotic syndrome, mumps and swelling of salivary glands (like inflammation of parotid gland). Relieves for Puffy Face 1. Dietary Methods Dietary modifications are helpful in relieving puffiness of face without requiring any other intervention. Maintain high hydration status by increasing your water intake to at least 2 liters per day. Salt osmotically attracts water and aggravates the symptoms of edema. Limiting your salt intake is extremely helpful if you have puffy face due to renal problem or hypertension. High alcohol intake is associated with dieresis (excretion of large amounts of water in urine). Eat Healthy and balanced diet that is rich in quality vitamins and minerals. 2. Regular Exercises Perform regular physical activity since sometimes the inflammatory reactions block lymphatics leading to puffiness of face. With regular physical therapy and simple stretching exercises you can relieve edematous swelling of the face and other parts of the body. 3. Homemade Remedies Home remedies are helpful in alleviating the symptoms of puffy face. You can try these remedies for speedy recovery: Cold Milk. In situations when the swelling on your face is due to an abscess or sore, application of cold milk with cotton ball is helpful in reducing the pain, swelling and inflammation by acting as a cleansing agent. Moreover, also wash your face throughout the day with cold water (without any soap). Cold Creams and Lotions. You can also store your creams and lotions in refrigerator (especially in hot humid days) to alleviate puffiness of face. Cold Compress. Cold compresses are helpful if you have developed an inflammatory or painful swelling due to trauma or underlying inflammation (abscess) 4. Sleeping Position
Changing your sleeping position also helps a great deal. Using higher pillows usually helps in reducing edema of face due to abnormal posture. However, caution must be maintained since high pillows or higher head support may also lead to neck-pain, insomnia or breathing difficulties. 5. Medications Depending upon the cause of puffy face, your healthcare provider may advise you antibiotics or anti-viral medications to relieve the symptoms due to bacterial or viral infections. You may also get benefitted from steroids if you have developed puffy face due to allergic reaction, anaphylaxis or insect bite. http://www.med-health.net/Puffy-Face.html 5. Why the PA found thoracic radiograph define opaque mass? Find the picture
Radiological examination is the most important examination is used to diagnose lung cancer. Lung cancer has a varied picture of radiology. This check is performed to determine tumor malignancy by looking at the size of the tumor, lymph nodes, and metastasis to other organs. Radiological examination can be done using computer tomography. In computer tomography lung cancer relationship can be seen with the thoracic wall, bronchi, and blood vessels clearly. Advantages of computer tomography not only show bronchus, but also the structure around the lesion and tumor invasion into the thoracic wall. Computed tomography also has a higher resolution, can detect small lesions and tumors that are hidden by the adjacent normal structures
Fig. 9-2. Carcinoma of the lung. A. The PA radiograph demonstrates a subtle increase in density at the inferior portion of the right hilum that would probably be unobserved without the lateral film. B. The lateral view demonstrates an obvious retrosternal abnormality ( arrow ). The mass was in the right upper lobe and was a primary lung cancer. It is critical to remember that a fluid level, and particularly an air fluid level, is not visible unless the beam is in a horizontal projection, regardless of the patient's position;
P.117 http://flylib.com/books/en/3.98.1.14/1/
http://www.pitt.edu/~super1/lecture/lec18121/003.htm 6. Why the result of PE facial anhidrosis,ptosis,miosis?
Horner syndrome
Key points • Horner syndrome is characterized clinically by miosis, ptosis, and anhidrosis. • The lesion is due to disruption of the oculosympathetic pathway. • Carotid dissection is a potentially life-threatening acute etiology. • Pharmacologic testing with cocaine or apraclonidine can confirm the clinical diagnosis of Horner syndrome. • Imaging of the entire oculosympathetic axis may be indicated in the evaluation of Horner syndrome. Historical note and nomenclature
The syndrome of ptosis, miosis, and anhidrosis due to a lesion in the sympathetic pathway to the eye is known commonly as Horner syndrome. Johann Friedrich Horner was a talented and well-respected 19th-century Swiss ophthalmologist. In 1869, he described a 40-year-old woman with headaches who had a right droopy eyelid, smaller right pupil, and right facial flushing. He attributed the findings to damage of the cervical sympathetic nerves to the eye. Although his case was not the first to report the clinical effects of damage to the cervical sympathetic nerves, his name has become an eponym for the triad of ptosis, miosis, and anhydrosis. Professor Horner is also remembered as the founder of Swiss ophthalmology. Because the French physiologist Claude Bernard described the signs of sympathetic injury in animals 17 years earlier in 1852, the syndrome is also called Bernard-Horner syndrome in some parts of the world (Pearce 1995). Clinical manifestations Horner syndrome is caused by a lesion of the sympathetic pathway supplying the head, eye, and neck. Ptosis. There is both upper and lower lid ptosis due to loss of sympathetic innervation to the superior and inferior tarsal muscles. The upper lid ptosis is usually mild and can be voluntarily overcome if the patient utilizes the levator palpebrae and frontalis muscles excessively as these are not innervated by the oculosympathetic nerves. One way to check for lower lid ptosis is to ask the patient to look upward slightly. In the eye with an oculosympathetic defect, the inferior corneal margin abuts the lower lid margin (upside down ptosis). In the normal eye, sclera is visible between the inferior corneal limbus and the lower lid margin. This lower lid ptosis is also known as "reverse" or "upside-down ptosis." Apparent enophthalmos. In the relaxed state, the combined upper and lower lid ptosis narrows the palpebral fissure and creates the false impression of enophthalmos (Thompson 1977;Miller 1985). Measurement with an exophthalmometer reveals the enophthalmos to be apparent only. Miosis. The anisocoria of a Horner syndrome is generally small, about 1.0 mm or less. The miosis (smaller pupil) results from a lack of an active pupillodilator due to an oculosympathetic defect; therefore, the anisocoria is greater in darkness than in room light. In ambient room light conditions, the anisocoria can be clinically inapparent if the parasympathetic pupilloconstrictor activity overshadows the unequal sympathetic pupillodilator activity between the 2 eyes. Therefore, it is important to always check the pupils in room light and in darkness as well as with added light. Dilation lag. A normal pupil will dilate promptly within 5 seconds after the light is turned off. This is chiefly due to sympathetic activation of the pupillodilator that "pulls" the pupil open. However, a Horner pupil lacks this activity and dilates slowly, over 15 to 20 seconds, from parasympathetic inhibition "letting go" of the pupilloconstrictor (Lowenstein and Loewenfeld 1950). Because the pupils need to be observed simultaneously in the dark, a camera with infrared viewing greatly facilitates the examination for dilation lag. Clinical photographs of the pupil may be useful for documentation of dilation lag. Using a flash Polaroid or digital camera, the decreasing anisocoria between 5 and 15 seconds in darkness can be easily recorded with static photographs. Finding a change (decrease) in anisocoria of 0.4 mm or more between 5 and 15 seconds after a light flash is 100% specific for Horner syndrome, but unfortunately, not all Horner patients demonstrate this finding (Kawasaki and Kardon 2004). Drowsiness causes miosis and obscures dilation lag, so arouse the patient before testing. The dilation lag may also only
be intermittently present, and the absence of the dilation lag does not rule out Horner syndrome (Crippa et al 2007). In the clinically suspect patient, pharmacologic testing must be pursued. When a patient is suspected of having a bilateral Horner syndrome, asymmetry of pupillary dilation and pharmacologic responsiveness can no longer be used for diagnostic purposes. Infrared computerized pupillography has been utilized to define dilation lag as the recovery time (in seconds) to baseline pupil size after a light flash and, thus, may be useful in detecting bilateral Horner syndrome because the recovery time is compared against established normative values, not the patient's contralateral pupil (Smith and Smith 1999). Anhidrosis. Because the sympathetic plexus accompanying the internal carotid artery innervates sweat glands only to the medial forehead (Salvesen 2001), facial anhidrosis does not occur significantly with postganglionic Horner syndrome. Among patients with central and preganglionic Horner syndrome, in which there is loss of the vasomotor sympathetic fibers to the face, the patient may or may not complain of decreased sweating on 1 side, depending on whether the patient sweats enough to notice the asymmetry. A clinical test for anhidrosis is the iodine starch test. Powdered starch is applied to both sides of the patient's face and the patient is warmed under a heating lamp for several minutes. Sweat turns the powder blue and shows areas of anhydrosis. Hemifacial sweating may also occur (Sarikaya 2011). Iris heterochromia. Unequal iris color is suggestive of a congenital Horner syndrome but is not pathognomonic. The iris on the side with Horner syndrome fails to develop normal ocular pigment during infancy and is, therefore, lighter in color (Weinstein et al 1980). Subclinical Horner syndrome. A "subclinical" Horner syndrome (ie, prior history of unilateral ptosis and miosis that seemingly resolved clinically) may still test positive for a defect in the oculosympathetic pathway using the pharmacologic cocaine test. Subclinical Horner syndrome has been reported with cervical cord lesions and carotid artery dissection (Leira et al 1998). Slavin reported 1 such case of a Horner syndrome without anisocoria due to underlying physiologic anisocoria (Slavin 2000). http://www.medlink.com/medlinkcontent.asp 7. Why does he have fever? 8. Why he has hoarse voice? Hoarseness is defined as an abnormal sound when you try to speak. This may be described as raspy, breathy, soft, tremulous or as changes in the volume of your voice. You may also experience pain or a strained feeling when trying to speak normally. A hoarse voice can be caused by anything that interferes with the normal vibration of the vocal cords, such as swelling and inflammation, polyps that get in the way of the vocal cords closing properly or conditions that result in one or both of the vocal cords becoming paralyzed. Hoarseness is also referred to by the medical term "dysphonia." http://lungcancer.about.com/od/Respiratory-Symptoms/a/Hoarseness.htm 9. Why does he decrease his apetite?
TNF menguluarkan enzim lipoproteinase lemak di jaringan menipis tampak kurus.
Gejala malaise sering ditemukan berupa anoreksia tidak ada nafsu makan, badan makin kurus ( berat badan turun ), sakit kepala, meriang, nyeri otot, keringat malam. Gejala malaise ini makin lama makin berat dan terjadi hilang timbul secara teratur. Hal tersebut dipengaruhi juga oleh proses inflamasi yang terjadi dalam tubuh pasien tersebut, pada inflamasi di produksi TNF ( Tumor Necrosis Factor ) yaitu sitokin untuk menghambat pertumbuhan tumor dan menghancurkan sel – sel tumor. Di lain pihak, TNF menyebabkan anoreksia yang hebat melalui efeknya pada pusat nafsu makan di hipotalamus. TNF menimbulkan hambatan pengosongan di lambung sehingga menimbulkan perasaan kenyang. Di samping itu TNF menghambat kerja enzim lipoprotein lipase, yaitu enzim yang memindahkan lemak dalam serum ke sel – sel lemak sehingga lemak disintesis dan di simpan. Dengan adanya TNF, cadangan lemak dalam jaringan menjadi sangat menipis sehingga penderita tampak kurus. Karena walaupun asupan nutrisi berkurang, tumor yang berkembang biak menyebabkan terjadinya peningkatan metabolisme.Selain itu TNF dalam jumlah besar dapat menyebabkan gangguan metabolisme berat seperti gula darah turun sampai kadar yang tidak memungkinkan untuk hidup. Hal ini disebabkan karena penggunaan yang berlebihan glukosa oleh otot dan hati dan gagal untuk manggantikannya. Badan penelitian dan pengembangan kesehatan. Survei kesehatan rumah tangga (SKRT) tahun 1995. Departemen Kesehatan Republik Indonesia, 1995.
Process of eating disorders-not eat or refuse to eat - an eating disorder or drink consumption with the type and amount of physiologically appropriate age, from
opening his mouth without force, chewing, swallowing up until well absorbed in the digestive tract without coercion and without vitamin and certain drugs. So in the process of eating disorder itself is a symptom or sign of irregularities, abnormalities and diseases that are happening in a person's body. While the psychological effects associated with eating behavior that is sometimes determined by environmental, social and mental that can be consciously controlled during the day such as eating habits, eating because of the delicacy of the food served to improve the taste, the condition of stress, anxiety and depression easily change diet . Actually appetite was associated with nerve signals that affect hormones and enzymes when the stomach is empty or loaded. Appetite can also occur at the level of taste sensors on the tongue, including the stomach and the hunger signals from the brain. The process begins when the nerves in the stomach and intestine where the brain receives information from the contents of the stomach and intestinal digestion and metabolism of nutrients from the heart, including an increase in glucose concentration after a meal causes the stimulation of the surrounding stomach and intestines into several neural networks, information is excitatory then forwarded to the hypothalamus in the brain There are two areas in hipothamus nerve signals (brain) that play a role in appetite (eating response) is an area called the satiety center (satiety system) and an area called the hunger center or center meal (feeding system). Some medical experts and health of appetite explains, there are several input signals that play a role in the regulation of the two regions appetite (eating response) and will result in eating behavior that the body needs these signal inputs diantaranta Kader Leptin, Ghrelin, Gastrointesyinal distension, Secretion Colecistokinin and usage levels of glucose and insulin sekresin. Each of these can be explained as follows: Leptin Levels Leptin is a hormone produced by cells in the adipose tissue (fat tissue). Leptin levels increased in proportion to the number of trigeliserida fat deposits in adipose tissue. The more fat stores more and more leptin is secreted, the presence of leptin will cause suppression of the desire to eat. The more levels of leptin, the appetite decreases, whereas the less leptin levels the greater the desire to eat. The main function of this hormone is the control of eating, especially regarding eating disorders, especially obesity. Ghrelin Levels Ghrelin is an appetite stimulant, mostly in production in the stomach, ghrelin is able to cause an increase in food intake and reducing consumption of fat reserves. Grelin also functions as a stimulant of growth hormone secretion (Growth Hormone), food intake and weight gain. Ghrelin secretion increases in negative energy balance conditions such as starvation, anorexia nervosa and others. And vice versa Ghrelin levels
decreased in positive energy balance condition such as after a meal, hyperglycemia and obesity. Gastrointestinal distention When the stomach and intestines filled with food then the nerves that are in the stomach and intestines will be stimulated, a nerve impulse signals are down to the core of the nerve tract, will be delivered to the central regulation of appetite in the brain (hypothalamus). There are two feedback signals will be issued by the otal signal satiety and hunger signals. In the state of Gastrointestinal distension or when the stomach and intestines filled, the brain releases a satiety signal, otherwise if the stomach and intestines to be empty, then the brain will emit a signal or signals are hungry eat. Secretion Colecistokinin (CCK) Secretion Colecistokinin (CCK) is a hormone secretion from the mucosal wall of the intestine (duodenum) during digestion of foods that contain fat. The existence of secretion Colecistokinin shows full signal. CCK also lead to an increase in the hormone serotonin in the hypothalamus. Serotonin is a hormone associated with feelings of calm (comfortable), in terms of eating will support a feeling of comfort after meals. Sherwood, Lauralee. Human Physiology. 6thed. USA: The Thomson Corporation. , 2007. Guyton A.C. Physiology of the Human Body. 5th ed. Philadelphia: W.B. Saunders Company. , 1979
10. Why he coughing up blood?
Paparan dari bahan – bahan seperti asap rokok, polutan ( karsinogenik ) dalam jangka waktu yang lama terinhalasi ke saluran pernafasan mengaktifkan reaksi imunitas berupa reaksi inflamasi bronkokonstriksi, hipervaskuler dan hipersekresi mukus apabila hal ini terus terjadi maka akan terjadi perubahan – perubahan seperti rusaknya silia dan perubahan metaplasia ( perubahan bentuk epitel bronkus ) pembuluh darah disekitarnya berdilatasi dan bila berlangsung terus menerus pembuluh darah tersebut bisa ruptur dan rusak darahnya bisa keluar dan bercampur dengan mukus mengaktifkan reseptor batuk batuk darah Arif N. Batuk darah dalam pulmonologi klinik. Bagian pulmonologi FKUI; Jakarta :1992, 179-183 11. Etiology ?
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Paparan atau inhalasi berkepanjangan suatu zat yang bersifat karsinogenik : o Asbestos mesotelioma jinak local/ganas difus dari pleura adalah tumor langka yang secara spesifik berkaitan dengan pajanan terhadap asbes. o Radiasi ion pekerja tambang uranium
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o Radon, arsen (mis. insektisida), kromium, nikel, polisiklik hidrokarbon, vinil klorida Kebiasaan merokok (aktif atau pasif) Polusi udara Genetic perubahan/mutasi beberapa gen yg berperan dalam kanker paru (Proto oncogen, Tumor suppressor gene, Gene encoding enzyme) Diet rendahnya konsumsi terhadap betakarotene, selenium & vit A Buku Ajar IPD ed IV jilid II. FK UI.
12. What are the risk factor?
Faktor yang mempengaruhi: Merokok (baik perokok aktif maupun perokok pasif) Bahaya industry Asbesbanyak digunakan diindustri bangunan. Pekerja berisiko terkena 10 kali lebih tinggi dibandingkan masayarakat umum. Mesotelioma jinak local/ganas difus dari pleura adalah tumor langka yang secara spesifik berkaitan dengan pajanan terhadap asbes. Uranium, kromat, arsen (misal: insektisida yang digunakan untuk pertanian), besi dan oksida besi . Polusi udara Faktor lain : makanan & kecenderungan familial Perokok yang makanannya rendah vitamin A memiliki risiko yang lebih besar untuk menjadi kanker paru. Anggota keluarga pasien kanker paru berisiko lebih besar terkena penyakit ini. Sylvia A. Price & Lorraine M. Wilson. Patofisiologi ed 6 vol 2. EGC. 13. Clinical manifestation? Ca bronkogenik : Batuk gejala umum yg sering diabaikan atau dianggap sebagai akibat merokok atau bronchitis Hemoptisis Gejala awal : mengi local & dispnea ringan akibat obstruksi bronkus Nyeri dada dapat timbul dalam berbagai bentuk perasaan sakit atau tidak enak akibat penyebaran neoplastik ke mediastinum Nyeri pleuritik bila terjadi serangan sekunder pada pleura akibat penyebaran neoplastik atau pneumonia Pembengkakan jari yg timbul cepat dikaitkan dg Ca bronkogenik (30% kasus NS CLC) Gejala2 umum : anoreksia, lelah, ↓ BB Gejala penyebaran intratorax atau extrathorax : Penyebaran local tumor ke struktur mediastinum suara serak akibat terserangnya saraf laringeus rekuren
14.
Disfagia keterlibatan esophagus Peralisis hemidiafragma keterlibatan saraf frenicus Penekanan VCS sindrom Vena cava (pelebaran vena di leher & edem pada wajah, leher & lengan atas) Nyeri dada atau temponade jantingnakibat penyebaran ke dinding dada atau pericardium secara terpisah Tumor2 yg berkembang di apex paru (tumor Pancoast) dapat melibatkan plexus brachialis nyeri & kelemahan pada bahu dan lengan bagian yg terkena; ganglion simpatikus dapat terkena sindrom Horner unilateral (ptosis & kontriksi pupil unilateral serta tidak adanya produksi keringat pada bag yg sama dg wajah) Gejala ekstrathorax bergantung pada tempat metastasis. Struktur yg sering terserang : KGB skalenus, kel adrenalis (50%), hati (30%), otak (20%), tulang (20%), ginjal (15%). Sindrom paraneoplastik : berkaitan dg kanker paru Sindrom endokrin (12%) Tumor sel oat : menghasilkan hampir seluruh hormone polipeptida, seperti hormone paratiroid (PTH), hormone adrenokortikotropik (ACTH), atau hormone antidiuretik (ADH)gejala hiperparatiroid, sindrom Cushing, sindrom ketidaktepatan sekresi ADH (SIADH) berhubungan dg retensi cairan & hiponatremia. Sindrom jar ikat rangka : jari tabuh (biasanya pada NS CLC) timbul pada 30% kasus dan osteoartropati hipertrofik (HOA) hingga 10% kasus (biasanya pada adenoCa) Gejala sistemik : anoreksia, ↓ BB, dan kakeksia pada 30% kasus adalah sindrom paraneoplastik yg tidak diketahui asalnya. Sylvia A. Price & Lorraine M. Wilson. Patofisiologi ed 6 vol 2. EGC. Classification?
Secara patologi, untuk menentukan terapi: a) Kanker paru sel kecil (small cell lung cancer, SCLC) Gambaran histologist khas : dominasi sel2 kecil hamper semua diisi mucus dg sebaran kromatin yg sedikit sekali tanpa nucleoli. Disebut juga “oat cell carcinoma” karena bentuknya mirip biji gandum. Sel ini cenderung berkumpul sekeliling pembuluh darah halus menyerupai pseudoroset. Sel2 yg bermitosis banyak sekali ditemukan begitu juga gambaran nekrosis. DNA yg terlepas myebabkan warna gelap sekitar pembuluh darah. b) Kanker paru sel tidak kecil (non small cell lung cancer, NSCLC) Termasuk didalamnya adalah epidermoid, adenokarsinoma, tipe-tipe sel besar/campuran dari ketiganya. Karsinoma sel sqamos berciri khas proses kreatinisasi & pembentukan “bridge” intraseluler. Secara sitologi adanya perubahan nyata dari dysplasia squamosa ke Ca insitu. Diagnosis terlokalisasi, diatasi dengan reseksi bedah. Buku Ajar IPD ed IV jilid II. FK UI.
Sumber : Buku Saku Patofisiologi Corwin Oleh Elizabeth J. Corwin 15. DD of opaque mass in lung? 16. What are the Therapy?
Sumber : Aplikasi Klinis Patofisiologi – Valentina L. Brashers 17. Supportive examination? 18. The complication? 19. Stage of lung malignancy?
System stadium TNM Internasional atau Kanker paru 1997 American Joint Committee on Cancer (dimodifikasi dari Mountain CF : Revisions in the international system for staging lung cancer, chest 111 : 1710-1717, 1997) : Gambaran TNM STATUS TUMOR PRIMER T0 Tx
Tis T1 T2
T3 T4
KETERLIBATAN KGB REGIONAL (N) N0 N1 N2 N3
DEFINISI Tidak terbukti adanya tumor primer Ca yg tersembunyi terlihat pada sitologi bilasan bronkus, tetapi tidak terlihat pada radiogram atau bronkoskopi Ca in situ (ditemukan sel tumor di suatu tempat & belum menyebar) Tumor berdiameter ≤ 3 cm dikelilingi paru atau pleura viseralis yg normal Tumor berdiameter > 3 cm atau ukuran berapapun yg sudah meyerang pleura viseralis atau mengakibatkan atelektasi yg meluas ke hilus; harus berjarak 2cm dari karina, tetapi tidak mengenai karina Ukuran tumor diameter 5 cm Tumor berukuran berapapun dg perluasan langsung pada dinding dada, diafragma, pleura mediastinalis, atau pericardium tanpa mengenai jantung, pembuluh darah besar, trachea, esophagus, atau korpus vertebra; atau dalam jarak 2 cm dari karina , tetapi tidak mengenai karina
Tidak dapat terlihat metastasis pd KGB regional Metastasis pd peribronkial dan/atau kelenjar2 hilus ipsilateral Metastasis pd mediastinal ipsilateral atau KGB subkarina Metastasis pd mediastinal atau KGB hilus kontralateral; KGB skalenus atau supraklavikular ipsilateral atau kontralateral
METASTASIS JAUH (M) M0
Tidak diketahui adanya metastasis jauh Metastasis jauh terdapat pd tempat tertentu (missal otak)
M1
KELOMPOK STADIUM Ca tersembunyi
Tx, N0, M0
Stadium 0 Stadium IA
Tis, N0, M0 T1, N0, M0
Stadium IB
T2, N0, M0
Stadium IIA
T1, N1, M0
Stadium IIB
T2, N1, M0 T3, N0, M0
Stadium IIIA
T1-T3, N1, N2, M0
Sputum mengandung sel2 ganas tetapi tidak dapat dibuktikan adanya tumor primer atau metastasis Ca in situ Tumor termasuk T1 tanpa adanya bukti metastasis pd KGB regional atau tempat yg jauh Tumor termasuk klasifikasi T2 dengan bukti metastasis pd KGB regional atau tempat yg jauh Tumor termasuk klasifikasi T2 dengan bukti hanya terdapat metastasis ke peribronkial ipsilateral atau hilus kelenjar limfe ; tidak ada metastasis ke tempat yg jauh Tumor termasuk klasifikasi T2 atau T3 dengan atau tanpa bukti metastasis ke peribronkial ipsilateral atau hilus kelenjar limfe; tidak ada metastasis ke tempat yg jauh Tumor termasuk klasifikasi T1,T2 atau T3 dengan atau tanpa bukti metastasis ke peribronkial ipsilateral
Stadium IIIB
T berapapun, N3, M0 T4, N berapapun, M0
Stadium IV
T berapapun, N berapapun, M1
atau hilus kelenjar limfe; tidak ada metastasis ke tempat yg jauh Setiap klasifikasi tumor dg metastasis ke hilus kontralateral atau KGB mediastinum atau ke skalenus atau kel limfe supraklavikular; atau setiap tumor yg diklasifikasikan sebagai T4 dg atau tanpa metastasis ke KGB regional; tidak ada metastasis ke tempat yg jauh Setiap tumor dengan metastasis jauh
Sylvia A. Price & Lorraine M. Wilson. Patofisiologi ed 6 vol 2. EGC. Non-small cell lung cancers (NSCLC) are assigned a stage from I to IV in order of severity.
In stage I, the cancer is confined to the lung.
In stages II and III, the cancer is confined to the lung and, possibly, the lymph nodes.
Stage IV cancer has spread outside of the lung to other parts of the body.
Small cell lung cancers (SCLC) are staged using a two-tiered system:
Limited stage (LS) SCLC refers to cancer that is confined to its area of origin in the lung and lumph nodes.
In extensive-stage (ES) SCLC, the cancer has spread beyond the lung to other parts of the body.
http://www.webmd.com/lung-cancer/guide/stages-of-lung-cancer 20. Diagnosis examination to evaluate lung malignancy
Sumber : Aplikasi Klinis Patofisiologi – Valentina L. Brashers 21. How is the prognosis of lung malignancy
