Medical

Semiology Review
Guidelines for 1 semester Exam
(Based on Professors material, McLeodss, Extended matching questions (EMQs) in Clinical Medicine and personal extras) Alessandro Motta, Medicine Class in English, 3rd Year, UVVG

Cardiology: diseases, cardiopathies, valvulopathies Respiratory: diseases and syndromes How to approach a cardiac patient? In order to understand this introductive chapter we have to take care about identify a normal situation and a pathological one and correlate signs and changes at the physical examination with a possible cardiovascular disease. The steps are: performing a correct anamnesis and a proper examination of the patient.
Why the anamnesis could help us in our investigation? There are many pathologies that could affects the heart specifically in pediatrics field (e.g. atrial or ventricular septal defects, the cor pulmunale in young males or the mitral valve defect in females) and others complications may spread in adult age because of infections or rheumatic fever occurred in childhood. Other factors that influence the anamnesis are geographical data, family story, physiological data, and of course personal history and social status.

At a general examination three main symptoms can be founded in cardiac patient: Pain Dyspnea Palpitation The typical pain in heart problems is called angina pectoris, and is the main manifestation of coronary disease, so the lack of oxygen in the main responsible. The typical angina comes with substernal pain and discomfort, a sense of constriction to the mediastinum, and a rate of duration and depth usually common to many patients; it starts with efforts. It also irradiates to the left shoulder until the arm and even in the dorsal side. Rest or assumption of nitroglycerine relieves it. The atypical angina meets just two of the abovementioned signs and the non-cardiac pain could meet just one of them.
Other types of cardiac pain are the following: Prinzimental angina, is a variation of this type, and is made by coronary spasms; it usually comes at same hours in night/day Non-ischemic pain, derived by pericarditis, aortic causes or hypertension

I suggest you also this site: http://www.fastbleep.com/medical-notes/ really cool and feature a large selection of notes in cardiology for medical students

The second sign is the dyspnea: we all know this means the difficulty in respiration. In this specific case is triggered by pulmonary stasis or low cardiac output. It comes with Cheyne-Stock respiration:

Other types of dy. are the executional (linked to the effort) and the at rest one that is related with orthopnea (e.g. how many pillows you need?). Episodes of paroxysmal dyspnea may occur: in nighttime, with frightening awakes of patients, with cardiac asthma or with acute pulmonary edema (emergency case).

Palpitations are a set of unpleasant sensations in which aware patients of an irregular, hard or rapid heartbeat. May be triggered by hyperactivity of CNS or by abnormal cardiac states. These could be enhanced by physical condition (coffee, smoking, effort and stress) or by any cardiopathy. How to perform a general physical exam? In this phase do not look directly at cardiac status by try to correlate some situations with it. Look at mental status, specific syndromes, physical attitudes, face and skin/mucosa, joints and so on. Any changes in one of these factors could suggest you a specific condition. E.g. a baby that prefer to rest in squatting position is probably doing that because his body need to distribute the blood to the brain, so it would suggest a congenital cardiopathy. How to perform a physical exam for cardiac diseases? The inspection is performed in the precordial area, the epigastrium and the cervical region (ant.).

Hence at palpation we should check for apex impulse (mitral area), thrill, pericardial rub and others. The apex impulse corresponds to a ventricular systole, so we have to pay attention for displacement in the area (a dilatation could present a bigger area) the amplitude/force that could rise in hypertrophies and volume overload. The thrill sounds like a murmur (cats purring) and could be heard as diastolic or systolic. The pericardial Rub is described as scratching or friction with leather and is audible in pericarditis. Other enhanced sounds are given by valve closure. In the auscultation of the heart we have to look back at the picture in the previous page and give a nice rehearse to the heart sounds meanings. This wonderful picture synthesizes murmurs and some pathological meanings. Always try to keep in mind a simple rule to auscultation: 1. Sound is LUB and corresponds to the beginning of systole, when mitral and tricuspid valve close 2. Sound is DUB and means the end of systole with the start of a new diastole. Comes with closure of aortic and pulmonary valves. 3. Sound is normal in childhood, pathological in adults: left ventricle problems 4. Sound formation is due atrial hypertrophy
I wont insist in hs. to avoid confusions

Now that well start with diseases I have to be transparent with you, professors presentations are perfect for his lessons in course room where him eviscerate the argument taking inspirations by those writings but I personally find a mess to ground my knowledge about syndromes and pathologies on those slides So I will take them in account by Id rather write case-by-case definitions and clinical aspects, or you and probably I too wont remember these notions for a long As Mr. Pop wrote in a ppt: I hope you wont memorize all these names, just get an Idea Here the list of diseases, I included what was most important in presentations and ECG findings:

Valvular heart diseases: Regurgitation/stenosis Mitral/Aortic Ischemic Cardiopathies: CAD, coronary artery disease Endocarditis Arrhythmias and conduction troubles Aortic Dissection Venous Diseases Cardiac Failure

Valvulopathies:

The regurgitation is a failure of valve closure, which leads to back flow of blood. The stenosis is the narrowing of valves when it is open. In mitral regurgitation a part of blood flows back from left ventricle to the respective atria, diminishing the output in the aorta. The acute form bring with it a pulmonary edema, the chronic form triggers an enlargement of right side, especially right atrium, with raised pressure in lungs in a long period of time. Causes of this disease may involve all the components of the valve (valve prolapse, chordae tendinee, dysfunction in papillary muscles). The valve itself gives the primary form, while the secondary one is given by dilation of left ventricle.

ECG findings: mitral P wave, hypertrophy of LV and RV, supraventricular arrhythmias. Mitral stenosis is more common in women, the valve cause an impediment to the blood normal flow, creating a pressure gradient and increasing pressure of left atrium (triggers embolism and pulmonary capillary increased pressure). The usual etiology is the rheumatic fever; it could be also congenital and degenerative. Clinical signs are jugular distension, ascites, edema and mitral facies (redness of cheeks). In this pathology is audible a murmur before the first sound, presystolic accentuation. ECG findings: mitral P wave, hypertrophy of LV and RV, supraventricular arrhythmias, atrial fibrillation. Aortic regurgitation means the diastolic blood flow from the aorta into the left ventricle. It has a chronic and an acute form, leads to left ventricular hypertrophy and heart failure. In acute phases as a result of pressure well notice pulmonary edema, usually is severe and leads to failure and cardiogenic shock. The murmur will result as a prolonged S2. ECG findings: tall R waves in V5, V6 and tall T waves too. Aortic Stenosis could be either congenital, degenerative or due to rheumatic fever. The pressure in the left ventricle triggers a hypertrophy of this last. The contractility diminishes, and so decreases the output leading to cardiac failure. The classic triad of clinical signs is: angina, syncope in exercise, dyspnea. Pulsus parvus et tardus: murmur with a crescendo-decrescendo systolic ejection, just after the first sound. ECG findings: Left Ventricle Hypertrophy

Coronary Artery Disease (CAD) triggers ischemic cardiopathies, this basically means an unbalance between oxygen need and intake. Main causes are atherosclerosis and embolism, and usually is a progressive disease that begins in childhood and manifest in adulthood, men are more affected and geographical area (nutritional factors) is highly important. Classification of CAD: Without pain: arrhythmias, sudden death With pain: stable or unstable angina and acute myocardial infarction Chronic, with a stable angina manifested in effort Acute syndromes, with unstable pain and acute myocardial infarction Acute Myocardial Infarction = ST segment elevation = Acute Coronary Syndrome (STEMI) ***STEMI: s-t elevation in myocardial infarction ECG findings: check the picture on the right; the T is hyper acute, pathological Q wave indicates necrosis (case E on picture) How to understand where is the infarct? Anterior: V2-V4 (less from V1to V6) Lateral: V5-V6, I, aVL Inferior: II, III, aVF *For completeness there is also a change in enzymes creatine kinase, troponin and lactate dehydrogenase, some days after the onset. I wont be more precise! The Endocarditis is an infection of the endocardial surface, including valves. There are intracardiac effects such as valvular insufficiency, congestive heart failure or myocardial abscesses, and there are also systemic signs (sterile/non sterile emboli and immunological changes). This picture synthesize all clinical findings:

Just the last reminder: a past bacteremia triggered by either surgical procedures, dental operations and other medical procedures could give in time a more dangerous endocarditis, mainly because those forms of bacteria in time could deposit in endocardium and vegetate. ECG findings? Are depending on which area of the endocardium or valves is affected, there is not a general rule. Arrhythmias and conduction troubles are generated by abnormalities in generation and/or conduction of electrical impulses in the normal network of the heart. At this point is important underline how changes can affect both Rate and Rhythm. Briefly now and case by case later: Atrial Fibrillation = upper heart chambers contract irregularly Bradycardia = slow heart rate Conduction Disorders = heart does not beat normally Premature contraction = early heart beat Tachycardia = very fast heart rate Ventricular Fibrillation = disorganized contraction of the lower chambers of the heart How conduction can be altered? Sympathetic stimulation increases it Vagal stimulation decreases it Ischemia and hypoxia decrease it Drugs (adrenergic = increase, Cholinergic = decrease) The Atrial Flutter is a condition of normal ventricular rhythm but in coexistence with rapid atrial contractions (200-350bpm). It could be triggered by right-sided heart dilation, mitral valve disease, ischemic heart disease, pulmonary embolism, thoracic surgery, hypoxia, and electrolyte disturbances. Give as consequences thromboembolism and cardiac failure.

The Atrial Fibrillation is different from the abovementioned; in this condition the atria depolarize rapidly and irregularly, usually resulting in an atrial rate more than 350/min. Various stages from the less to the most dangerous: paroxysmal, permanent, persistent (irreversible). Ventricular arrhythmia is a condition of multiple and disorganized ectopic beats, in this ECG you can see various QRS complexes spreading between two ordinary one, from one single ectopic each 1 normal beat until one ectopic each 4, or even two or three ectopic in sequence. P waves are usually hidden by those extra QRSs.

 In this picture you can appreciate probably the most severe form of arrhythmia: the ventricular fibrillation, cause of no mechanical response and of cardiac arrest. The Torsade de Pointes is a curious condition in which the ventricular arrhythmia triggers a twisting of the axis around the isoelectric line, with wide QRS complexes with strange morphology. Is given by hypokalemia or hypomagnesaemia, sum antidepressant drugs.

The Sino-atrial block is a lack of signal from SA node to the atrium that cannot depolarize. Have several levels: Type I: P-P interval shortens until one P wave is dropped Type II: a pause in the sinus rhythm is equal to a multiple of the PR interval (e.g. 1:2, 1:3) The Atrio-ventricular block is a consequence of ischemia, degeneration of His-Purkinje system, infections, immunological compliances, surgery or congenital disorders and has different degrees: AV 1: prolonged PR (more than O.2) AV 2: are named Mobitz 1 and 2, in the first there is a progressive PR enlargement until drops a QRS, in the second the PR distance is constant but the QRS drops in an unexpected way, and usually in mathematical ratios (e.g. 2:1, 3:1) AV 3 (complete): no relation between atria and ventricles usually accompanied by junctional rhythm. Bundle Branch blocks: When a bundle branch or fascicle becomes injured (due to underlying heart disease, myocardial infarction, or cardiac surgery), it may cease to conduct electrical impulses appropriately. This results in altered pathways for ventricular depolarization. In this picture you can understand a characteristic of the ECG findings in these pathologies. The QRS complex is wide and two complexes may be visible in one phase only. There are some typical changes that help you to discriminate a RBBB from a LBBB: In Right Block: M shape QRS in V1/V2, W shape QRS in V5/V6/I, (MARROW) In Left Block: W shape QRS in V1/V2, M shape QRS in V5/V6 (WILLIAM) Hemiblocks: The left bundle branch splits into 2 fascicles: the anterior and posterior fascicles. When conduction through one of the fascicles is blocked it is called an anterior or posterior hemiblock, respectively. Left anterior hemiblock is more common and causes left axis deviation on the ECG. Left posterior hemiblock causes right axis deviation on the ECG.

Bifascicular Block: This is a combination of right bundle branch block and either left anterior or left posterior hemiblock. The ECG will show RBBB with either left (anterior hemiblock) or right (posterior hemiblock) axis deviation. Trifascicular Block: This is when bifascicular block is associated with 1st degree heart block. Aortic Dissection is a pathological condition in which a false lumen is created into a tear of the intimal layer of the aorta, this decrease the pressure to the upper vessels. Just for completeness Im adding a picture showing the DeBakeys and Stanford classification here on right side of the page. Is linked by acute pain, usually decreased blood pressure with differences arm to arm and dyspnea. About venous disease there is not so much to talk and eviscerate so try just to keep in mid the pathogenesis of thromboembolism, that is contained in the Virchows triad as follows:

The Cardiac Failure first of all is a syndrome, and not a disease; so we should focus on discover the underlying cause. Arise from any condition that compromises the contractility of the heart, so the systolic or diastolic phases and the cardiac output too. This scheme is really a good way to synthesize the entire process:

There are many ways to classify heart failure depending on the parameters involved, but the 2 most common ones used are left/right heart failure and systolic/diastolic heart failure: Left heart failure common causes are ischemic heart disease, valvular heart disease, and hypertension. Affects the blood flow systemically to the brain and the rest of the body. Right ventricular heart failure common causes are chronic left heart failure resulting in back pressure to the right side of the heart, pulmonary hypertension, chronic lung disease, and infarction to the right side of the heart and adult congenital heart disease. Affects blood flow to the lungs. Systolic heart failure Insufficient contraction of the heart i.e. reduced ejection fraction. Diastolic heart failure Insufficient relaxation of the heart muscles during diastole and hence decreased cardiac output. Patient has signs and symptoms of heart failure but ejection fraction is normal i.e. >45-50%. Common in elderly hypertensive patients. It is important to remember that commonly patients have overlapping symptoms, as chronic left heart failure for instance, will eventually lead to right heart failure. And there are several symptoms that could help us in diagnose the genesis of the failure: Left heart failure: Tachypnea, orthopnea (shortness of breath on lying flat), paroxysmal nocturnal dyspnea i.e. PND (attacks of severe sudden shortness of breath that usually wakes the patient up at night), bi-basal crepitation, laterally displaced apex beat, gallop rhythm, murmurs, cyanosis. Right heart failure: Peripheral pitting edema, hepatomegaly, increased JVP, parasternal heave, ascites.

There are also characteristic features on a chest xray (ABCDE) that is often asked about in finals: Alveolar oedema (in a bats wings distribution) Kerley B lines (short white lines that run perpendicular to the pleura and is a sign of interstitial oedema) Cardiomegaly Upper lobe Diversion (prominent upper lobe vessels) Effusion (pleural)

I will not insist more about ECG and interpretation, if you need to rehearse it just pick up the physiopathology review I made, its all in there step by step. And Im happy to tell you that this is all we have to know about Cardiac System for this semester! Now we should start the respiratory system, which is much more easier in my opinion, why? Maybe because Ive faced it many times and because for any given pathology I do not have to think about ECG, hence Im always happy to see a nice X-ray (my field of future studies). Lets Start! In the next page of course ^_^ By the way I forgot to mention what semiology is, some key words and also basic principles of a good physical examination and how to elaborate a good clinic eye well Ill try to write something at the and of the work just as a reminder for you my dears.

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How to approach a respiratory patient?

Doesnt mean of course how to approach any person able to breath, just a patient that could have respiratory problems.

Main symptoms we would face in this chapter are dyspnea, cough, chest pain and wheeze (whistling sound in chest). The Dyspnea is the difficulty in breathing acts, it is important to understand its onset, duration, aggravation or relieving factors and associated symptoms. It could have respiratory causes which in generally means situations in the airways or pulmonary causes such as parenchyma, circulation and pleural (every aspect of the lung). Keep in mind that this symptom could be triggered by several non-respiratory causes such as chest wall injuries, neuromuscular, cardiac or psychiatric. Cough is either an involuntary reflex or a voluntary act. Initiated by stimulation of sensory receptors from the pharynx to the alveoli; a rapid increase in intra-thoracic pressure caused by contraction of respiratory muscles against a closed glottis, the glottis opens with an explosive release of air into the upper airway. The function of cough is to remove secretions or particles from the respiratory airways. Causes of the cough: Larynx, trachea, large airways: Infection, tumours, aspiration, gastro-esophageal reflux, foreign body, irritant dusts Small airways: Asthma, COPD, bronchiectasis, bronchiolitis, irritant dusts Alveoli: drugs (angiotensin-converting enzyme inhibitors), infection, left ventricular failure, irritant dusts A cough can be non-productive (dry) or productive (when sputum is coughed up). Hemoptysis is the expectoration (coughing up) of blood or of bloodstained sputum from the bronchi, larynx, trachea, or lungs (e.g., in tuberculosis or other respiratory infections or cardiovascular pathologies). Main causes are: Tumour: Lung cancer, bronchial metastasis Infection: Bronchiectasis, Tuberculosis, Lung abscess, Cystic fibrosis Vascular: Pulmonary infarction, Arteriovenous malformation, Vasculitis (Wegener's granulomatosis, Goodpasture's syndrome) Trauma: Inhaled foreign body, Chest trauma Iatrogenic: bronchoscopic biopsy, transthoracic lung biopsy Cardiac: Mitral valve disease, Acute left ventricular failure Hematological: Blood dyscrasias, Anticoagulation Chest pain is originated by pleura or chest wall in a respiratory patient, but it does not originate from lungs themselves. Causes: 1. Non-central Pleural: Infection, malignancy, pneumothorax, pulmonary infarction, connective tissue diseases (rheumatoid arthritis, systemic lupus erythematosus) Chest wall: malignancy, persistent cough, muscle sprains/tears- Coxsackie B infection, Tietze's syndrome (costochondritis), rib fracture, intercostal nerves compression, herpes zoster (intercostal nerves) 2. Central Tracheal: Infection, irritant dusts Cardiac: Massive pulmonary thromboembolism, Acute myocardial infarction/ischemia Esophageal: esophagitis Great vessels: Aortic dissection Mediastinal: Lung cancer, Thymoma, Lymphadenopathy, Mediastinitis

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At a thorax objective exam these should be your points of interests: Conformation: AP and transversal diameters The normal chest is bilaterally symmetrical and elliptical in cross-section scars of previous heart or lung surgery; swellings, marks and spots on the skin. 'barrel shaped thorax: Increased anteroposterior diameter compared with the lateral diameter Due to hyperinflation pulmonary emphysema, severe COPD the degree of chest deformity does not correlate with the severity of airways obstruction. Kyphosis and scoliosis= an exaggerated anterior curvature of the spine and scoliosis is lateral curvature. Pectus carinatum (pigeon chest) = a localized prominence of the sternum and adjacent costal cartilages often accompanied by indrawing of the ribs to form symmetrical horizontal grooves ('Harrison's sulci') above the costal margin Pectus excavatum (funnel chest) = localized depression of the lower end of the sternum or depression of the whole length of the sternum. Respiratory rate is the number of respirations per minute. Tachypnea is a respiratory rate > 18/min (15) Causes: fever, pneumonia, pulmonary edema, interstitial lung disease. A respiratory rate > 30/min is the most important prognostic sign associated with death in community-acquired pneumonia !!! bradypnea: crisis of asthma, opioids, raised intracranial pressure, hypothalamic lesions, and hypercapnia. The most important breathing patterns: Cheyne-Stokes breathing, or periodic respiration= a period of increasing rate and depth of breathing followed by diminishing respiratory effort and rate, usually ending in a period of apnea or hypopnea and the cycle then repeats. Hyperventilation is a common response to acute anxiety or emotional distress and is often associated with respiratory alkalosis. tetany and occasionally grand mal seizure can occur. Kssmaul respiration= Hyperventilation with deep, sighing respirations as a response to the reduced arterial pH- metabolic acidosis Biot resp.(ataxic respiration)= irregular type of breathing sign of neurologic damage irregular and unpredictable rate, rhythm, and depth Usually slow rate Stertorous respiration = a harsh, rattling, snoring sound, as a result from the vibration of relaxed oropharyngeal structures during sleep or coma, causing partial airway obstruction In Palpation there are three things to remember in a respiratory examination. Position of the Trachea - this is uncomfortable and should be done gently Chest expansion - should be done in at least 3 places, both front and back. Apex Beat Additionally, some perform tactile vocal fremitus (TVF) in palpation by applying the ulnar border of the right hand to points on the chest wall and asking the patient to say '99' to create palpable resonance. This can be used to effectively pick up pleural effusions (reduced TVF), or sometimes consolidation (increased TVF). (spunez treizece si trei, va rog!) In Percussion the chest should be percussed front and back, making sure to cover all lobes and paying particular attention to the bases.

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You should use your dominant hand's middle finger to percuss, and should use it to tap your middle finger from the opposite hand 2-3 times - this amplifies the sound. When percussing the apical segments of the lungs, use this technique in the supraclavicular fossae, but percuss the clavicle directly (i.e. you don't need your second hand). The technique takes some practice - especially to get the percussing motion to come from the wrist - but we all have chests to practice on (!) and when that's not appropriate you can tap tables, books, etc. This is a normal routine of percussion: Start at the apices - percuss one side, then the contralateral side at the same level - this provides comparison in order to increase the likelihood of detecting pathology. Move down through the anterior chest, percussing the intercostal spaces of each side alternately. Percuss in the axillae Ask the patient to lean forward and repeat on the back, ensuring you percuss right down into the bases. Sites for Auscultation are the same as those for percussion. The bell should be used in the supraclavicular fossae and the diaphragm elsewhere. On auscultation you are looking for: Breath sounds - vesicular (normal) or bronchial (pathological) Reduced air entry Added sounds Added sounds include: Wheeze Crepitation Pleural rub And now some syndromes affecting the respiratory tract, starting from Pneumonia, a nice synthetic picture:

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Pleural effusion is not a distinct disease but it is an important and common presentation of various conditions. Most frequently it is due to cardiac failure, pneumonia, or malignancy. It occurs when there is an increase in the volume of fluid in the pleural space (the space between the visceral pleura and parietal pleura which line the lungs and pulmonary cavity respectively). The normal volume of fluid in this space is between 10-20ml.

Symptoms Could be asymptomatic unless the volume of fluid is >300ml Shortness of breath (may only be on exertion) Cough (typically dry) Pleuritic chest pain Signs On observation the patient may have a raised respiratory rate and show signs of respiratory distress (e.g. use of accessory muscles, abdominal breathing, tracheal tug) On palpation there will be reduced chest expansion on the affected side. If the effusion is large there may be tracheal deviation away from the affected side On pecussion there will be stony dullness over the effusion On auscultation there will be absent or reduced breath sounds over the effusion with bronchial breathing directly above it. Main Causes: Transudates Cardiac failure Hepatic failure with cirrhosis Pulmonary embolism (10-20% are transudates) Exudates Pneumonia (parapneumonic effusion or emphysema) Malignancy (about 50% due to lung or breast) PE (80-90% are exudates) Rheumatoid arthritis Pneumothorax means the presence of air or gases in the pleural cavity, it could bear spontaneously or triggered by traumas, lung diseases, Marfan syndrome.

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COPD (chronic obstructive pulmonary diseases) is a group of diseases that include Chronic Bronchitis and Emphysema. Using the term COPD can be confusing and so it is important to know which pathology is occuring, although most patients have a combination of both diseases and smoking is the main cause. Chronic Bronchitis tends to be diagnosed clinically and is when the patient has chronic cough and sputum production for 3 months of a year for 2 consecutive years. Mucus glands and goblet cells increase in number and contribute to the reduced airway size by blocking the lumen with secretions. Emphysema is destruction of the alveolar walls creating large air sacs, decreasing the surface area for gaseous exchange. Large airspaces in the lung may also allow for gas trapping; the airways close prematurely and cause hyperinflation. It is believed that chronic inflammation is the method behind the alveolar wall destruction. Last but not least as promised here we are with main concepts in medical semiotic, its rather an introduction than the end of a work but not all donuts comes out with a hole so Semiology deals with symptoms and signs of diseases, gives the opportunity to a doctor to see and correlate a sign with a specific physiological or pathological condition. Symptom: is the subjective feeling of disease Sign: the objective parameter of change in the body In the steps for the final diagnosis we have to consider with the maxim importance the history of the patient, his familys medical relevant records, the physical examination where the semiology takes a key role and after further analysis and/or exams finally get the final diagnosis. What is a syndrome? Is the sum of all clinical manifestation common for different diseases, for example: Pain is a symptom, dyspnea too; both of them could be signs for tuberculosis or pleural syndrome, which are different! The principles of acting a proper examination by a doctor (or a medical student in our case) are: Medical communication, Polite, empathy, active listening, Do not judge! And also a non-verbal communication. Steps for accepting a patient in a health department: General data Reason of admittance Personal history Family history Social habits Current illness (if known) and story of the disease These are part of a process of great importance at the base of medicine named Anamnesis Thats it for this semester, this is my last review guys, see you after this short vacation time and may the force be with you, your beloved colleague, Alessandro Motta

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