Where such designations appear in this book, they have been printed with initial caps. McGraw-Hill .. CMDT Online-Transgender Health & Disease Prevention. a LANGE medical book you'd like more information about this book,.. Q Fever. Human Current. current-medical-diagnosis-and-treatmentpdf. a LANGE medical book you'd like more information about this book,. in their respective fields, CMDT offers the most current insights into symptoms, signs.
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Search Textbook Autosuggest Results. Chapter 1: CMDT Media Library. Collection of key diagnostic CMDT Flashcards cover image CMDT Flashcards, 2e. Current Medical Diagnosis & Treatment (CMDT ) is the 54th edition of this The book emphasizes the practical features of clinical diagnosis and patient nvrehs.info CMDT is available for free PDF download here. According to the author of CMDT , this book has been written keeping in mind the.
On physical examination, her neck reveals tender anterior cervical lymphadenopathy, and her tonsils are inflamed and exudative. Young age; sick contact; sore throat; fever; lack of cough; cervical adenopathy; exudative tonsils How to think through: Risk of subsequent rheumatic fever and glomerulonephritis.
How many Centor criteria are present in this patient? Four of four diagnostic criteria: If a rapid strep test result were negative in this case, what would be the appropriate management strategy? Antibiotic therapy in a patient with four of four the Centor criteria is reasonable regardless of the rapid test result. What other important infectious diseases present with pharyngitis in young adults and must be considered?
If infectious mononucleosis was a consideration, what antibiotic should be avoided because of the high frequency of associated rash? If the patient provides a history of a recent high-risk sexual encounter, should she receive an HIV antibody test now?
Detectable antibodies take between 3 weeks and 2 months to form in the majority of infected patients. An HIV viral load nucleic acid test would be more appropriate. About one-third of patients with infectious mononucleosis have secondary streptococcal tonsillitis requiring treatment. Ampicillin should routinely be avoided if mononucleosis is suspected because it induces a rash.
Sore throat may be severe, with odynophagia, tender adenopathy, and a scarlatiniform rash. Marked lymphadenopathy and a shaggy white-purple tonsillar exudate, often extending into the nasopharynx, suggest mononucleosis, especially if present in a young adult. He had a recent binge of alcohol use that ended 2 days before admission, and he woke up with these symptoms.
On physical examination, his temperature is His lower right lung field has inspiratory crackles on auscultation. A chest radiograph shows focal consolidation in the right middle and lower lobes. Alcohol history predisposing to aspiration; fever and chills; rigors; shortness of breath; cough with purulent sputum; tachypnea; consolidation on examination and radiograph; leukocytosis How to think through: Pneumonia is a clinical diagnosis in which symptoms, examination, white blood cell count, and chest radiograph are all considered.
Although these all point to a diagnosis of pneumonia in this case, what other causes are plausible? Aspiration pneumonitis, lung neoplasm, lung abscess, acute respiratory distress syndrome, bronchitis, tuberculosis, pulmonary embolism, congestive heart failure, atelectasis, drug reactions. What are the next diagnostic steps? Blood cultures; arterial blood gases. Pathogens and outcomes vary with epidemiologic risk factors.
This patient likely has community-acquired pneumonia CAP , but recent exposure to health care settings and immune status including HIV testing should be assessed. His alcoholism may indicate other substance abuse, and both increase the risk of tuberculosis. What pathogens are most likely in this case?
But empiric antibiotic coverage for both types may be important. Although Staphylococcus aureus pneumonia is uncommon, it is associated with morbidity, so coverage for it may be appropriate with severe disease and for patients requiring intensive care.
If this patient responds to antibiotic treatment within the first 2 to 3 days, its duration should be 7 days for most pathogens. Essentials of Diagnosis Fever or hypothermia, tachypnea, cough with or without sputum, dyspnea, chest discomfort, sweats or rigors or both Bronchial breath sounds or inspiratory crackles on chest auscultation, opacity on chest radiograph Leukocytosis Purulent sputum CAP occurs outside of the hospital; hospital-acquired pneumonia HAP occurs more than 48 hours after admission; ventilator-associated pneumonia VAP develops in a mechanically ventilated patient; health care—associated pneumonia HCAP occurs in community members with high health care facility exposures General Considerations May be bacterial e.
Symptoms and Signs Acute or subacute onset of fever, cough with or without sputum, and dyspnea may be present. Rigors, sweats, chills, pleurisy, chest discomfort, and hemoptysis are common. Fatigue, anorexia, headache, myalgias, and abdominal pain may be present. Physical findings include fever or hypothermia, tachypnea, tachycardia, decreased oxygen saturation, rales or abnormal breath sounds, and dullness to percussion. Laboratory Tests Sputum Gram stain, blood cultures, rapid influenza testing, or urine antigen assays for Legionella pneumophila and S.
All hospitalized patients should have complete blood count, chemistry panel, and arterial blood gas analysis. HIV testing should be considered in all adult patients. Imaging Studies Chest radiograph findings range from patchy airspace opacities to lobar consolidation with air bronchograms to diffuse alveolar or interstitial opacities. Clearing of opacities can take 6 weeks or longer. Diagnostic Procedures Sputum induction and fiberoptic bronchoscopy are indicated for patients who cannot provide samples or who may have Pneumocystis jiroveci or Mycobacterium tuberculosis pneumonia.
Thoracentesis with pleural fluid analysis should be performed in all patients with effusions. Endotracheal aspiration and fiberoptic bronchoscopy with lavage in patients with VAP. Medications Treatment is based on risk factors and severity of illness. Four days later, he develops shortness of breath and right-sided pleuritic chest pain. Cardiopulmonary examination is normal. Recent surgery; acute dyspnea; pleuritic chest pain; tachypnea and tachycardia; hypoxia oxygen desaturation ; signs of deep venous thrombosis DVT including unilateral calf tenderness and edema.
How to think through: This patient has sudden onset of dyspnea, chest pain, tachypnea, hypoxemia, and tachycardia. What is the differential diagnosis of this scenario? Myocardial infarction, pneumothorax, cardiac tamponade, pulmonary embolism [PE]. What features make PE more likely? Pleuritic quality of chest pain, normal cardiopulmonary examinations, post-surgical onset.
What are immediate management and diagnostic priorities in this unstable patient? Supplemental oxygen, intravenous access; electrocardiogram [ECG], chest radiography. If ECG shows only sinus tachycardia and chest radiography shows only clear lung fields, how should the possibility of PE be evaluated?
Helical CT scan. Is there a role for a D-dimer test? His CT scan shows extensive bilateral pulmonary emboli.
In this case, given that his blood pressure is likely below baseline, but he is not in shock, how might you better assess right heart strain? What treatment should you initiate regardless of the thrombolysis decision?
Heparin or low-molecular weight heparin [LMWH]. Is a workup for thrombophilia indicated? Less common symptoms and signs include fever, hemoptysis, cough, crackles rales , angina, and an accentuated pulmonary component of the second heart sound.
Homans sign is pain with forced dorsiflexion of the ankle and suggests DVT in the ipsilateral lower extremity; it is a rare finding. Acute respiratory alkalosis, hypoxemia, and widened arterial—alveolar O2 gradient A—a Do2 may be seen, but these findings are not diagnostic. D-dimer testing is very sensitive but is nonspecific for VT.
Imaging Studies The most common chest radiography findings are atelectasis, infiltrates, pleural effusions, Westermark sign focal oligemia with a prominent central pulmonary artery , and Hampton hump pleural-based area of increased density from intraparenchymal hemorrhage. Helical CT arteriography is the initial diagnostic study of choice because it is very sensitive and noninvasive, but it does require administration of intravenous radiocontrast dye.
Venous thrombosis studies include lower extremity Doppler ultrasonography and may establish the need for treatment, precluding invasive testing in patients with high suspicion for PE. Pulmonary angiography is the reference standard for the diagnosis of PE but is invasive.
Medications Full anticoagulation with heparin should begin with the diagnostic evaluation in patients with a moderate to high clinical likelihood of PE and no contraindications.
LMWHs are as effective as unfractionated heparin and do not require coagulation monitoring. Warfarin is an option for oral anticoagulation therapy.
The durations of treatment are 6 months for an initial episode with a reversible risk factor, 12 months after initial idiopathic episode, and 6 to 12 months to lifelong in patients with irreversible risk factors or recurrent disease. Thrombolytic therapy increases intracranial hemorrhage but is indicated in hemodynamically unstable patients.
Surgery Pulmonary embolectomy is an emergency procedure with a high mortality rate performed at few centers. Therapeutic Procedures Catheter devices that fragment and extract thrombus have been used on small numbers of patients. Inferior venal caval IVC interruption IVC filters may be indicated when a significant contraindication to anticoagulation exists or when recurrence occurs despite adequate anticoagulation.
IVC filters decrease the short-term incidence of PE but increase the long-term rate of recurrent DVT; thus, provision should be made for their removal at the time of insertion. He describes a right-sided fullness and tenderness over his cheek.
He has also had yellow-green drainage from his nose along with subjective fevers, halitosis, and malaise. He felt as though he was getting better 1 week ago, but then his symptoms returned worse than ever. On physical examination, his right maxillary sinus is tender to palpation and percussion.
Unilateral facial pain, pressure, and fullness; purulent drainage; fevers and halitosis; partial resolution with subsequent worsening; maxillary sinus tenderness on examination How to think through: Sinus pressure and nasal discharge, accompanied by headache, cough, or subjective fever, are a common constellation of findings in sinusitis.
The majority of cases are caused by viral rhinosinusitis, are self-limited, and are treatable symptomatically. The two main tasks for the clinician are to determine the likelihood of bacterial sinusitis and to rule out serious complications. What are the elements of the clinical history associated with bacterial sinusitis? What organisms are commonly implicated in bacterial sinusitis? Streptococcus pneumoniae, other streptococci, Haemophilus influenzae; possibly Staphylococcus aureus or Moraxella catarrhalis.
Eye involvement [proptosis, double vision], altered mental status, and facial erythema suggesting cellulitis. Immune compromise should heighten vigilance for such complications.
When should one consider sinus imaging or referral to an otolaryngologist for nasal endoscopy? Patients who receive appropriate antibiotic treatment and have no improvement at 4 weeks. What are first-line antibiotics for treatment or acute bacterial sinusitis?
What other treatments can help? Symptoms and Signs Bacterial rhinosinusitis can be distinguished from viral rhinitis when symptoms last longer than 10 days after onset or worsen within 10 days after initial improvement. Nonspecific symptoms include fever, malaise, halitosis, headache, hyposmia, and cough. Maxillary sinusitis presents with unilateral facial fullness, pressure, and tenderness over the cheek; pain may refer to the upper incisor and canine teeth.
Ethmoid sinusitis is usually accompanied by maxillary sinusitis; the symptoms are similar. Hospital-acquired sinusitis may present without any symptoms, is often associated with nasogastric tubes, and is a common source of fever in critically ill patients.
Laboratory Tests Diagnosis is usually made on clinical grounds alone. Imaging Studies Noncontrast coronal computed tomography scans are more cost effective than conventional films; provide a rapid and effective means to assess all of the paranasal sinuses, identify areas of concern, and direct therapy; and are indicated when symptoms persist longer than 4 to 12 weeks. Routine sinus series radiographs are not cost-effective but may be helpful in difficult-to-evaluate cases, when the patient does not respond to appropriate therapy, or when the patient has symptoms or signs of more serious infection e.
Procedures Nasal endoscopy is indicated when symptoms persist longer than 4 to 12 weeks. Medications Antibiotics should be given if symptoms last more than 10 to 14 days or if severe symptoms such as fever, facial pain, and periorbital swelling are evident on presentation.
After recent antibiotic use, levofloxacin or amoxicillin—clavulanate is appropriate. Second-line therapy includes amoxicillin—clavulanate or moxifloxacin. Hospital-acquired infections may require broad-spectrum agents.
Oral or nasal decongestants may be used for symptom improvement. Therapeutic Procedures For hospital-acquired sinusitis, removal of a nasogastric tube, improved nasal hygiene, and endoscopic or transantral cultures particularly in HIV-infected or other immunocompromised patients may be helpful. He describes the pain as a heavy pressure sensation that radiates down both arms and is 10 of 10 in intensity. His pain started while he was walking around his yard and improved, but did not resolve, with rest.
His medical history is significant for diabetes mellitus. He has smoked 1 pack of cigarettes per day for the past 50 years.
His mother died of a myocardial infarction MI at age 56 years. On heart examination, you hear an S4 gallop, and on lung examination, you hear bibasilar fine crackles. Advanced age; sudden onset of substernal chest pain radiating to the arms; pain worse with exertion; cardiac risk factors of diabetes mellitus, smoking, and family history; S4 gallop and crackles consistent with pulmonary edema; ECG with ST elevations in an inferior distribution How to think through: Radiation to the arms correlates strongly with cardiac chest pain.
To evaluate a patient with chest pain, first determine the likelihood of ACS as its cause; then stratify the risk for mortality to ensure timely intervention in high-risk patients.
Here the history alone strongly suggests ACS. Evidence of new heart failure confers high risk. What medications should be administered upon diagnosis? Aspirin; clopidogrel, heparin, or low-molecular-weight heparin [LMWH]; nitroglycerin; morphine, if needed.
His new heart failure is a relative contraindication. If the hospital lacks facilities for cardiac catheterization, how should he be managed? If transfer to another facility for percutaneous coronary intervention [PCI] within 90 minutes of first medical contact is not possible and barring contraindication, fibrinolytic therapy should be given. ST-segment elevation or left bundle branch block Immediate reperfusion treatment is warranted with PCI within 90 minutes preferred or thrombolysis within 30 minutes of arrival and within 6 to 12 hours of symptom onset General Considerations Results, in most cases, from an occlusive coronary thrombus at the site of a preexisting although not necessarily severe atherosclerotic plaque More rarely, may result from prolonged vasospasm, inadequate myocardial blood flow e.
Laboratory Tests Quantitative CK-MB creatine kinase myocardial band , troponin I, and troponin T elevations are seen as early as 4 to 6 hour after onset; they are almost always abnormal by 8 to 12 hours. Troponins may remain elevated for 5 to 7 days or longer and are not generally useful for evaluating suspected early reinfarction. Imaging Studies Chest radiograph: Primary PCI is the approach of choice in patients with absolute and many relative contraindications to thrombolytic therapy.
In patients with cardiogenic shock, early catheterization and percutaneous or surgical revascularization are the preferred management and have been shown to reduce mortality. Because an acute interventional approach carries a lower risk of hemorrhagic complications, it may also be the preferred strategy in many older patients.
He becomes short of breath after walking one block or up one flight of stairs. He awakens at night gasping for breath and has to prop himself up with pillows to sleep. His apical impulse is displaced to the left and downward. There are rales over both lower lung fields. There are two distinct cardiac murmurs: Chest radiography shows cardiomegaly and pulmonary edema. Echocardiography shows severe aortic regurgitation AR with left ventricular hypertrophy LVH and dilatation.
Progressive shortness of breath on exertion, paroxysmal nocturnal dyspnea, orthopnea; pulmonary edema and cardiomegaly indicating heart failure HF ; wide pulse pressure; hyperdynamic pulses; early diastolic murmur at the left sternal border; diastolic rumble at the apex Austin-Flint murmur ; echocardiogram diagnostic of AR with LVH and dilatation How to think through: This patient has symptoms dyspnea on exertion, paroxysmal nocturnal dyspnea, and orthopnea and signs rales of HF. Can a clinician generally distinguish between systolic, diastolic, and valvular cause based on symptoms?
Not reliably. The murmurs suggest a valvular cause. The diastolic murmur at the left upper sternal border and the apical diastolic rumble suggest AR. What other data help in the diagnosis of AR? The wide pulse pressure, high systolic blood pressure, and hyperdynamic carotid pulse are also characteristic of AR. What underlying processes cause AR? Rheumatic heart disease, congenitally bicuspid valve, infective endocarditis, hypertension, cystic medial necrosis, Marfan syndrome, aortic dissection, ankylosing spondylitis, and reactive arthritis.
Echocardiography is key to diagnosis and to monitoring progression of AR. Imaging by contrast computed tomography CT may be indicated to assess aortic root diameter or ascending aneurysm. How should this patient be managed? Blood pressure control with afterload reduction can decrease regurgitation. This patient is symptomatic, and elective valve replacement is indicated. Essentials of Diagnosis Usually asymptomatic until middle age; then presents with left-sided failure or chest pain Wide pulse pressure; diastolic murmur along the left sternal border ECG shows left ventricular hypertrophy; radiograph shows left ventricular LV dilatation Echocardiography with Doppler is diagnostic General Considerations Rheumatic heart disease is less common since the advent of antibiotics.
Nonrheumatic causes include congenitally bicuspid valve, infective endocarditis, hypertension, cystic medial necrosis, Marfan syndrome, aortic dissection, ankylosing spondylitis, and reactive arthritis. LVH occurs from both increased preload and afterload.
Symptoms and Signs High-pitched, decrescendo aortic diastolic murmur along the left sternal border without respiratory variation Water-hammer or Corrigan pulse: Imaging Studies Chest radiography shows cardiomegaly with LV prominence and sometimes aortic dilatation.
Doppler echocardiography confirms the diagnosis and estimates the severity. Serial echocardiographic assessments determine the timing of valve replacement. CT or magnetic resonance imaging can estimate aortic root size and exclude aneurysm. Cardiac catheterization helps quantify the severity and evaluates the coronary arteries. Medications Treatment of hypertension to decrease afterload can reduce the severity of regurgitation.
Urgent surgery is indicated in patients with acute AR. Mechanical valves last longer than tissue valves but require anticoagulation. While running in the park, he suddenly lost consciousness. He had no premonitory symptoms and no symptoms or deficits upon regaining consciousness.
For several weeks, he had had substernal chest pressure with exercise. He had no shortness of breath, dyspnea on exertion, orthopnea, or paroxysmal nocturnal dyspnea. As a child, he had had a heart murmur never further evaluated. The carotid pulse is weak and delayed in character. The lungs are clear.
There is no lower extremity edema. Electrocardiogram shows left ventricular hypertrophy LVH. Middle age; childhood murmur; syncope without prodrome or postictal phenomena; angina pectoris; no signs of heart failure yet ; narrow pulse pressure; pulsus parvus weak et tardus late ; systolic murmur at the base radiating to the carotids; S4 gallop; electrocardiogram showing LVH How to think through: With recent exertional substernal chest pressure then sudden syncope, what diagnoses are most likely?
Coronary artery disease, acute myocardial infarction MI , transient ventricular arrhythmia. However, the physical examination suggests valvular heart disease.
The diminished and delayed carotid artery pulse indicates severe AS. Why does he have a laterally displaced and sustained apical impulse?
LVH caused by a high-pressure gradient across the aortic valve. His childhood murmur suggests what predisposition to AS? Bicuspid aortic valve. What are the next steps in his management? Cardiac enzymes to rule out MI; echocardiography to assess the aortic valve; consultation to discuss aortic valve replacement.
Essentials of Diagnosis Diminished and delayed carotid pulses pulsus parvus et tardus Soft, absent, or paradoxically split S2 Harsh systolic murmur, classically crescendo—decrescendo, along the left sternal border, often radiating to the neck and sometimes associated with a thrill Electrocardiography ECG with LVH; calcified valve on radiography; echocardiography is diagnostic General Considerations Congenital bicuspid valve is the most common etiology in middle-aged patients.
The cause in elderly patients is usually valvular degeneration from progressive calcification. It is more frequent in men, smokers, and patients with hypercholesterolemia and hypertension. Coronary artery disease is often coincident because risk factors are the same. Differential Diagnosis Other causes of angina pectoris e. Imaging Studies Chest radiography or fluoroscopy may show an enlarged cardiac silhouette and calcified valve. Doppler echocardiography is usually diagnostic and can estimate the gradient across the aortic valve.
Cardiac catheterization provides confirmatory data, assesses hemodynamics, and excludes concomitant coronary artery disease. Medications Medical treatment may stabilize heart failure, but surgical intervention is definitive.
Lipid-lowering therapy may theoretically slow the progression of AS. Control of systemic hypertension is important to reduce excess afterload. Therapeutic Procedures and Surgery Aortic valve replacement is indicated for all symptomatic adult patients and those with LV dysfunction or peak gradient greater than 64 mm Hg by echocardiography or Doppler.
Balloon valvuloplasty is palliative in adolescents but ineffective for the long term in adults. Pericardial valves appear to last longer than porcine valves; neither requires warfarin.
Mechanical valves have longest life but require warfarin therapy. Percutaneous valve replacement may be an option for high surgical risk patients. For the past 5 months, he has noted intermittent substernal chest pressure radiating to his left arm. The pain occurs primarily when exercising vigorously and is relieved with rest. He has no associated shortness of breath, nausea, vomiting, or diaphoresis.
His medical history is significant for hypertension and hyperlipidemia. He is on atenolol and a low-fat diet. His father had died of a myocardial infarction MI at age 56 years. He has a pack-year smoking history and is currently trying to quit. Middle-aged man; intermittent pain with exercise and relieved with rest; substernal location with radiation to the arm; risk factors: When evaluating a patient with chest pain, first determine if the pain is acute in onset or progressive with features concerning for acute coronary syndrome ACS , pulmonary embolism, aortic dissection, pneumothorax, or another emergency.
But most patients with chest pain do not require emergent evaluation. What are the major CAD risk factors? Age, sex, family history, tobacco use, diabetes mellitus, hypertension, low high-density lipoprotein [HDL] cholesterol, high non-HDL cholesterol.
Could this be aortic stenosis? Based on history alone, it could be. Cardiac and carotid pulse examination will help distinguish. While other causes esophageal spasm or musculoskeletal pain are possible, the symptoms, long smoking history, and family history confer a high pretest probability of CAD.
There are several noninvasive CAD testing options; all involve a stressor exercise or pharmacologic and a detector ECG, echocardiography, nuclear medicine. Is medical therapy indicated at this point? Symptoms and Signs Myocardial ischemia: Differential Diagnosis Cardiovascular: The patient denies any symptoms but is worried about his weight and diet, which consists of many saturated fats.
Obese man; large waist circumference; elevated blood pressure; elevated serum triglyceride level; low HDL cholesterol level; insulin resistance consistent with the metabolic syndrome How to think through: This patient has a different, but equally important, pattern of dyslipidemia: The degree to which these abnormalities are independent predictors of CAD is debated because they so often travel with other metabolic abnormalities, collectively termed the metabolic syndrome.
What are the elements of this syndrome? What other secondary causes of hypertriglyceridemia should be considered? Alcohol abuse, hypothyroidism, nephrotic syndrome, familial disorders of triglyceride metabolism, and medications [e.
What is an important complication of elevated triglycerides, and is this patient likely to experience this complication? Should he receive targeted therapy to lower his triglycerides?
Not necessarily. Weight loss and reduction of CAD risk factors known to improve outcomes is the primary treatment strategy for dyslipidemia. The first interventions should be diet, exercise, blood pressure control, and a statin medication.
What medications lower triglycerides? Fibric acid derivatives [e. What downside might there be to prescribing nicotinic acid for this patient? Worsened glucose intolerance.
Essentials of Diagnosis Elevated serum total cholesterol or LDL cholesterol, low serum HDL cholesterol, or elevated serum triglycerides In severe cases associated with metabolic abnormalities, superficial lipid deposition occurs General Considerations Cholesterol and triglycerides are the two main circulating lipids.
Elevated levels of LDL cholesterol are associated with increased risk of atherosclerotic heart disease; high level of HDL cholesterol are associated with a lower risk. Familial genetic disorders are an uncommon, but often lethal, cause of elevated cholesterol.
Symptoms and Signs Dyslipidemia is usually asymptomatic. Extremely high levels of chylomicrons or very-low-density lipoprotein particles are associated with eruptive xanthomas. Very high LDL levels are associated with tendinous xanthomas. The metabolic syndrome consists of a large waist circumference, elevated blood pressure, elevated triglycerides, low HDL cholesterol, and elevated serum glucose level.
Differential Diagnosis Hypercholesterolemia elevated serum cholesterol Hypothyroidism, diabetes mellitus, Cushing syndrome, obstructive liver disease, nephrotic syndrome, chronic kidney disease, anorexia nervosa, familial hypercholesterolemia, idiopathic Drugs: Laboratory Tests Fasting lipid panel; screen for lipid disorders in patients older than age 35 years or with coronary heart disease risk factors, vascular disease, heart failure, or family history of premature heart disease Serum thyroid-stimulating hormone to screen for hypothyroidism Other tests only as indicated by symptoms and signs suggestive of a secondary cause LDL cholesterol is classified into five categories: Bile acid—binding resins e.
Fibric acid derivatives e. Exercise and moderate alcohol consumption can increase HDL levels. Reducing alcohol and fatty foods and controlling hyperglycemia are effective for hypertriglyceridemia.
He can no longer lie flat at night and uses four pillows to prop himself up in bed. On physical examination, he has bilateral crackles halfway up his lung fields, his jugular venous pulsations JVPs are elevated, and his lower extremities have pitting edema. Elderly man with CAD and previous MIs; shortness of breath; orthopnea; lung crackles from left-sided failure; elevated JVP and lower extremity edema from right-sided failure How to think through: Heart failure HF is a prevalent, important syndrome.
Prompt diagnosis and effective management improve morbidity, mortality, and quality of life. As in this case, HF diagnosis typically begins with a complaint of undifferentiated dyspnea on exertion. This patient also describes orthopnea. What additional symptoms also should be elicited? Exertional chest pain, paroxysmal nocturnal dyspnea, lower extremity edema, syncope or presyncope, palpitations. What cardiac pathologies can produce HF as well as the physical examination signs found in this patient?
Impaired systolic function, impaired diastolic function, and valvular disease. What physical examination sign should be present with systolic and diastolic dysfunction? Enlarged, sustained, displaced point of maximal impulse [PMI] at the apex. After a diagnosis of HF is made, the underlying cause should be identified. In this case, the patient has known CAD, and an echocardiogram or nuclear imaging study may show wall motion abnormalities consistent with ischemia or infarction.
What medication classes improve mortality and should be added if not already part of his regimen? A loop diuretic should be started for symptomatic relief immediately after assessment of electrolytes and renal function. Implantable cardiac defibrillator improves mortality. Biventricular pacing can significantly improve symptoms and systolic function in some patients.
Acute exacerbations may be caused by excessive salt intake, arrhythmias, or pulmonary emboli. High-output HF is caused by thyrotoxicosis, beriberi, severe anemia, or arteriovenous shunting. Systolic dysfunction is caused by MI, ethanol abuse, longstanding hypertension, viral myocarditis including HIV , or Chagas disease or is idiopathic. Laboratory Tests Complete blood cell count, serum electrolytes, creatinine, thyroid-stimulating hormone, ferritin Electrocardiography ECG to look for arrhythmia, MI, LV hypertrophy, conduction delays, repolarization changes B-type natriuretic peptide elevated in exacerbation; high negative predictive value Imaging Studies Chest radiography: Aldosterone blockers such as spironolactone or eplerenone decrease mortality.
Diuretics such as loop or thiazides reduce symptoms of fluid overload. Digoxin can reduce symptoms but does not have a mortality benefit. Inotropic agents e. He denies any symptoms. He also denies any recent caffeine or other stimulant use.
Elevated blood pressure on multiple occasions and after resting; African American ethnicity; no temporary cause How to think through: What are some causes of secondary hypertension? What prescription and over-the-counter medications and other substances might cause hypertension?
What dietary and lifestyle factors will most impact his blood pressure? Alcohol use, sodium intake. In the absence of other comorbidities, what would be your first choice antihypertensive agent? Is the patient likely to need more than one medication? How would you assess for end-organ damage?
What evidence might you find on cardiac and ophthalmic examination, standard laboratory studies, urinalysis, or electrocardiography ECG? What is the treatment goal for systolic blood pressure in this patient? What comorbid medical conditions would lower the treatment goal for systolic blood pressure to mm Hg? Diabetes, coronary artery disease [CAD], and chronic kidney disease. Resistant hypertension criteria mandate a regimen of three or more agents, including a diuretic.
A thiazide diuretic should generally be the first or second agent. Medications Initiation of drug therapy based on level of blood pressure, presence of target end-organ damage, and overall cardiovascular risk profile.
Choice of medication is based on presence of disease-specific indications e. Therapeutic Procedures Weight reduction, alcohol restriction, salt reduction, increased physical activity, smoking cessation Dietary changes DASH diet: Physical examination shows inspiratory crackles over the lower three-quarters of both lung fields, basilar dullness to percussion, hyperdynamic left ventricular LV impulse, brisk carotid upstroke, pansystolic murmur at the apex that radiates into the axilla, and S3 gallop.
Chest radiography shows Kerley B lines and bilateral pleural effusions consistent with acute pulmonary edema. Doppler echocardiography shows severe mitral regurgitation, and transesophageal echocardiography reveals a posterior mitral leaflet prolapsing into the left atrium LA and dyskinesis of basal lateral wall segment of the LV. The diagnosis is posterolateral myocardial infarction MI with acute mitral regurgitation resulting from papillary muscle ischemia and rupture.
Crushing chest pain and myocardial ischemia; shortness of breath; crackles, dullness to percussion, and S3 gallop and chest radiography indicating pulmonary edema; hyperdynamic LV, brisk carotid upstroke, and pansystolic murmur at the apex radiating to the axilla; echocardiogram diagnostic of mitral regurgitation How to think through: What complications of acute MI lead to acute HF?
LV myocardial dysfunction, rupture of the septum or LV free wall with tamponade, arrhythmia, or acute valvular dysfunction. What examination findings suggest acute mitral regurgitation as the cause of HF? The character of the murmur, hyperdynamic precordium, and brisk carotid upstroke. In acute MI, true rupture of the papillary muscles is much less common than papillary muscle dysfunction or displacement caused by LV dilatation.
With dysfunction or displacement, angiography and percutaneous revascularization are often first steps, the mitral regurgitation resolving with reperfusion. Here echocardiography reveals the posterior mitral leaflet prolapsing into the LA, suggesting papillary muscle rupture.
What is the optimum intervention? Emergent coronary artery bypass grafting with mitral valve repair or replacement. Imaging Chest radiography shows left atrial and ventricular enlargement.
Transesophageal echocardiography may reveal the cause, identify candidates for repair, and diagnose endocarditis. Medications Vasodilators decreases systemic vascular resistance and may stabilize acute mitral regurgitation while awaiting surgery.
Surgery Acute mitral regurgitation resulting from endocarditis, MI, and ruptured chordae tendineae often requires emergency surgery. Chronic regurgitation usually requires surgery when symptoms develop or in asymptomatic patients when the LV end-systolic dimension is larger than 4. Mitral valve replacement uses mechanical or bioprosthetic valves. Therapeutic Procedures Novel percutaneous approaches to mitral valve repair are being explored.
She has noted a fast heartbeat and a pounding sensation in her chest. In childhood, she had been ill for several weeks after a severe sore throat.
She has distended jugular venous pulses and rales at both lung bases Cardiac examination also reveals a soft, low-pitched diastolic decrescendo murmur, heard best at the apex in the left lateral decubitus position.
Dyspnea; tachycardic, irregularly irregular rhythm; atrial fibrillation on ECG; possible childhood rheumatic fever; jugular venous distention; pulmonary edema; diastolic decrescendo murmur at the apex and axilla; LA enlargement How to think through: Evaluation of palpitations is more urgent when they are associated with signs of hemodynamic compromise lightheadedness, syncope, or dyspnea. With the irregularly irregular pulse, an ECG is done, confirming atrial fibrillation.
Examination shows left heart failure HF with jugular venous distention and pulmonary edema. How might atrial fibrillation lead to subacute HF? New-onset atrial fibrillation alone may cause inefficient forward flow. In the chapters you will find comprehensive coverage of inpatient and outpatient care, focusing on the diagnostic tools relevant to day to day practice.
These are complemented by quick-access drug treatment tables, with indexed trade names and updated drug prices and ICD codes featured on the inside covers. You will find also diagnostic and treatment algorithms which present important information in an at-a-glance style. Up-to-date references provide peer-reviewed, evidence-based information.
Updated topics in this edition include topics in epidemiology, aetiology, and diagnosis and treatment recommendations; sections on asthma includes NAEPP guidelines and palpitations; more algorithms are provided throughout and there is increased coverage of Canadian and International Guidelines. The chapter on haemostasis and antithrombotic therapy has been improved.
Colour inserts have been expanded to 16 pages with the latest developments in HIV infection, including new drugs, recommended treatment regimens, and antiretroviral drug resistance. Alternative medicine and complementary therapies are represented with sections on mind-body medicine; clinical hypnosis; biofeedback; mindfulness meditation; stress reduction and cognitive therapy and guided imagery.
Any treatment that is done without diagnosis is very dangerous and life threatening. So, if you want to be a good doctor, first you would need to learn the process of diagnosis. And you would need to use the information properly and do treatments. Fortunately we have a book called current medical diagnosis and treatment pdf that can be used to learn the complete step by step process of diagnosis and treatment both.
Here is our brief review of CMDT It is one of the most popular book of medical diagnosis which is cleared from the number of editions of this book. Not only diagnosis, but is also provides a detailed knowledge about the treatment based on diagnosis.