Definition, Types, Risk factors, Pathogenesis, Complications, Diagnosis and Treatment of Hypertension

 Definition, Types, Risk factors, Pathogenesis, Complications, Diagnosis and Treatment of Hypertension .

DEFINITIONS:

Normal blood pressure – Systolic <120 mmHg and diastolic <80 mmHg

Elevated blood pressure – Systolic 120 to 129 mmHg and diastolic <80 mmHg

Stage 1 Hypertension – Systolic 130 to 139 mmHg or diastolic 80 to 89 mmHg

Stage 2 Hypertension – Systolic at least 140 mmHg or diastolic at least 90 mmHg

Types of Hypertension:

PRIMARY HYPERTENSION:

Hypertension without any know cause is called primary Hypertension. 

Risk factors for primary (essential) hypertension:

●Age – Advancing age is associated with increased blood pressure, particularly systolic blood pressure, and an increased incidence of hypertension.

●Obesity – Obesity and weight gain are major risk factors for hypertension and are also determinants of the rise in blood pressure that is commonly observed with aging.

●Family history – Hypertension is approximately twice as common in subjects who have one or two hypertensive parents, and multiple epidemiologic studies suggest that genetic factors account for approximately 30 percent of the variation in blood pressure in various populations.

●Race – Hypertension tends to be more common, be more severe, occur earlier in life, and be associated with greater target-organ damage in Black patients.

●Reduced nephron number – Reduced adult nephron mass may predispose to hypertension, which may be related to genetic factors, intrauterine developmental disturbance (eg, hypoxia, drugs, nutritional deficiency), premature birth, and postnatal environment (eg, malnutrition, infections).

●High-sodium diet – Excess sodium intake (eg, >3 g/day [sodium chloride]) increases the risk for hypertension, and sodium restriction lowers blood pressure in those with a high sodium intake.

●Excessive alcohol consumption – Excess alcohol intake is associated with the development of hypertension, and alcohol restriction lowers blood pressure in those with increased intake.

●Physical inactivity – Physical inactivity increases the risk for hypertension, and exercise (aerobic, dynamic resistance, and isometric resistance) is an effective means of lowering blood pressure.

●Insufficient sleep – Short sleep duration (eg, <7 hours per night) is associated with a higher risk of hypertension [21-23], and increasing the duration of sleep may lower blood pressure.

●Social determinants – Social determinants of health, such as low socioeconomic status, lack of health insurance, food and housing insecurity, and lack of access to safe spaces for exercise may underlie several of the above risk factors for hypertension (obesity, poor diet, physical inactivity, etc. These social factors likely account in large part for racial disparities in hypertension.

SECONDARY OR CONTRIBUTING CAUSES OF HYPERTENSION:

Hypertension with know cause is called secondary hypertension. 

Major causes of secondary hypertension include:

manifestations of Cushing syndrome".)

●Oral contraceptives, particularly those containing higher doses of estrogen

•Nonsteroidal antiinflammatory agents (NSAIDs), particularly chronic use 

●Antidepressants, including tricyclic antidepressants, selective serotonin reuptake inhibitors, and monoamine oxidase inhibitors

•Corticosteroids, including both glucocorticoids and mineralocorticoids

•Decongestants, such as phenylephrine and pseudoephedrine

•Some weight-loss medications

•Sodium-containing antacids

•Erythropoietin

•Cyclosporine or tacrolimus

•Stimulants, including methylphenidate and amphetamines

•Atypical antipsychotics, including clozapine and olanzapine

•Angiogenesis inhibitors, such as bevacizumab

•Tyrosine kinase inhibitors, such as sunitinib and sorafenib

●Illicit drug use – Drugs such as methamphetamines and cocaine can raise blood pressure.

●Primary kidney disease – Both acute and chronic kidney disease can lead to hypertension. 

●Primary aldosteronism – The presence of primary mineralocorticoid excess, primarily aldosterone, should be suspected in any patient with the triad of hypertension, unexplained hypokalemia, and metabolic alkalosis. However, up to 50 to 70 percent of patients will have a normal plasma potassium concentration. Other disorders or ingestions can mimic primary aldosteronism (apparent mineralocorticoid excess syndromes), including chronic licorice intake.

●Renovascular hypertension – Renovascular hypertension is often due to fibromuscular dysplasia in younger patients and to atherosclerosis in older patients. 

●Obstructive sleep apnea – Disordered breathing during sleep appears to be an independent risk factor for systemic hypertension.

●Pheochromocytoma – Pheochromocytoma is a rare cause of secondary hypertension. Approximately one-half of patients with pheochromocytoma have paroxysmal hypertension; most of the rest have what appears to be primary hypertension.

●Cushing's syndrome – Cushing's syndrome is a rare cause of secondary hypertension, but hypertension is a major cause of morbidity and death in patients with Cushing's syndrome.

●Other endocrine disorders – Hypothyroidism, hyperthyroidism, and hyperparathyroidism may also induce hypertension.

●Coarctation of the aorta – Coarctation of the aorta is one of the major causes of secondary hypertension in young children, but it may also be diagnosed in adulthood.

Symptoms:

severe headaches

chest pain

dizziness

difficulty breathing

nausea

vomiting

blurred vision or other vision changes

anxiety

confusion

buzzing in the ears

nosebleeds

abnormal heart rhythm

COMPLICATIONS OF HYPERTENSION:

●Left ventricular hypertrophy (LVH)

●Heart failure, both reduced ejection fraction (systolic) and preserved ejection fraction (diastolic) 

●Ischemic stroke

●Intracerebral hemorrhage

●Ischemic heart disease, including myocardial infarction and coronary interventions

●Chronic kidney disease and end-stage kidney disease 

DIAGNOSIS OF HYPERTENSION:

Classification Systolic and diastolic readings

●Normal systolic: less than 120 mm Hg

diastolic: less than 80 mm Hg

●Elevated systolic: 120–129 mm Hg

diastolic: less than 80 mm Hg

●High blood pressure systolic: 130 mm Hg or higher

diastolic: 80 mm Hg or higher

Laboratory testing:

●Electrolytes (including calcium) and serum creatinine (to calculate the estimated glomerular filtration rate)

●Fasting glucose

●Urinalysis

●Complete blood count

●Thyroid-stimulating hormone

●Lipid profile

●Electrocardiogram

●Calculate 10-year atherosclerotic cardiovascular disease risk

TREATMENT:

Nonpharmacologic therapy:

●Dietary salt restriction – In well-controlled randomized trials, the overall impact of moderate sodium reduction is a fall in blood pressure in hypertensive and normotensive individuals of 4.8/2.5 and 1.9/1.1 mmHg, respectively. The effects of sodium restriction on blood pressure, cardiovascular disease, and mortality as well as specific recommendations for sodium intake, are discussed in detail elsewhere.

●Potassium supplementation, preferably by dietary modification, unless contraindicated by the presence of chronic kidney disease or use of drugs that reduce potassium excretion.

●Weight loss – Weight loss in overweight or obese individuals can lead to a significant fall in blood pressure independent of exercise. The decline in blood pressure induced by weight loss can also occur in the absence of dietary sodium restriction [53], but even modest sodium restriction may produce an additive antihypertensive effect. The weight loss-induced decline in blood pressure generally ranges from 0.5 to 2 mmHg for every 1 kg of weight lost.

●DASH diet – The Dietary Approaches to Stop Hypertension (DASH) dietary pattern is high in vegetables, fruits, low-fat dairy products, whole grains, poultry, fish, and nuts and low in sweets, sugar-sweetened beverages, and red meats. The DASH dietary pattern is consequently rich in potassium, magnesium, calcium, protein, and fiber but low in saturated fat, total fat, and cholesterol. A trial in which all food was supplied to normotensive or mildly hypertensive adults found that the DASH dietary pattern reduced blood pressure by 6/4 mmHg compared with a typical American-style diet that contained the same amount of sodium and the same number of calories. Combining the DASH dietary pattern with modest sodium restriction produced an additive antihypertensive effect. These trials and a review of diet in the treatment of hypertension are discussed in detail elsewhere.

●Exercise – Aerobic, dynamic resistance and isometric resistance exercise can decrease systolic and diastolic pressure by, on average, 4 to 6 mmHg and 3 mmHg, respectively, independent of weight loss. Most studies demonstrating a reduction in blood pressure have employed at least three to four sessions per week of moderate-intensity aerobic exercise lasting approximately 40 minutes for a period of 12 weeks. 

●Limited alcohol intake – Women who consume two or more alcoholic beverages per day and men who have three or more drinks per day have a significantly increased incidence of hypertension compared with nondrinkers. Adult men and women with hypertension should consume, respectively, no more than two and one alcoholic drinks daily.

Pharmacologic therapy:

●Thiazide-like or thiazide-type diuretics

●Long-acting calcium channel blockers (most often a dihydropyridine such as amlodipine)

●Angiotensin-converting enzyme (ACE) inhibitors

●Angiotensin II receptor blockers (ARBs)

Combination therapy:

Single-agent therapy will not adequately control blood pressure in most patients whose baseline systolic blood pressure is 15 mmHg or more above their goal. Combination therapy with drugs from different classes has a substantially greater blood pressure-lowering effect than doubling the dose of a single agent, often with a reduction in side effects seen with a higher dose of monotherapy. When more than one agent is needed to control the blood pressure, we recommend therapy with a long-acting ACE inhibitor or ARB in concert with a long-acting dihydropyridine calcium channel blocker. Combination of an ACE inhibitor or ARB with a thiazide diuretic can also be used but may be less beneficial when hydrochlorothiazide is used. ACE inhibitors and ARBs should not be used together. 

Prevention:

Do:

•Eat more vegetables and fruits.

•Sit less.

•Be more physically active, which can include walking, running, swimming, dancing or activities that build strength, like lifting weights.

•Get at least 150 minutes per week of moderate-intensity aerobic activity or 75 minutes per week of vigorous aerobic activity.

•Do strength building exercises 2 or more days each week.

•Lose weight if you’re overweight or obese.

•Take medicines as prescribed by your health care professional.

•Keep appointments with your health care professional.

Don’t:

•Eat too much salty food (try to stay under 2 grams per day)

•Eat foods high in saturated or trans fats

•Smoke or use tobacco

•Drink too much alcohol (1 drink daily max for women, 2 for men)

•Miss or share medication.

Macleod's Clinical Examination 14th Edition pdf free download

 Macleod's Clinical Examination 14th Edition pdf free download 

Download

About The Authors:

J Alastair Innes

BSc PhD FRCP(Ed)

Consultant Physician, Respiratory Unit, Western General Hospital, Edinburgh; Honorary Reader in Respiratory Medicine, University of Edinburgh, UK

Anna R Dover

PhD FRCP(Ed)

Consultant in Diabetes, Endocrinology and General Medicine, Edinburgh Centre for Endocrinology and Diabetes, Royal Infirmary of Edinburgh; Honorary Clinical Senior Lecturer, University of Edinburgh, UK

Karen Fairhurst

PhD FRCGP General Practitioner, Mackenzie Medical Centre, Edinburgh; Clinical Senior Lecturer, Centre for Population Health Sciences, University of Edinburgh, UK

Illustrations by Robert Britton and Ethan Danielson

Contents:

SECTION 1 PRINCIPLES OF CLINICAL HISTORY AND EXAMINATION

1 Managing clinical encounters with patients

2 General aspects of history taking

3 General aspects of examination 

SECTION 2 SYSTEM-BASED EXAMINATION

4 The cardiovascular system

5 The respiratory system

6 The gastrointestinal system

7 The nervous system

8 The visual system

9 The ear, nose and throat

10 The endocrine system 

11 The reproductive system 

12 The renal system

13 The musculoskeletal system

14 The skin, hair and nails

SECTION 3 APPLYING HISTORY AND EXAMINATION SKILLS IN SPECIFIC SITUATIONS

15 Babies and children

16 The patient with mental disorder Stephen Potts

17 The frail elderly patient

18 The deteriorating patient

19 The dying patient

SECTION 4 PUTTING HISTORY AND EXAMINATION SKILLS TO USE

20 Preparing for assessment

21 Preparing for practice

 OXFORD HANDBOOK OF CLINICAL MEDICINE 10th Edition pdf free download 

Download

Authors:

Jan B. Wilkinson

Tim Raine

Kate Wiles

Anna Goodhart Catriona Hall

Harriet O'Neill

Contents:

1 Thinking about medicine

2 History and examinations

3 Cardiovascular medicine

4 Chest medicine

5 Endocrinology 6 Gastroenterology

7 Renal medicine

8. Haematology

9 Infectious diseases

10 Neurology

11 Oncology and palliative care

12 Rheumatology 13 Surgery

14 Clinical chemistry

15 Eponymous syndromes 

16 Radiology

17 Reference intervals, etc.

18 Practical procedures

19 Emergencies 20 References

Index

Early warning score

 Cardiac arrest 

 Boards and Beyond | Step 2/3 | Video Lectures | Free Download | March 2023 |

Download

Contents:

Behavioral Sciences

9 files

Cardiology

6 folders 1 file

Emergency medicine 3 folders 1 file

Endocrinology 4 folders-1 file

Epidemiology 13 files

Gastroenterology 6 folders - 1 file

Hematology and Oncology

3 folders 1 file

Infectious Diseases 4 folders 1 file

Musculoskeletal (Rheumatology)

10 files

Neurology 

5 folders 1 file

Obstetrics and Gynecology 3 folders 1 file

Pediatrics

4 folders. 1 file

Psychiatry

5 folders. 1 file

Pulmonary Critical care 3 folders 1 file

Renal and Genitourinary

5 folders-1 file

Surgery and Anesthesia 3 folders-1 file

BoardsBeyond23C_Checklist_2020_2.pdf

207.4 KB Sep 16, 2021, 22:14

White Coat Companion 2022 OPT.pdf 186.73 MB

Pathogenesis, Clinical features, Diagnosis, and Management of Community Acquired Pneumonia

 INTRODUCTION:

Community-acquired pneumonia (CAP) is a leading cause of morbidity and mortality worldwide. The clinical presentation of CAP varies, ranging from mild pneumonia characterized by fever and productive cough to severe pneumonia characterized by respiratory distress and sepsis. Because of the wide spectrum of associated clinical features, CAP is a part of the differential diagnosis of nearly all respiratory illnesses.

DEFINITIONS:

Community-acquired pneumonia (CAP) refers to an acute infection of the pulmonary parenchyma acquired outside of the hospital.

●Nosocomial pneumonia refers to an acute infection of the pulmonary parenchyma acquired in hospital settings and encompasses both hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP).

•HAP refers to pneumonia acquired ≥48 hours after hospital admission.

•VAP refers to pneumonia acquired ≥48 hours after endotracheal intubation.

Risk factors:

Older age – The risk of CAP rises with age. The annual incidence of hospitalization for CAP among adults ≥65 years old is approximately 2000 per 100,000 in the United States. This figure is approximately three times higher than the general population and indicates that 2 percent of the older adult population will be hospitalized for CAP annually .

Chronic comorbidities – The comorbidity that places patients at highest risk for CAP hospitalization is chronic obstructive pulmonary disease (COPD), with an annual incidence of 5832 per 100,000 in the United States [7]. Other comorbidities associated with an increased incidence of CAP include other forms of chronic lung disease (eg, bronchiectasis, asthma), chronic heart disease (particularly congestive heart failure), stroke, diabetes mellitus, malnutrition, and immunocompromising conditions.

Viral respiratory tract infection – Viral respiratory tract infections can lead to primary viral pneumonias and also predispose to secondary bacterial pneumonia. This is most pronounced for influenza virus infection.

Impaired airway protection – Conditions that increase risk of macroaspiration of stomach contents and/or microaspiration of upper airway secretions predispose to CAP, such as alteration in consciousness (eg, due to stroke, seizure, anesthesia, drug or alcohol use) or dysphagia due to esophageal lesions or dysmotility.

Smoking and alcohol overuse – Smoking, alcohol overuse (eg, >80 g/day), and opioid use are key modifiable behavioral risk factors for CAP.

Other lifestyle factors – Other factors that have been associated with an increased risk of CAP include crowded living conditions (eg, prisons, homeless shelters), residence in low-income settings, and exposure to environmental toxins (eg, solvents, paints, or gasoline).

MICROBIOLOGY:

Common causes — Streptococcus pneumoniae (pneumococcus) and respiratory viruses are the most frequently detected pathogens in patients with CAP.

The most commonly identified causes of CAP can be grouped into three categories:

●Typical bacteria

•S. pneumoniae (most common bacterial cause)

•Haemophilus influenzae

•Moraxella catarrhalis

•Staphylococcus aureus

•Group A streptococci

•Aerobic gram-negative bacteria (eg, Enterobacteriaceae such as Klebsiella spp or Escherichia coli)

•Microaerophilic bacteria and anaerobes (associated with aspiration)

●Atypical bacteria ("atypical" refers to the intrinsic resistance of these organisms to beta-lactams and their inability to be visualized on Gram stain or cultured using traditional techniques)

•Legionella spp

•Mycoplasma pneumoniae

•Chlamydia pneumoniae

•Chlamydia psittaci

•Coxiella burnetii

●Respiratory viruses

•Influenza A and B viruses

•Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)

•Other coronaviruses (eg, CoV-229E, CoV-NL63, CoV-OC43, CoV-HKU1)

•Rhinoviruses

•Parainfluenza viruses

•Adenoviruses

•Respiratory syncytial virus

•Human metapneumovirus

•Human bocaviruses

PATHOGENESIS:

CAP has been viewed as an infection of the lung parenchyma, primarily caused by bacterial or viral respiratory pathogens. In this model, respiratory pathogens are transmitted from person to person via droplets or, less commonly, via aerosol inhalation (eg, as with Legionella or Coxiella species). Following inhalation, the pathogen colonizes the nasopharynx and then reaches the lung alveoli via microaspiration. When the inoculum size is sufficient and/or host immune defenses are impaired, infection results. Replication of the pathogen, the production of virulence factors, and the host immune response lead to inflammation and damage of the lung parenchyma, resulting in pneumonia (figure 3).

With the identification of the lung microbiome, that model has changed [19-21]. While the pathogenesis of pneumonia may still involve the introduction of respiratory pathogens into the alveoli, the infecting pathogen likely has to compete with resident microbes to replicate. In addition, resident microbes may also influence or modulate the host immune response to the infecting pathogen. If this is correct, an altered alveolar microbiome (alveolar dysbiosis) may be a predisposing factor for the development of pneumonia.

In some cases, CAP might also arise from uncontrolled replication of microbes that normally reside in the alveoli. The alveolar microbiome is similar to oral flora and is primarily comprised of anaerobic bacteria (eg, Prevotella and Veillonella) and microaerophilic streptococci. Hypothetically, exogenous insults such as a viral infection or smoke exposure might alter the composition of the alveolar microbiome and trigger overgrowth of certain microbes. Because organisms that compose the alveolar microbiome typically cannot be cultivated using standard cultures, this hypothesis might explain the low rate of pathogen detection among patients with CAP.

In any scenario, the host immune response to microbial replication within the alveoli plays an important role in determining disease severity. For some patients, a local inflammatory response within the lung predominates and may be sufficient for controlling infection. In others, a systemic response is necessary to control infection and to prevent spread or complications, such as bacteremia. In a minority, the systemic response can become dysregulated, leading to tissue injury, sepsis, acute respiratory distress syndrome, and/or multiorgan dysfunction.

CLINICAL PRESENTATION:

The clinical presentation of CAP varies widely, ranging from mild pneumonia characterized by fever, cough, and shortness of breath to severe pneumonia characterized by sepsis and respiratory distress. Symptom severity is directly related to the intensity of the local and systemic immune response in each patient.

●Pulmonary signs and symptoms – Cough (with or without sputum production), dyspnea, and pleuritic chest pain are among the most common symptoms associated with CAP. Signs of pneumonia on physical examination include tachypnea, increased work of breathing, and adventitious breath sounds, including rales/crackles and rhonchi. Tactile fremitus, egophony, and dullness to percussion also suggest pneumonia. These signs and symptoms result from the accumulation of white blood cells (WBCs), fluid, and proteins in the alveolar space. Hypoxemia can result from the subsequent impairment of alveolar gas exchange. On chest radiograph, accumulation of WBCs and fluid within the alveoli appears as pulmonary opacities.

●Systemic signs and symptoms – The great majority of patients with CAP present with fever. Other systemic symptoms such as chills, fatigue, malaise, chest pain (which may be pleuritic), and anorexia are also common. Tachycardia, leukocytosis with a leftward shift, or leukopenia are also findings that are mediated by the systemic inflammatory response. Inflammatory markers, such as the erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and procalcitonin may rise, though the latter is largely specific to bacterial infections. CAP is also the leading cause of sepsis; thus, the initial presentation may be characterized by hypotension, altered mental status, and other signs of organ dysfunction such as renal dysfunction, liver dysfunction, and/or thrombocytopenia.

Diagnosis:

A chest X-ray looks for inflammation in your lungs. A chest X-ray is often used to diagnose pneumonia.

Blood tests, such as a complete blood count (CBC) see whether your immune system is fighting an infection.

Pulse oximetry measures how much oxygen is in your blood. Pneumonia can keep your lungs from getting enough oxygen into your blood. To measure the levels, a small sensor called a pulse oximeter is attached to your finger or ear.

A blood gas test may be done if you are very sick. For this test, your provider measures your blood oxygen levels using a blood sample from an artery, usually in your wrist. This is called an arterial blood gas test.

A sputum test, using a sample of sputum (spit) or mucus from your cough, may be used to find out what germ is causing your pneumonia.

A blood culture test can identify the germ causing your pneumonia and also show whether a bacterial infection has spread to your blood.

A polymerase chain reaction (PCR) test quickly checks your blood or sputum sample to find the DNA of germs that cause pneumonia.

A bronchoscopy looks inside your airways. If your treatment is not working well, this procedure may be needed. At the same time, your doctor may also collect samples of your lung tissue and fluid from your lungs to help find the cause of your pneumonia.

A chest computed tomography (CT) scan can show how much of your lungs are affected by pneumonia. It can also show whether you have complications such as lung abscesses or pleural disorders. A CT scan shows more detail than a chest X-ray.

A pleural fluid culture can be taken using a procedure called thoracentesis, which is when a doctor uses a needle to take a sample of fluid from the pleural space between your lungs and chest wall. The fluid is then tested for bacteria.

DIFFERENTIAL DIAGNOSIS:

Congestive heart failure with pulmonary edema

•Pulmonary embolism

•Pulmonary hemorrhage

•Atelectasis

•Aspiration or chemical pneumonitis

•Drug reactions

•Lung cancer

•Collagen vascular diseases

•Vasculitis

•Acute exacerbation of bronchiectasis

•Interstitial lung diseases (eg, sarcoidosis, asbestosis, hypersensitivity pneumonitis, cryptogenic organizing pneumonia)

TREATMENT:

Outpatient antibiotic therapy:

For most patients aged <65 years who are otherwise healthy and have not recently used antibiotics, we typically use oral amoxicillin (1 g three times daily) plus a macrolide (eg, azithromycin or clarithromycin) or doxycycline. Generally, we prefer to use a macrolide over doxycycline.

This approach differs from the American Thoracic Society (ATS)/Infectious Diseases Society of America (IDSA), which recommend monotherapy with amoxicillin as first line and monotherapy with either doxycycline or a macrolide (if local resistance rates are <25 percent [eg, not in the United States]) as alternatives for this population [26]. The rationale for each approach is discussed separately. (See "Treatment of community-acquired pneumonia in adults in the outpatient setting", section on 'Empiric antibiotic treatment'.)

●For patients who have major comorbidities (eg, chronic heart, lung, kidney, or liver disease, diabetes mellitus, alcohol dependence, or immunosuppression), who are smokers, and/or who have used antibiotics within the past three months, we suggest oral amoxicillin-clavulanate (875 mg twice daily or extended release 2 g twice daily) plus either a macrolide (preferred) or doxycycline.

Inpatient antibiotic therapy:

For patients without suspicion for MRSA or Pseudomonas, we generally use one of two regimens: combination therapy with a beta-lactam plus a macrolide or monotherapy with a respiratory fluoroquinolone. Because these two regimens have similar clinical efficacy, we select among them based on other factors (eg, antibiotic allergy, drug interactions). For patients who are unable to use either a macrolide or a fluoroquinolone, we use a beta-lactam plus doxycycline.

●For patients with known colonization or prior infection with Pseudomonas, recent hospitalization with IV antibiotic use, or other strong suspicion for pseudomonal infection, we typically use combination therapy with both an antipseudomonal beta-lactam (eg, piperacillin-tazobactam, cefepime, ceftazidime, meropenem, or imipenem) plus an antipseudomonal fluoroquinolone (eg, ciprofloxacin or levofloxacin). The selection of empiric regimens should also be informed by the susceptibility pattern for prior isolates.

●For patients with known colonization or prior infection with MRSA or other strong suspicion for MRSA infection, we add an agent with anti-MRSA activity, such as vancomycin or linezolid, to either of the above regimens. We generally prefer linezolid over vancomycin when community-acquired MRSA is suspected (eg, a young, otherwise healthy patient who plays contact sports presenting with necrotizing pneumonia) because of linezolid's ability to inhibit bacterial toxin production.Ceftaroline is a potential alternative for the treatment of MRSA pneumonia but is not US Food and Drug Administration approved.

PREVENTION:

The three primary pillars for the prevention of CAP are:

●Smoking cessation (when appropriate)

●Influenza vaccination for all patients

●Pneumococcal vaccination for at-risk patients

FIRST AID for the USMLE STEP 2 CK-10th Edition.pdf Free Download

 FIRST AID for the USMLE STEP 2 CK-10th Edition.pdf Free Download 

How to Use This Book?

We have made many improvements and added several new features to this edition of First Aid for the USMLE Step

2 CK. In particular, we have added more tables, charts, and images throughout the text to facilitate studying. We

encourage you to read all aspects of the text to learn the material in context. We have also included comments in

the margins and additional vignette questions to periodically test your knowledge of key concepts. These questions

are located in the lower corner of certain pages. To prevent peeking at the answers, you’ll find the answer on the

back of the same page in the lower corner. These questions are not always representative of test questions.

To practice for the exam and simulate the actual test day, you can use the USMLE-Rx Step 2 CK Qmax question

test bank (www.usmle-rx.com), which was developed by the First Aid author team. If you are constantly on the

move, use the USMLE-Rx Step 2 CK app for smartphones. The question bank and this text are more than enough

to allow many students to ace the exam.

Good luck!

Download

Contents:

SECTION 1: GUIDE TO EFFICIENT EXAM

PREPARATION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

USMLE Step 2 CK—Computer-Based Testing Basics . . 2

Defining Your Goal.................................. 7

Study Resources . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

Test-Day Checklist . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

Testing Agencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

SECTION 2: DATABASE OF HIGH-YIELD FACTS . . . 15

How to Use the Database . . . . . . . . . . . . . . . . . . . . . . . . . . 16

Cardiovascular . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

Dermatology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55

Endocrinology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89

Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119

Ethics and Legal Issues . . . . . . . . . . . . . . . . . . . . . . . . . . . 135

Gastrointestinal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143

Hematology/Oncology . . . . . . . . . . . . . . . . . . . . . . . . . . . 179

Infectious Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211

Musculoskeletal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253

Neurology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 275

Obstetrics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 315

Gynecology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 353

Pediatrics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 391

Psychiatry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 445

Pulmonary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 477

Renal/Genitourinary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 503

Surgery and Emergency Medicine . . . . . . . . . . . . . . . . 533

Rapid Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 563

SECTION 3: TOP-RATED REVIEW RESOURCES . . 589

How to Use the Database . . . . . . . . . . . . . . . . . . . . . . . . 590

Disclaimer/Conflict-of-Interest Statement . . . . . . . . 591

Comprehensive . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 592

Question Banks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 592

Internal Medicine, Emergency Medicine,

Family Medicine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 593

Neurology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 593

OB/GYN . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 594

Pediatrics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 594

Psychiatry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 595

Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 595

Commercial Review Courses . . . . . . . . . . . . . . . . . . . . . 596

Appendix I: Acronyms and Abbreviations . . . . . . . . . 597

Appendix II: Common Laboratory Values . . . . . . . . . 605

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 607

About the Authors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 639

Diabetes Mellitus

 Introduction of Diabetes:

Diabetes mellitus is taken from the Greek word diabetes, meaning siphon - to pass through and the Latin word mellitus meaning sweet.

Diabetes mellitus (DM) is a metabolic disease, involving inappropriately elevated blood glucose levels. DM has several categories, including type 1, type 2, maturity-onset diabetes of the young (MODY), gestational diabetes, neonatal diabetes, and secondary causes due to endocrinopathies, steroid use, etc. The main subtypes of DM are Type 1 diabetes mellitus (T1DM) and Type 2 diabetes mellitus (T2DM), which classically result from defective insulin secretion (T1DM) and/or action (T2DM). T1DM presents in children or adolescents, while T2DM is thought to affect middle-aged and older adults who have prolonged hyperglycemia due to poor lifestyle and dietary choices. The pathogenesis for T1DM and T2DM is drastically different, and therefore each type has various etiologies, presentations, and treatments.

Etiology of Diabetes:

In the islets of Langerhans in the pancreas, there are two main subclasses of endocrine cells: insulin-producing beta cells and glucagon secreting alpha cells. Beta and alpha cells are continually changing their levels of hormone secretions based on the glucose environment. Without the balance between insulin and glucagon, the glucose levels become inappropriately skewed. In the case of DM, insulin is either absent and/or has impaired action (insulin resistance), and thus leads to hyperglycemia.

Type 1 Diabetes Mellitus:

T1DM is characterized by the destruction of beta cells in the pancreas, typically secondary to an autoimmune process. The result is the absolute destruction of beta cells, and consequentially, insulin is absent or extremely low.

Type 2 Diabetes Mellitus:

T2DM involves a more insidious onset where an imbalance between insulin levels and insulin sensitivity causes a functional deficit of insulin. Insulin resistance is multifactorial but commonly develops from obesity and aging.

The genetic background for both types is critical as a risk factor. As the human genome gets further explored, there are different loci found that confer risk for DM. Polymorphisms have been known to influence the risk for T1DM, including major histocompatibility complex (MHC) and human leukocyte antigen (HLA).

T2DM involves a more complex interplay between genetics and lifestyle. There is clear evidence suggesting that T2DM is has a stronger hereditary profile as compared to T1DM. The majority of patients with the disease have at least one parent with T2DM.

Monozygotic twins with one affected twin have a 90% likelihood of the other twin developing T2DM in his/her lifetime.[3] Approximately 50 polymorphisms to date have been described to contribute to the risk or protection for T2DM. These genes encode for proteins involved in various pathways leading to DM, including pancreatic development, insulin synthesis, secretion, and development, amyloid deposition in beta cells, insulin resistance, and impaired gluconeogenesis regulation. A genome-wide association study (GWAS) found genetic loci for transcription factor 7-like 2 gene (TCF7L2), which increases the risk for T2DM.[4][5] Other loci that have implications in the development of T2DM include NOTCH2, JAZF1, KCNQ1, and WFS1.

Maturity-onset diabetes of the young (MODY):

MODY is a heterogeneous disorder identified by non-insulin-dependent diabetes diagnosed at a young age (usually under 25 years). It carries an autosomal dominant transmission and does not involve autoantibodies as in T1DM. Several genes have implications in this disease, including mutations to hepatocyte nuclear factor-1-alpha (HNF1A) and the glucokinase (GCK) gene, which occurs in 52 to 65 and 15 to 32 percent of MODY cases, respectively.[8][9] The genetics of this disease are still unclear as some patients have mutations but never develop the disease, and others will develop clinical symptoms of MODY but have no identifiable mutation.

Gestational diabetes:

Gestational diabetes is essentially diabetes that manifests during pregnancy. It is still unknown why it develops; however, some speculate that HLA antigens may play a role, specifically HLA DR2, 3, and 4. Excessive proinsulin is also thought to play a role in gestational diabetes, and some suggest that proinsulin may induce beta-cell stress. Others believe that high concentrations of hormones such as progesterone, cortisol, prolactin, human placental lactogen, and estrogen may affect beta-cell function and peripheral insulin sensitivity.

Several endocrinopathies, including acromegaly, Cushing syndrome, glucagonoma, hyperthyroidism, hyperaldosteronism, and somatostatinomas, have been associated with glucose intolerance and diabetes mellitus, due to the inherent glucogenic action of the endogenous hormones excessively secreted in these conditions. Conditions like idiopathic hemochromatosis are associated with diabetes mellitus due to excessive iron deposition in the pancreas and the destruction of the beta cells.

Pathophysiology:

A patient with DM has the potential for hyperglycemia. The pathology of DM can be unclear since several factors can often contribute to the disease. Hyperglycemia alone can impair pancreatic beta-cell function and contributes to impaired insulin secretion. Consequentially, there is a vicious cycle of hyperglycemia leading to an impaired metabolic state. Blood glucose levels above 180 mg/dL are often considered hyperglycemic in this context, though because of the variety of mechanisms, there is no clear cutoff point. Patients experience osmotic diuresis due to saturation of the glucose transporters in the nephron at higher blood glucose levels. Although the effect is variable, serum glucose levels above 250 mg/dL are likely to cause symptoms of polyuria and polydipsia.

Insulin resistance is attributable to excess fatty acids and proinflammatory cytokines, which leads to impaired glucose transport and increases fat breakdown. Since there is an inadequate response or production of insulin, the body responds by inappropriately increasing glucagon, thus further contributing to hyperglycemia. While insulin resistance is a component of T2DM, the full extent of the disease results when the patient has inadequate production of insulin to compensate for their insulin resistance. 

Chronic hyperglycemia also causes nonenzymatic glycation of proteins and lipids. The extent of this is measurable via the glycation hemoglobin (HbA1c) test. Glycation leads to damage in small blood vessels in the retina, kidney, and peripheral nerves. Higher glucose levels hasten the process. This damage leads to the classic diabetic complications of diabetic retinopathy, nephropathy, and neuropathy and the preventable outcomes of blindness, dialysis, and amputation, respectively.

History and Physical:

During patient history, questions about family history, autoimmune diseases, and insulin-resistant are critical to making the diagnosis of DM. It often presents asymptomatically, but when symptoms develop, patients usually present with polyuria, polydipsia, and weight loss. On physical examination of someone with hyperglycemia, poor skin turgor (from dehydration) and a distinctive fruity odor of their breath (in patients with ketosis) may be present. In the setting of diabetic ketoacidosis (DKA), clinicians may note Kussmaul respirations, fatigue, nausea, and vomiting. 

Funduscopic examination in a patient with DM may show hemorrhages or exudates on the macula. In frank diabetic retinopathy, retinal venules may appear dilated or occluded. The proliferation of new blood vessels is also a concern for ophthalmologists and can hasten retinal hemorrhages and macular edema, ultimately resulting in blindness. While T1DM and T2DM can present similarly, they can be distinguished based on clinical history and examination. T2DM patients are typically overweight/obese and present with signs of insulin resistance, including acanthosis nigricans, which are hyperpigmented, velvety patches on the skin of the neck, axillary, or inguinal folds. Patients with a longer course of hyperglycemia may have blurry vision, frequent yeast infections, numbness, or neuropathic pain. The clinicians must ask the patient bout any recent skin changes in their feet during each visit. The diabetic foot exam, including the monofilament test, should be a part of the routine physical exam.

Evaluation:

The diagnosis of T1DM is usually through a characteristic history supported by elevated serum glucose levels (fasting glucose greater than 126 mg/dL, random glucose over 200 mg/dL, or hemoglobin A1C (HbA1c exceeding 6.5%) with or without antibodies to glutamic acid decarboxylase (GAD) and insulin.

Fasting glucose levels and HbA1c testing are useful for the early identification of T2DM. If borderline, a glucose tolerance test is an option to evaluate both fasting glucose levels and serum response to an oral glucose tolerance test (OGTT). Prediabetes, which often precedes T2DM, presents with a fasting blood glucose level of 100 to 125 mg/dL or a 2-hour post-oral glucose tolerance test (post-OGTT) glucose level of 140 to 200 mg/dL.

According to the American Diabetes Association (ADA), a diagnosis of diabetes is through any of the following: An HbA1c level of 6.5% or higher; A fasting plasma glucose level of 126 mg/dL (7.0 mmol/L) or higher (no caloric intake for at least 8 hours); A two-hour plasma glucose level of 11.1 mmol/L or 200 mg/dL or higher during a 75-g OGTT; A random plasma glucose of 11.1 mmol/L or 200 mg/dL or higher in a patient with symptoms of hyperglycemia (polyuria, polydipsia, polyphagia, weight loss) or hyperglycemic crisis.[24] The ADA recommends screening adults aged 45 years and older regardless of risk, while the United States Preventative Service Task Force suggests screening individuals between 40 to 70 years who are overweight.

To test for gestational diabetes, all pregnant patients have screening between 24 to 28 weeks of gestation with a 1-hour fasting glucose challenge test. If blood glucose levels are over 140mg/dL, patients have a 3-hour fasting glucose challenge test to confirm a diagnosis. A positive 3-hours OGTT test is when there is at least one abnormal value (greater than or equal to 180, 155, and 140 mg/dL for fasting one-hour, two-hour, and 3-hour plasma glucose concentration, respectively).

Several lab tests are useful in the management of chronic DM. Home glucose testing can show trends of hyper- and hypoglycemia. The HbA1c test indicates the extent of glycation due to hyperglycemia over three months (the life of the red blood cell). Urine albumin testing can identify the early stages of diabetic nephropathy. Since patients with diabetes are also prone to cardiovascular disease, serum lipid monitoring is advisable at the time of diagnosis. Similarly, some recommend monitoring thyroid status by obtaining a blood level of thyroid-stimulating hormone annually due to a higher incidence of hypothyroidism.

Treatment / Management:

The physiology and treatment of diabetes are complex and require a multitude of interventions for successful disease management. Diabetic education and patient engagement are critical in management. Patients have better outcomes if they can manage their diet (carbohydrate and overall caloric restriction), exercise regularly (more than 150 minutes weekly), and independently monitor glucose. Lifelong treatment is often necessary to prevent unwanted complications. Ideally, glucose levels should be maintained at 90 to 130 mg/dL and HbA1c at less than 7%. While glucose control is critical, excessively aggressive management may lead to hypoglycemia, which can have adverse or fatal outcomes.

Since T1DM is a disease primarily due to the absence of insulin, insulin administration through daily injections, or an insulin pump, is the mainstay of treatment. In T2DM, diet and exercise may be adequate treatments, especially initially. Other therapies may target insulin sensitivity or increase insulin secretion by the pancreas. The specific subclasses for drugs include biguanides (metformin), sulfonylureas, meglitinides, alpha-glucosidase inhibitors, thiazolidinediones, glucagonlike-peptide-1 agonist, dipeptidyl peptidase IV inhibitors (DPP-4), selective, amylinomimetics, and sodium-glucose transporter-2 (SGLT-2) inhibitors. Metformin is the first line of the prescribed diabetic medications and works by lowering basal and postprandial plasma glucose. Insulin administration may also be necessary for T2DM patients, especially those with inadequate glucose management in the advanced stages of the disease. In morbidly obese patients, bariatric surgery is a possible means to normalize glucose levels. It is recommended for individuals who have been unresponsive to other treatments and who have significant comorbidities.[29] The GLP-1 agonists liraglutide and semaglutide correlate with improved cardiovascular outcomes. The SGLT-2 inhibitors empagliflozin and canagliflozin have also shown to improve cardiovascular outcomes along with potential renoprotection as well as prevention for the development of heart failure.

Regular screenings are necessary since microvascular complications are a feared complication of diabetes. Regular diabetic retinal exams should be performed by qualified medical personnel to assess for diabetic retinopathy. Neurologic examination with monofilament testing can identify patients with neuropathy at risk for amputation. Clinicians can also recommend patients perform daily foot inspections to identify foot lesions that may go unnoticed due to neuropathy. Low-dose tricyclic antidepressants, duloxetine, anticonvulsants, topical capsaicin, and pain medications may be necessary to manage neuropathic pain in diabetes. Urine microalbumin testing can also assess for early renal changes from diabetes with albuminuria greater than 30mg/g creatinine along with the estimated GFR. The antiproteinuric effect of the angiotensin-converting enzyme (ACE) inhibitors and the angiotensin receptor blockers (ARBs) makes them the preferred agents to delay the progression from microalbuminuria to macroalbuminuria in patients with both Type 1 or Type 2 diabetes mellitus.

The FDA has approved pregabalin and duloxetine for the treatment of diabetic peripheral neuropathy. Tricyclic antidepressants and anticonvulsants have also seen use in the management of the pain of diabetic neuropathy with variable success. 

The ADA also recommends regular blood pressure screening for diabetics, with the goal being 130 mmHg systolic blood pressure and 85 mmHg diastolic blood pressure. Pharmacologic therapy for hypertensive diabetics typically involves angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, diuretics, beta-blockers, and/or calcium channel blockers. The ADA recommends lipid monitoring for diabetics with a goal of low-density lipoprotein cholesterol (LDL-C) being less than 100 mg/dL if no cardiovascular disease (CVD) and less than 70 mg/dl if atherosclerotic cardiovascular disease (ASCVD) is present. Statins are the first-line treatment for the management of dyslipidemia in diabetics. The ADA suggests that low dose aspirin may also be beneficial for diabetic patients who are at high risk for cardiovascular events; however, the role of aspirin in reducing cardiovascular events in patients with diabetes remains unclear.

Complications:

Regardless of the specific type of diabetes, complications involve microvascular, macrovascular, and neuropathic issues. Microvascular and macrovascular complications vary according to the degree and the duration of poorly control diabetes and include nephropathy, retinopathy, neuropathy, and ASCVD events, especially if it is associated with other comorbidities like dyslipidemia and hypertension.[45] One of the most devastating consequences of DM is its effect on cardiovascular disease (ASCVD). Approximately two-thirds of those with DM will die from a myocardial infarction or stroke.[46] In T2DM, fasting glucose of more than 100 mg/dL significantly contributes to the risk of ASCVD, and cardiovascular risk can develop before frank hyperglycemia.

DM is also a common cause of blindness in adults aged 20 to 74 years in the United States. Diabetic retinopathy contributes to 12000 to 24000 new cases of blindness annually, and treatments generally consist of laser surgery and glucose control.

Renal disease is another significant cause of morbidity and mortality in DM patients. It is the leading contributor to end-stage renal disease (ESRD) in the United States, and many patients with ESRD will need to start dialysis or receive a kidney transplant.[49] If the albuminuria persists in the range of 30 to 300 mg/day (microalbuminuria), it seems to be a predictable earliest marker for the onset of diabetic neuropathy. Once macroalbuminuria (greater than 300 mg/24 hr) sets in, the progression to ESRD hastens up. The random spot urine specimen for measurement of the albumin-to-creatinine ratio is a quick, easy, predictable method that is the most widely used and preferred method to detect microalbuminuria. Two of three tests, done over a six month showing a persistent level greater than 30 mcg/mg creatinine, confirms the diagnosis of microalbuminuria.

DM is also the leading cause of limb amputations in the United States; this is primarily due to vasculopathy and neuropathy associated with DM. Many patients who develop neuropathy need to have regular foot exams to prevent infection from wounds that go unnoticed.

The duration of diabetes is the most crucial risk factor for the development of diabetic retinopathy. In people with type 1 diabetes, it typically sets in about 5 years after disease onset. Hence it is recommended to start the yearly retinal exams in these patients about five years after diagnosis. Among patients with type 2 diabetes, many patients might already have retinal changes at the time of diagnosis. Approximately 10% at ten years, 40% at 15 years, and 60% at 20 years will have nonproliferative retinal disease. In these patients, the recommendation is to start the yearly retinal screening at the time of diagnosis. Study after study has shown that reasonable glycemic control favorably affected the onset and progression of diabetic retinopathy. Uncontrolled blood pressure is an added risk factor for macular edema. Lowering the blood pressure in patients with diabetes thus also affects the risk of progression of the retinopathy. Injection of antibodies vascular endothelial growth factor (anti-VEGF) agents are generally in use as the initial therapy in cases of macular edema. In cases of nonproliferative diabetic retinopathy, pan-retinal photocoagulation is being used. In cases of diabetic proliferative retinopathy, combined modalities of anti-VEGF agents and pan-retinal photocoagulation are now in use. Sudden loss of vision can occur for several reasons in patients with diabetes mellitus, the most common being vitreous hemorrhage. Less common causes that merit consideration include vascular occlusion (central retinal vein or branch vein occlusion involving the macula), retinal detachment, end-stage glaucoma, and ischemic optic neuropathy.

Furthermore, evidence suggests that T2DM may also contribute to cancer development, specifically bladder cancer, in those using pioglitazone.[50] Patients using metformin had improved cancer-specific survival in those with prostate, pancreatic, breast, and colorectal cancers. However, it is unclear how metformin plays a role in modulating cancer in patients with diabetes.

Those with gestational diabetes are at a higher risk for cesarean delivery and chronic hypertension. Pregnant patients with T2DM generally have a better prognosis in terms of neonatal and pregnancy complications compared to those with T1DM. Generally, neonates of DM mothers will present with hypoglycemia and macrosomia.

The most acute complication of DM is diabetic ketoacidosis (DKA), which typically presents in T1DM. This condition is usually either due to inadequate dosing, missed doses, or ongoing infection.[53] In this condition, the lack of insulin means that tissues are unable to obtain glucose from the bloodstream. Compensation for this causes the metabolism of lipids into ketones as a substitute energy source, which causes systemic acidosis, and can be calculated as a high anion-gap metabolic acidosis. The combination of hyperglycemia and ketosis causes diuresis, acidemia, and vomiting leading to dehydration and electrolyte abnormalities, which can be life-threatening. In T2DM, hyperosmolar hyperglycemic syndrome (HHS) is an emergent concern. It presents similarly to DKA with excessive thirst, elevated blood glucose, dry mouth, polyuria, tachypnea, and tachycardia. However, unlike DKA, HHS typically does not present with excessive urinary ketones since insulin still gets produced by pancreatic beta cells. Treatment for DKA or HHS involves insulin administration and aggressive intravenous hydration. Careful management of electrolytes, particularly potassium, is critical in the management of these emergent conditions.

 BRS Physiology Seventh Edition Download Free Pdf

Physiology

SEVENTH EDITION

Linda S. Costanzo, Ph.D.

Professor of Physiology and Biophysics

School of Medicine Virginia Commonwealth University Richmond, Virginia

Download

Contents:

1. CELL PHYSIOLOGY

I. Cell Membranes

II. Transport Across Cell Membranes

III. Osmosis

IV. Diffusion Potential, Resting Membrane Potential, and Action Potential

V. Neuromuscular and Synaptic Transmission

VI. Skeletal Muscle

VII. Smooth Muscle

VIII. Comparison of Skeletal Muscle, Smooth Muscle, and Cardiac Muscle

Review Test

2. NEUROPHYSIOLOGY

I. Autonomic Nervous System (ANS) II. Organization of the Nervous System

III. Sensory Systems

IV. Motor Systems

V. Higher Functions of the Cerebral Cortex VI. Blood-Brain Barrier and Cerebrospinal Fluid (CSF)

VII. Temperature Regulation

Review Test

3. CARDIOVASCULAR PHYSIOLOGY

I. Circuitry of the Cardiovascular System

II. Hemodynamics

III. Cardiac Electrophysiology

IV. Cardiac Muscle and Cardiac Output V. Cardiac Cycle

VI. Regulation of Arterial Pressure

VII. Microcirculation and Lymph

VIII. Special Circulations

IX. Integrative Functions of the Cardiovascular System: Gravity, Exercise,

and Hemorrhage Review Test

4. RESPIRATORY PHYSIOLOGY

I. Lung Volumes and Capacities II. Mechanics of Breathing

III. Gas Exchange

IV. Oxygen Transport V. CO₂ Transport

VI. Pulmonary Circulation

VII. V/Q Defects

VIII. Control of Breathing

IX. Integrated Responses of the Respiratory System

Review Test

5. RENAL AND ACID-BASE PHYSIOLOGY

I. Body Fluids

II. Renal Clearance, Renal Blood Flow (RBF), and Glomerular Filtration

Rate (GFR)

III. Reabsorption and Secretion

IV. NaCl Regulation

V. K* Regulation

VI. Renal Regulation of Urea, Phosphate, Calcium, and Magnesium VII. Concentration and Dilution of Urine

VIII. Renal Hormones

IX. Acid-Base Balance

X. Diuretics

XI. Integrative Examples

Review Test

6. GASTROINTESTINAL PHYSIOLOGY

I. Structure and Innervation of the Gastrointestinal Tract

II. Regulatory Substances in the Gastrointestinal Tract

III. Gastrointestinal Motility IV. Gastrointestinal Secretion

V. Digestion and Absorption

VI. Liver Physiology Review Test

7. ENDOCRINE PHYSIOLOGY

I. Overview of Hormones

II. Cell Mechanisms and Second

Messengers III. Pituitary Gland (Hypophysis)

IV. Thyroid Gland

V. Adrenal Cortex and Adrenal Medulla

VI. Endocrine Pancreas-Glucagon and Insulin

VII. Calcium Metabolism (Parathyroid Hormone, Vitamin D, Calcitonin) VIII. Sexual Differentiation

IX. Male Reproduction

X. Female Reproduction

Review Test

Comprehensive Examination

APPENDIX A.KEY PHYSIOLOGY TOPICS FOR USMLE

STEP 1 APPENDIX B.KEY PHYSIOLOGY EQUATIONS FOR USMLE

STEP 1

APPENDIX C.NORMAL BLOOD VALUES

Index

 Boards & Beyonds USMLE STEP 1 Videos with English Subtitles 2023 Free Download 

Today, in this article, we are going to share with you Board and Beyond USMLE STEP 1 2023 for free download. We hope that our readers will find these videos helpful in their learning.

Boards & Beyond provides an online virtual curriculum to supplement your coursework and provide a comprehensive review for the USMLE Step 1 exam all in one place! Instead of buzzwords or mnemonics, we emphasize understanding of the basic and clinical sciences, so that the students can study more effectively and build a foundation to succeed in medical school, on Step 1, and beyond.

Download

Checklist of Board and Beyond USMLE STEP 1 2023 List of Videos

Below is the complete checklist of Board and Beyond USMLE STEP 1 2023 free download which you will be able to access here:

1. Basic Pharmacology

2. Behavioral Science

3. Biochemistry

4. Biostats

5. Cardiology

6. Cell Biology

7. Dermatology

8. Endocrinology 9. Gastroenterology

10. Genetics

11. Hematology

12. Immunology

13. Infectious Disease 14. Musculoskeletal

15. Neurology

16. Pathology

17. Psychiatry

18. Pulmonary

19. Renal

20. Reproductive

Dietary Approaches to Stop Hypertension (DASH diet).

DASH stands for Dietary Approaches to Stop Hypertension.

The DASH diet is a healthy-eating plan designed to help prevent or treat high blood pressure, also called hypertension. It also may help lower cholesterol linked to heart disease, called low density lipoprotein (LDL) cholesterol.

High blood pressure and high LDL cholesterol levels are two major risk factors for heart disease and stroke.

Foods in the DASH diet are rich in the minerals potassium, calcium and magnesium. The DASH diet focuses on vegetables, fruits and whole grains. It includes fat-free or low-fat dairy products, fish, poultry, beans and nuts.

The diet limits foods that are high in salt, also called sodium. It also limits added sugar and saturated fat, such as in fatty meats and full-fat dairy products.

DASH diet and sodium:

The standard DASH diet limits salt to 2,300 milligrams (mg) a day. That amount agrees with the Dietary Guidelines for Americans. That's about the amount of sodium in 1 teaspoon of table salt.

A lower sodium version of DASH restricts sodium to 1,500 mg a day. You can choose the version of the diet that meets your health needs. If you aren't sure what sodium level is right for you, talk to your health care provider.

DASH diet: What to eat:

The DASH diet is a balanced eating plan that gives choices of what to eat. The diet helps create a heart-healthy eating style for life. There's no need for special foods or drinks. Foods in the diet are at grocery stores and in most restaurants.

When following DASH, it is important to choose foods that are:

Rich in potassium, calcium, magnesium, fiber and protein.

Low in saturated fat.

Low in salt.

DASH diet: Suggested servings:

The DASH diet provides daily and weekly nutritional goals. The number of servings depends on daily calorie needs.

Here's a look at the recommended servings from each food group for a 2,000-calorie-a-day DASH diet:

Grains: 6 to 8 servings a day. One serving may be 1/2 cup of cooked cereal, rice or pasta, 1 slice of bread or 1 ounce dry cereal.

Vegetables: 4 to 5 servings a day. One serving is 1 cup raw leafy green vegetable, 1/2 cup cut-up raw or cooked vegetables, or 1/2 cup vegetable juice.

Fruits: 4 to 5 servings a day. One serving is one medium fruit, 1/2 cup fresh, frozen or canned fruit, or 1/2 cup fruit juice.

Fat-free or low-fat dairy products: 2 to 3 servings a day. One serving is 1 cup milk or yogurt, or 1 1/2 ounces cheese.

Lean meats, poultry and fish: six 1-ounce servings or fewer a day. One serving is 1 ounce of cooked meat, poultry or fish, or 1 egg.
Nuts, seeds, or dry beans and peas: 4 to 5 servings a week. One serving is 1/3 cup nuts, 2 tablespoons peanut butter, 2 tablespoons seeds, or 1/2 cup cooked dried beans or peas, also called legumes.
Fats and oils: 2 to 3 servings a day. One serving is 1 teaspoon soft margarine, 1 teaspoon vegetable oil, 1 tablespoon mayonnaise or 2 tablespoons salad dressing.
Sweets and added sugars: 5 servings or fewer a week. One serving is 1 tablespoon sugar, jelly or jam, 1/2 cup sorbet or 1 cup lemonade. 

DASH diet: Alcohol and caffeine:

Drinking too much alcohol can increase blood pressure. The Dietary Guidelines for Americans recommends that men limit alcohol to no more than two drinks a day and women to one or less.

The DASH diet doesn't talk about caffeine. How caffeine affects blood pressure isn't clear. But caffeine can cause blood pressure to rise at least briefly.

If you have high blood pressure or if you think caffeine affects your blood pressure, think about cutting down. You might talk to your health care provider about caffeine.

What is Pirola, the new variant of the Coronavirus?

What to Know About the New BA 2.86 COVID Variant?

 The CDC and the World Health Organization have dubbed the BA 2.86 variant of COVID-19 as a variant to watch. 

  So far, only 26 cases of "Pirola," as the new variant is being called, have been identified: 10 in Denmark, four each in Sweden and the United States, three in South Africa, two in Portugal, and one each the United Kingdom, Israel, and Canada. BA 2.86 is a subvariant of Omicron, but according to reports from the CDC, the strain has many more mutations than the ones that came before it. 

  With so many facts still unknown about this new variant, we asked experts what people need to be aware of as it continues to spread.

 What is unique about the BA 2.86 variant? 

It is unique in that it has more than three mutations on the spike protein," said Purvi Parikh, MD, an infectious disease expert at New York University's Langone Health. The virus uses the spike proteins to enter our cells. 

This "may mean it will be more transmissible, cause more severe disease, and/or our vaccines and treatments may not work as well, as compared to other variants," she said.

Good news ― hospital admissions with Covid plateaued last week, and at levels lower than recent troughs. none of this has anything to do with new variant BA.2.86 ("Pirola") which is a tiny tiny proportion of sequenced cases. "Eris" (EG.5.1) still not dominant either.

What do we need to watch with BA 2.86 going forward? 

"We don't know if this variant will be associated with a change in the disease severity. We currently see increased numbers of cases in general, even though we don't yet see the BA.2.86 in our system," said Heba Mostafa, PhD, director of the molecular virology laboratory at Johns Hopkins Hospital in Baltimore. 

"It is important to monitor BA.2.86 (and other variants) and understand how its evolution impacts the number of cases and disease outcomes," she said. "We should all be aware of the current increase in cases, though, and try to get tested and be treated as soon as possible, as antivirals should be effective against the circulating variants." 

What should doctors know?

Parikh said doctors should generally expect more COVID cases in their clinics and make sure to screen patients even if their symptoms are mild.

"We have tools that can be used – antivirals like Paxlovid are still efficacious with current dominant strains such as EG.5," she said. "And encourage your patients to get their boosters, mask, wash hands, and social distance."

How well can our vaccines fight BA 2.86?

"Vaccine coverage for the BA.2.86 is an area of uncertainty right now," said Mostafa. 

In its report, the CDC says scientists are still figuring out how well the updated COVID vaccine works. It's expected to be available in the fall, and for now, they believe the new shot will still make infections less severe, new variants and all. 

If you weren't already aware, BA.2.86 (Pirola) is in the US Midwest%u2014probably the first time a major variant has been seen in the Midwest before the major US coastal cities. 

Prior vaccinations and infections have created antibodies in many people, and that will likely provide some protection, Mostafa said. "When we experienced the Omicron wave in December 2021, even though the variant was distant from what circulated before its emergence and was associated with a very large increase in the number of cases, vaccinations were still protective against severe disease." 

What is the most important thing to keep track of when it comes to this variant?

According to Parikh, "it's most important to monitor how transmissible [BA 2.86] is, how severe it is, and if our current treatments and vaccines work." 

Mostafa said how well the new variants escape existing antibody protection should also be studied and watched closely. 

What does this stage of the virus mutation tell us about where we are in the pandemic?

The history of the coronavirus over the past few years shows that variants with many changes evolve and can spread very quickly, Mostafa said. "Now that the virus is endemic, it is essential to monitor, update vaccinations if necessary, diagnose, treat, and implement infection control measures when necessary."

With the limited data we have so far, experts seem to agree that while the the variant's makeup raises some red flags, it is too soon to jump to any conclusions about how easy it is to catch it and the ways it may change how the virus impacts those who contract it.

How do viruses mutate, exactly?

 It is natural for all viruses to mutate over time and such changes are particularly common in viruses that have RNA as their genetic material, as in the case of coronaviruses and influenza viruses.

Once a virus enters the human body, its genetic material — RNA or DNA — enters the cells and starts making copies of itself which can infect the other cells. Whenever an error occurs during this copying process, it triggers a mutation.

Occasionally, a mutation comes along when the genetic mistakes that are introduced while copying prove to be advantageous for the virus — these help the virus copy itself or enter human cells more easily. Whenever a virus is widely circulating in a population, the more it spreads and replicates, its chances of mutating increases.

What differentiates Pirola?

Speaking to the Yale School of Medicine, Anne Hahn, a postdoctoral associate who leads the Yale SARS-CoV-2 Genomic Surveillance Initiative, said that this is a “much more interesting subvariant”, when compared to the Omicron subvariant known as XBB.1.9. That variant initially spread quickly but did not overwhelm populations at a significant scale.

The same report noted that it has been detected by surveillance labs in Israel and Denmark and later in labs in England, South Africa, and the United States.

According to Fortune, new data released on Twitter on Friday evening by Ben Murrell, a researcher at the Karolinska Institutet in Sweden, showed that blood samples taken last week performed better than expected when it came to neutralising BA.2.86.

Dr Eric Topol, a professor of molecular medicine at Scripps Research and founder and director of the Scripps Research Translational Institute, said in a tweet that the findings offer a more positive outlook for how new boosters might protect against the highly mutated variant.

What precautions need to be kept in mind against this new variant?

Roberts said that the US Centres for Disease Control and Prevention’s (CDC) preliminary report says there is not enough evidence right now to conclude whether Pirola could lead to more severe disease, death, or hospitalisation. “We don’t yet know how transmissible it is, and it’s very possible it doesn’t spread that well and we would see this peter out in a couple of weeks,” Dr Roberts said.
He added, “But it’s important to remember that it’s still the same virus at its core, so the same prevention methods — masking, vaccination, and hand-washing, among others — can help people avoid infection.”

Sources:

CDC: "Risk Assessment Summary for SARS CoV-2 Sublineage BA.2.86."

Purvi Parikh, MD, assistant professor, NYU Langone Health, New York City. 

Heba Mostafa, PhD, director, molecular virology laboratory, Johns Hopkins Hospital, Baltimore.

GISAID: "Tracking of hCoV-19 Variants."