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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2866_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Preface
- •Contents
- •Introduction
- •Prevention
- •Harm Reduction
- •Decision-Making/Differential Diagnosis
- •Screening
- •Health Maintenance
- •References
- •Physical Exam
- •Vaccinations
- •Introduction
- •Symptoms
- •Other History
- •Physical Exam
- •Lab Tests
- •Differential Diagnosis
- •Treatment
- •Prevention
- •Long Covid
- •References
- •Introduction
- •Provider Perspectives
- •Portable Medical Summary
- •Education
- •Employment
- •Specialist-Dominated Care
- •Internist-Dominated Care
- •Condition-Specific Medical Knowledge
- •Medication Reconciliation/Polypharmacy
- •Secondary Medical Conditions
- •Behavioral Health
- •Health Maintenance
- •Sexual Health
- •Sexual Abuse
- •Contraception
- •Cervical Cancer Screening
- •Health Disparities
- •Ethical Considerations
- •Conclusion
- •References
- •Introduction
- •Outpatient Assessment
- •Social History
- •Medications
- •Functional Assessment
- •Geriatric Syndromes
- •Delirium
- •Confusion Assessment Method (CAM): Short version [14]
- •Delirium Evaluation
- •Depression
- •Medication Management
- •Preventing Future Falls
- •Polypharmacy
- •Sensory Loss
- •Vision
- •Hearing Loss
- •Osteoporosis
- •Sleep Disorders
- •Advanced Care Planning
- •Home Care
- •References
- •History
- •Palliative Care/Hospice Care
- •Constipation
- •Nausea/Vomiting
- •Pain
- •Conclusion
- •References
- •Introduction
- •Definitions
- •Decision-Making
- •Identification
- •Key History
- •Workup
- •Management
- •Risky or Unhealthy Alcohol Use
- •Risky Opioid Use or OUD
- •References
- •Introduction
- •History
- •Physical Exam
- •Type 1 Diabetes
- •Type 2 Diabetes
- •Lifestyle Changes
- •Metformin
- •GLP-1 Receptor Agonists (Exenatide, Liraglutide, Dulaglutide, Lixisenatide)
- •DPP-4 Inhibitors (Sitagliptin, Saxagliptin, Linagliptin, Alogliptin)
- •SGLT-2 Inhibitors (Canagliflozin, Dapagliflozin, Empagliflozin, Ertugliflozin)
- •Thiazolidinediones (Pioglitazone)
- •Alpha-Glucosidase Inhibitors (AGIs) (Acarbose, Miglitol)
- •Insulin
- •References
- •Subclinical Hypothyroidism
- •Treatment Challenges
- •Hyperthyroidism
- •Brief Introduction
- •Key H&P
- •Decision-Making/Differential Diagnosis
- •Treatment
- •Graves’ Disease
- •Hypothyroidism
- •Brief Introduction
- •Key H&P
- •Decision-Making/Diagnosis
- •Treatment
- •Overt Hypothyroidism
- •Radioactive Iodine (RAI)
- •Surgery
- •Treatment: Subclinical Hyperthyroidism
- •Thyroid Nodules
- •Brief Introduction
- •Key H&P
- •Decision-Making/Differential Diagnosis
- •Treatment
- •References
- •Introduction
- •History
- •Medical History
- •Family History
- •Social History
- •Physical Exam
- •Decision-Making/Differential Diagnosis
- •Screening Population
- •Testing Lipid Levels: Fasting vs. Non-fasting
- •Treatment
- •Treatment Strategies
- •Lifestyle Modification
- •Statins
- •Fibrates
- •Fish Oil
- •Other Non-statin Medications
- •Monitoring After Initiating Therapy
- •References
- •Introduction
- •History
- •Who Should Lose Weight?
- •Treatment
- •Diet
- •Physical Activity
- •Pharmacotherapy
- •Long-Term Follow-Up After Uncomplicated Bariatric Surgery
- •References
- •Brief Introduction
- •Decision-Making/Differential Diagnosis
- •Acute Cough
- •Subacute Cough
- •Chronic Cough
- •Evaluation/Investigation
- •Disease-Specific Features
- •Acute Cough
- •Subacute Cough
- •Chronic Cough
- •Treatment
- •References
- •Introduction
- •Sudden-Onset Dyspnea
- •Acute-Onset Dyspnea
- •Episodic Dyspnea
- •Chronic Dyspnea
- •Treatment
- •References
- •Introduction
- •Acute Sinusitis
- •Chronic/Recurrent Sinusitis
- •Physical Findings
- •Diagnosis
- •Diagnostic Tests
- •Additional Evaluation
- •References
- •Introduction
- •Decision-Making/Differential Diagnosis
- •Key H&P
- •Rapid Antigen Detection Tests
- •Treatment
- •Symptomatic Treatment
- •References
- •Introduction
- •ICSD3 Classifies Sleep Disorders into Seven Major Categories [4]
- •Prevalence
- •Sleep History
- •STOP-Bang Questionnaire
- •Understanding ESS Score
- •Focused Physical Exam
- •Definition
- •Risk Factors
- •Pathophysiology
- •Diagnosis
- •Treatment: OSAHS/SDB (Usual Therapy)
- •References
- •Brief Introduction
- •Decision-Making/Differential Diagnoses
- •Physical Examination
- •Measuring Blood Pressure
- •Diagnostic Studies
- •Clinical Quality Measure
- •Assessment
- •Treatment
- •Lifestyle Management
- •Pharmacological Interventions
- •Refractory or Resistant Hypertension
- •References
- •Chest Pain
- •History
- •Physical Exam
- •Differential Diagnosis
- •Potentially Life-Threatening
- •Acute Coronary Syndromes
- •Aortic Dissection
- •Pulmonary Embolism
- •Pneumothorax
- •Non-Life-Threatening Causes
- •Gastroesophageal Reflux Disease
- •Pleuritic Chest Pain
- •Cervical Angina
- •Pericarditis
- •Chronic Angina
- •Herpes Zoster
- •Muscular Pain
- •Rib Fracture
- •Costochondritis
- •Esophageal Spasm
- •Diagnostic Testing
- •Electrocardiogram
- •Blood Testing
- •Imaging
- •Chest X-Ray
- •X-Ray C-Spine
- •Transthoracic Echocardiogram
- •References
- •Introduction
- •Laboratory Evaluation
- •Hypoproliferative Anemias
- •Microcytic Anemia
- •Differential Diagnosis
- •Iron Deficiency Anemia
- •Epidemiology
- •Pathophysiology
- •Key History
- •Physical Exam
- •Laboratory Evaluation
- •Diagnosis
- •Treatment
- •Normocytic Anemia
- •Differential Diagnosis [6]
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Diagnosis
- •Treatment
- •Macrocytic Anemia
- •Differential Diagnosis [2]
- •Megaloblastic Anemia
- •Vitamin B12 Deficiency
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Diagnosis
- •Folic Acid Deficiency
- •Hyperproliferative Anemia
- •Hemolytic Anemia
- •Intrinsic Hemolytic Anemia
- •Sickle Cell Anemia
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Diagnosis
- •Treatment
- •Thalassemia
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Hereditary Spherocytosis (HS)
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Glucose-6-Phosphate Dehydrogenase Deficiency (G6PD Deficiency)
- •Epidemiology
- •Pathophysiology
- •History Physical Exam
- •Laboratory Evaluation
- •Extrinsic Hemolytic Anemia
- •Autoimmune Hemolytic Anemia
- •Warm Autoimmune Hemolytic Anemia (WAHA)
- •Epidemiology
- •Pathophysiology
- •Laboratory Evaluation
- •Cold Autoimmune Hemolytic Anemia
- •Epidemiology
- •Pathophysiology
- •Laboratory Assessment
- •Conclusion
- •References
- •Introduction
- •Differential Diagnosis
- •Decision-Making/Treatment
- •References
- •Introduction
- •Decision-Making/Differential Diagnosis
- •Papulosquamous
- •Psoriasiform
- •Pityriasiform
- •Lichenoid
- •Erythroderma
- •Eczematous
- •Dermal
- •Vascular
- •Vesiculobullous
- •Infectious
- •Autoimmune, Intraepidermal
- •Autoimmune, Subepidermal
- •Noninflammatory
- •References
- •Introduction
- •Decision-Making/Differential Diagnosis
- •Non-scarring Alopecias
- •Androgenetic Alopecia
- •Focal Hair Loss
- •Diffuse Hair Loss
- •Scarring Alopecia
- •Lymphocytic
- •Acne Keloidalis
- •Neutrophilic
- •References
- •Introduction
- •Key H&P
- •History
- •Medications
- •Social History
- •Physical Examination
- •Differential Diagnosis
- •Decision-Making
- •Treatment
- •References
- •Introduction
- •Key H&P
- •History
- •Physical Examination
- •Differential Diagnosis
- •Intrinsic Shoulder Pain
- •Decision-Making
- •Treatment
- •Rotator Cuff Injury
- •Adhesive Capsulitis
- •References
- •Introduction
- •Key H&P
- •History
- •Medications
- •Social History
- •Physical Examination
- •Differential Diagnosis
- •Decision-Making
- •Treatment
- •Pharmacotherapy
- •Non-pharmacotherapy
- •References
- •Introduction
- •Decision-Making/Differential Diagnosis
- •Vertigo
- •Central vs. Peripheral Vertigo
- •BPPV
- •Meniere’s Disease
- •Labyrinthitis/Vestibular Neuritis
- •Migrainous Vertigo
- •Presyncope
- •Disequilibrium
- •Lightheadedness
- •Dix-Hallpike Maneuver
- •Nystagmus
- •Hearing Evaluation
- •Romberg Testing
- •Other Diagnostic Testing
- •Treatment
- •BPPV
- •Vestibular Neuritis/Labyrinthitis
- •Meniere’s Disease
- •Disequilibrium
- •Presyncope
- •Lightheadedness
- •References
- •Introduction
- •History

Chapter 6. Substance Use Disorder
ents in Scotland: record linkage, validation, and investigation
of risk-factors. PLoS One. 2015;10(11):e0141073. https://doi.
org/10.1371/journal.pone.0141073.
32. Kakko J, Svanborg KD, Kreek MJ, Heilig M. 1-year retention
and social function after buprenorphine-assisted relapse prevention treatment for heroin dependence in Sweden: a randomised,
placebo-controlled trial. Lancet. 2003;361(9358):662–8. https://
doi.org/10.1016/S0140- 6736(03)12600- 1.
33. Liebschutz JM, Crooks D, Herman D, etal. Buprenorphine treatment for hospitalized, opioid-dependent patients: a randomized
clinical trial. JAMA Intern Med. 2014;174(8):1369–76. https://doi.
org/10.1001/jamainternmed.2014.2556.
34. Medications for opioid use disorder: for healthcare and addiction professionals, policymakers, patients, and families [Internet].
Rockville (MD): Substance Abuse and Mental Health Services
Administration (US); 2018.
35. Mattick RP, Breen C, Kimber J, Davoli M.Buprenorphine maintenance versus placebo or methadone maintenance for opioid
dependence. Cochrane Database Syst Rev. 2014;2:CD002207.
https://doi.org/10.1002/14651858.CD002207.pub4.
36. Gowing L, Ali R, White JM, Mbewe D. Buprenorphine for
managing opioid withdrawal. Cochrane Database Syst Rev.
2017;2(2):CD002025. https://doi.org/10.1002/14651858.
CD002025.pub5. PMID: 28220474; PMCID: PMC6464315
3 7. Robbins JL, Englander H, Gregg J. Buprenorphine micro-
dose induction for the Management of Prescription Opioid
Dependence. J Am Board Fam Med. 2021;34(Suppl):S141–6.
https://doi.org/10.3122/jabfm.2021.S1.200236.
38. Fareed A, Patil D, Scheinberg K, Blackinton Gale R, Vayalapalli
S, Casarella J, Drexler K. Comparison of QTc interval prolongation for patients in methadone versus buprenorphine
maintenance treatment: a 5-year follow-up. J Addict Dis.
2013;32(3):244–51. https://doi.org/10.1080/10550887.2013.824333.
39. McCance-Katz EF, Sullivan LE, Nallani S. Drug interactions of clinical importance among the opioids, methadone
and buprenorphine, and other frequently prescribed medications: a review. Am J Addict. 2010;19(1):4–16. https://doi.
org/10.1111/j.1521- 0391.2009.00005.
40. Pacific southwest addiction technology transfer center. SBIRT
training: participant guide. 2013.
155

Part II
Endocrine

Chapter 7
Diabetes
AriGeliebter
Abbreviations
A1C Hemoglobin A1C
AGIs Alpha-glucosidase inhibitors
DM Diabetes mellitus
DPP-4 Dipeptidyl peptidase 4
GLP-1 Glucagon-like peptide-1
SGLT-2 Sodium-glucose cotransporter-2
T1D Type 1 Diabetes
T2D Type 2 Diabetes
TZD Thiazolidinediones
Introduction
Diabetes mellitus (DM) is a heterogeneous, complex, and
chronic disease in which glycemic regulation and control are
progressively lost, leading to hyperglycemia. Diabetes can lead
to many adverse short- and long-term consequences for
A. Geliebter (*)
Comprehensive Endocrinology, PC, Maywood, NJ, USA
e-mail: ageliebter@comprehensiveendo.com
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2022
E. Sydney et al. (eds.), Handbook of Outpatient Medicine,
https://doi.org/10.1007/978-3-031-15353-2_7
159

160
A. Geliebter
patients, and diabetic management is focused on mitigating
these adverse outcomes [1]. Studies such as the UKPDS,
DCCT, and ACCORD have demonstrated that achieving glycemic control can significantly reduce many DM complications, especially microvascular complications [2–4]. More
recently, the introduction of GLP-1 agonists and SGLT2 inhibitors has been shown to potentially improve cardiovascular and
renal outcomes in selected patients [5, 6]. A new diagnosis of
DM has major ramifications for patients, providers, and the
healthcare system overall. Effective management not only
includes glycemic management but also management of coexisting conditions such as hypertension and hyperlipidemia.
Patients may become overwhelmed by the complexity of DM
control and the myriad of recommendations given by their
healthcare providers, thus jeopardizing their ability to achieve
treatment aims and to impact quality of life. A patient-centered
approach remains the foundation for successful management
of DM and the prevention of DM-related complications [1].
Much has been written about the high prevalence of DM in
the USA.As many as 34.2 million people, or 10.5% of the US
population, have diabetes as of 2018, and nearly a quarter of
adults are unaware of their diagnosis [7]. Given the great benefit of tight glycemic control early in the disease process, identification and screening high-risk individuals remains a priority.
The majority of patients fall into one of the two categories,
type 1 diabetes or type 2 diabetes [8].
• Type 1 diabetes (T1D): an autoimmune disease in which
the insulin-producing beta cells are destroyed, leading to
an insulin-deficient state. Overall, about 5% of all patients
with diabetes have T1D [9]. While the majority of T1D
patients are diagnosed at a relatively young age, a new
diagnosis of T1D can occur later in life. The rate of beta
cell destruction is variable, and patients with T1D may still
produce varying amounts of insulin for some time. T1D
patients eventually become dependent on exogenous insu-
lin administration to maintain glycemic control.
• Type 2 diabetes (T2D): a disease state in which glycemic
control is lost due to a combination of factors, including

Chapter 7. Diabetes
insulin resistance and relative insulin insufficiency.
Approximately 90–95% of all patients with diabetes have
T2D [7]. The average age at diagnosis of T2D is older than
of T1D; however T2D has also been increasingly diag-
nosed in younger ages.
• Other DM types: gestational DM, maturity-onset diabetes
of the young (MODY), drug-induced DM, drug or chemi-
cal induced diabetes, destruction of the exocrine pancreas
from cystic fibrosis or pancreatitis.
• Pre-DM: a state in which patients do not meet criteria for
DM, but glucose levels are abnormal. Studies have demon-
strated that pre-DM often progresses to overt DM, and
thus early intervention is considered important.
161
Diagnosis ofDM
DM is commonly diagnosed based on the following ADA
criteria [8]:
1. Fasting plasma glucose of ≥126mg/dL (fasting for 8h).
2. A1C≥6.5%.
3. Classic symptoms of hyperglycemia + plasma glucose of
≥200mg/dL.
4. Two-hour plasma glucose of ≥200mg/dL after a 75-gram
oral glucose load.
Pre-DM is diagnosed with the following ADA criteria [8]:
1. Fasting plasma glucose of 100–125mg/dl.
2. A1C 5.7–6.4%.
3. Two-hour plasma glucose of 140–199g/dL after a 75-gram
oral glucose load.
A single test is typically insufficient for the diagnosis of
DM and should be repeated to confirm the diagnosis.
Distinguishing between T1D and T2D may initially be difficult. A careful history and physical examination may suggest a specific diagnosis, but final confirmation usually occurs
over time. While diabetic ketoacidosis (DKA) is often the
hallmark of T1D, it can also occur on occasion in some T2D

162
A. Geliebter
patients as well. Similarly, while certain characteristics such as
obesity and dyslipidemia are more common in T2D patients,
they can be encountered in T1D patients and thus cannot be
used to definitively classify a disease type. When T1D is suspected, autoimmune markers such as antibodies to islet cells
and insulin, GAD65, IA-2 and IA-2β, and ZnT8 can be used
to help aid in the diagnosis [8]. Insulin secretion can also be
assessed in the ambulatory setting by measuring a C-peptide
level in the setting of hyperglycemia, with a low value being
more consistent with insulin-deficiency and T1D.
Screening forDM
Given the large number of patients with undiagnosed diabetes, an evidence-based screening program is important.
According to the US Preventive Services Task Force, the
following patient populations without obvious diabetes symptoms should be screened in the ambulatory setting [10]:
• Patients aged 35–70 who are overweight (BMI≥ 25) or
obese (BMI≥30).
• Consider earlier screening for overweight or obese patients
from a population with a higher prevalence of diabetes,
such as American Indians/Alaskan Natives, Blacks,
Hispanics/Latinos, or Native Hawaiians/Pacific Islanders.
• Consider earlier screening at BMI ≥ 23 for Asian
Americans.
The USPSTF suggests repeat testing of high-risk patients
every 3years [10].
Key H&P inEarly DM
The symptoms and signs of DM are often due to the presence
of hyperglycemia. The early stages of DM may often be
asymptomatic when the hyperglycemia is mild, but a comprehensive history and physical exam might suggest the
diagnosis.

Chapter 7. Diabetes
163
History
The classic symptoms of polyuria, polydipsia, and weight loss
are consistent with the osmotic diuresis that can accompany
hyperglycemia. Additionally, symptoms such as fatigue, malaise, and blurry vision may be present as well. When T1D is
suspected, patients should be asked about the presence of
any co-existing autoimmune diseases such as vitiligo and primary hypothyroidism.
Physical Exam
There are few exam findings specific to DM.Cutaneous findings such as acanthosis nigricans and skin tags may suggest
the presence of insulin resistance.
Healthcare Maintenance inthePatient
withDiabetes [11]
• Annual eye exam
• Annual monofilament test or other test for detecting
neuropathy
• A1C every 3–6months depending on control
• Annual lipid panel
• Annual spot urinary albumin-to-creatinine ratio
• Blood pressure at every visit
• Annual influenza vaccine and pneumococcal vaccine at
appropriate intervals
• COVID-19 vaccination
Treatment ofDM
Effectively treating DM requires a patient-centered approach
that includes lifestyle modification, glycemic control, and
management of comorbid conditions such as obesity, hyper-

164
A. Geliebter
tension, and dyslipidemia. Patients with DM are at significantly increased risk for cardiovascular disease including
myocardial infarction and stroke, as well as retinopathy and
nephropathy, and mitigating these risks remains a primary
goal of DM management and treatment [1].
DM complications can be divided into microvascular (retinopathy, nephropathy, neuropathy) and macrovascular (CV
disease) categories. Intensive glycemic control has been associated with significant reductions in microvascular complications in both T1D and T2D and in macrovascular complications
in T1D [2–4]. Importantly, while intensive glycemic control
has not been consistently found to reduce macrovascular
complications in T2D, SGLT2 inhibitors and GLP1 agonists
have been shown to mitigate cardiovascular complications in
high-risk patients [5, 6]. Additionally, cardiovascular risk can
be improved by aggressively addressing the traditional risk
factors of hypertension, hyperlipidemia, smoking cessation,
and weight loss.
A1C Treatment Goals in DM [12, 13].
• 6–6.5%: for patients who can achieve tight glycemic con-
trol without hypoglycemia or other adverse effects of
treatment
• <7%: for most nonpregnant patients without significant
hypoglycemia
• <8%: for patients with limited life expectancy or where
adverse effects of treatment are significant
Type 1 Diabetes
Insulin therapy is required in the management of T1D, and a
comprehensive guide to T1D management is beyond the
scope of this resource.
Patients with T1D require both basal and prandial insulin
administration. Insulin can be administered with multiple
daily injections or using an insulin pump (continuous subcutaneous insulin infusion). Prandial insulin should account for
the anticipated carbohydrate intake and pre-meal sugars, and

Chapter 7. Diabetes
a personalized assessment for prandial insulin requirements
is a crucial part in the successful glycemic management in
T1D. Self-monitoring of glucose should be performed both
pre-meal and post-meal to assess adequacy of the insulin
regimen. A continuous glucose monitoring (CGM) has been
associated with A1C reductions [14] and is generally considered the standard of care for all patients with type 1 diabetes.
The current generation of hybrid closed-loop pump systems
has shown promise in reducing hypoglycemia and improving
overall glycemic control.
165
Type 2 Diabetes
The American Diabetes Association (ADA) and the
American Association of Clinical Endocrinologists (AACE)
have published comprehensive treatment guidelines for T2D
[1, 13]. While there are many different treatment approaches
for patients with T2D, it is important that the chosen
approach be understood and agreed upon by both patient
and provider for the highest chances of success.
Lifestyle Changes
Lifestyle changes remain a backbone of treatment for most
patients with T2D as they may partially correct the insulin
resistance and impaired insulin secretion associated with the
disease. These changes include weight loss, increased physical
activity, and smoking cessation. Caloric restriction is a critical
aspect of successful weight loss, and nutritional counseling
and support with realistic goals can help patients make the
appropriate changes to their diet necessary for weight loss
[13]. Meal planning for the diabetic patient requires an
understanding of the glycemic index of carbohydrate containing foods. Educating patients regarding meal composition
and portion size is also essential. Patients should be given a
prescription for increased physical activity advising 30–45min
4–5 times/week of aerobic exercise.

166
A. Geliebter
Motivated patients with newly diagnosed DM with an
A1C ≤7.5% may be tried on a 3–6-month trial of lifestyle
changes alone but should be started on pharmacotherapy if
glycemic targets are not reached. In the majority of patients,
lifestyle changes alone are insufficient to achieve sustained
adequate glycemic management, and pharmacotherapy will
be necessary.
Pharmacological Therapy inT2D
Pharmacological therapy is eventually needed in most
patients with T2D. Since early achievement of tight glycemic
control has been associated with overall improved outcomes,
it is imperative that pharmacological therapy adequate to
achieve glycemic goals be initiated early in the disease course.
There are several pathophysiological defects in T2D, and
combination therapies that address several of these defects
should be considered in all patients [15].
The choice of therapy should be tailored to fit each
patient’s individual glycemic goals while balancing the potential adverse effects of therapy including hypoglycemia. In
adults with recently diagnosed T2D and without significant
comorbidities such as established cardiovascular disease,
intensive therapy sufficient to achieve an A1C of 6.0–6.5%
should be initiated to reduce microvascular and macrovascular disease [13]. In adults with a longer diabetes course, with
established cardiovascular disease or other significant comorbidities, the risk of hypoglycemia and other adverse events
associated with the intensive therapy begins to outweigh the
potential benefits, and a more lenient A1C target of 7.0–8.0%
is appropriate. See Fig. 7. 1 for a suggested pharmacological
approach to glycemic management in T2D treatment.
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