Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2866_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •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 21. Alopecia
439
Key History andPhysical Exam
Various diagnostic tools can help differentiate types of alopecia. A detailed history and physical examination will point to
the diagnosis of most non-scarring and some scarring alopecias, though a skin biopsy may be required.
History
• Description: duration (acute vs. chronic), location, degree
of hair loss, distribution (diffuse vs. patchy), symptoms
including pruritus, redness, pain, or infection.
• Hair practices: tight ponytails, braids, weaves, use of “hot
combs,” chemical treatment.
• Recent changes to medications; chemotherapeutic agents.
• Medical problems: recent illnesses or surgeries, pregnancy,
thyroid disorder, iron deficiency, autoimmune disorders,
malnutrition.
• Emotional or psychological stressors.
• Family history.
Physical Exam
1. Gross inspection of hair:
(a) Generalized, patterned, or focal hair loss.
(b) Density of hair, presence of broken hairs, vellus (thin,
downy premature hair) vs. terminal hairs (thick, strong
mature hair).
2. Inspection of scalp:
(a) Absence of follicular ostia and scar tissue: scarring
alopecias.
(b) Papules, pustules, scaling, perifollicular erythema.
3. Diagnostic procedures:
(a) Hair pull test (useful for telogen efuvium) [1]:
• Performed by grasping a small portion of hair and
gently applying traction while sliding the fingers
along the hair shafts.
– Normal: 1–2 hairs removed.
– Abnormal: ≥6 hairs.

440
C. Barranco and K. Krishnamurthy
(b) Direct microscopic inspections of hair shaft [1]:
• Exclamation point hairs: distal end broader than
proximal end; seen in alopecia areata.
• Anagen hairs: elongated, distorted bulb with
attached outer root sheath.
• Telogen hair: club-shaped bulb.
(c) “Hair growth window” (useful for trichotillomania):
• Repeatedly (weekly) shaving a small area of
involved scalp to demonstrate normal regrowth.
(d) Scalp biopsy (useful for scarring alopecias) [1]:
4. Laboratory testing (useful for androgenetic alopecia,
females particularly):
(a) Total and free testosterone and dehydroepiandros-
terone sulfate.
Treatment (Table21.1) [1–4, 6, 8–10]
General Measures
• Treat underlying medical problems: thyroid disorder or
iron deficiency.
• Discontinue any possible contributing medications, especially in telogen effluvium.
• Advise patient of importance of changing hair practices:
traction alopecia or CCCA.
• Psychological intervention may be needed for
trichotillomania.
Clinical Pearls
• A thorough history and physical examination of the hair
and scalp are key to determining the type of alopecia.
• Treat underlying medical conditions and remove any
potentially exacerbating medications.
• A change in hair practices, especially in African American
women, is often necessary.
• Check nails for pitting in alopecia areata and check the
ears for signs of discoid lupus.

Chapter 21. Alopecia
441
References
1. Bolognia J, Jorizzo JL, Schaffer JV.Dermatology. Philadelphia:
Elsevier Saunders; 2012.
2. Elston D, Bergfeld W.Cicatricial alopecia (and other causes of
permanent alopecia). Disorders of hair growth. NY: McGrawHill; 1994.
3. Barth JH. Hair patterns: hirsuties and baldness. Current concepts in pathogenesis and management. Drugs. 1988;35(1):83–91.
4. Olsen EA, Messenger AG, Shapiro J, Bergfeld WF, Hordinsky
MK, Roberts JL, etal. Evaluation and treatment of male and
female pattern hair loss. J Am Acad Dermatol. 2005;52:301–11.
5. Trueb R. Androgenetic alopecia. In: European handbook of
dermatological treatments. Berlin Heidelberg: Springer-Verlag;
2015. p.55–65.
6. Alkhalifah A, Alsantali A, Wang E, McElwee KJ, Shapiro
J. Alopecia areata update: Part II. Treatment J Am Acad
Dermatol. 2010;62(2):191–202.
7. Zhou C, et al. Alopecia areata: an update on etiopathogenesis, diagnosis, and management. Clin Rev Allergy Immunol.
2021;61:403–23.
8. Mubki T, etal. Evaluation and diagnosis of the hair loss patient.
J Am Acad Dermatol. 2014;71(3):415–e1.
9. Grant J, Chamberlain S. Trichotillomania. Am J Psychiatry.
2016;173:9.
10. Malkud S. Telogen effluvium: a review. J Clin Diagn Res.
2015;99(6):1195–2211.
11. Lenzy YM, et al. Central centrifugal cicatricial alopecia. In:
Clinical cases in skin of color. NewYork: Springer; 2015. p.51–60.
12. Udompanich S, etal. Hair and scalp changes in cutaneous and systemic lupus erythematosus. Am J Clin Dermatol. 2018;19:679–94.

Part VI
Orthopaedic

Chapter 22
Knee Pain
MitsuyoKinjo
Introduction
The knee is the largest articular surface of any joint in the
body. By convention, musculoskeletal pain lasting less than
6weeks is defined as acute, whereas pain lasting longer than
6weeks is chronic.
Important elements of the history are whether acute knee
pain began following recent trauma or overuse during regular
activity and if the pain increases with activity. If the pain
developed after trauma, the presentation is likely caused by
the specific activity or traumatic injury.
Key H&P
First, ask patients if the knee pain is acute or chronic. A
detailed history should be asked to assess if acute knee pain
developed following recent trauma or overuse. If the knee
pain is unrelated to acute trauma or overuse during regular
M. Kinjo (*)
Division of Rheumatology, Department of Medicine, Okinawa
Chubu Hospital, Uruma City, Okinawa, Japan
© 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_22
445

446
M. Kinjo
activity, ask if the knee pain occurs with activity. The patient
is then instructed to pinpoint the location of the pain. If the
knee pain is not related to activity, ask if any systemic symptoms or signs are present.
History
Knee pain is the tenth most common complaint in the ambulatory setting [1]. Knee pain is classified as acute or chronic.
Acute joint pain is defined as knee pain lasting less than
6weeks.
• Did pain develop following an injury or increasing activity
level?
• Did the knee pop at the time of injury? (ligamentous tear
or fracture).
• Did you twist the knee while you were sustaining the knee
flexed? (meniscus tear).
• Is the pain exacerbated by activity? Does the knee feel
stiff?
• Is the pain with activity worse while walking on uneven
surface, walking up and down stairs, movements requiring
knee flexion, or pivoting? (ligaments or meniscus tear).
• In which anatomic quadrant of the knee is the pain
located? Can you point where the pain is with one finger
(anterior, lateral, medial, or posterior)?
• Is the knee pain intermittent or constant?
• Is the knee pain worse after exercise?
• Do you feel the knee is getting stuck in place? Does the
knee give way during walking or climbing stairs without
pain preceding the episode?
• Are there any symptoms or signs of systemic illness? Is
there any fever, chills, night sweats, weight loss, fatigue, or
rash?
• Do you have morning stiffness? Is there pain at night?
• Is there any other joint pain or swelling?

Chapter 22. Knee Pain
Knowing the detailed traumatic event is helpful. If the
knee is twisted while in a flexed position, meniscus tear is
suggested [2]. The clicking, catching, or locking of the knee
and delayed onset of knee effusion are frequently appreciated in the meniscal injury. Patellofemoral pain is common
among active females in the second and third decade of life.
The knee pain is anterior around or under the patella and
worsens with squatting, running, or prolonged sitting [3]. Pain
from the degenerative osteoarthritis tends to be accompanied
by stiffness and is worse with exercise or activity. Knee pain
in osteoarthritis can be anteromedial or more generalized on
the medial side of the tibiofemoral joint, or anterior in the
patellofemoral joint [4].
447
Past Medical andSurgical History
Systemic conditions including rheumatic diseases, thyroid
disease, hyperparathyroidism, hemochromatosis, or sarcoidosis could be causes of knee pain. Sickle cell disease increases
the risk of septic arthritis and osteomyelitis. Hemophilia or
other bleeding disorders can cause hemarthrosis from minor
trauma. Patients should be asked regarding any old injury or
surgery to the lower extremities.
History of gout or psoriasis, infections including sexually
transmitted diseases such as gonorrhea, and Lyme disease
should also be asked.
Medications
History of prior treatment with analgesics, nonsteroidal antiinflammatory drugs, intra-articular injections of
corticosteroids, or hyaluronic acid should be asked. Side
effects of systemic glucocorticoids could be linked to avascular necrosis of the bone (AVN), especially in patients with
systemic lupus erythematosus. AVN is characterized by
insidious onset of unilateral or bilateral knee pain exacerbated by weight- bearing activity.

448
M. Kinjo
Social History
The clinician should explore the patient’s history of exercise
tolerance and daily activity including the use of an ambulatory assist device and walking capability.
Physical Examination
Knee is examined using a systematic approach. First compare
the affected and unaffected joints. Inspection, palpation,
range of motion, strength, assessment of joint stability, and
special tests to detect focal conditions should be included.
When inspecting the knee, the clinician should assess gait,
swelling, ecchymosis and other signs of injury, muscle atrophy,
alignment, and skin changes. If the patient can execute a duck
walk, the knee is free from pathology of ligament, meniscus,
or joint. The alignment of the knee, whether varus (bowlegged) or valgus (knock-kneed) deformity, predisposes the
patient to osteoarthritis.
Palpation of both knees includes the skin temperature,
medial and lateral joint lines, bursae, and posterior knee.
Joints are normally cooler than surrounding skin, and if the
joint feels warm compared to the back of the hand, it indicates inflammation. If the patient can pinpoint localized pain,
attention should be paid to specific structures in that location
(Fig.22.1). With the patient’s knee flexed at a 90° angle, place
your thumbs on the tibial tuberosity and palpate the patellar
tendon. Patellar tendinitis is suspected if the patient complains of pain at the inferior pole of the patella. If there is a
tenderness over the medial anterior aspect of the tibia below
the knee, pes anserine bursitis is suggested [5]. Pain on the
medial joint line may indicate osteoarthritis of the medial
compartment, medial collateral ligament injury, or a medial
meniscal tear. Lateral joint line tenderness suggests similar
conditions of the medial counterpart. Focal pain at the lateral
femoral condyle is indicative of iliotibial band syndrome.
Diffuse tenderness along the joint line is often caused by

Chapter 22. Knee Pain
449
Medial Femoral
epicondyle
Tibial plateau
Tibiofemoral joint
Tibial tuberosity
Biceps femoris
tendon
Lateral femoral
epicondyle
Common
Peroneal nerve
Fibula Head
F . Anterior knee
degenerative, inflammatory, or infectious pathologies.
Evaluation for a joint effusion should be determined. Effusion
is seen as fullness or swelling in the suprapatellar pouch.
Ballottement of the patella can confirm the knee effusion. In
the case of small effusions, “milking” of the fluid from the

450
M. Kinjo
suprapatellar pouch to the patella and noting a parapatellar
bulge can confirm effusions as small as 10cc or less.
If the patient has diminished active but intact passive
range of motion (ROM), it suggests a problem outside the
joint. Common reasons are structural disruption of the muscle tendon unit, excessive pain, or motor nerve damage.
Diminished ROM is often caused by a mechanical problem
inside the joint such as a torn meniscus. If the patient has
crepitus and retropatellar pain when the patella is being compressed during active extension, patellofemoral syndrome or
patellofemoral arthritis is suggested.
Vascular assessment includes palpating the lower extremity pulses of the dorsalis pedis, posterior tibial, and popliteal
arteries.
Referred pain to the popliteal space originates from the
fifth lumbar (L5) nerve root and sacroiliac joint, and referred
pain to the lateral aspect of the knee originates from the S1
nerve root, hip joint, trochanteric bursa, and femur.
Provocative maneuvers are only tested when initial history
and examination suggest specific conditions.
The MCL valgus test is performed with knee at 0 and at 30
degrees of flexion [6]. The knee is braced by placing one hand
along the lateral aspect of the knee joint and applying a valgus force to the knee while the ankle is held in a neutral position. The MCL functions as the primary restraint at both
flexion angles. At 30° of knee flexion, capsule and cruciate
ligaments provide no secondary restraints to valgus stress.
Thus, positive valgus test at 0° suggests injury to both the
MCL and cruciate ligament, but positive test at 30° suggests
isolated MCL injury. Focal tenderness at the collateral ligament and opening of the joint line with this stress testing
compared to the unaffected knee suggests collateral ligament
injury. To perform the LCL varus stress test, place one hand
along the medial aspect of the knee joint and hold the ankle,
applying varus force to the knee while keeping the ankle in a
neutral position.
Anterior and posterior cruciate ligament (ACL and PCL)
damage can be elicited by the drawer test. With the affected
Соседние файлы в папке Библиотека им академика М.И. Перельмана
