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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 21. Alopecia
Acne
Keloidalis
Cellulitis
Scarring
(Cicatricial)
Dissecting
CCCA
Lupus
Discoid
429
Alopecia
(MPHL)
Hair Loss
Male Pattern
Female
Pattern Hair
Loss (FPHL)
Anagen
Effluvium
Non-Scarring
(Non-cicatricial)
Diffuse Pattern (Androgenetic) Lymphocytic Neutrophillic Mixed
Telogen
Effluvium
Focal
Traction Tr ichotillomania
Areata
Alopecia
F . Hair loss algorithm

430
C. Barranco and K. Krishnamurthy
telogen effluvium and anagen effluvium. Patterned alopecia,
also known as androgenetic, includes female pattern hair loss
and male pattern hair loss.
Decision-Making/Differential Diagnosis
The first step to assessing hair loss is to determine whether a
scarring or non-scarring process is occurring. Generally
speaking, scarring alopecia includes forms of alopecia where
the hair follicles are permanently lost. Some alopecias, including alopecia areata, androgenetic alopecia, and traction alopecia, may demonstrate a non-scarring process early in the
disease course and permanent hair loss in later stages.
Non-scarring Alopecias
Androgenetic Alopecia
(Synonyms: Male Pattern and Female Pattern Hair Loss
[MPHL and FPHL], Common Balding, Hereditary Balding
or Thinning)
Androgenetic alopecia represents the most common sub-
type of the non-scarring alopecias and in fact is the most
common cause of hair loss overall. It is due to a genetically
determined sensitivity to androgens of the scalp hair follicles
[1]. It can begin any time after puberty, when androgens begin
to be synthesized [3, 4].
Features:
• Gradual thinning without noticeable shedding.
• Strong genetic disposition, with a high concordance among
monozygotic twins.
• Male pattern hair loss: symmetric and progressive, typically affecting the frontoparietal area with frontal recession as well as vertex thinning (Fig.21.2).

Chapter 21. Alopecia
F . Classic pattern of androgenetic alopecia in a male
involving the bitemporal and crown of the scalp [5]
431
• Female pattern hair loss: diffuse central thinning of the
crown with preservation of the frontal hairline. A
“Christmas tree” pattern results with widening of the central part width (Fig.21.3).
• Treatment options include antiandrogenic medications
(Table21.1).
Focal Hair Loss
Alopecia Areata. This is usually a hair-specific autoimmune
phenomenon in which T-cells interact with follicular antigens.
It is characterized by abrupt onset usually before the second
decade [2]. Alopecia areata can be associated with other

C. Barranco and K. Krishnamurthy
432
F . Classic “Christmas tree” pattern seen in androgenetic
alopecia in a female [5]
T . Non-scarring alopecia treatment
Androgenetic
alopecia
• Minoxidil 5% topical solution (1mL BID)
• Finasteride 1mg/day × at least 3months
(with oral contraceptives)
• Spironolactone 100–200mg/day
• Surgical hair transplant

Chapter 21. Alopecia
T . (continued)
Alopecia areata • Intralesional steroid 2.5–5mg/mL (0.5–1- cm
intervals)
• Topical clobetasol propionate 0.05%
ointment, desoximetasone 0.25% cream, or
betamethasone valerate foam BID
• Diphencyprone (DCP) and squaric acid
dibutyl ester (SADBE): 0.001% for 2weeks
and gradually increase weekly over time
(0.01%, 0.1%, 0.2%, 0.5%, 1%, and 2%)
• Topical minoxidil
• Topical anthralin
• Systemic corticosteroids (for totalis or
universalis): 40mg triamcinolone IM
monthly or daily oral prednisone tapered
over 6–8weeks
433
Trichotillomania
Telogen
effluvium
Scarring alopecia treatment
Discoid lupus
Erythematosus
Central
centrifugal
Cicatricial
alopecia
Dissecting
cellulitis
Acne keloidalis
• Behavioral modification therapy, hypnosis,
insight-oriented therapy
• Clomipramine 25mg daily, gradually
increase to 100mg/day (divided with meals)
over 2weeks
• Treat underlying thyroid or iron deficiency
• Reassurance
• Oral hydroxychloroquine.
• Topical, oral, or intralesional corticosteroids.
• Combination of doxycycline or minocycline
+ topical clobetasol or fluocinonide.
• Oral isotretinoin (0.5–1.5mg/kg daily until
4months after achieving a clinical remission).
• Doxycycline+potent topical corticosteroids.

434
cd
C. Barranco and K. Krishnamurthy
ab
ef
F . Clinical variants of alopecia areata (AA). (a) Classic
round patch of hair loss seen in alopecia areata. (b) Multiple round
patches of hair loss. (c) Reticulate pattern of AA. (d) Ophiasis pattern: band- like loss of hair across the temporal and occipital scalp.
(e) Sisaipho pattern. (f) Alopecia universalis [7]
autoimmune diseases, including Hashimoto’s thyroiditis, vitiligo, inflammatory bowel disease, and type I diabetes [6]
(Fig.21.4).
Features:
• Typically presents as discrete bare patches of hair loss, in a
patchy or multifocal distribution.
• Other presentations include:
• Alopecia totalis: loss of all scalp hair.
• Alopecia universalis: loss of all scalp and body hair.
• Ophiasis pattern: band-like pattern of hair loss that occurs
along the periphery of the temporal and occipital scalp.
• Alopecia involving the beard area.
• Multiple treatment options are available, including but not
limited to corticosteroids, topical immunotherapy
(SADBE, Table21.1), excimer laser therapy.
Traction Alopecia. Occurs due to physical stress on the
hair follicle secondary to tight hairstyles, including ponytails,
braids, and hair weaves:
• Hair thinning mainly noted along the marginal hairline—
frontally, temporally, and occipitally [2]
• Mostly affects African Americans.

Chapter 21. Alopecia
Trichotillomania. Can have various presentations, but
there will be rough, irregular patches of hair loss with broken
or twisted hairs on closer examination. It is a result of intentional pulling of hair from the scalp [1]:
• Onset in childhood and more commonly seen in females
(4:1 ratio) [8].
• Grouped with DSM IV OCD disorders.
• Patients may pull hairs out from other hair-bearing areas
such as the eyebrows, eyelashes, face, extremities, and
pubic area.
• Treatment options include behavioral modification and
clomipramine [1, 9] (Table21.1).
435
Diffuse Hair Loss
1. Telogen Efuvium. Patients experience excessive hair
shedding over the entire scalp:
• Often preceded by a physical or emotional stressor
approximately 3 months prior to the start of the hair
loss.
• Acute telogen effluvium, <3-months duration; chronic
telogen effluvium, >6-months duration.
• Causes include severe infections, postsurgical, postpar-
tum, hypothyroidism, anemia, malnutrition, and drugs
(especially beta-blockers) [10].
• In many instances, a discernible precipitating cause can-
not be found. Chronic telogen effluvium may be a precursor to patterned hair loss.
2. Anagen Efuvium. Abrupt and striking loss of hair (90%
of hairs are in anagen phase):
• It typically is caused by chemotherapy.
• Occurs within days to weeks of initiation and is entirely
reversible.
• Hair regrowth typically occurs after a delay of
3–6months.

436
C. Barranco and K. Krishnamurthy
Scarring Alopecia
Generally refers to all forms of alopecia in which there is
permanent loss of hair follicles. Clinically, one will observe a
smooth scalp with absence of follicular ostia and replacement
with scar tissue. Patients may experience symptoms, including
pain, itching, erythema, and burning sensations. This occurs as
a result of continued inflammation that targets the follicle.
Histopathologic correlation is often needed. As such, the
classification scheme is typically divided into the type of
inflammatory infiltrate involved: lymphocytic, neutrophilic,
or mixed [2] (Fig.21.1).
Lymphocytic
Central Centrifugal Cicatricial Alopecia (CCCA)
(Fig.21.5)
• A chronic, progressive disease with eventual spontaneous
burnout.
• Alopecia centered on the crown or vertex and expands
peripherally in a symmetric fashion.
• It is found almost exclusively in African Americans.
• Early and mild disease can be effectively treated. Longacting oral tetracycline and topical corticosteroid can usually halt progression (Table21.1).
Discoid lupus erythematosus. A form of cutaneous lupus
erythematosus that occurs most commonly on the face, ears,
and scalp (Fig.21.6):
• Discoid lesions usually demonstrate erythema, epidermal
atrophy, and dilated, plugged follicular ostia.
• Central hypopigmentation with peripheral hyperpigmentation is evident in dark-skinned individuals.
• Patients typically do not have systemic disease.
• Diagnosis requires biopsy.

Chapter 21. Alopecia
437
F . Central centrifugal cicatricial alopecia. Characteristic central scarring alopecia that will eventually expand centrifugally [11]

438
ab
C. Barranco and K. Krishnamurthy
F . (a) Figure A demonstrates a fibrotic plaque with
peripheral hyperpigmentation and central hypopigmentation, which
are classic findings in the scarring alopecia of discoid lupus. (b)
Enhanced view of a scarring alopecic plaque of discoid lupus showing loss of hair follicles centrally, follicular keratotic plugging, and
central hypopigmentation with peripheral hyperpigmentation [12]
Mixed Neutrophilic andLymphocytic
Acne Keloidalis
• Presents with small, firm papules and pustules on the
occipital scalp and posterior neck.
• Usually affects young African American men and occasionally women and rarely will be seen in Caucasians.
• Often seen in conjunction with CCCA, but the cause
remains uncertain.
Neutrophilic
Dissecting cellulitis. Involves multiple, firm scalp nodules
most often on the mid-posterior vertex and upper occiput:
• A part of the “follicular occlusion triad.”
• It most often affects young adult black men.
• Over time, the nodules become boggy, fluctuant, and interconnected and will discharge purulent material.
1
Group of disorders in which the hair follicle becomes blocked with
keratin, including hidradenitis suppurativa, acne conglobata, and dissecting cellulitis.
1
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