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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 20. Rash
419
• Diagnostic procedures:
– Potassium hydroxide (KOH) prep: identifies dermato-
phyte infection.
Positive test: presence of hyphae (long, slender,
refractile filaments that cross multiple cell walls).
Tinea versicolor is diagnosed by presence of “spaghetti and meatballs” appearance, which represents
hyphae and spores [3].
– Mineral oil prep: identifies scabies or Demodex mites.
Positive test: observe mite, eggs, or feces (scybala) for
scabies. Observe mite for Demodex. Mineral oil used.
– Wood’s lamp (365nm) [4]:
Findings in different skin conditions:
• Vitiligo: milky white appearance.
• Tinea versicolor: yellow or orange glow.
• Tinea capitis: Microsporum species fluoresce bluegreen, Trichophyton schoenleinii fluoresces dull blue.
• Erythrasma: coral-pink color due to
Corynebacterium.
• Pseudomonas: fluoresces green.
• Porphyria: red-pink fluorescence of skin.
– Nikolsky sign: positive if lateral pressure causes shear-
ing of the epidermis from the dermis. This indicates an
intraepidermal process.
– Asboe-Hansen sign: positive if gentle pressure on the
blister causes lateral expansion of the blister. This also
indicates an intraepidermal process.
– Diascopy: pressing on a lesion with a glass slide to see
whether or not redness blanches out. Purpura is nonblanching often indicating vasculitis.
– Skin biopsy: rashes not responding to conventional treat-
ment require a biopsy. For autoimmune conditions, two
punch biopsy samples should be taken, one for H&E and
one for direct immunofluorescence (DIF). The DIF
specimen should be obtained from uninvolved perilesional skin for suspected immunobullous processes.
• Treatment: Please see diagnostic and treatment (Figs.20.9,
20.10, 20.11, 20.12, 20.13, and 20.14).

420
A. Howell and K. Krishnamurthy
Reaction
Pattern
Red and
Scaly?
Papulo-
squamous
Refer to Papulo-
squamous
algorithm
Eczematous?
Refer to
“eczema”
algorithm
No surface
change?
Refer to
“dermal”
algorithm
Blanchable
erythema or
purpura?
Refer to
“vascular”
algorithm
Blisters?
VesiculaobullousVascularDermalEczema
Refer to
“vesicullaobullous”
algorithm
F . Approach to rashes based on clinical reaction patterns
Clinical Pearls
• A broad differential diagnosis based on a rash’s reaction
pattern is helpful in diagnosing the rash.
• Consider common rashes first and rule out life-threatening
rashes quickly.
• Perform a KOH on most scaly rashes.
• Erosion and/or ulceration can represent an initial vesiculobullous eruption.
• Punch biopsies (3–5mm) should be used for nonresponding or undiagnosed rashes, and a DIF should be performed
for vesiculobullous eruptions.DisclaimerThis research was
supported (in whole or part) by HCA Healthcare and/or
an HCA Healthcare affiliated entity. The views expressed
in this presentation represent those of the author and do
not necessarily represent the official views of HCA
Healthcare or any of its affiliated entities.

immuneossupprossi
Chapter 20. Rash
421
PAPULOSQUAMOUS
and scale
(>90% BSA)
Diifuse rodness
Lichenoid Erythroderma
Pityriasiform
plunar, pruritic
Purple, polygonal
Tan to red or
hypopigmented
with scant scale
solos
trunk palms and
Red-brown, scaly,
tree” distribution
Oval, “christmas
plaquos
Annular, scaly
CTCL or Drug
Psoriasis/Eczema,
Drug-induced LPLichen planus (LP)Tinea versicolor
syphilis
Secondary
Pytyriasis RoseaTinea corporation
Care
Supportive
steroids
Tropial or oral
storoids, oral
metronidazole
Tropical/Intralesional
difucan
Tropical
ketaconazole,
solenlum sulfide
IM penicillin
Reassurance
antidungals
Tropical or oral
Pilaris
Dermatitis
Psoriasis
Oral rotnoids
immuneosupprossives
Ketoconazole
cream/shampoo
ve
calcipotriene
Tropical storoids,
biologies
F . Algorithm for rashes with papulosquamous reaction patterns
Fallicular red-
orange plaquos
Psoriasiform
Greasy scale
Thick,
scaly plaquos
Pityriasis Rubra
Seborrhetic

422
A. Howell and K. Krishnamurthy
ECZEMA
Vesicular, weeping,
irregular or linear
shape
Acute Contact
Dermatitits
Tropical and/or
oral steroids
Scale, crust forms
Subtract Eczema Chronic Eczema
Tropical steroids
Lichenified
hyperpigmented,
scaly
Tropical steroids,
moisturization,
bleach baths,
immunosupperssives
F . Algorithm for rashes with eczematous reaction patterns

Chapter 20. Rash
423
DERMAL
Inflammatory InfectiousSubcutaneous
Linear nodules
with lymphadenitis
nodule
Necrotic ulcerative
plaque
red indurated
Well-demarcated
Red-brown
indurated plaques
small papules
Annular groups of
Atypical
Cat-scratch
Sporotrichosis,
Mycobacterium,
Sarcoidosis Erysipelas Deep fungal
annulare
Granuloma
Antibiotics
Antifungals or
AntibioticsAntifungals
steroids
Tropical or
intralesional
steroids
intralesional
Tropical and/or
photosensitivity
Malar erythema +
Erythema, pain
warmth, edema
Erythematous
tender nedules
Lupus
Erythemaaosus
Panniculitis Cellulitis
steroids
Antimalarials,
Antibiotics
colchicine
NSAIDs, steroids,
F . Algorithm for rashes with dermal reaction patterns

424
A. Howell and K. Krishnamurthy
VASCULAR
Erythema
AnnulateGyrate
ulceration
Purpura to
Palpable purpura
with dusky centre
Targetoid papules
desquarnation
Diffuse bullae and
Toxin-mediated
ECMVasculopathy
Vasculitis
vs. Septic)
(Hypersensitivity
Erythema
Multiforme
SJS/TEN
Kawasaki)
fever, TSS,
(SSSS, Scarlet
amoxicillin
Doxycycline or
cause
Treat underlying
cause
Treat underlying
Acyclovir
care
unit supportive
Stop drug, brun
section)
(see vascular
Various treatments
and paules
“toxic erythem”
Erythematous macules
Hives or wheals
Drug EruptionViral ExanthemUrticaria
drug
Remove
offending
Antihistamines Supportive Care
F . Algorithm for rashes with vascular reaction patterns

Chapter 20. Rash
vesicles in
Small superficial
intertriginous areas
Noninflammatory
Miliaria Crystallina
cooling measures
425
VESICULOBULLOUS
Tarda
alcohol, estrogen
with sun exposure,
Acral blisters worse
(+) Nikolsky (+) Nikolsky
soles
Vesicles on buccal
mucosa, pains, and
Infections Inflammatory
Porphyria Curanea
Tense bulfae on
trunk, fliexual areas
oral invlovemant
Flaccid blister with
Coxsackie
DermatomalNondermatomal
Phlebotomy
Sun protection,
Hydroxychloroquine,
Bullous PemphigoldPemphigus vulgaris
Supportive thearapy
Herpes zosterHSV
Prednisone,
Doxycycyline &
Prednisone,
Acyclovir, Valacyclovir
Niacinamide,
immunosupperessives
Azathioprine
Grouped vesicles on
an erythematous base
Acyclovir, Valacyclovir
F . Algorithm for rashes with vesiculobullous reaction patterns

426
A. Howell and K. Krishnamurthy
References
1. Gropper CA. An approach to clinical dermatologic diagnosis based on morphologic reaction patterns. Clin Cornerstone.
2001;4(1):1–14.
2. Drage LA. Life-threatening rashes: dermatologic signs of four
infectious diseases. Mayo Clin Proc. 1999;74(1):68–72.
3. Santistevan J, Long B, Koyfman A.Rash decisions: an approach
to dangerous rashes based on morphology. J Emerg Med.
2017;52(4):457–71.
4. Bolognia J, Schaffer JV, Cerroni L.Dermatology. Philadelphia:
Elsevier Saunders; 2018.
5. Stern RS. Exanthematous drug eruption. N Engl J Med.
2012;366:2492–501.
6. Pickert A. An approach to vasculitis and vasculopathy. Cutis.
2012;89(5):E1–3.
7. Norman GR, Rosenthal D, Brooks LR, Allen SW, Muzzin LJ.The
development of expertise in dermatology. Arch Dermatol.
1989;125(8):1063–8.
8. Baroni A, et al. Vesicular and bullous disorders: pemphigus.
Dermatol Clin. 2007;25:597–603.
9. Ghatan H. Dermatologic differential diagnosis and pearls.
NewYork: Parthenon; 2002.

Chapter 21
Alopecia
ClaraBarranco andKarthikKrishnamurthy
Introduction
Alopecia (or hair loss) includes a group of disorders in which
there is an absence of hair where it is usually present. More
than 35 million men and 21 million women in the USA experience hair loss. The incidence is highest in Caucasians, followed by Asians, African Americans, and Native Americans.
Though a common problem, hair loss can cause a considerable amount of emotional and social stress to patients.
Moreover, it presents a challenge for practitioners, as there
are multiple etiologies with similar clinical presentations.
Understanding the normal hair cycle is key in assessing
alopecias. There are three main phases of the hair follicle
“This research was supported (in whole or in part) by HCA Healthcare
and/or an HCA Healthcare affiliated entity. The views expressed in this
publication represent those of the author(s) and do not necessarily represent the official views of HCA Healthcare or any of its affiliated
entities.”
C. Barranco · K. Krishnamurthy (*)
Department of Dermatology, Orange Park Hospital,
Orange Park, FL, USA
© 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_21
427

428
C. Barranco and K. Krishnamurthy
cycle: anagen (active growth), catagen (regression), and telogen (rest). Approximately 85–90% of hair follicles are in the
anagen phase, while 10–15% are in the telogen phase, and
less than 1% in the catagen phase. There are approximately
100,000 hair follicles on the scalp, and, on average, 50–100
hairs are normally lost every day [1]. Hair loss becomes a
clinical problem when there are localized patches of hair loss
or when the number of hairs lost daily exceeds the normal
amount. Progressive thinning and excessive shedding of the
scalp hair are the two most common hair complaints
reported [2].
The alopecias are divided into two main categories: scar-
ring (or cicatricial) and non-scarring (or non-cicatricial) alopecias (Fig.21.1). When assessing a patient with alopecia, it is
important to consider the chief complaint as stated by the
patient, the chronicity, the age at onset, whether there is a
pattern to the areas of hair loss, and if there have been any
major stressors, physical or emotional, in the patient’s life.
Androgenetic alopecia, also referred to as female or male
pattern hair loss, is the most common type of hair loss due to
hormonal effects at the level of the follicle and is what most
patients refer to as “balding.” Generalized thinning is most
commonly seen in alopecia areata, in which the etiology is
autoimmune, or telogen effluvium, in which some physiologic
stressor initiates abnormal shedding [2]. Other causes of hair
loss include autoimmune conditions, underlying systemic
problems like thyroid disease and iron deficiency, infections
of the scalp, inflammatory processes, and habitual practices.
Regardless of the underlying cause, both physical and psychological stress can exacerbate any form of hair loss.
Alopecia is characterized into scarring and non-scarring
categories. Scarring can be divided based on the predominant
cell type: lymphocytic, neutrophilic, and mixed. This category
includes discoid lupus, central centrifugal cicatricial alopecia,
dissecting cellulitis of the scalp, and acne keloidalis. Nonscarring alopecia can be divided based on its distribution.
Focally distributed alopecias include alopecia areata, traction
alopecia, and trichotillomania. Diffuse distribution includes
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