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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

398
V. J. Cabrera
ultrasonography can also reveal if there is chronic venous
insufficiency and a transthoracic echocardiogram (TTE)
could be obtained if history and physical are concerning for
heart failure. Ultrasound examination of the inferior vena
cava diameter and collapsibility may also provide information about hypervolemia.
By directing therapy at correcting the underlying capillary
hemodynamic disturbance, development of edema can be
stopped or reversed. Lifestyle and dietary modification in
conjunction with pharmacotherapy are useful in the longterm management. For the common systemic causes, treatment of the underlying condition is indicated. For those with
chronic venous insufficiency, mechanical therapies such as leg
elevation and compression stockings, as well as judicious
diuretic therapy, are useful, although caution should be taken
in those with peripheral arterial disease. Deep venous thrombosis is treated with anticoagulation therapy and cellulitis
with antibiotics. In medication-induced edema, the culprit
medication should be discontinued if possible, and in those
with heart failure, cirrhosis, and nephrotic syndrome, cautious
use of diuretics and salt restriction can be initiated. Caution
to avoid volume depletion with diuretics must be exerted.
Patients should be monitored for electrolyte disturbances
and changes in urea and serum creatinine, watching for signs
of volume depletion. For patients with nephrotic syndrome,
higher doses of diuretics might be required. For those with
diuretic resistance, the use of diuretic combinations could be
required.
Clinical Pearls
• A thorough history and physical examination are
essential.
• Chronic venous insufficiency and cellulitis have common
manifestations: peripheral edema, increase in skin tem-
perature, and erythema. Have in mind that cellulitis is usu-
ally a unilateral process.

Chapter 19. Edema
399
Don’t Miss This!
• Deep vein thrombosis presents with acute limb swelling in
a patient with risk factors (e.g., immobilization) but could
be bilateral in patients with malignancy.
• Compartment syndrome presents with acute limb swelling,
tense skin, and decreased peripheral pulses.
• Heart failure presents with peripheral edema ± pulmonary
edema, jugular venous distention, and ascites.
• Recheck medication list and do not forget over-the-
counter medications: common things are common!
• Think of central venous stenosis causing upper extremity
edema in patients with history of central catheter
placement.
• Facial edema and dilated neck veins are findings of supe-
rior vena cava syndrome.
References
1. Cho S, Atwood JE. Peripheral edema. Am J Med.
2002;113(7):580–6.
2. Ely JW, Osheroff JA, Chambliss ML, Ebell MH. Approach
to leg edema of unclear etiology. J Am Board Fam Med.
2006;19(2):148–60.
3. Blankeld RP, Finkelhor RS, Alexander JJ, Flocke SA, Maiocco J,
Goodwin M, etal. Etiology and diagnosis of bilateral leg edema
in primary care. Am J Med. 1998;105(3):192–7.
4. Trayes KP, Studdiford JS, Pickle S, Tully AS.Edema: diagnosis and
management. Am Fam Physician. 2013;88(2):102–10.
5. Messerli FH.Vasodilatory edema: a common side effect of anti-
hypertensive therapy. Curr Cardiol Rep. 2002;4(6):479–82.
6. Frishman WH. Effects of nonsteroidal anti-inammatory drug
therapy on blood pressure and peripheral edema. Am J Cardiol.
2002;89(6A):18D–25D.
7. Nesto RW, Bell D, Bonow RO, Fonseca V, Grundy SM, Horton
ES, et al. Thiazolidinedione use, uid retention, and congestive
heart failure: a consensus statement from the American Heart
Association and American Diabetes Association. Diabetes Care.
2004;27(1):256–63.

400
V. J. Cabrera
8. Stemmer R. A clinical symptom for the early and differential
diagnosis of lymphedema. Vasa. 1976;5(3):261–2.
9. Wells PS, Anderson DR, Rodger M, Forgie M, Kearon C, Dreyer
J, etal. Evaluation of D-dimer in the diagnosis of suspected deep-
vein thrombosis. N Engl J Med. 2003;349(13):1227–35.

Part V
Dermatologic

Chapter 20
Rash
AlexanderHowell andKarthikKrishnamurthy
Introduction
Rashes are common problems encountered in all facets of
healthcare that often represent a diagnostic conundrum, even
at times to the most experienced dermatologist. Many conditions produce rashes that appear very similar clinically, and
the differences distinguishing them are often subtle, or only
apparent on histopathology. It is important that the correct
differential diagnosis be made initially. Many conditions can
be exacerbated by incorrect treatments or delay of therapeutic intervention, leading to significant morbidity in some
cases and, rarely, mortality. When approaching rashes, it is
helpful to generate a good differential diagnosis by categorizing the rash based on its reaction pattern. Presented here is
an algorithmic approach to rashes that begins with five
previously described reaction patterns: papulosquamous,
eczematous, vascular, dermal, and vesiculobullous [1]. Each
reaction pattern is then subcategorized based on nuances in
the appearance, texture, and symptoms of various skin
conditions.
A. Howell · K. Krishnamurthy (*)
Department of Dermatology, Orange Park Medical Center,
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_20
403

404
A. Howell and K. Krishnamurthy
Decision-Making/Differential Diagnosis
The initial step in approaching a rash is to create a detailed
description of the rash. A good description includes primary
morphology, secondary change, color, shape, configuration,
and distribution (see H and P).
Next, categorize the reaction pattern based on your
description:
• Papulosquamous rashes are red scaly rashes.
• Eczematous rashes are red and itchy and can have scale,
crust, and lichenification (accentuation and thickening of
skin markings).
• Dermal rashes are rashes with no surface (or epidermal)
change.
• Vascular rashes are red and may be blanching or
non-blanching.
• Vesiculobullous rashes are rashes with blisters of varying
sizes.
In general, consider common conditions first while at the
same time ruling out life-threatening conditions promptly
(i.e., severe drug reactions such as Stevens-Johnson syndrome
[SJS], toxic epidermal necrolysis [TEN], drug reaction with
eosinophilia and systemic symptoms, urticaria with angioedema, staphylococcal scalded skin syndrome [SSSS], toxic
shock syndrome [TSS] , erythroderma, meningococcemia,
rocky mountain spotted fever [RMSF], bacterial endocarditis,
necrotizing fasciitis, etc.) [2, 3].
Papulosquamous
Generally speaking, this reaction pattern includes rashes with
red, scaly papules and plaques.

Chapter 20. Rash
405
Psoriasiform
Psoriasis. Well-demarcated, red plaques with thick overlying
scale. Common locations include extensor surfaces (knees,
elbows), scalp, palms, and soles. Nail findings can aid in the
diagnosis and include pitting, oil spots, and onycholysis
(Fig.20.1).
Seborrheic dermatitis. Erythema with overlying greasy scale
in a “seborrheic distribution” (oil- and hair- bearing areas).
Associated with HIV, Parkinson’s disease, and other neu-
rologic conditions [4].
Pityriasis rubra pilaris. Reddish-orange scaly plaques, kera-
totic follicular papules, or palmoplantar keratoderma.
Distinct areas of uninvolved skin referred to as “islands of
sparing” are characteristic.
Tinea corporis. Annular or ring-shaped red, scaly plaques.
Raised border has more scale than the clearer center of
the lesion [4].
F . Plaque psoriasis. Thick, red plaques with sharply
demarcated borders and overlying silvery scale

406
A. Howell and K. Krishnamurthy
Pityriasiform
Pityriasis rosea. Oval-shaped pink to red scaly thin plaques
in “Christmas tree” distribution along the body folds.
Often a herald patch appears a few days before the other
smaller lesions. Located mostly on the trunk, it can
involve extremities. This can occur on the face in African
Americans.
Secondary syphilis. Small red to brown scaly papules with
involvement of the palms and soles.
Tinea versicolor. Tan to red or hypopigmented thin plaques
with fine scale. These are typically located on the upper
chest, upper back, and neck.
Lichenoid
Lichen planus (LP) five Ps. Purple, polygonal, planar, and
pruritic plaques. “Wickham striae” may be present. Lower
extremities are a common location, but some people have
mucosal and penile lesions. Drug-induced LP is associated
with NSAIDs, diuretics, ACE inhibitors, and beta-blockers
[4] (Fig.20.2).
Erythroderma
Erythroderma is generalized erythema and scaling that
affects >90% of the body surface area. The underlying causes
include preexisting dermatoses (atopic dermatitis, psoriasis,
seborrheic dermatitis), cutaneous T-cell lymphoma, or drug
reactions [4] (Fig.20.3).
Eczematous
1. Acute eczema. Weeping, vesicular erythematous papules
and plaques that are very itchy. Geometric or linear con-
guration indicates an “outside job” and is a clue to diag-
nosis [1]. Includes acute allergic/irritant contact dermatitis
and dyshidrotic eczema.

Chapter 20. Rash
407
F . Lichen planus. Purple, polygonal, planar plaques on the
anterior lower extremity

408
A. Howell and K. Krishnamurthy
F . Erythroderma. Generalized erythema and exfoliative
scaling in a patient with underlying psoriasis
2. Subacute eczema. Eczematous lesions that progress, form-
ing scaly crust.
3. Chronic eczema. Characterized by lichenication, hyper-
pigmentation, and thicker scaly plaques.
Atopic dermatitis. Common in children, but can also be
seen in adults. Located in flexural areas. It is associated with
asthma, allergies, and an “itch-scratch” cycle. A diagnostic
clue is that the middle part of the back (where the patient
cannot reach to scratch) will be spared (Fig.20.4).
Stasis dermatitis. Typically seen on the lower extremities in
elderly individuals. Underlying venous insufficiency, varicose
veins, and edema are present. Hyperpigmentation occurs
from hemosiderin deposition. Itching and overlying scale
occurs.
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