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96 CHAPTER 5: Nonregional Systems and Diseases
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for energy, leading to ketosis and ketoacidosis. With chronic disease there is
progressive microvasculature injury in the eyes, glomeruli, nerves, and large
vessel atherosclerosis. Symptoms include polydipsia, polyuria, polyphagia,
weight loss, and weakness. Physical ndings are dryness of the skin and
acetone on the breath. After ≥15 years, symptoms and signs of peripheral
neuropathy, atherosclerosis, renal insufciency, and retinopathy may be seen.
Diabetes mellitus type-2.
Hyperglycemia results from persistent hepatic gluconeogenesis despite elevated circulating insulin levels. Patients are usually obese adults, although it
is seen increasingly in children. There is a strong familial predisposition and
an increased risk in some ethnic groups (e.g., Hispanics and Pima Indians).
The metabolic abnormalities are like those of type-1 diabetes, but less acute, so
many patients escape detection until complications (e.g., myocardial infarction, neuropathy, retinopathy, or renal insufciency) bring them to medical
attention. Polyuria and polydipsia are gradual in onset and less pronounced
than in type-1.
Hypoglycemia. Low blood glucose results from increased insulin effects
or decreased hepatic glucose production. Hypoglycemia is a common self-
misdiagnosis associated with nonspecic complaints related to autonomic
activity, e.g., sweating, shakiness, ushing, anxiety, or nausea. True symptoms
of hypoglycemia are neuroglycopenic, e.g., dizziness, confusion, tiredness, dysarthria, headache, and difculty thinking, resulting from brain dysfunction.
Inadvertent or surreptitious use of insulin or hypoglycemia-inducing medications is the most common cause of hypoglycemia, usually in patients with
known diabetes. Insulinoma is rare and reactive hypoglycemia (alimentary
hypoglycemia) is an unproven concept.
Disorders of Thyroid Function: Changes in thyroid size and consistency
are frequently associated with disturbances of function. Thyroid hormone
excess or deciency alters physiology producing physical signs. Determine
thyroid size and morbid anatomy, assess thyroid function, and estimate the
likelihood of cancer. Thyroid mass is assessed by history, inspection, and
palpation. Thyroid function is assessed by symptoms and signs of hypo- or
hyperthyroidism, paying attention to the pulse, pulse pressure, eyes and face,
voice, skin and hair, stretch reexes, affect, and mood. Clinical hypotheses are
tested in the lab. The presence or absence of malignancy can only be determined by obtaining tissue. See Chapter 7, pages 256 and 258 for discussion of
goiter and thyroid nodules.
Insulin resistance is the primary disorder.
Abnormalities of thyroid function. L-Thyroxine (T4) production is con-
trolled by thyrotropin (thyroid stimulating hormone, TSH) released from the
anterior pituitary under the control of hypothalamic thyrotropin-releasing
hormone (TRH). T4 and triiodothyronine (T3) are released from the thyroid
follicles in a ratio of 20:1. In peripheral tissues T4 is converted to the active
hormone T3, at a rate specic to each tissue. T4 and T3 inhibit TRH release
from the hypothalamus and pituitary TSH release. Thyroid hormones bind to
thyroid hormone receptors in the nucleus. Binding of this complex to thyroid
response elements of multiple genes affects gene transcription and cellular
metabolism.
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Hypothyroidism. Underproduction of thyroid hormone slows the metabo-
lism of all tissues producing cellular, organ, and whole-body hypofunction.
Myxedema, the most severe form, manifests as soft-tissue thickening consequent to interstitial mucopolysaccharide accumulation. Symptoms: Patients
complain of fatigue, loss of energy, decreased concentration, coldness, constipation, and weight gain despite decreased food intake. The onset is often
gradual and overlooked.
out edema. The expression is placid and good-natured. Responses are slow.
Speech is slow, and the voice is hoarse from vocal cord thickening. There is
a paucity of motion (hypokinesia); movements are slow and deliberate. There
is generalized weakness, but muscle wasting, and paralysis are absent. Slow
muscle relaxation is seen and felt when testing knee and ankle reexes; it is as
if the part were “hung up.” The tongue may be large and awkward. The skin is
cool, dry, and thick, often with scaling difcult to distinguish from ichthyosis.
The palms and circumoral skin may be yellow from carotenemia. The hair is
dry, coarse, and easily broken. The nails are also dry and brittle. The only ocular sign is periorbital edema. Cardiovascular signs include reduced strength of
myocardial contraction manifest as a reduced apical impulse and pulse contour. Angina and heart failure may be present at diagnosis or be manifest with
thyroid hormone replacement. Pericardial effusion (ECG with low-voltage
QRS complexes), ascites, and ankle edema occur without heart failure. The
ventricular rate is normal or slow. Dysrhythmias are rare. The blood pressure
is normal or there is moderate elevation of both systolic and diastolic pressure.
Constipation is common resulting in tympanites suggesting ileus. Menorrhagia is common. Thinking is slowed (bradyphrenia), patients are irritable and
emotionally labile, and may develop depression. Myxedema coma is a rare but
grave condition that paradoxically does not require the patient to be comatose.
Hyperthyroidism.
creases the metabolic rate producing changes in all organ systems. Sympathetic nervous system stimulation accounts for many symptoms and
signs. Symptoms: Patients initially feel energetic and are often happy to be
losing weight. They progressively develop tremor, sweaty skin, frequent
defecation, and weight loss despite increasing food intake.
are alert and vigilant, responses to questions are quick and the emotions
are labile. The face is thin with sharp features. Spontaneous movement
is increased (hyperkinesia). The voice is normal, but speech cadence is accelerated. There is often quadriceps weakness; the patient pushes with
the arms to rise from a chair. Reexes are normal or hyperactive with unsustained clonus; in patients taking β-blockers this may be the only sign
of hyperthyroidism. There is almost always a ne tremor. The skin is thin,
moist, and sweaty; the hair is ne and oily. The ngernails may separate
from the matrix (onycholysis); usually only one or two pairs of nails are involved. Lid lag is frequent. Cardiovascular signs include tachycardia and
increased strength of myocardial contraction manifest by an accentuated
apex beat and sharp heart sounds. Angina and congestive failure may be
precipitated in patients with coronary artery disease. The systolic blood
pressure is slightly elevated, the diastolic diminished, so the pulse pressure is widened. There is a high incidence of atrial brillation. Defecation
may be more frequent; the onset of true diarrhea is a grave prognostic
sign. Extracellular uid does not accumulate unless cardiac failure occurs.
Signs: The face is rounded, relaxed, and puffy with-
Overproduction or ingestion of thyroid hormone in-
Signs: Patients
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Menses are usually normal; occasionally there is oligomenorrhea. Mental
status changes include irritability, emotional lability, and depression; occasionally, a manic state develops.
Graves disease (diffuse toxic goiter).
producing TSH-independent hyperplasia and increased T4 release. Myxomatous
inltration of the extraocular muscles produces exophthalmos and abnormalities of gaze.
bruit results from increased blood ow through the tortuous thyroid arteries.
The eye signs occur at any time and initially can be unilateral. The signs are lid
lag, lid spasm, lacrimation, chemosis, periorbital edema, periorbital inltration
with mucopolysaccharides, and exophthalmos (proptosis; Chapter 7, page 196,
Fig. 7-29). Often there is paresis of extraocular muscles, usually involving one or
two symmetrical pairs; isolated weakness of the two superior recti is common.
Firm, nontender, pink, well circumscribed areas of elevated skin over the shins
known as pretibial myxedema usually occurs in association with the ophthalmopathy. Similar skin thickening on the dorsal ngers or toes is thyroid acropachy.
Hashimoto thyroiditis. Lymphocytic thyroid inammation produces indu-
ration and gradual loss of function. This is the most common cause of hypo-
thyroidism; it occurs most commonly in women after the fth decade. The
gland is rm, only slightly enlarged, nontender, and nodules may be present.
Postpartum thyroiditis.
mon following normal pregnancy. Onset is usually 3–6 months postpartum
signaled by signs of either hyper- or hypothyroidism. The latter is often confused with the fatigue and stress of caring for a newborn. The gland is diffusely enlarged and nontender. It usually resolves over a period of months.
De Quervain thyroiditis, viral thyroiditis.
roid from viral infection or postinfectious inammation releases thyroid hormone from damaged follicles producing hyperthyroidism with depressed
TSH and low iodine uptake. The patient may complain of pain with swallow-
ing which is frequently referred to the ear. The gland is unusually rm and
rather small with one or more, often tender, nodules. In the acute phase the
patient may be euthyroid or hyperthyroid.
The thyroid is diffusely enlarged, usually ≤2x normal. A thyroid
Painless inammation of the thyroid gland is com-
Autoantibodies activate the TSH receptor
Acute inammation of the thy-
Adrenal Disorders
Corticosteroid excess—Cushing syndrome. Hypercortisolism results from
adenoma or adenocarcinoma of the adrenal cortex, excess adrenocorticotropic hormone (ACTH) from a pituitary adenoma, corticosteroids treatment, or ectopic ACTH production. Patients present with weakness, weight
gain, amenorrhea, and/or back pain. Physical ndings include hypertension,
moon face, acne, thoracic kyphosis, supraclavicular fat pads, hypertrichosis,
wide purple striae on the abdomen and thighs, and peripheral edema.
Primary adrenal insufciency—Addison disease.
ure results from autoimmune, ischemic, or hemorrhagic destruction of
the gland resulting in cortisol and mineralocorticoid (aldosterone) deciency and increased circulating ACTH. Increased stimulation of pituitary
Primary adrenal fail-
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proopiomelanocortin synthesis and ACTH release causes a secondary increase
in melanocyte-stimulating hormone.
Symptoms include weakness, fatigue,
lethargy, nausea and vomiting, diarrhea, weight loss, abdominal pain, and
salt craving. Physical exam may reveal reduced hair growth, hypotension
(especially orthostatic), dehydration, mottled skin pigmentation, and pigmented buccal mucosa, lips, vagina, and rectum. Cause to be considered
include tuberculosis, fungal infection, other granulomatous processes, amyloidosis, hemochromatosis, tumor metastases, antiphospholipid antibody
syndrome, or autoimmune destruction.
Secondary adrenocortical insufciency. Pituitary insufciency with
decreased ACTH production or inadequate recovery of ACTH responsiveness following prolonged corticosteroid administration leads to inadequate
cortisol levels. Symptoms and signs are less prominent than with primary
adrenal failure because the mineralocorticoid axis remains intact. Symptoms
are often precipitated when relative cortisol deciency appears in a setting of
increased cortisol demand, e.g., infection, trauma, or surgery.
Disorders of Parathyroid Function
Hyperparathyroidism. An adenoma, hyperplasia, or neoplasia of a parathy-
roid gland leads to excessive secretion of parathyroid hormones (PTH) causing bone resorption and inhibition of renal tubular phosphate reabsorption.
Hyperparathyroidism may be primary or secondary to hypocalcemia (renal
insufciency, hypercalciuria) activating the parathyroid glands. In some cases
of secondary hyperparathyroidism, the gland becomes autonomous, tertiary
hyperparathyroidism.
Primary hyperparathyroidism is most common in
women in the third to fth decades. Onset is insidious and often detected by
abnormal calcium on serum chemistries drawn for another reason. The clinical
triad of peptic ulcer, urinary calculi, and pancreatitis suggests the diagnosis.
Symptoms can include muscle weakness or stiffness, anorexia, nausea, constipation, polyuria, polydipsia, weight loss, deafness, paresthesias, bone pain,
and renal colic. Signs include band (calcic) keratitis, hypotonia and weakness, fragility fractures, and skeletal deformities.
Hypoparathyroidism. This occurs spontaneously or from removal or dam-
age to the parathyroid glands during thyroidectomy. Inadequate parathyroid hormone secretion leads to hypocalcemia and hyperphosphatemia.
Symptoms are nervousness, weakness, paresthesias, muscle stiffness and
cramps, headaches, and abdominal pain. Tetany with spontaneous carpopedal spasm may be seen or is induced by ination of a blood pressure
cuff on the arm (Trousseau sign). A facial twitch on light percussion over
the facial nerve is Chvostek sign. Other signs are hair loss, cataracts, and
papilledema.
Vitamin D deciency. Vitamin D
ence of sunlight. It is converted to the active 1,25-dihydoxycholecalciferol
form sequentially in the liver (25-hydorxylation) and kidney (1-hydroxylation). Vitamin D deciency is common especially in older and/or chroni-
cally ill persons in northern latitudes. African Americans and darkly
pigmented individuals of other ethnic backgrounds are especially at risk.
is synthesized in the skin under the inu-
3
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Diets low in milk products supplemented with vitamin D are another risk
factor. In addition to osteomalacia manifest as low bone density and leading
to secondary hyperparathyroidism, patients frequently complain of diffuse
persistent musculoskeletal pain. Anyone presenting with these risk factors or
complaints should be evaluated for vitamin D.
Disorders of Pituitary Function.
Acromegaly and gigantism. See Chapter 13, page 581.
Cushing disease.
Prolactinoma.
adenoma or macroadenoma suppresses FSH and LH secretion and induces
lactation.
decreased libido and hypogonadotropic hypogonadism. Headache suggests
a macroadenoma.
Hypopituitarism.
or granuloma leading to progressive pituitary insufciency with decreased
thyroid, adrenal cortex and gonadal function. Symptoms are those of multi-
ple endocrine failure; hypogonadal symptoms are a common early indication.
are characteristic. Signs include hypothermia, bradycardia, hypotension, skin
atrophy, pallor, hypotonia, areolar depigmentation, loss of axillary and pubic
hair, and atrophy of sex organs.
Sheehan syndrome. Hemorrhage and shock during obstetrical delivery
causes hypopituitarism secondary to pituitary necrosis. Symptoms include
failure of lactation, amenorrhea, lethargy, sensitivity to cold, and diminished
sweating. There is ne wrinkling of the skin, hair loss, depigmentation of the
skin and areola, and mammary and genital atrophy.
Women present with galactorrhea and amenorrhea, men with
See Cushing Syndrome, page 98.
Increased prolactin secretion by a functioning pituitary micro-
The pituitary gland is destroyed by tumor, injury, infarct,
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CLINICAL VIGNETTES AND QUESTIONS
Case 5-1
A 32-year-old man presents with 2 weeks of fever, fatigue, anorexia,
sore throat, and headache. He has multiple sexual partners and used
intravenous drugs on and off in the last 2 years. On examination he has
generalized lymphadenopathy and a widespread maculopapular rash.
QUESTIONS:
1. What is the most likely diagnosis?
2. What is the differential diagnosis of generalized lymphadenopathy?
Case 5-2
You are examining a 23-year-old man with high fever, pharyngitis,
and lymphadenopathy. He has prominent cervical lymphadenopathy
(posterior cervical lymph nodes are more pronounced compared to
anterior). You also notice some lymphadenopathy in the axillary and
inguinal areas.
QUESTIONS:
1. What is the differential diagnosis of cervical lymphadenopathy?
2. Describe some characteristics of mycobacterial cervical node infec-
tion (scrofula).
3. What is the most likely diagnosis?
A 26-year-old man is brought to the emergency room after becoming
confused at work while preparing his lunch. He started an exercise program this morning to lose weight. He remembers getting sweaty, shaky,
extremely hungry, and seeing double. He appeared confused to coworkers and seemed to be struggling to focus on things around him. He has
had similar episodes for 6 months if he skips breakfast, but never this
severe. Eating a snack resolves the symptoms; today he improved with
orange juice. He does not take any medications and denies any illicit
substances. Vital signs are normal and his BMI is 30.
QUESTIONS:
1. What is the most likely etiology for this patient’s symptoms?
2. What is Whipple’s triad and what does it indicate?
3. What is the most likely diagnosis in this patient?
4. What is the most common cause for this presentation?
Case 5-3
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Case 5-4
A 55-year-old woman is found to have multiple hard nontender right
axillary lymph nodes during a routine screening examination. No upper
extremity lesion or source of infection is found.
QUESTIONS:
1. What is the drainage area for axillar lymph nodes?
2. What is the differential diagnosis for axillary lymphadenopathy?
3. What is the most likely cause?
Case 5-5
You are planning a lymph node examination on a 70-year-old man with
unexplained weight loss.
QUESTION:
1. When examining lymph nodes, which features of the lymph nodes
are essential to forming your differential diagnosis?
CHAPTER 6
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The Skin and Nails
Every clinician should be able to characterize skin lesions, identify common
conditions, and recognize cutaneous signs of systemic disease.
PHYSIOLOGY OF THE SKIN AND NAILS
Skin protects the body from injury, infection, heat, and uid loss and is a
major intermediary for sensing the outside world. It is continuous with
the mucous membranes at body orices. The dermis is rich in blood vessels that constrict to conserve heat or dilate dissipating heat via radiation,
conduction, and convection aided by sweating. Dermal and subcutaneous fat provide insulation assisting heat conservation. Impermeability is
maintained with tight junctions formed by intercellular adhesion molecules. Integrity of the dermis depends upon interlacing collagen bundles
and elastic tissue.
The skin contains specialized structures including hair follicles, sebaceous and sweat glands, and location specic special sensory structures. The
skin is also an immunologic organ. Intradermal Langerhans cells, reproducing
within the epidermis, are activated by foreign antigens. They then migrate
to regional lymph nodes presenting antigens to T-lymphocytes initiating an
immune response.
FUNCTIONAL ANATOMY OF THE SKIN AND NAILS
Skin Layers: The layers of the skin are the epidermis, dermis, and subcutane-
ous tissue.
Epidermis.
layer; it has four layers. The keratinized nonliving cells of the outer keratin layer (stratum corneum) are stratied and overlapping, the outermost cells
sloughing regularly (desquamation). Underlying the stratum corneum are the
granular layer (stratum granulosum), spinous layer (stratum spinosum), and
basal layer (stratum basale). The living cells in these layers, mostly keratinocytes, get nourishment from the dermis and are held together by proteins,
including desmosomes. Melanocytes in the lower epidermis contain melanin, whose concentration is determined by genetics, sunlight, injury repair,
and hormones. The epidermis contains a visible network of furrows that
are exaggerated over joints. The epidermis thickens in areas of high friction
such as palms and soles. A basement membrane separates the epidermis
from the dermis. The epidermis attaches to the basement membrane by
hemidesmosomes.
103
The avascular epidermis (Fig. 6-1) is the most supercial
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FIG. 6-1Principal Skin Structures.
Dermis and subcutaneous tissue. The supercial papillary dermis forms pap-
illary extensions surrounded by epidermis and containing rich capillary and
nerve networks. The deeper reticular dermis contains blood vessels, lymphatics,
nerves, and fat cells surrounded by collagen bundles mixed with elastic bers.
The dermal appendages, including hair follicles, apocrine glands, eccrine sweat
glands, and holocrine sebaceous glands, extend into this layer. The deep reticular dermis merges with the subcutaneous layer. In general, the dermis is thicker
over dorsal and lateral than over ventral and medial surfaces. It is thickest over
the back and extremely thin over the eyelids, scrotum, and penis.
Skin Associated Structures.
Fingernails. Fingernails frequently show signs of systemic disease. The
nails grow throughout life, providing a record of nutritional disturbances.
Changes in the visible nailfold capillaries are signs of systemic disease. The
nail plate is a hard, semitransparent convex rectangle, transverse radius of
curvature of which is shorter than its longitudinal radius (Fig. 6-2). The nail
plate adheres to the nail bed, a layer of modied skin studded with narrow
longitudinal ridges containing a rich capillary network giving the nail plate
its pink color. The proximal third of the nail bed is the matrix composed of
partially cornied cells containing keratohyalin granules. This is where new
nail is added to the nail plate forcing it distally. The matrix as seen through
the nail plate is the white lunula. The proximal root of the nail plate is buried
in a dermal pouch. The lip of the pouch is the mantle terminating in the cuticle.
The distal nail plate not adherent to the bed is the free edge; the body is the
intervening portion. The sides of the nail plate are buried in lateral nail folds
of skin and cuticle. The nail plate elongates continuously from the root and
thickens from the matrix. The time for growing a new ngernail is ~6 months,
faster in youth than in old age.
Toenails. Toenails undergo the same changes as ngernails, but most are less
pronounced. It takes 12–18 months for a toenail to regrow.
Functional Anatomy of the Skin and Nails 105
Free margin
Nail fold
Nail sulcus
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Cuticle
FIG. 6-2Fingernail Anatomy. The nail plate is formed by the cells of the matrix and extruded distally to the free margin where the plate separates from the nail bed. The lunula marks the extent of the matrix under
the nail plate.
Nail plate overlying
Nail bed (pink)
Lunula
(white)
Lateral
sulcus
Long papillary
ridges
Free margin
Nail plate
Nail bed
Lunula
Cuticle
Mantle
Matrix
Root
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