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76 CHAPTER 4: Vital Signs, Anthropometric Data, and Pain
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CLINICAL VIGNETTES AND QUESTIONS
Case 4-1
A 34-year-old male presents with confusion and increasing muscle stiffness. He recently started treatment for paranoid schizophrenia. His
physical examination is notable for temperature 38.6°C, heart rate 115,
blood pressure 148/94, and respiratory rate of 22. He is diaphoretic,
tremulous and has “lead pipe rigidity.”
QUESTIONS:
1. What is the differential diagnosis of this presentation?
2. What is the most likely diagnosis?
3. What physical examination ndings differentiate serotonin syn-
drome from this diagnosis?
Case 4-2
You have been asked to evaluate an 18-year-old man in the emergency
room with a rst episode of diabetic ketoacidosis. The arterial pH is 7.14.
QUESTIONS:
1. Describe the expected respiratory pattern of this patient. What is it
called?
2. What other conditions can also cause this respiratory pattern?
3. How does this respiratory pattern differ from Cheyne–Stokes respi-
rations?
4. Describe the physiology of Cheyne–Stokes respirations.
5. What underlying conditions cause Cheyne–Stokes respirations?
A 63-year-old man complains of lightheadedness when getting out of
bed in the morning and when standing from a seated position. One year
ago he was diagnosed with Parkinson disease without tremor. He has
not improved on carbidopa/levodopa. He also has urinary incontinence
and erectile dysfunction. His recumbent blood pressure and pulse are
128/84 and 72; his standing blood pressure and pulse are 105/72 and 75.
QUESTIONS:
1. What is notable about the BP and pulse changes and what does this
indicate?
2. What are causes of orthostatic (postural) hypotension?
3. What is the most likely diagnosis?
4. Name some subtypes of this diagnosis.
Case 4-3
Clinical Vignettes and Questions 77
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Case 4-4
A 72-year-old man presents to a walk-in clinic with a laceration. Before
interviewing the patient you review his vital signs noting a blood pres-
sure of 155/65 and heart rate of 94.
QUESTIONS:
1. What is notable about the blood pressure?
2. What is the physiology of a widened pulse pressure?
3. What are possible causes of the widened pulse pressure?
4. What heart valve condition is associated with a widened pulse pres-
sure and what physical examination ndings are associated with this
condition?
CHAPTER 5
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Nonregional Systems and Diseases
Several physiologic systems are located within multiple body regions and
are assessed continuously during the exam. Diseases of these systems most
commonly present with nonspecic constitutional symptoms and recognition
depends on integrating all exam ndings. This concept is captured by the saying “he who knows syphilis knows medicine.”
CONSTITUTIONAL SYMPTOMS
Constitutional symptoms are those that relate to the body or a person as a
whole. They are combined with physical exam and laboratory ndings to
make 1–3 general physiologic hypotheses. For example, a middle-aged patient
presenting with anorexia, weight loss, and night sweats suggests neoplasm,
chronic infectious or inammatory disease, or possibly Addison disease.
Fatigue: Fatigue results from serious organic disease, mood disorders, or
deconditioning. Patients describe decreased energy and endurance during
usual activities. Clinical fatigue incorporates three components, present to
variable degrees in individual patients: inability to initiate activity (perception of generalized weakness in the absence of objective ndings); reduced
capacity to maintain activity (easy fatigability); and difculty with concentration, memory, and emotional stability (mental fatigue). It is important to
distinguish fatigue from shortness of breath, muscle weakness, and sleepiness. Fatigue can complicate any chronic disease, e.g., anemia, hypothyroidism, hyperthyroidism, and autoimmune or neurologic disorders.
History should determine the severity and temporal pattern of fatigue as
follows: Onset—abrupt or gradual and relationship to an event or illness.
Course—stable, improving or worsening, duration and daily pattern, factors
that alleviate or exacerbate symptoms, and impact on daily life. Symptoms
suggesting underlying occult medical illness should be explored in a detailed
review of systems, including presence of weight loss or night sweats. The
history should include screening questions for psychiatric disorders (particularly depression, anxiety disorders, somatoform disorders, and substance
abuse). When a complete history, physical examination, and screening laboratory evaluation do not nd a specic explanation, consider deconditioning,
depression, sleep disorders, and myalgic encephalomyelitis/chronic fatigue
syndrome (ME/CFS).
CLINICAL OCCURRENCE: These are examples only and not meant to be
all-encompassing. Congenital: Muscular dystrophies, mitochondrial myopathy; Endocrine: Hypothyroidism, hyperthyroidism, Addison disease, hypopituitarism, hypoparathyroidism, hypogonadism; Degenerative/Idiopathic:
ME/CFS, inclusion body myositis, amyotrophic lateral sclerosis, multiple
sclerosis, dementia; Infectious: Tuberculosis, infectious mononucleosis,
DDX:
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Constitutional Symptoms 79
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hepatitis, following other viral illnesses, hookworm infestation, HIV infection;
Inammatory/Immune: Systemic lupus erythematosus (SLE), rheumatoid
arthritis (RA), polymyositis, dermatomyositis, vasculitis, myasthenia gravis;
Metabolic/Toxic: Hypokalemia, hypocalcemia, hypomagnesemia, hypona-
tremia, anemia, uremia, hypoglycemia, congestive heart failure, drugs (e.g.,
β-blockers, sedatives, opioids, anticholinergics), alcohol; Neoplastic: Acute
and chronic leukemia, myelodysplastic syndromes, myeloproliferative syndromes, solid tumors, lymphomas; Psychosocial: Disordered sleep, depression, deconditioning, overwork and overtraining, insomnia, chronic anxiety;
Vascular: Claudication, strokes.
Appetite Disturbance: Appetite is controlled by the hypothalamus under
the inuence of multiple hormones, metabolites, neural afferents (especially vagal visceral afferents), and cortical inputs reecting emotional and
cognitive state. Disturbances in any of these systems change appetite.
Anorexia.
Lack of appetite is anorexia. Appetite loss is nonspecic but a sen-
sitive indicator of disease and mood disorders. When caloric expenditure is
unchanged, anorexia results in weight loss.
CLINICAL OCCURRENCE: Endocrine: Adrenal insufciency, hypothy-
roidism, hypopituitarism; Degenerative/Idiopathic: Dementia, anosmia;
Infectious: Hepatitis, any acute or chronic systemic infection; Inammatory/
Immune: Inammatory cytokines (interleukin-1, tumor necrosis factor) sup-
press appetite, so any systemic inammatory process can lead to anorexia;
Mechanical/Traumatic: Gastrointestinal obstruction, dysphagia,; Metabolic/
Toxic: Advanced kidney disease, advanced liver disease, drugs (e.g., amphet-
amines, and stimulants); Neoplastic: Malignancy, especially when metastatic
or regionally advanced; Psychosocial: Depression, delirium, poverty, social
isolation, abuse, school problems, anorexia, and bulimia nervosa; Vascular:
Vasculitis, stroke.
Polyphagia.
Increased or insatiable appetite is uncommon. If calorie intake
exceeds expenditure weight is gained, if not weight is unchanged or lost.
Balance includes calories expended doing muscle work, ingested calories
wasted from vomiting, maldigestion/malabsorption, and calories absorbed
but subsequently lost, e.g., glucosuria and proteinuria.
CLINICAL OCCURRENCE: Endocrine: Diabetes, hyperthyroidism, insu-
linoma, hypothalamic disorders; Genetic: Prader-Willi; Metabolic/Toxic:
Malnutrition (protein, essential fatty acids), drugs (e.g., corticosteroids, cannabinoids), iron deciency;
Neoplastic: Insulinoma; Psychosocial: Bulimia,
binge eating syndrome, night eating syndrome.
Abnormal eating behaviors. Behaviors associated with selection, acquisition, preparation, serving, and eating of food are culturally determined and
socially important. Changes in food-related behaviors suggest medical, psychiatric, and social problems. See Chapter 15, page 726.
CLINICAL OCCURRENCE: Endocrine: Pregnancy; Degenerative/Idiopathic:
Anosmia; Infectious: Hookworm infestation; Metabolic/Toxic: Iron de-
ciency, trace metal deciency; Neoplastic: Food preferences and taste are frequently disturbed by malignant disease, especially with liver involvement;
Psychosocial: Psychosis, delusions.
80 CHAPTER 5: Nonregional Systems and Diseases
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Pica. An unusual craving leads to ingestion of clay, paint chips, plaster, laundry starch, and ice chips. Old paint ingestion causes lead poisoning and laundry starch contributes to obesity and hypochromic anemia.
Thirst Disturbance: Water depletion (increased osmolarity and serum sodium)
triggers thirst as does moderate to severe extracellular volume depletion.
Antidiuretic hormone (ADH) is released increasing water intake and water
reabsorption in renal collecting ducts. A defect in the production of ADH or the
response of the renal collecting duct to ADH leads to water loss and persistent
thirst.
Increased thirst—polydipsia. Thirst indicates a water decit and/or
intravascular volume depletion. Distinguish between isolated water loss
(increased osmolarity with normal extracellular volume), loss of extracellular volume alone (normal osmolarity, but decreased volume), and combined
losses of extracellular volume and water (increased osmolarity and decreased
volume). Most common considerations are diabetes insipidus (central or
nephrogenic), diabetes mellitus, hemorrhage, hypotension of any cause,
diuretic overuse, dry mouth, psychogenic polydipsia.
Decreased thirst—hypodipsia.
tant diabetes insipidus is seen with congenital or acquired hypothalamic
structural lesions or hypothalamic stroke.
Constitutional Syndromes and Diseases
Myalgic encephalomyelitis/Chronic fatigue syndrome. The cause is
unknown. It usually occurs after a viral illness in young to middle-aged adults.
The case denition requires new onset of fatigue not related to exertion and
not relieved by rest, resulting in substantial limitation of previous occupational, educational, social, or personal activities. The fatigue must have been
present for more than 6 months and should be able to be alleviated by rest.
Additionally, postexertional malaise lasting >24 hours and unrefreshing sleep
are required to make the diagnosis. Either cognitive impairment or orthostatic
intolerance should also be present. Other symptoms like short-term memory
loss, sore throat, tender cervical or axillary nodes, muscle pain, polyarthralgias
without arthritis, and gastrointestinal impairment may be present.
Diabetes insipidus. Central diabetes insipidus (decreased ADH/vasopressin production) and nephrogenic diabetes insipidus (renal unresponsiveness
to ADH) result in an excessive, constant water diuresis. Patients present with
an unquenchable thirst, polydipsia, and polyuria with a low urine-specic
gravity.
Adipsic diabetes insipidus. Both thirst and ADH secretion are impaired
making patients vulnerable to recurrent hypernatremia. Once called essential hypernatremia, this disorder is now called adipsic diabetes insipidus or
central diabetes insipidus with decient thirst. Causes are congenital and
acquired central nervous system lesions, the most common being septo-optic
dysplasia, germinoma, clipping or rupture of anterior communicating artery
aneurysms, craniopharyngioma, and central nervous system sarcoidosis.
A defect in thirst with or without concomi-
The Immune System 81
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THE IMMUNE SYSTEM
Understanding immune system disorders and how they present requires
understanding normal immune system physiology. For practical purposes,
the immune system has innate, nonspecic, and adaptive components. The
latter has evolved more recently. Disorders of innate immunity are often
quantitative or qualitative disorders of neutrophils and macrophages. These
are discussed with the hematopoietic system. Disorders of adaptive immunity are described below.
Serious congenital immune system disorders present in infancy or childhood and are beyond our scope. Acquired immunologic deciencies present at any age and are divided into defects of antibody production (humoral
immunity) and defects of cell-mediated immunity. Because humoral immunity requires functioning T-cells for proper regulation, defects in cell-mediated
immunity are often accompanied by impaired humoral immunity.
Patients with an altered immune system present with a variety of illnesses, most commonly infections, neoplasms, autoimmune disorders, or
a combination. This can be the result of a common primary problem (e.g.,
immunosuppressive drugs), or the presence of a neoplastic disease (e.g., multiple myeloma), severe autoimmune disease (e.g., SLE), chronic infections
(e.g., HIV/AIDS, tuberculosis) and chronic systemic illnesses (advanced
renal and liver disease). Treatments of neoplastic and autoimmune disorders
are often highly immunosuppressive. Iatrogenic immunosuppression is the
most commonly encountered immunodeciency.
Defects in humoral immunity commonly present with infections by
encapsulated bacteria (Streptococcus pneumonia, Haemophilus inuenzae,
Neisseria meningitidis, and Neisseria gonorrhoeae) that require opsonizing
antibodies for control. Since the spleen is needed to clear the blood of opsonized bacteria, rapidly overwhelming infection may occur post-splenectomy.
All patients contemplating splenectomy should receive immunization for
Streptococcus pneumonia, Haemophilus inuenzae, and Neisseria meningitidis.
Patients with defects in cellular immunity have an increased risk for neoplasms and infections by intracellular pathogens (e.g., tuberculosis) and
opportunistic bacterial, viral, and fungal organisms.
The major autoimmune diseases (SLE, RA, vasculitis syndromes,
Addison disease, etc.) are discussed elsewhere. Isolated autoimmune hormone deciencies are common (thyroid, ovary, adrenal, pituitary, islet cells),
less common is autoimmune polyglandular syndrome with multiple hormone deciencies.
Common Immunodeficiency Syndromes
HIV infection and acquired immunodeciency syndrome (AIDS). HIV
infection progressively destroys CD4 cells impairing cellular and humoral
immunity. AIDS is dened as <200 CD4 cells/mm
ness, opportunistic infection, or AIDS-associated neoplasm. Infection is
acquired by unprotected sexual intercourse (male homosexuals and heterosexuals of both sexes) intravenous drug use, contact with infected body
uids, and vertical transmission from mother to newborn. Opportunistic
infections include parasites (Pneumocystis jeroveci, Toxoplasmosis encephalitis,
and Cryptosporidium enteritis), viruses (cytomegalovirus, Epstein–Barr virus,
3
or an AIDS-dening ill-
82 CHAPTER 5: Nonregional Systems and Diseases
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herpes simplex, herpes zoster, and human herpes virus-8), fungi (candidiasis,
cryptococcal meningitis, coccidioidomycosis, histoplasmosis, aspergillosis),
bacteria (salmonella, Strep. pneumoniae, H. inuenzae), mycobacteria (Mycobacte-
rium tuberculosis, M. avium complex), listeria, Treponema pallidum, and nocardia.
Symptoms and Signs. Acute HIV infection is a nonspecic viral syndrome,
often with exanthem, easily mistaken for Ebstein–Barr virus infection. After
a latent period of several years, the patient develops an immunosuppressive
syndrome manifest as lymphadenopathy, weight loss, dermatitis, opportunistic infections, and malignancies (e.g., Kaposi sarcoma, central nervous system
lymphoma, human papillomavirus-associated anal, and cervical carcinomas).
Common variable immunodeciency.
ration decreases immunoglobulin production and circulating levels of IgG,
IgM, and/or IgA. It presents with chronic or recurrent sinusitis and pneumonia. Risk of non-Hodgkin lymphomas is increased.
An acquired defect of B-cell matu-
THE LYMPHATIC SYSTEM
The normal lymphatic system is essential for recognition and response to
foreign antigens. Lymphocytes circulate out of capillary blood into tissue,
then to lymph nodes, and back to blood via the thoracic duct which empties into the left subclavian vein. Macrophages and Langerhans cells (antigen-presenting cells) migrate from peripheral sites with processed antigen,
which they present to T-cells and B-cells in the lymph nodes. T-cells circulate
from the capillary circulation to the lymphatics and nodes and then back into
the circulation until presented with an antigen specic to their T-cell receptor; recognition leads to activation and proliferation, generating an immune
response. Disorders of the lymphatics produce only three physical signs: palpable lymph nodes, red streaks in the skin from supercial lymphangitis, and
lymphedema.
Lymph Node Examination: Examination is primarily by palpation though
enlarged nodes may be visible by inspection, especially with oblique light.
Record these characteristics of palpable lymph nodes: number, size, consistency, mobility, tenderness, warmth, and whether they are discrete or matted
together. Procedures for examining the major lymph node beds are described
below. All lymph node–bearing areas should be palpated when searching for
generalized lymphadenopathy. The spleen should always be examined as
part of the lymphatic system examination.
Palpating cervical lymph nodes. With the patient sitting, palpate from
behind with the ngertips. Use this sequence for exam: (1) submental, midline
under the chin and both sides; (2) submandibular, under the jaw near its angle;
(3) jugular (anterior triangle), along the sternocleidomastoid’s anterior border; (4) supraclavicular, behind the middle of the clavicle; (5) posterior triangle,
posterior and behind the upper half of the sternocleidomastoid; (6) postau-
ricular, behind the ear over the mastoid; (7) preauricular, in front of the tragus;
(8) suboccipital, under the occiput and to either side; and (9) pre-trapezius, in
front of the upper border of the trapezius (Fig. 5-1). Examine the drainage
region of an enlarged node, e.g., anterior cervical triangle—the anterior third
The Lymphatic System 83
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FIG. 5-1Superficial Lymph Nodes of the Neck. Neck palpation reliably detects lymphadenopathy when each
group of nodes is examined systematically. The drawing contains a numbered scheme for examining nine node groups in
sequence.
of the scalp and face, posterior cervical triangle, and occiput—the posterior
two-thirds of the scalp.
Palpating axillary, infraclavicular, and supraclavicular lymph nodes.
With
the patient sitting, the right hand palpates the left axilla and the left hand the
right axilla (Fig. 5-2A). Relax the arm and axillary muscles by holding the
wrist with the other hand, elevating the arm toward the chest. Examine with
the palm toward the chest wall, the ngers pointing obliquely toward the axillary apex. Next, rest their hand on the examining arm, while the examiner’s
other hand supports their shoulder. The central node group on the thoracic
wall (Fig. 5-3) is examined by rmly raking the ngers along the chest wall
feeling for enlarged nodes. With the arm elevated examine the lateral axillary
nodes along the axillary vein medial to the proximal humerus. With the arm
still elevated, palpate the pectoral group under the lateral edge of the pectoralis major muscle. From behind with the arm raised, palpate the subscapular nodes under the anterior edge of the latissimus dorsi muscle. Palpate the
infraclavicular group under the clavicle. Enlargement in the supraclavicular
group is sought by feeling the soft tissues above and behind the clavicle (Fig.
5-2B). Repeat on the other side using the opposite hand for the exam.
Palpating inguinal lymph nodes.
Palpate at and just below the inguinal
ligament and distally along the course of the greater saphenous vein.
Diseases and Syndromes of Lymphocytes, Lymph Nodes, and Plasma Cells.
Lymphadenopathy. Lymph node enlargement results from a stimulated
regional or systemic immune response, direct infection of the node, which
can lead to suppuration, deposition of intracellular or extracellular material, or inltration with neoplastic cells. Describe their distribution, location
and number, size, mobility, consistency (uctuant, soft, rm, hard), surface
(smooth, irregular), and any tenderness, warmth, and/or sinus tracts. Perform
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FIG. 5-2Palpation of Axillary and Supraclavicular Lymph Nodes. A. Axilla: Position the patient’s upper
arm close to the chest to relax the axillary muscles. Rest the patient’s arm on the examining right arm while supporting the
shoulder with the left hand. Palpate the left axilla by sliding the right hand toward the axillary apex with palm toward the
chest wall. The approximated fingers are extended so the pulps feel the ribs and chest wall. Rake the examining fingertips
from apex down the chest wall. Enlarged nodes will slide under the fingertips. The positions are reversed to examine the right
side. B. Supraclavicular fossa.
FIG. 5-3Axillary Lymph Node Groups. Note that the lateral axillary group is on the inner aspect of the upper
arm, near the axillary vein. The subscapular group lies deep to the anterior edge of the latissimus dorsi muscle. The
pectoral group is behind the lateral edge of the pectoralis major muscle.
a meticulous skin and soft tissue exam of the involved region looking for
inammation, infection, or neoplasm. Pain and tenderness suggest inammation and/or infection; painless lymphadenopathy is more likely neoplastic. Fluctuant nodes suggest suppurating bacterial, mycobacterial, or fungal
infection. Fixation of the nodes to underlying tissue is most common with
metastatic carcinoma and chronic inammation. Matting together of nodes
suggests lymphoma or chronic inammation.
Generalized lymphadenopathy. Lymphadenopathy occurring simultaneously in multiple lymphatic beds, especially above and below the diaphragm,
suggests a systemic process, usually infectious, inammatory or neoplastic.
The Lymphatic System 85
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CLINICAL OCCURRENCE: Congenital: Niemann–Pick disease, Gaucher
disease;
sive lymphadenopathy (Rosai–Dorfman disease);
Degenerative/Idiopathic: Sarcoidosis, sinus histiocytosis with mas-
Infectious: Bacteria- Scarlet
fever, brucellosis, Lyme disease, secondary syphilis, tularemia, bubonic
plague, cat-scratch fever, Whipple disease, melioidosis, scrub typhus;
Mycobacteria- Tuberculosis, atypical mycobacteria; Viruses- Rubella, rube-
ola, infectious mononucleosis, HIV;
Chagas disease, kala-azar, toxoplasmosis;
Protozoa- African trypanosomiasis,
Fungi- Sporotrichosis; Helminths-
Filariasis; Ectoparasites- Scabies; Inammatory/Immune: RA, Still disease,
dermatomyositis, SLE, amyloidosis, serum sickness, drug allergy, graft-vshost disease, hyper IgM syndrome; Metabolic/Toxic: Drugs (e.g., diphenyl-
hydantoin), berylliosis, silicosis; Neoplastic: Hodgkin disease, non-Hodgkin
lymphoma, chronic lymphocytic leukemia, systemic mastocytosis, metastatic
carcinomas.
Lymphedema. Lymphatic obstruction drainage by whatever cause leads to
distal edema from accumulation of interstitial uid with a high protein content. Patients present with progressive painless swelling of a body part, which
can be massive. Initially the edema may pit, but over time brosis leads to
woody thickening without pitting. Lymphatic injury can result from surgery,
irradiation, trauma, and neoplastic obstruction. Longstanding lymphedema
is associated with an increased risk for lymphangiosarcoma.
DDX: The edema
may pit at rst, but characteristically is not pitting.
Filariasis (wuchereriasis).
Lymphatic infestation with Wuchereria bancrofti
or Brugia malayi larvae follows the bite of an infected mosquito. There is
inammation and later scarring with lymphatic obstruction and lymph-
Headache, photophobia, vertigo, fatigue, low-grade fever, and
edema.
myalgia are common symptoms. Acute signs include conjunctivitis, orchitis,
lymphangitis, and lymphadenopathy; later, obstruction of lymphatic and
venous drainage produces edema, hydrocele, and elephantiasis of breasts,
scrotum, vulva, or legs.
Inoculation lesion with regional lymphadenopathy.
Infectious agents are
inoculated into the skin and subcutaneous tissue by trauma, contamination
of broken skin, and bites of arthropods and larger animals including humans.
The extent of inoculation site inammation varies with the infecting organism. Local reactions may progress to ulceration and/or necrosis with eschar
formation. Spread through subcutaneous lymphatics toward regional lymph
nodes is marked by cutaneous inammation, streaking, and induration.
CLINICAL OCCURRENCE: Infectious: Bacterial- Streptococcal infections,
syphilitic chancre, anthrax, erysipeloid, ulceroglandular tularemia, bubonic
plague, rat-bite fever, cat-scratch disease, nocardia, actinomycosis, glanders;
Mycobacteria- Inoculation tuberculosis, atypical mycobacteria; Rickettsia-
Scrub typhus, boutonneuse fever, South African tick fever, Kenya typhus,
rickettsialpox; Fungi- Sporotrichosis; Viruses- Herpes simplex; Helminths-
Filariasis, trypanosomiasis, leishmaniasis; Neoplastic: Melanoma, squamous
cell carcinoma, lymphangioleiomyomas.
Suppurative lymphadenopathy. Lymph node suppuration is caused by streptococci, staphylococci, bovine tuberculosis, actinomyces, lymphogranuloma
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