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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3156_Библиотеки_им_академика_М_И_Перельмана.pdf
• >50 y old
• Female
• Weight loss
• Signs specic to
particular tumor site
• Further workup
according to the
suspected primary
tumor site
• Alkaline
phosphatase
• Bone scan
• Breast cancer
• Ovarian cancer
• Metastatic disease
• >50 y old
• Male
• Urinary complaints
• Prostate mass on
rectal examination or a
diffusely enlarged hard
prostate
• Prostate-specic
antigen
• Alkaline
phosphatase
• Bone scan
• Ultrasound-guided
prostate biopsy
• Prostate cancer
• >60 y old
• Bone pain
• Weight loss
• Fatigue
• Pallor
• Hepatomegaly
• Splenomegaly
• Tenderness over
bones
• CBC (anemia)
• Serum and
urine protein
electrophoresis
• Creatinine
• Erythrocyte
sedimentation rate
• Multiple myeloma (6)
D. Medications/vitamins
• Lithium
• Furosemide
• Thiazide diuretics
• Aminophylline
• Teriparatide
• Physical examination
normal or shows signs
of hypercalcemia
• Repeat serum
calcium (elevated)
• Other serum
electrolyte values
may be abnormal
• Medication use
• Calcium-based
antacids
• Normal or shows signs
of hypercalcemia
• Phosphate
• BUN
• Creatinine
• Bicarbonate
• Milk-alkali syndrome
• Vitamin pill use
• Bone pain
• Headaches
• Normal physical
examination or
tenderness over bones
• Papilledema
• Repeat serum
calcium
• Vitamin D level
• Serum phosphate
and chloride levels
• For vitamin A
overuse, serum
retinyl esters
• Vitamin D overdose
• Vitamin A overdose
TABLE 17.7.1 Evaluation of the Patient with Hypercalcemia (Continued)
History Physical examination Testing Diagnosis
(Continued)
388
E. Other
• Prolonged bed rest or
chair rest
• Physical examination
normal or shows signs
of hypercalcemia
• Consider
DEXA scan for
osteoporosis
• Immobilization
• History of acute renal
failure
• Physical examination
normal or shows signs
of hypercalcemia
• BUN
• Creatinine
• Urinalysis
• Chronic or diuretic
phase of acute renal
failure
• Fever
• Fatigue
• Malaise
• Anorexia
• Cough
• Dyspnea
• Retrosternal chest
discomfort
• Polyarthritis
• Findings dependent
on sites involved
• Erythema nodosum
• Uveitis
• Lymphadenopathy
• CBC
(lymphocytopenia)
• Chest X-ray
• Pulmonary
function testing
• Transbronchial
biopsy
• Sarcoidosis or other
granulomatous
disease
• Family history of
hypercalcemia
• May be normal
or show signs of
hypercalcemia
• Low 24-h urine
calcium level
• Familial hypocalciuric
hypercalcemia
CBC, complete blood count; BUN, blood urea nitrogen; CT, computed tomography; DEXA,
dual-energy X-ray absorptiometry.
IV. DIAGNOSIS. See Table 17.7.1. Calcium levels above 12.5 mg/dL can be life threatening. In
such situations, one should perform an electrocardiogram and begin treatment immediately,
because cardiac arrest, convulsions, or coma can occur. Further testing can be performed while
the serum calcium is lowered.
REFERENCES
1. Bushinsky DA, Monk RD. Calcium. Lancet 1998;352:306–311.
2. Potts JT, Juppner, H. Disorders of the parathyroid gland and calcium homeostasis. In: Longo DL, ed.
Harrison’s principles of internal medicine, 18th ed. New York, NY: McGraw Hill, 2011:3096–3120.
3. ASBMR (2009) Chapter 67. Non-parathyroid hypercalcemia. In: Horwitz MJ, Hodak SP, Stewart AF,
eds. Primer on the metabolic bone diseases and disorders of mineral metabolism. Hoboken, NJ: Wiley. doi:
10.1002/9780470623992.ch67
4. Al Zahrani A, Levine MA. Primary hyperparathyroidism. Lancet 1997;349:1233–1238.
5. Stewart AF. Hypercalcemia associated with cancer. N Engl J Med 2005;352:373–379.
6. Mundy GR, Guise TA. Hypercalcemia of malignancy. Am J Med 1997;103:134–145.
TABLE 17.7.1 Evaluation of the Patient with Hypercalcemia (Continued)
History Physical examination Testing Diagnosis
389
17.8
Hyperkalemia
Nathan Falk and Joshua P. Brautigam
I. BACKGROUND. Hyperkalemia is defined as a serum potassium (K
+
) >5.0 mEq/L. The preva-
lence of hyperkalemia in hospitalized patients is between 1% and 10% (1). Hyperkalemia can
be life threatening secondary to cardiac manifestations when K
+
> 6.5 mEq/L (2).
II. PATHOPHYSIOLOGY. Hyperkalemia can be divided into four etiologic groups: spurious,
redistribution abnormalities, renal disorders (impaired excretion), and hormone deficiencies.
Spurious hyperkalemia in a healthy patient, most commonly caused by hemolysis during phle-
botomy, can also be seen in cases of thrombocytosis, leukocytosis, and repeated fist clenching in
blood drawing. The most common redistribution abnormality is acidosis. The most frequently
occurring renal disorders leading to impaired excretion are renal failure with a concomitant
potassium load and/or medication involvement. The primary cause of endocrinologic hyperka-
lemia is uncontrolled diabetes.
III. EVALUATION. Hyperkalemia is usually not sustained unless there is a disorder of the potas-
sium regulatory system. In an otherwise healthy individual, routine screening of potassium
is not indicated. Potassium should be monitored in patients on certain medications (see
Table 17.8.1), with acid–base disorders, with abnormalities in renal function and disorders of
aldosterone secretion. These patients are at risk for potentially fatal hyperkalemia (6).
IV. DIAGNOSIS. The initial diagnostic approach begins with a clinical history, review of medi-
cations, and physical examination. Hyperkalemia is usually asymptomatic; however, it can
present with muscle weakness, flaccid paralysis, ileus, and characteristic electrocardiographic
(ECG) changes (1). Arrhythmias occur at high levels of K
+
and if K
+
rises very rapidly in its
concentration. The earliest ECG changes are tall, peaked T waves, followed by the loss of the
P wave, then widening of the QRS complex, and finally development of a sine wave rhythm that
can precipitate into ventricular fibrillation and asystole. Hyperkalemia can be life threatening
even when the ECG is normal, as nearly one-half of patients with K
+
> 6.0 mEq/L will have
a normal ECG (1). Laboratory testing is required to determine serum potassium level. Patients
with a K
+
≥ 6.5 mEq/L require immediate cardiac evaluation.
TABLE 17.8.1 Evaluation of the Patient with Hyperkalemia
History Physical examination Testing Diagnosis
A. Spurious (3)
Laboratory reading
is “hemolysis” on
electrolyte panel
Healthy patient
Repeat serum K
+
testing; normalized
in redrawn sample
Hemolysis in
collection tube
Platelet count
>1 million
Healthy patient, except
for disorder causing
thrombocytosis
Repeat platelet count
with heparinized
specimen
Thrombocytosis
(platelets release
K
+
during clotting)
WBC count >200,000
Healthy patient, except
for underlying disorder
causing leukocytosis
Repeat WBC
count with rapid
processing/spinning
down specimen
Leukocytosis
(Continued)
390
TABLE 17.8.1 Evaluation of the Patient with Hyperkalemia (Continued)
History Physical examination Testing Diagnosis
K
+
normalized in
repeat draw with
careful draw
technique
Healthy patient
Repeat serum K
+
Tight or prolonged
tourniquet or st
clenching during
blood draws
B. Redistribution (4)
Acidosis Often no signs specic
to acidosis in an
otherwise ill patient
• Immediate ECG
• Monitor cardiac
rhythm
• ABG
• Sequential testing
pH < 7.35
• β-blockers
• Angiotensin-
converting enzyme
inhibitors
• Angiotensin-receptor
blockers
• Cardiac glycosides
• Neuromuscular
blocking agents
• Salt substitutes
• Trimethoprim
• Pentamidine
No signs of hyperkalemia.
Physical examination
may reveal underlying
illness leading to
medication use
• Immediate ECG
• Cardiac rhythm
should be monitored
Medication/diet effect
• Crush injury
• Tissue breakdown
Bruising, other signs of
trauma, or a necrotic
wound
• Immediate ECG
• Monitor cardiac
rhythm
Cell breakdown
Rhabdomyolysis Signs of cell injury, heat
stroke, crush injury
• Urinalysis for
myoglobin
• BUN/creatinine
• Immediate ECG
• Monitor cardiac
rhythm
Cell breakdown and
kidney dysfunction
Large bruise or
hematoma
Hematoma • Immediate ECG
• Monitor cardiac
rhythm
Hematoma
breakdown
Muscle contraction in
marathon runners
Endurance athlete Cell breakdown and
muscle release
of K
+
• Cachexia
• Symptoms related
to the etiology of the
cachexia
• Cachectic
• Signs related to reason
for cachexia
• Immediate ECG
• Monitor cardiac
rhythm
Tissue catabolism
(Continued)
391
Hemolytic anemia • Pallor
• Petechiae
• Orthostatic
hypotension
• Bleeding from any
orice
• Immediate ECG
• Monitor cardiac
rhythm
• CBC
Hemolysis
• Other signs as related
to the etiology of
hemolytic anemia
Hyperkalemic periodic
paralysis (5)
Quadriplegia with
sparing of the cranial
nerves
Transient hyper K
+
C. Renal disorders
Use of potassium-
sparing diuretics
(e.g., triamterene,
spironolactone)
• BUN
• Creatinine
• Creatinine clearance
may be low
• FE
K+
Diuretic use
History of treatment
for a Pneumocystis
carinii infection
• BUN
• Creatinine
• Normal creatinine
clearance
Trimethoprim or
pentamidine effect
Known creatinine
clearance <50
• Creatinine clearance
• Immediate ECG,
monitor cardiac
rhythm
Renal insufciency
or failure with a
potassium load
Systemic lupus
erythematosus
• Malar rash
• Discoid rash
• Recurrent oral ulcers
• Focal neurologic
decits
• ABG
• Creatinine clearance
• FE
K+
• Evaluation of
underlying disease
Decreased GFR
Sickle cell disease
or trait
• BUN
• Creatinine
• Creatinine clearance
may be low
• Low FE
K+
• Evaluation of
underlying disease
Decreased GFR
TABLE 17.8.1 Evaluation of the Patient with Hyperkalemia (Continued)
History Physical examination Testing Diagnosis
(Continued)
392
Amyloidosis • Signs due to
amyloidosis
• BUN
• Creatinine
• Creatinine clearance
may be low
• Low FE
K+
• Evaluation of
underlying
disease
Decreased GFR
D. Hormone deficiency
Diabetes • Signs of DKA • Evaluate for DKA
• Check ECG/cardiac
rhythm
• Sequential testing
Acidosis causing
redistribution with
K
+
/H
+
exchange
Pseudo and actual
aldosterone
d eciency
• Hyperpigmentation
• Hypotension
• Weight loss
• Vomiting
• Aldosterone levels
• Renin levels
• Check ECG/cardiac
rhythm
• Cosyntropin
stimulation test
Addison’s disease
Heparin use • Aldosterone
levels
• Check ECG/cardiac
rhythm
Aldosterone excretion
low second to
heparin
WBC, white blood cell; ECG, electrocardiogram; CBC, complete blood count; ABG, arterial blood
gases; BUN, blood urea nitrogen; FE
k+
, low fractional excretion of potassium; GFR, glomerular
ltration rate; DKA, diabetic ketoacidosis.
TABLE 17.8.1 Evaluation of the Patient with Hyperkalemia (Continued)
History Physical examination Testing Diagnosis
REFERENCES
1. Hollander-Rodriguez JC, Calvert JF Jr. Hyperkalemia. Am Fam Physician 2006 Jan 15;73(2):
283–290.
2. Halperin ML, Kamel KS. Potassium. Lancet 1998;352(9122):135–140.
3. Wallach J, ed. Interpretation of diagnostic tests, 6th ed. New York, NY: Little, Brown and Company,
1996.
4. Gennari F. Disorders of potassium homeostasis: hypokalemia and hyperkalemia. Crit Care Clin
2002;18:273–288.
5.
Evers S, Engelien A, Karsch V, et al. Secondary hyperkalemic paralysis. J Neurol Neurosurg Psychiatry
1998;64(2):249–252.
6.
Humes HD, DuPont HL, eds. Kelley’s textbook of internal medicine, 4th ed. Philadelphia PA:
Lippincott-Raven.
393
17.9
Hypokalemia
Nathan Falk
I. BACKGROUND. Hypokalemia is one of the most common electrolyte abnormalities found in
basic laboratory electrolyte panels. Although the definition varies, hypokalemia is generally said
to occur when serum potassium (K
+
) concentration falls below 3.6 mEq/L.
II. PATHOPHYSIOLOGY. With the exception of factitious causes (leukemic patients with extreme
leukocytosis, where K
+
is taken up by the abnormal white blood cells), true hypokalemia results
from increased potassium excretion, transcellular shift, or decreased dietary intake of potassium.
Most commonly, hypokalemia is caused by abnormal losses of potassium through the gastroin-
testinal tract or kidney (see Table 17.9.1). The most common of these causes is iatrogenic via
diuretic use leading to K
+
depletion. Both the loop (blocked resorption in the loop of Henle)
and thiazide diuretics (block resorption in early distal tubule) contribute to the development
of hypokalemia. Sodium and chloride delivery are increased by the diuretics, resulting in the
secretion of K
+
. Further K
+
loss is fostered by increased magnesium excretion, which is also
linked to the loop and thiazide diuretics. Other medications, metabolic alkalosis, renal tubular
acidosis, and aldosteronism due to systemic diseases and genetic disorders are implicated in the
development of hypokalemia (5).
III. EVALUATION. See Table 17.9.1.
IV. DIAGNOSIS. See Table 17.9.1.
TABLE 17.9.1 Evaluation of the Patient with Hypokalemia
History Physical examination Testing Diagnosis
A. Gastrointestinal
losses (1)
• Emesis
• Nasogastric drainage
• Pyloric/duodenal
obstruction
• Pancreatic stulas
• Diarrhea
• Laxative abuse
• Colonic neoplasms
• Often no signs on
physical examination
• Generalized muscle
weakness
• Constipation
• Cachexia
• Abdominal
examination for signs
of peritonitis
or localized pain
• Serum electrolytes
• Spot urine electrolytes
if needed
• Urine and serum
osmolality as needed
• Stool electrolytes as
appropriate
• Electrocardiogram
(look for “U” waves
or, if rapidly replacing
potassium by the
intravenous route,
look for arrhythmias)
Gastrointestinal
potassium losses
(Continued)
394
(Continued)
B. Renal losses (2)
• Diuretics (loop or
thiazide)
• Osmotic diuresis
(uncontrolled diabetes)
• Metabolic alkalosis
(vomiting/diarrhea)
• Primary
hyperaldosteronism
• Cortisol-responsive
aldosteronism
• Congenital adrenal
hyperplasia
• Liddle’s syndrome
• 11β-hydroxysteroid
dehydrogenase
deciency
• Bartter syndrome
• Gitelman’s syndrome
• Inappropriate secretion
of antidiuretic hormone
• Hypomagnesemia
• Licorice use
• Corticosteroids
• Renal tubular acidosis
• Renal artery stenosis
• As above
• May also ask about
history of diabetes or
use of loop or thiazide
diuretics
• As above
• May also check for
ketones, blood sugar,
serum pH
Renal potassium
losses and
congenital
syndromes
C. Transcellular
shift(3, 4)
• Bronchodilators
• Antihistamines
• Tocolytics
• Theophylline
• Caffeine
• Insulin
• Delirium tremens
• Hyperthyroidism
• Familial hypokalemic
periodic paralysis
• Barium toxicity
• As above
• May also ask about
alcohol abuse and
careful medication
history
• As above
• May also check for
serum alcohol level,
drug screen as
appropriate
Drug therapy
and systemic
diseases
TABLE 17.9.1 Evaluation of the Patient with Hypokalemia (Continued)
History Physical examination Testing Diagnosis
395
• Pancreatitis
• Congestive heart
failure
• Toxic shock
• Pleural effusion
• Ascites
• Anasarca
• Burns (second/third
degree)
D. Inadequate intake
• Anorexia/bulimia
• Forced vomiting or
diarrhea for any reason
• Neurotic spitting
• Poor diet
• As above
• May also check for
evidence to support
the history such as
weight loss, staining,
or pitting of the teeth
• As above Patient excesses
TABLE 17.9.1 Evaluation of the Patient with Hypokalemia (Continued)
History Physical examination Testing Diagnosis
REFERENCES
1. Gennari F. Disorders of potassium homeostasis: hypokalemia and hyperkalemia. Crit Care Clin
2002;18:273–288.
2. Huang C, Kuo E. Mechanism of hypokalemia in magnesium deficiency. J Am Soc Nephrol
2007;18:2649.
3. Rastergar A, Soleimani M. Hypokalemia and hyperkalemia. Postgrad Med J 2001;77:759–764.
4. Clausen T. Hormonal and pharmacological modification of plasma potassium homeostasis. Fundam
Clin Pharmacol 2010;24:595.
5. Gennari F. Current concepts: hypokalemia. N Engl J Med 1998;339(7):451–458.
396
Diagnostic Imaging
Abnormalities
Enrique S. Fernandez
CHAPTER 18
18.1
I. BACKGROUND. Breast cancer is currently the most common noncutaneous malignancy and
the second leading cause of cancer death among women in the United States. Widespread
screening with mammography and advances in treatment have resulted in decreased mortality
from breast cancer. Currently, there are differing recommendations regarding screening and
concerns about the effects of false-positive results. Since most women will have a mammogram
either as a screening recommendation or a found breast mass, clinicians need to be able to
discuss the role of mammography and subsequent results with patients.
II. PATHOPHYSIOLOGY
A. Etiology.
The exact etiology of breast cancer is unknown but is believed to be due to
aberrations in cell cycle regulation. Breast cancer can have a genetic predisposition with the
most common mutations, BRCA1 and BRCA2, occurring in about 5–10% of breast cancers
(1, 2). No single environmental or dietary exposure has been directly linked to a specific
genetic mutation. Growth-enhancing mammotropic hormones affect the number of target
cells and the likelihood of spontaneous mutations. The number of mammary tissue-specific
stem cells, which are determined in early life, affect the risk of breast cancer. Their differen-
tiation occurs during pregnancy and is protective (3).
The breasts are composed of fat, connective tissue, lymphatics, lobules which are the
milk-producing glands, and ducts connecting lobules to the nipple. Breast cancers often
arise from the duct or lobule and can be either in situ or invasive. Ductal carcinomas are
more common, with invasive ductal carcinoma occurring in about 70% of cases (1, 3).
Ductal carcinoma in situ tends to be more localized, while lobular carcinoma in situ shows
a diffuse distribution in the breast.
Invasive ductal carcinoma shows the highest prevalence in women who are premeno-
pausal or in early menopause. It is composed of heterogeneous cells arranged in single rows.
Invasive lobular carcinoma is composed of small homogenous cells that invade the stroma
and is often multifocal and bilateral. Estrogen, progesterone, and Herceptin protein recep-
tors (HER2) play a role in tumorigenesis and regulation of breast cancer. They are also
important markers for prognosis and used for targeted treatment. Tumors with overexpres-
sion of HER2 have a poorer prognosis (3).
Other less common types of breast cancer include inflammatory breast cancer, medul-
lary cancer (younger women), phyllodes tumor, angiosarcoma, mucinous carcinoma (older
women), mixed tumors, and Paget’s disease involving the nipple.
Abnormal Mammogram
Abbie Jacobs
397