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12 Laboratory Medicine in Psychiatry and Behavioral Science
Alkaline phosphatase (ALP) (continued)
Increased levels (continued) • Liver disease: cirrhosis, alcohol use disorder, hepatitis,
cholestasis, cancer (primary or metastatic), infectious
mononucleosis, diabetes, Gilbert’s syndrome
• Bile duct obstruction
• Gallbladder disease
• Bone disease: cancer (primary or metastatic), Paget’s dis-
ease, osteomalacia, rickets, osteogenesis imperfecta
• Hyperparathyroidism (with elevated calcium)
• Hyperthyroidism
• Infarction (myocardial or pulmonary)
• Hodgkin’s disease
•Lung or pancreatic cancer
• Ulcerative colitis
• Peptic ulcer disease
• Amyloidosis
•Sarcoidosis
• Bowel infarction or perforation
• Chronic renal failure
• Congestive heart failure
• Hepatotoxic drugs
Decreased levels • Hypothyroidism
• Pernicious anemia and other anemias
• Malnutrition
• Magnesium or zinc deficiency
• Milk-alkali syndrome
• Celiac sprue
• Congenital hypophosphatasia
Interfering factors ALP levels increase at room temperature and in refrigera-
tion; tests should be run the same day as collection.
ALP levels decrease if blood is anticoagulated.
People older than 50
years may have 1.5 times the normal
level of
ALP without pathology.
Elevated ALP levels are seen in pregnancy and after meno-
pause.
ALP levels increase after fatty meals.
Elevation in ALP is seen for several days after albumin infu-
sion.
A very large number of drugs are associated with ALP ele-
vation, including all psychotropic drug classes and nearly all
members of each class.
Cross-references Alcohol Use Disorder
Cirrhosis
Liver Function Tests
https://t.me/med1917
13 Laboratory Tests
Alkaline phosphatase (ALP) (continued)
American Association for Clinical Chemistry: Testing.com. Available at: https://www.testing.com/tests.
Accessed May 2021.
Fischbach FT, Fischbach MA: A Manual of Laboratory and Diagnostic Tests, 10th Edition. Philadelphia,
PA, Wolters Kluwer Health/Lippincott Williams and Wilkins, 2018
Giannini EG, Testa R, Savarino V: Liver enzyme alteration: a guide for clinicians. CMAJ 172:367–379, 2005
Reust CE, Hall L: Clinical inquiries: what is the differential diagnosis of an elevated alkaline phosphatase
(AP) level in an otherwise asymptomatic patient? J Fam Pract 50:496–497, 2001
https://t.me/med1917
14 Laboratory Medicine in Psychiatry and Behavioral Science
Alprazolam level
Type of test Blood
Background and explanation
of test
Benzodiazepines are Schedule IV sedative-hypnotic drugs
used to treat anxiety and insomnia. Alprazolam is a fast- to
intermediate-acting drug with a half-life that varies consid
-
erably among individual patients. In general, levels are
checked when either overdose or noncompliance is sus
-
pected or to detect use without a prescription.
Relevance to psychiatry and
behavioral science
On postmortem study, brain alprazolam levels were more
than twice those in blood in cases in which alprazolam was
judged not to have been a contributing cause of death. Tox
-
icity with chronic benzodiazepine ingestion may be mani-
fested as confusion, disorientation, memory impairment,
ataxia, decreased reflexes, and dysarthria. With acute over-
dose, the patient may exhibit somnolence, confusion, ataxia,
decreased reflexes, vertigo, dysarthria, respiratory depres
-
sion, and coma. More serious consequences usually involve
co-ingestion of alcohol or other sedatives.
Preparation of patient None needed
Indications • Screening for drug use
• Suspicion of overdose
•
Signs of toxicity in a treated patient
• Suspected noncompliance with prescribed therapy
Reference range 10–40 ng/mL with low-dose therapy (1–4 mg/day)
50–100 ng/mL with high-dose therapy (6–9 mg/day)
Critical value(s) Above upper limits noted
Increased levels • Overdose
•Overuse
• Poor metabolism
• Hepatic encephalopathy
Decreased levels Noncompliance
Interfering factors None
Cross-references Benzodiazepines
ARUP Laboratories: Alprazolam, in Lab Test Directory. Salt Lake City, UT, ARUP Laboratories, 2021.
Available at: https://ltd.aruplab.com/Tests/Pub/0090010. Accessed May 2021.
Skov L, Holm KM, Johansen SS, Linnet K: Postmortem brain and blood reference concentrations of al-
prazolam, bromazepam, chlordiazepoxide, diazepam, and their metabolites and a review of the liter-
ature. J Anal Toxicol 40(7):529–536, 2016
https://t.me/med1917
15 Laboratory Tests
Ammonia
Type of test Blood
Background and explanation
of test
Ammonia is a waste product made by intestinal bacteria and
other cells during protein digestion. Under normal condi
-
tions, ammonia is transformed in the liver to urea, which can
be excreted by the kidneys. If this cycle malfunctions, am
-
monia can build up in the blood, affecting acid-base balance
and brain function. In acute hepatic failure, with a rapid rise
in ammonia levels, there is a reasonable correlation of ve
-
nous ammonia levels with arterial ammonia levels and of
arterial ammonia with brain glutamine levels. In chronic he
-
patic insufficiency, correlations are much less robust.
Relevance to psychiatry and
behavioral science
Routine blood tests do not include ammonia assays, in part
because of the unreliability of ammonia sampling. Unless
there is clinical suspicion of ammonia elevation based on the
patient’s history or exam findings, the ammonia level is not
checked. For this reason, hyperammonemia may be under-
diagnosed in some settings. Elevated ammonia levels can be
found in hepatic failure due to alcoholic cirrhosis, hepatitis,
and Wilson’s disease, among other conditions. Acute hyper
-
ammonemia is associated with delirium and other mental
status changes as well as seizures. In severe cases, coma and
death from brain herniation can supervene. When acute hy
-
perammonemia is suspected, the ammonia level should be
ordered and checked stat because this represents a medically
urgent situation. This order is also critical to the accuracy of
the test, because ammonia levels increase with the break
-
down of proteins during blood storage. Chronic hyperam-
monemia has less severe symptoms because of
compensatory changes in ammonia metabolism and damp
-
ening of excitatory effects on the brain.
Preparation of patient If possible, patients should fast for 8 hours except for water
and should not smoke for 2 hours before testing.
Indications • Workup for mental status changes
• Workup for lethargy and vomiting in a child after viral
illness
• Diagnosing hepatic encephalopathy
• Diagnosing Reye’s syndrome
• Monitoring severity of hepatic disease and response to
treatment
• Evaluating genetic urea cycle disorders
• Monitoring patients on hyperalimentation
Reference range Dependent on what is measured:
• Measured as NH
3
, adults: 15–60 μg/dL
• Measured as N, adults: 15–45 μg/dL
Critical value(s) NH
3
>200 μmol/L
https://t.me/med1917
16 Laboratory Medicine in Psychiatry and Behavioral Science
Ammonia (continued)
Increased levels • Liver disease, especially after a precipitant such as GI
bleeding or electrolyte imbalance
• Decreased blood flow to the liver
• GI hemorrhage
• GI tract infection with distention and stasis
• Reye’s syndrome (with decreased glucose levels)
•Renal failure
• Total parenteral nutrition
• Heritable defects in urea cycle enzymes (can appear at
any age)
• Use of valproic acid (especially in patients with carnitine
deficiency)
• Other drugs, including barbiturates, diuretics, and
opioids
Decreased levels • Hypertension
• Antibiotics such as neomycin
Interfering factors Sampling techniques greatly affect ammonia values.
Hemolysis, use of a tight tourniquet, clenching fist, or allow-
ing sample to sit increases ammonia levels, as does exercise
or other muscular exertion and smoking.
Cross-references Alcohol Use Disorder
Cirrhosis
Hepatic Encephalopathy
Hepatitis, Viral
Blanco Vela CI, Bosques Padilla FJ: Determination of ammonia concentrations in cirrhosis patients: still
confusing after all these years? Ann Hepatol 10(Suppl 2):S60–S65, 2011
Cohn RM, Roth KS: Hyperammonemia, bane of the brain. Clin Pediatr (Phila) 43:683–689, 2004
Fischbach FT, Fischbach MA: A Manual of Laboratory and Diagnostic Tests, 10th Edition. Philadelphia,
PA, Wolters Kluwer Health/Lippincott Williams and Wilkins, 2018
Kundra A, Jain A, Bang a A, et al: E valuation of plasma ammonia levels in patients with acute liver failure
and chronic liver disease and its correlation with the severity of hepatic encephalopathy and clinical
features of raised intracranial tension. Clin Biochem 38:696–699, 2005
https://t.me/med1917
17 Laboratory Tests
Amylase
Type of test Blood
Background and explanation
of test
Amylase is an enzyme produced by the parotid glands and
the pancreas that facilitates digestion of complex carbohy
-
drates. It enters the circulation in large amounts when the
salivary glands or pancreas is inflamed and is e xcreted by
the kidneys. The most important use of amylase testing is to
diagnose acute pancreatitis, although lipase is more specific
for this condition. In acute pancreatitis, the serum amylase
level begins to rise 2 hours after onset, peaks at 24 hours,
and persists for 2–4 days. Amylase appears in the urine with
a lag time of 6–10 hours and persists for 7–10 days.
Amylase can also be high in macroamylasemia. In this condi-
tion, amylase is bound to immunoglobulin, forming a mol-
ecule that is poorly filtered by the kidney because of its large
size. Macroamylasemia does not cause symptoms but is as
-
sociated with other diseases such as ulcerative colitis, celiac
disease, HIV infection, and rheumatoid arthritis. It is also
seen in apparently healthy patients. Macroamylasemia can
be distinguished from acute pancreatitis by measuring
urine amylase, which is low in macroamylasemia and high
in acute pancreatitis.
Relevance to psychiatry and
behavioral science
Amylase is elevated along with lipase in pancreatitis, and
certain populations are at particular risk, including patients
with alcoholism (especially males), gallstones (especially fe
-
males), and hyperlipidemia and those treated with medica-
tions such as valproate, corticosteroids, or isoniazid.
Amylase of salivary origin may be elevated in patients with
eating disorders that include purging behaviors.
Preparation of patient Patients should fast for ≥ 2 hours before testing.
Indications Diagnosis and monitoring of patients with acute pancreati-
tis, although lipase alone may be sufficient for this purpose
Reference range Adults ≤60 years: 25–125 U/L
Adults >60 years: 24–151 U/L
Critical value(s) Amylase ≥ 3 times the upper limit of normal is one criterion
for acute pancreatitis.
Increased levels • Pancreatitis
• Other pancreatic disease or trauma
• Eating disorder with purging
• Partial gastrectomy
• Appendicitis, peritonitis
• Perforated peptic ulcer
•TBI
•Shock
• Mumps or other salivary gland/duct inflammation or
obstruction
https://t.me/med1917
18 Laboratory Medicine in Psychiatry and Behavioral Science
Amylase (continued)
Increased levels (continued) • Acute cholecystitis (stone in the common bile duct)
• Intestinal obstruction
• Ruptured ectopic pregnancy
• Macroamylasemia
Decreased levels • Pancreatic insufficiency, pancreatectomy
• Liver disease, hepatitis
• Cystic fibrosis
Interfering factors Anticoagulated blood and lipemic serum interfere with
results.
Pregnancy and diabetes increase levels.
Drugs that increase amylase levels include clozapine, desip-
ramine, donepezil, mirtazapine, risperidone, valproate, and
numerous non-psychotropic medications, including
NSAIDs, acetaminophen, many opioids, and steroids.
Drugs that decrease amylase levels include anabolic ste-
roids, cefotaxime, propylthiouracil, zidovudine, and others.
Cross-references Lipase
Pancreatitis, Acute
American Association for Clinical Chemistry: Testing.com. Available at: https://www.testing.com. Ac-
cessed May 2021.
Boxhoorn L, Voermans RP, Bouwense SA, et al: Acute pancreatitis. Lancet 396 (10252):726–734, 2020
Fischbach FT, Fischbach MA: A Manual of Laboratory and Diagnostic Tests, 10th Edition. Philadelphia,
PA, Wolters Kluwer Health/Lippincott Williams and Wilkins, 2018
Ghio L, Fornaro G, Rossi P: Risperidone-induced hyperamylasemia, hyperlipasemia, and neuroleptic
malignant syndrome: a case report. J Clin Psychopharmacol 29:391–392, 2009
Ismail OZ, Bhayana V: Lipase or amylase for the diagnosis of acute pancreatitis? Clin Biochem
50(18):1275–1280, 2017
https://t.me/med1917
19 Laboratory Tests
Angiography, computed tomography (cerebrovascular)
Type of test Imaging
Background and explanation
of test
In CT angiography, cerebral vasculature and tissues are ex-
amined using CT technology along with administration of
contrast dye. This modality is used in the acute setting to
evaluate new-onset headache, TIA, suspected stroke, bleed
-
ing from a cerebral aneurysm or arteriovenous malforma-
tion, and other events (as noted in the Indications section
below). Compared to magnetic resonance angiography
(MRA), CT angiography is superior in the detection of acute
blood.
Relevance to psychiatry and
behavioral science
Patients with stenotic lesions, aneurysms, vascular malfor-
mations, and other cerebrovascular conditions may exhibit
associated psychiatric signs and symptoms, and CT angiog
-
raphy may be helpful in the diagnostic workup. Psychia-
trists should be familiar with this modality and be able to
explain what is involved to patients under their care, even
though the test may be ordered by other specialists. Ex
-
tremely detailed and lifelike images can now be obtained
via an image processing technique—three-dimensional cin
-
ematic rendering—that facilitates exploration of and teach-
ing about cerebral vasculature.
Preparation of patient See Computed Tomography Scan, Head
Indications • Sudden-onset severe or unilateral headache
• Suspected carotid or vertebral dissection
•Ipsilateral Horner syndrome
• Suspected carotid vascular disease: asymptomatic
cervical bruit and/or risk factors
• TIA involving carotid or vertebrobasilar territories
(combined with head CT)
• New focal neurological deficit (combined with head CT)
• Risk of unruptured aneurysm with positive family
history (combined with noncontrast head CT)
• Known subarachnoid hemorrhage
• Known parenchymal hemorrhage
• Acute ataxia (head and neck; combined with CT)
Reference range No vascular stenosis, occlusion, dissection, dilatation,
abnormal communication, or extravasated blood
Abnormal test • Atherosclerotic stenosis or occlusion
• Disease or aneurysm of the aorta
• Aneurysm or arteriovenous malformation in the brain
• Intracerebral or intracranial hemorrhage
• Vascular injury from trauma
• Hypervascular tumor or tumor invasion of vasculature
https://t.me/med1917
20 Laboratory Medicine in Psychiatry and Behavioral Science
Angiography, computed tomography (cerebrovascular) (continued)
Interfering factors Any motion artifact results in poor imaging. Patients who
are agitated or unable to comprehend instructions to mini
-
mize motion from swallowing and breathing cannot be
studied.
Carotid artery overlap (internal with external on each side)
makes it difficult to view an individual vessel.
Cross-references Computed Tomography Scan, Head
Stroke
Caton MT Jr, Wiggins WF, Nunez D: Three-dimensional cinematic rendering to optimize visualization of
cerebrovascular anatomy and disease in CT angiography.J Neuroimaging 30(3):286–296, 2020
Fauci AS, Braunwald E, Kasper DL, et al (eds): Harrison’s Principles of Internal Medicine, 17th Edition.
New York, McGraw-Hill, 2008
Hopyan J, Ciarallo A, Dowlatshahi D, et al: Certainty of stroke diagnosis: incremental benefit with CT
perfusion over noncontrast CT and CT angiography. Radiology 255:142–153, 2010
https://t.me/med1917
21 Laboratory Tests
Angiography, magnetic resonance (cerebrovascular)
Type of test Imaging
Background and explanation
of test
Magnetic resonance angiography (MRA) is an application
of MRI that images blood flow and highlights pathology of
blood vessels. It can be performed with or without contrast
medium, although contrast can aid visualization. The scan
takes 15–30 minutes. Compared with CT angiography, MRA
is superior in the resolution of adjacent tissues.
Relevance to psychiatry and Patients with stenotic lesions, aneurysms, vascular malfor-
behavioral science mations, and other cerebrovascular conditions may exhibit
associated psychiatric signs and symptoms. MRA may be
helpful in the diagnostic workup.
Preparation of patient No pretest preparation is needed. MRA is not performed on
patients with implanted metal devices, including pacemak
-
ers, defibrillators, cochlear implants, metal heart valves,
pumps, neurostimulators, certain prostheses, and certain
intrauterine devices. For surgical implants reported to be
MRI compatible, the brand, style, and serial number should
be requested to confirm compatibility. MRA is not advised
for pregnant patients or patients with epilepsy.
Indications • Sudden-onset severe or unilateral headache
• Suspected carotid or vertebral dissection
• Ipsilateral Horner syndrome
• Suspected vascular disease in carotid or vertebrobasilar
arteries
• Surgical planning for carotid artery disease (with carotid
duplex study)
• TIA involving carotid or vertebrobasilar territories
(combined with head MRI)
• New focal neurological deficit (combined with head MRI)
• Risk of unruptured aneurysm with positive family
history
• Follow-up study for a known arteriovenous malforma-
tion or aneurysm
• Known parenchymal hemorrhage
• Ataxia, acute (head and neck; with MRI)
• Evaluation of pulsatile tinnitus
Reference range No vascular stenosis, occlusion, dissection, dilatation,
abnormal communication, or extravasated blood seen
Abnormal test • Atherosclerotic stenosis or occlusion
• Aneurysm or arteriovenous malformation in the brain
• Intracerebral or intracranial hemorrhage
• Vascular injury from trauma
• Hypervascular tumor or tumor invasion of vasculature
https://t.me/med1917