By K. Sancho. University of Tennessee Health Science Center. 2018.

Increased Direct (Conjugated): Note: Determination of the direct bilirubin is usually unnecessary with total bilirubin levels <1 generic renagel 800 mg amex gastritis diet 21. Liberated when proinsulin is split to insulin; levels suggest endogenous production of insulin Decreased: Diabetes (decreased endogenous insulin) cheap renagel 800 mg without a prescription gastritis diet , insulin administration (factitious or therapeutic), hypoglycemia C-REACTIVE PROTEIN (CRP) • Normal = none detected • Collection: Tiger top tube A nonspecific screen for infectious and inflammatory diseases, correlates well with ESR. Increased: Bacterial infections, inflammatory conditions (acute rheumatic fever, acute RA, MI, transplant rejection, embolus, inflammatory bowel disease), last half of pregnancy, oral contraceptives, some malignancies CA 15-3 Used to detect breast cancer recurrence in asymptomatic patients and monitor therapy. Lev- els related to stage of disease Increased: Progressive breast cancer, benign breast disease and liver disease Decreased: Response to therapy (25% change considered significant) CA 19-9 • <37 U/ml (SI:<37 kU/L) • Collection: Tiger top tube Primary used to determine resectability of pancreatic cancers (ie, >1000U/mL 95% unresectable) Increased: GI cancers such as pancreas, stomach, liver, colorectal, hepatobiliary, some cases of lung and prostate, pancreatitis CA-125 • <35 U/mL (SI: <35 kU/L) • Collection: Tiger top tube Not a useful screening test for ovarian cancer when used alone; best used in conjunction with ultrasound and physical examination. Rising levels after resection predictive for recur- rence Increased: Ovarian, endometrial, and colon cancer; endometriosis; inflammatory bowel disease; PID; pregnancy; breast lesions; and benign abdominal masses (teratomas) 4 Laboratory Diagnosis: Chemistry, Immunology, and Serology 61 CALCITONIN (THYROCALCITONIN) • <19 pg/mL (SI: <19 ng/L) • Collection: Tiger top tube Increased: Medullary carcinoma of the thyroid, C-cell hyperplasia (precursor of medullary carcinoma), small (oat) cell carcinoma of the lung, newborns, pregnancy, chronic renal insufficiency, Zollinger–Ellison syndrome, pernicious anemia. If it is not within nor- mal limits, a corrected calcium can be roughly calculated by the following formula. Aldosterone decreases 2 h later from baseline in normals or essential hypertension, but does not suppress in pa- tients with aldosteronism. For renovascular hypertension, the PRA increases >12 ng/mL/h and an absolute increase of 10 ng/mL/h plus a 400% increase in PRA if pretest level <3 ng/mL/h and >150% over baseline if the pretest PRA was >3 ng/mL/h. Patient must be supine in a nonstimulating environment with IV access to obtain sample. Catecholamine Plasma (Supine) Levels Norepinephrine 70–750 pg/mL (SI: 414–4435 pmol/L) Epinephrine 0–100 pg/mL (SI: 0–546 pmol/L) Dopamine <30 pg/mL (SI: 196 pmol/L) Increased: Pheochromocytoma, neural CREST tumors (neuroblastoma), with extra- adrenal pheochromocytoma, norepinephrine may be markedly elevated compared with epi- nephrine. CHLORIDE, SERUM • 97–107 mEq/L (SI: 97–107 mmol/L) • Collection: Tiger top tube Increased: Diarrhea, renal tubular acidosis, mineralocorticoid deficiency, hyperalimen- tation, medications (acetazolamide, ammonium chloride) Decreased: Vomiting, diabetes mellitus with ketoacidosis, mineralocorticoid excess, renal disease with sodium loss CHOLESTEROL • Total • Normal, see Table 4–1; see also LIPID PROFILE/CHOLESTEROL SCREEN- ING, page 79, and Figure 4–4, see page 80. Levels <45 mg/dL associated with increased risk of CAD Increased: Estrogen (females), regular exercise, small ethanol intake, medications (nicotinic acid, gemfibrozil, others) Decreased: Males, smoking, uremia, obesity, diabetes, liver disease, Tangier disease Low-Density Lipoprotein Cholesterol (LDL, LDL-C) • 50–190 mg/dL (SI: 1. Can be seen in some normals and neonates COLD AGGLUTININS • <1:32 • Collection: Lavender or blue top tube Most frequently used to screen for atypical pneumonias. Complement C3 • 85–155 mg/dL, (SI: 800–1500 ng/L) Decreased levels suggest activation of the classical or alternative pathway, or both. Increased: RA (variable finding), rheumatic fever, various neoplasms (gastrointestinal, prostate, others), acute viral hepatitic, MI, pregnancy, amyloidosis Decreased: SLE, glomerulonephritis (poststreptococcal and membranoproliferative), sepsis, SBE, chronic active hepatitis, malnutrition, DIC, gram-negative sepsis Complement C4 • 20–50 mg/dL (SI: 200–500 ng/L) Increased: RA (variable finding), neoplasia (gastrointestinal, lung, others) Decreased: SLE, chronic active hepatitis, cirrhosis, glomerulonephritis, hereditary an- gioedema (test of choice). Complement CH50 (Total) • 33–61 mg/mL (SI: 330–610 ng/L) Tests for complement deficiency in the classical pathway. Increased: Acute-phase reactants (tissue injury, infections, etc) Decreased: Hereditary complement deficiencies CORTISOL, SERUM •8AM, 5. Organisms identified in- 4 Laboratory Diagnosis: Chemistry, Immunology, and Serology 65 clude Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae, and group B Streptococcus. CREATINE PHOSPHOKINASE (KINASE) (CP, CPK) • 25–145 mU/mL (SI: 25–145 U/L) • Collection: Tiger top tube Used in suspected MI or muscle diseases. Increased: Renal failure (prerenal, renal, or postrenal obstruction or medication- induced [aminoglycosides, NSAIDs, others]), gigantism, acromegaly, ingestion of roasted meat, false-positive with DKA Decreased: Pregnancy, decreased muscle mass, severe liver disease CRYOGLOBULINS (CRYOCRIT) <0. Should be collected in nonantico- agulated tubes and transported at body temperature. Positive samples can be analyzed for immunoglobulin class, and light-chain type on request. Increased: Serial measurements 10–14 days apart with a 4× increase in titers or a single 4 IgM >1:8 is suspicious for acute infection. Low-Dose Test: After collection of baseline serum cortisol and 24-h urine-free cortisol levels, dexamethasone 0. ERYTHROPOIETIN (EPO) • 5–36 mU/L (5–36 IU/L) • Collection: Tiger top tube EPO is a renal hormone that stimulates RBC production. Female Normal Values Follicular phase 25–75 pg/mL Midcycle peak 200–600 pg/mL Luteal phase 100–300 pg/mL Pregnancy 1st trimester 1–5 ng/mL 2nd trimester 5–15 ng/mL 3rd trimester 10–40 ng/mL Postmenopause 5–25 pg/mL Oral contraceptives <50 pg/mL Male Prepubertal 2–8 pg/mL Adult 10–60 pg/mL ESTROGEN/PROGESTERONE RECEPTORS These are typically determined on fresh surgical (breast cancer) specimens. The presence of the receptors is associated with a longer disease-free interval, survival from breast cancer, and increased likelihood of responding to endocrine therapy. ETHANOL (BLOOD ALCOHOL) • 0 mg/dL (0 mmol/L) • Collection: Tiger top tube; do not use alcohol to clean venipunc- ture site, use povidone-iodine Physiologic changes can vary with degree of alcohol tolerance of an individual. Vi- tamin B12 deficiency can result in the RBC unable to take up folate in spite of normal serum folate levels. Increased: Folic acid administration Decreased: Malnutrition/malabsorption (folic acid deficiency), massive cellular growth (cancer) or cell turnover, ongoing hemolysis, medications (trimethoprim, some anticonvul- sants, oral contraceptives), vitamin B12 deficiency (low RBC levels), pregnancy FOLLICLE-STIMULATING HORMONE (FSH) • Males: <22 IU/L • Females: nonmidcycle <20 IU/L, midcycle surge <40 IU/L (Midcycle peak should be two times basal level • Postmenopausal 40–160 IU/L • Collection: Tiger top tube Used in the workup of impotence, infertility in men, and amenorrhea in women Increased: (Hypergonadotropic >40 IU/L) postmenopausal, surgical castration, gonadal failure, gonadotropin-secreting pituitary adenoma Decreased: (Hypogonadotropic <5 IU/L) prepubertal, hypothalamic and pituitary dys- function, pregnancy FTA-ABS (FLUORESCENT TREPONEMAL ANTIBODY ABSORBED) • Normal = nonreactive • Collection: Tiger top tube FTA-ABS may be negative in early primary syphilis and remain positive in spite of ade- quate treatment. Positive: Syphilis (test of choice to confirm diagnosis after a reactive VDRL test), other treponemal infections can cause false-positive (Lyme disease, leprosy, malaria) FUNGAL SEROLOGIES • Negative <1:8 • Collection: Tiger top tube This is a screening technique for complement-fixed fungal antibodies, which usually detects antibodies to Histoplasma capsulatum, Blastomyces dermatitidis, Cryptococcus neo- formans, Aspergillus species, Candida species, and Coccidioides immitis. Increased: Zollinger–Ellison syndrome, medications (antacids, cimetidine, others) py- 4 loric stenosis, pernicious anemia, atrophic gastritis, ulcerative colitis, renal insufficiency, and steroid and calcium administration Decreased: Vagotomy and antrectomy GGT (SERUM GAMMA-GLUTAMYL TRANSPEPTIDASE, SGGT) • Male 9–50 U/L • Female 8–40 U/L • Collection: Tiger top tube Generally parallels changes in serum alkaline phosphatase and 5 -nucleotidase in liver disease.

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Brain damage from chronic the hangover order renagel 800mg with amex gastritis colitis diet, a condition characterized by headache quality 400 mg renagel gastritis diet , ethanol consumption can be especially severe in the nausea, sweating, and tremor. The fetal alcohol syndrome has three primary features: microcephaly, prenatal growth Treatment for Acute Intoxication deficiency, and short palpebral fissures. Other character- Generally, no treatment is required for acute ethanol in- istics include postnatal growth deficiency, fine motor toxication. Allowing the individual to sleep off the ef- dysfunction, cardiac defects, and anomalies of the exter- fects of ethanol ingestion is the usual procedure. A definite risk of producing Hangovers are treated similarly; that is, no effective fetal abnormalities occurs when ethanol consumption remedy exists for a hangover, except for controlling the by the mother exceeds 3 oz daily, the equivalent of amount of ethanol consumed. For example, prompt treat- ment is required if the patient is in danger of dying of Treatment for Alcoholism respiratory arrest, is comatose, has dilated pupils, is hy- pothermic, or displays tachycardia. The immediate concern in the treatment of alcoholics is Treatment for severe ethanol overdose is generally detoxification and management of the ethanol with- supportive. Once the patient is detoxified, long- lieved by intravenous administration of hypertonic term treatment requires complete abstinence, psychiatric mannitol. Hemodialysis can accelerate the removal of treatment, family involvement, and frequently support ethanol from the body. If ethanol is taken after disulfiram administration, blood acetalde- hyde concentrations increase 5 to 10 times, resulting in Alcoholism vasodilation, pulsating headache, nausea, vomiting, se- Alcoholism is among the major health problems in most vere thirst, respiratory difficulties, chest pains, orthosta- countries. In certain tive drugs, is expressed as drug-seeking behavior and is cases, marked respiratory depression, cardiac arrhyth- associated with a withdrawal syndrome that occurs after mias, cardiovascular collapse, myocardial infarction, abrupt cessation of drinking. The ethanol withdrawal acute congestive heart failure, unconsciousness, convul- syndrome is characterized by tremors, seizures, hyper- sions, and sudden death have been reported. Hepatic fatty infiltration and cirrhosis are common ticraving drugs, for example serotonin uptake inhibitors, 416 IV DRUGS AFFECTING THE CENTRAL NERVOUS SYSTEM dopaminergic agonists, and opioid antagonists. The only of the most abundant receptors in the CNS, and its dis- treatment that has shown considerable promise is one tribution within the brain reflects the pharmacological that uses the opioid antagonist naltrexone. High receptor densities in the extrapyramidal motor system and the cerebellum are consistent with the actions of cannabinoids on many MARIJUANA forms of movement. The effects of cannabinoids on cog- nition and memory may be due to the relatively dense The hemp plant, or cannabis (Cannabis sativa), contin- receptor populations in the hippocampus and cortex. The dried leaves and flowering tops of the medial striatum and nucleus accumbens suggests an as- plant are referred to as marijuana, and it is typically sociation with dopamine neurons hypothesized to me- smoked in pipes or rolled as cigarettes. Hashish is a solid black resinous material obtained from the leaves of the plant and is usually smoked in a pipe. Pharmacological Actions Central Nervous System Chemistry Marijuana produces a distinctive behavioral syndrome that is easily distinguished from that of most other The major psychoactive constituent in marijuana use is 9 drugs. The most prominent feature is the initial period -tetrahydrocannabinol (THC), the prototypical can- of euphoria, or high, which has been described as a nabinoid. Euphoria is fre- of cannabinoids, they lack behavioral activity with the quently followed by a period of drowsiness or sedation. Pharmacokinetic Aspects The subjective effects of marijuana vary from indi- 9 vidual to individual as a function of dose, route of ad- -THC is readily absorbed when marijuana is smoked. Motor coordination also may decrease, espe- dynamics of smoking (number of puffs, spacing, hold cially in situations requiring highly complex motor skills, time, and lung capacity) substantially influence how such as flying an airplane and driving an automobile. Although oral ingestion of mari- 9 Increased appetite is frequently attributed to smok- juana produces similar pharmacological effects, -THC ing marijuana. Impairment on particularly in treating emesis arising during chemo- various performance measures related to driving skills 9 therapy. This time discordance between blood concentrations of 9-THC and effects has The most consistent pharmacological effect produced made it difficult to establish a meaningful relationship by marijuana is tachycardia, which is closely associated between blood concentrations and effects. There is relatively lit- 9-THC is rapidly distributed to all tissues despite tle effect on blood pressure unless large quantities of being tightly bound by plasma proteins. Traces of 9-THC have been found vasodilatory, which results in the characteristic conjunc- in adipose tissue more than 30 days after the subject tival reddening following marijuana smoking.

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The urinary [Cl−] >10 mEq/L trusted 400mg renagel gastritis diet 2012, and these disorders do not respond to NaCl administration buy discount renagel 800 mg gastritis low stomach acid. RESPIRATORY ACIDOSIS: DIAGNOSIS AND TREATMENT Respiratory acidosis is a primary rise in pCO with a compensatory rise in plasma [HCO −]. Marked obesity (Pickwickian syndrome) 8 Treatment of Respiratory Acidosis Improve Ventilation: Intubate patient and place on ventilator, increase ventilator rate, reverse narcotic sedation with naloxone (Narcan), etc RESPIRATORY ALKALOSIS: DIAGNOSIS AND TREATMENT Respiratory alkalosis is a primary fall in pCO2 with a compensatory decrease in plasma [HCO −]. Iatrogenic mechanical overventilation Treatment of Respiratory Alkalosis Correct the underlying disorder. The second type of information gained from a blood gas level, in addition to acid–base results, pertains to the level of oxygenation. Usually, results are given as pO2 and oxy- gen saturation (See Table 8–1 for normal values in page 162). Oxygen saturation at any given pO2 is influenced by temperature, pH, and the level of 2,3-DPG as shown in Figure 8–4. Pneumothorax O2 dissociation curve of blood at 37°C 100 90 80 70 60 O2 affinity O2 affinity 50 (shift to right) (shift to left) 40 acidosis alkalosis hypoxemia hypothermia 30 fever banked blood increased decreased 20 2,3 DGP 2,3 DGP 10 0 0 10 20 30 40 50 60 70 80 90 100 110 120 Blood oxygen tension (pO2) FIGURE 8–4 Oxyhemoglobin dissociation curve. Congenital heart disease: Tetralogy of Fallot, transposition, etc 8 SAMPLE ACID–BASE PROBLEMS In each of the following examples, use the technique for blood gas interpretation on page 163 in this chapter to identify the acid–base disorder. Step 3: pCO > 44 and [HCO −] is not < 22, so it represents a respiratory acidosis. This patient has a chronic res- 3 piratory acidosis due to hypoventilation (simple acid–base disorder). Step 3: [HCO −] is < 22 mEq/L and pCO is not > 44, so this is a metabolic acidosis. This patient has a lactic acidosis following a car- diopulmonary arrest (simple acid–base disorder). This patient had a metabolic acidosis due to dia- betic ketoacidosis and a concomitant respiratory alkalosis due to early sepsis and fever (mixed acid–base disorder). Step 3: pCO < 36 and the [HCO −] is not >26, thus a respiratory alkalosis is present. This patient has a respiratory acidosis due to pregnancy and a relative secondary meta- bolic alkalosis due to vomiting. Because the actual bicarbonate was higher than expected, this must be a mixed metabolic gap acidosis and metabolic alkalosis. The patient has a metabolic gap acidosis from DKA and a metabolic alkalosis from the vomiting. Step 1: 17 mmol/L actual gap −10 mmol/L normal gap 7 mmol/L expected change in [HCO –] from normal 3 Step 2: 24 mmol/L normal [HCO–] 3 −7 mmol/L expected change in [HCO –] 3 17 mmol/L expected change in [HCO –] 3 Actual bicarbonate is 10 mmol/L and not the expected 17 mmol/L if there was a pure metabolic gap acidosis. Since the actual bicarbonate is lower than expected, there must be a 8 mixed metabolic gap acidosis and metabolic nongap acidosis. The patient has a metabolic nongap acidosis from diarrhea and a metabolic gap acidosis from the alcoholic ketoacidosis. In the absence of hypokalemia and with normal renal function, most of this is excreted in the urine. Potassium is easily interchanged between intracellular and extracellular stores under conditions such as acidosis. Potassium demands increase with diuresis and building of new body tissues (anabolic states). Routine administration is not needed in the absence of specific indications, such as parenteral hyperalimentation, massive diuresis, ethanol abuse (frequently needed) or preeclampsia. During starvation, caloric needs are supplied by body fat and protein; the majority of protein comes from the skeletal muscles. The administration of at least 100 g of glucose/d reduces protein loss by more than one-half. Virtually all IV fluid solutions supply glucose as dextrose (pure dextrorotatory glucose). COMPOSITION OF PARENTERAL FLUIDS Parenteral fluids are generally classified based on molecular weight and oncotic pressure. Colloids have a molecular weight of >8000 and have high oncotic pressure; crystalloids have a molecular weight of <8000 and have low oncotic pressure.

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Increased knowledge in this field should ally the number of negative episodes can be reduced renagel 800 mg discount treating gastritis over the counter. In time cheap renagel 800mg mastercard gastritis diet livestrong, these advances will improve the prac- The cytochrome P450 system is a group of related tice of medicine and become the standard of care. Stein, PhD 918 GALE ENCYCLOPEDIA OF GENETIC DISORDERS Phenotype see Genotypes and phenotypes Nerve cells have specialized extensions called dendrites and axons. Stimulating a nerve cell triggers nerve impulses, or signals, that speed down the axon. These nerve impulses then stimulate the end of an axon to release chemicals called neurotransmitters that spread IPhenylketonuria out and communicate with the dendrites of neighboring nerve cells. Definition Many nerve cells have long, wire-like axons that are Phenylketonuria (PKU) can be defined as a rare covered by an insulating layer called the myelin sheath. PKU is the most serious form of a class of nine levels in the blood and brain can produce nerve cells diseases referred to as “hyperphenylalaninemia,” all of with abnormal axons and dendrites, and cause imperfec- which involve above normal (elevated) levels of pheny- tions in the myelin sheath referred to as hypomyelination lalanine in the blood. This loss of myelin can “short circuit” PKU, mental retardation, is the result of consuming nerve impulses (messages) and interrupt cell communi- foods that contain the amino acid phenylalanine, which is cation. It patients who have not maintained adequate dietary con- is the most common genetic disease involving amino acid trol. PKU is incurable, but early, effective treat- PKU can also affect the production of one of the ment can prevent the development of serious mental inca- major neurotransmitters in the brain, called dopamine. PKU patients who do not consume enough tyrosine in Description their diet cannot produce sufficient amounts of dopamine. This is the only Some preliminary research suggests that nerve cells role of PAH in the body. A lack of PAH results in the of PKU patients also have difficulty absorbing tyrosine. Above normal who receive sufficient dietary tyrosine still experience levels of phenylalanine are toxic to the cells that make up some form of learning disability. Teratogens are any IQ (intelligence quotient) tests provide a measure of substance or organism that can cause birth disorders in a cognitive function. They generally very large molecules composed of strings of may require special tutoring and need to repeat some of smaller building blocks or molecules called amino acids. The body grams may experience problems with typical academic breaks down proteins from food into individual amino tasks such as math, reading, and spelling. Ten years of age seems to be an impor- sues, and are the key components of enzymes, antibodies, tant milestone for PKU patients. PKU and the human nervous system People with PKU tend to avoid contact with others, The extensive network of nerves in the brain and the appear anxious, and show signs of depression. KEY TERMS It is also interesting to note that people with PKU are less likely to display such habits as lying, teasing, and active Amino acid—Organic compounds that form the disobedience. There are 20 types of research findings are still quite preliminary and more amino acids (eight are “essential amino acids” extensive research is needed to clearly show how abnor- which the body cannot make and must therefore mal phenylalanine levels in the blood and brain might be obtained from food). Genetic profile Enzyme—A protein that catalyzes a biochemical reaction or change without changing its own PKU symptoms are caused by alterations or muta- structure or function. Mutations in the PAH gene prevent the liver from producing ade- Gene—A building block of inheritance, which quate levels of the PAH enzyme needed to break down contains the instructions for the production of a phenylalanine. The PAH gene and its PKU mutations are particular protein, and is made up of a molecular found on chromosome 12 in the human genome. Each gene is detail, PKU mutations can involve many different types found on a precise location on a chromosome. The term autosomal means that the gene for inheritance and expression of a genetic mutation. A recessive genetic trait, such as PKU, is one true or chronological age and multiplies that ratio that is expressed—or shows up—only when two copies by 100. A person with one normal and one PKU gene is Metabolism—The total combination of all of the called a carrier. A carrier does not display any symptoms chemical processes that occur within cells and tis- of the disease because their liver produces normal quan- sues of a living body.

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