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Lab Dx III Review for Final Exam

LAB Dx III Spring 2009 FINAL EXAM STUDY OBJECTIVES


Environmental Tox Testing

1. What can aid you in deciding appropriate testing for toxins?
--history (exposures)

2. What is the best test for accurate determination of total body heavy metal burden?
“No single test exists for accurate determination of the total body heavy metal burden” (though a provocative urine challenge test “gives best estimate of body burden”)

3. What are the specimens of choice for assessing short-term acute and chronic exposures to heavy metals?
Blood is the best specimen for assessing short-term acute exposure (see slide 12 for how acute)
Urine is best for chronic toxicity

4. Be familiar with the mechanisms of heavy metal toxicity
Mechanisms of metal toxicity usually multiple:
--Enzyme/cofactor inhibition or potentiation
--Disruption of membrane and other transport processes
--Decreases in neuronal function and nerve conduction
--Ability to bind to sulfhydryl groups on proteins and amino acids

5. Know the classic CBC picture of lead poisoning. What are the “normal” blood lead levels in children and adults? In Oregon, what do you need to do if a patient’s blood lead levels are above “normal?”
--Lead interferes with heme synthesis by diminishing delta-ALA dehydrase activity. This results in microcytic-hypochromic anemia with Basophilic stippling dt RNA accumulation in RBCs.
--“Normal” blood levels: Kids<10 ug/dl; Adults<25ug/dl
--In Oregon, blood levels in excess of normals must be reported to Oregon Health Division within one week

6. What should you do if hair analysis indicates high levels of toxic metals?
If hair analysis indicates high levels of toxic metals, you should follow up by blood or provocative urine testing.

7. What is the general principle behind “provocative challenge testing” for heavy metals? What is the route of excretion of the heavy metals with this method?
Provocative challenge testing involves administering a water soluble chelating agent (DMPS i.v. or DMSA p.o. or rectally) to draw the heavy metals out of their hiding places, back in to the blood and then out through the Kidneys.

8. What tests do you need to run prior to administration of DMSA? Why?
CMP, CBC and CCLR are required before administration of either DMSA or DMPS, to ensure kidneys are working.

9. What is the order of “binding affinity” of DMSA to heavy metals?
DMSA binds Pb>Hg>As>Cd>Ni. Whereas DMPS does NOT cross the blood brain barrier, DMSA might. In rats, DMSA was found to be the most efficient chelator for brain mercury.

10. What is the specimen of choice to assess the “natural” route of heavy metal excretion? What factors might influence the test results?
Fecal elimination is the #1 ‘natural’ route of excretion for most heavy metals, as metal forms complexes with glutathione in the liver, 90% of which are secreted into bile. Stool test results may be influenced by heavy metals in the diet that are being excreted without being absorbed.

11. What is the mechanism of toxicity for cholinesterase-inhibiting insecticides? What symptoms might you see as a result? In addition to “SLUDGE,” expect to see or hear such signs as miosis, muscle fasciculations, rales, wheezes, ↑’d bowel sounds. Patient may also report blurred vision due to spasm of ciliary muscles.
--Cholinesterase-inhibitors prevent acetylcholine breakdown-->acetylcholine buildup in synapses-->twitching, paralyzed breathing, convlusions, and sometimes death.
--SLUDGE: Saliva/sweating, Lacrimation, Urination, Diarrhea, Gastric motility (borborygmus), Emesis
--Cholinesterase-inhibitors can be found in organophosphate and carbamate pesticides.

12. How would you diagnose chlolinesterase poisoning? Be aware of factors that may influence the test results (other than the pesticide itself).
--Diagnose cholinesterase poisoning by testing RBC cholinesterase of whole blood for True Cholinesterase AND and plasma cholinesterase for “pesudocholinesterase”. Take a baseline when the worker has not been exposed to CI’s for at leaset 30 days; subsequent depression indicates a poisoning (15-25% depression → slight poisoning; 35-50% → severe poisoning).
-You can also find low Pseudocholinesterase with hepatitis, cirrhosis, malnutrition, chronic alcoholism and BCP use; low True RBC Cholinesterase with Hemolytic Anemia.
13. What specimens might you want to analyze for DDT and its metabolites? Why?
Blood and breast milk can be analyzed for DDT and DDE. Adipose readily stores DDT metabolites, so fat biopsies may be analyzed for DDE levels.
14. What is the specimen of choice for monitoring exposure to the herbicide glyphosate? Is this herbicide potentially carcinogenic?
Glyphosate (aka “Roundup”) is a non-selective, broad spectrum herbicide that is difficult to measure in environmental samples.
-24-hour urine levels are used to monitor exposure to glyphosate
-Non-Hodgkins Lymphoma patients were 2.3 times more likely to have had contact with glyphosate; Roundup also contains other substances known as Polyoxyethyleneamines which are contaminated with dioxane, a suspected carcinogen
15. What are the specimens of choice for determining exposure to chlorophenoxy herbicides? What time frame do you have for testing after exposure?
Chlorophenoxy herbicide (eg, Agent Orange) exposure is monitored for using Gas-liquid chromatography analysis of blood or urine samples and must be tested for ASAP because it will be excreted in 24-72 hours (but the DNA damages is long lasting)
16. What signs or symptoms might indicate solvent exposure? What is the main specimen of choice when looking for solvent metabolites? Be familiar with the metabolites of benzene, toluene, and ketones. Where are solvents typically stored in the body?
-Solvent exposure symptoms include
respiratory irritation (including pneumonitis and pulmonary edema),
eye irritation (burning, tearing, pain)
dermatitis(red, itchy, blistered skin dt breakdown of skin fats and oils dt acute contact w/solvent)
CNS depression (as though drunk; can progress to coma, convulsions, death)
Heart arrhythmia
Benzene exposure can cause aplastic anemia and leukemia
Vinyl chloride has been known to cause hepatic angiosarcoma
-Urine is tested for solvent metabolites
-Benzene: urinary phenol; aplastic anemia
Toluene: urinary hippuric acid
Ketones: aceto-acetic acid in urine/blood
-Solvents are typically stored in adipose
17. Why is it advisable to order chemistry testing in cases of methanol poisoning? What results would prompt you to consider this as a diagnosis?
-Methanol poisoning leads to severe metabolic acidosis, and so it is important to check arterial blood gases, serum electrolytes, BUN and creatinine, glucose, ketones and osmolarity. (Methanol levels can also be measure directly in the blood)
-??results to prompt diagnosis?
18. When might you suspect nitrate/nitrite toxicity? What happens when a person is over-exposed to these substances? What test would you order to assess this?
-Nitrate/Nitrate toxicity is assessed using Methemoglobin Blood Levels. The most common sources of nitrates/nitrites are wells contaminated from agricultural runoff, and those used to preserve meats.
-Sxs of nitrate/nitrite toxicity depend on blood levels of methemoglobin:

Methemoglobin conc. Clinical Findings
10-20% Central cyanosis or asymptomatic
20-45% CNS depression, dyspnea
45-55% Coma, shock, convulsions
>70% Death common

babies less than 1 year old are particularly susceptible, developing “Blue Baby Syndrome”; Nitrates/nitrites cause the formation of methemoglobin (Fe3+ instead of Fe2+), which holds O2 more tightly than hemoglobin, and so O2 is not readily delivered to tissues.

Essential Element Testing
19. Be able to ascertain the defining characteristics of “trace elements” & “macro-minerals”? Of the various specimens used to assess mineral status, which one is believed to provide the best correlation with nutritional status?
-Trace elements are required in very small amounts for proper functioning of the body (the 13 are Iron, Copper, Zinc, Selenium, Iodine, Silicon, Boron, Cobalt, Chromium, Molybdenum, Vanadium, Manganese, Nickel)
-Macro-minerals are found in total “body concentrations much higher vs. trace elements” The 6 macro-minerals are Calcium, Magnesium, Phosphorus, Sodium, Potassium and Chloride.
-“Intracellular mineral content may provide BEST correlation with nutritional status”
20. What are the hair analysis advantages & disadvantages?
-Hair Pros: sample is easy to obtain; fair screening took for specific essential mineral balance (can somewhat indicate storage over time) and of heavy metals; can be used to test Drugs of Abuse
-Hair Cons: Poor standardization between labs; easily contaminated by pools, dyes, product; perception as legitimate has been damaged by bad advertising; interpretation is not straight forward—highs or lows may not correspond to excesses and deficiency in the body;
21. Know the hair growth rate and understand when this occurs during the growth cycle.
-During the anagen phase, hair grows at 1cm/month
-Hair phases are
Anagen—growth phase—2-4 years
Catagen—transition phase—1-2 weeks
Telogen—resting phase—5-6 weeks
--then hair breaks off/falls out and a new hair begins to grow in anagen
22. Where is a hair sample best collected & what might you advise a patient to do before your collection? When is hair NOT suitable for analysis?
-Hair samples are best collected closest to the scalp, unless it may be contaminated in which case pubic hair may be used.
-Prior to collection, some labs recommend the use of “No more tears” shampoo x2 weeks
-Hair is NOT suitable for analysis if it has been dyed, permed, straightened or otherwise chemically treated.
23. Toxic elements in hair: Know that finding them in hair is NOT “hard and fast” evidence of causation of abnormalities. That understood, be familiar with associations for the following: aluminum in kids; mercury; lead; selenium; manganese.
-Aluminum is elevated in children with behavioral difficulties and in Alzheimer’s patients; Al tends to accumulate in bone and brain more so than in hair—this may depend on age of exposure, with more Al landing in bones during bone-building years
-Mercury levels are 2-3x higher in the hair of dentists and dental assistants than in support staff; hair Hg may correlate with # of amalgam fillings, and does correlate with fish congestion; Hg levels are also higher in MS patients relative to non-MS controls.
-Hair lead and cadmium correlate with reduced intelligence scores.
-Hair Selenium provides good reflection of dietary intake and body sufficiency; Se is required for glutathione production; low levels of Se are associated with lung and breast ca, and may reflect low iodine.
-Manganese is found high hair levels of patients suffering from ALS.
24. Know correlations between mercury and other hair minerals.
“Mercury in the body tends to make hair essential elements vary widely. Mercury is not excreted effectively when calcium levels are high in the hair.”
25. What causes high levels of calcium & magnesium in hair? What might low hair sulfur indicate?
-Patients with high P:Ca ratio showed hair Ca up to 3x normal
-Magnesium in the hair correlates with diet and supplementation levels. Increased levels reflect bone mobilizations. High levels have been reported in patients with dyslexia and Prader-Willi syndrome (in which the satiety center in the brain doesn’t work); decreased levels are linked to diabetic complications, autism and skin disorders
-Low hair Sulfur can indicate insufficiency in Phase II biotransformation sulfation reaction; reflect malabsorption; reflect insufficient intake of quality proteins.
26. Know the interpretations for hair zinc analysis, hair chromium analysis & hair rubidium analysis.
-High Zinc levels almost always reflect maldistribution of Zn or frank deficiency (note: Sudden Zn deficiency arrests hair growth); high zinc with low copper may indicate mineral displacement by mercury; high zinc correlated with elevated cholesterol
-Decreased Zinc hair levels mbdt prolonged Zn deficiency, which mb associated with dietary def, anorexia, vegetarianism, hyperactivity, age, atherosclerosis, poverty, hypogeusia, IDDM, beta-thal
-Chromium hair levels may be a useful indicator of body status: hair concentration is over 100x blood concentration, which is an easier level to measure
-Rubidium hair levels reflect intake and status in body tissues.
27. Know the best sample for measuring each of the following minerals: Copper, magnesium, potassium, zinc, manganese.
Best sample for measuring…
Copper: serum Ceruplasmin
Magnesium: WBC/RBC intracellular content
Potassium: RBC reflects tissue content, is a good indicator of total body stores
Zinc: WBC is best choice; serum is NOT a good indicator, and RBC is unreliable.
Manganese: whole blood—reflects soft tissue levels
28. Know how to interpret the “zinc tally” test.
With 10ml held in the mouth for 10 seconds, lack of taste or delayed taste suggests zinc deficiency (hypoguesia is a symptom of zinc deficiency); immediate taste suggests adequate zinc status. (Dr. W got more specific in class with the directions off the bottle. The immediate taste should be foul, like battery acid, to indicate adequate zinc; if you taste something immediately but it tastes like dirty water, that may still indicate inadequate zinc status.)

Therapeutic Drug Monitoring
29. Know what is meant by therapeutic window or therapeutic index. Why is it advisable to monitor drugs with a low TI?
-“The Therapeutic Index is the Ratio of the Median Toxic Dose to the Median Effective Dose; a narrow (low) T.I. means that the amount of drug that produces toxic effects is close to the dosage that exerts therapeutic effects”—and therefore they need to be monitored carefully, to keep the levels in therapeutic range but out of toxic range.
30. Know definitions for the terms half-life and steady state, and the implications of steady state. How many half-lives are required after starting drug therapy to achieve steady state?
-Half-life: time required for a 50% reduction in serum drug concentration
-Steady state: occurs when the rate of drug entering the body equals the rage of drug elimination
-Typically, 4 to 5 half-lives are required after starting drug therapy to achieve steady state
31. Know why one would want to monitor therapeutic drugs and when you would start doing so.
One would want to monitor therapeutic drugs…
-when there is a “narrow therapeutic window”;
-if the therapeutic effect is not met with standard dosing;
-if toxicity symptoms occur on standard dosing;
-to ensure that adequate blood concentrations are reached
-to determine if a disease is present that is known to affect drug absorption, protein binding,
metabolism or excretion
-to reveal possible drug interaction
-in combination drug therapy (eg, multiple anticonvulsants at same time)
-to reveal noncompliance
-for medico legal considerations (amingoglycoside antibiotics)?
-when there is a change in patient status or dosage
I’m not sure if that answers the question or not. I can’t find anything on “when you would start doing
so” apart from the above indications. The “why” is encompassed there too…
32. Know the difference between peak and trough drug levels, and the significance of elevated or decreased peak and trough drug levels.
-Peak levels correlate with toxicity. They are usually reached 1-2 hours p p.o., 1 hour p IM or ½ hour p IV
-Trough levels correlate with proper therapeutic ranges (if blood level remains w/in the therapeutic range). Trough is usually reached 15-30 minutes before the next scheduled dose. If trough level is in toxic range, this is a strong indication of toxicity
-Trough should be kept IN the therapeutic range; Peak should be kept OUT of the toxic range (ideally, both should be within the therapeutic range)
33. Know factors that influence blood levels of therapeutic drugs.
-route of administration: IV>IM>PO in terms of speed
-drug absorption—altered by GI motility, pH, malabsorption, food interactions, etc.
-Drug transport—plasma protein binding; protein-bound drugs are not metabolically active
-Drug uptake by target tissues—molecules must reach target site and penetrate cells
-Drug distribution—lipid soluble vs. non lipid soluble
-Drug tissue utilization
-Drug metabolism (wholly or partly detox’d by liver, fast vs. slow metab; rates of metab are critical!)
-Drug excretion, usually by kidneys
-Dosage—size and frequency
-Patient age (infants and adults given same amt per wt unit; kids get 2x that; elderly get less)
-Wt based dosing more effective than arbitrary, fixed dosage schedules
-Drug interactions
-Peak or trough (residual) levels
-Pt compliance, or lack thereof
-foods accelerating or decelerating p450 system enzymes (eg, grapefruit)
34. Know the timing of sample collection for therapeutic drug monitoring for toxic effects and therapeutic effects.
?? I’m not entirely sure what she’s getting at with this one, but (slides 12 and 15):
-“Blood draw is a ‘snapshot’ of the moment; if toxicity symptoms develop, best to get sample then, if possible. Exception! Digoxin is best 6-8 hours after last dosage”
-“BOTH peak and trough should be within the therapeutic range”
Peak is associated with toxicity, reached between ½-2 hours after dose depending on how administered
-you don’t want the peak in the toxic range
Trough is associated with proper therapeutic range, usually reached 15-30 min before next dose is due
-you don’t want the trough below the therapeutic range
35. Know what parameters are noted to insure specimen integrity for toxicology
-Exact drug or drugs to be assayed
-patient age AND WEIGHT
-time elapsed from last dose to sample collection
-drug dose
-route of administration
-other: reason for assay, list of other meds taken
36. What is the role of the liver and kidneys in processing drugs.
?? the liver metabolizes drugs; the kidneys excrete them and their metabolites
37. Know how one drug’s effects on the liver might affect liver processing of other drugs. How might kidney disease and hypoalbuminemia affect drug levels?
-Drugs can either induce or inhibit the activity of CYP enzyme responses; be aware that a newly introduced drug, then, may end up decreasing or increasing the serum concentration of the first drug
-Hypoalbuminism will increase the concentration of “free” active drug, as most drugs bind to plasma proteins to some extent.
-Elimination of drugs is primarily renal, and so may be compromised by impaired renal function.
38. Be able to match the active ingredient with the drug of abuse being tested.
-Marijuana: THC
-Cocaine: benzoylecgonin metabolite
-PCP (Phencyclidine): “drug or metabolites detectable in urine 6-18 hours after use”
-Amphetamines: also doesn’t mention a different active ingredient
-Opiates (methadone, morphine, heroin, codeine): conjugated glucuronide metabolites
39. Know that most labs measure TOTAL drug concentrations, and why those with “normal” drug levels may experience toxic effects.
-Most labs measure Total drug concentration (free+protein-bound); in hypoalbuminism, a greater proportion of the drug will be unbound (=active) and so pts may experience toxic effects with “normal” levels.
40. Know the specimen of choice for screening for drugs of abuse and the means of assuring specimen integrity and confirmation of + screens. Know the average length of time that drugs of abuse can be detected in the specimen of choice.
-Screening for drugs of use or abuse is usually done on urine. Specimen may be obtained hours or days after drug use; drug metabolic products exist in urine at detectable levels for longer periods than in blood.
-Assure specimen integrity by recording: temperature, specific gravity, creatinine level, color
-Positive screens must be confirmed by another equally accurate method, and usually by a diff. facility.
-I don’t think they care for specifics, but here they are:
Marijuana appears in 1 hour, persists 1-3 and up to 60 days
Cocaine appears in 1-4 hours, persists 2-3 and up to 20 days
PCP appears 6-18 hours, for up to 3 days
Amphetamines appear in 3 hours, persist for 1-2 days
Opiates appear within 2 hours, persist for 2-3 days
41. Know factors that can interfere with drug screening for opiates.
OTC pain relievers, cough suppressive medicines containing codeine
42. What is the sample of choice for determining when a person last used cocaine?
Serum levels must be used to determine timing of cocaine use.
Pregnancy & Neonatology
43. Measurement of HCG is the test of choice for “diagnosing” pregnancy. Where is HCG produced? When is HCG detectable in serum and urine?
-hCG is produced by the blastocyst w/in 24 hours of implantation/7 days post conception
-within 1-2 days after implantation, serum hCG levels elevate above 5IU/L (= + preg test); + Urine preg tests occur 3-4 days after implantation; serum levels are higher than urine levels for about the first month
44. Know the interfering factors for urine pregnancy testing.
-False negatives may occur with very dilute urine and too early in pregnancy
-False positives may occur with proteinuria, hematuria, excess pituitary gonadotropin; hCG injections
45. How reliable are serum and urine tests for diagnosing ectopic pregnancy? Know the normal rate of increase for serum quantitative HCG. How might that be different in cases of ectopic pregnancy? What is the significance of decreasing quantitative serum HCG levels? When would you expect HCG levels to return to normal after an ectopic pregnancy is removed?
-Urine and qualitative serum tests will detect pregnancy when hCG reaches a certain low level (urine tests will be positive in 65-95% of ectopic pregnancies), but cannot diagnose ectopic pregnancy. Qualitative serum hCG, though, can be useful to evaluate the integrity of a pregnancy
-Normally, hCG levels will double every 48 hours; suspect ectopic pregnancy with < 66% increase in 48 hours
-Decreasing quantitative hCG levels indicates diminished viability of the placenta, as in threatened miscarriage or embryonal/fetal demise
-“Following removal of ectopic tissue, hCG levels should return to <5 IU/ml within 4 weeks”
46. What are some other causes of elevated HCG levels & just how elevated are they?
Tumors (testicular seminoma, ovarian dysgerminoma, some lung/stomach/pancreas neoplasms)
In Gestational Trophoblastic Diseases (eg, Hydatidiform mole, Choriocarcinoma), will see hCG levels 3-100x greater than nml pregnancy
47. If you compared the results of a Hgb, HCT, and comprehensive metabolic panel (CMP) pre-conception to those during pregnancy, what changes would you expect to see? (Hemodilution versus hemoconcentration)
**depends in part on when in pregnancy we’re talking about! According to these notes…:*
-early pregnancy blood volume increase may dilute: lower Hgb, HCT, BUN, Creatinine and albumin
-after the 24th week gestation, often see elevated blood glucose levels
-later in pregnancy, with adequate protein intake, BUN may increase (may also increase with HTN post 20th week gestation, to reflect renal insufficiency)
48. Considering the incubation period for hepatitis, is it possible for a woman with a negative HBsAg test to be infected with the Hepatitis B virus?
Yes. Incubation period is 5 weeks to 6 mos, so recent exposure may not be seen
49. Know when the various types of HDN manifest (e.g., first pregnancy, second, etc.). What is the main cause of Hemolytic Disease of the Newborn today?
-HDN due to Rh incompatibilities (Rh- mom; Rh + fetus) affects 2nd and future pregnancies
-HDN due to “unexpected antibodies” like anti E, anti-Kell, anti-Duffy can occur in first pregnancy
??main cause of HDN today??
50. Why are urine dipstick tests done during prenatal visits? What should you do if the dipstick reading shows > protein?
??-urine dips are done in-office to check for glucose, protein, urinary tract infection
??-same as if woman was not pregnant? Repeat the test, then figure out why it’s high?
51. When is the glucose challenge screen for gestational diabetes performed? Know the criteria for proceeding with a full OGTT & diagnosis.
-Gestational DM Screen is done at 24-28 weeks gestation.
-Mom drinks 50gm glucose load; blood is drawn 1 hour later. If glucose is >140mg/dl, require 3-hour OGTT.
-with 3-hour OGTT: obtain FBS; drink 100gm glucose; draw blood hourly x3 hours.
-GD cutoff levels: Fasting> 105mg/dl;
1-hour > 190
2 hour 165
3-hour > 145 mg/dl
Dx based on fasting > 105, any 2 hourly values > cutoffs, or any value > 200mg/dl
52. At what point during pregnancy are Group B Strep cultures collected?
35-37 weeks
53. What is the purpose of performing Triple Screens and Quad Screens? When is it collected? What is the most common reason for increased AFP?
Triple Screen and Quad Screen are done at 16-18 weeks gestation to asses risk of Neural Tube Defects, Down’s Syndrome/Trisomy 21 & Trisomy 18. AFP is increased in neural tube defects, and can also be increased in multiple pregnancies, but the most common reason for increased AFP is underestimation of fetal gestational age.
54. What is the pH of vaginal secretions vs. Amniotic fluid & why is this valuable?
pH can be used to determine if watery discharge is amniotic fluid or vaginal secretions
vaginal secretions are acidic, 4.5-5.5; amniotic fluid is alkaline, 7.0-7.5
55. When would you order ABO, Rh, and Direct Coombs testing on neonates?
ABO always determined on babies born to O moms
Rh always performed on babies born to Rh negative moms
Direct Coombs (aka DAT) should be done on babies in above categs, or in any case of neonatal jaundice
56. What conditions result in neonatal jaundice? What bilirubin values are associated with kernicterus?
-Physiologic neonatal jaundice occurs when the liver is immature, lacking enzymes for bilirubin conjugation
-total bilirubin must be kept below 15mg/dl to avoid kernicterus and mental retardation
57. Know specifics for neonatal PKU & thyroid function testing, including where to collect the samples. What can cause false positive PKU testing?
-PKU test is performed on a heel stick blood sample, 3 days after birth, and preferably after the infant has been fed milk; this may be false positive in premature infants and invalid in babies less than 5lbs. If blood test not done in the hospital, uring PKU can be done after 6 weeks of age
-T4 levels are tested at same time as PKU, on same heel-stick; at 3 days, T4 should be 11-22ug/dl
58. Pregnancy Induced hypertension is now called? What are the symptoms in a pregnant woman?
“Gestational Hypertension”
Mild: high BP, water retention; Severe: h/a, blurred vision, inability to tolerate bright light, fatigue, N/V, urinating small amounts, pain in the URQ, SOB, tendency toward easy bruising

Pulmonary Function Tests & Oxygen Saturation
59. What are the indications for pulmonary function testing?
-preoperative evaluation of respiratory status;
-dx of pulmonary disease (obstructive vs. restrictive);
-quantifying pulmonary disability;
-managing patients with known pulmonary disease
60. What do the FVC and FEV1 tests measure? How can you be sure the patient is performing maximum inspiratory and expiratory efforts?
FVC is maximum volume forcefully exhaled after maximal inspiration
FEV1 is volume of air forcefully exhaled in one second
-?to ensure pt is performing maximal efforts, repeat test 3 times?
61. Know the changes in spirometry tests for obstructive vs. restrictive lung diseases. Know examples of each type of lung disease.
-Obstructive lung disease: can’t get air out, e.g. asthma, chronic bronchitis
FVC shows reduced flow rates and normal lung volumes, but with reduced FEV1
-Restrictive lung disease: can’t get as much air in; mbdt biologic agents (TB, virus, mycoplasma), physiologic agents (radiation, gasses, fumes), restrictive ventilator function (asbestosis, other scarring-type diseases)
FVC is decreased, but flow rates (including FEV1) are normal


Celiac, Saliva & Miscellaneous
1. Urinary Indican Testing: Is useful for indicating what?
Intestinal dysbiosis
2. What three serological markers are used to screen for Celiac disease?
-Tissue Transglutaminase IgA (tTG)
-Anti-Endomysial Ab (EMA)
-Antigliadin Ab (AGA)
3. What HLA marker is used to diagnose Celiac disease?
HLA DQ2 (and DQ8)
4. What immunoglobulins are involved in the pathogenesis of Celiac?
IgA and IgG—not IgE
5. What dermatologic skin manifestation is seen with Celiac, what increased malignancies?
Dematitis Herpetiformis
Increased rates of:
Adenocarcinoma of the small intestine (by 33x)
Thyroid ca (23x)
Esophageal ca (11.6x)
Non Hodgkins Lymphoma (9.1x)
Melanoma (5x)
6. How do you diagnose gluten allergy vs. Wheat allergy?
--as the notes have it laid out is below; but is that right? Or can one have an IgE allergy to gluten, and an IgG allergy to wheat, too?--
Wheat allergy is an IgE diagnosed with RAST testing; see classic allergy-anaphylaxis signs
Gluten allergy is IgG; may see eosinophilic gastritis; may be called “gluten intolerance”
7. ASI: How many cortisol levels are taken throughout the day? When is the lowest and highest natural cortisol level?
?? not in our notes? Highest in the morning, lowest at midnight
8. ASI: What is Pregnenalone steal?
??(not in our notes?) when pregnenolone is shunted to make stress hormones instead of sex hormones

Endocrine Part 3: Menstrual Cycles
1. What is the significance of low estrogen levels during the follicular phase of the cycle?
E2 secretion is stimulated by pituitary gonadotrophins FSH and LH. E2 in the follicular phase is a direct marker of follicle quality.
2. What is the significance of elevated estradiol levels in males?
A tumor of the testicles may elevate estradiol in males
3. How do estrogen levels influence secretion of LH? How do the LH & FSH levels differ in primary & secondary hypogonadism? In infertility?
-Via hypothalamic feedback, prior to ovulation, high estrogen levels increase LH (positive feedback); after ovulation, rising estradiol and progesterone levels inhibit LH release (negative feedback) {slide 12}
-In primary hypogonadism, FSH and LH will be high (trying to get the ovaries to respond)
-In secondary hypogonadism LH and FSH are low.
-In infertility, a low serum LH to FSH ratio on day 2 or 3 of the menstrual cycle may be an early biomarker of poor ovarian response.
4. How do FSH & LH levels change after menopause? At what point of a “normal” menstrual cycle would FSH & LH levels be the highest?
-In menopausal women, “a high serum FSH to LH ratio has been observed”. *note that the FSH and LH
have switched in their spots in the ration relative to infertility; in other words, I think we see the same
thing in both of these—a high FSH to LH OR a low LH to FSH. Thoughts, anyone?
-In a normal cycle, FSH and LH are highest midcycle, just before ovulation.
5. What are the indications for testing progesterone? How do the levels change over the course of a “normal” menstrual cycle? What happens to progesterone production in anovulatory cycles?
Test Progesterone to
-confirm ovulation in infertility therapy
-detect defects in the luteal phase
-monitor progesterone replacement therapy
-with hCG, to identify ectopic pregnancy
-Progesterone peaks in the luteal phase (second half of cycle), decreasing approximately four days prior
to menses. In pregnancy, it remains elevated to maintain the fetus.
-In anovulatory cycles, progesterone isusually low.
6. What are the effects of increased Prolactin levels? What difference in prolactin levels might be seen between nursing & non-nursing mothers?
-Prolactin levels climb during pregnancy to suppress gonadal function and allow the production of milk
-Notes say, “during pregnancy, prolactin levels climb steadily to 10-20x nonpregnant levels; levels drop
after pregnancy”

7. How might decreased LH levels influence testosterone levels? What are potential causes of increased testosterone levels in women? What changes might occur in such women?
-LH stimulates Leydig Cell production of testosterone—so decreased LH may lead to decreased testosterone levels.
-In women, may see increased testosterone with PCOS, ovarian tumors, adrenal tumors, and Cushing’s syndrome. This can lead to virilization (clitoral enlargement, increased muscle strength, acne, hirsutism, frontal hair thinning, deepening

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