Adv chemistry exam 2

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Thyroid anatomy:
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TSH vs fT4 graph
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Female pituitary & sex steroids through course of menstrual period, and pregnancy
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Primary adrenal Insufficiency:
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Cushing’s disease
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cushing's disease
supraclavicular fat deposits (buffalo hump)
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cushing's disease
moon face (corticosteroid-induced lipodystrophy)
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Grave’s disease
primary hyperthyroidism
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thyroid eye disease
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Aromatic steroid hormones
cholesterol, progesterone, estrone, androstenedione, testosterone, 17B-estradiol
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Hypothalamic-Pituitary portal circulation
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What pituitary hormone in excess causes goiter?
Prolonged elevation of TSH (thyroid stimulating hormone) levels due to iodine or hypothyroidism
What pituitary hormone deficiency causes adrenal atrophy and failure?
Deficiency in production of ACTH (adrenocorticotropic hormone)
Anterior pituitary hormones:
SH (Thyroid-stimulating hormone), ACTH (adrenocorticotropic hormone), HGH (Human Growth hormone), LH (Luteinizing hormone), FSH (stimulating follicle hormone), PRL (prolactin)
Posterior pituitary hormones:
Oxytocin, antidiuretic hormone (arginine vasopressin)
Most common two pituitary adenomas
Somatotrophs Growth Hormone Prolactin
Effect of hyperprolactinemia in males and females
Suppresses ovulation in both genders - Males: infertility, lactation in male, breast development - Females: infertility, menstrual irregularity
Negative feedback players on TRF/TSH & ACTH
TRF/TSH: Triiodothyronine (T3) ACTH: Cortisol
Components of POMC
Secretion of ACTH and melanocyte stimulating hormones. Y-MSH, ACTH (a-MSH and CLIP), and B-Lipotropin (Y-lipotropin (B-MSH), B-endorphin) ACTH secreted as part of Proopiomelanocortin (POMC) precursor with melanocyte stimulating hormones
Function of thyroglobulin in physiology & thyroid cancer
Synthesized by follicular cells Thyroglobulin (TG): useful as a post-treatment tumor marker of residual thyroid cancer Useful tumor marker for post-treatment for differentiated thyroid cancer (recurrence)
ID Most potent thyroid hormone & most potent androgen
Thyroid hormone: T3 (Triiodothyronine) Androgen: Dihydrotestosterone (DHT)
Match receptor type (Tyrosine Kinase)
T3 (Triiodothyronine)
Match receptor type: GCPR (G-protein coupled receptor)
trophic hormones – TSH (Thyroid stimulating hormone)
Match receptor type: Nuclear Steroid (glucocorticoid receptor
cortisol, thyroxine (T4), Triiodothyronine (T3)
What laboratory test(s) aid in identifying Congenital Hypothyroidism
Spot test for babies
What laboratory test(s) aid in identifying Chronic lymphocytic (Hashimoto’s) thyroiditis
autoantibody panels: serum anti-TPO, blocking TSIs or less sensitive anti-TG -- Anti TSH receptor antibody panel, Anti TPO, anti-thyroglobulin
What laboratory test(s) aid in identifying Graves’ disease
Autoantibody TSI, Antibodies screen or panel. Includes some of Hashimoto’s tests like Anti-TSH receptor antibody panel, Anti-TPO, anti-thyroglobulin test
What laboratory test(s) aid in identifying Subclinical hypothyroidism
perform a panel for T3, T4, TSH. Results Normal T3 and T4, high TSH
What laboratory test(s) aid in identifying Cushing’s Syndrome and Diseases
-Disease due to pituitary adenoma (Secondary cause of cortisol excess). -Syndrome caused by cortisol excess from Stress, Cushing’s disease (cortisol excess from pituitary adenoma), Cushing’s syndrome (cortisol excess from any cause), Adrenal adenoma, Ectopic ACTH syndrome (paraneoplastic syndrome)
What laboratory test(s) aid in identifying Primary Adrenal Insufficiency (Addison’s disease)
-Cosyntropin Stimulation test (Cosyntropin is hR ACTH fragment. Low dose stimulation (1ug) elicits cortisol peak of >18 ug/dL. (Used for suspected cortisol insufficiency) -Dexamethasone suppression test (used for suspected cortisol excess)
What laboratory test(s) aid in identifying 21-hydroxylase (Congenital Adrenal Hyperplasia)
elevated 17-beta-hydroxyprogesterone levels, androgen, and cortisol
What laboratory test(s) aid in identifying Growth Hormone deficiency
provocative testing: stimulation tests using insulin-induced hypoglycemia or GHRH or suppression test. low IGF-1 (insulin-like growth factor-1 – surrogate marker – synthesized by liver). -IGF-1 assay is preferred for GH deficiency or excess. -GH secretion by pituitary adenoma: 75g oral glucose load suppression – adenoma not suppressed
Thyroid storm (Thyrotoxic crisis):
heart - acute exacerbation of thyrotoxicosis and presenting cardiac abnormalities.
Low T3, Low T4, high TSH. Severe hypothyroidism, Unresponsive hypometabolic state. Treatment: replacement hormone (levothyroxine).
Adrenal crisis (adenosine crisis)
hypoglycemia, hyperkalemia, mineralocorticoid deficiency, fluid imbalance.
Primary hyperthyroidism (Grave’s disease)
thyroid stimulating immunoglobulins (autoantibodies -TSI) activate TSH receptors causing over secretion of T4 and T3. Low TSH.
Secondary hyperthyroidism
pituitary function issue. Decreased TSH
Tertiary hyperthyroidism
hypothalamic issue. Decreased TSH.
Clinical findings of primary, secondary, and tertiary hyperthyroidism
anxiety, emotional lability, weak, tremor, palpitations, heat intolerance, increased perspiration, weight loss despite normal or increased appetite (thyroid storm/thyrotoxicosis
lab tests for primary, secondary, and tertiary hyperthyroidism
low TSH, overt hyperthyroidism <0.05 mU/L. TSH levels suppressed by feedback loop cause high thyroid hormone. Diagnoses by radioiodine uptake
Primary hypothyroidism
increased serum TSH. Low Free T4
Secondary hypothyroidism
due to pituitary TSH deficiency. TSH normal or low. FT4 low.
Tertiary hypothyroidism
due to hypothalamic TRH deficiency
Clinical findings of primary, secondary, and tertiary hypothyroidism
fatigue, cold intolerance, weight gain, constipation, dry skin, myalgia, menstrual irregularities, bradycardia, hypertension, delayed relaxation phase of deep tendon reflexes (myxedema coma)
lab tests for primary, secondary, and tertiary hypothyroidism
elevated TSH, low Free T4. Majority of patients with Hashimoto’s (autoimmune thyroiditis) have elevated thyroid peroxidase (TPO) autoantibodies
Primary adrenal insufficiency (Addison’s disease)
deficiency in glucocorticoids or mineralocorticoids resulting in adrenocortical insufficiency resulting in destruction or dysfunction of Cortex. Produces renal wasting and potassium retention leading to severe dehydration. Hypotension, hyponatremia, hyperkalemia, and acidosis
Secondary adrenal insufficiency
deficiency in secretion of pituitary ACTH (adrenocorticotropic hormone). Caused by exogenous glucocorticoid therapy.
Tertiary adrenal insufficiency
deficiency in secretion of corticotropin-releasing hormone (CRH) from hypothalamus.
clinical findings in adrenal insufficiency
weak and fatigue, anorexia, weight loss, GI issues, nausea, vomiting, hyperpigmentation
lab tests in adrenal insufficiency
Cosyntropin stimulation test and rapid ACTH stimulation test. Hypoglycemia, hyperkalemia, hyponatremia, hypotension.
Cushing’s syndrome
from any cause including stress
Cushing’s disease
cortisol excess from pituitary adenoma, ACTH
clinical findings in cushing's
striae, supraclavicular and other fat deposits (buffalo hump, moon-face), delayed wound healing, impaired immune response.
lab tests for cushing's
Plasma ACTH, salivary, and 24 hr urinary cortisol, dexamethasone suppression test
21-Hydroxylase deficiency (CAH)
over secretion of adrenal androgens in females
clinical signs of 21-Hydroxylase deficiency (CAH)
females: excess adrenal androgens, virilization of fetus due to androgen excess, acne, hirsutism, clitoromegaly. males: (Hercules)
tests for 21-Hydroxylase deficiency (CAH)
neonatal testing of elevated 17-beta-hydroxyprogesterone levels
Cosyntropin stimulation test
Cosyntropin is hR ACTH fragment with biological activity towards adrenal receptors. Low dose stimulation elicits cortisol peak >18 ug/dL in 1-2 hrs.
Dexamethasone suppression test
has potent negative feedback on ACTH release. High dose: 8 mg, most people with Cushing’s disease suppress, those with ectopic ACTH syndrome do not. Low dose: 1mg, AM cortisol >14, Cushing’s syndrome suspected.
Thyrogen stimulation test
synthetic TSH given to stimulate thyroid and unmask residual cancer
Provocative test
for growth hormone excess and deficiency – suppression and stimulation GH secretion by pituitary adenoma: 75g oral glucose load suppression – adenoma not suppressed GH deficiency: stimulation tests using insulin-induced hypoglycemia or GHRH
Iodine Deficiency
causes goiter (enlargement) – hypothyroidism – main one
Rate limiting step in steroid biosynthesis induced by ACTH
Conversion of cholesterol to Pregnenolone
Identify TPO inhibitors
Methimazole Propylthiouracil (PTU)
Liver failure
low TBG, low SHBG, low CBG
Chronic illness
low SHBG, low CBG, low TBG
high TBG, high SHBG, High CBG
Total hormone levels
low TBG, low CBG, low SHBG cause low total hormone total T4 less informative than free T4
Tumor marker for medullary Thyroid Cancer
Salivary Cortisol:
used for accurate free cortisol levels in patients with abnormal serum-binding proteins. best in sensitivity and specificity for Cushing’s syndrome. Not normal nadir for people with Cushing’s
24-hr urinary Free cortisol tests
diagnosis of Cushing syndrome. Great for cortisol excess – poor for cortisol deficiency (adrenal insufficiency) – lacks sensitivity at low levels because low cortisol excretion can be found in normal levels of urine
Thyroid hormones
T3 and T4 bound by albumin, TBG and Transthyretin. Free (unbound) TH are biologically active in combination with TH nuclear receptors and feedback loops. Responsible for oxidative metabolism at acceptable level for life – temperature, fever (metabolism high)
cortisol bound to albumin and CBG with free cortisol circulating. Plasma free cortisol is a biologically active cortisol regulated for ACTH
Diurnal rhythm of testosterone
highest levels early morning lowest levels at midnight
Diurnal rhythm of Cortisol
peak early morning. - 8 AM cortisol: 10-20 ug/mL. - 4PM cortisol: 3-10 ug/mL. - During sleep: <5 ug/mL
Diurnal rhythm of ACTH
peak early morning. - 8AM ACTH: 10-50 pg/mL. - 4PM ACTH: <20 pg/mL. - During sleep: 5-10 pg/mL
Biochemical markers of Pheochromocytoma & Paragangliomas
Normal doubling time of hCG in first trimester v. ectopic pregnancy
First trimester: 2-3 days (doubling) Ectopic pregnancy: does not meet doubling time criterion – flat line
urinalysis screening
Neural tube closure defects
screening at 15-20 gestation. Alpha-fetoprotein measured first in maternal serum (MSAFP).
Fetal lung maturity
lecithin-sphingomyelin ratio (L/S ratio) (2:1) indicator. Phosphatidyl choline/glycerol (PC) another indicator (delayed in maternal DM). Thin layer chromatography detection
Differentiating urine from amniotic fluid
creatinine levels lower in amniotic fluid than urine. Fern test. pH (amniotic fluid 7.1-7.3, urine 4.5 – 6.0)
Cell free DNA screening (cf-DNA)
ratio of cell-free DNA from fetus and mom compared to determine trisomy Also determines gender of the fetus and X/Y chromosomal abnormalities
Trisomy 21:
Down syndrome
Trisomy 18
Edwards syndrome
Trisomy 13
Patau syndrome
TLC (Thin Layer chromatography)
stationary phase: thin layer (coated plate) hydrophobic or hydrophilic stationary phase mobile: solvent that mixes up the liquid phase
GC (Gas chromatography)
stationary phase: capillary columns, coils can be packed with material (inside the column) mobile phase: volatile gas (hydrogen) affinity for either stage a compound that has equal affinity for both stages
which of the following pathways is responsible for maintaining the change in water balance (increase in volume)
renin angiotensin aldosterone axis
method for neonatal screening tests
tandem mass spectrometry (MS/MS)
Identify major indications for monitoring therapeutic drugs
Compliance: medication has adverse effects toxicity levels may be close to therapeutic ranges (Digoxin, lithium)
When should peak and trough drug levels be collected
peak: above minimum 15-30 minutes after intravenous injections or infusions 30-60 minutes after intramuscular injections 1 hours after drug taken orally trough: below maximum -immediately before next dose is given
Preferred methods for detecting aspirin, ethanol, and alcohols other than ethanol
Can be measured by enzymatic technique exploiting NADH production by ADH Or identified and quantified by Gas chromatography
major metabolites of methanol
formic acid
major metabolites of ethylene glycol
glycolic acid oxalic acid
major metabolites of isopropanol
major metabolites of ethanol
acetaldehyde acetate
lethal ethanol concentration
50-100 mL 300-500 mg/dL
lateral flow immunoassay
-sample pad is the first stage of the absorption process -conjugate pad stores conjugated labels and antibodies will get sample -binding reagents on nitrocellulose membranes will bind to the target -colored lines will form -sample will pass through membrane into absorbent pad -absorbent will absorb excess samples
Volume of distribution
relative proportion of drug in plasma, target tissues and organs. Volume of plasma into which a fixed concentration of drug is dissolved
MEC (minimum effective concentration)
minimum plasma concentration of a drug needed to achieve sufficient drug concentration at the receptors to produce desired pharmacologic response
MTC (Maximum therapeutic concentration)
highest dose of drug or treatment that does not cause unacceptable side effects
Peak level
highest level of drug in blood
Trough level
lowest level of drug in blood – occurs after drug has been broken down and metabolized by the body
altering one or more functional groups of a chemical compound into similar (derivative) compound
Retention time
ime that a solute spends in column or time spent in stationary or mobile phases
M/Z ratio (mass to charge ratio)
ratio of an ion’s mass to its charge