front 1 purpose of sertoli cell | back 1 testis formation and spermatogenesis |
front 2 feedback loop from sertoli cells, from leydig cells? | back 2 Inhibin, secreted by the Sertoli cell, is believed to be involved in a feedback loop from the testis to the pituitary to inhibit FSH production leydig -> testosterone -> inhibit LH |
front 3 The first and rate-limiting step in steroidogenesis is | back 3 the conversion of cholesterol to pregnenolone by a single enzyme, CYP11A1 |
front 4 most circulating testosterone is bound to what 2 proteins | back 4 ALB, SHBG |
front 5 diurnal variation of testosterone, highest when, lowest when | back 5 highest 6 AM, lowest midnight |
front 6 two metabolites of testosterone | back 6 DHT and ee2 |
front 7 lab results of hypergonadotropic hypogonadism | back 7 low T, high FSH, LH |
front 8 most common human sex chromosome abnormal | back 8 Klinefelter syndrome |
front 9 hypergonadotropic hypogonadism or hypogonadotropic hypogonadism: sertoli cell-only syndrome (rare, lack of germ cells), Turner, Kallmann, hyperPRL, T2D, Klinefelter, androgen insensitivity syndrome (female phenotype of 46, XY), mumps (rare), pituitary tumor | back 9 hyper-hypo: Turner syndrome, Klinefelter, androgen insensitivity syndrome (female phenotype of 46, XY), mumps (rare), sertoli cell-only syndrome (rare, lack of germ cells) hypo-hypo: Kallmann, hyperPRL, T2D, pituitary tumor |
front 10 lab results of hypogonadotropic hypogonadism | back 10 low T, low or inappropriate normal GnRH, FSH, LH |
front 11 Initial laboratory testing for male hypogonadism should include | back 11 early morning (8:00–10:00 AM) measurement of serum testosterone, prolactin, FSH, and LH levels |
front 12 figure 17.2 page 455 | back 12 later |
front 13 what test to distinguish between secondary and tertiary gonadotropic disorders | back 13 GnRH stimulation test |
front 14 most widely available and cost-effective mode of testosterone therapy | back 14 parenteral T |
front 15 3 tests should be done following a testosterone replacement therapy | back 15 PSA, hematocrit, lipid panel |
front 16 produces the hormones estrogen and progesterone -> what cell type in ovary | back 16 corpus luteum |
front 17 The onset of puberty -> increasing what hormones | back 17 FSH, LH |
front 18 typical duration of menstrual cycle | back 18 25-35 days |
front 19 During follicular phase, low estrogen results in + or - FB? | back 19 negative FB |
front 20 what happens during follicular phase | back 20 FSH and LH released -> follicle development and preparation for ovulation |
front 21 what happens during luteal phase | back 21 corpus luteum -> progesterone increases, thicken uterus lining |
front 22 how many hypothalamic pituitary endocrine gland axis? | back 22 4 (GHRH, GnRH, TRH, CRH) |
front 23 which of these are symptoms of hypogonadotropic hypogonadism in females: amenorrhea, low energy, osteoporosis, premature ovarian failure? | back 23 amenorrhea, low energy, osteoporosis |
front 24 premature ovarian failure is primary or secondary hypogonadism, this is the result of what abnormality? | back 24 primary, result of Turner syndrome |
front 25 lab result of FSH and ee2 levels for Turner syndrome | back 25 FSH>30 and ee2<20 (high FSH and low ee2) |
front 26 what does + beta-HCG mean? | back 26 pregnancy |
front 27 most common treatment for hyperPRL | back 27 dopamine agonist |
front 28 symptoms of polycystic ovary syndrome | back 28 hirsutism, overweight, infertility, hypertension |
front 29 Iodiopathic hirsutism -> which of the following is the most prominent increase in lab result: total T, free T, DHEAS? | back 29 free T |
front 30 polycystic ovary syndrome -> which of the following is the most prominent increase in lab result: total T, free T, DHEAS? | back 30 free T |
front 31 congenital adrenal hyperplasia -> which of the following is the most prominent increase in lab result: total T, free T, DHEAS? | back 31 DHEAS |
front 32 ovarian tumors -> which of the following is/are the most prominent increase in lab result: total T, free T, DHEAS? | back 32 both total and free T |
front 33 adrenal tumors -> which of the following is the most prominent increase in lab result: total T, free T, DHEAS? | back 33 DHEAS |
front 34 what functional part of parathyroid gland that responds to low or high calcium level | back 34 calcium-sensing receptors (CSR) |
front 35 which is not function of PTH? A. increase renal tubule calcium reabsorb | back 35 B -> should be "increase phosphate excretion" |
front 36 functions of skin, liver, kidney in synthesis of vitamin D | back 36 skin: 7-dehydrocholesterol -(UV)-> vit D3 liver: D3 -> 25OH-vitamin D kidney: 25OH-vitamin D -> 1,25(OH)2 vitamin D |
front 37 most common cause for secondary hyperparathyroidism is | back 37 chronic renal failure (or kidney diseases) |
front 38 2 main types of bones in skeleton | back 38 cortical (long bones) and trabecular (vertebrae) |
front 39 what type of bone is preferentially lost in primary hyperPTH | back 39 cortical bone |
front 40 what are bone resorption markers | back 40 pyridinium crosslinks, hydroxyproline, Tartrate-resistant acid phosphatase (TRAP), telopeptide |
front 41 what are bone formation markers | back 41 alkaline phosphatase, osteocalcin, procollagen peptides |
front 42 primary hyperPTH->what is the lab result for serum Ca, serum Phos, PTH, 25-OH-D, 1,25-D, urine Ca, serum Cl, serum ALP, metabolic acidosis/alkalosis | back 42 hyperCa, hypoP, high PTH, low 25-OH-D, high 1,25-D, high urine Ca, hyperCl, metabolic acidosis, high serum ALP |
front 43 most common PTH testing assay | back 43 sandwich ELISA |
front 44 associated with secondary hyperPTH is hypercalcemia or hypocalcemia | back 44 hypocalcemia (without active vit D -> low Ca and PTH released too much to compensate) |
front 45 people with CKD (chronic kidney disease) -> lab results for serum phos, 1,25-D, serum Ca, PTH | back 45 hyperphosphatemia, low 1,25-D, hypocalcemia, high PTH |
front 46 people with FHH (familial hypocalciuric hypercalcemia) -> lab results for serum Mg, PTH, CSR (normal or mutation), end-organ (normal or damaged), surgery (yes or no) | back 46 elevated serum Mg, PTH, mutant CSR, normal end-organ, surgery ineffective |
front 47 Addison disease -> hypercalcemia or hypocalcemia | back 47 hypercalcemia (low aldosterone so high osmolality -> more concentrated Ca in blood) |
front 48 hyperthyroidism -> hypocalcemia or hypercalcemia | back 48 hypercalcemia |
front 49 people with hypoparathyroidism -> lab results for serum calcium, urine calcium, serum phosphate, PTH level | back 49 your blood calcium level is low, your blood phosphate level is high, and your parathyroid hormone level is low, hypercalciuria (risk of kidney stones) |
front 50 what is ricket | back 50 softening and weakening of bones in children, usually because of an extreme and prolonged vitamin D deficiency |
front 51 lab finding for both ricket and osteomalacia | back 51 secondary hyperPTH |
front 52 what is the most prevalent metabolic bone disease in adults | back 52 osteoporosis |
front 53 osteoporosis happens more to female or to male | back 53 female |
front 54 the following diseases are potential for developing osteoporosis, except what: Cushing syndrome, hyperPTH, disorder of vitamin D, hyperthyroidism, adrenal insufficiency | back 54 adrenal insufficiency |
front 55 4 hormones secreted by the kidneys | back 55 renin, erythropoietin, 1,25-D, prostaglandins |
front 56 substances reabsorbed in proximal tubule | back 56 Na, Cl, H2O, glucose |
front 57 substances secreted in proximal tubule | back 57 H+, drugs |
front 58 what leaves the descending loop and what leaves the ascending loop of Henle | back 58 water leaving the descending loop and sodium and chloride leaving the ascending loop |
front 59 substances secreted by the distal tubule | back 59 NH3 |
front 60 substances reabsorbed in distal tubule | back 60 K, H2O |
front 61 substances reabsorbed in collecting duct | back 61 urea |
front 62 substances secreted by the collecting duct | back 62 NH3, H+ |
front 63 where is urea synthesis | back 63 liver |
front 64 is CRE reabsorbed by the tubules | back 64 no |
front 65 primary ECF cation | back 65 Na |
front 66 main ICF cation | back 66 K |
front 67 CRE clearance formula | back 67 (conc urine CRE clr)*(vol U24h)*1.73 divided by (serum CRE conc)*1440min*A |
front 68 Cockcroft-Gault formula for eGFR | back 68 GFR=(140-age)*weight*0.85(if female) divided by 72*(serum CRE) |
front 69 clinical significance of CysC what testing method? | back 69 rise more quickly than CRE in AKI, useful in early changes of kidney function immunoassay |
front 70 clinical significance of B2M | back 70 elevated -> indicate inflammation, renal failure, organ rejection (transplant patient) |
front 71 clinical significance of myoglobin what testing method | back 71 serum level elevated -> skeletal and cardiac muscle injury, can cause renal failure IA |
front 72 what level of ALB to CRE ratio is diagnostic of ALBuria | back 72 greater than 30 mg/g |
front 73 the first FDA-cleared test to diagnose patient developing moderate to severe AKI | back 73 Nephrocheck |
front 74 preferred what time for urine specimen collection | back 74 initial morning, midstream catch -> analysis within 1 hour (RT) or 8 hours (fridge, 2-8C) |
front 75 possible instability outcomes for urine specimens | back 75 bacteria -> false-pos nitrite test, urea degraded to NH3 and elevate pH, CO2 loss to atm -> elevate pH |
front 76 normal urine pH range | back 76 4.7-4.8 |
front 77 Four major types of cardiovascular disease | back 77 Coronary Heart Disease Cerebrovascular disease Peripheral arterial disease Aortic atherosclerotic disease |
front 78 Chest pain, heart attack, heart failure -> what cardiovascular disease | back 78 CHD(Coronary) |
front 79 Blood supply cut off to the brain, stroke, Transient ischemic attack (mini stroke)-> what cardiovascular disease | back 79 Cerebrovascular disease |
front 80 Blockage in the arteries of extremities-> what cardiovascular disease | back 80 PAD(Peripheral) |
front 81 Aneurysms, tears in thoracic or abdominal aorta-> what cardiovascular disease | back 81 Aortic atherosclerosis |
front 82 blood vessel lumen narrows due to lipid plaque formation-> what cardiovascular disease | back 82 Atherosclerosis (chronic) |
front 83 Chest pain, ischemia(lack of blood supply) that ranges from angina( no cell death); acute myocardial infarction (cell death)-> what cardiovascular disease | back 83 Acute coronary syndrome (ACS) |
front 84 3-protein complex cardiac marker w/ high sensitivity & specificity (gold standard) | back 84 Troponin (TnT, TnI, TnC) |
front 85 Cardiac Markers for diagnosis of ACS or acute MI | back 85 CK-MB, troponin |
front 86 Cardiac Markers to differentiate lung disease from heart failure | back 86 BNP and NT-proBNP |
front 87 biomarkers to diagnose pulmonary embolism | back 87 troponin, BNP and NT-proBNP, D-dimer |
front 88 cardiac markers for CV risk stratification | back 88 troponin, CRP, HCY |
front 89 nonspecific biomarkers of cardiac dysfunction | back 89 BNP and NT-proBNP |
front 90 Symptoms of heart failure | back 90 Shortness of breath, fatigue, lower extremity edema |
front 91 recommended laboratory clinical tests for heart failure | back 91 from the AU: ISE, BUN/CRE, glucose, liver enzymes (AST, ALT, LD), lipid panel from the Centaur: TSH, BNP others: blood count, UA, ECG |
front 92 Measurement of what peptide is helpful in distinguishing cardiac from noncardiac causes of dyspnea? | back 92 B-type natriuretic peptide (BNP) |
front 93 Which peptides are elevated in patients with ventricular dysfunction and cardiac hypertrophy? | back 93 BNP & NT-proBNP |
front 94 An acute marker for inflammation that is used in evaluation of CVD & CHD risk | back 94 C-Reactive protein (CRP) |
front 95 When an embolus becomes lodged within the pulmonary arteries | back 95 Pulmonary embolism |
front 96 Elevated concentrations of this amino acid is the common factor leading to arterial damage | back 96 Homocysteine |
front 97 Blood test that is indicative of current or recent coagulation and subsequent fibrinolysis | back 97 D-dimer test |
front 98 Cells responsible for the liver's regenerative properties. | back 98 Hepatocytes |
front 99 Macrophages that engulf debris, toxins, and bacteria. | back 99 Kupffer cells |
front 100 Liver performs 4 functions | back 100 Excretion, Secretion, Metabolism, Detoxification |
front 101 major heme waste product | back 101 Bilirubin |
front 102 is insoluble in water and cannot be conjugated by the liver | back 102 unconjugated bilirubin |
front 103 conjugation of bilirubin occurs in the presence of which enzyme | back 103 uridine diphosphate glucuronosyltransferase(UDPGT) |
front 104 french word that means yellow | back 104 jaundice |
front 105 clinical condition in which scar tissue replaces healthy liver tissue | back 105 cirrhosis |
front 106 used to describe a group of disorders caused by infectious, metabolic, toxic, or drug-induced diseases -> build up fats in liver | back 106 Reye’s Syndrome |
front 107 Three scoring of bilirubin, INR (how much time for blood to clot), creatinine, age, WBC count, BUN, and albumin levels | back 107 MELD Score (Model for End-Stage liver disease) |
front 108 colorless end product of bilirubin metabolism oxidized by intestinal bacteria to brown pigment | back 108 Urobilin |
front 109 test measure liver function of removing NH3 | back 109 ammonia concentration, GGT |
front 110 purpose of Ehrlich reagent | back 110 most quantitative method for urobilinogen |
front 111 bilirubin analysis -> testing methods involve diazo reagent and a red-purple product which method uses an accelerator (caffeine-benzoate) | back 111 Malloy-Evelyn Jendrassik-Grof (uses accelerator) |
front 112 decreased GFR, anemia, high BUN, CRE, edema; hyaline and granular cast, RBC cast; direct injury, drug, bacteria | back 112 acute glomerulonephritis |
front 113 scarring, slight proteinuria and hematuria, uremia as first signs | back 113 chronic glomerulonephritis |
front 114 massive proteinuria and hypoALBemia, lipid everywherer | back 114 Nephrotic syndrome |
front 115 microorganisms, high nitrite, bacteriuria, leukocytes in urine, hematuria, WBC cast | back 115 pyelonephritis (infection) |