ABIM 2015 - Endocrine Flashcards

Question

What results on the ORAL 2-HOUR 75 g GLUCOSE TOLERANCE TEST are considered POSITIVE for GESTATIONAL DIABETES (NOT DM)?

Answer 1

FASTING: ≥92 mg/dL 1-HOUR: ≥180 mg/dL 2-HOUR: ≥153 mg/dL

Answer 2

Normal FASTING Plasma Glucose

Answer 3

Normal RANDOM Plasma Glucose

Answer 4

Normal HbA1c

Answer 5

GESTATIONAL DIABETES

Answer 6

GESTATIONAL DIABETES

Answer 7

EXCLUDED: 30, previous H/O gestational diabetes or Polycystic Ovarian Syndrome - "PCOS", previous fetus with MACROSOMIA (large baby >4,500 g), FAMILY H/O DM, or NON-WHITE

Answer 8

LIFESTYLE MODIFICATIONS (diet and exercise), INSULIN (if these changes are not sufficient) or ORAL agents (METFORMIN and GLYBURIDE if INSULIN is refused)

Answer 9

PREGNANT WOMEN (gestational diabetes or otherwise)

Answer 10

In women who have been DIAGNOSED with GESTATIONAL DIABETES in a previous pregnancy

Answer 11

CHILDHOOD OBESITY

Answer 12

Because their HORMONAL ACTIONS are ANTAGONISTIC to INSULIN

Answer 13

SULFONYLUREAS

Answer 14

DIET and EXERCISE

Answer 15

HbA1c (measuring the glycosylated Hb)

Answer 16

Every 3 MONTHS if patient's therapy is being adjusted and every 6 MONTHS if on STABLE therapy

Answer 17

HbA1c, because it will be FALSELY lowered due to the presence of ERYTHROCYTES that are not 120 days old

Answer 18

Average daily blood glucose in HbA1c of 7.0 - 154 mg/dL | Average daily blood glucose in HbA1c of 8.0 - 183 mg/dL

Answer 19

ATHEROSCLEROSIS (due to inflammatory state of DM)

Answer 20

MODERATE EXERCISE for at LEAST 150 min/WEEK

Answer 21

LIFESTYLE MODIFICATIONS (diet, exercise, weight loss)

Answer 22

They RISE!! because exercise INDUCES hepatic gluconeogenesis and no insulin was taken (as patient did not eat breakfast yet)

Answer 23

BARIATRIC surgery (BMI >40)

Answer 24

Because in TYPE 2 DM, the LOSS of pancreatic β-cell function is PROGRESSIVE in ADDITION to underlying INSULIN RESISTANCE

Answer 25

LIFESTYLE MODIFICATIONS (diet, exercise, weight loss) AND START a NON-INSULIN agent (METFORMIN)

Answer 26

1. ORAL for control of POST-PRANDIAL BLOOD GLUCOSE [sulfonylureas (glipizide, -"ride, mide, zide"), α-glucosidase inhibitors (acarbose, voglibose -"bose"), meglitinides (rapaglinide, -"glinide") and dipeptidyl peptidase-4 inhibitors (sitagliptin, -"gliptin") 2. INJECTABLE that SLOW GASTRIC EMPTYING and SUPPRESS GLUCAGON (by the pancreas) - pramlintide, exenatide, liraglutide -"tide" 3. INSULIN

Answer 27

SULFONYLUREAS (glybuRIDE, chlorpropaMIDE) as these two in particular, have LONG HALF-LIVES and can cause PROFOUND HYPOglycemia (DEADLY) as well as their association with MYOCARDIAL DAMAGE (MI)

Answer 28

gliclaZIDE and glimepiRIDE

Answer 29

Third-generation SULFONYLUREAS NOT associated with myocardial damage (MI) as the act EXCLUSIVELY on pancreatic β-cells (not also on myocardial cells)

Answer 30

ADD INSULIN (ie NPH insulin at BEDTIME + DAYTIME METFORMIN)

Answer 31

LONG-ACTING forms of insulin

Answer 32

At BEDTIME or FIRST THING in the MORNING

Answer 33

BASAL + PRE-PRANDIAL INSULINS (same as used in TYPE 1 DM)

Answer 34

Because patients with TYPE 1 DM are VERY SENSITIVE to INSULIN and those with TYPE 2 DM have a variable RESISTANCE to insulin

Answer 35

0.5 - 1.5 units/kg/day

Answer 36

1/2 of the DAILY dose is given as the BASAL (NPH insulin) INSULIN and the remainder of the DAILY dose is given in THREE (3) injections BEFORE EACH MEAL (ideally, these 3 injections would be approximated to the meal's carbohydrate content ie 1 unit for every 10-15 g of carbs and 1 unit for every 25 mg/dL the PRE-PRANDIAL glucose level was above 100 mg/dL for TYPE 2 DM and for every 50 mg/dL over 100 mg/dL in TYPE 1 DM)

Answer 37

Because they can cause more FREQUENT and UNPREDICTABLE HYPOglycemia and WEIGHT GAIN

Answer 38

SULFONYLUREAS (only gliclaZIDE and glimepiRIDE are safe to use)

Answer 39

METFORMIN (Biguanide)

Answer 40

α-glucosidase inhibitors (acarbose, voglibose -"bose")

Answer 41

THIAZOLIDINEDIONES (-"glitazones") - these cause HF, MI, macular edema, osteoporosis and bladder cancer - DO NOT USE

Answer 42

rosiGLITAZONE ("not so rosy" - THIAZOLIDINEDIONES)

Answer 43

MEGLITINIDES (rapaGLINIDE, nateGLINIDE)

Answer 44

BOTH have the SAME mechanism of action (STIMULATING INSULIN SECRETION from PANCREATIC β-cells) HOWEVER, of the sulfonylureas, ONLY gliclaZIDE and glimepiRIDE are safe to use as the rest cause MYOCARDIAL DAMAGE and PROFOUND HYPOglycemia in OLDER patients and those with RENAL dysfunction

Answer 45

ORLISTAT (Lipase Inhibitor)

Answer 46

SLOW GASTRIC EMPTYING and SUPPRESS GLUCAGON SECRETION by the pancreas (can cause pancreatitis, N/V and rashes)

Answer 47

RAPID-ACTING INSULINS (onset 5-15 min, peaks 45-90 min lasts 2-4 hrs)

Answer 48

LISPRO, ASPART, GLULISINE

Answer 49

SHORT-ACTING (not rapid) - (onset 30 min-1 hr, peaks 2-4 hrs, lasts 4-8 hrs)

Answer 50

BASAL (long-acting) - (onset 1-3 hrs, peaks 4-10 hrs, lasts 10-18 hrs) - so if you take it first thing in the morning, it will be ready for LUNCH and if you take it at bedtime, it will be ready for BREAKFAST

Answer 51

DETEMIR and GLARGINE have NO PEAKS (steady blood levels)

Answer 52

PLASMA GLUCOSE and HbA1c (plasma glucose should be taken frequently ie BEFORE MEALS and BEDTIME or EVERY 6 HOURS if NPO)

Answer 53

D/C PO agents May continue the PO agents IF patients ARE EATING PO EXCEPT SULFONYLUREAS (glipizide, -"ride, mide, zide") and MEGLITINIDES (rapaglinide, -"glinide") as these can cause HYPOglycemia if PO food intake is unpredictable or stopped

Answer 54

METFORMIN (Biguanide)

Answer 55

THIAZOLIDINEDIONES (-"glitazones")

Answer 56

140-180 mg/dL with IV INSULIN (for all other patients NO LOWER than 90 and NO HIGHER than 180 mg/dL when taken RANDOMLY post-prandially with 140 mg/dL fasting and pre-prandially )

Answer 57

BASAL INSULIN (due to the potential wide swings in blood glucose)

Answer 58

Give 1/2 of the DAILY dose as the BASAL (NPH insulin) INSULIN and give the remainder of the DAILY dose in THREE (3) injections BEFORE EACH MEAL (ideally, these 3 injections would be approximated to the meal's carbohydrate content ie 1 unit for every 10-15 g of carbs and 1 unit for every 25 mg/dL the PRE-PRANDIAL glucose level was above 100 mg/dL for TYPE 2 DM and for every 50 mg/dL over 100 mg/dL in TYPE 1 DM)

Answer 59

INSULIN-DEFICIENCY (induces hepatic gluconeogenesis worsening HYPERglycemia as well as the HYPERglycemia that occurs from dietary GLUCOSE in the absence of INSULIN)

Answer 60

New-Onset TYPE 1 DM, UNDER-DOSING of INSULIN and MISSED INSULIN DOSING (alone or in the setting of infection or serious illness)

Answer 61

BLOOD GLUCOSE: ~400-500 mg/mL

Answer 62

BLOOD GLUCOSE: ~200-250 mg/mL (because the liver gets slowly depleted of glycogen stores (pt who isn't eating) used for gluconeogenesis and glucose rises slowly until the liver is depleted or the process of gluconeogenesis is hampered (by the injured liver) and fatty acid breakdown and ketogenesis occur because glucose is still not available to the cells/organs that require it in the continued absence of insulin - which stops lipolysis)

Answer 63

INDUCED HEPATIC GLUCONEOGENESIS (glucose production by the liver from glycogen stores) due to the ABSENCE of INSULIN

Answer 64

HYPERglycemic HYPERosmolar Syndrome (HHS) - a SEVERE HYPERosmolar NON-KETOTIC HYPERglycemia with VERY HIGH GLUCOSE LEVELS (>700 mg/dL) and NORMAL SERUM HCO3¯ (24 meq/L)

Answer 65

HYPERglycemia

Answer 66

HYPERglycemia

Answer 67

POTASSIUM (K⁺) administration, because ALTHOUGH SERUM K⁺ levels "appear" normal, they do so because INTERcellular K leaked out into the serum and INSULIN administration RAPIDLY moves the K⁺ BACK INTO THE CELLS resulting in severe HYPOkalemia (decreased SERUM K⁺)

Answer 68

SERUM GLUCOSE: HOURLY | ELECTROLYTES: every 2-4 HOURS

Answer 69

>20,000!!!!!

Answer 70

USUALLY NOT (so absence of a fever, does NOT r/o infection)

Answer 71

When SERUM HCO3¯

Answer 72

AMYLASE (can be >1000 units/L)

Answer 73

BLOOD GLUCOSE

Answer 74

HYPERglycemic CRISES

Answer 75

Change the IVF's from NS (or from 1/2 NS "0.45% NS" if serum Na became normal or HIGH) to D5 1/2 NS "5% Dextrose 0.45% NS"

Answer 76

REDUCE the RATE to 0.02-0.05 units/kg/hr MAINTAINING the BLOOD GLUCOSE at a level between 150-200 mg/dL until the INCREASED anion gap METABOLIC Acidosis is RESOLVED in DKA (gap is due to the keto acids - the "unmeasured anions") as there is NO ACIDOSIS in HYPERglycemic HYPERosmolar Syndrome (HHS)

Answer 77

Give IV KCl 20-30 meq/hr via CENTRAL LINE until K >3.3 meq/L, then ADD 20-30 meq of KCl to EACH LITER of IVF and KEEP SERUM K⁺ between 4.0-5.0 meq/L

Answer 78

START INSULIN & IVF, DO NOT GIVE K⁺

Answer 79

GIVE Na-BICARBONATE (NaHC03¯) AND KCl over 2 HOURS (DO NOT give sodium bicarbonate if pH >6.9)

Answer 80

GROWTH HORMONE (anterior pituitary bg

Answer 81

Due to the ACTIVATION of the ADRENAL GLANDS by the brain (via adrenocorticotrophic hormone ACTH) and resulting RELEASE of CATECHOLAMINES epinephrine and norepinephrine

Answer 82

SEVERE HYPOglycemia and IMPENDING SEIZURES and LOSS of CONSCIOUSNESS as well as focal neurologic signs such as HEMIparesis

Answer 83

HYPOglycemia (liver and muscles take up blood glucose to replenish glycogen after exercise and the liver's ability to induce gluconeogenesis in the setting of alcohol consumption is impaired)

Answer 84

Attributing HYPOglycemic symptoms to alcohol INTOXICATION

Answer 85

Their HYPOglycemic SYMPTOMS may NOT be apparent or recognized even by the patient (due to deteriorated response) - treat by reducing insulin dose and increasing carbohydrate intake for a blood glucose level between 150-200 mg/dL to "RESET" the body's ability to "SENSE"

Answer 86

~28-29 mg/dL (HbA1c of 6.0 - blood glucose of 126; HbA1c of 7.0 - blood glucose of 154; HbA1c of 8.0 - blood glucose of 183) - [183-154=29, 154-126=28, etc.)

Answer 87

Verify that the BLOOD GLUCOSE is

Answer 88

ANOTHER person should help by ADMINISTERING SUBLINGUAL GLUCOSE (or IV or SQ glucagon, depending on setting)

Answer 89

When they are at CHRONICALLY elevated BLOOD GLUCOSE LEVELS (poorly controlled diabetic) >200 mg/dL and then LOWERED closer to the normal range by medications or lifestyle changes (maintaining consistency resets the patient's symptom threshold)

Answer 90

RETINAL damage - EDEMA, HARD EXUDATES, TINY HEMORRHAGES - (this is why ALL patients with TYPE 1 DM must be checked by ophthalmologist 5 years AFTER diagnosis, then ANNUALLY and why ALL patients with TYPE 2 DM must be checked AT TIME OF DIAGNOSIS, then ANNUALLY) - in pregnant women with either type of DM, diabetic retinopathy must be SCREENED for in FIRST TRIMESTER and checked EVERY TRIMESTER, then ANNUALLY

Answer 91

BACKGROUND or "NON-PROLIFERATIVE" diabetic retinopathy)

Answer 92

PROLIFERATIVE diabetic retinopathy - leads to RETINAL DETACHMENT

Answer 93

TEMPORARY (reversible) WORSENING of the retinopathy

Answer 94

LASER PHOTOCOAGULATION (retinopathy) and FOCAL LASER THERAPY (edema)

Answer 95

LOSS of PERIPHERAL vision, however CENTRAL vision is preserved

Answer 96

INTRA-OCULAR injections of INHIBITORS of Vascular Endothelial Growth Factors (VEGF-I) bevaciZUMAB and ranibiZUMAB every 4-8 WEEKS

Answer 97

HYPERglycemia causes DIRECT, PROGRESSIVE damage to the GLOMERULAR BASEMENT MEMBRANE

Answer 98

URINE microalbumin (and protein) using the Urine PROTEIN:Cr (30-300 mg/g indicate microalbuminuria)

Answer 99

Episodes of SEVERE HYPERglycemia

Answer 100

PERIPHERAL Diabetic Neuropathy (can cause CARPAL TUNNEL syndrome and MERALGIA PARESTHETICA - numbness in OUTER THIGH)

Answer 101

TOPICAL CAPSAICIN cream, low-dose TCA's (amitriptyline), SSRI's/SNRI's (sertraline, citalopram/venlafaxine, duloxetine) IF NOT SUFFICIENT with ABOVE, use GABAPENTIN, PREGABALIN, carbamazepine, phenytoin (NO OPIATES)

Answer 102

Diabetic AMYOTROPHY

Answer 103

CHARCOT Foot Deformity (bony degeneration of a weight-bearing joint)

Answer 104

DIABETICS with damage to AUTONOMIC NERVES

Answer 105

Pancreas stops secreting insulin and Hepatic glycogenolysis (breakdown of stored glycogen) supplies glucose to maintain BLOOD GLUCOSE LEVELS >70 mg/dL

Answer 106

The PANCREAS, it STIMULATES the LIVER to break down stored GLYCOGEN into GLUCOSE

Answer 107

Growth Hormone INHIBITS the actions of INSULIN in states of MODERATE HYPOglycemia (

Answer 108

In MODERATE HYPOglycemia (

Answer 109

PROTIENS (amino acids) and FAT (free fatty acids) are converted into GLUCOSE and KETONES

Answer 110

When HEPATIC GLYCOGEN stores are EXHAUSTED - 8 HOURS - (by the pancreatic action of GLUCAGON and the adrenal action of CORTISOL) or by SEPSIS, EXTREME STARVATION, LIVER DYSFUNCTION (alcohol) or CORTISOL and thus ACTH deficiency (ADDISON disease - chronic adrenal insufficiency)

Answer 111

Insulinoma (VERY RARE), Injecting Insulin (absence of the C-peptide) and taking ORAL Sulfonylureas or Meglitinides (BOTH INDUCE INSULIN secretion by pancreatic β-cells - in which case C-peptide WILL be present)

Answer 112

1. HYPOglycemic SYMPTOMS are present | 2. LOW BLOOD GLUCOSE (

Answer 113

INPATIENT 72-HOUR FAST while REGULARLY measuring BLOOD GLUCOSE, PRO-INSULIN (insulin precursor: insulin-C-peptide complex), INSULIN, C-peptide, β-hydroxybutyrate (ketone produced in the absence of insulin) and SULFONYLUREA/MEGLITINIDE levels

Answer 114

1. HIGH LEVELS of BOTH INSULIN and C-peptide (because insulinomas CAUSE the PANCREAS to release too much endogenous insulin) 2. CT abdomen/EUS to confirm and SURGERY to remove

Answer 115

Psychiatric Evaluation

Answer 116

1. Observe patient and MEASURE BLOOD GLUCOSE when SYMPTOMS occur, NOT with the oral glucose tolerance test as you MAY INDUCE more SYMPTOMS 2. Treat by RECOMMENDING SMALL, FREQUENT meals just as you would for someone who DID have a gastric BYPASS surgery

Answer 117

PROLACTIN (because this is the ONLY pituitary hormone whose CONTINUOUS hypothalamic generated signal through the pituitary stalk is an INHIBITORY one via DOPAMINE, whereas for ALL other PITUITARY hormones, the signal is a SECRETORY one)

Answer 118

Injury to the pituitary stalk (because PROLACTIN is the ONLY pituitary hormone whose CONTINUOUS hypothalamic generated signal through the pituitary stalk is an INHIBITORY one via DOPAMINE, whereas for ALL other PITUITARY hormones, the signal is a SECRETORY one)

Answer 119

HYPOTHALAMUS (also hypersexuality and somnolence)

Answer 120

PRIMARY pituitary TUMORS and their TREATMENT (surgery, radiation) followed by EXTRA-PITUITARY lesions (meningioma, germinoma, craniopharyngioma, Rathke cleft cyst - congenital)

Answer 121

HEMOCHROMATOSIS, LANGERHAN's Cell Histiocytosis (a lymphoproliferative disease where abnormal "Langerhan cells" proliferate from bone marrow and also affect SKIN with face/chest/abd rash and LYMPH NODES), TB, SARCOIDOSIS

Answer 122

Vascular diseases that cause INFARCTION (subarachnoid hemorrhage can do this as well) of the PITUITARY resulting in HYPOpituitarism

Answer 123

LYMPHOCYTIC HYPOPHYSITIS

Answer 124

HYPOpituitarism

Answer 125

Pituitary APOPLEXY (tumor-caused infarct/hemorrhage into the pituitary)

Answer 126

- GLUCOCORTICOID REPLACEMENT due to ACTH deficiency (HYDROCORTISONE) and IVF's - DEXTROSE - Replacement of TSH, LH, FSH and GH are NOT emergent)

Answer 127

SHEEHAN SYNDROME (blood loss/hypotension DURING CHILDBIRTH - "SHE couldn't HANdle it")

Answer 128

CENTRAL (CNS) ADRENAL INSUFFICIENCY (due to ACTH deficiency)

Answer 129

RADIATION therapy

Answer 130

ACTH deficiency, because of associated CORTISOL deficiency (hydrocortisone) and ALDOSTERONE deficiency

Answer 131

LOSS of MUSCLE, INCREASED FAT, LOSS of STRENGTH and STAMINA, DECREASED BONE DENSITY, INCREASED cardiovascular RISK

Answer 132

ALDOSTERONE (rening-angiotensin-aldosterone)

Answer 133

CORTISOL (hydrocortisone) - replaced by PREDNISONE and other steroids

Answer 134

TESTOSTERONE (although only ~10% in men as the rest is produced by the testicles)

Answer 135

CATECHOLAMINES (EPInephrine and NOREPInephrine)

Answer 136

Growth Hormone (GH) - LOSS of MUSCLE, INCREASED FAT, LOSS of STRENGTH and STAMINA, DECREASED BONE DENSITY, INCREASED cardiovascular RISK and DECREASED QUALITY OF LIFE (decreased sensation of "well being")

Answer 137

By testing for the level of Insulin-like Growth Factor 1 (IGF-1) which is what the LIVER makes after exposure to GH by the PITUITARY gland - IT WOULD BE LOW or testing for GHRH (growth hormone releasing hormone), glucagon or arginine

Answer 138

Amenorrhea, Breast Atrophy, Vaginal Dryness, Reduced Libido, Erectile Dysfunction, Loss of Muscle/Bone Mass and Anemia (men) AND possible GALACTORRHEA (if HYPERprolactinemia is the cause as it suppresses GnRH secretion by the hypothalamus and thus suppressed LH and FSH secretion by the pituitary)

Answer 139

DECREASED LH and FSH resulting in HYPOgonadotropic HYPOgonadism (reduced ESTROGEN production and reduced OVULATION, OSTEOPOROSIS)

Answer 140

MRI or CT of the head (look for a lesion)

Answer 141

When it is caused by or there is concomitant HYPERprolactinemia (suppresses GnRH secretion by the hypothalamus and thus suppressed LH and FSH secretion by the pituitary)

Answer 142

Treated with LEVOTHYROXINE and progress checked with T4 levels and CLINICAL SYMPTOMS, NOT TSH (as TSH is not released by the pituitary in this condition)

Answer 143

Treated with HYDROCORTISONE or PREDNISONE, adjusted clinically

Answer 144

1. MEN: TESTOSTERONE (and injected LH/FSH if FERTILITY is desired) 2. WOMEN: low-dose COMBINED oral contraceptives or estrogen/medroxyprogesterone (and injected LH/FSH if FERTILITY is desired)

Answer 145

Injected LH/FSH

Answer 146

Treated with GH supplementation, adjusted to maintain IGF-1 levels in the mid-normal range (higher doses for women on oral estrogens)

Answer 147

Treated with DESMOPRESSIN (vasopressin "ADH" analogue)

Answer 148

VIA direct NEURAL stimulation, NOT through a "hormone-releasing-hormone" as is done for the anterior pituitary hormones

Answer 149

LOW/NORMAL ACTH and LOW CORTISOL (because the LOW cortisol level, although signaling the HYPOTHALAMUS to release CRH so that the PITUITARY RELEASES ACTH, however because either something is wrong with the hypothalamus or the pituitary, ACTH is not increased and CORTISOL is low)

Answer 150

HIGH! (because the LOW cortisol level signals the HYPOTHALAMUS to release CRH so that the PITUITARY RELEASES ACTH and both the hypothalamus and pituitary are normal)

Answer 151

ADDISON Disease - PRIMARY ADRENAL INSUFFICIENCY due to the effects of ELEVATED ACTH

Answer 152

ADDISON Disease - PRIMARY ADRENAL INSUFFICIENCY due to the effects of ELEVATED ACTH

Answer 153

Because the ALDOSTERONE produced in the outermost portion of the ADRENAL CORTEX is NOT CONTROLLED by the HYPOTHALAMUS/PITUITARY but SEPARATELY by the KIDNEYS/LUNGS/LIVER renin-angiotensin-aldosterone system

Answer 154

ADDISON Disease - PRIMARY ADRENAL INSUFFICIENCY

Answer 155

Suppression of the secretion of CRH (hypothalamus) and therefore ACTH (pituitary) by EXOGENOUS CORTICOSTEROID administration (prednisone, megestrol - appetite stimulant used in HIV and cancer patients, etc.) >2-3 WEEKS

Answer 156

Because OTHER pituitary hormones would ALSO be deficient, not JUST ACTH

Answer 157

By measuring the SERUM TSH (NORMAL/low) AND T4 (LOW) which would be due to understimulation of the THYROID gland due to a LOW TRH (hypothalamic) or TSH (pituitary) issue where these should be HIGH if the T4 was low (NEED BOTH TSH and T4)

Answer 158

HYPOthyroidism

Answer 159

Without a concomitant central cause, the TSH level would be HIGH (T4 and T3 would be low but not necessary) as the properly-functioning hypothalamic/pituitary axis is trying to STIMULATE an ABNORMAL THYROID gland

Answer 160

Serum T4 - would also be LOW (because this would demonstrate the problem to be CENTRAL - hypothalamic/pituitary)

Answer 161

EUTHYROID SICK-SYNDROME (thyroid if normal and the lab abnormalities are caused by the sickness)

Answer 162

During stress such as WATER DEPRIVATION (loss of a patient's usual access to water) or PREGNANCY (due to placental vasopressinase - a placental enzyme that degrades vasopressin causing the "partial" release of vasopressin to now become insufficient)

Answer 163

Diabetes Insipidus (DI)

Answer 164

SIADH - look for a cancer

Answer 165

Water Deprivation test to DIFFERENTIATE between DIABETES INSIPIDUS (DI) and PRIMARY POLYDIPSIA (psychogenic)

Answer 166

Pituitary MICROadenoma 1 cm

Answer 167

Most are NON-FUNCTIONAL adenomas | Most COMMON FUNCTIONAL pituitary tumor is the PROLACTINOMA (prolactin >200 ng/mL)

Answer 168

Multiple Endocrine Neoplasia - 1 (MEN-1) the 3 P's

Answer 169

Visual Field Defects (optic chiasm), HEADACHES, compressive effect on the remaining pituitary with HYPOpituitarism

Answer 170

FOLLOW-UP with MRI and HORMONAL ANALYSIS (HYPO/HYPER) INCLUDING SERUM PROLACTIN level, check for VISUAL FIELD DEFECTS

Answer 171

Tests that MUST be done for ALL masses in the SELLA TURCICA whether found INCIDENTALLY or not

Answer 172

Hormone Replacement Therapy (HYPOpituitarism) or SURGERY (if functional - except prolactinomas - serum prolactin >200 ng/mL)

Answer 173

Serial Follow-up Evaluataions

Answer 174

The OPTIC CHIASM

Answer 175

Pituitary tumors

Answer 176

Likely hemorrhagic infarction of the tumor (Pituitary Apoplexy)

Answer 177

VERY RARELY, more commonly due to a NON-PITUITARY lesion such as a CYSTIC TUMOR (craniopharyngioma or Rathke cleft cyst - congenital) or metastases

Answer 178

SURGICAL RESECTION of ALL Pituitary tumors that are FUNCTIONAL (secrete hormone) or those that are >1 cm (MACROADENOMAS) EXCEPT PROLACTINOMAS (prolactin >200 ng/mL) - treated with DOPAMINE agonists (dopamine inhibits prolactin secretion)

Answer 179

RADIATION THERAPY

Answer 180

PITUITARY Prolactinoma - serum prolactin >200 ng/mL - (cabergoline or bromocriptine)

Answer 181

HYPERprolactinemia

Answer 182

Pituitary Prolactinoma - serum prolactin >200 ng/mL - (benign adenoma)

Answer 183

Tumor (hypothalamic, sellar) affecting the pituitary STALK, HYPOthyroidism, Cirrhosis, Kidney Failure (Cr

Answer 184

Antidopaminergic (block dopamine secretion which inhibits prolactin secretion)

Answer 185

Serum Prolactin >200 ng/mL (normal is 5-20 ng/mL)

Answer 186

GH (because HYPOTHALAMIC secretion of GnRH is INHIBITED by the INCREASED SECRETION of HYPOTHALAMIC DOPAMINE (negative inhibitory response to HYPERprolactinemia)

Answer 187

MRI of the PITUITARY gland

Answer 188

HYPERprolactinemia (treat with dopamine agonists - cabergoline or bromocriptine, NOT SURGERY - as tumors typically shrink by >50% with medical therapy ALONE)

Answer 189

STILL NO SURGERY, treat with dopamine agonists - cabergoline or bromocriptine - as tumors typically shrink by >50% with medical therapy ALONE

Answer 190

Consult PSYCHIATRY

Answer 191

LOW-DOSE ESTROGEN in the form of ORAL CONTRACEPTIVES with regular monitoring of PROLACTIN levels

Answer 192

CABERGOLINE (except TSH-secreting adenomas which require OCTREOTIDE)

Answer 193

When serum prolactin levels have been NORMAL (5-20 ng/mL) >2 YEARS and NO VISIBLE tumor on MRI with close follow-up (50% recurrence rates)

Answer 194

SURGICAL RESECTION (endonasal transsphenoidal)

Answer 195

There are VISUAL FIELD DEFECTS due to optical chiasm compression by the PROLACTINOMA

Answer 196

THEY BOTH INCREASE in SIZE

Answer 197

Start BROMOCRIPTINE (preferred agent), TRANSSPHENOIDAL SURGERY or DELIVERY if appropriate (timing)

Answer 198

ONCE BREASTFEEDING has STOPPED (not safe in breastfeeding)

Answer 199

NO, also, prolactin levels are of no value during pregnancy

Answer 200

ACROMEGALY due to a GH-secreting pituitary tumor (adenoma)

Answer 201

ACROMEGALY due to a GH-secreting pituitary tumor (adenoma) - due to their higher RISK for Colon Cancer

Answer 202

Serum Insulin-like Growth Factor - 1 (IGF-1) - HIGH | -Rarely, an oral glucose tolerance test measuring GH levels can be done and if a level

Answer 203

Because GH secretion by the pituitary is PULSATILE and not consistent

Answer 204

The BONY changes

Answer 205

OCTREOTIDE/lanreotide (can also use cabergoline) as well as adjuvant RADIATION therapy

Answer 206

PEGvisomant

Answer 207

These are most commonly found as MACROadenomas (>1 cm) and may be causing MASS effect with visual field loss and other symptoms such as HA and well as HYPOpituitarism - the recommendations is that ALL MACROADENOMAS be surgically removed EXCEPT for prolactinomas because these respond well and rapidly to DOPAMINE-agonists (cabergoline and bromocriptine) in both reduction of hormone and shrinkage. In contrast, ALL FUNCTIONAL pituitary tumors require SURGICAL resection regardless of size, again EXCEPT prolactinomas

Answer 208

MONITORING with MRI every 6-12 months to assess for symptom development and growth

Answer 209

OCTREOTIDE/lanreotide

Answer 210

Thyroxine (T4 - made by the thyroid gland) and Triiodothyronine (T3 - some made by the thyroid gland, the MAJORITY made by peripheral tissues - LIVER & KIDNEY that convert T4)

Answer 211

THYROTOXICOSIS

Answer 212

free T4 and free T3 (unbound) | When these are BOUND (to thyroxine-binding-globulin "TBG") the hormones are INACTIVE and reflect STORED hormone reserves

Answer 213

IODINE (requirements increase in pregnancy/lactation)

Answer 214

Serum free T4 (reflects biologically-active, UNBOUND T4 made by the thyroid gland) - if LOW, then the problem is CENTRAL because there is no negative-feedback inhibition of the pituitary or hypothalamus yet TSH is low

Answer 215

When looking for T3 thyrotoxicosis (excess T3)

Answer 216

When suspecting a SUBACUTE THYROIDITIS or SURREPTITIOUS ingestion of thyroid hormone (T4 or T3) or followed as a tumor marker in thyroid cancer

Answer 217

Thyroglobulin (Tg) STORES the thyroid hormones T4 and T3 made in the thyroid gland after contact with IODINE (iodination) and SECRETES it in response to TSH (most of T3 is made by peripheral tissues - LIVER & KIDNEY - after conversion of T4) some of the Thyroglobulin (Tg) itself is also secreted and thus measurable

Answer 218

GRAVES Disease (TSH-receptor Stimulating (TSI) and Blocking (TBII) Ab's - an autoimmune HYPERthyroidism disease

Answer 219

When suspecting HASHIMOTO Thyroiditis (an autoimmune HYPOthyroidism disease)

Answer 220

In a NON-PREGNANT, NON-BREASTFEEDING patient, to determine the cause of THYROTOXICOSIS (excess T4 (thyroxine) due to ANY cause) by examining the UPTAKE PATTERN

Answer 221

Serum TSH (normal 0.5-5.0 µU/mL)

Answer 222

BOTH TSH and freeT4

Answer 223

BOTH would be elevated (unless, rarely only the free T3 level was high, due to T3 thyrotoxicosis)

Answer 224

NO, because it can be conserved even when HYPOthyroidism is severe and therefore of NO diagnostic value in this setting

Answer 225

HASHIMOTO thyroiditis

Answer 226

GRAVES disease

Answer 227

1. NOTHING (EXCEPT in WOMEN who either ARE or wish to BECOME PREGNANT, serial measurements of anti-TPO Ab's are appropriate due to the HIGH risk for INFERTILITY, PRETERM DELIVERY and MISCARRIAGE) 2. Presence of these Ab's suggests a FUTURE risk of autoimmune thyroid disease

Answer 228

anti-thyroid peroxidase Ab's (anti-TPO) - NOT anti-TBG

Answer 229

1. ABNORMAL TSH is the ONLY indication to treat 2. YES, for WOMEN who either ARE or wish to BECOME PREGNANT, serial measurements of anti-TPO Ab's are appropriate due to the HIGH risk for INFERTILITY, PRETERM DELIVERY and MISCARRIAGE

Answer 230

Serum anti-TSI and anti-TBII Ab's [anti-TSH receptor Ab's: "anti-TSI - Thyroid Stimulating Immunoglobulin (TSI)" and "anti-TBII - Thyrotropin-Binding Inhibitory Immunoglobulin (TBII)"]

Answer 231

- BOTH cause it to be INCREASED - [Thyroglobulin (Tg) STORES the thyroid hormones T4 and T3 made in the thyroid gland after contact with IODINE (iodination) and SECRETES it in response to TSH (most of T3 is made by peripheral tissues - LIVER & KIDNEY - after conversion of T4) some of the Thyroglobulin (Tg) itself is also secreted and thus measurable

Answer 232

- DECREASED (because TSH would be LOW thus inhibitory) - [Thyroglobulin (Tg) STORES the thyroid hormones T4 and T3 made in the thyroid gland after contact with IODINE (iodination) and SECRETES it in response to TSH(most of T3 is made by peripheral tissues - LIVER & KIDNEY - after conversion of T4) some of the Thyroglobulin (Tg) itself is also secreted and thus measurable

Answer 233

Serum THYROGLOBULIN (Tg) because it would be LOW - this is the ONLY way to be able to tell that the observed THYROTOXICOSIS (excess of thyroid hormone, mainly free T4 and some free T3) is NOT due to ENDOGENOUS secretion of thyroid hormone but rather by an EXOGENOUS source

Answer 234

1. Serum THYROGLOBULIN (Tg) - can be used as an effective tumor marker in these well-differentiated cancer types (in UNDIFFERENTIATED or POORLY-DIFFERENTIATED thyroid cancers "RAS-mutations" such as "ANAPLASTIC Thyroid Cancer (ATC) - due to altered cell morphology, measuring thyroglobulin would not be helpful) 2. The presence of anti-THYROGLOBULIN Ab's (anti-Tg) and therefore, the PRESENCE of these Ab's MUST ALSO be measured

Answer 235

WELL-DIFFERENTIATED Cancers (the cancer cells and therefore their secreted products look SIMILAR to normal tissue)

Answer 236

Because the IODINE is TAKEN UP by the NORMAL and CANCEROUS THYROID cells causing their DESTRUCTION due to their RADIATION effects

Answer 237

CALCITONIN should be measured in ALL patients with THYROID NODULES or THYROID DYSFUNCTION that have a FAMILY H/O MEDULLARY THYROID CANCER with features of the FAMILIAL Multiple Endocrine Neoplasia - 2 (MEN-2) - PHEOCHROMOCYTOMA & MEDULLARY THYROID CANCER (can include parathyroid cancer - 2a or mucosal neuromas and Marfan disease 2b) or those with POSITIVE BIOPSY (of a thyroid nodule - US-guided FNA) for Medullary Thyroid Cancer

Answer 238

The possibility of PRESENCE, RECURRENCE or PERSISTENCE of MEDULLARY THYROID CANCER

Answer 239

Radioactive Iodine Uptake scan (RAIU-scan) - would be HIGH (>30% after 24 hrs or HIGH-NORMAL, where normal uptake is between 5-25%)

Answer 240

Radioactive Iodine Uptake scan (RAIU-scan) - would be LOW (

Answer 241

DIFFUSE UPTAKE of radioactive iodine

Answer 242

NO!! it is due to POSTPARTUM THYROIDITIS

Answer 243

HYPERthyroidism

Answer 244

HYPERthyroidism (thyrotoxicosis caused by ENDOGENOUS thyroid gland overactivity with resulting EXCESS production of thyroid hormones)

Answer 245

HYPERthyroidism (thyrotoxicosis)

Answer 246

THYROTOXICOSIS

Answer 247

YES!! (which is why although found with HASHIMOTO thyroiditis, the presence of these are not SUFFICIENT for the diagnosis of HASHIMOTO thyroiditis requiring testing for TSH and CLINICAL evidence of HYPOthyroidism)

Answer 248

Thyroid US

Answer 249

1. A TSH-secreting PITUITARY tumor (serum "α-TSH >1) - "α-TSH" suggests pituitary source 2. MRI

Answer 250

When there is a PERIPHERAL TISSUE (LIVER, KIDNEY) RESISTANCE to the thyroid hormone (free T4)

Answer 251

GRAVES disease

Answer 252

GRAVES disease via anti-TSH RECEPTOR Ab's (TSH-receptor Stimulating (TSI) and Blocking (TBII) Ab's)

Answer 253

GRAVES OPHTHALMOPATHY (exophthalmos, diplopia, conjunctival irritation)

Answer 254

GRAVES disease (autoimmune HYPERthyroidism)

Answer 255

β-blocker ATENOLOL (cardioselective β-blocker)

Answer 256

METHIMAZOLE or PROPYLTHIOURACIL (used in PREGNANCY), radioactive Iodine (I-131), or surgery

Answer 257

LIVER toxicity (elevated LFT's) - thus a BASELINE CBC and LFT's are REQUIRED prior to initiating treatment

Answer 258

PERMANENT HYPOthyroidism (the entire gland is destroyed) - in 2-3 months AFTER treatment, REQUIRING thyroid hormone replacement with LEVOTHYROXINE

Answer 259

Establishing a EUTHYROID (normal thyroid) state

Answer 260

TOXIC MULTINODULAR GOITER (palpable nodules or overall enlargement) and TOXIC ADENOMA

Answer 261

- THYROTOXICOSIS (HYPERthyroidism due to excess free T4 and free T3 secretion) - Use of MRI or US is recommended in these patients

Answer 262

US of the thyroid to assess for cancer and need for biopsy (US-guided FNA)

Answer 263

ABLATION with either RADIOACTIVE Iodine (I-131) or with SURGERY

Answer 264

GOITER causing compression/obstruction

Answer 265

An ACTIVE, hormone-secreting (free T4, free T3) nodule

Answer 266

It would show a SINGLE "HOT" (active, functional) nodule because it would take up the RADIOACTIVE Iodine (I-131) whereas the REST of the gland which is NORMAL, would be suppressed by the effects of the VERY HIGH TSH that the pituitary gland is secreting trying to inhibit the overactive thyroid which has an autonomous nodule secreting thyroid hormone

Answer 267

A NODULE that is noted in areas of the RAIU-scan with DECREASED uptake that signifies a NON-FUNCTIONAL thyroid nodule that is NOT secreting hormones and is a distinct MASS lesion

Answer 268

CONFIRMATION that is is a NODULE by US, followed by a BIOPSY (US-guided FNA) BEFORE starting and TREATMENT ("COLD" nodules have a much higher risk of being CANCER than "HOT" nodules

Answer 269

Ablation with RADIOACTIVE Iodine (I-131) or if not responsive sufficiently to this therapy, SURGERY

Answer 270

DESTRUCTIVE thyroiditis (destruction of thyroid tissue that results in follicle disruption with release of pre-formed thyroid hormone - free T4 and free T3 into the circulation)

Answer 271

VIRAL INFECTION

Answer 272

SUBACUTE Thyroiditis (caused by a viral infection)

Answer 273

POSTPARTUM Thyroiditis (will require levothyroxine)

Answer 274

With levothyroxine for 6 months, then with SLOW TAPER to check if function had been restored and ONGOING monitoring for RECURRENCE

Answer 275

- In SILENT and POSTPARTUM Thyroiditis, β-blocker (ATENOLOL) is used for the THYROTOXIC phase and LEVOTHYROXINE for the HYPOthyroid phase if needed (prolonged/permanent phase) - In SUBACUTE (de Quervain) Thyroiditis, the PAIN is treated with NSAID's and STEROIDS

Answer 276

The DESTRUCTIVE thyroiditis diseases [SUBACUTE (de Quervain) thyroiditis, SILENT thyroiditis and POSTPARTUM thyroiditis]

Answer 277

AMIODARONE (others are INF-α, IL-2 and lithium)

Answer 278

Those with TOXIC MULTINODULAR GOITER (palpable nodules or overall enlargement) and TOXIC ADENOMA most commonly caused by the activation of the expression of a MUTATION in the TSH-RECEPTOR gene that can lead to AUTONOMY of FUNCTION of the THYROID gland with secretion of EXCESS free T4 and free T3 from the affected thyroid NODULES

Answer 279

- DIRECT cause - anti-thyroid drugs (methimazole or propylthiouracil) - INDIRECT cause - STEROIDS - BOTH can be used as well (methimazole + steroids) when unsure and if unresponsive, SURGERY

Answer 280

Subclinical HYPERthyroidism

Answer 281

-They should be TREATED (methimazole or radioactive iodine - I-131) BECAUSE they are at HIGH-RISK for CARDIAC (including a-fib), CNS and BONE disease

Answer 282

HASHIMOTO thyroiditis and IATROGENIC (amiodarone, lithium, INF-α, IL-2 - the same meds that can cause hyperthyroidism, surgery, radiation, etc.)

Answer 283

CELIAC disease (often occurs with autoimmune thyroid disease such as HASHIMOTO thyroiditis)

Answer 284

Anti-TPO Ab's as these would suggest likely HASHIMOTO thyroiditis

Answer 285

Thyroid US and if NODULE is found, MUST BIOPSY (US-guided FNA)

Answer 286

LEVOTHYROXINE (taken 1 HOUR BEFORE meals or 2-3 HOURS AFTER meals, Ca or Iron - containing supplements

Answer 287

1. TSH 0.5-4.3 µU/mL (normal is 0.5-5.0 µU/mL) | 2. If >80 yo the TSH range is 1.0-7.0 µU/mL)

Answer 288

Subclinical HYPOthyroidism (can have HYPERlipidemia and elevated CRP)

Answer 289

They should be TREATED with LEVOTHYROXINE TREAT ALL women who DESIRE PREGNANCY to achieve a TSH level between 0.5-0.25 µU/mL (the normal, physiologic TSH range in pregnancy)

Answer 290

PREGNANCY TSH Range is between 0.1-2.5 µU/mL

Answer 291

THYROID CANCER

Answer 292

Serial Follow-Up

Answer 293

REPEAT BIOPSY (US-guided FNA)

Answer 294

BREAST, MELANOMA, KIDNEY

Answer 295

Thyroid LYMPHOMA

Answer 296

Those that are found in the setting of HYPOthyroidism (

Answer 297

Check serum free T4 and free T3

Answer 298

RAIU-scan to assess etiology of HYPERthyroidism and look for possible "COLD" nodules (which must then be confirmed by US and BIOPSIED - US-guided FNA)

Answer 299

Thyroid US and US-guided FNA BIOPSY as well as LABS looking for thyroid Ab's

Answer 300

If they currently HAVE or HAD MEDULLARY THYROID CANCER treatment/resection and you are following them for disease PROGRESSION or RECURRENCE OR if they have a FAMILY H/O MEDULLARY THYROID CANCER or MEN-2

Answer 301

If they currently HAVE or HAD WELL-DIFFERENTIATED (follicular/papillary) THYROID CANCER treatment/resection and you are following them for disease PROGRESSION or RECURRENCE

Answer 302

MALIGNANT NODULE

Answer 303

BENIGN NODULE

Answer 304

NON-CONTRAST CT or MRI (CT-scans with dye should be avoided as they can trigger thyrotoxicosis in a patient with a toxic adenoma or toxic multinodular goiter)

Answer 305

SUPPRESSED or LOW in the setting of HIGH free T4 and/or free T3 (suggests toxic adenoma or toxic multinodular goiter)

Answer 306

≥1 cm (or ≥0.5 cm if worrisome US features or in patients with RISK factors)

Answer 307

THYROIDECTOMY

Answer 308

THYROIDECTOMY

Answer 309

MONITOR every 6-12 MONTHS with follow-up evaluations AND REPEAT FNA BIOPSY if SIGNIFICANTLY CHANGED in SIZE or APPEARANCE, BUT if STABLE >18 MONTHS, re-evaluate every 3-5 YEARS

Answer 310

HASHIMOTO thyroiditis

Answer 311

COSMETIC INTERVENTION desired by the patient

Answer 312

SIMPLE GOITER (monitor clinically only, no US needed as there are no nodules)

Answer 313

US-guided FNA BIOPSY, because of HIGH-RISK for LYMPHOMA in this setting

Answer 314

MEDULLARY THYROID CANCER (expresses CALCITONIN) - "plasmacytoid, spindle, round or polygonal cells on biopsy"

Answer 315

Medullary Thyroid Cancer (expresses CALCITONIN)

Answer 316

≥45 Stage I - ≤2 cm, no invasion, no LN ≥45 Stage II - >2 cm ≤4 cm, no invasion, no LN Stage III - >4 cm, local invasion, any LN Stage IV - mets or mediastinal LN's

Answer 317

THYROIDECTOMY + RADIOACTIVE Iodine (I-131) + LEVOTHYROXINE (enough to suppress TSH to 0.1-0.5)

Answer 318

When the TUMOR is SOLITARY and

Answer 319

CRITICALLY-ILL patients (also have LOW free T4 - POOR PROGNOSIS)

Answer 320

EUTHYROID SICK SYNDROME (DO NOT TREAT THYROID)

Answer 321

APPROXIMATELY 8 WEEKS

Answer 322

INCREASE her LEVOTHYROXINE by 50% (because there will be less free T4 and free T3 available as ESTROGEN increases thyroxine-binding-globulin "TBG" which binds (stores) more of the free T4 and free T3 and MAINTAIN her TSH level between 01-2.5 µU/mL

Answer 323

Because the maternal Human Chorionic Gonadetropin (HCG) cross-reacts (due to a commonly-shared α-subunit) with the TSH-receptors stimulating thyroid hormone production (does NOT cause HYPERthyroidism)

Answer 324

GRAVES disease (HYPERthyroidism) - REFER TO ENDOCRINOLOGIST and HIGH-RISK OBSTETRICIAN

Answer 325

THYROID EMERGENCIES

Answer 326

THYROID STORM - an EMERGENCY!!!

Answer 327

Antithyroid drugs (METHIMAZOLE or PROPYLTHIOURACIL) + IODINE + IV STEROIDS + β-blockers (atenolol) ± lithium

Answer 328

MYXEDEMA COMA - an EMERGENCY!!!

Answer 329

FIRST, check a RANDOM CORTISOL level (to ensure no concomitant adrenal insufficiency), THEN, give IV BOLUS OF LEVOTHYROXINE + IV STEROIDS (in case of adrenal insuficiency) and then daily IV LEVOTHYROXINE until can be changed to ORAL

Answer 330

Adrenal ALDOSTERONE (mineraloCORTICOID) is controlled by the RENIN (kidney) - ANGIOTENSIN (LUNG-angiotensin-I/LIVER angiotensin-II) SYSTEM (NOT by the pituitary or hypothalamus)

Answer 331

PITUITARY or HYPOTHALAMIC disease/injury, MEDICATIONS, EXOGENOUS STEROIDS, CRANIAL RADIATION, HEAD TRAUMA

Answer 332

EXOGENOUS use of STEROIDS (PREDNISONE, etc.) which suppress CRH and ACTH secretion resulting in ADRENAL CORTICAL ATROPHY causing the adrenal to be unable to secrete adequate CORTISOL especially in STRESS conditions

Answer 333

ACUTE ADRENAL INSUFFICIENCY

Answer 334

They suppress the adrenal glands resulting in ADRENAL INSUFFICIENCY

Answer 335

PRIMARY ADRENAL INSUFFICIENCY with decreased ALDOSTERONE levels and HIGH RENIN LEVELS

Answer 336

PRIMARY or CENTRAL ADRENAL INSUFFICIENCY with DECREASED ADREAL ANDROGENS (DHEA/DHEAS)

Answer 337

PRIMARY or CENTRAL ADRENAL INSUFFICIENCY with DECREASED ADRENAL CORTISOL

Answer 338

ADDISON disease and ADDISONIAN CRISIS

Answer 339

STRESS (illness, surgery) due to the nature of ADDISON disease which affects the ENTIRE adrenal gland with the loss of BOTH glucocorticoids (CORTISOL) and mineralocorticoids (ALDOSTERONE) - NOT usually seen in SECONDARY adrenal insufficiency due to the preservation of the renin-angiotensin-aldosterone system

Answer 340

Adrenal Insufficiency

Answer 341

NORMAL AM: 7-28 µg/dL NORMAL PM: 2-18 µg/dL Stimulated (LOW DOSE): ≥18 µg/dL Suppressed (overnight, given at 11pm, checked at 8am):

Answer 342

Minimal to NO increase (because in PRIMARY adrenal insufficiency, the entire adrenal gland is affected and does not respond to ACTH or its analogues) - BOTH CORTISOL and ALDOSTERONE are LOW, ACTH is HIGH

Answer 343

Serum CORTISOL will INCREASE in this setting as the NORMAL adrenal gland responds to the ACTH analogue. ALDOSTERONE will be NORMAL and unaffected as there is NO central control of aldosterone.

Answer 344

LOW in BOTH (but not typically replaced as not essential for survival)

Answer 345

HYDROCORTISONE (more physiological than prednisone) - however prednisone and dexamethasone are used as they are longer-acting and more convenient for patients

Answer 346

UNDERDOSING: ADDISONIAN CRISIS OVERDOSING: CUSHING Syndrome

Answer 347

FLODROCORTISONE

Answer 348

During times of STRESS (illness, surgery)

Answer 349

Mineralocorticoid used to replace ALDOSTERONE in a patient with PRIMARY ADRENAL INSUFFICIENCY

Answer 350

Cushing SYNDROME - SIGNS and SYMPTOMS caused by EXCESS steroid exposure due to ANY cause [PRIMARY (adrenal adenoma), SECONDARY (exogenous meds OR increased ACTH from pituitary adenoma OR ECTOPIC ACTH-secreting tumor - carcinoid), TERTIARY (excess CRH produced by hypothalamic adenoma)

Answer 351

1. Cushing SYNDROME - SIGNS and SYMPTOMS caused by EXCESS steroid exposure due to ANY cause [PRIMARY (adrenal adenoma), SECONDARY (exogenous meds OR increased ACTH from pituitary adenoma OR ECTOPIC ACTH-secreting tumor - carcinoid), TERTIARY (excess CRH produced by hypothalamic adenoma) 2. Cushing DISEASE - when Cushing syndrome is caused by a SECONDARY (exogenous meds OR increased ACTH from pituitary adenoma OR ECTOPIC ACTH-secreting tumor - carcinoid) OR TERTIARY (excess CRH produced by hypothalamic adenoma) cause 3. ectopic Cushing SYNDROME is Cushing syndrome caused by an ectopic focus of ACTH secretion such as by an ectopic (not adrenal, pituitary or hypothalamic) TUMOR such as a CARCINOID tumor or part of a PARANEOPLASTIC syndrome 4. PRIMARY Cushing SYNDROME is Cushing syndrome that is caused by an ADRENAL adenoma

Answer 352

CUSHING SYNDROME

Answer 353

24-HOUR Urine free-CORTISOL (3x - 4x normal is diagnostic) IF the increase is NOT this HIGH, one of the other two tests is required for confirmation (dexamethasone suppression test or late-night salivary test)

Answer 354

These conditions INCREASE corticosteroid-binding globulin levels (cortisol-binding proteins) in the serum, binding MORE of the available and bioactive "FREE cortisol" levels thus in a NORMAL patient (normal adrenal/pituitary/hypothalamic axis), revving UP production of cortisol so that more of the available FREE cortisol exists in the serum, thus creating the FALSE impression that the total serum cortisol level measured (measures total + free cortisol) is HIGH where that is NOT the case as the AMOUNT of free CORTISOL, the BIOLOGICALLY ACTIVE HORMONE is in FACT LOWER (since more of it became bound to increased binding proteins)

Answer 355

These conditions DECREASE the corticosteroid-binding globulin levels (cortisol-binding proteins) in the serum, binding LESS of the available and bioactive "FREE cortisol" levels thus in a NORMAL patient (normal adrenal/pituitary/hypothalamic axis), slowing DOWN production of cortisol because more of the FREE cortisol now exists in the serum (due to less proteins available to bind it), thus creating the FALSE impression that the total serum cortisol level measured (measures total + free cortisol) is LOW where that is NOT the case as the AMOUNT of free CORTISOL, the BIOLOGICALLY ACTIVE HORMONE is in FACT HIGHER (since more of it became UN-bound due to the decreased circulating binding proteins )

Answer 356

Serum ACTH level (will differentiate between primary - adrenal adenoma/carcinoma, secondary - pituitary adenoma, tertiary - hypothalamic and ectopic - ACTH-producing tumor like CARCINOID or a paraneoplastic syndrome)

Answer 357

POSSIBILE causes: pituitary/hypothalamic/ectopic source NEXT: MRI head (look for PITUITARY/hypothalamic cause), if negative could be a SMALL tumor - CT chest/abdomen, OCTREOTIDE scan (carcinoid) first and if this is negative too, consider B/L inferior petrosal sinus (venous) sampling for small pituitary/hypothalamic tumors not showing up on MRI

Answer 358

POSSIBLE: adrenal ADENOMA (small, homogeneous, fatty tumor) vs. adrenal CARCINOMA (larger, irregular, vascular) NEXT: CT-scan of the ADRENALS - SURGICAL RESECTION of BOTH followed by STEROID replacement

Answer 359

Up to a YEAR after surgery, there will be ACTH deficiency which requires STEROID replacement, endogenous ACTH production usually resumes. If RESIDUAL disease exists, can treat with RADIATION therapy together wit MEDS that inhibit CORTISOL synthesis by the adrenal glands (KETOCONAZOLE, METYRAPONE or MITOTANE)

Answer 360

Because in the setting of ADRENAL SECRETION (not exogenous) of LARGE QUANTITIES of CORTISOL, the mineralocorticoid (ALDOSTERONE) also INCREASES with expected retention of Na and therefore Water with resulting HYPERvolemia (HTN), K⁺ wasting (HYPOkalemia) and thus HYPERkaluria as well as H¯ wasting with METABOLIC Alkalosis

Answer 361

LOW DOSE - suppresses CORTISOL in a NORMAL patient with no pathology in ENDOGENOUS cortisol production (normal adrenals, pituitary, hypothalamus and NO ectopic ACTH source) - suggesting EXOGENOUS etiology HIGH DOSE - NEGATIVE FEEDBACK INHIBITION of PITUITARY and HYPOTHALAMUS ACTH production but has NO effect on ECTOPIC ACTH or ADRENAL TUMORS

Answer 362

THOROUGH assessment for signs of CANCER and HORMONE HYPERsecretion (catecholamines, cortisol, aldosterone) even without overt symptoms If 70 yo and >6 cm

Answer 363

B/L ADRENAL HYPERplasia vs METASTATIC CANCER

Answer 364

Adrenal ALDOSTERONE-secreting ADENOMA (not cancer) - treated with aldosterone-receptor blocking agents SPIRONOLACTONE (can cause GYNECOMASTIA, decreased LIBIDO, IMPOTENCE, MENSTRUAL irregularities) or EPLERENONE - BOTH are CONTRAINDICATED in PREGNANCY

Answer 365

Monitoring with a SINGLE FOLLOW-UP CT-scan ONCE 6-12 MONTHS after initial finding. If there are ANY changes on imaging or clinical symptoms, evaluate biochemically AGAIN

Answer 366

PHEOCHROMYCYTOMA (MEN-2, neurofibromatosis, Von-Hippel-Lindau)

Answer 367

NEVER treat with β-blockers ALONE as this WORSEN the HTN, always START with α-blockers, and THEN add the β-blockers (same treatment pre-surgery) - can use LABETALOL (combination α & β blocker) and nitroprusside if HTN occurs DURING SURGERY

Answer 368

PHEOCHROMYCYTOMA (MEN-2, neurofibromatosis, Von-Hippel-Lindau)

Answer 369

A radio-labeled medication, METAIODOBENZYLGUANIDINE (MIBG) is used for SCINTIGRAPHIC localization of the primary tumor and its potential metastases

Answer 370

PRIMARY HYPERaldosteronism - ADDISON disease (hyperpigmentation) - caused by ADRENAL ADENOMA or ADRENAL HYPERplasia (unilateral or B/L)

Answer 371

Likely PHEOCHROMOCYTOMA (MEN-2, neurofibromatosis, Von-Hippel-Lindau)

Answer 372

Likely PRIMARY HYPERaldosteronism

Answer 373

>15 ng/dL (or pALDOSTERONE:pRENIN >20) are diagnostic Using the RATIO test is BEST especially in patients taking ACE-I's/ARB's or direct renin inhibitors NEITHER test can be done in a patient taking aldosterone-receptor antagonists (SPIRONOLACTONE or EPLERENONE)

Answer 374

It REMAINS elevated (>10 ng/dL) and is NOT SUPPRESSED because of the autonomous ALDOSTERONE production by the ADRENAL gland independent of the RENIN-ANGIOTENSIN system (in a normal person, the plasma aldosterone would decrease to

Answer 375

K⁺-supplementation, because giving a SODIUM load will EXACERBATE the HYPOkalemia

Answer 376

Treatment with aldosterone-receptor blocking agents SPIRONOLACTONE (can cause GYNECOMASTIA, decreased LIBIDO, IMPOTENCE, MENSTRUAL irregularities) or EPLERENONE BOTH are CONTRAINDICATED in PREGNANCY

Answer 377

MALIGNANCY

Answer 378

MITOTANE (like metyrapone and ketoconazole, this med acts to suppress adrenal function)

Answer 379

LEYDIG cells ("ladies!") - located in the interstitial space, OUTSIDE the seminiferous tubules

Answer 380

SERTOLI cells ("Sir!") - located WITHIN the seminiferous tubules where the sperm are made

Answer 381

MORNING (metabolized to dihydrotestosterone in the prostate and estrogen in fat) AM Testosterone >350 ng/dL is NORMAL AM Testosterone

Answer 382

- free-Testosterone is 2% - BOUND-Testosterone is 98% (44% bound TIGHTLY to Sex Hormone-Binding Globulin - SHBG and 54% bound LOOSELY to Albumin - freely dissociates from albumin) - THEREFORE, BIOAVAILABLE Testosterone is free-Testosterone + Albumin Bound-Testosterone - SHBG INCREASES with age (less available, bioactive testosterone) and DECREASES with OBESITY (more available, bioactive testosterone) - THEREFORE, in OLDER or FAT MEN, serum FREE-Testosterone is a BETTER measure of Testostrone

Answer 383

PRIMARY HYPOgonadism (due to testicular failure)

Answer 384

KLEINFELTER Syndrome (XXY) - Y is for male sex, X is for female sex (followed by Cryptorchidism and Varicocele)

Answer 385

ACQUIRED PRIMARY HYPOgonadism in MEN

Answer 386

SECONDARY HYPOgonadism (due to PITUITARY - LH/FSH/HYPOTHALAMIC - GnRH failure)

Answer 387

CONGENITAL SECONDARY HYPOgonadism (due to PITUITARY - LH/FSH/HYPOTHALAMIC - GnRH failure)

Answer 388

ACQUIRED SECONDARY HYPOgonadism (due to PITUITARY - LH/FSH/HYPOTHALAMIC - GnRH failure)

Answer 389

TESTOSTERONE, ESTRADIOL (estrogen) - converted by fat in men, DIHYDROTESTOSTERONE - converted by the prostate AND INHIBIN-B (produced by testicular sertoli cells)

Answer 390

HYPOgonadism

Answer 391

- Check the SERUM free-Testosterone level and if ALSO LOW, patient is DIAGNOSED with HYPOgonadism - NOW serum LH & FSH should be measured (to determine primary or secondary HYPOgonadism) - IF HIGH (primary - w/o h/o testicular injury, check for Kleinfelter karyotype XXY) an IF LOW or NORMAL (secondary - check for prolactinemia, hemochromatosis - high transferrin/ferritin - and ANY other pituitary deficiencies AND do an MRI, especially if testosterone

Answer 392

Testosterone Replacement Therapy for HYPOgonadism

Answer 393

GEL (hydroalcoholic) - all testosterone replacement types require follow-up with testosterone level testing and evaluation for potential development of adverse effects (increased Hct >54%, worsened OSA, BPH >1.4 in one year or >0.4 in 6 months, dyslipidemia, increased RISK of prostate cancer and cardiovascular events)

Answer 394

ANDROGEN ABUSE (injectable/oral testosterone, HCG, DHEA, aromatase inhibitors and androstenedione supplements)

Answer 395

SEMEN analysis (for sperm count) after abstaining from sex for 48-72 HOURS - if abnormal, repeat once more

Answer 396

GYNECOMASTIA (physiologic during neonatal and adolescent periods only)

Answer 397

Detection of SUB-AREOLAR GLANDULAR tissue

Answer 398

Testicular US FIRST (if estradiol was also elevated), if NEG for mass - CHEST/ABD CT to detect possible malignancy, if NEG, do adrenal CT/MRI for possible adrenal malignancy and if NEG - likely peripheral aromatase activity if obese. IF after all of this is done and STILL NEG, if BOTH LH and Testosterone are elevated - androgen insensitivity syndrome

Answer 399

FSH INCREASES slightly (causing recruitment of ovarian follicles - the saccular structures within the ovary that contain the EGG) and an INCREASE of ESTRADIOL (stimulating endometrial proliferation), inducing LH-receptors in the OVARIES, which in turn causes an INCREASE of LH (surge) causing OVULATION and the LUTEAL PHASE due to the POSITIVE FEEDBACK ACTIVATION by ESTRADIOL of the PITUITARY gland. LH also stimulates ANDROGEN production (by the THECA cells that line the FOLLICLES) which is aromatized to ESTROGEN (inside the inner GRANULOSA cells of the FOLLICLE by FSH). After the LH surge (and thus OVULATION - the expulsion of the EGG from the now mature FOLLICLE) the empty FOLLICLE which now becomes the CORPUS LUTEUM, secretes BOTH ESTRADIOL and PROGESTERONE. If NO CONCEPTION (fusion of a sperm with the EGG) occurs, as the CORPUS LUTEUM begins to INVOLUTE (atrophy and disappear), the DECLINING PROGESTERONE LEVELS lead to MENSTRUAL BLEEDING and the cycle begins again. If pregnancy DOES occur, the HCG produced by the CONCEPTUS (fusion of the SPERM and EGG) ARRESTS the INVOLUTION of the CORPUS LUTEUM which continues to secrete PROGESTERONE as does the developing PLACENTA and thus NO BLEEDING OCCURS

Answer 400

They are ANOVULATORY (no ovulation took place)

Answer 401

PRIMARY AMENORRHEA (NORMAL body hair and BREAST development)

Answer 402

PREGNANCY (if this is NEG, 50% will have a CHROMOSOMAL abnormality - gonadal dysgenesis "defective development of the gonads" and 15% will have an anatomic abnormality - uterus, vagina or cervix)

Answer 403

TURNER SYNDROME (45,X) - (PRIMARY OVARIAN INSUFFICIENCY) - short stature, webbed neck, low set ears and low hairline on back of neck, no breasts

Answer 404

SECONDARY AMENORRHEA

Answer 405

SECONDARY AMENORRHEA

Answer 406

Polycystic Ovarian Syndrome (PCOS), Hypothalamic disorders, HYPERprolactinemia (direct GnRH inhibition by prolactin), HYPERthyroidism (due to weight loss), HYPOthyroidism (due to INCREASED hypothalamic TRH secretion which also stimulates prolactin secretion which inhibits GnRH) and Primary Ovarian Insufficiency

Answer 407

SECONDARY AMENORRHEA due to FUNCTIONAL HYPOTHALAMIC AMENORRHEA

Answer 408

Primary OVARIAN Insufficiency

Answer 409

Turner Syndrome (45,X), Fragile X Carrier, Autoimmune Disease and CHEMO/RADIATION therapy

Answer 410

Pituitary MRI

Answer 411

Assess for ESTROGEN DEFICIENCY (Progesterone challenge test - if bleeding occurs within a WEEK of taking progesterone, she is making enough estrogen and perhaps has PCOS, if NO BLEEDING occurs, she is NOT making enough estrogen likely due to HYPOTHALAMIC causes - do a pituitary MRI)

Answer 412

The presence of EITHER an OVARIAN or ADRENAL tumor causing "virilization"

Answer 413

DHEAS, TSH, Prolactin, Total Testosterone and 17-hydroxyprogesterone

Answer 414

HIGH levels of 17-hydroxyprogesterone (due to deficiency of the 21-hydroxylase enzyme)

Answer 415

1. Pelvic US and Adrenal CT to exclude tumors | 2. Adrenal CT to exclude a medullary tumor (one that secretes androgens OR cortisol)

Answer 416

Criteria for diagnosis of PCOS (2 of the 3 are needed)

Answer 417

Polycystic Ovarian Syndrome (PCOS)

Answer 418

Irregularities with the menstrual cycle (oligomenorrhea, light bleeding, irregular bleeding, prolonged or shortened cycles)

Answer 419

INSULIN RESISTANCE

Answer 420

Weight Loss & Exercise, COMBINED Oral Contraceptive Pills (to treat Menstrual Irregularities and HYPERandrogenism) + Spironolactone (if persistent hirsutism and acne after 6 months) and METFORMIN for INSULIN RESISTANCE (with acanthosis nigricans) and if INFERILITY is present, CLOMIPHENE is added (estrogen agonist)

Answer 421

INFERTILITY (can be caused by even MILD thyroid or prolactin irregularities) - check male sperm count and ovulatory function by checking the progesterone level mid-luteal phase (highest level)

Answer 422

REFERRAL to REPRODUCTIVE ENDOCRINOLOGIST

Answer 423

Normal serum Ca 9.0-10.5 mg/dL | 60% is BOUND to plasma proteins or complexed with ANIONS, the rest is FREE and controls physiologic actions

Answer 424

Absorbed: intestine (by Eliminated: kidney Stored: bone

Answer 425

The PARATHYROID glands have a cell membrane Calcium-Sensing Receptor (CSR) that monitors the PLASMA free (IONIZED) Ca levels. As circulating levels of plasma free (IONIZED) Cal levels INCREASE, the Calcium-Sensing Receptor (CSR) causes PTH secretion to DECREASE and when plasma free (IONIZED) levels are LOW, the Calcium-Sensing Receptor (CSR) causes PTH secretion to INCREASE

Answer 426

PTH acts on: 1. Activating BONE RESORPTION (breakdown of bone by osteoclasts, essentially mining the stored Ca) 2. Induces DISTAL CONVOLUTED TUBULE reabsorption of Ca 3. Stimulates KIDNEY production of 1,25-dihydroxyvitamin D, the ACTIVE form of vitamin D which acts on the SMALL INTESTINE enterocytes to INCREASE ABSORBTION of Ca

Answer 427

HYPERcalcemia (>12 mg/dL) - when serum Ca >14 mg/dL symptoms of LETHARGY, DISORIENTATION and COMA can occur

Answer 428

MEN-1 and MEN-2

Answer 429

-MALIGNANCY DIRECT: (Multiple Myeloma, Breast Cancer, Lymphoma) -MALIGNANCY INDIRECT: PTH-related protein (squamous cell carcinoma, breast/ovary adenocarcinoma, renal cell carcinoma, transitional cell carcinoma, T-cell lymphoma) -Granulomatous Disease: SARCOIDOSIS, TB OTHER: HYPERthyroidism, Adrenal Insufficiency, Thiazides

Answer 430

FACTITIOUS HYPERcalcemia - INCREASED levels of the PLASMA proteins that BIND Ca (HIV, chronic HEPATITIS, Multiple Myeloma) - as the free (IONIZED) Ca⁺² remains normal

Answer 431

Serum PTH levels and EITHER serum free (IONIZED) Ca⁺² levels or if no increased plasma proteins, the serum total Ca

Answer 432

PRIMARY HYPERparathyroidism (PTH-mediated HYPERcalcemia with a LOW serum PHOS)

Answer 433

When the cause is PRIMARY HYPERparathyroidism (PTH-mediated HYPERcalcemia)

Answer 434

When the cause is Vitamin D INTOXICATION (hypervitaminosis D)

Answer 435

PRIMARY HYPERcalcemia (PTH-mediated HYPERcalcemia) usually due to a PARATHYROID ADENOMA (the other causes are parathyroid hyperplasia and parathyroid cancer)

Answer 436

The SEVERITY (how HIGH is the serum Ca level) and the CHRONICITY (how QUICKLY did the levels rise from normal

Answer 437

Chronic HYPERcalcemia symptoms

Answer 438

DO NOT RESTRICT dietary Ca nor Vit D supplementation as doing so will WORSEN bone loss and further elevate serum PTH

Answer 439

BISPHOSPHONATES

Answer 440

CINACALCET - a calcimimetic

Answer 441

FAMILIAL HYPOcalciuric HYPERcalcemia (CASR gene mutation), NO TREATMENT NEEDED

Answer 442

BECAUSE in FAMILIAL forms (MEN-1 and MEN-2), where there is a FAMILY H/O (Pituitary adenoma, PARATHYROID hyperplasia, Pancreatic tumors - 1); or (Medullary thyroid cancer, Pheochromocytoma, PARATHYROID hyperplasia -2a) ALL FOUR (4) parathyroid glands may be affected by the hyperplasia REQUIRING evaluation of ALL FOUR (4) glands during surgery

Answer 443

BEFORE: evaluate for a possible PHEOCHROMOCYTOMA DURING: evaluate ALL FOUR (4) parathyroid glands for HYPERplasia and CHECK for a possible MEDULLARY THYROID CANCER

Answer 444

1. CANCER (Multiple Myeloma, Breast Cancer, Lymphoma) | 2. If NO cancer is found, CHECK for Vitamin D INTOXICATION or 1,25-duhydroxyvitamin D production by SARCOIDOSIS or TB

Answer 445

SURGERY for parathyroidectomy

Answer 446

CANCER (Multiple Myeloma, Breast Cancer, Lymphoma)

Answer 447

B-cell LYMPHOMA

Answer 448

PTH-related PROTEIN "PTHrP" which acts in the SAME way as PTH causing HYPERcalcemia by BONE resorption and DECREASING Ca EXCRETION by the kidneys with INCREASED EXCRETION of PHOSPHATE resulting in serum HYPERcalcemia, HYPOphospatemia with a LOW serum PTH (suppressed) but when measured, a HIGH PTHrP

Answer 449

1. Aggressive IVF's (NS) HYDRATION + DIURETICS 2. IV Bisphosphonates (ZOLENDRONATE/Pamidronate) to stop osteoclast activity on bone resorption (causes osteoclast apoptosis) 3. SQ CALCITONIN injection 4. Hemodialysis 5. If caused by Vitamin D intoxication, give STEROIDS

Answer 450

STOP INTESTINAL ABSORPTION with STEROIDS (prednisone)

Answer 451

``` Serum ALBUMIN (binds free Ca in the serum) For EACH 1 g/dL the serum Alb is ```

Answer 452

HYPOparathyroidism with resulting HYPOcalcemia | Other causes of HYPOcalcemia without HYPOparathyroidism are pancreatitis, rhabdomyolysis and tumor lysis syndrome

Answer 453

HYPOparathyroidism

Answer 454

Iatrogenic INJURY or REMOVAL of the PARATHYROID glands

Answer 455

HUNGRY-BONE SYNDROME

Answer 456

DiGeorge Syndrome ("Did George have parathyroids?")

Answer 457

MAGNESIUM (HYPOmagnesemia) - PTH can be LOW, NORMAL or HIGH

Answer 458

pseudoHYPERparathyroidism

Answer 459

RICKETS (Type I - vit D dependent AND Type II - vit D resistant)

Answer 460

RICKETS Type I (vitamin D dependent)

Answer 461

RICKETS Type II (vitamin D resistance - a receptor defect)

Answer 462

Check MAGNESIUM and Vitamin D

Answer 463

SLOW replacement with IV Ca-GLUCONATE until SYMPTOMS are relieved, then switch to PO (making sure than any existing Mg and Vit D deficiencies are ALSO treated)

Answer 464

Oral Ca + Vitamin D (replenishing their stores first)

Answer 465

Indefinite - because the absence of PTH causes the absence of 1α-hydroxylase in the kidney thus no hydroxylation of the stored vitamin D into the active form. Serum Ca must be maintained in the LOW-normal range to prevent HYPERcalciuria and formation of kidney STONES

Answer 466

Ca - between 1,000-2,500 mg (1,200-2,000 if >50 yo) | Vitamin D3 - between 600-4,000 units (800-4000 if >50 yo)

Answer 467

OSTEOPOROSIS (tested by Bone Mineral Density - reflects bone Ca-content)

Answer 468

OSTEOPOROSIS

Answer 469

OSTEOPENIA

Answer 470

PROXIMAL FEMUR and LUMBAR SPINE

Answer 471

HIP fracture (from associated complications such as PE and PNA)

Answer 472

Bone-absorbing OSTEOCLASTS (destroyers) STIMULATED by PTH, create "RESORPTION PITS" in the BONE liberating the mined Ca into the BLOOD, a portion of which becomes BOUND to Albumin and the rest exists as the BIOACTIVE free Ca (sensed by the sensor cells of the parathyroid glands which regulate Mg-dependent PTH secretion). The OSTEOBLASTS then FILL-IN these "RESORPTION PITS" with new, RAW bone MATRIX which is then MINERALIZED with HYDROXYAPATITE to become mineralized BONE With ADVANCING AGE, less and less new BONE is MADE compared to how much is RESORBED resulting in DECLINING BONE MASS and INCREASED RISK of fractures

Answer 473

It COUNTERACTS the actions of parathyroid hormone (PTH) and INHIBITS HYPERcalcemia (it reduces blood Ca) by INHIBITION of Ca absorption by the INTESTINE, INHIBITS OSTEOCLASTS and STIMULATES OSTEOBLASTS and INHIBITS KIDNEY REABSORPTION of Ca INCREASING its EXCRETION

Answer 474

In the PERI-MENOPAUSAL and EARLY-MENOPAUSAL periods due to ESTROGEN DEFICIENCY

Answer 475

Dual-Energy X-ray Absorptiometry (DEXA) which yields T-scores and Z-scores

Answer 476

The T-score (the NUMBER of standard deviations (SD) a patient's Bone Mineral Density is HIGHER or LOWER than the MEAN reference value of a young, healthy sex-matched 30 yo)

Answer 477

DEXA test (t-score/z-score) for osteoporosis and osteopenia

Answer 478

Because although T-scores may improve SLIGHTLY, the patient's FRACTURE RISK improves by 30-50%

Answer 479

Because HYPERthyroidism and MEDULLARY THYROID CANCER can cause EXCESS CALCITONIN release with resulting HYPOcalcemia and HYPERparathyroidism

Answer 480

TESTOSTERONE deficiency

Answer 481

BONE LOSS and FRACTURES

Answer 482

It means that for other people of the same sex and age, the patient is BELOW the expected rate of bone loss INDICATING that OTHER factors besides AGE are contributing to their BONE LOSS

Answer 483

Women ≥65 | ALL others with RISK FACTORS

Answer 484

A patient's ABSOLUTE FRACTURE RISK over the next 10 YEARS | FRAX - Fracture Risk Assessment

Answer 485

OSTEOPOROSIS (reduction of fractures of 30-60% over 2-3 years)

Answer 486

BISPHOSPHONATES

Answer 487

TERIPARATIDE (PTH analogue) - although CHRONIC elevation in serum PTH results in BONE LOSS, the use of this medication which provides TRANSIENT PTH SPIKES rather than CHRONIC exposure creates a desired ANABOLIC effect - the ONLY ANABOLIC agent AVAILABLE

Answer 488

RALOXIFENE (bone-selective estrogen receptor modulator) - NOT for men

Answer 489

CALCITONIN

Answer 490

Because of its HIGH RISK for OSTEOSARCOMAS

Answer 491

PHARMACOLOGIC TREATMENT (bisphosphonates, etc.)

Answer 492

Assess for MEDICATION ADHERENCE or an UNRECOGNIZED CAUSE (CANCER)

Answer 493

OSTEOMALACIA (can be confirmed by bone biopsy if needed)

Answer 494

RICKETS (Types I &II) Type I - vitamin D dependent Type II - vitamin D resistance - a receptor defect

Answer 495

OSTEOMALACIA (can be confirmed by bone biopsy if needed)

Answer 496

OSTEOMALACIA (can be confirmed by bone biopsy if needed)

Answer 497

Cholecalciferol (Vitamin D3) + CALCIUM

Answer 498

25-hydroxyvitamin D (the STORAGE form of Vitamin D)

Answer 499

50,000 Units/WEEK of ERGOCALCIFEROL (Vitamin D2) x 8 WEEKS followed by a confirmation of NORMAL serum 25-hydroxyvitamin D

Answer 500

Serum 25-hydroxyvitamin D

Answer 501

PAGET disease of bone

Answer 502

Evaluate for OSTEOSARCOMA as he has PAGET disease of bone

Answer 503

NUCLEAR BONE SCAN (X-rays should ALSO be done, to exclude metastatic disease)

Answer 504

2 MONTH course of RISEDRONATE or an INJECTABLE bisphosphonate (ZOLENDRONATE, Pamidronate)

Answer 505

CALCITONIN (SQ injection and Intranasal)

Answer 506

By serial measurements of serum Alk. Phos., check every 3-6 months and RETREAT as necessary as well as AUDIOMETRY testing when skull is involved

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ABIM 2015 - Endocrine Flashcards

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