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232 Cards in this Set
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What is the difference between endocrine and exocrine glands?
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endocrine glands secrete hormones directly into blood
exocrine glands secrete products into ducts |
Physiolgoy p317
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In the adrenal gland, which layers secrete which hormones?
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adrenal cortex:
-zona glomerulosa mainly secretes aldosterone -zona fasciculata mainly secretes cortisol -zona reticularis mainly secretes DHEA and DHEA-S andrenal medulla: secretes epinephrine and norepinephrine |
Physiology p322
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Which hormone measurement is more important, free or total?
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free
only free can diffuse out of capillaries and encounter target cells |
Physiology p323
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What is the function of aldosterone?
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↑ sodium and water retention
↑ potassium and hydrogen excretion in urine long-term regulation of BP |
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What are the major organs that exrete or metabolize hormones?
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kidneys
liver |
Physiology p324
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How long do free and bound hormones stay in blood?
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free hormones stay in blood for minutes to an hour
bound hormones stay in blood several hours to days |
Physiology p324
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Name a synthetic form of cortisol and its indication.
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prednisone
used to suppress inflammatory and allergic reactions |
Physiology p325
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What is a tropic hormone?
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hormone that stimulates secretion of another hormone
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Physiology p327
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What are the 4 broad categories of endocrine diseases?
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1. hyposecretion
2. hypersecretion 3. target-cell hyporesponsiveness 4. target-cell hyperresponsiveness |
Physiology p327
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What are 3 causes of primary hyposecretion?
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1. glandular injury
2. enzyme deficiency 3. dietary deficiency |
Physiology p327
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How can you differentiate between primary and secondary hyposecretion?
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administer tropic hormone
if gland responds → 2° hyposecretion if gland fails to respond → 1° hyposecretion |
Physiology p327
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How can you differentiate between primary and secondary hypersecretion?
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measure hormone and tropic hormone concentrations
if both elevated → 2° hypersecretion if tropic hormone diminished (due to negative feedback) → 1° hypersecretion |
Physiology p328
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What is diuresis?
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loss of excess water in urine
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Physiology p331
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What is the classic triad of diabetes symptoms?
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1. polyuria (increased urination)
2. polydypsia (increased thirst) 3. polyphasia (increased fluid intake and appetite) |
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What is the normal range for A1C?
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4.8-5.6
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Why is A1C used to moniter diabetes?
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AC1 levels are proportional to glucose levels over past 2 months
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What does A1C measure?
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control of glucose over past 2 months
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What are the indications for ordering hemoglobin A1C?
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screening for diabetes
monitoring of long-term glucose control in diabetic patients |
Interpreting Laboratory Data p2
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What is menopause?
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cessation of menses due to aging or bilateral oophorectomy
no menstruation for 1 year |
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In endocrinology, primary dysfunction means?
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problem originates in a particular gland
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What is the etiology of menopause?
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aging
bilateral oophorectomy premature menopause: ovarian failure and menstrual cessaton <40y/o often d/t genetic or autoimmune |
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In endocrinology, secondary dysfunction means?
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problem outside gland causes effect to other gland or tissue
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What is the clinical presentation of menopause?
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~51y/o if d/t aging
hot flashes night sweats vaginal dryness dyspareunia mood changes → anxiety, depression etc. thinned vaginal mucosa → pale smooth vaginal mucosa small cervix and uterus ovaries non-palpable |
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Where is the pituitary located?
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base of brain
attached to hypothalamus via infundibular stalk |
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What is the diagnostic workup of menopause?
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elevated FSH and LH
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What is another name for the anterior pituitary?
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adenohypophysis
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What is the management of menopause?
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1. for hot flashes → consider estrogen/progestin therapy or SSRIs
2. for vaginal atrophy → lubrications, vaginal creams, estradiol vaginal ring 3. calcium and vitamin D supplements 4. monitor for osteoporosis and treat accordingly 5. if vaginal bleeding occurs following menopause → R/O endometrial cancer 5. provide education and support and referral to midlife discussion groups 6. if surgical menopause → immediate estrogen therapy that is then tapered |
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The anterior pituitary produces and stores its own hormones, true or false?
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true
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How long does menopause last?
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menstruation diminishes until absent usually over 1-3 year period
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The posterior pituitary produces and stores its own hormones, true or false?
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false
only stores hormones produced by hypothalamus |
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What are hot flashes?
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feeling of intense heat over face and trunk
flushing sweating worse following oophorectomy may occur at night and cause insomnia and fatigue |
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What is another name for the posterior pituitary?
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neurohypophysis
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What is the controversy behind menopause-associated hormone replacement therapy?
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estrogen-progestin therapy increased risk of cardiovascular disease, cerebrovascular disease and breast cancer
can consider prescribing if early menopause + severe hot flashes but d/c after 3-4 years |
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List hormones produced by the anterior pituitary.
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growth hormone (GH)
adrenocorticotropic hormone (ACTH) follicle-stimulating hormone (FSH) leutinizing hormone (LH) thyroid stimulating hormone (TSH) |
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How long do hot flashes typically last?
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2-3 years
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What is a mnemonic for remembering the hormones produced by the anterior pituitary?
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GPA is B FLAT:
G = GH P = prolactin A = above produced by acidophil cells B = below produced by basophil cells F = FSH L = LH A = ACTH T = TSH |
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What is the origin, regulation, and function of growth hormone?
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ORIGIN:
anterior pituitary REGULATION: + GHRH from hypothalamus - somatostatin FUNCTION: stimulates growth stimulates carbohydrate, protein and lipid metabolism |
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What is the origin, regulation, and function of adrenocorticotropin?
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ORIGIN:
anterior pituitary REGULATION: + corticotropin releasing hormone (CRH) from hypothalamus (often released in response to stress) - glucocorticoid negative feedback FUNCTION: stimulates adrenal cortex to secrete glucocorticoids (including cortisol) to resist stressors |
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GH deficiency can cause?
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short stature in children
weakness obesity increased cardiac mortality in adults |
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What is the origin, regulation and function of insulin?
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ORIGIN:
B-cells of islet of langerhans of pancreas REGULATION: + hyperglycemia, amino acids, digestive hormones (IGF, GIP, GLP), parasympathetic stimulation - epinephrine, sympathetic stimulation |
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What is the origin, regulation, and function of prolactin?
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ORIGIN:
anterior pituitary REGULATION: + PRH (prolactin releasing hormone) from hypothalamus - PRH (prolactin inhibiting hormone) from hypothalamus FUNCTION: stimulates lactation decreases estrogen in women and testosterone in men |
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What is the ddx for short stature?
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familial
small for a GH deficiency skeletal dysplasias Turner syndrome Prader-Willis Down syndrome pyschosocial dwarfism |
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What is the diagnostic workup for short stature?
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Radiograph of left hand and wrist for bone age
Complete blood count (to detect chronic anemia or infection) Erythrocyte sedimentation rate (often elevated in collagen-vascular disease, cancer, chronic infection, and inflammatory bowel disease) Urinalysis, blood urea nitrogen, and serum creatinine (occult renal disease) Serum electrolytes, calcium, and phosphorus (renal tubular disease and metabolic bone disease) Stool examination for fat, serum tissue transglutaminase, or endomysial antibody (malabsorption or celiac disease) Karyotype (in girls) Thyroid function tests: free thyroxine (FT4) and thyroid-stimulating hormone (TSH) IGF-1 and IGF-binding protein 3 (IGFBP-3) |
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Define hirsutism.
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excessive terminal hair growth that appears in a male pattern in women
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HIRSUTISM DDX
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idiopathic
familial PCOS → increased testosterone Cushing’s syndrome acromegaly steroidogenic enzyme defects malignancy medications |
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HIRSUTISM CLINICAL PRESENTATION
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increased sexual hair (upper lip, chin, chest, abdomen)
increased sebaceous gland activity (acne) irregular menstruation, amenorrhea, anovulation defeminization (↓ breast size, loss of feminine adipose tissue) virilization (frontal balding, muscularity, clitoromegaly, deepened voice) |
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HYPOGONADISM MALE
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ETIOLOGY:
caused by deficient testosterone secretion by the testes 1. pituitary pathology → insufficient gonadotropin secretion (hypogonadotropic) 2. testicle pathology (hypergonadotropic) 3. both Hypogonadotropic Hypogonadism ↓ FSH and LH may be d/t normal aging, obesity, poor health may be d/t Cushing’s syndrome, adrenal insufficiency, growth hormone excess or deficiency, thyroid hormone excess or deficiency, hyperprolactinemia, GnRH agonist therapy for prostate cancer Hypergonadotropic Hypogonadism ↑ FSH and LH viral infection (mumps), irradiation, cancer chemotherapy, autoimmunity, myotonic dystrophy, uremia, XY gonadal dysgenesis, partial 17-ketosteroid reductase deficiency, Klinefelter syndrome, and male climacteric. Klinefelter syndrome – testes firm, fibrotic, small, and nontender, gynecomastia, tall stature, greater than arm span CLINICAL PRESENTATION: decreased libido erectile dysfunction gynecomastia fatigue, hot sweats, depression infertility decreased body, axillary, beard, or pubic hair lose muscle mass and gain weight due to an increase in subcutaneous fat DIAGNOSTIC WORKUP: testosterone – nonfasting morning specimens if hypergonadotropic hypogonadism ↑serum FSH and LH if hypogonadotropic hypogonadism ↓ serum FSH and LH mild anemia DXA MANAGEMENT: Testosterone replacement is the usual treatment for hypogonadism. 1st-line = Topical testosterone gel Patch, IM, or PO also avaliable |
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Kussmaul respirations are associated with?
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diabetic ketoacidosis
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What is the most common cause of hyperpituitarism?
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adenoma
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What is the etiology of diabetes insipidus?
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1° d/t ADH deficiency or resistance resulting in reduced water reabsorption
2° d/t kidney dysfunction resulting in reduced water reabsorption 1 ° central diabetes insipidus: unknown genetic autoimmune 2° central diabetes insipidus: cause may be: damage to hypothalamus or pituitary via trauma, infection, neoplasm, iatrogenic, etc. nephrogenic diabetes insipidus: genetic pyelonephritis ATN renal amyloidosis Sjogren's syndrome sickle cell anemia hypokalemia chronic hypercalcemia myeloma medications |
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What is the clinical presentation of diabetes insipidus?
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polydipsia
polyuria hypernatremia if insufficient fluid intake |
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What is the diagnostic workup of diabetes insipidus?
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UA → low specific gravity, otherwise normal
24 hour urine for volume and creatinine → 2-20L, otherwise R/O vasopressin challenge test for suspected central cause → decreased polydipsia and polyuria ADH for suspected nephrogenic cause → elevated ADH MRI of hypothalamus and for lesions |
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What is the management of diabetes insipidus?
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1. if mild → adequate fluid intake
2. if central or preganancy → desmopressin acetate 3. avoid corticosteroids which increase renal free water clearance 4. wear medical alert bracelet in case unable to drink adequate fluids d/t mental status changes, bed-bound, etc. |
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What is another name for ADH?
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vasopressin
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What is the origin, regulation, and function of ADH?
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ORIGIN:
produced in hypothalamus stored in posterior pituitary REGULATION: + dehydration FUNCTION: stimulates insertion of aquaporins in distal tubule and collecting duct → increasing water reabsorption |
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What is the vasopressin challenge test?
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ordered for suspected diabetes insipidus
urine measured 12 hours before desmopressin acetate given desmopressin acetate given subcutaneously, intranasally or via IV urine measured 12 hours after desmopressin given which acts as a synthetic ADH replacement if central diabetes insipidus present → reduction in polydipsia and polyuria if nephrogenic diabetes insipidus present → no reduction |
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What is the etiology of acromegaly?
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usually pituitary adenoma
rarely genetic → MEN 1 rarely ectopic secretion of GHRH or GH → lymphoma, hypothalmic tumor, pancreatic tumor McCune-Albright syndrome Carney syndrome |
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What is the clinical presentation of acromegaly?
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occurs in adults
excessive growth of jaw, hands, feets, and internal organs HA, weakness visual field loss (temporal hemianopsia) enlarged hat, ring and shoe size soft, doughy, sweaty handshake deepened voice d/t hypertrophy of pharynx and laryngx weight gain macroglossia carpal tunnel obstructive sleep apnea HTN cardiomegaly DM arthritis hyperhidrosis cystic acne acanthosis nigricans hypogonadism if pituitary adenoma also secreting prolactin or pressing on normal pituitary tissue |
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What is the diagnostic workup of acromegaly?
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comprare patient to older photos
elevated random serum IGF-1 → usually 5x normal give 75mg glucose and measure GH one hour later → R/O if not elevated glucose prolactin liver enzymes and BUN (failure can elevate GH) calcium and phos TSH and FT4 MRI |
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What is the management of acromegaly?
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1. surgery then observation
2. if refractory to surgery → dopamine agonist, somatostatin, or pegvisomant 3. if refractory to medical management → radiation |
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How does GH affect IGF-1?
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GH stimulates release of IGF-1 from liver and other tissues
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What are the most common complications of agromegaly?
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cardiovascular disorders
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GH can be elevated by what normal physiologic conditions?
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eating
exercise |
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What is the etiology, diagnostic workup, and management of gigantism?
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same as acromegaly
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What is the clinical presentation of gigantism?
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occurs if manifests before growth plate closure
extremely tall and thin |
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acromegaly
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gigantism
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What is the etiology of hypothyroidism?
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impaired thyroid gland (autoimmune)
TSH deficiency (pituitary) medications → amiodarone chemotherapy radiation surgery HepC associated with increased risk affects 1% of population affects 5% >60y/o |
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What is the clinical presentation of hypothyroidism?
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fatigue
lethargy HA weakness myalgias muscle cramps weight gain cold intolerance hoarseness exertional dyspnea constipation menorrhagia arthralgias paresthesias depression diastolic HTN bradycardia skin pallor or yellowing (carotenemia) xerosis thinning hair thin brittle nails goiter puffy face and eyelids peripheral edema Raynaud syndrome delayed return of DTRs carpal tunnel |
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What is the diagnostic workup of hypothyroidism?
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anemia
hyponatremia hyperlipidemia elevated TSH (if primary) decreased FT4 |
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What is the management of hypothyroidism?
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levothyroxine
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What are the complications of hypothyroidism?
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myxedema coma
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What is the most common cause of hypothyroidism?
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Hashimoto thyroiditis
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Myxedema coma is a complication of what disorder?
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hypothyroidism
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What is hypothyroidism?
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endocrine condition characterized by thyroid hormone deficiency
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What is the clinical presentation of myxedema coma?
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lymphedema
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What is the etiology of myxedema coma?
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complication of hypothyroidism
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What are the types of thyroiditis?
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Hashimoto's thyroiditis
subacute thyroiditis suppurative thyroiditis Reidel's thyroiditis |
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What is the most common thyroid disorder in the U.S.?
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hashimoto's thyroiditis
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What is the clinical manifestation of hashimoto's thyroiditis?
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slow onset
thyroid enlarged, rubbery, non-tender symptoms of hypothyroidism |
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What is the etiology of hashimot's thyroiditis?
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autoimmune → B-cells invade thyroid gland → often progresses to hypothyroidism
6x more common in women, usually middle-aged associated with iodine dietary supplementation, medications, radiation |
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What is another name for hashimoto's thyroiditis?
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chronic lymphocytic thyroiditis
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What is the diagnostic workup of hashimoto's thyroiditis?
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high TSH
low FT4 antithyroid peroxidase antibody antithyroglobulin antibody |
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What is the management of hashimoto's thyroiditis?
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1. if minimally enlarged thyroid + no thyroid hormone deficiency → observation
2. if enlarged thyroid + hypothyroidism → levothyroxine 3. if goiter → T4 to suppress TSH and shrink goiter |
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What is the etiology of subacute thyroiditis?
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viral infection
often follows URTI peak incidence occurs in summer most commonly affects young and middle-aged women |
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What is the clinical presentaiton of subacute thyroiditis?
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acute
fatigue low-grade fever painful enlarged thyroid +/- radiation to ears dysphagia may progress to thyrotoxicosis for several weeks then hypothyroidism for 4-6 months can also cause hyperthyroidism |
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What is the diagnostic workup of subacute thyroiditis?
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markedly elevated ESR
low antithyroid antibody titers |
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What is the management of subacute thyroiditis?
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1. treatment empiric
2. symptomatic treatment → aspirin 3. thyrotoxicosis → propranolol 4. transient hypothyroidism → T4 5. symptoms may last weeks to months depending on development of thyrotoxicosis and hypothyroidism → usually resolves within 12 months → but hypothyroidism may persist |
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What is the different types of hyperthyroidism?
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Grave's disease
toxic multinodular goiter thyroid crisis or "storm" subacute thyroiditis |
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What is the most common cause of hyperthyroidism?
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Grave's disease
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What is the etiology of Grave's disease?
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autoimmune → autoantibodies bind to TSH receptor of thyroid cell membrane → stimulate hyperfunctioning
familial tendency risk increased if dietary iodine supplementation affects 8x more women than men onset 20-40y/o |
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What is Grave's disease?
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type of hyperthyroidism characterized by increased secretion of thyroid hormone
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What is the clinical presentation of Grave's disease?
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thyroid → diffusely enlarged, hyperplastic
eye changes assymetric or bilateral upper eyelid retraction (Dalrymple sign), lid lag with downward gaze (von Graefe sign), weakness of upward gaze (Stellwag sign), staring appearance (Kocher sign), conjunctivitis, chemosis, exophthalmos, diplopia, corneal dryness, vision changes exophthalmos acropachy pretibial myxedema |
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What is the diagnostic workup of hyperthyroidism
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↓ TSH
↑ T4, FT4, T3, FT3, thyroid resin uptake |
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What is the clinical presentation of toxic multinodular goiter?
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thyroid → enlarged, palpable nodules
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What is the clinical presentation of general hyperthyroidism?
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restlessness, nervousness, fatigue, weakness, muscle cramps, weight loss, pruritis, sweating, palpitations, angina pectoris, frequent bowel movements, irregular menstruation
fever, warm moist skin, fine hair, onycholysis, fine resting finger tremors, hypperflexia exertional dyspnea, forceful PMI, sinus tachycardia, PACs, atrial tachycardia, atrial fibrillation, pulmonary HTN, cardiomyopathy, CHF |
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What is the clinical presentation of subacute thyroiditis?
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thyroid → moderately enlarged, tender
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What is the etiology of toxic multinodular goiter?
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goiter
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What is the most common cause of goiter?
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iodine deficiency
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Goiter can be associated with hypo- or hyperthyroidism, true or false?
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true
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What are the complications of hyperthyroidism?
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hypercalcemia
osteoporosis nephrocalcinosis gynecomastia, decreased libido, erectile dysfunction, decreased sperm motility cardiac arrhythmia, HF opthalmopathy dermopathy thyroid storm |
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What is the initial treatment for thyroid storm?
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propranolol
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What is thyroid storm?
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complication of untreated hyperthyroidism
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What is the clinical presentation of thyroid storm?
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worsened hyperthyroid symptoms
tachycardia marked elevation of body temperature (105-106F) weakness sweating anxiety disorientation SOB chest pain HF |
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What is the etiology of thyroid storm?
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pregnancy
infection MI excessive dose of hyperthyroid meds abrupt discontinuation of hyperthyroid meds radioactive iodine thyroidectomy |
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ENDEMIC GOITER
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ETIOLOGY:
d/t iodine deficiency – no access to iodized salt or living in areas with iodine-depleted soil high incidence of congenital hypothyroidism (deafness, short stature, low IQ) and cretinism high incidence of goiter (aggravated by smoking, pregnancy) CLINICAL PRESENTATION: goiter – very large, multinodular, hypo or hyperthyroidism, compressive symptoms DIAGNOSTIC WORKUP: usually normal TSH and T4 (sometimes hypo or hyperthyroidism) ↑ serum thyroglobulin no antithyroid antibodies PREVENTION: add iodine to salt MANAGEMENT: iodine and vitamin A thyroidectomy if hyperthyroidism, compressive symptoms, cosmetic reasons |
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THYROID CANCER
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ETIOLOGY:
Papillary thyroid carcinoma most common Follicular thyroid carcinoma 14% Medullary thyroid carcinoma 3% Anaplastic thyroid carcinoma 2% female:male ratio 3:1 CLINICAL PRESENTION: often asymptomatic if large → neck discomfort, dysphagia, hoarsness thyroid → palpable, firm, nontender nodule lymphadenopathy metastasis to lymph nodes, bone, lung Medullary thyroid carcinoma → flushing and persistent diarrhea DIAGNOSTIC WORKUP: normal thyroid function tests ↑ serum thyroglobulin neck US RIA CT, MRI, PET MANAGEMENT: Surgery thyroxine replacement thyroid carcinomas resistant to chemotherapy Radioactive Iodine (131I) Therapy Thyroid remnant ablation Surveillance |
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MYXEDEMA COMA
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ETIOLOGY:
complication of hypothyroidism usually following thyroidectomy or ablative therapy may also be d/t trauma, infection, CVA, anesthesia, medication, surgery usually occurs if >60y/o, female, winter after cold exposure CLINICAL PRESENTATION: hypothyroidism CNS depression hypothermia hypotension bradycardia hypoventilation hyporeflexia consciousness disturbances, coma |
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What is the origin, regulation, and function of PTH?
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ORIGIN:
parathyroid glands REGULATION: + hypocalcemia - hypercalcemia FUNCTION: release of calcium from bone to increase plasma calcium increases calcium resorption in kidney decreases phosphate resorption in kidney increases 1,25(OH) vitamin D production |
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What is bone resorption?
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process by which osteoclasts breakdown bone → releasing minerals into blood
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HYPOPARATHYROIDISM
ETIOLOGY |
thyroidectomy
parathyroidectomy neck irradiation autoimmune abnormal magnesium genetic congenital |
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HYPOPARATHYROIDISM
CLINICAL PRESENTATION |
irritability
altered mental status abdominal and muscle cramps parasthesias of lips, hands and feet hyperreflexia carpopedal spasms tetany convulsions Chvostek sign (facial muscle contraction on tapping the facial nerve) Trousseau sign (carpal spasm after application of a sphygmomanometer cuff) dry scaly skin, loss of eyebrows, thin brittle nails |
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HYPOPARATHYROIDISM
DIAGNOSTIC WORKUP |
hypocalcemia
hyperphosphatemia ↓ urine calcium normal alkphos hypomagnesemia may exacerbate symptoms ↓ PTH |
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HYPOPARATHYROIDISM
MANAGEMENT |
calcium
vitamin D magnesium if abnormal |
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HYPERPARATHYROIDISM
ETIOLOGY |
excessive PTH secretion → hypercalcemia
parathyroid adenoma parathyroid hyperplasia parathyroid carcinoma genetic MEN 1 MEN 2A 3x more common in women usually >50y/o |
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HYPERPARATHYROIDISM
CLINICAL PRESENTATION |
often detected incidentally
fatigue mental status changes polyuria constipation HTN renal calculi bone pain (d/t chronic bone resorption d/t chronically elevated PTH) rarely pathologic fractures muscular weakness parasthesias hyporeflexia |
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HYPERPARATHYROIDISM
DIAGNOSTIC WORKUP |
hypercalcemia
↑ urine calcium low-normal serum phosphate ↑ urine phosphate normal-elevated alkphos ↑ PTH vitamin D deficiency |
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HYPERPARATHYROIDISM
MANAGEMENT |
if asymptomatic → no treatment, drink adequate fluids, avoid immobilization, avoid calcium supplements and thiazide diuretics
if symptomatic → parathyroidectomy |
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HYPOCALCEMIC CRISIS
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usually occurs after parathyroidectomy
tetany mental status changes establish airway IV calcium glutonate oral calcium vitamin D magnesium transplantation of parathyroid gland removed during prior surgery |
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"Bones, stones, abdominal groans, psychic moans, with fatigue overtones" describes what disease?
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hyperparathyroidism
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HYPERCALCEMIC CRISIS
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severe mental status changes
calcium >15 hospitalization IV saline |
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PSEUDOHYPOPARATHYROIDISM
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genetic disorder
resistance to PTH (as opposed to decreased production of PTH seen in hypoparathyroidism) similar symptoms to hypoparathyroidism hypocalcemia hyperphosphatemia normal PTH genetic testing calcium and vitamin D supplementation |
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What is the etiology of Cushing's syndrome?
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Cushing's syndrome (60%):
spontaneous excessive corticosteroid production by adrenal glands (rare) high-dose corticosteroids Cushing's disease: benign pituitary adenoma → ACTH hypersecretion by anterior pituitary 3x more common in women non-pituitary ACTH-secreting neoplasm ACTH from unknown source benign adrenal adenoma → excessive cortisol secretion independent of ACTH |
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What is the clinical presentation of Cushing's syndrome?
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moon facies
buffalo hump supraclavicular fat pads central obesity thin extremities thin skin hirsutism purple striae acne superficial skin infections muscle wasting poor wound healing polydipsia polyuria olgiomenorrhea or amenorrhea erectile dysfunction psychological changes HTN osteoporosis avascular bone necrosis |
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What is the diagnostic workup of Cushing's syndrome?
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leukocytosis
lymphocytosis hypokalemia hyperglycemia glucosuria ↑ serum cortisol ↑ urine free cortisol dexamethasone suppression test → lack of suppression |
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What is the management of Cushing's syndrome?
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1. surgical resection of pituitary adenoma
2. corticosteroids |
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What is Cushing's syndrome?
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endocrine disorder characterized by hypercortisolism
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What is the origin, regulation, and function of cortisol?
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ORIGIN:
adrenal cortex REGULATION: + ACTH - negative feedback by cortisol FUNCTION: promotes gluconeogenesis and hyperglycemia mobilizes fat for energy metabolism protein catabolism depressess inflammatory and immune responses |
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What is pheochromocytoma?
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tumor of the sympathetic nervous system that arises from adrenal medulla → secretes epinephrine and norepinephrine → HTN, tachyarrhythmias
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What is the etiology of pheochromocytoma?
|
germline mutation
type 2 von Hippel–Lindau (VHL) disease MEN 2A MEN 2B rare |
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What is the clinical presentation of pheochromocytoma?
|
"attacks" → spontaneous or triggered by bending, lifting, exercise, stress, procedures, drugs, surgery
attacks typically cause: HA perspiration palpitations anxiety/sense of impending doom tremor HTN orthostatic HTN pallor followed by flushing as attack subsides hypotension syncope tachyarrhythmias |
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What is the diagnostic workup of pheochromocytoma?
|
1. plasma fractionated free metanephrines
2. 24 hour urine fractionated metanephrines and creatinine 3. abdominal CT |
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What is the management of pheochromocytoma?
|
1. HTN management prior to surgery → a-blockers, CCBs, B-blockers
2. surgery |
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What are the complications of pheochromocytoma?
|
hypertensive crisis
fatal cardiac arrhythmia |
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What is the patient education of pheochromocytoma?
|
measure BP daily and during attacks
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What is acute adrenal insufficiency (adrenal crisis)?
|
emergency characterized by insufficient cortisol
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What is the etiology of acute adrenal insufficiency?
|
chronic adrenocortical insufficiency (Addison's disease)
pituitary gland disorders may occur in following situations: 1. adrenal insufficiency + stress 2. adrenal insufficiency + sudden withdrawal of adrenocortical hormone 3. adrenalectomy 4. pituitary necrosis 5. hypoadrenalism + thyroid hormone 6. bilateral adrenal injury 7. etomidate |
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What is the clinical presentation of acute adrenal insufficiency?
|
fever
nausea vomiting diarrhea abdominal pain weakness confusion hypotension dehydration hyperpigmentation |
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What is the diagnostic workup of acute adrenal insufficiency?
|
eosinophilia
hyponatremia hyperkalemia hypoglycemia ↑ BUN cosyntropin stimulation test -cosyntropin (synthetic ACTH) given via IM injection -cortisol drawn in 30-60 minutes -normally, cortisol >20 mcg/dL -if adrenal crisis, cortisol <20 mcg/dL cortisol |
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What is the management of acute adrenal insufficiency?
|
1. draw cortisol
2. immediate IV hydrocortisone and saline 3. then IV hydrocortisone phosphate or hydrocortisone sodium succinate 4. empiric broad-spectrum antibiotics 5. then oral hydrocortisone 6. determine degree of permanent adrenal insufficiency and cause |
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What are the complications of acute adrenal insufficiency?
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lack of treatment leads to shock and death
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What do the adrenal glands secrete?
|
CORTEX:
cortisol aldosterone testosterone MEDULLA: epinephrine norepinephrine |
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What is Addison's disease?
|
adrenal gland disorder characterized by chronic deficiency of cortisol, aldosterone, and adrenal androgens
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What is the etiology of Addison's disease?
|
autoimmune destruction of adrenal glands (80%)
TB bilateral adrenal hemorrhage adrenoleukodystrophy lymphoma, metastatic carcinoma, coccidioidomycosis, histoplasmosis, cytomegalovirus infection (more frequent in patients with AIDS), syphilitic gummas, scleroderma, amyloid disease, and hemochromatosis congenital presents by 15y/o uncommon |
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What is the clinical presentation of Addison's disease?
|
fever, fatigue, weakness, anorexia, weight loss
nausea, vomiting, diarrhea anxiety, irritability skin hyperpigmentation → especially nipples, creases, joints, pressure areas vitiligo (10%) sparse axillary and pubic hair longitudinal banding of nails abdominal pain myalgias arthralgias amenorrhea hypotension small heart |
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What is the diagnostic workup of Addison's disease?
|
anemia
neutropenia eosinophilia lymphocytosis hyponatremia hyperkalemia hypercalcemia ↑ BUN ↑ ACTH ↓ cortisol cosyntropin test CT if not clearly autoimmune |
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What is the managment of Addison's disease?
|
1. if mild → hydrocortisone
2. if more severe → fludrocortisone 3. increase dosing if stress 4. treat infections promptly and vigorously |
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What are the complications of Addison's disease?
|
susceptibility to infection
associated autoimmune diseases complications of underlying disorder (i.e. TB) |
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what drugs are filtered by glomerulus not reabsorbed to to size so water is excreted with them
|
osmotic diuretics (mannitol isorbide)
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What is the etiology of primary hyperaldosteronism?
|
excessive aldosterone production → increased sodium retention and decreased plasma renin → increased renal potassium excretion → hypokalemia
adrenal adenoma (Conn syndrome) unilateral or bilateral adrenal hyperplasia genetic |
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What is the clinical presentation of primary hyperaldosteronism?
|
HTN
HA muscle weakness parasthesias paralysis tetany polydipsia polyuria |
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What is the diagnostic workup of primary hyperaldosteronism?
|
↑ plasma aldosterone
↑ urine aldosterone ↓ plasma renin hypokalemia |
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What is the management of primary hyperaldosteronism?
|
1. CT scan to screen for adrenal carcinoma
2. if Conn syndrome → adrenalectomy or long-term therapy with spironolactone or eplerenone 3. if bilateral adrenal hyperplasia → spironolactone or eplerenone |
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What are the complications of primary hyperaldosteronism?
|
severe or drug-resistant HTN
cardiovascular complications |
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What is the patient education of primary hyperaldosteronism?
|
monitor BP daily when beginning meds
spironolactone may cause breast tenderness and gynecomastia |
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What is the most common cause of refractory HTN in youth and middle-aged populations?
|
primary hyperaldosteronism
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What are the requirements when testing for aldosterone and renin?
|
withhold certain anti-hypertensives
withhold diuretics x 3 weeks consume unrestricted high sodium intake be out of bed for at least 2 hours and seated for 5–15 minutes before the blood draw draw blood between 8 am and 10 am |
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Discuss oral glucose tolerance test.
|
if the fasting plasma glucose level is < 126 mg/dL but DM still suspected
eat a minimum of 150–200 g of carbohydrate per day x 3 days preceding the test fast after midnight preceding the test day perform test in morning due to diurnal variation in oral glucose tolerance give adults 75 g of glucose in 300 mL of water give children are 1.75 g of glucose per kilogram of ideal body weight drink within 5 minutes do not smoke or be active during test draw blood at 0 minutes and 120 minutes after drinking glucose 0 minute normal = <100 mg/dL (DM indicated if ≥126) 120 minute normal = <140 mg/dL (impaired glucose tolerance if 140-199, DM indicated if >200) false-positives may occur if malnutrition, infection, stress, bed-bound, oral contraceptives, diuretics, corticosteroids, excess thyroxine, phenytoin, nicotinic acid, psychtropics |
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What is the diagnostic workup of diabetic ketoacidosis?
|
• hyperglycemia > 250 mg/dL
• serum bicarbonate < 15 mEq/L • serum positive for ketones • acidosis with blood pH < 7.3 |
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DIABETIC KETOACIDOSIS
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ETIOLOGY:
complication of type I DM (but may occur in type II DM + severe stress such as trauma or sepsis) may be initial presentation of DM d/t increased requirements of insulin during trauma, infection, MI, surgery d/t insulin pump leakage or failure d/t poor compliance life-threatening CLINICAL PRESENTATION: polyruria, polydipsia → fatigue, nausea, vomiting → mental stupor → coma fruity breath rapid deep breathing dehydration signs hypotension tachycardia DIAGNOSTIC WORKUP: • hyperglycemia > 250 mg/dL • serum bicarbonate < 15 mEq/L • serum positive for ketones • acidosis with blood pH < 7.3 plasma glucose of 350–900 mg/dL serum ketones at a dilution of 1:8 or greater hyperkalemia (serum potassium level of 5–8 mEq/L), slight hyponatremia (serum sodium of approximately 130 mEq/L) hyperphosphatemia (serum phosphate level of 6–7 mg/dL) elevated blood urea nitrogen and serum creatinine acidosis may be severe (pH ranging from 6.9 to 7.2, and serum bicarbonate ranging from 5 mEq/L to 15 mEq/L) PCO2 is low (15–20 mm Hg) related to hyperventilation. Fluid depletion is marked, typically about 100 mL/kg. central nervous system depression or coma occurs when the effective serum osmolality exceeds 320–330 mosm/L. MANAGEMENT: mild diabetic ketoacidosis = pH between 7.25 and 7.30 moderate ketoacidosis = pH between 7.0 and 7.24 + alert or drowsy severe ketoacidosis = pH < 7.0 + stupor. if mild → treat in ER if moderate or severe → admit to ICU restore plasma volume and tissue perfusion, reduce blood glucose and osmolality, correct acidosis, replace electrolytes, and identify and treat cause |
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HYPERGLYCEMIC HYPEROSMOLAR COMA
|
d/t mild to moderate hyperglycemia
ETIOLOGY: second most common form of hyperglycemic coma characterized by severe hyperglycemia in the absence of significant ketosis + hyperosmolality + dehydration. occurs in occult or mild diabetes usually precipitated by infection, MI, stroke, drugs, peritoneal dialysis, surgery usually middle-aged to elderly underlying CKD or CHF common CLINICAL PRESENTATION: may be insidious over a period of days or weeks weakness, polyuria, and polydipsia lethargy, confusion →convulsions → coma profound dehydration no Kussmaul respirations DIAGNOSTIC WORKUP: • Hyperglycemia > 600 mg/dL. • Serum osmolality > 310 mosm/kg. • No acidosis; blood pH above 7.3. • Serum bicarbonate > 15 mEq/L. • Normal anion gap (< 14 mEq/L). • No ketosis MANAGEMENT: Fluid Replacement Insulin Potassium Phosphate mortality rate of hyperglycemic hyperosmolar coma is more than ten times that of diabetic ketoacidosis, chiefly because of its higher incidence in older patients, who may have compromised cardiovascular systems or associated major illnesses and whose dehydration is often excessive because of delays in recognition and treatment. |
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LACTIC ACIDOSIS:
|
ETIOLOGY:
characterized by accumulation of excess lactic acid in the blood overproduction of lactic acid (tissue hypoxia), deficient removal (hepatic failure), or both (circulatory collapse) can cause accumulation common in any severely ill patient suffering from cardiac decompensation, respiratory or hepatic failure, septicemia, or infarction of bowel or extremities uncommon in DM but occasionally occurs with metformin tx + metformin contraindication (renal failure) CLINICAL PRESENTATION: marked hyperventilation if secondary to tissue hypoxia or vascular collapse → presentation variable if spontaneous → rapid onset over a few hours, normal BP, no cyanosis, peripheral circulation good DIAGNOSTIC WORKUP: • Severe acidosis with hyperventilation. • Blood pH below 7.30. • Serum bicarbonate < 15 mEq/L. • Anion gap > 15 mEq/L. • Absent serum ketones. • Serum lactate > 5 mmol/L. MANAGEMENT: Treat underlying cause |
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What is the Dawn phenomenon and Somogyi effect?
|
Dawn phenomenon. The dawn phenomenon is the end result of a combination of natural body changes that occur during the sleep cycle and can be explained as follows. Between 3:00 a.m. and 8:00 a.m., your body starts to increase the amounts of counter-regulatory hormones (growth hormone, cortisol, and catecholamines). These hormones work against insulin's action to drop blood sugars. The increased release of these hormones, at a time when bedtime insulin is wearing out, results in an increase in blood sugars. These combined events cause your body's blood sugar levels to rise in the morning.
Somogyi effect. Named after the doctor who first wrote about it, this condition is also called "rebound hyperglycemia." Although the cascade of events and end result -- high blood sugar levels in the morning -- is the same as in the dawn phenomenon, the cause is more "man-made" (a result of poor diabetes management) in the Somogyi effect. The term refers to pattern of high morning sugars preceded by an episode of hypoglycemia (with no symptoms). Your blood sugar may drop too low in the middle of the night, so your body counters by releasing hormones to raise the sugar levels. This could happen if you took too much insulin earlier or if you did not have enough of a bedtime snack. Is Your Type 1 Diabetes Under Control? Which of the Two Conditions Is Causing the High Blood Sugar Levels? To determine which of the two above conditions is causing your high blood sugar level, your doctor will likely ask you to check your blood sugar levels between 2:00 a.m. and 3:00 a.m. for several nights in a row. If your blood sugar is consistently low during this time, the Somogyi effect is suspected (too much nighttime insulin or too small of a bedtime snack for the insulin given). If the blood sugar is normal or high during this time period, the dawn phenomenon (increases in counter-regulatory hormone) is more likely to be the cause. How Can Morning High Blood Sugar Be Corrected? Once you and your doctor determine how your blood sugar levels are behaving during the nighttime hours, he or she can advise you about the changes you need to make to better control them. Options that your doctor may discuss include: Changing the time you take the long-acting insulin in the evening so that its peak action occurs when your blood sugars start rising. Changing the type of insulin you take in the evening Taking extra insulin overnight if you find that overnight your blood sugars are progressively elevated. Here, the additional insulin would help lower high morning blood sugars. Switching to an insulin pump, which can be programmed to release additional insulin in the morning |
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What is reactive hypoglycemia?
|
hypoglycemia that occurs shortly after eating
occurs in non-diabetics cause unknown eat less sugar eat smaller more frequent meals |
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|
What is Turner syndrome?
|
sex-linked genetic disorder that occurs in women characterized by partial or complete absence of an X chromosome
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What is the etiology of Turner syndrome?
|
genetic
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What is the clinical presentation of Turner syndrome?
|
hypogonadism → manifesting as absent or incomplete development at puberty
small breasts sparse pubic hair primary amenorrhea short stature epicanthal folds high-arched palate webbed neck wide-spaced nipples short 4th metacarpals HTN renal abnormalities emotional disorders |
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What is the diagnostic workup of Turner syndrome?
|
blood karyotype → 45,XO or X chromosome abnormalities or mosaicism
elevated FSH and LH normal GH and IGF-1 |
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What is the management of Turner syndrome?
|
1. US or MRI of chest and abdomen to R/O cardiac or renal abnormalities
2. for short stature → GH injections daily 3. for hypogonadism → begin estrogen therapy at 12y/o and when growth stops add progestin 4. monitor for cardiac problems (100-fold increased risk for aortic dissection), renal problems, DM, osteoporosis |
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|
Turner syndrome
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|
What is menopause?
|
cessation of menses due to aging or bilateral oophorectomy
no menstruation for 1 year |
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|
What is the etiology of menopause?
|
aging
bilateral oophorectomy premature menstration: ovarian failure and menstrual cessaton <40y/o often d/t genetic or autoimmune often due to |
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What is the clinical presentation of menopause?
|
~51y/o if d/t aging
hot flashes night sweats vaginal dryness dyspareunia mood changes → anxiety, depression etc. thinned vaginal mucosa → pale smooth vaginal mucosa small cervix and uterus ovaries non-palpable |
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What is the diagnostic workup of menopause?
|
elevated FSH and LH
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What is the management of menopause?
|
1. for hot flashes → consider estrogen/progestin therapy or SSRIs
2. for vaginal atrophy → lubrications, vaginal creams, estradiol vaginal ring 3. calcium and vitamin D supplements 4. monitor for osteoporosis and treat accordingly 5. if vaginal bleeding occurs following menopause → R/O endometrial cancer 5. provide education and support and referral to midlife discussion groups 6. if surgical menopause → immediate estrogen therapy that is then tapered |
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|
How long does menopause last?
|
menstruation diminishes until absent usually over 1-3 year period
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|
What are hot flashes?
|
feeling of intense heat over face and trunk
flushing sweating worse following oophorectomy may occur at night and cause insomnia and fatigue |
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|
What is the controversy behind menopause-associated hormone replacement therapy?
|
estrogen-progestin therapy increased risk of cardiovascular disease, cerebrovascular disease and breast cancer
can consider prescribing if early menopause + severe hot flashes but d/c after 3-4 years |
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|
How long do hot flashes typically last?
|
2-3 years
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|
When does menarche usually occur in the U.S.?
|
11-15y/o
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|
What is primary amenorrhea?
|
failure of menses to appear
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|
When should amenorrhea be workup up?
|
at age 14 if no menarche + either:
1. no breast development 2. height in lowest 3% othewise at age 16 |
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|
What is the etiology of primary amenorrhea?
|
hypothalamic-pituitary causes
hyperandrogenism ovarian causes uterine causes pseudohermaphroditism athletics dieting anorexia nervosa stress illness pregnancy |
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What is the clinical presentation of primary amenorrhea?
|
no menarche
dependent on cause |
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|
What is the diagnostic workup of primary amenorrhea?
|
HCGP
FSH LH prolactin TSH FT4 if low-normal FSH and LH +/- high prolactin → order MRI for suspected hypothalmic or pituitary tumor |
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|
What is the management of primary amenorrhea?
|
treat underlying cause
permanent hypogonadism treated with ERT |
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What is secondary amenorrhea?
|
absence of menses for 3 consecutive months in women who have passed menarche
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|
What is the etiology of secondary amenorrhea?
|
pregnancy
stress illness dieting eating disorder athletics hypothalmic-pituitary causes hyperandrogenism premature ovarian failure uterine causes menopause |
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What is the clinical presentation of secondary amenorrhea?
|
no menses for 3 consecutive months
dependent on cause |
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|
What is the diagnostic workup of secondary amenorrhea?
|
HCGP
FSH LH prolactin TSH |
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|
What is the management of secondary amenorrhea?
|
dependent on cause
|
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|
What is the most common cause of secondary amenorrhea?
|
pregnancy!!!
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|
What is osteoporosis?
|
↓ bone matrix and mineral
|
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|
What is osteomalacia?
|
intact bone matrix
↓ bone mineral |
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|
What is osteopenia?
|
bone mineral density lower than normal
bone mineral density T-score between -1.0 and -2.5 precursor to osteoporosis |
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|
What is the interpretation of DXA?
|
bone mineral density in typically expressed in gm/cm2
bone mineral density reported as standard deviation of young normal mean the following results are based on post-menopausal white women: T score –1.0: normal T score –1.0 to –2.5: osteopenia T score < –2.5: osteoporosis T score < –2.5 + fx: severe osteoporosis |
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|
What are the indications for DXA?
|
at risk for osteoporosis or osteomalacia
diminished bone density on radiograph pathologic fracture |
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|
What does DXA measure?
|
bone density of lumbar spine and hip
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|
|
OSTEOPOROSIS
|
↓ bone matrix and mineral
increased rate of bone resorption causes include: genetic disorders hypogonadism estrogen deficiency in women (menopause) androgen deficiency in men hyperparathyroidism thyrotoxicosis Cushing's syndrome malignancy malnutrition malabsorption alcohol cigarettes immobilization asymptomatic until fx ↑ risk of spine, hip, pelvis and wrist fx ↓ height normal PTH, calcium, phosphate, alkaline phosphatase ↓ vitamin D DXA T score –1.0: normal T score –1.0 to –2.5: osteopenia T score < –2.5: osteoporosis T score < –2.5 + fx: severe osteoporosis treatment indicated if: women + osteoporosis person + fragility fx consider prophylaxis if advanced osteopenia adequate sun exposure or vitamin D supplementation calcium supplementation bisphosphonates raloxifene estrogen calcitonin |
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|
What is the prevention for osteoporosis and pathologic fx?
|
eat adequate calories, calcium and protein
avoid alcohol and smoking low-impact exercise to increase muscle strength and prevent falls high-impact exercise (jogging or stair-climbing) to increase bone density weight training to increase bone density and muscle strength balance exercises to prevent falls avoid immobilization fall prevention measures – cane, walker, adequate lighting, handrails adequate sun exposure vitamin D supplementation reduce or d/c corticosteroids |
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|
OSTEOMALACIA
|
ETIOLOGY:
defective skeletal mineralization in adults (AKA rickets in children) caused by any condition that results in inadequate calcium or phosphate mineralization of bone osteoid commonly caused by vitamin D deficiency due to low sun exposure, malnutrition, or malabsorption also caused by genetic conditions, poor nutrition (dietary calcium deficiency, alcoholism), phosphate deficiency, malignancy, anticonvulsants, aluminum toxicity CLINICAL PRESENTATION: proximal muscle weakness d/t calcium deficiency – especially pelvic girdle bone pain and tenderness pathologic fx with little or no trauma DIAGNOSTIC WORKUP: ↓ 25(OH) vitamin D Hypocalcemia Hypocalcuria hypophosphatemia ↑ alkphos (high serum alkaline phosphatase may be present in severe osteomalacia but not osteoporosis) radiographs DXA ↓ bone density MANAGEMENT: adequate sun exposure – 15 minutes 2x weekly without sunscreen adequate vitamin D from diet – salmon, mackerel, tuna, sardines, cod liver oil vitamin D supplementation – 1000 IU daily if frank vitamin D deficiency → prescribe ergocalciferol if poor nutrition or malabsorption → calcium supplementation |
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|
PAGET'S DISEASE OF THE BONE
|
ETIOLOGY:
characterized by ≥1 bony lesions having high bone turnover and disorganized osteoid formation → bones become vascular, weak, and deformed cause unknown genetic component most common in >40y/o and men CLINICAL PRESENTATION: usually discovered incidentally d/t ↑alkphos or radiographic findings can involve just one bone (monostotic) or multiple bones (polyostotic), particularly skull (increased hat size, HA), femur, tibia, pelvis, and humerus pain in involved or adjacent bone → bone softening → kyphosis, bowed tibias, frequent “chalkstick” fx with slight trauma degenerative arthritis DIAGNOSTIC WORKUP: ↑alkphos radiographs – osteolytic with focal radiolucencies in the skull or advancing flame-shaped lytic lesions in long bones → sclerosis → thickening and deformity COMPLICATIONS: arthritis if immobilization → hypercalcemia and renal calculi if skull involvement → cranial nerve palsies, vision loss, hearing loss if vertebral involvement → spinal cord compression, radiculopathy, paralysis osteosarcoma MANAGEMENT: if asymptomatic → surveillance, serial alkphos 1st-line = bisphosphonates contraindicated in patients with a history of esophagitis, esophageal stricture, dysphagia, hiatal hernia, or achalasia given cyclically – 1st course of therapy → 3 month break → repeat take with 8 oz of water to prevent pill-induced esophagitis do not lie down for 30 minutes following ingestion may experience increase in pain at onset of therapy which subsides with further tx; flu-like symptoms common; jaw osteonecrosis rare IV bisphosphonates more effective than oral and indicated if cannot tolerate oral, but more systemic adverse effects (hypocalcemia, postinfusion fever, fatigue, myalgia, bone pain, ocular problems, rarely uveitus and AKD) use of calcitonin use has declined dramatically with the introduction of more potent bisphosphonates |
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|
What is MEN 1?
|
familial multiglandular endocrine tumor syndrome
affects 2-10 in 100,000 may present in childhood or adulthood presentation varies hyperparathyroidism may include pituitary, parathyroid, endopancreatic, and non-endocrine tumors gene testing hypercalcemia |
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What are multiple endocrine neoplasias?
|
autosomal dominant genetic disorders causing a predisposition in the development of tumors, especially tumors involving endocrine glands
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|
What characterizes MEN 2A?
|
medullary thyroid cancers, pheochromocytomas, Hirschsprung disease
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What characterizes MEN 2B?
|
medullary thyroid cancers, pheochromocytomas, Marfan-like habitus, mucosal neuromas, intestinal ganglioneuroma, delayed puberty
|
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|
What characterizes MEN 1?
|
tumors of the parathyroid glands, endocrine pancreas and duodenum, pituitary, adrenal, thyroid; lipomas and facial angiofibromas
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|
What are the electrolyte disturbances that occur in beer potomania?
|
large alcohol consumption → dietary sodium and protein insufficiency → dilutional hyponatremia
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|
What are the electrolyte disturbances that occur in aldosteronsim?
|
hypernatremia
hypokalemia increased bicarb |
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|
What are the electrolyte disturbances that occur in diabetes insipidus?
|
diabetes insipidus → dehydration → hypernatremia
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|
What is aldosteronism?
|
oversecretion of aldosterone from adrenal glands independent of renin
aldosterone causes increased sodium and water reabsorption and potassium excretion |
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|
What are the normal and critical values for serum calcium?
|
NORMAL:
8.5-10.5 mg/dL CRITICAL: <6.5 mg/dL >13.5 mg/dL |
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|
What are the normal and critical values for serum magnesium?
|
NORMAL:
1.8-3.0 mg/dL CRITICAL: <0.5 mg/dL >4.5 mg/dL |
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|
What are the normal and critical values for serum phosphate?
|
NORMAL:
2.5-4.5 mg/dL CRITICAL: <1.0 mg/dL |
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|
What is serum fructosamine?
|
formed by glycosylation of serum proteins (primarily albumin)
test evaluates glucose control in last 1-3 weeks (average lifespan of plasma proteins) fingerstick or venipuncture used to monitor DM instead of A1C when: recent change in diet recent change in tx pregnancy blood loss hemolytic anemia abnormal hemoglobin (sickle cell disease etc) results depend on albumin normally 200–285 mcmol/L when the serum albumin level is 5 g/dL results will be lower if abnormally low albumin d/t hepatic or renal disease correlates with A1C HbA1c = 0.017 x serum fructosamine level (mcmol/L) + 1.61 serum fructosamine 317, 375, and 435 mcmol/L = A1C 7%, 8%, and 9% respectively |
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|
What is the MOA of alpha-glucose inhibitors?
|
delay intestinal glucose absorption
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|
List nonsulfonylurea insulin stimulators.
|
repaglinide
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|
List alpha-glucose inhibitors.
|
acarbose
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|
List incretins.
|
exenatide
sitagliptin |
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List biguanides.
|
metformin
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|
List thiazolidinediones.
|
pioglitazone
rosiglitazone |
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|
REPAGLINIDE
|
INDICATIONS:
DM II – adjunctive therapy if not adequately controlled by metformin CONTRAINDICATIONS: hepatic or renal dysfunction MOA: nonsulfonylurea insulin stimulator similar to sulfonylureas causes brief but rapid impulse of insulin ADVERSE EFFECTS: weight gain hypoglycemia INTERACTIONS: PEAK LEVEL AND DURATION: PATIENT EDUCATION: |
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ACARBOSE
|
INDICATIONS:
Type II DM – adjunctive therapy CONTRAINDICATIONS: diabetic ketoacidosis cirrhosis GI tract disorders MOA: competitive inhibitor of pancreatic a-amylase and intestinal brush border a-glucosidases → delayed digestion of carbs and absorption of glucose ADVERSE EFFECTS: flatulence diarrhea abdominal pain increased liver enzymes INTERACTIONS: PEAK LEVEL AND DURATION: PATIENT EDUCATION: take with first bite of meal flatulence tends to decrease in frequency and intensity over time |
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|
LEVOTHYROXINE
|
INDICATIONS:
hypothyroidism pituitary TSH suppression CONTRAINDICATIONS: hypersensitivity recent MI recent thyrotoxicosis uncorrected adrenal insufficiency use with caution if elderly, cardiovascular disease, swallowing disorders do not use for weight control MOA: unknown ADVERSE AFFECTS: • fever • headache • nausea • vomiting • diarrhea • stomach cramps • sensitivity to heat • excessive sweating • increased appetite • nervousness • irritability • tremor • insomnia • temporary hair loss • weight loss • changes in menstrual cycle INTERACTIONS: increases effect of vitamin K anatagonists PATIENT EDUCATION: take with 8oz of water on empty stomach 30-60min before breakfast may take several weeks for symptoms to improve requires 6-8 weeks for full effect continue taking even if feel well call immediately if experience rapid HR or chest pain |
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PROPRANOLOL
|
INDICATIONS:
unlabeled/investigational use for thyrotoxicosis HTN angina pectoris V-tach arrhythmias essential tremor MI prevention migraine prevention CONTRAINDICATIONS: hypersensitivity severe bradycardia 2nd or 3rd-degree heart block uncompensated CHF cardiogenic shock asthma COPD pheochromocytoma use with caution if DM (may mask hypoglycemia), hyperthyroidism (may mask thyrotoxicosis), myasthenia gravis or psychiatric disease (may cause CNS depression), renal or hepatic dysfunction MOA: non-selective B-adrenergic blocker → competitively blocks B1 and B2 adrenergic stimulation → decrease in BP, HR, myocardial contractility and O2 demand ADVERSE EFFECTS: • fatigue • dizziness • rash • upset stomach • vomiting • constipation • diarrhea • insomnia INTERACTIONS: increased or decreased with alcohol PATIENT EDUCATION: take same time everday do not stop abruptly → may result in HTN, tachycardia or ischemia call immediately if experience • hypotension, arrhythmia, sore throat, SOB, chest pain, unusual bleeding, swelling of the feet or hands, unusual weight gain |
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PROPYLTHIOURACIL (PTU)
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INDICATIONS:
hyperthyroidism (palliative treatment prior to radioactive iodine therapy or surgery) thyrotoxic crisis only give if allergic or can't tolerate methimazole or in 1st trimester of pregnancy CONTRAINDICATIONS: pregnancy breast feeding hypersensitivity use with caution if bone marrow depression or liver dysfunction MOA: inhibits synthesis of thyroid hormones by blocking oxidation of iodine in thyroid gland ADVERSE EFFECTS: • dizziness • nausea • vomiting • difficulty tasting food • hair loss • neck swelling • myalgias • arthralgias • parasthesias INTERACTIONS: decreases effect of vitamin K anatagonists PATIENT EDUCATION: take same time everyday in relation to meals (i.e. always with meals or always without meals) take even if feel well requires periodic monitoring of CBCDP, HFP, TSH, FT4, PT |
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METHIMAZOLE
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INDICATIONS:
hyperthyroidism (palliative treatment prior to radioactive iodine therapy or surgery) thyrotoxic crisis CONTRAINDICATIONS: pregnancy breast feeding hypersensitivity use caution if bone marrow depression or hepatic dysfunction MOA: inhibits synthesis of thyroid hormones by blocking oxidation of iodine in thyroid gland ADVERSE EFFECTS: INTERACTIONS: decreases effect of vitamin K anatagonists PATIENT EDUCATION: take same time every day in relation to meals (i.e. always with meals or always between meals) requires periodic monitoring of CBCDP, HFP, TSH, FT4, PT |
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What is the starting regimen and monitoring for levothyroxine in a newly diagnosed patient with hypothyroidism?
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starting dose and rate of adjustment dependent on age, weight, chronic disease (especially CAD), symptom duration, and TSH level
if young and healthy: start at 50-100 mcg/d if >50y/o or comorbidities: start at 25-50 mcg/d to avoid angina, arrhythmias or HF symptomatic improvement occurs in 2-4 weeks full effect occurs 6-8 weeks monitor TSH and adjust dose after 6-8 weeks if young and healthy → adjust in 25-50 mcg increments until euthyroid if >50y/o or comorbidities → adjust in 25 mcg increments until euthyroid decrease dose if cardiac symptoms if pregnant → refer to endocrinologist → requires increase up to 50% in 25-50 mcg increments every 4-6 weeks |
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List available thyroid replacement therapies.
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levothyroxine (T4)
levotrix (T4/T3 combination) |
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What are the pros and cons of thyroid replacement therapies?
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LEVOTHYROXINE (T4):
well tolerated LIOTRIX (T4/T3 combo): unecessary since body converts T4 into T3 in appropriate amounts does not improve outcomes compared to T4 data insufficient to support use potential side effects can easily take too much side effects rapid due to short half-life can cause HTN, tachycardia, angina especially avoid in elderly switch to levothyroxine |
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LIOTRIX
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INDICATIONS:
hypothyroidism T4/T3 combination does not improve outcomes cost not justified |
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What is Amour thyroid and why shouldn't it be prescribed?
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Amour thyroid
brand of dessicated thyroid from pigs should not be used due to large variation in amount of thyroid from batch to batch |
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