Endocrinology 5

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Endocrinology 5
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2011-07-18 23:49:08
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DPAP2012 Endocrinology
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Endocrinology flashcards made by previous students
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  1. Axial skeleton:
    15 % of skel mass; verts, pelvis, skull; majority of cancellous bone (most of Ca efflux from this); 80 % of metabolic activity
  2. Appendicular Skeleton
    85 % of skel mass; long bones; majority of cortical bone; 20 % of metabolic activity
  3. Hypercalcemia S/S
    serum Ca >10.5 mg/dL; altered mentation, N/V; polyuria, polydipsia, stones
  4. Hypercalcemia pathogenesis
    accel bone resorption by osteoclasts (PTH, 1,25 (OH)D, IL-1, IL-6, TNF-alpha); enhanced GI absorption of Ca (vit D); hypercalcemia represents eclipsed renal capacity to excrete Ca load ( ie, hypercalciuria also present)
  5. Hypercalcemia: causes
    inc skeleton resorption (primary hyperPTH; malig); inc GI absorption (milk-alk syn); both inc skel resorp & GI absorption (granulomatous: sarcoid, TB, fungal);
  6. Primary hyperPTH mnemonic
    Bones, stones, moans & groans
  7. Primary hyperPTH evolving clin spectrum
    more recently, less about stones & bone dz, more asymptomatic
  8. Hypercalcemia: nonpharm tx
    Tx underlying cause; enhance calciuresis: Fluids (2-3 L / day po for mild; IV saline for severe / Ca > 13); loop diuretics (only after volume repletion); furosemide
  9. Hypercalcemia: Pharm tx: Inhibit osteoclastic resorption:
    bisphosphonates (pamidronate IV; zoledronic acid for malig-related hypercalc); calcitonin (transient benefit d/t tachyphylaxis); cinacalcet; Last line: plicamycin, gallium nitrate
  10. Hypercalcemia: Pharm tx: Inhibit osteoclast resorption/reduce GI absorption:
    Glucocorticoids (prednisone; solumedrol)
  11. Chvostek sx =
    twitching of face and upper lip in response to tapping inferior to TMJ joint
  12. Trousseau sx =
    inflate BP cuff, leave it there; pt gets carpal spasm
  13. If suspect pt is hypocalcemic, measure 1,25-D?
    No; measure 25-OH D
  14. Acute Hypocalcemia S/S
    tetany, twitching, paresthesia; Chvostek sx; Trousseau sx; seizures; laryngo or bronchospasm; long QT; arrhythmia; hypotension
  15. Chronic Hypocalcemia S/S
    ectopic calcification (basal ganglia); EPS; parkinsonism; dementia; cataracts; abnml teeth; dry skin
  16. Most common cause of hypocalcemia
    surgically induced hypoPTH
  17. Hypocalcemia Tx
    Vit D (25 OH D deficiency): Calcium (2000-4000 mg/day); ergocalciferol / cholecalciferol if 25 OH D deficient; Calcitriol if 25 OH D sufficient
  18. Osteomalacia =
    Defective bone matrix mineralization d/t: inadequate Ca & phosphorus; deficient mineralizn mechm in presence of normal Ca / phosphorus
  19. Osteomalacia in childhood is:
    rickets
  20. Osteomalacia symptoms
    diffuse bone pain (esp pelvis), waddling gait, mx weakness, fractures & pseudofractures (Looser’s zones) of long bones, ribs, pelvis
  21. Osteomalacia: causes
    Vitamin D disorders; Hypophosphatemia (inherited disorders); Mineralization disorders
  22. Osteomalacia: Tx
    Vitamin D (25 OH D def): Ca (1500-2000 mg/day); ergocalciferol (D2-Drisdol) cholecalciferol (D3); Calcitriol (for hypophosphatemic osteomalacia)
  23. Paget’s Disease =
    Localized disorder of bone remodeling
  24. Paget’s Dz: initiating lesion is:
    inc bone resorption (giant multicellular osteoclasts); bone formation and mineralization is normal, though of irregular woven type
  25. Paget’s Dz: most commonly affects:
    pelvis, femur, spine, skull and tibia
  26. Paget’s Dz: Sx
    pain, bowing, fracture, HA, hearing loss; elevated alk phos (hallmark); bone turnover markers often elevated
  27. Paget’s Dz: Tx
    Inhibit osteoclast resorption/ bone formation: bisphosphonates; calcitonin
  28. More abundant; precursor to T3
    T4
  29. exerts majority of thyroidal hormone effects:
    T3
  30. Circulating T3 & T4
    most is pro-bound; unbound = regulator for negative feedback inhibition mechanism
  31. Thyroid hormones control:
    O2 consumption CHO & protein metabolism, electrolyte mobilization & conversion of carotene to Vitamin A; also lipid synth & metab
  32. Thyroid & insulin req in DM
    Hypo: dec insulin req, inc chol/TG; hyper = inc insulin req, dec chol/TG
  33. Amt TBG affects:
    amt serum T3 & T4 (not physiologic thyroid status, which is affected by free hormone)
  34. TBG can be measured:
    directly or by T3 uptake
  35. Factors increasing TBG
    Estrogens (inc serum TBG, so low T3 uptake value)
  36. Factors decreasing TBG
    Androgens or adrenocorticosteroid, low protein states (nephrotic syndrome or hepatic failure): dec serum TBG, so high T3 uptake value
  37. T3 uptake =
    indirect measure of pt’s Total T4; the higher the T3 uptake, the higher the pt’s T4 level
  38. Thyroid state & T3 uptake:
    Hyper: high T3 uptake; hypo: low T3 uptake
  39. FTI (T7) =
    total T4 x T3 uptake; FTI low: hypo; FTI high: hyperthyroid
  40. Most common calculation method for free hormone
    FTI (takes into account both absolute hormone level & binding capacity of TBG)
  41. Hyperthyroidism labs
    Depressed TSH; Elevated FT4, T3 Uptake, FTI
  42. Hypothyroidism labs
    Elevated TSH; Depressed FT4, T3 Uptake, FTI
  43. Euthyroid, High TBG (eg, PG)
    Sl low TSH; Free T4 nml or sl high; low T3 Uptake
  44. Euthyroid, Low TBG (eg nephrotic syn)
    TSH variable; Total T4 low to normal; Elevated T3 Uptake
  45. ThRH stimulating test evaluates:
    entire thyroid-pituitary-hypothalamus feedback loop
  46. TSH levels don’t rise in:
    primary hypopituitarism & states of altered thyroid homeostasis
  47. TSI test
    IgG Ab vs thyroid cell TSH rec's; 78% Graves pts are pos; test to monitor tx; titers rise with relapse
  48. hypometabolism with low T3/T4; +/- low FTI & nml TSH; If reverse T3 (inactive product from T4 metabolic breakdown) is elevated =
    euthyroid sick syndrome
  49. Thyroid screening
    USPSTF: no recs; ATA: TSH screen start at 35 yo & q5 yrs (sooner if risk factors or sx)
  50. Thyroglobulin Ab >1:100 suggestive of:
    autoimmune thyroiditis
  51. Microsomal Ab >1:32 titer correlates with:
    autoimmune thyroiditis
  52. Graves dz: predictors of remission
    small goiter (decreases w/thianamides); FT3 predominance; neg TSI titer
  53. GH stimuli include:
    exercise, hypoglycemia hi protein diet, acute starvation & oral contraceptives (secondary to estrogen)
  54. GH deficiency seen in:
    obesity & corticosteroid therapy
  55. Pituitary adenoma diagnosed by:
    CT or MRI of brain to evaluate sella turcica
  56. GH lab testing
    GH on fasting AM samples (often not diagnostic); GH Stimu tests (hyperglycemia normally suppresses GH secretion); GH remains elevated in acromegaly
  57. 3 causes of pituitary dwarfism:
    pit tumor (1/3); pit damage (1/3); Pure GH deficiency (1/3)
  58. pituitary dwarfism: IGF-1 & GH
    Useful to compare IGF-1 levels to GH; IGF-1 is low whenever GH is deficient; IGF1 more stable than GH; mediate GH fx on sk mx
  59. IGF-1 levels influenced by:
    nutrition (low levels in malnutrition)
  60. Prolactin prodn driven by:
    automatic/constant unless inhibited
  61. Most common disorder involving excess pituitary secretion
    Prolactinomas
  62. ACTH measurement
    rarely measured directly (d/t lability)
  63. 2 actions of ADH
    Alters the permeability of renal collecting tubules to water; Causes vasoconstriction
  64. ADH is secreted when serum osmo exceeds:
    285 mOsm/L
  65. Central DI:
    Hypothalamic origin; ADH production or release is deficient
  66. Nephrogenic DI:
    Kidneys fail to respond to normal or even elevated levels of ADH
  67. ADH measurement
    usually unmeasurable; 2.3-3.1 pg/mL
  68. Pt ADH deficient, urine osmo: ≤300 mOsmkg
    urine osmo: <300 mOsmkg (nml pt; ovenight urine is ≥800)
  69. H2O deprivation test: fx of exogenous ADH
    Central DI: urine osmo will increase; Nephrogenic DI: urine osmo will not change
  70. SIADH caused by:
    excessive levels of ADH active material of non-pituitary origin
  71. SIADH labs:
    low serum osmolality, low serum sodium & high urine osmolality
  72. ADH problems: tests
    DI: H2O deprivation; SIADH: water loading test
  73. Water loading study results
    (1L H2O; hourly urine/serum x 5 hrs) Normal: urine osmo < serum osmo; SIADH: urine osmo > serum osmo
  74. PTH labs
    can measure Ca, PO4, Mg, PTH directly; Alk phos assoc w/osteocyte activity (higher in growing kids, M>F, or mets)
  75. Vit D metabolites
    responsible for absorption of dietary calcium & phosphate in intestines; enhance PTH fx on mobilization of skeletal Ca & PO4
  76. Vit D labs
    can directly measure Vit D & metabolites
  77. IGF's fn:
    IGF’s mediate the effect of GH on skeletal muscle
  78. Aldosterone made in:
    zona glomerulosa
  79. Aldosterone fn
    reabsorption of sodium and excretion of potassium; prevention of hypovolemia & hyperkalemia
  80. Cortisol fn
    counters fx of insulin; anti-inflam
  81. Cortisol level highest:
    in AM; in stress & exercise
  82. Primary AI involves:
    AKA Addison dz; all 3 zones of adrenal (so potl insuff of cortisol & aldost)
  83. Addison dz: Ddx can be narrowed by:
    considering the abruptness of disease onset
  84. Primary AI: abrupt onset: etiology
    Adrenal hemorrhage, necrosis, thrombosis; meningococcal sepsis (Waterhouse-Friderichsen Syn); pseudo; coag dz; mets ca w/ bleed
  85. Primary AI: slow onset: etiology
    Auto-immune Adrenalitis; infxs Adrenalitis; Mets ca; congenital Adrenal Hyperplasia (CAH); Adrenomyeloneuropathy
  86. Primary AI: clin findings
    Hyperpigmentation (due to xs ACTH); Salt craving; Hyponatremia; Hyperkalemia; Vitiligo, pallor; auto-immune thyroid dz; CNS sx in adrenomyeloneuropathy
  87. Secondary/tert AI: slow onset: etiology
    Pit tumor / surgery / rad; Craniopharyngioma ; Isolated ACTH def; Megace (glucocorticoid-like action); LT g’corticoid tx; Sarcoidosis; Hypothalamic tumor
  88. AM cortisol results:
    >18: r/o AI; <3: R/I AI; btw this range: need dynamic testing
  89. ACTH stim test
    250 mcg Cosyntropin; measure cortisol before & 30 & 60 min after injxn; pre or post >18: R/O AI
  90. AI dx: labs
    AM cortisol (low); ACTH stim (low); plasma ACTH (>100: primary AI) (nml: 5-45 R/O primary AI; find cause of secondary/tert AI)
  91. Adrenal crisis tx
    Tx HYPOTENSION w/ volume (2 to 3 L of NS or D5NS); Give IV DEXAMETHASONE 4mg or IV HYDROCORTISONE 100mg (Dex preferred bc it won’t interfere w/ further dx testing & is long acting)
  92. Chronic AI: maint tx
    Hydrocortisone 20mg AM / 10mg PM; Dex; prednisone
  93. Tx chronic primary AI: besides cortisol, must also tx insuff of:
    aldosterone: Fludrocortisone; check for postural HypoTN, orthostasis, serum K, renin; poss inc dose summer (inc persp Na loss) & dec dose in HTN (do not d/c altogether); NO K sparing diuretics for anti-HTN Rx
  94. AI Prophylaxis: Steroids in Surgery
    Give pre-op hydrocortisone / continue 24 hrs; cut dose by 50% after first 24 h; cut dose by 50% each day until return to maint level (small procedures: give single dose of HC IV before procedure)
  95. Cushing syn: ACTH-indept:
    Adrenal lesion: next step is adrenal CT; exogenous source; Plasma ACTH level is low (< 5 pg/mL)
  96. Cushing syn: ACTH-dependent:
    Plasma ACTH level is normal or high (>15 pg/mL); Either ectopic production OR Pituitary adenoma = Cushing dz
  97. Diagnosis: ACTH-dept: distinguish btw ectopic vs pituitary:
    CRH-Stimulation test; HD Dex suppression; Petrosal Sinus Sampling; Octreotide scintigraphy to localize ectopic source; MRI
  98. Cushing syn: tx
    Surg Resection; Transphenoidal microsurgical removal (if sure Cushing dz); Bilateral Adrenalectomy (uncommon); Pharmacologic adrenal blockade
  99. Hirsutism / virilization: etiology
    Idiopathic (Familial); PCOS; Androgen-secreting adrenal adenomas or carcinoma; Ovarian tumors; Glucocorticoid resistance
  100. Hirsutism / virilization: etiology: ACTH-dependent causes
    Congenital Adrenal Hyperplasia; ACTH-dependent Cushing Syn
  101. PCOS LH:FSH ratio
    >2.0 common
  102. Androgen-secreting adrenal adenomas
    Rare; high serum androgen conc remain elevated despite Dex suppression
  103. Androgen-secreting adrenal ca prevalence
    More common than adenomas
  104. Androgen-secreting adrenal carcinomas
    usu > 5 cm at dx; Very high DHEA, DHEA sulfate; No response to HD Dex Suppression
  105. Hirsutism / virilization: lab eval
    Serum testost (total & free); androstenedione (>1000: ovar adrenal neoplasm); DHEAS (>700: adrenal source of androgen xs; Need adrenal CT to detn if hyperplasia or ca)
  106. Hirsutism / virilization: Imaging
    Pelvic Exam & US; Abd CT (esp adrenal glands/ fine cuts): adenoma / ca / hypertrophy
  107. CAH
    Enzyme defects in adrenal steroid hor synth -> insuff cortisol +/-mineralocorticoid; classically with an assoc androgen excess
  108. CAH: classical forms
    Salt-wasting form; Virilizing Syndromes
  109. CAH: nonclassical forms
    Late-onset: women = hirsutism & menstrual irreg which can mimic PCOS; Men/boy: androgen excess can be asymptomatic
  110. Hirsutism / virilization: Tx
    Stop any offending meds; Med tx options; Interventional tx options (Postmeno F can undergo lap bilat oophorectomy, if scans are nml; small hilar cell tumors of ovary may not be visible on scans
  111. PCOS Tx options
    Oral Contraceptives (beware DVT); Metformin; Anti-androgen ( if NOT PG): Aldactone (spironolactone), Finasteride, Flutamide
  112. Primary hyperaldosteronism: clin findings
    Hypertension; Mx Sx (d/t hypokalemia): cramping, weakness, periodic paralysis; Often few clinical findings at all (often suspected after lab abnormalities)
  113. Primary hyperaldosteronism: labs
    Chem7 (Hypokalemia, Metab alkalosis); Serum renin & aldosterone ( Aldo/renin ratio >20 is suspicious); 24-hr urine aldost (high in setting of low renin (<5mcg/dL) suspicious); Saline-loading; 18-OH corticosterone
  114. Primary hyperaldosteronism: labs: 18-OH corticosterone
    indicative of aldosterone producing adenoma (APA)
  115. Primary hyperaldosteronism: imaging
    Abd CT (esp of adrenals); Adrenal vein sampling: for localization (cath of left an&d right adrenal veins & the IVC, looking for lateralization of elevated aldosterone level
  116. Primary hyperaldosteronism: issues in eval
    S/b off Aldactone; CCB; ACEI (consider in-house eval); At least 150mEq of sodium intake daily (to suppress aldosterone prodn)
  117. Primary hyperaldosteronism: presenting forms
    APA (Conn’s); Bilateral Hyperplasia of the Zona Glomerulosa (if bilat, need remove both); Primary adrenal hyperplasia; Adrenal carcinoma
  118. Primary hyperaldosteronism: Tx: Aldosterone Producing Adenoma:
    surgical (effective only in patients with unilateral disease)
  119. Primary hyperaldosteronism: Tx: IHA or poor surgical candidate:
    med tx: Mineralocorticoid receptor antagonists: Spironolactone (DOC) or Eplerenone; CCB; ACEI
  120. Pheochromocytoma =
    dz of adrenal medulla (site of catecholamine prodn)
  121. Pheochromocytoma: 5 P’s
    pain; pallor (ortho hypoTN); palpitations; pressure (HTN); perspiration
  122. Pheochromocytoma; rule of 10
    10% of dz are: extra-adrenal; bilateral; familial; malignant; not assoc w/ HTN
  123. Pheochromocytoma: Dx
    24 hr urine (for Catecholamines & Metabolites: Metanephrines / VMA); Serum metanephrines/ plasma catecholamines; Imaging
  124. Pheochromocytoma: Tx : First:
    Alpha Adrenergic-Blockade first; Beta-blockade next if nec; NEVER start before alpha-blockade (can lead to worsened hypertensive crises); CCB (may be better tolerated than alpha-blockade)
  125. Pheochromocytoma: Tx:
    Surgical resection is tx of choice (May req open lap); Need adequate a-blockade pre-op; Watch for post-op comps(Labile BP; Post-resection hypoTN/ shock; Hypoglycemia)
  126. TBG is increased / decreased by:
    inc by estrogen, decreased by androgen
  127. Fx of illness on T3 / T4
    Severe illness or starvation decrease total T3 and free T3, increase rT3, no change of free T4 (euthyroid sick syndrome)
  128. Thyroid functional assessment
    131-Iodine Uptake; Measured at 24 hours; Normal 15-30%
  129. Thyroid imaging
    Thyroid scan (99m Tc); US (good for nodules); CT; MRI; PET
  130. Graves dz: etiology
    Auto-antibody reacting with the TSH receptor (TSI, 80-95% pos)
  131. Graves dz: eval
    Symmetric non-tender goiter (80%) (bruit is pathognomonic); Ocular findings (30%); Pretibial myxedema; TSH, Free T4, Free T3; Thyroid uptake and scan
  132. Subacute thyroiditis (early) AKA:
    de Quervain’s
  133. Silent or painless thyroiditis (early) AKA:
    Hashitoxicosis
  134. thyroiditis (early): course:
    hyperthy (1-3 mo); then hypothy (1-3 mo); then euthyroid
  135. hypothyroid prevalence
    2% of US F (0.2% US M); 1 in 4000 newborns
  136. Hypothyroid etiology (3)
    Primary; goitrous; central
  137. Hashimoto etiology
    cytotoxic anti-thy Ab's (80-90% antithyroglobulin); >50 yo
  138. toxic multinodular goiter etiology
    multicell autonomic fn
  139. toxic multinodular goiter exam & Tx
    >50 yo; lg irreg nod thy; TSH, FT4, FT3, uptake & scan; Rx RAI
  140. Toxic nodule: etiology
    activation of TSH receptors via rec gene mutation
  141. Toxic nodule: exam
    30-40 yo; lg irreg nod thy; onycholysis; TSH, FT4, uptake & scan; Rx RAI
  142. subacute thyroiditis etio
    TH leak d/t viral infxn -> thy gland destn
  143. subacute thyroiditis: exam
    Fever; lg irreg very tender thy; TSH, FT4, FT3, thyroglobulin, ESR, uptake & scan(result: zero)
  144. subacute thyroiditis: Tx
    ASA/ NSAIDs; prednisone
  145. silent thyroiditis: etio
    transient autoimmune dysfn (often post-partum); sudden onset of hyperthyroid
  146. silent thyroiditis: exam & Tx
    lg nod thy; TSH, FT4, FT3, anti-thy Ab (30%), uptake & scan; Rx beta blocker
  147. levothyroxine AE
    Osteoporosis; Inc cardiac contractility; Inc risk of A-fib; Allergic rxn dye in tablets
  148. Multinodular goiters
    2-4% prev in iodine-sufficient areas; F 5-15 x M; multifactorial; genetic cause?
  149. Multinodular goiters: tx
    thyroxine suppression of TSH; surg if obstruction
  150. Thy nodule/neoplasia: exam
    benign hx; s/s hypo or hyper; tender nod; FH hypo, nod, or goiter
  151. Thyroid nodule: eval for neoplasm
    TSH; US (80%); FNA. Scan = no value
  152. Tx for Graves dz
    PTU (esp for PG/BF)(TID); Tapazole (qd)
  153. Cytomel =
    T3 drug
  154. Cytomel AE
    inc cardiotoxicity risk
  155. Armour thyroid: problems
    Unpredictable hormonal stability; allerg rxn risk; Lacks bioequivalence among brands
  156. PTU works within:
    17 weeks
  157. Tapazole works within:
    6 wks (w/fewer AE)(QD dosing, so better compliance than PTU TID)
  158. PTU & Tapazole AE:
    Benign rash; potl agranulocytosis; hepatotoxicity
  159. Surgery for hyperthyroid: subtotal or total thyroidectomy: indicated in:
    pts with obstructions, malignancy, pregnancy in 2nd trimester, or those with contraindications to RAI or thioamides
  160. Tx of choice for hyperthyroid in US:
    radioactive I ablation (CI in PG)
  161. Hyperthyroid tx adjuncts:
    beta-blockers; c'steroids (dec action of thy hormone & imm response in Graves); Iodine (blocks thy hor release)
  162. PTU / Tapazole: If miss a dose:
    take as soon as remember. Double up doses if necessary!
  163. Tx for thyroid storm
    PTU; Propranolol; Corticosteroid; Iodide; Supportive measures; mortality 20%
  164. Myxedema Coma: findings
    Emergency: elderly in winter; Hypothermia; Resp depression; Unconsciousness
  165. Myxedema Coma: tx
    stat IV levothyroxine; then check labs
  166. hypothyroid Tx: T4/T3 ratios
    Liotrix 4:1; thyroglobulin 2.5:1; armour = not consistent
  167. thyroid replacement tx dosing
    <45 yo 100%; > 45 or LT/severe dz 50%; CVD or >65 25%; PG: inc dose by 50%
  168. Hyperthyroid tx monitoring
    TT4 & FTI after 4-6 wks; after change in tx; then q 6-12 mo (for RAI: TSH/FT4 qmo)
  169. test used to evaluate overall cortisol production
    24 hr urine cortisol (AKA urine free cortisol)
  170. preferred test for Cushing syn
    24 hr urine cortisol
  171. 24 hr urine cortisol specimen
    5 mL (frozen, fridge, or preservative) within 4 hr of collection
  172. ACTH levels indicate:
    High: Addison; low: secondary AI
  173. Increased ACTH d/t:
    Cushing dz; Addison; ectopic ACTH-producing tumors
  174. Decreased ACTH d/t:
    adrenal tumor; steroid medication; hypopituitarism
  175. Acute AI: lab findings
    Low cortisol; Hyperkalemia; Hyponatremia; Elevated BUN; Hypoglycemia
  176. Cushing: lab dx
    24 hr urine cort; Dex suppression test; high PM cortisol
  177. Cushing: to detn cause of xs cortisol:
    Plasma ACTH level; HD Dex supp test; CRH stimulation test; Imaging (CT, MRI, US)
  178. Secondary hyperaldosteronism
    More common than primary; usu d/t renal artery stenosis (curable by surg/angioplasty)
  179. Renin & aldosterone: body position
    levels rise following assumption of an upright position
  180. Elevation of 17-KS indicates:
    tumor or hyperplasia of adrenal cortex
  181. adrenal x-rays to:
    look for calcifications (poss d/t TB)
  182. adrenal CT/MRI to:
    evaluate the size & shape of the adrenal glands & pituitary
  183. 17-OCHS & 17-KS useful to:
    detn cause of Cushing’s syn
  184. Cushing other findings
    Hyperglycemia; Glycosuria; Leukocytosis; Lymphocytopenia; Hypokalemia
  185. 17-OCHS very high in:
    ectopic ACTH secretion
  186. Hirsutism/virilization labs:
    Inc plasma & urine 17-KS; inc plasma ACTH
  187. interfering substance in urine metanephrine analysis
    peppers
  188. VMA
    useful in dx & f/u of pheochromocytoma; present in larger amts than other catecholamines

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