21 | Thyroid Flashcards

Question

regulation of iodide uptake by thyroid gland

Answer 1

- iodine is impt regulator of TH production - rate limiting step in synthesis is iodide transport from bloodstream into follicular cell - competitive inhibitors of NIS (perchlorate, can cause hypothyroidism if at toxic levels, also can be given clinically for hyperthyroidism) can sig. affect thyroid gland function

Answer 2

- protection against sudden excess in I- intake, which would cause excess TH output - involves inhibition of iodination - physiological inhibition of hormonogenesis by WC effect w/ normal function is only 26-50 hrs - after, thyroid escapes from inh by adapting to higher I- levels, and resumes almost normal synthesis - may be due to down-regulation of NIS prod. would dec I- transported into follicle regardless of high serum I- levels, return biosynthesis to normal and release inh

Answer 3

- T3 + T4 secretion at 80-100 and 5 microgm/day - majority is bound to circulating plasma proteins (thyroxine binding globulin TBG, albumin + transthyretin, prod by liver) - tiny unbound amount determines metabolic rate of many tissues - all T4 in bloodstream from gland sec vs only 20% of T3. rest of T3 from intracellular deiodinase activity in periphery - T3 is physiologically relevant TH at tissue level, 90% of occupancy of nuclear thyroid hormone rec bound by T3

Answer 4

- T4 has a larger, more tightly bound extracellular pool with slower (t1/2=7days) turnover rate (T3 t1/2=1day) - metabolic rate is much faster for T3 than T4 (22 vs 1 L/day)

Answer 5

- THs into cells via PM carrier, cellular uptake plays role in regulating TH bioactivity - THs bind to non-histone protein nuclear receptors in conjuction w/ thyroid hormone response elements (TRE) - binding activity affects types and rates of translation of various RNAs in cells for enz and other cellular products - TH + its receptor interact with genes uniquely responsive to TH - response of tissue varies and is proportional to amount of nuclear TH rec in specific tissue ex: liver + myocardial tissue have large amount, and respond with large changes in protein synth and enzyme patterns. spleen + testis have small amounts, not very influenced by TH

Answer 6

- TH stimulates anabolic and catabolic pathways of metabolism, supports balance - in adults, regulates body weight, basal metabolism, oxygen req - physiological effects from 1. TH action on protein expression an activity 2. metabolic increase due to increase body temp 3. enhanced sensitivity to catecholamines - inc metabolic activity inc body's need for O2, met by various inc. - stimulation of metabolic pathways by TH is accompanied by inc need for energy

Answer 7

increases - glycogenolysis - gluconeogenesis - glucose oxidation - lypolysis - protein synthesis + degredation (net tends to be catabolic)

Answer 8

hyper: tachycardia, hand tremors hypo: bradycardia, slow physical response

Answer 9

- TH maintains normal gut motility and intestinal transit time - hyper: diarrhea - hypo: constipation

Answer 10

TH acts on multiple different effects to produce desired physiological response - TH stimulates CVS activity by increasing HR, stroke vol, CO, pulse pressue - concerted response by influencing electrical activity, cardiac contractility, NT activity, O2 use, alteration of cardiac tissue and proteins in myocytes

Answer 11

- normal whole body growth can't happen without enough TH even with normal GH levels - without TH, normal differentiation is impaired, decreased height + physical maturation. bone age of hypothyroidic children is lower.

Answer 12

- begins prenatal , completed 2-3 yo - untreated hypothyroidism leads to sever and irreversible mental retardation - iodide deficiency is major preventable cause in the world - may impair function in adults - treat with oral T4 or iodine

Answer 13

- axis dev independently from moths - thyroid gland early in first trimester - fetal TSH in pituitary and iodine conc in thyroid at end of first trimester - axis actively functioning by mid-gestation - as its developing, during first half, TH is fetal plasma derived from months

Answer 14

- during pregnancy, mother's thyroid gland inc production of TH - might lead to hyperthyroidism if not for parallel inc in thyroxine binding globulin (TBG) - compensatory mechanism that allows total TH pool to inc without raising free TH levels

Answer 15

- immature fetal thyroid lacks auto-reg mechanisms - can't regulate large exogenous loads of iodine - down regulation of NIS as an escape mechanism from Wolff-Chaikoff inhibition isn't fully dev in fetus - chronic fetal exposure to excess iodine can lead to prolonged inhibition, causing hypothyroidism in utero

Answer 16

- increased basal metabolic rate - increased appetite to maintain weight, weight loss, hyperdefecation, nervousness, tremors, tachycardia, larger pulse pressure, increased SV + CO, lower systemic vascular resistance, dec circ times, thin + smooth skin, inc heat production + intolerance - older patients may have "non-classical" symptoms: atrial fibrillation, weight loss, and muscle weakness as only manifestations - acute emergency: thyroid storm (grave's test for Ab to distinguish)

Answer 17

- slowing of metabolic rate with cold intolerance, lethargy, fatigue, dementia, thick + dry skin, constipation, bradycardia - slower metabolic rate may inc cholesterol levels and slower metabolism of drugs and toxins - thin hair, puffy face, mental changes, mood disturbance - LDL is markedly decreased, reduced clearance of cholesterol, inc risk of atherosclerosis - acute emergency: myxedema coma

Answer 18

- most common cause of hyperthyroidism - cause by autoantibodies against TSH receptor - Abs bind to rec and activate it, mimicking action of TSH - goiter caused by over-stim of thyroid - patients show signs and symptoms of hyperthyroidism and exophthalmos - deposition and accumulation of mucopolysaccharides behind eyes, causing to protrude out - if untreated can lead to systolic hypertension, cardiac arrhythmias, remodeling of heart muscle and congestive heart failure. also at risk of osteoporosis, both osteoclastic and osteoblastic activity inc - net effect is catabolic.

Answer 19

- most common cause of hypothyroidism - characterized by non-stimulating autoantibodies against thyroid gland proteins (anti TPO, peroxidase, TSH-rec, NIS) that eventually destroy the gland - goiter due to inflammation and lymphocytic infiltration of the gland due to immune attack in early stage - later, the destroyed gland atrophies

Answer 20

- inflammation of thyroid gland - i.e. silent and post-partum thyroiditis - may show over months hyperthyroidism followed by hypothyroidism then return to euthyroidism - hyperthyroidism not caused by excess hormone biosynth b/c inflammation reduces ability to synth new TH - rather, autoimmune attack on gland leads to "leaking" of pre-synthesized hormone stored in gland - initially leads to hyperthyroidism, lasts 2-3 mo - as stored supply is depleted and while biosynth is low, hypothyroid state produced - as inflammation goes away, gland resumes normal fucntion and euthyroid state reach - often self-resolves, can treat with beta-blockers to reduce symptoms

Answer 21

- occurs in susceptible women in first year after childbirth, 9% - since symptoms mimic others (i.e. depression), many cases may be unnoticed - during pregnancy, immune suppression dev in mother to tolerate fetus, but after birth rebounds and in predisposed women can lead to autoantibody prod and thyroid inflammation - after a year treated as chronic hypothyroidism

Answer 22

- in thyroid dysfunctional states, can affect reproductive function - most females with thyroid disease present during reproductive years, can appear as altered menstrual cycle - primary hypothyroidism, feedback from low free T3 can stim hypothalamic overproduction of TRH, leading to overprod of prolactin - can lead to galactorrhea and inh GnRH sec, causing amenorrhea (loss of period) - hyperthyroidism can cause altered sex hormone levels that can interfere with normal gonadotropin secretion + reproductive function - either extreme can cause impotence and/or infertility

Answer 23

- aim to decrease overproduction of THs w/ drugs that inh TH synthesis and/or drugs that inhibit peripheral effect of TH - surgery or radioactive iodine therapy to desotroy tissue can dec excessive TH production - create stable hypothyroid state than can be treated

Answer 24

- hormone replacement therapy with exogenous oral T4 | - has longer half life

21 | Thyroid Flashcards

(48 cards)