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56 Cards in this Set

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thyroid follicular cells secrete

thyroid hormones promote

thyroid parafollicluar secrete?
-T4, 20% T3, rest is converted in peripheral tissue T4-T3

-growth, energy, hear tproduction

-calcitonin-tone down calcium blood levels
thyroid hormone syntehsis
1. Iodine transport across epithelial cell BM

2. Thyroglobulin gene transcription

3. iodine + tyrosin + thyroglobulin

4. I- coupling to from T3-T4 catalyzed by thyroid peroxidase

5. thyroid hormone bound to Tg stores in follicular lumen

6. transported back and released
thyroid Hormone Transport

TBG increase/decrease
-bound to plasma proteins(TBG)

-Asses fxn consider T3/T4 free plasma not just overal hormone lvels

-TBG increase w/ prgenancy, birth control, tamoxifen- raising total plasma T4 but euthyroid

-TBG decrease w/ glucosteroids, protein loss, and heparin, reducing total plasta T4 but euthyroid
Graves disease
caused by?
Additional to usual hyperthyorid sx?
-TSH AB stim-->excessive hormone production

-exophthalmos(occular proptosis): bilateral/unilateral, independent of thyroid levels
-spasm of upper lid due to inflammation into orbital tissues and muscles which leads to eye being pushed outwards and compression of optic nerve

-Pretibial myxedema: thickening of skin-->orange peal
Rgulation of thyroid

Hypothalamus
Pituitary
-feedback mechansim? what do hyp/hyper have?
thyroid
1. Hypothalamus-TSH acts on pituitary

2. Pituitary: takes fdbk from TSH and acts releases TSH(AP)-->growth of thyroid, idodide uptake, release of T3/T4
-TSH regulated by T3 cells, negative feedback

- hypothyroidisim: low T3/T4, high TSH
-Hyper: high free T3/T4, low TSH

3. thyroid: regulated by infrathyroid iodide levels, TSH.
-excess levels inhbiti resposne to TSH, depletion enhances response
thyroid Strom
what is it?
sx?
follows?
accelearted hyperthyroidism

-fever, prostration, severe tachycardia(A-fib), extreme sweating, restlessness, dehydration, shock

-follows prolonged hyperthyorid state, related to increased binding sites for catecholamines
Role of TSH receptor
-binds TSH--> T4/T3

-also binds TSH-Receptor stimulating Abs, TSH-receptor blocking Abs
Toxic Adenoma
caused by?
diagnosed?
-overproduction of hormone by single autonomous adenoma, rest of gland supressed

-hot spot on thyroid scan
Hyperthyroidism
also called?
represents?
sx?
signs?
-increase lvels of thyroid hormone(any cause)

Sx: overheating(heat intolerance) palpitations, dypnea, polyphagia(hungry panda), anxiety, nervousness, insomnia, increased stool freuency/diarrhea, weight loss, fatigue

Signs:
-rapid heart rate, tremors, WARM/MOIST, palmar erythema, nervous
-eyes pop out
-thyroid gland may or may not be nenlarged
toxic nodular goiter
-autonomous sites of overproduction of hormones, multiple hot spots
Subacut thyroiditis
caused by?
limited?
-post viral condition, dammage/inflammation causes leakage of performed hormones in follicular space so circulating levels are lower than other types of hyperthyroidisim
Factitious hyperthyroidism
-ingestion of thyroid hormones by medical personnel

-hamburger toxicosis- thyroid ground in beef neck muscles
Hyperthyroidism Treatment
-decrease hormone production by inhibiting thyroid peroxidase enzyme

-counteract peripheral effect: drugs like beta-blockers

-Radioactive iodine- shrink gland, knocks out entire gland

-Surgery-partila or totla thyroidectomy
Hypothyroidism
also known as?
Sx?
-decrease in thyroid hormone levels

-cold intolerance, lethargy, myalgias, athralgia, depression, parasthesia, distortion of taste, smell, bizarre sense of humor, psychosis
Signs of hypothyroidism
-cool coarse, dry yellow skin
-puffiness(periorbital edema)
-brittle hiar
-weight gain, deep harsh voice, slow reflexes
-constipation
-hyptoension, pericardial and pleural effusions, bradycardia, anemia
-myxedeme coma(end stage)
-weakness, hypothermia, stupor, hypoventiliation, hypoglycemia, coma, death
Causes of Hypothyrodisim
-autoimmune
-hashimotos
-raised TSH receptor blocking ABs
-Iatrogenic
-Iodine deficiency
Hashimotos thyroiditis(chronic lymphocytic thyroiditis)

caused by?
also assoicated with?
-raised levels of thyroid peroxidase antibody

-mitral valve prolapse
Hypothyroidism Treatments
1. Replacement of T4 hormone

2. Combination therapy with T4, T3 is promoted but provides little benefit
thyroid Disease Diagnosis
Serology Test
Iodine metabolism
Imaging(ultrasound)
Serology Tests for thyroid disease
TSH:
low = hyper
high = hypo

Free T4-change

Autoimmune hypothyroidism: antithyroid antibodies
Iodine Metabolism Test
-Radioactive iodine uptake: measures amount of radioactive iodine taken up by thyorid gland overtime

-good for subacute thyroiditis
dental implications
Hyperthyroidism:
-thyroid storm, epinephrine sensitivity
Hypothyroidism:
-myxedeme coma, sensitivty to depressents(lose ability to cope with hypoxia or hypercapnia-->can stop breathing)
Calcium homeostasis:
-in plasma?
-healthy?
-55% bound to albumin or citrate/po4
-can be changed by certain meds
-unbound-Ca2+ = active form
-maintain constant level of Ca@+ in ECF, amount you lose = amount eat
Calcium Regulation:
controlled by:
Parathyroid hormone
vitamin D

Ca levels:

can inhibit release of PTH, decrease levels sitmulate PTH
fxn of PTH
-increase outflow of Ca into ECF via:
Kindey: 1,25 OH2 vitamin D production-->retention of Ca, excrete PO4

-Bone: resorption/release of Ca and PO4

-GI tract: increases intestinal Ca absorption
vitamin d 12OH2 D3 fxn
-mediates Ca absoprtion in intestine and promotes bone formation
Hashimotos thyroiditis(chronic lymphocytic thyroiditis)

caused by?
also assoicated with?
-raised levels of thyroid peroxidase antibody

-mitral valve prolapse
Hypothyroidism Treatments
1. Replacement of T4 hormone

2. Combination therapy with T4, T3 is promoted but provides little benefit
thyroid Disease Diagnosis
Serology Test
Iodine metabolism
Imaging(ultrasound)
Serology Tests for thyroid disease
TSH:
low = hyper
high = hypo

Free T4-change

Autoimmune hypothyroidism: antithyroid antibodies
Iodine Metabolism Test
-Radioactive iodine uptake: measures amount of radioactive iodine taken up by thyorid gland overtime

-good for subacute thyroiditis
dental implications
Hyperthyroidism:
-thyroid storm, epinephrine sensitivity
Hypothyroidism:
-myxedeme coma, sensitivty to depressents(lose ability to cope with hypoxia or hypercapnia-->can stop breathing)
Calcium homeostasis:
-in plasma?
-healthy?
-55% bound to albumin or citrate/po4
-can be changed by certain meds
-unbound-Ca2+ = active form
-maintain constant level of Ca@+ in ECF, amount you lose = amount eat
Calcium Regulation:
controlled by:
Parathyroid hormone
vitamin D

Ca levels:

can inhibit release of PTH, decrease levels sitmulate PTH
fxn of PTH
-increase outflow of Ca into ECF via:
Kindey: 1,25 OH2 vitamin D production-->retention of Ca, excrete PO4

-Bone: resorption/release of Ca and PO4

-GI tract: increases intestinal Ca absorption
vitamin d 12OH2 D3 fxn

disfxn causes?
-mediates Ca absoprtion in intestine and promotes bone formation

-rickets in children, osteomalacia in adults
Calcitonin fxn
-opposite of vitamin D
-reduces circulating Ca/PO4 levels by inhibting osteolcast bone resoprtion
-increase Ca-->stims calcitonin
-naturually has no effect on calcium blaance but synthetic versions can used for therapy
other hormones involved in calcium homeostasis
-Sex Steroids: etrogens-->anabolic/protective effects, lack of -->resorption

-Glucocorticoids: bone thinning/reduction of bone density by inhibiting ostelbasts

-thyroid hormone: increase Ca realease from bone. Deficiency can lead to reduced skeletal growth(cretinisim)

-growth hormone:
promotes growth of bone and cartilage, excessive can cause abnormal growth(gigantism, acromegaly)
Hypercalcemia Sx
-non-specific: malaise, fatigue, headaches, diffuse pains(calcium deposition in soft tissues)

-renal: plyuria, nephrolithiasis, urnary obstruction

-gastrointestinal: nausea, vomiting, anoreixa, constipation

-musculoskeletal: weak, myopathy, bone cysts, osteoporosis

-neuropsychiatric: lethargic, ataxia, psychosis, stupor, coma

-mestatis calcificaiton- in eyes, skin kidney

stones bone and abdominal groans and psychic moans
Primary Hyperparathyroidism:
-high PTH, serum Ca, low PO4

-Sx releated to elevated Ca

-Osteitis Fibrosa Cystica(von Recklinghausens bone disease)
-High PTH-->subperiosteal bone resorption-->marrow fibrosis, cystic reparative lesions(brown tumors)

-causes bone pains/vetebral fractures
-metastatic calcification(renal stones)
Hypercalcemia Malignancies
-local osteolytic process in bone from invading cancer

-can rasie calcium through PTHrP
Hypercalcemia other causes:
-Sarcoidosis and other granulomatous diseases-->increase Ca absorption
-granuloma cells convert Vit D to inactive-->lower bone deposition(vit D) and drive up PTH production(less Ca absorbed)

-too much milk
hypercalcemia treatments
-treat underlying cause
-drugs(bisphosphonates to inhibit bone resorption)
Hypocalcemia:
Sx
-realted to neuromuscular excitability OR deposition of calcium in soft tissues(not cause and effect)

-parethesias of lips, fingers, muscle cramps, spasms, tetany, restlessness, depression, seizures

-chovstek: tapping of facil nerve
-trousseaus-carpal spasm
-EKG changes: delayed repolarization
Hypocalcemia
causes?
treatment?
-hypoparathyroidism:
-idiopathic or post surgical thyroidectomy
-glandular damage from iron overload(thalassemia), copper overload(wilsons), autoimmune destruction
-renal failure-reduced vit D level, resistance to PTH action
-decrease vit. D intake/metabolism
-pancreatitis, crush injuries, citrated blood transfusion

-treatment: Ca IV or Vitamin D
Bone mass trends?
Osteoporosis:
characterized by?
-Gain most bone during adolescence, after 35 start losing
-bone health dependent on levels of exposure to nutrients, hormones, physical activities, genetics

-decrease in denisty and microarchitecture of bone
Classification of Osteoporosis:
Type 1: bone loss acceleartion following menopause
-loss of estrogen which promoted bone deposition, also has protective effect against cytokine mediated osteoclast activation

Type 2: constant bone loss related to other conditions
-drugs, endocrine disease, malabsorption, immobilization
Clinical Presentation of Osteoporosis:
-asymptomatic unless fracture

-vertebral fracture via minimal stress from recurrent small fractures over time(loss of height and classic hump)

-fracture of wrist, hip, ribs, pelvis, humerus
-hip fracture via minimal traumua-->pulmonary embolism, infection
Effects of aging
Deficient:
-Vit D production in skin
-12OHD3 production in kidneys-->decrease intestinal absoprtion-->decrease plasma calcium

-->increase PTH-->increase bone resoprtion
Osteoporosis Diagnosis
-Dual Energy Xray Absorptiomtry for bone desnity

-osteopenia: 1-2.5 SD below peak bone mass
-osteoporsis: 2.5 SD below peak bone mass


-Quantitative computed tomography
Osteoporosis Treatment/Prvention
-Calcium and Vitamin D
-Estrogen repalcement(progestin)
-Bisphosphonates: prevent bone resporption but may increase jaw bone necrosis

-selective estrogen receptor modulators-effective but have sig. side effects

-intranasal calcitonin
-excercise
Pituitary Gland:
hormones?
AP:
Growth Horme(GH): on organs
Prolactin(PRL) : breasts
ACTH: adrenal glands
TSH:thyroid gland
LH/FSH

Posteiror:
ADH vsopressin
Anterior Pituitary general problems
-hypersecretion of hormones secondary to an adenoma

-hyposecretion of hormones-via compression, damage or infarct

-local damage of expanding tumor: visual problems
AP Hypersecretion SX
Hyperprolactinemia :
females: galactorrhea, irreuglar mesnes, amenorrhea

Males: loss of

Growth Hormone: acronmegaly in adults, gigantism in kids

ACTH: cushings

TSH: hyperparathyroidism
AP hyposecretion
Prolactin: no breast feed

LH/FSH:
kids: delay puberty
Men: decrease libido, impotence, infertility
Women: menstrual irregularity, amenorrhea, hot flushes, dypareunia

TSH: hypoparathyroidism
ACTH: adrenal insufficiency, Addisons
Posterior Pituitary
-ADH deficient: Diabetes insipidus
-excessive dilute urine-->polydipsia

-Syndrome of inappropriate ADH Secretion(SIADH)
-excessive water retention, hyponatermia