Physiology - Block 1 - Part 4

davidwurbel7's version from 2015-06-07 04:37


Question Answer
The coupling of one MIT and one DITTriiodothyronine (T3)
The coupling of two DITThyroxine (T4)
TG is a glycoprotein containing large quantities of this amino acidTyrosine
Na+ - I- cotransport pumps iodide against its concentration gradientIodide Trap Mechanism
Thiocyanate & Perchlorate anions inhibitsNa+ - I- Cotransport Pumps
Propyl Thiouracil, Methimazole & Carbimazole inhibit this enzymeThyroid Peroxidase
Enzyme that converts T4 to T3 in the peripheral tissue5' Deiodinase
Iodination is catalyzed byThyroid Peroxidase
Which form of thyroid hormone is the more biologically activeT3
High levels of I- inhibit the organification and synthesis of thyroid hormoneWolff-Chaikoff Effect
Coupling of one MIT and one DIT or two DIT is catalyzed byThyroid Peroxidase
Medication given to persons exposed to nuclear radiation in the event of a nuclear disasterPotassium iodide
Enzyme that recycles iodine in the follicular epithelial cells after the release of T3 and T4Thyroid Deiodinase
TRH deficiencyTertiary Hypothyroidism
TSH deficiencySecondary Hypothyroidism
Thyroid peroxidase deficiency or TSH receptor defectsPrimary Hypothyroidism
Antibodies that targets thyroglobulin and thyroid peroxidase resulting in hypothyroidismHashimoto's Thyroiditis
Antibodies that targets TSH receptors causing excitation leading to hyperthyroidismGraves' Disesase
Thyroxine Binding Globulin (TBG) is produced in which organLiver
In the target tissues, this thyroid hormone binds more strongly to the nuclear receptorT3
In the plasma, this thyroid hormone binds more strongly to Thyroxine Binding Globulin (TBG)T4
Enzyme that converts T4 to reverse T3 (rT3)5-Monodeiodinase
Test for thyroid functionRadioactive Iodine
Decreased T3, T4, Increased TSH, Increased TRHPrimary Hypothyroidism
Decreased TSH, Decreased T3, T4, Increased TRHSecondary Hypothyroidism
Decreased TRH, Decreased TSH, Decreased T3, T4Tertiary Hypothyroidism
Increased T3, T4, Decreased TSH, Decreased TRHPrimary Hyperthyroidism
Increased TSH, Increased T3, T4, Decreased TRH Secondary Hyperthyroidism
Increased TRH, Increased TSH, Increased T3, T4Tertiary Hyperthyroidism
This hormone act synergistically with GH & Somatomedins to promote bone formationThyroid Hormone
This hormone causes the maturation of the CNS in which formation of synapses, myelination of nerve fibers during the perinatal periodThyroid Hormone
Thyroid hormone increases the BMR in all tissues except inCNS
Palpitations are seen in this condition as a result of an increase in heart rateHyperthyroidism
β-adrenergic blocking drug, is used in Hyperthyroidism to treat palpitations that blocks both β1 and β2 adrenergic receptorsPropranolol
Increases formation of LDL receptors in liver which increases hepatic removal of cholesterol from circulationThyroid Hormone
Increases glucose absorption from GIT, increases Glycogenolysis & Gluconeogenesis; Increases blood glucose levels; Increases LipolysisThyroid Hormone
Overall effect of Thyroid hormones on protein metabolismCatabolic
Increased metabolic rate - polyphagia. Increased heat production - causes sweating, heat intolerance. Increased Cardiac output (Palpitations), increased BP. Tremor (increased β-adrenergic activity). Weight loss, weakness (increased Protein catabolism). Exophthalmos, Goiter, Pretibial Myxedema (Dermopathy), irritability, increased excitabilityGrave's Disease
Exophthalmos and Pretibial Myxedema (Dermopathy) are classical signs ofGrave's Disease
Patient has features of Hyperthyroidism with Exophthalmos. Presence of peri -orbital and retro-orbital edema because of Cytokine release which is an inflammatory mediator. Sympathetic over-activity causes lid retraction, giving rise to a Staring LookThyrotoxicosis
Propylthiouracil/Methimazole- Blocks Peroxidase enzyme which is used to treatHyperthyroidism
Thyroidectomy, Iodine(I131) which destroys follicular cells, β-blockers like propranolol are done to treatHyperthyroidism
Causes of this condition include Hashimoto’s Thyroiditis, Subacute thyroiditis (de Quervain thyroiditis) or painful thyroiditis), Thyroidectomy, Pituitary adenoma, Tumors impinging on Hypothalamus, Shehan’s syndrome, Iodine deficiency (Not in the USA), Drug induced (Amiodarone, Lithium,), Radioactive Iodine 131- (Treatment for grave’s disase )Hypothyroidism
Most common cause of hypothyroidism. Antibodies are produced which destroy Thyroglobulins & Thyroid peroxidase enzyme (TPO). Results in inflammation leading to structural damage of the Thyroid gland.There will be decreased levels of Thyroid Peroxidase (TPO) enzymeHashimoto’s Thyroiditis
On TSH administration, if T3, T4 increasesSecondary Hypothyroidism
On TSH administration, if T3, T4 DOES NOT increasePrimary Hypothyroidism
When monitoring a patient on thyroid hormone replacement therapy, this marker is usedTSH
Decreased metabolic rate and O2 consumption, Decreased heat production (cold intolerance), Dry and cold skin, Decreased appetite, Weight gain, Decreased Cardiac output, hypoventilation, Lethargy, mental slowness, Psychosis (Myxedema Madness), Ptosis, peri-orbital edema, Goiter, Constipation, Hoarseness in speech, Deep tendon reflexes with slow relaxation phase, Anemia, myxedema, (accumulation of mucopolysaccharides), Beta-Carotenemia, Menstrual irregularities, AmenorrheaHypothyroidism
Results from untreated postnatal hypothyroidism, Individuals often appear normal following delivery but may display respiratory difficulty, jaundice, hyperglossia, feeding problems and hypotonia; defective myelination in axons of cortical neurons leading to mental retardationCretinism
Percentage of uptake of 123Iodine is decreasedHypothyroidism
Percentage of uptake of 123Iodine is increasedHyperthyroidism


Question Answer
9-11 mg/dL or 4.3 to 5.3 mEq/L is the normal range in the blood forCalcium
Has Ca+2 & Phosphate (PO4) saltsHydroxyapatites
[Ca+2] x [PO4 ] = a constantSolubility Product
[Ca+2] x [PO4 ] > Solubility product has this effect on boneBone Deposition
[Ca+2] x [PO4 ] < Solubility product has this effect on boneBone Resorption (Demineralization)
Decreased serum Ca 2+ increases secretion ofPTH
Actions of PTH produces an increase in serum [Ca 2+ ] and decrease in serumPhosphate
PTH receptors are present on only this class of cells in the bonesOsteoblasts
Osteoblasts release this in response to PTH receptorCytokines (IL-6 and RANK-L)
Inhibits renal Phosphate reabsorption in this part of the kidneyProximal Tubule
PTH increases renal Calcium reabsorption in this part of the kidneyDistal Tubule
PTH stimulates activity of 1α- Hydroxylase in kidneys and increases formation of 1,25 DHCC which in turn increases absorption of Ca 2+ and Phosphate inIntestine
In the kidneys, PTH increases the formation of this, which increases absorption of Ca 2+ and phosphate in the intestine1,25, Dihydrocholecalcipherol
Primary Hyperparathyroidism is most commonly caused byParathyroid Adenoma
Increased serum [Ca 2+] - Hypercalcemia; Decreased serum Phosphate - Hypophosphatemia; Increased urinary Phosphate excretion -Hyperphosphaturia; Increased bone resorption due to increased osteoclasts (osteitis fibrosa cystica); Increased serum Calcium predisposes to Nephrocalcinosis (Calcium stones in kidney); Eventually, Nephrocalcinosis may cause Renal tubular damage causing Polyuria; Renal stones (Nephrolithiasis)Primary Hyperparathyroidism
Stones within the urinary tract (most likely made of calcium)Nephrolithiasis
Deposition of calcium in the medulla of the kidney due to hypercalcemiaNephrocalcinosis
Common causes include Vitamin D deficiency and Chronic renal failure. Increased demand for calcium in pregnancy. PTH is elevated in both conditions. Parathyroid gland is normalSecondary Hyperparathyroidism
Common causes include inadequate sun exposure, malabsorption of Vitamin D, enzyme deficiencies in the pathway of activation of Vitamin DVitamin D Deficiency
Blood serum levels for Ca+2 high, PTH high, PO4 lowVitamin D Deficiency
Blood serum levels for Ca+2 high, PTH high, PO4 highRenal Failure
Long-term secondary hyperparathyroidism which eventually leads to hyperplasia of the parathyroid glands and a loss of response to serum calcium levelsTertiary Hyperparathyroidism
Blood profile very similar to primary hyperparathyroidism but low PTH. Hypercalcemia, Hypophosphatemia, HyperphosphaturiaHumoral Hypercalcemia of Malignancy
Furosemide (inhibits calcium reabsorption) Etideonate (Inhibits bone resorption) is used to treat hypercalcemia in patients with thisHumoral Hypercalcemia of Malignancy
Most commonly seen as a consequence of Thyroid surgeryHypoparathyroidism
Clinically presents with Decreased serum [Ca 2+] - Hypocalcemia & Tetany. Hyperphosphatemia & decreased urinary Phosphate excretion. Decreased cAMP levelsHypoparathyroidism
Clinical features of include neuromuscular hyperexcitability - there is decreased threshold for excitability of nerve fibers as there is less of calcium to stop activity of Sodium channels. Laryngeal spasm - is a life threatening complication. Carpopedal spasm - Flexion of thumb & wrist with hyperextension of metacarpophalangeal & interphalangeal jointsTetany
Flexion of thumb & wrist with hyperextension of metacarpophalangeal & interphalangeal jointsCarpopedal Spasm
Decreased threshold for excitability of nerve fibers as there is less of calcium to stop activity of Sodium channelsNeuromuscular Hyperexcitability
Is a life threatening complication of TetanyLaryngeal Spasm
Trousseau's sign and Chvostek's sign are clinical signs ofTetany
Pseudohypoparathyroidism Type 1a is also known asAlbright’s Hereditary Osteodystrophy
Inherited autosomal dominant disorder in which the Gs protein for PTH in kidney & bone are defective. When PTH binds to its receptors in these tissues, it does not activate Adenylyl cyclase. This leads to resistance to actions of PTH in the target organsPsuedohypoparathyroidism
Occurs due to inadequate dietary intake, inadequate exposure to sunlight, Renal & Liver diseases. Leads to - Rickets in children and osteomalacia in adults Vitamin D Deficiency
Deformed bones. Bow Legs (Knock Knees) - due to bowing of weight bearing areas. Thickening of wrists & ankles. Retarded growth & dentition. Widening of epiphyseal cartilaginous plates. Frontal bossing.Rickety RosaryRickets
Excessive osteoclastic functions with breakdown of bone matrix, leads to a decrease in bone mass and bone mineral density which can lead to an increased risk of fracture. Bone formation cannot keep pace with bone resorption. Characterized by weakened bonesOsteoporosis
(Insert 6.48 table)