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123 Cards in this Set
- Front
- Back
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Skeletal location of pituitary
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Sella Turnica of the sphenoid bone
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Symptom of pituitary growth
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Loss of visual field and accuity as a result of compresion of the optic chiasm
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Posterior Pituitary Origin
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Neural process grows down from the diencephalon becoming the median eminence and neurohypophysis consisting mostly of hypothalamic neurons
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Origin of anterior pituitary
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Rahtke's Pouch grows up from roof of mouth forming the adenohypophysis
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Hormones of the Anterior Pituitary
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Prolactin (PRL)
Growth Hormone (GH) Thyroid Stimulating Hormone (TSH) Adrenocorticotropic Hormone (ACTH) Follicle-Stimulating Hormone (FSH) Luteinizing Hormone (LH) |
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Function of TSH
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Stimulates secretion of Thyroid Hormone
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Function of ACTH
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Stimulates release of cortisol
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ACTH Cell Type and target
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Corticotroph
Adrenal Glands |
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TSH cell type and target
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Thyrotroph
Thyroid Gland |
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GH cell type and target
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Somatotroph
All Tissues |
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Vessels from hypothalamus to anterior pituitary
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hypophyseal-portal circulation
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Hypothalamic Hormone Stimulating ACTH
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Corticotropin-Releasing Hormone (CRH)
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Hypothalamic Hormone Stimulating TSH and PRL
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Thyrotropin-Releasing Hormone (TRH)
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Hypothalamic Hormone Stimulating GH
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Growth Hormone-Releasing Hormone (GHRH)
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Hypothalamic Hormone Inhibiting GH
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Somatostatin
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Release characterisitics of Hypothalamic Releasing Hormones
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Secretion is in pulses to maintain Anterior Pituitary sensitivity. Constant stimulation downregulates Anterior Pituitary receptors
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Function of GH
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Direct Effect (Adult): Metabolic; Binds receptor on adipocytes stimulating lypolysis
Indirect Effect (Adolescence): Stimulates IGF-1 production in liver which causes cellular growth |
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Molecular action of GH
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Binds GHR releasing associated JAK2 tyrosine kinase initiating phosphorylation cascade. Phosphorylation of STAT Transcription Factors causes gene transcription
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Effects of GH on Chondrocytes
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Increases Amino Acid uptake, Protein synthesis, DNA/RNA synthesis, Chondroitin Sulfate, Collagen, Cell Size and number= Linear Growth
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Effects of GH on Metabolism
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Increases Plasma Glucose and FFA's
Decreases Plasma Amino Acids and Urea |
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Effects of GH on Muscle
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Increases Amino acid uptake and protein synthesis
Decreases Glucose uptake = Increase Lean Body Mass |
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Effects of GH on Adipose
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Decrease Glucose uptake
Increase Lypolysis = Decrease Adipose cell size |
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Secretion of GH
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10 Pulses per day
Nocturnal peak 1hr after stage 3/4 Highest levels during puberty 50% drop on levels every 7 years after puberty |
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Cause and Effect of Dwarfism
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Pre-pubescent GH deficiency
Retarded Skeletal growth Poor muscle development Excessive subcutaneous fat |
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SX of adult GH deficiency
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Lethargy
Central Obeisity Increased CV disease Decreased Bone Density |
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Cause & Effect of Gigantism
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Pre-pubescent GH excess typically from pituitary tumors
Glucose intolerance/hyperinsulinism CV hypertrophy |
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Cause & Effect of Acromegaly
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Post-pubescent GH excess
Coursening of features from bone and connective tissue overgrowth Think Skin Decreased Subcutaneous fat Glucose intolerance and diabetes |
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Thyroid functional anatomy
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Follicular cells (Cuboidal Epithelial) arranged in a sphere arround a lumen, the Colloid, where Thyroid hormone is stored. TSH stimulates enlargement of follicular cells forcine thyroid hormone out of the Colloid
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Three steps of Thyroid hormone synthesis
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Iodide Metabolism
Tyrosine Iodination Coupling of iodinated molecules with thyroglobulin (by TPO) |
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Hormones of the Thyroid
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Thyroxine (T4)
Triiodothyronine (T3) |
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Iodide Metabolism
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I- enters follicular cells by secondary active transport via electrochemical gradient and a 2NA-1I Symporter in the basal membrane (Called an iodide trap)
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Tyrosine iodination
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Tyrosine is glycosylated and exocytosed into the colloid
Iodide is carried into the colloid by pendrin. Thyroid Peroxidase (TPO) Oxidizes and incorporated Iodide into tyrosine to produce either 3-Monoiodotyrosine (MIT) or 3,5-Diiodotyrosine (DIT) |
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Coupiling of Iodinated molecules
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Thyroid Peroxidase (TPO) couples either two DIT or one MIT and one DIT to produce Thyoxine or Triiodothyronine respectively
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Conversion of T4 to T3
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Once released from the thyroid, 3,5,3',5'-tetraiodothyronine is activated in the periphery by either 5'-monodeiodinase to 3,5,3'-Triiodothyronine (T3) or 5-monodeiodinase to 3,3',5'-Triiodothyronine (Reverse T3/rT3)
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What causes decrease in conversion of T4 to T3 and increase in T4 to rT3
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Cortisol inhibits 5'-monodeiodinase shunting convertion of T4 from T3 to rT3. Fasting, Malnutrition, Physical Trauma (Burn injury). Deactivates T4 to an inactive form to slow metabolism, decrease temperature and enzyme activity, and conserve energy.
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Binding proteins of T4/T3
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T4/T3 are hydrophobic, require transport molecules
70% bound to Thyroxine-Binding Globulin (TBG) 29% bound to albumin Very low levels of free hormone, but free hormone is active and responsible for effects and feedback |
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Regulation of Free/Bound T4 ratio
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↓ in free T4 is reversed by dissociation of bound T4
Change in [TBG] is compensated for by ↑/↓ T4 release by thyroid **Alterations in TBG do not disturb ratio if Thyroid gland is normal |
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Effect of Thyroid-Stimulating hormone (TSH)
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Stimulates growth and vascularity of thyroid gland
Stimulates most steps in thyroid hormone synthesis Iodide Uptake and oxidation Iodination and coupling Edocytosis of colloid Thyroglobulin Proteolysis |
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Regulation of TSH
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T4/T3 has a negative feedback effect on the Anterior pituitary
Repression of TSH gene Suppression of TSH release Down-regulation of TRH Receptors |
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What hormones does Somatostatin Inhibit
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Anterior Pituitary:
Growht Hormone (GH) Thyoid Stimulating Hormone (TSH) Pancreas: Insulin (SS from delta cells) Glucagon |
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Where is Thyroxin Binding Globulin (TBG) synthesized?
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Liver
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What is the half-life of T4 and why is it so long?
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6 Days
T4 has a much higher binding affinity for Thyroxin-binding hormone (TBG) |
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Why is T3 the biologically active hormone?
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T3 has a much higher binding affinity for active receptors
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When treating hypothyroidism, why is it better to give synthetic T4 than T3?
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T4 is a better mimic of biological conditions (Biologically more T4 produced)
T4 has a longer Half-Life |
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MOA of T4/T3
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T4/T3 enters the cell via carrier mediated transport →T4 is converted to T3 in the target cell → T3 binds to nuclear receptors causing DNA transcription and protein synthesis.
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Physiological effects of T3 on target cells
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Stimulates bone and CNS maturation
↑BMR ↑Mitochondiral # and size ↑O2 consumption ↑Na-K ATPase ↑Protein Synthesis and Degredation (Net Catabolic) ↑Heat Production ↑Metabolism ↑Glucose Absorbtion ↑Glycogenolysis ↑Gluconeogenesis ↑Lipolysis ↑Cardiac output ↑HR and SV ↑SBP and ↓DBP |
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Describe Sympathomimetic effect of Thyroid Hormones
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Actions of T4/T3 resemble those if increased SNS activity
Reinforces CV respose to Epi/NE by ↑β-adrenergic receptor number, Coupling to Adenylate Cyclase, ↑cAMP |
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Cause & Effect of Creatinism
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Adolescent Hypothyroidism
Impaired growth of cerebral and cerebellar cortex Impaired proliferation of axons and dentrides Impaired myelinization |
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S/SX of Adult Hypothyroidism
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↓BMR → cold intolerance
Lethargy Somnolence (Dowsiness) Mental Slowness Muscle Aches Decreased Reflexes Decreased Sweating Weight Gain Myedema (Mucopolysaccharide acculumation under eyes causing edema) Goiter Amenorrhea Constipation |
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Causes of Hypothyroidism
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Primary (Thyroid Failure)
Secondary (Pituitary/Hypothalamic Failure) Iodide Insufficiency |
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What causes formation of a goiter?
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Increases TSH or TSH like peptide (Thyroid Stimulating Immunoglobulins TSI)
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Cause & Effect of Graves Disease
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Hyperthyroidism
Exopthalamos (Forward displacement of eyes), Lid Retraction Pretibital Myxedema (Hyaluronic Acid and Chondroitin Sulfate accululation in dermis) ↑BMR → Heat Intolerance Restlessness Palpatations Muscle Weakness Bruit over thyroid Goiter |
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Causes of Hyperthyroidism
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Primary Hyperthyroidism (Graves Disease)
Autoimmune disease involving TSH receptor, Thyroid Stimulating Immunoglobulins (TSI) Secondary Hyperthyroidism Excess TSH/TRH Hypersecreting Thyroid Tumor |
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Lab tests for Thyroid function
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Measure TOTAL T4/T3 and TSH levels in blood
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What are the layers and associated hormone classes of the adrenal cortex
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Zona Glomerulosa-Mineralocorticoids (Aldosterone)
Zona Fasciculata- Glucocorticoids (Cortisol) Zona Reticularis- Androgens |
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What Hormones are produced in the Adrenal Medulla?
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Catecholamines (Epi/NE)
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What does ACTH effect?
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Stimulates all steps in synthesis of Cortisol, Adrenal Androgens, and Aldosterone
** Only CORTISOL feeds back Stimulates cell hyperplasia via IGF-1 |
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Precursor of ACTH
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Preproopiomelanocortin (POMC)
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For what hormones is ACTH a precursor for?
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Melanocyte-Stimulating Hormone (MSH)
Corticotropin-Like Intermediate Peptide (CLIP) |
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Describe secretion of Cortisol
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Cortisol is secreted diurnaly and under stress
Secretion is pulsatile , amount of secretion does not vary, frequency of secretion pulse varies |
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What effect doe stress have on cortisol release?
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Can override the negative feedback inhibition
Stress enhances CRH-ACTH release |
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What is the half-life of cortisol and how is it transported in the blood?
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70 Minutes
Mostly transported by Corticosteroid-Binding Globulin (CBG), also by Abumin, 5% unbound |
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Cortisol MOA
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Adrenal steroids diffuse into the cell → Receptor bound to Heat-Shock Proteins (HSP) is activated, HSP released → Activated receptor binds to and activated steroid response element → gene transcription and protein synthesis
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Effects of Cortisol
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(Most of Cortisols effects are Permissive, not initiate but enhances)
4 important functions: Stimulates Gluconeogenesis in response to low blood glucose Increases protein and lipid breakdown (For GNEO) Anti-inflamatory effect Immunosuppressive |
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Cortisol effect on metabolism
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↑Blood Glucose (cost of protein and lipids)
Mobilizes protein and lipids ↑GNEO and responsiveness to glucagon and Epi ↓ Insulin dependant glucose uptake in muscle and adipose ↓Blocks Insulin-suppresion on hepatic glucose production Permissive for lipolytic effects of catecholamines ↑Body Fat ↑appetite (CNS effect) Stimulates lipogenesis in adipose of face and trunk causing accumulation in those areas ↑Protein breakdown by inhibiting AA utilization =Cortisol is a catabolic, anti-anabolic, diabetogenic hormone |
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Stress induced Cortisol cumulative effect
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Accentuates hyperglycemia and accelerates protein loss
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Cortisol effect on Muscle
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Basal levels are required for normal contractility
Excess levels cause muscle atrophy through protein wastage |
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Cortisol effect on Bone
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Decreases bone formation
↓Vitamin D synthesis and blocks its action(Ca absorbtion from GI) ↑Urinary Ca excretion ↑Apoptosis of Osteoblasts and osteocytes Stimulates osteoclasts increasing bone resorbtion |
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Actions of 1,25 Vitamin D
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Increases dietary Calcium absorbtion
Increases dietary Potassium absorbtion Increased bone reabsorbtion of calcium and phosphate |
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Cortisol effects on vasculature
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Maintains normal BP
Permits responsivenes to angiotensin ↓Permeability of vasculature (Can cause hypertension) |
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Cortisol effect on kidneys
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↑GFR by ↓ preglomerular resistance and ↑ plasma flow
Feedsback and inhibits ADH (Vasopressin) |
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Cortisol effect on CNS
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Acts on receptors in the hippocampus (Memory), reticular activating system (state of arousal), and Autonomic Nuclei of the Brainstem altering perceptual and emotional function
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Cortisol effect on development
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Facilitates in utero maturation of lungs, GI, CNS, Retina, and Skin
↑Surfactant Synthesis |
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Cortisol effect on immune system
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Inhibits many steps in inflamation and immune system responses
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Cause & Effect of Cushing's Syndrome
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Hypersecretion of Cortisol
Redistribution of body fat, Central Obeisity and Moon face with thin extremities Atrophy of skin and dermal connective tissue Thinning of bone Muscle wasting Easy Bruising Delayed Healing Hypertension Diabetes |
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Two types of Cushing's Syndrome
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1. ACTH Dependent (Results in Adrenocortical Hyperplasia) (Most common)
a. Pituitary Microadenoma (Cushing's Disease) b. ACTH Ectopic Tumor c. CRH Ectopic Tumor 2.ACTH Independent (Results in Adrenocortical Atrophy) a. Adrenal tumor b. Iatrogenic (Induced by medical teatment) |
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Hypercortisolism Diagnostic Test
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Dexamethasone Suppression test
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Explain Dexamethasone Suppression Test
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(Dexamethasone is a synthetic glucocorticoid with high affinity for cortisol receptor)
1. 1-md overnight suppression test (Screening) Normal: Drop in Cortisol level Abnormal: No drop in Cortisol 2. 8-mg overnight suppression test (Diagnostic) Hypothalamic/Pituitary Hyperfunction-50% drop in Cortisol (ACTH Dependent) Adrenal Hyperfunction **or Ectopic ACTH tumor- No drop in Cortisol (ACTH Independent) 3.Tesing ACTH level will differentiate b/w Adrenal tumor and Etopic ACTH Tumor. High ACTH=Ectopic ACTH Tumor Low ACTH Adrenal Tumor |
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Cause & Effect of Addison's Disease
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Primary Adrenal Insufficiency- Autoimmune destruction of adrenal cortex leads to deficiency in cortisol, adrenal androgens, aldosterone, and high ACTH due to loss of Negative Feedback
Causes Hyperpigmentation, Weakness, Depression, Weighloss, Hypotension. |
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What causes hyperpigmentation in Addison's Disease?
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Excess amounts of ACTH becomes degraded into Melanocyte-Stimulating Hormone (MSH) causing hyperpigmentation
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Cause & Effect of Secondary Adrenal Insufficiency
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Ususaly Iatrogenic and results in ACTH hyposecretion from receiving GCC medication excessively suppressing ACTH. Once off medication, there is a lack of ACTH available.
Causes same symptoms as Addison's Disease without Hyperpigmentation |
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Hypocortisolism Diagnostic Test
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ACTH Stimulation Test
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Describe ACTH Stimulation Test
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Test evaluates Adrenal Cortex ability to respond to ACTH
1.Rapid ACTH Test (Screening)- Injection of Cosyntropin (ACTH Analogue) Normal- Increase in Cortisol Abnormal- No increase 2. Prolonged ACTH Test (Diagnostic)- IV injection of ACTH Primary Adrenal Insufficiency-Low Cortisol (Gand is destroyed) Secondary Adrenal Insufficiency- Moderate increase in Cortisol (Sluggish Response) |
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What causes Congenital Adrenal Hyperplasia?
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An enzyme blockage that results in low Cortisol levels results in High ACTH causing Adrenal Hyperplasia
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Anabolic hormones
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Promote Synthesis and Store Energy
Insulin Growth Hormone (GH) |
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Catabolic Hormones
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Break down Fuel stores and release energy (ATP Production)
Cortisol Glucagon Catecholamines |
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Functions of the pancreas
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Exocrine: Produces digestive enzymes
Endocrine: Produces Insulin (Beta-Cells), Glucagon (Alpha-Cells), and Somatostatin (Delta-Cells) |
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Describe morphology of insulin
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Consists of 2 polypeptides, Alpha and Beta connected by 2 disulfide bridges.
Beta-chain contains core biological function (B24 + B25) Alpha-chain contains speces-specific sites |
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Secretion of Insulin
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Insulin is synthesized preproinsulin (Signal peptide+C-peptide+Insulin). Signal peptide and C-peptide are cleaved producing proinsulin ans insulin respectively.
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Clearance of Insulin
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The liver removes 50% of insulin in a single pass (Insulin half-life= 4-6 minutes). The liver does not remove C-Peptide- C+I released in 1:1 ratio, diagnostically useful
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Insulin Receptors
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Tyrosine Kinase Receptors
2A+2B subunits Receptors can be downregulated (internalized)(Diabetes) or Upregulated (Exercise and Fasting) |
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Insulin physiologic effects
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↓Lipolysis
↓Proteolysis ↓Gluconeogenesis |
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Biphasic Secretion of Insulin
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Early Phase: Initial burst of insulin 10 minutes after a meal (Fusion of docked insulin granules) sensitizes receptors
(Absent in DMII) Late Phase: Gradual increase in insulin (Mobilisation from pool) |
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Factors Stimulating Insulin Secretion
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Metabolic Components
Glucose Amino Acids Fatty Acids Ketones Hormonal Componenets Growth Hormone Glucagon Intesinal Nutrients GI Hormones (Incretins: Glucagon-Like Peptide 1 (GLP-1)and Gastric Inhibitory Peptide (GIP)) |
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What effect does Incretins have on Insulin release
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Incretins (Glucagon-Like Peptide 1 (GLP-1)and Gastric Inhibitory Peptide (GIP)) are released by the GI increase insulin release before glucose rises in blood and enhances Insulin reaction to glucose
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Factors Inhibiting Insulin Secretion
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Insulin
Epinephrine Serotonin |
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Major Tissues Insulin Acts on
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Liver: Inhibits glucose production
Muscle: Promotes glucose uptake and protein synthesis Adipose Tissue: Increases storage of fatty acids |
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Glucose Transporters and function
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Glut1&3: Ubiquitous- Insulin Independent, Mediates basal glucose uptake, High glucose affinity
Glut2:Pancreatic B-cells+Hepatic Cells- Insulin Independent, Low affinity for glucose (Regulatory Capacity) Glut4: SK Muscle, Heart, Adipose Tissue- Transporters are internally sequestered and require Insluin signal |
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Steps of Insulin secretion regulation
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Glucose is transported into the cell vie Glut2 and converted to Pyruvate+ATP+NADPH
Increase in ATP and NADPH closes K+ Channel Closing K+ causes depolarization and opening of voltage gated Ca++ channel Increased Ca++ trigger exocytosis of Insulin granules |
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How do Sulfonylurea drugs increase insulin release
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Sulfonylurea drugs close ATP-Sensitive K+ channels causing influx of Ca++ and exocytosis of Insulin granules
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What is the effect of insulin on FFA conversion in the liver?
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Insulin present: FFA's converted to VLDL and Triglycerides
Insulin absent: FFA's converted into Ketone acids. May result in Ketoacidosis (Only brain is capable of utilizing Ketone Acids for ATP production (During starvation)) |
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Characteristics of Diabetes Millitus
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Absolute or Reative deficiency of insulin/excess of Glucagon
Absolute-Lack of Insulin production Relative- Insensitivity to Inslulin Causes Hyperglycemia and 3 "Poly's" Polyurea- Excess glucose acts as osmotic diuretic Polydipsia- Dehydration from osmotic diuresis Polyphagia- Resistance of Insulin receptors in hypothalamus regulating appetite + Low Intracellular Glucose |
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Diet which predisposes DMII
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High Fat Diet, Not High Sugar Diet
Trans-fats increase risk Polyunsaturated fats decrease risk by increasing membrane fluidity |
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Link between obeisity and Diabetes
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Obeisity causes increase in Tumor Necrosis Factor-A (TNF-A) causing inflamation and alters insulin receptor
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Risk factors for DMII
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High trans-fat diet
High glycemic index foods (processed carbs and high fructose corn syrup) Meat & Iron Low Vitamin D (Vit. D reduces systemic inflamation) Low activity Smoking Genetics (More so than DM1) |
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Insulin and glucose levels in developing diabetes
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Insulin Resistance- Euglycemia + Hyperinsulinemia (Excess insulin produced to control glucose)
Impaired Glucose Tolerance- Hyperglycemia + Hyperinsulinemia (Cells increse resistance to high levels of insulin) Diabetic- Hyperglycemic+Hypoinsulinemic (Insulin production is exhausted and blood glucose is unregulated) |
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Most common cause of insulin resistance
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Post-receptor defect
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Pathophysiology of Hyperglycemia
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Tissues with Glut1 receptors allow high amounts of glucose into cells
This causes Advanced Glycation End Products- Glucose molecules binding to cellular proteins causing disfunction High amounts of glucose in cells alters metabolism of glucose into deleterious forms. |
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Complications of hyperglycemia
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Kidney Failure
Cardiovascular Disease Retinopathy Microvascular (Resulting in amputation) |
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What hormones are involved in the Counter-Regulatory response
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Occurs during hypoglycemia <40mg/dl
GH, Epi, NE, Cortisol, and Glucagon all act on the liver to increase glucose production |
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Effects of Glucagon
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Mobilization of Glucose in the liver
Increase Gluconeogenesis Increase Glycolysis Increases Ketogenesis in the liver Directs FFA to B-oxidation to Ketone Acids |
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Glucagon synthesis
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Synthesized as preproglucagon, converted to proglucagon, and glucagon
Increase synthesis Low Glucose Low FFA Epi/NE Inhibit Synthesis High Glucose+FFA Somatostatin Insulin |
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PTH increases serum Ca++ in what ways
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1. Activates osteoclasts to release Ca++ from bone (resorption)
2. Icreases reabsorption in distal tubules (kidneys) 3. Activation of Vitamin D to increase Ca absorption from the GI tract. |
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What is the function of PTH
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Regulation of blood Ca++ and PO4- by:
Increasing bone resorbtion Increase kidney resorbtion of Ca++ Increase PO4- secretion in kidney Increase convertion of 25-hydroxycholecalciferol to 1,25-Dihydroxycholecalciferol |
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What is the function of Calcitonin
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Calcitonin inhibits osteoclast activity and is stimulated by hypercalcemia
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What can result from excess Vitamin D
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Excess bone resorbtion and demineralization
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Actions of 1,25-Dihydroxycholecalciferol
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Increases transcription of Calcium binding protein, increasing intestinal absorbtion of Ca++ and PO4-
Increases reabsorbtion of Ca++ in distal tubules |
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Vitamin D Regulation
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PTH regulates 1-alpha-hydroxylase, the enzyme responsible for converstion of 25-hydroxycholecalciferol to 1,25-Dihydroxycholecalciferol
(Occurs in the kidney) |
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↓ PTH, ↑ Ca, ↑ phosphate
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Secondary Hypoparathyroidism due to excess Vitamin D
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↑ PTH, ↓ Ca, ↓ phosphate
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Secondary Hyperparathyroidism: Vitamine D deficiency
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↓ PTH, ↓ Ca, ↑ phosphate
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Primary Hypoparathyroidism: Surgical Removal of Parathyroid or Autoimmunity
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↑ PTH, ↑ Ca, ↓ phosphate
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Primary Hyperparathyroidism: Parathyroid Adenoma or Ectopic Parathyroid Secreting Tumor
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Composition of Bone
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Phosphate and Calcium precipitate forming Hydroxyapatite in the osteoid matrix
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