Endocrine Physiology Flashcards

Question

Prolactin Pathophysiology

Answer 1

Excess: Hyperprolactinemia ▪ Gonadal dysfunction, amenorrhea (no menstruation), reduced libido * Treatment: Dopamine (DA) agonist treatment/tumor removal Deficiency: Hypoprolactinemia * Gonadal dysfunction, impaired lactation

Answer 2

Excess: Pituitary diabetes (Hyperglycemia) Deficiency: * Hypopituitarism: failure of the pituitary gland to produce one or more of its hormones partially or completely * Panhypopituitarism: inadequate or absent production of all the anterior pituitary hormones

Answer 3

TSH: Stimulates thyroid gland growth and thyroid hormone synthesis * Glycoprotein hormone: - Contains sugar residues- - 2 subunits: α and β: Biological activity resides in β subunit - Sugars are essential for biological activity, promote receptor recognition, prevent hormone degradation Actions of thyroid hormone: ↑ Metabolic rate and heat production; enhancement of growth and CNS development; enhancement of sympathetic activity T4 - 4 iodines; precursor to T3 (larrge amount) T3- more biologically active

Answer 4

An exocrine gland in early development - Colloid: site of thyroid hormone synthesis (it is extracellular which is different from other glands) - Follicular cells: surrounds the cavity with the colloid. When they are active, they increase in size, the colloid decreases in size

Answer 5

Glycoprotein synthesized in rough ER of follicular cells and secreted into colloid * Contains numerous tyrosine residues that provide a template for thyroid hormone synthesis * NOT a binding protein Steps: 1. I2 from IF cotransported with sodium ->cell 2. iodine ions diffuse into the lumen 3. thyroglobulin is synthesized in the follicular cell -> colloid. Iodine is oxidized and attached to tyrosine of thyroglobulin (MIT and DIT) 4. MIT or DIT is added to a DIT (coupling) - 20x more T4 than T3 5. Endocytosis of thyroglobulin with attached T3 and T4 6. Lysozymes release T3 and T4 7. Secretion

Answer 6

Thyroid hormone binding proteins (most bound hormone due to it being hydrophobic) ‒ Only 0.03 % of plasma T4 and 0.5 % plasma T3 free 3 binding proteins: * TBG → Thyroid-binding globulin (T4 and T3) ‒ Most important * TBA → Thyroid-binding albumin (T4 and T3) * TBPA → Thyroid-binding pre-albumin (T4 only) - Affinity for T4 is much higher than T3 - T3 most often comes from deiodase converting T4 -> T3

Answer 7

1. No specific target sites 2. Latent, long-lasting responses 3. Increases oxygen and glucose uptake by most tissues and increases basal metabolic rate (BMR) → CALORIGENESIS other actions: - Neural activity: ↑ irritability, mentation, beta-receptors; decrease reflex times - Cardiovascular action: via beta-receptors (↑ SNS, heart rate, contraction) - Intermediary metabolism: Carbohydrate absorption; decrease plasma cholesterol - Growth and development: Psychogenic / physical; growth hormone (GH) synergy

Answer 8

‒ Membrane-bound → linked to channels which allow glucose and oxygen to be taken up into the cell ‒ Cytoplasmic → roles in intracellular storage of thyroid hormone or production of ATP in mitochondria ‒ Nuclear → effects on protein synthesis

Answer 9

Excess: – Hyperthyroidism – ↑ BMR Primary thyroid dysfunction: ▪ ↑ T3, T4, toxic goitre/nodules Secondary (Pituitary, ↑ TSH) or tertiary (↑ TRH) dysfunction: ▪ Goitre Grave’s Disease: ▪ Long Acting Thyroid Stimulating (LATS) antibodies against the TSH receptor (Goitre) Deficiency: – Hypothyroidism – ↓ BMR – Endemic goitre - Iodine deficiency and Primary thyroid dysfunction, ↓ T3 → ↑ TSH → Goitre – Hashimoto’s Thyroiditis ▪ Antibodies against T3 or T4 or thyroglobulin (Goitre) – Secondary (Pituitary, ↓ TSH) or tertiary (↓ TRH) dysfunction (Central hypothyroidism, **atrophic** thyroid) In utero: cretinism; severely stunted mental and physical development; Irreversible – In adults: myxedema; accumulation of hyaluronic acid and mucus edema under the skin

Answer 10

Hypothalamus releases CRH/ADH -> anterior pitutary releases ACTH (Stimulates adrenal blood flow, adrenal growth and adrenal steroidogenesis) -> adrenal cortex produces cortisol, aldosterone and other products Zones: Glomerular zone → Aldosterone → No metabolism - Conn's syndrome: ↑aldosterone = ↑Na+, ↓K+ = hypertension and kypokalemia, alkalosis Fascicular zone → Cortisol → Intermediate metabolism Reticular zone → Androgens → Sex characteristics

Answer 11

Gradual fall during the day, rise during sleep Action: Intermediary metabolism: ‒ Increases blood glucose through anabolic effects on the liver and catabolic effects on other tissues ▪ Stimulates gluconeogenesis in the liver ▪ Stimulation of triglyceride breakdown in adipose tissue ▪ Stimulation of the breakdown of skin, connective tissue and muscle These actions lead to ... Mobilizes glucose for brain/heart use (Glucose sparing) ‒ ↑ substrate availability (↑ tissue catabolism, ↓ synthesis) ‒ ↑ substrate uptake by the liver ‒ ↑ gluconeogenesic enzymes ‒ ↑ glycogenolysis the stress hormone: Prevents inflammation, Prevents autoimmunity, mobilizes glucose (Glucocorticoid action)

Answer 12

Addison's disease: primary - reduced adrenal secretions = Hypotension, anorexia, weight loss, weakness Cushing's disease: secondary; exposed to high levels of cortisol - due to pituitary (most common), adrenal, or ectopic (tumour that produces ACTH) umour

Answer 13

‒ DHEA (Weak androgen, 20 % testosterone potency) synthesized in zona reticularis ‒ Converted to testosterone/estrogens in other tissues ‒ Involved in secondary sexual characteristics (Axillary hair), libido in females and is a source of estrogen in postmenopausal women Adrenogenital syndrome: ‒ Results from excess androgens (therefore less aldosterone and less cortisol) from the adrenal cortex = increased testosterone and masculinity

Answer 14

Embedded in the thyroid gland (4) Source of hormone: chief cells in gland Action: Plasma calcium (Ca2+) ↑ * Plasma phosphate (PO43-) ↓ * Kidney: ↑ Ca2+ reabsorption↓ PO43-reabsorption, ↑ vitamin D3 activation * Bone: ↑ bone resorption * GIT: Indirect effect by ↑ vitamin D3 formation - high levels of calcium and vitamin D3 (1,25 (OH)2D3) inhibits. Stimulated by low calcium

Answer 15

– Bones, stones and abdominal groans * ↑ PTH, ↑ Ca2+, ↓ PO43-, ↑ 1,25 (OH)2D3 * Soft tissue calcification (Kidney stones) * Weak bones, fractures (Bone resorption) * GIT dysfunction Causes: Primary - Normal plasma Ca2+ 9 - 10.5 mg/dL; calcification when Ca2+levels 10 - 12 mg/dL; death at 17 mg/dL Secondary - ↓ Ca2+, ↑ PTH – In rickets/osteomalacia (↓ 1,25 (OH)2D3) ▪ Impaired GI uptake of Ca2+ – In renal failure ▪ Impaired renal reabsorption of Ca2+

Answer 16

Primary hypothyroidism:↓ PTH, ↓ Ca2+, ↑ PO4 3-, ↓ 1,25 (OH)2D3 – ↑ neuromuscular activity ▪ ↓ Ca2+, ↓ threshold for excitation, resulting in repetitive responses, reduced accommodation – Tetany (Ca2+ 6 mg/dL) – Asphyxia-death (Ca2+ 4 mg/dL) Trousseau’s Sign: Involuntary contraction of the carpal muscles, due to hypocalcemia and tetany Chvostek’s Sign: tap nerve on face = snarl Pseudohypoparathyroidism: – ↑ PTH, ↓ Ca2+, ↑ PO4 3-, ↓ 1,25 (OH)2D3 – Tissue insensitivity to PTH action

Answer 17

Parafollicular cells (C-cells) release calcitonin (Peptide hormone) Stimulus: ↑ plasma Ca2+ Effects of calcitonin: Plasma calcium (Ca2+) ↓, Plasma phosphate (PO43-) ↓ * Kidney: ↓ Ca2+ reabsorption, ↓ PO43-reabsorption, ↓ vitamin D3activation * Bone: ↓ bone resorption * GIT: ↓ Ca2+ absorption No excess or deficiency syndromes Treatment of postmenopausal osteoporosis – In the absence of estrogen, PTH action on bone is not antagonized Treatment of Padget’s Disease – Characterized by excessive osteoclast activity

Answer 18

Cholesterol -> 7-dehydrocholesterol (UV light) ->Vitamin D3 Synthesis of vitamin D3: - skin accounts for >90% of cholecalciferol (D3), - <10% from diet in the form of cholecalciferol and ergocalciferol (D2) - At first very weak activity -> liver forms slightly more active 25-hydroxy vitamin D -> kidney forms very active 1,25-dihydroxy vitamin D and inactive 24,25 Effects of 1,25-dihydroxy vitamin D: * Plasma calcium (Ca2+) ↑, Plasma phosphate (PO43-) ↑ * Kidney: ↑ Ca2+ reabsorption, ↑ PO43-reabsorption * Bone: Promote PTH actions * GIT: ↑ absorption of Ca2+ and PO43-: main site of action -> induces synthesis of vitamin D channels (lumen), binding proteins, ATPase (basolateral) Stimulus: ↑ PTH, low Ca2+ - it is a steroid hormone - Protein-bound in plasma (Transcalciferin) and acts through nuclear receptors

Answer 19

Deficiency: ↓ Vit D, ↓ Ca2+ → poor bone formation ↓ Vit D, ↓ Ca2+, ↑ PTH → ↑ bone resorption – Rickets in juveniles: Bow-Legged and Knock-Kneed – Osteomalacia in adults * Excess: – VD toxicity -> hypercalcemia (soft tissue calcification)

Answer 20

Alpha cells → Glucagon 25 % - stimulate delta and beta Delta cells → Somatostatin 10 % (paracrine) - inhibits alpha and beta Beta cells → Insulin 60 % - inhibits alpha SNS: ↑ glucagon, ↓ insulin PSNS: ↑ insulin, ↑ glucagon

Answer 21

Insulin: nutrients -> stored forms = lower blood glucose - Primary stimulant of insulin secretion: high plasma glucose - structure: Proinsulin - Weak insulin-like activity; C-peptide - Weak insulin-like activity Glucagon: breakdown of stored forms of energy = increase blood glucose stimulated by nutrients (↓ glucose, ↑ amino acids), GIT hormones (↑ gastrin, CCK, ↓ secretin) and neural stimuli (↑ stress (Sympathetic), ↑ food (Parasympathetic)) actions: – Glucose:↓ glycogenesis, ↑ gluconeogenesis, ↑ glycogenolysis – Lipid: ↑ lipolysis, ↓ lipogenesis – Protein: (Minor) degradation

Answer 22

Diabetes mellitus: Insulin deficiency/glucagon excess - Cardinal symptoms of Diabetes Mellitus: Polyuria = ↑ dilute urine, Glucosuria (Glycosuria) = ↑glucose, Polydipsia = excessive thirst, Polyphagia = excessive hunger Type 1: (Insulin-dependent or juvenile-onset) – Destruction of the β-cells resulting in decreased insulin release ▪ Autoimmune disease where immune system incorrectly target insulin-producing β-cells – Treated with insulin injections – Prevalence: 10 - 20 % Type 2: (Insulin-independent or adult-onset) – Associated with insulin resistance ▪ Target cells have decreased response to insulin ▪ May have normal or high plasma insulin levels ▪ Receptor downregulation – Associated with obesity – Prevalence: 80 - 90 % - treated by diet and weight reduction

Answer 23

Causes: ▪ Insulin-secreting tumor ▪ Insulin overdose ▪ Reactive hypoglycemia (Hypersensitive beta cells) – Symptoms: ▪ Hypoglycemia ▪ Sympathetic activation ▪ Insulin shock – Treatment: – Glucose for diabetics – Low carbohydrates for reactive hypoglycemia

Endocrine Physiology Flashcards

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