Nervous system vs Endocrine system?
Endocrine is slower and more sustained control over long term processes
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| Term | Definition |
|---|---|
Nervous system vs Endocrine system? | Endocrine is slower and more sustained control over long term processes |
What are the 2 glandular systems? | 1. Exocrine glands: empty secretions into body cavities or onto body surfaces by tubular ducts
2. Endocrine glands: ductless glands that release secretions internally into bloodstream |
What are the 2 types of hormones? | - Steroids: cholesterol
- Proteins: amines, peptides |
Do secretory vesicles expose hormones to proteolytic degradation? | No, they protect them from it |
Secretory vesicles provide a _____ mechanism to the site of ______ | - Transport (microtubules/microfilaments)
- Release (plasma membrane) |
What type of release mechanism do secretory vesicles use? | Exocytosis, vesicle is incorporated into plasma membrane |
What are the 2 types of hormones in plasma? | - Bound
- Free |
Which hormone is biologically active? | Free |
T/F: Plasma hormones are inactive when bound to binding protein | True |
How does protein binding of plasma hormones provide a reservoir for target sites? | - Increase solubility/conc of lipid soluble and thyroid hormones |
How does protein binding of plasma hormones protect hormones from degradation by liver/plasma enzymes? | By increasing size |
How does protein binding of plasma hormones provide a buffer against changes in hormone conc? | By inactivating free hormones |
Why is hormone secretion dynamically regulated? | Maintain steady state around range/point that varies w/ age |
What happens when negative feedback of hormones takes place? | - Inhibits secretion when circulating levels are high
- Increased secretion when circulating levels are low |
What is the first requisite for hormonal action? | Binding of hormone to receptor |
In the "Lock and Key" saying, what is the receptor and what is the hormone? | Lock: Receptor
Key: Hormone |
What are the 2 types of hormone receptors? | Nuclear and Cytoplasmic |
What is the purpose of Nuclear receptors?
2 | - Steroid/thyroid hormones
- Genomically mediated through protein synthesis |
What is the purpose of Cytoplasmic receptors?
2 | - Intracellular T for cytosol-insoluble steroids
- Reservoir storage and organelle actions for thyroid hormones |
What happens during down regulation?
4 | - At high hormone conc to prevent over-activity
- Decreased receptor synthesis
- Internalized membrane receptors
- Dislocation of receptor system |
What does desensitization/sensitization do to the Lock structure? | Conformational change in shape |
What 2 things happen at high hormone conc to prevent over-activity? | - Down regulation (less receptors)
- Desensitization (less affinity) |
What happens during up regulation?
2 | - At low hormone conc to increase activity
- Increased receptor synthesis |
What 2 things happen at to low hormone conc to increase activity? | - Up regulation (More receptors)
- Sensitization (more affinity) |
Why does down regulation happen with coated pits? | Allow proteins hormones to enter cell |
What are 3 types of endocrine dysfunction? | 1. Primary defect in synthesis
2. Defect in regulation
3. Defect in hormone action |
Posterior pituary vs Anterior pituitary, which one has neural tissue? | Posterior P: neural tissue
Anterior P: non-neural tissue (Rathke's pouch) |
What are the posterior P hormones?
2 | - ADH/vasopressin: SON
- Oxytocin: PVN |
What is the mechanism for vasoconstriction?
2 | - Contract BV smooth muscle
- Increase BP
Only at high conc |
What is the mechanism for ADH?
3 | 1. Increase permeability for renal collecting duct (increase # water channels)
2. VC reduces glomerular filtration rate
3. Contraction reduces size of glomerulosa cells = reduces SA for filtration |
What are the 2 factors affecting secretion of ADH/vasopressin? | - Plasma volume
- Plasma osmolarity |
What is ADH secretion increased by?
4 | - Stress
- Heat
- Nicotine
- Caffeine |
What is ADH secretion decreased by? | - Cold
- Alcohol |
What deficiency does problem with ADH production cause? | Hypothalamic/central diabetes insipidus |
What deficiency does problem of ADH action cause? | Nephrogenic diabetes insipidus |
How is syndrome of inappropriate ADH (SIADH) caused? | Problem of ADH production (feedback failure)
- Excess |
What is polyuria? | Large amounts of dilute urine |
What is polydipsia? | Excessive thirst and fluid intake |
How is the #/amp of growth hormone release episodes increased?
3 | - Dark
- Sleep
- Fasting |
T/F: Frequent meals high in glucose/FA increase growth hormone release? | False, it suppresses it |
What is Type 1 dwarfism caused by? | Defect in GH production |
What is laron-type dwarfism caused by?
3 | - Defect in GH action
- GH levels no deficient
- IGF-1 levels are deficient |
What are the components of sompatopause?
4 | - GH deficiency in adults
- Increased fat/decreased lean mass
- Metabolic disturbance
- Impaired immunity |
What is acromegaly? | Excess GH production in adult |
What are the actions of prolactin?
3 | - Gonadal modulation: pro when gonadal acitivity is low
- Mammary gland grows
- Lactation |
What are prolactin releasing factors? PRF
2 | - TRH
- Oxytocin |
What are gonadal steroids for prolactin secretion?
2 | - E/T increase
- Progesterone decrease |
What is Hyperprolactinemia? is there treatment? | Excess
- Dopamine |
What is Hypoprolactinemia? | Deficiency |
What is hyperglycemia? | Pituitary diabetes
- Excess |
What is hypopituitarism? | Failure of P gland to produce hormones partially or completely |
What is panhypopituitarism? | Absent production of all anterior pituitary hormones |
What stimulates thyroid gland growth? | Peptide produced by pituitary thyrotrophs |
What subunits are in the glycoprotein hormone? | Alpha & Beta |
Where do biological activities happen in glycoprotein hormones? | In beta subunit |
Where is thyroglobulin secreted and synthesized? | Synthesized: in rough ER of follicular cells
Secreted: into colloid |
What kind of residues does thyroglobulin provide a template for thyroid hormone synthesis? | Tyrosine |
What is thyroxine (T4) converted to in peripheral tissues? | T3 |
Is T3 more or less biologically active than thyroxine? | More |
T/F: thyroglobulin is a binding protein | False |
What are the thyroid binding proteins?
3 | - Thyroid-binding globulin
- Thyroid binding albumin
- Thyroid binding pre albumin |
What is calorigenesis? | Increasing oxygen and glucose uptake by tissues
- increase BMR |
Is thyroid hormone action long or short responses? | Long |
What is thyroid hormone effect on BMR? | Increase |
What is thyroid hormone effect on heat production? | Increased O2 and glucose uptake = calorigenic effect = increased heat |
What is thyroid hormones effect on neural activity? | Increased irritability and beta receptors, decreased reflex times |
Does thyroid hormone increase or decrease plasma cholesterol? | Decrease |
What 3 types of thyroid hormone receptors are there? | - Membrane bound
- Cytoplasmic
- Nuclear |
What are membrane bound thyroid hormone receptors? | Linked to channels which allow glucose and O2 to be taken into cell |
What are cytoplasmic thyroid hormone receptors? | Intracellular storage of TH or production of ATP in mito |
What are nuclear thyroid hormone receptors? | Effect protein synthesis |
T/F: TH's are hydrophobic | True, even though they contain tyrosine residues |
What is caused by an excess in thyroid excess? | Hyperthyroidism |
What is graves disease cause by? | LATS antibodies against the TSH receptor |
What is caused by a deficiency in thyroid hormone? | Hypothyroidism |
Does hypothyroidism cause an increase or decrease in BMR? | Decrease |
What is an endemic goitre? | Iodine deficiency
- decreased T3 and increased TSH |
What does hashimoto's thyroiditis cause? | Antibodies against T3 or T4 or thyroglobulin |
What is a thyroid hormone deficiency in utero called? | Cretinism
- stunts metal and physical development |
What is the buildup of hyaluronic acid and mucus edema under the skin called? | Myxedema |
What is ACTH produced by? | Produced pituitary corticotrophs |
What does ACTH stimulate? | Adrenal BF, growth and steroidogenesis |
What zone is aldosterone in? | Glomerulosa |
What does angiotensis II stimulate? | Alodesterone release from adrenal cortex in response to decreased ECF volume/low blood [Na] |
What is intermediary metabolism? | Increased blood glucose through anabolic effects on liver and catabolic effects on other tissues |
What does intermediary metabolism do for gluconeogenesis? | Stimulate it in the liver (anabolic) |
What does intermediary metabolism do for triglyceride breakdown? | Stimulates it in adipose tissue w/ glycerol and FA release into blood (catabolic) |
What does intermediary metabolism do for skin breakdown? | Stimulates it and breaks down connective tissue and muscle to release AA (catabolic) |
Does glucocorticoid increased or decrease substrate availability? | Increase (increase tissue catabolism, decrease synthesis) |
Does glucocorticoid increased or decrease substrate uptake by the liver? | Increase |
Does glucocorticoid increased or decrease gluconeogensic enzymes? | Increase |
Does glucocorticoid increased or decrease glycogenolysis? | Increased |
What does cortisol do?
3 | - Prevent inflammation
- Prevent autoimmunity
- Mobilize glucose |
Where is DHEA (adrenal androgen) synthesized? | Zone reticularis |
What are adrenal androgens converted to? | Testosterone and estrogen |
What is adrenogenital syndrome? | Excess androgens from adrenal cortex |
What are the 2 hypercalcemic hormones? | - Parathyroid hormone (PTH)
- Vitamin D (VD) |
What is the hypocalcemic hormone? | Calcitonin (CT) |
What does PTH do to plasma Calcium and Phosphate? | - Ca: Increase
- PO4: Decrease |
What does PTH do to Ca, PO4, and VD in the kidney? | - Ca: increase reabsorption
- PO4: decrease reabsorption
- VD: increase activation |
What does PTH do to bones? | Increase bone resorption |
What effect does PTH have on GIT? | Increase VD formation |
What inhibits PTH secretion? Hypercalcemia or Hypocalcemia? | Hypercalcemia inhibits
Hypocalcemia stimulates |
Where does PTH come from? | Parathyroid gland (chief cells) |
What 3 things does Hyperparathyroidism affect? | Bones
Stones
Abdominal groans |
What does Hyperparathyrodism do to PTH, Ca, PO4, and VD? | - PTH, Ca, VD: increase
- PO4: decrease |
What is the "stones" part of hyperparathyroidism? | Soft tissue calcification = Kidney stones |
What is the "bones" part of hyperparathyroidism? | Weak bones, fractures (bone resorption) |
What is the "abdominal groans" part of hyperparathyroidism? | GIT dysfunction |
What are the Ca levels of kidney stones? | 10-12 mg/dL |
What is Ca levels of death? | 17 mg/dL |
What are the effects on Ca and PO4 during secondary hyperparathyroidism? | Ca: Decrease
PO4: increase |
What are the effects on Ca and VD during secondary hyperparathyroidism in rickets? | Impaired GI uptake of Ca
Decreased VD |
What are the effects on Ca during secondary hyperparathyroidism in renal failure? | Impaired renal reabsorption of Ca |
What are the effects on PTH, Ca, PO4, and VD during primary hypoparathyroidism? | PTH, Ca, VD: Decrease
PO4: increase |
What is primary hypoparathyroidism's effect on neuromuscular activity? | Decreased Ca = decreased threshold for excitation = repetitive responses |
What is trousseau's sign? | Involuntary contraction of carpal muscle due to hypocalcemia and tetany
- Hypoparathyroidism |
What are the effects on PTH, Ca, PO4, and VD during pseudohypoparathyroidism? | PTH, PO4, VD: increase
Ca: decrease |
What are C-cells? | Parafollicular cells
- Release calcitonin
- Peptide hormone |
What are the effects of calcitonin on plasma Ca and PO4? | Decrease both |
What are the effects of calcitonin on Ca, PO4, and VD in the kidney? | Decrease all reabsorption/activation |
What are the effects of calcitonin on bones? | Decreased bone resorption |
What is the stimulus for calcitonin secretion? | Increased plasma Ca |
What are the effects of VD on plasma Ca and PO4? | Increase both |
What are the effects of VD on Ca and PO4 in the kidney? | Increase both reabsorption |
What is the effect of VD on bones? | Promote PTH actions |
What does a deficiency in VD cause? | - Rickets in juvenils
- Osteomalacia in adults |
What is sympathetic stimulation for glucagon and insulin? | Glucagon: Increase
Insulin: Decrease |
What is parasympathetic stimulation for glucagon and insulin? | Glucagon: Increase
Insulin: Increase |
What is the purpose of insulin? Anabolic or catabolic? | - Convert nutrients into stored forms to lower blood glucose
- Anabolic |
What is the purpose of glucagon? anabolic or catabolic? | - Breakdown stored forms of energy to increase blood glucose
- Catabolic |
What are glucagon effects on glucose for glycogenesis, gluconeogenesis, glycogenolysis? | Glycogenesis: decrease
Gluconeogenesis & glycogenolysis: increase |
What are glucagon effects on lipids for lipolysis and lipogenesis? | Lipolysis: increase
Lipogenesis: decrease |
Is diabetes mellitus a glucagon deficiency or excess? | Excess; insulin deficiency |
What is type I diabetes? | - Beta cells destructed = decreased insulin release |
What is type II diabetes? | - target cells have decreased response to insulin
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