Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
61 Cards in this Set
- Front
- Back
|
Where is 85% of extracellular PO4 and 99% of Calcium is found?
|
-hydroxyapatite crystals of bone: Ca10(PO4)6(OH)2
|
|
|
Total plasma Ca++?
|
2.1-2.55 mM/L
|
|
|
equation for CO2 to H+ and HCO3.
|
CO2 + H2O ----> H2CO3 -----> H+ + HCO3
|
|
|
Symptoms of Hypocalcemia
|
-neuromuscular irritablility
-numbness -parasthesias -tetantic muscle contractions (hands feet and larynx) -epilepsy -arrythmias -osteoporosis |
|
|
Hypercalcemia
|
-decreased neuromuscular excitability
-decreased neurotransmission -muscle weakness -decreased GI motility -Arrhythmias -Hypertension -Hypercalciuria (kidney stones) -increased bone mass |
|
|
osteolysis
|
the osteocyte-osteoblast network transfers calcium from bone fluid to blood
|
|
|
Osteoprotegerin
|
-cytokine, inhibits differentation of macrophages into osteoclasts
-blocks RANK-RANK ligand interaction between osteoblasts/stromal cells and osteoclasts precursors |
|
|
What hormone stimulates osteoprotegerin?
|
-estrogen
|
|
|
RANK (Receptor Activator of Nuclear Factor kappa B)
|
-membrane protein expressed on osteoclasts and activates osteoclasts upon binding
-On dendritic cells and involved in immune signaling -ligand found on surface of stomal cells, osteoblasts and T cells |
|
|
What is bone formation inhibited by?
|
cortisol
|
|
|
What is bone resorption inhibited by?
|
Calcitonin
|
|
|
Function of 1,25-(OH)2 Vitamin D (Calcitrol)
|
-stimulates increase calcium Mg++ and PO4 absorption by GI tract ( and other tissues)
|
|
|
Alpha S G protein
|
-Stimulates adenyly cyclase, increase cAMP
-cAMP stimulates protein kinase A - |
|
|
How does Vibrio cholerae toxin produce diarrhea?
|
-adds ADP-ribose to alpha s subunit resulting in alpha S subunit activation.
-This increases cAMP and causes diarrhea |
|
|
Alpha I subunit
|
-inhibtis enzyme adenylyl cyclase = decreased cAMP
|
|
|
Alpha q subunit
|
-activates phospholipase C which cleaves phosphatidylinositol-1,4,5-triphosphate (IP3) and diacylglycerol (DAG)
-IP3 stimulates Ca++ channels to increase cytosolic calcium -DAG and calcium stimulate the activity of protein kinase C |
|
|
Genetic disorders of decreased G alpha s protein function?
|
-pseudohypoparathryroidisms
-albright's hereditatry osteodystrophy |
|
|
Genetic disorders of increased G alpha s protein function?
|
-McCune-albright Syndrome
-Fibrous dysplasia -cushing syndrome -thyrotoxicosis |
|
|
primary hyperparathyroidism
|
-PTH secreting tumor
-Hypercalcemia -hypercalcuria and hypophosphatemia -increased bone reabsorption |
|
|
What cranial nerve deficit is seen with medial medullary syndrome?
|
Tongue def towards lesion - CN12 "lick your wounds"
Contra Spastic Hemiparesis - Pyramids |
|
|
secondary parahyperthyroidism
|
-decreased Ca++
-increased PTH |
|
|
What is calcitrol stimulated by? Where is it produced?
|
-Stimulated by PTH and hypophsophatemia
-produced in the kidney |
|
|
Where is calcitonin released? What controls its release?
|
-Parafollicular cells ( C cells) of the thyroid gland (neural crest origin)
-secreted in response to high serum Ca++ (and also gastrin) |
|
|
What is the main action of calcitonin?
|
-Inhibits bone resorption
-osteoclast inactivation -increased urinary phosphate excretion |
|
|
What is calcitonin used to treat?
|
-paget's disease and osteoporosis
|
|
|
Disorders of Vitamin D deficiency?
|
-Rickets and osteomalacia
|
|
|
Disorders of excess Vitamin D?
|
-hypercalcemia, hyperphosphatemia and hypermagnesemia
-calcification of soft tissue -kidney stones |
|
|
List glucose transport proteins and where they are found?
|
-Glut-1 is in most cells
-Glut-2 liver, kidney and beta cells -Glut-4 increased by insulin in adipocytes and muscle cells |
|
|
Somatostatin
|
-pancreatic hormone produced bu delta cells, and inhibits the secretion of both insulin and glucagon.
-found in hypothalamus wher it is used to control the release of growth horomone |
|
|
What anabolic and catabolic reactions does insulin effect?
|
-increases: Glycogenesis, protein synthesis, lipogenesis and glycolysis
|
|
|
graves disease
|
-Hyperthyroidism caused by antibodies that bind the TSH receptors and mimic TSH effects
-Thyroid stimulating antibody (TSI) present in the blood -most common in older women |
|
|
Primary hyperthyroidism
|
-TH producing tumor
-initial stages of thyoiditis |
|
|
Secondary Hyperthyroidism
|
-autoimmune (graves disease
-TSH producing tumor |
|
|
Primary hypothyroidism
|
-failure of the gland
-Autoimmune (hashimoto's disease) -infection -other - genetic, toxins |
|
|
secondary hypothyroidism
|
-TRH and/or TSH deficiency
-Dietary: iodine deficiency |
|
|
Hashimotos disease
|
-caused by antibodies against thyroid gland proteins and/or antibodies that bind TSH receptor (10%) and block TSH effects
|
|
|
Cushing's syndrome
|
-Hypersecretion of glucocorticoids (cortisol)
-redistribution of fat (moon face), spindly extremities. -wound healing is poor, infections -tumors: adrenal (primary) - excess cortisol and pituitary (secondary) - excess ACTH -Iatrigenic (too many glucocorticoid meds) |
|
|
Primary hyperaldosteronism
|
-increased aldosterone secretion
-supression of renin -hypertension and hypokalemia |
|
|
Conn's syndrome
|
-unilateral adrenal adenoma producing aldosterone
-idiopathic hyperaldosteronism or bilateral adrenal hyperplasia |
|
|
secondary hyperaldosteronism
|
-high blood pressure caused by increased Na+ retention
-Hypokalemia, metabolic alkalosis -ANP compensation of ECF volume -can be caused by high renin/angiotension activity |
|
|
treatment for secondary hyperaldosteronism
|
-remove cause
-give spironolactone (binds aldosterone receptor; aldosterone antagonist) |
|
|
primary Adrenocortical abnormalities
|
-adrenal cortex disorder resulting in abnormal hormone production
|
|
|
secondary Adrenocortical abnormalities
|
-abnormal hormone production caused by disorder somewhere other than the adrenal cortex
-pituitary (CRH/ACTH) -other (renin-angiotension)(ectopic ACTH) |
|
|
Addison's disease
|
-deficient cortisol, aldosterone and androgens
-low BP, dehydration bc decreased Na+ in blood, excess K+, hypoglycemia, lethargy and weakness -skin darkening (high ACTH with MSH activity) |
|
|
Congenital adrenal hyperplasia
|
-defective enzyme in cortisol synthesis pathway
-21-hydroxylase (P450c21) (90% of CAH) and 11-hydroxylase (P450c11) -Adrenogenital syndrome: excess androgen production and inappropriate masculinization |
|
|
What are CRH, ACTH and cortisol release affected by?
|
-genetic programming and environmental factors:
-circadian factors -feedback regulation -hypoglycemia -inflammation (cytokines) -physical stress -psychological stress -age |
|
|
What is the immediate effect of PTH on bone?
|
-stimulates osteolysis (osteoblasts and osteocytes)
-Calcium transfer from ECF is the immediate short term effect |
|
|
Alpha 1 adrenergic receptor
|
-couple to phospholipase C (PLC) though G protein
-excitatory response in effector cells (smooth muscle contraction) |
|
|
Alpha 2 adrenergic receptor
|
-located on adrenic neuron presynaptic terminals, and usually act through G proteins
-inhbit adenylyl cyclase -inhibition of secretion of NE, insulin and gastric secretions |
|
|
Beta 1
|
-increase heart contractility
-kidney renin release -Beta adrenergic receptors usually act through G proteins that stimulate adenylyl cyclase and increase cytoplasmic cAMP levels |
|
|
Beta 2
|
-inhibit smooth muscle contraction and stimulate glucose release from liver
-Beta adrenergic receptors usually act through G proteins that stimulate adenylyl cyclase and increase cytoplasmic cAMP levels |
|
|
Beta 3
|
-adrenergic receptors found in adipose tissue stimulate lypolysis
-Beta adrenergic receptors usually act through G proteins that stimulate adenylyl cyclase and increase cytoplasmic cAMP levels |
|
|
What type of receptor does PTH act on to produce it's effects?
|
-G protein acts to increase cAMP, IP3/DAG
|
|
|
What type of receptor does calcitrol act on to produce it's effects?
|
-transcription factor receptor
|
|
|
What type of receptor does calcitonin act on to produce it's effects?
|
G-protein associated receptor
|
|
|
What does leptin inhibit?
|
-inhibits appetite
-orexogenic (NPY/AgRP) neurons |
|
|
What does leptin stimulate?
|
-alpha-MSH/CART
-medial hypothalamus |
|
|
alpha MSH
|
-a MC4 agonist and inhibits feeding behavior
|
|
|
agrouti-related protein (AgRP)
|
-a MC4 antagonist that blocks alpha MSH actions resulting in stimulation of feeding behavior
|
|
|
What simulates insulin release?
|
-Hyperglycemia
-amino acids, K+ FFA/ketoacids -GIP -Glucagon-like peptide (GLP-1) -Glucagon -Parasympathetic innervation (acetocholine-m receptor) -Sulfaonylurea drugs (K+ chnnels closed) |
|
|
What inhibits insulin release?
|
-hypoglycemia
-somatostatin -exercise -leptin -insulin -sympathetic innervation (alpha2 receptor inhibition, beta2 receptor stimulation minor) -diazoxide drugs (K channels open) |
