Endocrinology Flashcards
(126 cards)
NAD+ regeneration under anaerobic conditions.
regeneration under aerobic conditions
NADH transfers protons to pyruvate to form lactate (via lactate dehydrogenase) and regenerate NAD+
NAD+ is converted to NADH in TCA cycle, NADH is converted to NAD+ in electron transport chain when making ATP
NAD+ is required in which reaction?
convert glyceraldehyde-3-phosphate to 1-3-bisphosphoglycerate (via glyceraldehyde-3-phosphate dehydrogenase)
glycogen phosphorylase- pathway, action, activation
glycolytic pathway, breaks down glycogen for energy in during muscle contraction (cleaves glucose-1-P until 4remain before a branch point). activated by phosphorylation once cAMP becomes activated by epinepherine
carnitine-def, function, vit needed for synthesis
amino acid responsible for transport of fatty acids into mitochondria for beta-oxidation. need vit C for synthesis
amt of pyruvate in cells. synthesized how?
large amt usually not limiting factor for glycolysis. formed from PEP (phsophoenolpyruvate) via pyruvate dehydrogenase in glycolysis
citrate- pathway, formation, inhibits
TCA cycle, condensation of acetyl-CoA with oxaloacetate (via citrate synthase)
chronic renal failure leads to what levels of Ca2+ , phosphorous and PTH? why?
elevated PTH and low serum Ca2+ due to 2nd hyperparathyroidism. also causes high phosphorus levels. low 1,25 Vit D b/c 1-alpha hydroxylase (in kidneys) is low. also kidney is responsible for excreting phosphorus
low Ca2+ -high PTH (2) -low PTH (2) high Ca2+ -high PTH (3) -low PTH (2)
low Ca2+
-not eating enough, chronic renal failure (2nd parathyroidism)
-hypoparathyroidism (surgical removal, autoimmune, Di George)
high Ca2+
-because of high PTH, hyperplasia, adenoma, carcinoma (1ary parathyroidism)
-eating too much, cancer (PTH-independent hypercalcemia)
neurophysins. mutations cause? made where? and released into circulation where?
carrier proteins for oxytocin and vasopressin (ADH) from production in paraventricular (oxytocin) and supratoptic (ADH) nuclei to release in axons of posterior pituitary. point mutation in neurophysin II leads to diabetes insipidus (too little ADH)
- made in neuronal cell bodies of paravent and supraoptic neclei
- releeased into circulation form axon terminals in posterior pituitary gland
principle source of blood glucose after 24 hrs
12-18 hrs
gluconeogenesis-glucose is formed from lactate glycerol and glucogenic amino acids
glycogenolysis-breakdown of glycogen
In glycolysis which enzymes are unidirectional? what enzymes in gluconeogensis are used to bypass them?
1-hexokinase (glucose to glucose-6-phosphate), 2-phosphofructokinase (fructose-6-phosphate to fructose 1,6 bisphosphate), and 3-pyruvate kinase (PEP to pyruvate)
3-pyruvate carboxylase- converts pyruvate to oxaloacetate (in mitochondria)- require B7 cofactor
*oxaloacetate is shunted to cytosol via malate shuttle
-phophoenolpyruvate carboxykinase (PEPCK) (converts oxaloacetate to phosphoenolpyruvate)-in cytosol
2-fructose1,6-bisphosphatase (converts fructose 1,6 bisphosphate to fructose-6-phsophate)-in cytosol
1-glucose-6-phosphatase (converts glucose-6-phosphate to glucose)- in ER
major steps in glycogenolysis
glycogen to glucose-1-phosphate
glucose-1-phosphate to glucose-6-P
first fatty acid made by acetyl CoA during lipogenesis in the fed state
palmitate acid- pg 115 FA
chemical name for HMG CoA
3-hydroxy-3methylglutaryl-coenzyme A
most common cause of hypothyroidism in US
Hashimoto disease (autoimmune destroys thyroid)
forms of thyroid hormone most active form inactive form Thyroid hormone that regulates feedback of TSH secretion (it's affect on other form levels) enzyme that converts one to the other
T3, T4, and T3r T4 (produced the most) T3r T3 (decreased TSH, T4, and T3r) type II deiodinase (within hypothalamus and pituitary gland) comverts T4-T3 for feedback inhibition. other enzymes convert T4 to T3 or T4 to T3r but not T3 to T3r.
common endocrine cause of elevated CK levels
other causes?
hypothyroidism-(leads to muscle wasting)
HMG-CoA inhbitors,
autoimmune disease (polymyositis/dermatomyositis)
muscular dystrophies (Duchenne or Beckers)
why is an increased risk of osteoporosis (loss of bone density) with a prolactin secreting pituitary adenoma?
prolactin inhbits GnRH which leads to hypogonadism which can lead to decrease esterogen (esp in women) leading to accelerated bone loss
genetic triad of gastric ulcers with pitutary adenoma, and parathyroidism
MEN type I disease 3Ps (parathyroidism, peptic ulcer (usually from gastrin secreting cancer in pancreas) and pituitary adenoma
mechanism of insulin resistance in overweight pts (type II D)
marker for insulin deficiency in Type I D
- increased levels of FFA and serum TG- can lead to Diabetes type II
- increased beta-hydroxybutyrate levels
homocystinemia role of in vascular disease
can cause atherosclerosis
symptoms in pheochromocytoma vs carcinoid syndrome
- catecholamine release-HTN, tachycardia, HA, diaphoresis, and tremors
- produces 5-hydroxyindoleacetic acid (HIAA); Hypotension, facial flushing, bronchospasm, diarrhea
treatment for mothers with gestational diabetes
diet and light exercise or if that doesn’t work
insulin, avoid oral hypoglycemic meds b/c of risk of fetal hyperinsulinemia and hypogycemia
shape of coccicioides immitis vs cryptocococcus neoformans
- spherules (round structures with endospores)-causes fungal lung disease and disseminated mycosis
- narrow budding yeast with round or oval encapsulated cells