Endocrinology Flashcards
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
glucagon effects which organ in type 1 diabetes. not pancreas b/c
- causes increase production of glucose from liver
- beta cells in pancreas are absent. or else glucagon would stimulate insulin release. note glucagon is released from alpha cells in pancreas
21-hydroxylase deficiency-male vs female presentation, hormone levels, ion levels, presentation
- males have normal genitalia and females have ambiguous genitalia
- low cortisol and aldosterone, increased androgens and ACTH
- increased renin, 17-hydroxyprogesterone
- hyperkalemia, hyponatremia
- hypotension, vomiting
pt with delayed puberty plus anosmia- problem which secretion of which hormone?
Kallmann syndrome.
GnRH-secreting neurons fail to migrate from olfactory placode to hypothalamus
Name 1 high yield preventative intervention in almost every UMSLE pt?
smoking cessation!!!!!
histological description of
- zona glomerulosa
- zona fasciculata
- zona reticularis
- medulla
- cells are rounded or arched clusters
- foamy appearing cells in columns
- basophilic cells in anastomosing cords
- shape interface between cortex and medulla-chromaffin cells with deeply basophilic cytoplasm
neurons that innervate sweat glands and chromaffin cells release? a part of which autonomic nervous system?
acetylcholine, sympathetic
note* all other preganglonic neurons in sympathetic nervous secrete Ach.
most postganglionic cells in sympa secret? two exceptions?
NE
- sweat glands-ACh
- chromaffin cells- catecholamines (80% epi and 20% NE)
reduction of which hormone can biliary stones? why not secretin?
- cholecystokinin-reduced gallbladder contractility
- causes steatorrhea and decreased GI mobility
describe vitamin D production
- a 2 step process with sunlight UV (ring opening) and heat (isometization) converts 7-dehydrocholestreol (aka provitmain D3) to cholecalciferaol (vitamin D3)
- form here vitamin D3 or plant D2 undergoes two hydroxlyation steps to form active vitamin D
- the first hydroxylation step occurs in liver with cytochrome P450 enzyme 25-hydroxlyase (vitamin D to 25-hydroxy vitamin D aka calcidiol)
- kidney enzyme 1-alpha hydroxylase converts calcidiol to calcitrol (1,25 dihydroxy vitamin D)
how can kidney compensate for increased amounts of 1,25 dihydroxy vitamin D?
kideny has enzyme 24-hydroylase that can convert calcidiol (25-hydroxy vitamin D) to 24,25 dihydroxy vitamin D an inactive substance
GH causes release of what hormone from where? disease is called (in children? adults?)
defective growth hormone receptors leads to what syndrome? associated hormone levels?
- causes linear growth by inducing release of IGF-1 from liver
- gigantism in children and acromegaly in adults
- Laron dwafism=high serum growth hormone and low IGF-1
total body iron is regulated by which acute phase reactant? mech? how does it enter circulation? how is iron transported in body?
through hepcidin.
- prevent release of iron bound by ferritin in intestinal epithelial cells and by macrophages.
- enters circulation through ferroportin (basolateral iron transporter)
- travels in bloodstream on transferrin (delivers to bone marrow for heme production)
inactivating mutations in which enzyme results in mild hyperglycemia that can be exacerbated by pregnancy
glucokinase
McArdle’s syndrome-aka, pathway problem, enzyme missing, presentation
type 5 glycogen storage disease
- glycogenolysis
- myophosphorylase an isoenzyme of glycogen phosphorylase (glycogen to glucose -1 phosphate)
- exercise intolerance, myoglobinuria, and muscle pain with physical activity
name serious complication of antithyroid medications. name 2 examples of such medication
- agranulocytosis (watch for pts who presents with fever)
- methimazole or PTU
lung mass and hyponatremia suggests? urine concentration? body fluid volume?
- small cell lung carcinoma causing SIADH
- over concentration of urine and increased Na+ excretion
- normal body fluid volume
when is GTP synthesized in TCA cycle? when is GTP used in gluconeogenesis?
- by succinyl-CoA synthetase (succinyl CoA to succinate)
- hydrolysis of GTP is required for phosphorylation and decarboxylation of oxaloacetate to PEP by phophoenolpyruvate carboxykinase
FSH stimulates release of what from where?
LH stimulates release of what from where?
- inhibin B form Sertoli cells
- testosterone from Leydig cells
central DI
partial vs complete
- more than 10% increase in urine osmolality following administration of vasopression during a water deprivation test suggest partial central DI
- if response is more than 50% increase than it’s complete central DI
pt has excessive thirst and increased urine production: 2 possible outcomes if water deprivation test is normal
- normal test (two consecutive urine samples show >30mOsm/kg change)
- primary polydipsia-excessive consumption of water (usually female pt with overt mental illness)
- postobstructive polyuria- increased urinary output. pt with recent surgical (Foley catheter) relief from some sort of urinary obstruction
visceral obesity- def and prognosis factor for?
- waist to hip ratio (visceral fat to subcutaneous fat)
- determinant of insulin resistance
hyperactive jaw jerk reflex-def, vairant of which sign, indicative of which ion imbalance
- tap on jaw elicits masseter muscle spams
- variant of Chovstek’s sign(tap on facial nerve anterior to ear causes facial muscle contraction)
- low serum Ca2+ level <7.0mg/dL
role of phosphodiesterase
termination of effects of hormones that act by cAMP or cGMP GPCR messenger systems
which drug can be used to treat BPH and androgenetic alopecia? mech?
Finasteride
-suppress peripheral conversion of testosterone to dihydrotestosterone
- drug that decreases Leydig stimulation by LH
- drug that decreases Leydig androgen synthesis
- drug that decreases peripheral androgen aromatization
- drugs the impairs androgen receptor interaction
- GnRH agonists used in a continuous fashion (leuprolide)
- ketoconazole (weak anti-androgen) also used to inhibit steroid production by adrenals
- aromatase inhbitor (anastrozole/exemestane) used in postmenopausal women with breast cancer
- flutamide, used to treat prostate cancer but not BPH
17 alpha hydroxlyase deficiency vs 5 alpha reductase deficiency
- impairs synthesis of androgens (males appear female and females have normal genitalia), hypogonadism, HTN, and hypokalemia
- defective conversion of testosterone to dihydrotestosterone (males have ambiguous genitalia) but develop 2ndary sexual characteristics. no problems with HTN, or K+ levels.
