Endocrine Flashcards
Bisphosphanates
promote osteoclast apoptosis; inhibit osteoclast activity (used as tx for menopause induced bone fragility / osteoporosis)
What are some etiologies for hypercalcemia?
primary hyperPTHism, hyperthyroidism, thiazide diuretics, acute renal failure, adrenal insufficicency
What are some sx of hypercalcemia?
bone pain/athralgias (remodling effects); skel m weakness, neopholithiasis (kidney stones), shortened QT interval
What are some sx of hypocalcemia?
neuromuscular hyperexcitablity; Trousseau’s sign (inflate BP cuff –> carpal spasm); cardiac arrhythmia; prolongued QT interval
What are some etiologies for hypocalcemia?
hypoPTHism; pseudophypoPTHism
What are some symptoms of primary hyperPTHism?
(hypercalcemia due to parathyroid adenoma: cortical loss in bone, skel m weakness, cardiac m: shortened QT, calcifications in cardiac m; impaired smooth m fxn: GI, calcifications in arteries; CNS (depression, dementia, stupor) Renal: if severe, nephogenic diabetes incipidus (from CaSR activity blocking Aquaporin and NKCC activity, AVP resistant condition)
What is the function of CaSR?
senses molar amt of [Ca2+] in forming urine
What effect does Ca2+ have on cardiac action potentials?
Ca2+ is key in duration of plateau phase in myocyte/purkinje potential. Ca2+ dictates the rapid depol phase of pacemaker potentials.
What are the effects (and conditions) of hyperphosphatemia? (ie: on GFR and bone remodeling)
sick nephron model: -significantly reduces GFR -PTH can’t block PO4 reabsorption, so even more PO4 is reabsorbed -remodeling is negatively affected bc calcitriol (which is made in PCT under influence of PTH) and bone reabsorption is impaired -this leads to Ca2+ ppt and metastatic calcifications -EFFECT: hypocalcemia (and associated signs/sx)
What are the causes and effects of hypophostphatemia?
Most common etiology: increase in PO4 excretion that accompanies hyperPTHism; if severe, due to alcoholism Effects: (severe) decrease in [2,3-diphosphoglycerate], so increased affinity of Hb for O2, so O2 cannot offload to tissues –> skel muscle weakness and sometimes skel muscle necrosis (ie: rhabdomyolysis)
What are the causes and effects of Rickets?
Rickets = calcitriol deficiency/resistance PRIOR to epiphyseal plate closure (in adults, it is called osteomalacia) Calcitriol deficiency induces increased PTH-dependent elimination of PO4 in urine, and the inability to absorb dietary Ca2+ SSx: bone pain, tenderness, diminished bone density/mineralization, HYPOPHOSPHATEMIA, HYPOCALCEMIA, HYPOCALCIUREA.
What is Thyroid Peroxidase?
-Catalyzes oxidation, iodination, and coupling in TH production -exists almost exclusively in apical membrane of follicular cell
What does 5’deiodenase do?
Convert T4 to T3 NB: 5-diodinase converts T4 into rT3
Why does T4 have a longer half-life than T3?
It has higher affinity for carrier proteins like thyroxine binding globulin, transthyetin, and albumin these CPs act as mobile reservoirs
How does TH act in brown adipose tissue?
TH + SNS –> upregulates expression of UCP-1 (uncoupling protein 1) UCP-1: translocates to mito can triggers leakage of H+ across inner mito membrane to “short-circuit” the chain, allowing O2 to be used at high rates but little AP is synthesized,s o most energy is lost as heat
