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142 Cards in this Set
- Front
- Back
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what blocks peripheral utilziation of glucose in DKA
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glucagon and insulin deficiency
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what causes dka osmotic diuresis
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hyperglycemia
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low insulin/glucagon ration
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stimulates HSL
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3 abnormalities in type 2 dm
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impaired insulin, insulin resistance, excellive hepatic glucose production
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type 2DMconcotdance
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90%
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MODY
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maturity onset diabetys of the young
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exocrine pancerase DM
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chronic pancreatitis, cystic fibrosis, hemochromatosis
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endocrinopathies that cause diabets
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acromegaly, cushings, glucocorticoids
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infections that cause diabets
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cosacki B, cytomegalovirus
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how many b cells must be lost to get secondary or acquired type of diabets in chronic pancreatitis
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80%
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acute complications of diabetes
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DKA and Hyperglycemic Hyperosmolar State
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major chornic complicaitons in DM
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vascular lesions
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capillary microangiopathy is caused by
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chronic hyperglycemia it's what causes retinopathy, nephtopath and neuropathy
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by 20 years what's up with DM kidneys
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75% of type 1 and 20% of type 2 progress to nephrotic syndroem and ESRD that requires dialysis or transplant
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commonest cuase of death in diabetitcs
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MI
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commonest nontraumatic cause of amputation
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diabetes macrovascular comps
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hyperlipdiemia in dm
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activated lipoprotein lipase leads to increased triglycerides, ldl and decreased hdl and an in crease in platelty adhesivness
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gross diabetic kidney
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smaller and granular pitted surface and thin cortex
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how long in dm until bm thickeing
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10 yers
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diffuse glomerulosclerosis
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in diabets, htn and elderly, kw lesion is psecific
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lens in dm
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osmotic swelilng and change in visual acuity
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anterior chamber in dm
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increased veg f
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preproinsulin mad ein
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rer
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when is proinsulin made
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from preproinsulin after entry into RER
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insulin is made in
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membrane bound granules after golgi (trans golgi)
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trypsin like enzyme
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cleave insulin
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glucagon b cell receptor
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Gas, AC cAMP, PKA voltage dependten Ca channel releases insulin
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glucose into be tel
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ATP is manufacture.. Increase atp sensitve K channel stopping excretion of K, hyperpolarization and ca enters through voltage dependent
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alpha 2 b cell receptor
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Gai… opent K chanenel and decreases calcium channle and thus less insulin secreted
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glucose receptor of betacells
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glucokinase
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aa's that stim insulin
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leucine arginine
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fatty acid s and ketone bodies and insulin
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weak stimuli
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pancreati chormones and insuli
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glucagon and insulin deficiency
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CCK GIP
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GI hormones increase insulin
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hypercalcemia
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stims insulin
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all known insulin secretagogs
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increase intracellular calcium
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GLP-1
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increases cAMP (increased inslin by turing off K/ATP channel) also activate EPAC2
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increases b cell proliferation and decreased b cell apoptosis
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GLP-1 and IGF-1
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insulin muscle
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enhances transcription of hexokinase, activates glycogen synthase,increases hexokinase and hphophofructokinase and pyruvte dehydrogenase activti…
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insulin receptor action
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autophophorylates and activates serine threonine kinases
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serine thronine kinases
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activae othe rkinase via phosphylation
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IRS
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protein phosphatase that is activated by serine thrionine kinase and dephosphyorlates many proteins phosphorylated by PKA (opposite of glucagon which activates PKA)
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how does insulin insert glut 4
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P13K activates PIP2, PI3 activated PDK (PDK activates PKB (inserts ) and mTOR (70-S6 activation and translation of mRNA)
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mTOR
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target of rapamycin
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PHAS-1
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activated by mTOR and PHAS-1 resease initiation factor promoting translation
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GSK-3
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glycogen synthase kinase 3 also activated by PDK (PIP 2. P13K)
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GRB2
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also activated by insulin activate ME and MAPK
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glucagon is mediated bia
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cAMP and PKA… leading to conersion of glycogen phospholabe b to phosphoylase a.. Increases phosphorylase
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glucaon ____ phosphorylase
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increases glycogen phophorylase
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what inactivase glycogen phosphorylase
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pyruvate kinase
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low insulin and high glucagon
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fatty acid oxition rates go up due to CAT I activated by low malonyl CoA
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PEPCK
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transcription increased by glucagon
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EPI NORE
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increase HSL (fat), glygogenolysis and glycolis (calorigenic via PKA in uscle) and liver Ca2_ glycogenolysis
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GH
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HSL adipocytes, deceras sens of cells to insuilin
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Corisol
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decerases ssens to insulin, mobilized protein from muscle, permissive action on adiocytes
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thyroxine
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uncouples ox phos
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why codl extermities in DKA
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extracellular fluid depletion due to sodium depletion
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% of patients comatose in DKA
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10
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insulin to glucagon ratio falls
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increased hepatic glucose and ketoe production (starvation)
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what leads to vomiting in DKA
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ketonaemia
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what leads to loss of water na and k in dka
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vomiting, hyperventilation (water only) and osmtic diuresis
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what leads to acidosi in dka
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low gfr= less renal h, and kenonaemia
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carnitine
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glucagon increases carnitine and which increases acyl CoA to acyl carnitine to Aceytle co a to Ketone
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Oxaloacetate in DKA
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diverted to make glucose instead of acetyl CoA so ketone bodiees produced
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fat in parathryoid adenoma
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no contrast to usual
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commonest cause of primary hyperparathyroidism
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parathryoid adenoma
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Parathyroid hyperplasian and MEN
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1/3 of cases of parathryoid hyperplasia associated with MEN I and MEN Iia
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parathyroid carcinoma
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5%
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water clear cells predominate and clustures of pink appearing (oxyphi) cells
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primary parthyroid hyperlasia
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secondary parathyroid hyperplasia
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principally in CKD, but also in vitamin d deficinecy, intestinal malabsorption, fancoinand renal tuubular acidosis
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most common causes of hypercalcemia
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primary hyperparathyroidism and hypercalcemia of malignancy
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cancer associated hypercalcemia
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local osteolicic hypercalcemia (20%) # 1 is humoral hypercalcemia of malignancy (75-80%) vitamin d secreiting lymphoma and ectopic PTH (very rare)
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how does granulomatous disease cause hypercalcemia
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mediated by vitamin d (activated macrophages in granulmomas produce 1 alpha hydroxylase) steroid suppress this converion and return serum calcium to nomral
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familial hypocalciurmc hypercalcuria
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autosomal dominant disorder… reduced activity is Calcium receptor CaSR
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lithium
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causes hypercalcemia in 10%
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thiazides
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can worse or provoke hypercalcemia in bordelin situations
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often what are sympsoms of hypercparathryoid
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none
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classic manifestations of primary hyperparathyroidism
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kidney stones and severe bone disases and more vague malais, musclular weakness, depression, osteopeeni
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typical phpt pt
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over 40 woman usually elderly who has few or no symptoms cleraly tied to PTH…
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must ID PTH using
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two site immunometric techinique
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EKG in hypercalcemia
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prolonged QT
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HTN in hypercalcemia
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some find it is more frequent, bute rarely improved with parathryoid surgery
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EKG changes in hypoparathryodi
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condcution abnromalities
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eyes in hypoparatyroid
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cataracks
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22q.11.2
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digeorge syndrome… microeletion syn region controls pharyngeal development
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CATCH 22
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Digeoge Cardiac, abnormal facies, thymic aplasia, cleft palate hypoglycmia
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origin of parathyroid
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inferior 3 superior 4
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thymus origin
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3 pouch
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most common hypopartharyoid
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iatrogenic
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thymic hypopasia and imunodeficnecy
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digeorge syndrome… microeletion syn region controls pharyngeal development
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ID DiGeorge
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FISH
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candidiasis, ectodermal dystrophy and adnreal insufficney
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Type 1 autoimmune Polyglandular syndroem AIRE
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Isolated famillial hypoparathryoid ism
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ad or ar
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PCAR
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ad hypo PTH, calcium receptor activating mutation
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autosomal recessive famillal hypparathroidism
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inactivating mutation in pth gene
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tyep Ia spseudohyoparathyroisim
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GNAS gene on 20q13.2-14.4 causing deficinecy of GsA
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inheritance of type I pseudo PTH
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maternal allele
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fail to show nora increase in urinary cAMP following IV PTH
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Type 1A pseudohypoparthyroid
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hypogonadotropic hypogonad in female
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multihormone resistance pseudo hypo pth tsh fsh and LH deficine due to cAMP problems
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short stature, obeisity, round face, short metacarpal and metatarsal bones BRACHYDACTYLY (short fingers and toes), ocular and dental MR
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albright hereditay osteodystrophy… pseudo PTH 1a
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pseudopseudo hypoparathryoidism
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usually in type 1 a famlis but have normal parathroid founction and normal urinary cAMP in response to PTH… mutant allelle is from fatehr and since father allele normally under express ed inkidney no PTH or kidney effects
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TYPE II pseudo hypoparthyroid
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defect in signal transduction pathway (PKA in cAMP dependent) that low Ca due to blunted response (normal PTH)
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sone bone, moans and abdominal goranes
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lytic bone lesions, renal sones, and pareatitis= hyperparthyroidism
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tertiary hyperparathryoidism
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paratthyroid become autonomus and after renal transpor t the pth continues to hyperfunciton
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VIPoma
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men 1 (diarrhea hypokalemia achlorhydria
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insulinoma
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hMEN 1
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glucagonoma
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glucose intolerance MEN 1
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gastrinoama
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severe peptic ulser MEN I
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medullary carcinoma of thryoid
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type 2, 2A or 2B
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hyerparathryoid an dmne
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1 or 2A
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mucosla neuromas of mouth
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men 2b (or III)
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marfanoid features
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men 2b (or III)
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men no parathryodi
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2B
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htn and hirsuiism in iatrogenic cushings
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no
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tumor producin CRF(H)
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rare but can cause cushing syndrome
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corticotropin independint cushings
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cortisol is produced by eoplastic adreocortical tissues ans supressins CRH and corticotropin
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majority of coritcotroin independent cushings
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adrenal cortical carcinoma (80%)
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large borwn back nodules in adrenal
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autonomous micronodular hyperplasia… autoantibodies to ACTH receptors that promote adrenocortical growth and steroid sytnhesis
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htn and hypokalemai
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conn syndrome primare aldesteronism
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glucose in elderly
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posprandial level s up by 1mg/dl after 20, insigifact increase in fasting glucose
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post challenge hyperglycemia
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in some older adults
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why change in glucse response to measl in elderly
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increased body fat decreased muscle mass, decreased IGF-1 and IG r, and decerased glut 4
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why older adults ast risk for hypoglycemia
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decreased glycogen stores, incresed chronic disease, decreased caloric intake, increased comorbidity
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dm prevalence in elderly
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15-20% over 65, 90% type II
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life reduction in DM
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10 year
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risk of blindess in dm
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increased by 40
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A1C in elderly
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target less than 8, less than 7 normally
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bp for elderly
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140/80
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ldl for elderly
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<100
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TSH 5-10
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normal in elderly normall .3-5
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sublinical hypothryoism
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15% in elderly high tsh normlal free t4
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vit min d
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decreased between 60-90 years of age,
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BMD less than
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2.5 SD's for osteoporosi
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cortisol levels with age
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stay same
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ocortisol response to stress and age
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increased and return to baselin slow
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most common cause of adrenal failure in older adults
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glucocorticoids
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dhea levels
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down with age
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dehydration
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reserves, thirst drive,renal response to adh, kideney, polypharmacy, low aldosteron levels,
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gh with age
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decreased, decreased strench, muslce mass, bone
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testosterone in elderly
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degreased… common adnrogen deficnys (testicular failure) inc horonically ill
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sig of low testosterone
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osteoporisis, muscle wasting, anemia, loss of libidio, cognitive decline
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factors contributing to udnernutions
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depression, poverty, living alone, dementia swallowing, chronic diseaase, medicaiton, acute illness, surger
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