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140 Cards in this Set
- Front
- Back
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Cortisol Function
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Gluconeogenesis by proteolysis, thin skin
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Epinephrine function
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Gluconeogenesis and Glycogenolysis in liver/adrenal cortex
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GH function
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Gluconeogenesis by proteolysis in liver→ IGF-1 “somatomedin” to growh plates
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GIP function
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Enhances insulin action in pancrease→ post-prandial hypoglycemia
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GIP syndromes
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Dumping sndrome: seen after Bilroth II procedure
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Dumping Syndrome Features
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Increased osmotic load dumped into duodenum, causes osmotic diarrhea, can also cause postprandial (reactive) hypoglycemia. Insulin resistance over time (Type 2DM)
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Motilin function
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Stimulates primary peristalsis, MMC in duodenum
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Secretin function
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Secretion of bicarb, inhibits gastrin, tightens pyloric sphincter
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Somatostatin function
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Inhibits secretin, motilin, CCK
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VIP function
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Inhibits secretin, motilin, CCK
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ADH stimulated by
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Stress, high osmolarity
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Diabetes insipidus –Nephrogenic Tx
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THiazide diuretics (paradoxical effect)
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DI- Central DI Tx
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DDAVP
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Serum Na<115 is what disease
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SIADH (too much ADH)→ pee Na/retain H20
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Causes of SIADH
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Pain, Carbamezapine, Amphotericin B, Cancer, Increased ICP, Restrictive lung disease
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SIADH Tx:
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Fluid restriction (Turn IV down) or Demecocylcine/Li (ADH antagonists)
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Sx when Na<120
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Seizures, arrhythmias (tx: 3% NS)
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Psychogenic Polydipsia lab
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Low plasma osmolarity, appropriate ADH levels
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POMC (propiomelanocortin) is?
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Opio (B-endorphin-feel no pain) Melano-MSH (dark sin), Cortin (ACTH)
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Conn Syndrome Sx and Lab values
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HTN, H/A, muscle weakness, Decreased Renin
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Conn’s syndrome Test
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24 hr urine Aldo on high salt diet
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Conn’s syndrome Tx:
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ACE-I (increase K+), Spironolactone (blocks Aldo), Adrenalectomy
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Salt craving, Hyperpigmentation, Orthostatic Hypotension
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Low Cortisol
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Addison’s Disease Tx
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Hydrocortisone
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Addisonian Crisis
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Fever, change in mental status, ab pain, Orthostatic Hypotension (Tx: hydrocortisone)
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Water-house Friderichsen syndrome Tx
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Emergent Methylprednisolone
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Purulent Fallopian Tubes to Adrenals, to liver
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Adrenals (Waterhouse-Friderichsen-N.meningitidis), Liver (Fitz-Hugh-Curtis- N.gonorrhea)
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Nelson’s syndrome
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Pt w/ cushing had bilateral adrenalectomy, years later has hyperpgimentation+ visual problems d/t unsuppressed pituitary adenoma (Increased ACTH)
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Neuroblastoma
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Adrenal tumor in Kids, high spontaneous regression rate, Ab mass, Dancing eyes “hypsarrhytmia”, Dancing feet “myoclonus”
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Contraindicated in Pheochromocytoma
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B-blocks (unopposed Alpha stimulation causes rapid Increase in BP)
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Pre-op Pheochromocytoma Tx
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14d Phenoxybenazmine+ Fluid Load (increase NA+ diet)
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Operative Tx Pheochromocytoma
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Phentolamine (blocks Alpha Nonspecific)→ adrenalectomy→ increase NE/Epi→ HTN crisis→ B1 blocker (everythigns blocked except B2)→ depending on IVF to keep BP up…
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Insulin is stimulated by, inhibited by
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Stimulated (hyperglycemia, Stress, B2 receptors), Decreased (alpha2 receptors)
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DM Tx to slow progression of Nephropathy
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ACE-I
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DM type I genetics
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HLA-DR3 and HLA-DR4
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Acanthosis Nigracans <50
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<50=DM type II
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Acanthosis Nigracans >50
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>50= Stomach Ca
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Dawn Phenomenon
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3 am Increase glucose d/t GH (Tx: Increase PM insulin)
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Somogy Effect
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3 am decreased glucose→ 6 am Increased glucose (Tx: decrease pm insulin)
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Factitious Hypoglycemia
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d/t insulin injection (increase insulin, Decreased C-peptide)
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Erythrasma
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Rash in skin folds, coral red Wood’s lamp, micrococcus infection
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Erythrasma Tx
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Erythromycin
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Syndrome X
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Metabolic syndrome (Pre-DM=HTN, Dyslipidemia, Hyperinsulinemia)
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Syndrome X Dx
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Fasting glucose 111-125 AND Glucose challenge 140-200 mg/dl
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Syndrome X Tx
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Metformin
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Tight glycemic control will decrease risk of?
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Retinopathy, nephropathy, neuropathy, Fetal abnormalities
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What activities decrease Glucose in blood?
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Alcohol, Exercise, Pregnancy, Delayed Gastric Emptying
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How do you Diagnose DM?
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Random glucose >200 w/ sx OR Fasting glucose>126 (w/ 1x repeat) OR Glucose Challenge (75g>200 @2 hrs)
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What is the physiology of DM Retinopathy?
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Weak capillary BM: leak plasma→ Retina. (Microaneursysms, Hard exudates (sharp demarcation), Dot-blot hemorrhages, Flame hemorrhages)
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What do you see in Pre-Proliferative DM retinopathy?
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Edema of Macula, Infarction of retina (hypoxia)→ soft exudates, “cotton-wool spots”
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What do you see in PROLIFERATIVE DM retinopathy?
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Neovascularization, Ruptures, Heal→ collagen pulls→ retinal Detatchment
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HbA1c measures?
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Glycemic control over past 3 months= RBC lifespan
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What is a good glycmic control? When do you get a false positive?
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<6%= good HbA1c. False+ w/ Hemolytic Anemia
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What hormones have the same Alpha Subunits?
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LH, FSH, TSH, B-hCG
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Short Acting insulin?
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Lispro, Regular, Asparte
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Intermediate acting insulin?
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NPH, Lente
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Long Acting Insulin?
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Glargine, Ultralente
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What are Weight Gain differentials?
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Obesity, Hypothyrodism, Depression, Cushing’s, Anasarca
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Diet modifications for Type 2 DM?
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Low sat fats, and Exercise (weight loss upregulates insulin receptors)
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Sulfonylureas, Alpha-glucosidase inhibitors, Biguanides,
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1st generation sulfonylureas AE
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Weight gain, Hypoglycemia* (Chlorpropramide- SIADH), Tolbutamide, Tolazamide
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Glipizide, Glyburide (like 1st but inhibit gluconeogenesis and enhance peripheral glucose uptake)
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Where is glyburide metabolized?
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Kidney
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Sulfonylurea Overdose Treatment?
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Dextrose, then Octreotide (inhibits insulin secretion)
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Inhibits Gluconeogenesis. AE: reacts w/ IV dyes, severe metabolic acidosis
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What are the Meds to tx DM type II
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Thiazolidinediones: Incrase insulin sensitivity, check ALT/AST
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Pancrease Delta cells and Duodenum. Goes nowhere has Paracrine function
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Inhibits secretin, motilin, CCK
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cAMP
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High insulin, Glucagon
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Somatostainoma will cause?
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Steatorrhea, gallstones and DM like sx
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Duodenum. Goes to Pancrease and GB
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Secretion of Bicarb, Inhibits: gastrin. Tightens pyloric sphincter. cAMP
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Secretin is stimulated by?
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Low pH
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What stimulates CCK release, inhibits?
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Simulated by Fat, Inhibited by High pH
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Enhances insulin action⇒ post-prandial hypoglycemia
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Low pH, glucose
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Chromium
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High pH>2
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Parathyroid Chief cells
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Bone, kidney
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Low Ca, high Phosphate
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Parathryoid→ PTH. Stomach→ Pepsin
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Both decreased
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Calcium decreased, Phosphate Increased (vice versa in HyperPTH)
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Activates Osteoclasts (needs Vit A and Mg)→ High Ca2+
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In Proximal Tubule→ waste phosphoruous→ Low PO4. In Distal tubules→ Activates 1-Alpha Hydroxylase→ activate Vit D
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GI (stimulates Ca-binding protein→ High PO4). Kidney DT
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Cholecalciferol (D3)
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Calcifediol (25-OH)VitD2 (from 1-Alpha hydroxylase activated by PTH)
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Vitamin D in kidney?
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Calcitriol (1,25-OH2) vit D
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Primary Parathyroid Adenoma (MEN1,2), 2ndary Renal failure, Sarcoidosis
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Increased PTH and Ca2+, Decreased Phosphate. SX: “Bones-osteoclasts, Groans- pancreatitis (gi upset,ulcers), Stones- kidney, stones, Moans- psychosis”
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Subperiosteal thinning (erosion). MC- Medial side of 2nd and 3rd
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Decrease Calcium (Furosemide, Calcitonin, Bisphophonates). Parathyroidectomy (Decrase Ca2+→ can cause Bells palsy)
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Cant absorb/secrete→ Pseudohypo profile: Increased PTH and
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Oral Ca2+ (decrease Phosphate to avoid metastatic calcifications)
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Bad kidney PTH RECEPTOR (increased PTH, Decreased Ca, increased Phosphate)
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Pseudo-hypo-parathyroidism presentation and clinical syndrome:
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Sausage digits (short 3rd/5th digits), Albright’s Osteodystrophy,
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G-protein defect→ no cAMP (Increased PTH, phosphate, normal calcium)
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Familial Hypocalciuria Hypercalcemia:
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Decreased Calcium excretion (urine Ca<200)
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Oral/GI neuromas (MENIII)
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Thryoglobulin: I-Tyr-MIT (or DIT) in colloid
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5’-monodeiodinase
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Liver: T4→ T3, and when ur Sick T4→ rT3 (inactive storage when your sick)
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Exopthalmos is seen in:
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Graves, Histiocytosis X, Carvernous sinus thrombosis
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Enopthalmos is seen in:
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Horner’s
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Exopthalmos, Pretibial (hard) myxedema, increased risk of Myasthenia graivs
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Graves Disease TX
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Radio-iodine ablation+ Prednisone (for eyes)
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Subactue granulomatous Thyroidistis (viral Ix invades thyroid→ painful jaw)
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Neutrophils, lymphocytes, histiocytes, multinucleated giant cells= Mixed cell infiltration
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Increased ER, Tender/warm thyroid, Lid lag, Decreased Uptake
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Dequervain’s Tx
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Propanolol/PTU or Methimazole
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. Post partum (Immune system attacks after pregnancy→ attacks
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Benign “toxic” adenoma in old people→ increased radioactive
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(+)= Hyperthyroid/Adenoma. Non= THyroiditis. Low= Folicular
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Check free T4.
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FNA
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Iodine scan→ FNA (if cold)
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5-HT, TSH, Nipple stimulation
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Prolactin 1st> GH>FSH/LH (secondary amenorrhea, male impotence)>TSH (hypothyroid), ACTH
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No somatomedin receptors
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Midget
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=Laron Dwarf: abnormal FGF receptors (extremeties only)
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Osteoperosis
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More OsteoCLASTIC activity> osteoblastic. Loss of bone matrix or osteoid
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Osteomalacia
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Loss of mineralization= soft bone
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Osteopetrosis
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Decreased Osteoclast activity. Too much bone, Thick +Heavy bone. Oblierates BM. Bone is too thick and inflexible
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Osteopenia
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Loss of Bone mass, bone matrix and mineralization is lost
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Osteitis Deformans
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=Paget’s Disease of bone. Increased Osteoclastic activity (increase bone breakage and bone building). Normal serum calcium at first, increased LAP
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Paget’s Disease increased risk for? Genetics, Virus?
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10% increase risk of Bone Cancer. Paramyxovirus. Increased P53, oncogene gain function
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Paget’s disease Tx
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Bisphophonates, +/- Calcitonin
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Osteosclerosis
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Scarring of bone, occur in any inflammation of bone
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