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95 Cards in this Set
- Front
- Back
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group of disorders characterized by glucose intolerance
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DM
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what does the insulin produced by the beta cells of the pancreas caise
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decreases the BG by inhibiting glycogen breakdown and facilitates entry of glucose into the tissues
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what % of the population does DM affect
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2-5%
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what results when tissues fail to utilize glucose
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hyperglycemia
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Type I diabetes (IDDM) pts present with ...
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polyuria, polydipsia, polyphagia, and often rapid weight loss
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which type of DM has an abrupt onset
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IDDM - type 1
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pts with NIDDM present with what symptoms
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thirst, pruitis and fatigue. (obesity is present in 60-90% of these pts)
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list the 4 types of DM
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type 1, type 2, secondary, Impaired glucose tolerance (IGT), gestational
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most common form of DM
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NIDDM
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Form of DM that occurs in those less than 30 yo
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IDDM
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Form of DM that occurs in those over age 30
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NIDDM
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Form of DM that is common with ketosis
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IDDM
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Form of DM in which pts are of normal weight
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IDDM
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which gene region is associated with IDDM
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HLA
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Form of DM that is associated with islet cell antibodies
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IDDM
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what is usually the root cause of insulins' ineffectiveness in NIDDM
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insulin receptor defect
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what is the normal Hemoglobin A1c?
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3-6%
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what is A1c
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level of circualting glucose for the previous 2-3 months (RBC life span is 120 days)
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you can diagnose DM by oral glucose tolerance test or by a certain level fasting plasma glucose level..what are those levels
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-fasting plasma glucose greater then 140 on more then one occasion or oral glucose tolerance test above 200 at 2 hours and at another time between 0 and 2 hours
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how do you perform an oral glucose tolerance test
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75g of glucose dose dissolved in 300 ml water after overnight fast
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you have a symptomatic NIDDM who cannot be controlled by diet alone, what is the tx
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oral hypoglycemics like sulfonylureas
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what are 2 acute complications of DM
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-ketoacidosis, hyperosmolar non-ketotic hyperglycemic coma, infection, hypoglycemia
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what are 4 chronic complications of DM
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-atherosclerosis, retinopathy, nephropathy, neuropathy
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what are the precipitating factors for ketoacidosis in DM
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infection, omission of insulin, new onset diabetes
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Physiological characterisitcs of ketoacidosis in DM
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pH < 7.2, hyperglycemia, hyperventilation, inc anion gap, hyponatremia, hyperkalemia, inc BUN/Cr, ketones in blood and urine
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what is an anion gap
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the HCO3- lost is replaced by Cl-, to keep the anion gap normal
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what are the physical symptoms of ketoacidosis
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-polyuria, polydypsia, N/V, abd pain, dehydration, altered mental status, acetone halitosis
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why do those with absolute insulin def lead to diabetic ketoacidosis
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insulin def leads to inc lypolysis, inc fatty acids in the blood and thus ketosis
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what is the tx for ketoacidosis
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-fluids to restore intravascular volume, , bicarbonate, K relacement, insulin, monitor electrolytes, phosphate
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why is phosphate used in the tx of ketoacidosis
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insulin increases cellular uptake of phosphate and decreases plasma levels
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what is the glucose level when hyperosmolar non-ketotic hyperglycemic coma start
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greater then 600 mg/dL (more common in type 2)
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what is the tx for hyperosmolar non-ketotic hyperglycemic coma
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fluid replacement, insulin, electrolytes (esp K and phosphate)
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DM pts are more at risk due to the triopathy...which is
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neuropathy, vascular insufficency, immunopathy
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Dm at at risk for infections; one reason is the dec immune system...why is it decreased
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-due to granulocyte(WBC) depletion and defective phagocyte ingestion
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DM are at risk for infection...how does their nephropathy play a role in this
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-the nephropathy can compromise antibiosis
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hypoglycemia is glucose below 50 mg; list three things that can cause it
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-imbalance btwn insulin and glucose, reactive( insulin secretion vs absorption of food), insulin overproduction
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what can cause insulin overproduction that leads to hypoglycemia
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pancreatic tumor or alcohol ingestion
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whipples triad is a collection of three criteria that suggest a pts symptoms result from hypoglycemia
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-symptoms caused by hypoglycemia, BG below 40 at time of symptoms, relief of symptoms following admin. of glucose
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what is the somogyi phenomenon
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-hypoglycemia that causes rebound hyperglycemia, in which the body responds by releasing stored glucose from the muscles and liver to counter balance a rapid drop in blood glucose.
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why do Dm get vascular problems in the feet
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-due to atherosclerosis of the foot arteries
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why does retinopathy (damage to retina) occur in DM
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--due to microvascualr retinal changes
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why do DM get diffuse neprhopathy
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-too much sugar causes damage and widening of glomerular BM and mesangial cell thickening
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why do DM get nodular nephropathy
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-accumulation of PAS positive material at the glomular tufts and hyalinization of afferent glomular arterioles(causes inc protein in urine)
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what do PAS stains work on
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carbohydrates
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how do you treat the nephropathy of DM
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-stricter control of blood sugar, control of HTN and decrease protein in diet
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Radiculopathy
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-problem at the nerve root causing pain and dermatome sensory loss
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mononeuropathy
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mixed nerve problem with vascular, pain, weakness, sensory loss, reflex change
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polyneuropathy
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nerve terminal problem(muscle) that has sensory loss in stocking glove, absent reflex and mild weakness
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amyotrophy
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nerve terminal problem (muscle) with anterior thigh pain with weakness
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autonomic neuropathy
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sympathetic ganglion problem with postural hypotension, impotence, gastropathy, anhydrosis, arthropathy
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what are the pathogenic mechanisms that cause the neuropahty in DM
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-sorbitol pathway, occlusion of vasa nervosum, dec nerve myoinositol, dec nerve conduction, altered myelin synthesis and def repair, autonomic disorders, nerve growth factors
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what is myoinositol
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needed for normal nerve fxn
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what is the vasa nervosum
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-contains the small arterioles that supply a nerve
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how do your tx the neuropathy of DM
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-antidepressents like amitriptyline, anticonvulsant like carbamazapine, topicals like capsaicin, analgesics and sedatives
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what antidepressent dose of antidepressents like amitriptyline or nortriptyline be used to tx DM neuropathy
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10-25 mg qd of ami, 300mg nort
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what causes Diabetic charcot foot
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-neuropathy (loss of pain perception, propriocepton and sympa activity) also trauma from inc weight bearing promotes joint degeneration and subluxation
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what are the 3 stages of diabetic charcot foot
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development, colescence, reconstruction
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what happens in the dvlp stage of charcot
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this is the destructive phase, with joint laxity, subluxation and osteochondral fragmentation
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what happens in the coalescence phase of charcot
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absorption of debris and fusion of larger fragments to adjacent bone
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what happens in the reconstruction phase of charcot
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revascularization and remodeling of bone and fragments
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list vascular features of charcot
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bounding pulse, erythema, swelling, warmth
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list the neuropathic features of charcot
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absent/dminished pain, proprioception, vibration and DT reflexes
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list the skeletal features of charcot
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rocker bottom foot, medial tarsal subluxation, digital subluxation, crepitus, hypermobility
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list the cutaneous features of charcot
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ulcer, hyperkeratosis, infection, hyperhydrosis
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treatment for charcot foot
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casting/immobilization, accomative foot gear, reconstructive surgery
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what is the cornerstone of diabetic foot ulcer tx
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-prevention with adequate shoe gear, proper hygiene, control of blood sugar, frequent inspection
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what should a DM BG be prior to surgery
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btwn 100 and 200
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Other then DM pt BG btwen 100 and 200 prior to surgery, what else do you want to know about their metabolic balance
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-normal vitals and electrolytes, renal and hepatic status, preop EKG
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how should a DM pt be managed during minor surgical procedures
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-give oral nutrition immed post-op, no change in diet, oral hypoglycemic or insulin regimine, monitor glucose 1 hr before and 1 hr after surgery
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how should a DM pt be managed during major surgical procedures as far as their diabetic meds go
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-discontinue oral hypoglycemics the morning before the day of surgery, if on insulin and a controlled diabetic give 1/2 the dose the morning of curgery
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what is considered a controlled diabetic
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BG less then 250
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what should BG be intraoperative and postopertive be
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100-200
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how do you keep the BG from 100-200 during surgery
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Preop: IV with 1000 mL D5W w/ 40mEq/L of KCl run at 100mL/hr (dec in pts with CHF or renal failure); give 1/2 normal dose of insulin, continue IV fluids at 80 mL/hr, monitor BG every 4-6 hours
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what is D5W
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5% dextrose
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where does insulin for DM pts come from
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-beef, pork or human
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what is the main SE of insulin drug therapy
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hypoglycemia
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insulin can be rapid acting, intermediate and prolonged acting; which are rapid
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crystalline zinc or regular
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intermediate acting insulin
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isophane or NPH(neutral protamine hagedorn)
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prolonged insulin
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protamine zinc and ultralente
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humalog
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lispro (fast acting)
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with what pts are oral hypoglycemics used
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NIDDM
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what are the SE of oral hypoglycemics
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GI disturbances, hypoglycemia, pruitus, nausea, anemia
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what is the mechanism of oral hypoglycemics
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-stimulate insulin release from beta cells, reduce serum glucagon levels, inc binding of insulin to target tissues
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Biguanide
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metformin; antihyperglycemic (not hypoglycemic)
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how does metformin work
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-dec intestional glucose absorption, inc peripheral glucose uptake, inc insulin-mediated glucose uptake, dec hepatic glucose production
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what is the major SE of metformin
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lactic acidosis
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what is the dose of metformin
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500 mg tablets BID
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Rezulin
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Troglitazone; antidiabetic agent that lowers BG by improving target cell response to insulin
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mechanism of action of Rezulin
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binds to nuclear receptors PPAR
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what do the nucelar receptors PPAR do
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regulate the transcription of insulin responsive genes critical for the control of glucose and lipid metabolism
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when and how is rezulin used
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-used in Type 2 as an adjunct to diet/exercise and in combo with sulfonylurea, or with a sulfonylurea and metformin, or with insulin
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if insulin isnt working to control a DM 1 BG, what can be added to their drug therapy
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-Rezulin
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sulfonylurea (glipizide, tolbutamide)
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-hypoglycemic drug used in NIDDM that inc secretion of insulin from beta cells
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if sulfonylurea and metformin combo (glipizide-metformin) doesnt work to control BG in a NIDDM, what can you add to their therapy
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Rezulin
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what is the major contraindication of rezulin
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-severe idiosyncratic liver cell injury; so dont use in those with liver dz or elevated ALT
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