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47 Cards in this Set
- Front
- Back
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DM 2
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-dual defect: increased insulin resistance, imapired insulin secretion (by b cell)
-obesity --> inc insulin resistance --> DM2 -strong genetic pre-disposition -N. americans, AA, hispanics, asian -strong FM -increasing worldwide |
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clinical features of DM2
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-obese
-adult onset -non-insulin dependent (NIDDM) (slide 17) |
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risk factors for DM2
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Family History of DM2
Obesity Physical Inactivity Race/Ethnicity History of Gestational Diabetes, or delivery of baby >9 lbs Polycystic Ovarian Disease, or Acanthosis nigricans Hypertension, Low HDL, or High Triglycerides |
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metabolic syndrome
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-inc insulin resistance
-abd obesity -low HDL -high TGs -HTN -inc risk of DM and CV disease |
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goals of diabetes mgmt
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1. glycemic targets: A1c <7% (Am. dibetes assoc.) A1c <6.5 (american college of endocrinology); FG 80-120; post-prandial glucose (2h) <160
2. lipid targets: LDL <100; <70 if prevalant CV dz; HDL >40; TG <150 3. BP targets: <130/80 4. aspirin 5. preventing acute and longterm DM complications -annual eye exams, foot exams -screening for urine micro-albuminuria |
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ABCs of DM
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A1c: sugar control
BP Cholesterol -all diabetics should know their ABCs |
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oral diabetic agents
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-OHAs (oral hypoglycemic agents)
-only for type 2 DM -DM2 dual defect |
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insulin secretagogues
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-increase B cell insulin production
-Sulfonlyureas: Chlorpropamide, Glyburide -Rapid acting insulin secretogogues: Repaglinide, Nateglinide |
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Sulfonlyureas
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-MOA: Bind to Sulfonylurea receptor on Beta cell, and increase insulin release from pancreatic beta cells
-full effect within 2 wks -A1c drop expected: 1.5-2% -metablized by liver or kidney -given once a day or BID -cheap, long experience, rapid effect -SE: wt gain, risk of hypoglycemia -Caution: renal failure, liver dz, CHF, elderly |
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rapid acting insulin secretagogues
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-Repaglinide, Nateglinidie
-MOA: Insulin secretagogues; bind to separate site than the Sulfonylureas receptor -quick in, quick out: Decreased risk of hypoglycemia than longer acting secretagogues (SUs), esp in elderly, renal failure, CHF patients -Hypoglycemia can occur; More expensive ($60/mo); Weak effect: A1c drop 0.7% (20-30mg/dl) |
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insulin sensitisers
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-metformin
-TZDs -dec peripheral insulin resistance inprove insulin sensitivity -DO NOT cause hypoglycemia -efficacy comparable to SUs -more $$ |
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Metformin
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MOA: Acts at the LIVER, and the skeletal muscle, to decrease peripheral insulin resistance
-excreted unchanged by kidney -low risk of hypoglycemia -promotes WT LOSS -A1c drop 1.5-2%; 50-60mg/dL drop in sugars SE: GI (tend to improve over time) |
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Lactic acidosis
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-Phenformin,another biguanide drug was withdrawn in the past due to increased risk of lactic acidosis, and deaths
-Metformin rarely causes lactic acidosis -must be stopped in pt with renal insufficiency -also caution in pt with h/o CHF, due to inc risk of hypoxic lactic acidosis |
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Metformin and Contrast Media
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-Diabetics have increased risk of contrast nephropathy, and so metformin must be held before any procedure where patient may receive IVP/CT scan Dye. After the procedure, recheck renal function, and if normal, may resume metformin thereafter
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TZDs
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-Thiazolodinediones; 'Glitazones'
-Pioglitazone, Rosiglitazone, Troglitazone -MOA: PPAR-gamma agonists; Work at Muscle,liver, and adipose tissue, decreasing peripheral insulin resistance -low risk of hypoglycemia -A1c drop of 1.5-2% -$$$$$ -promote fluid retention and wt gain -caution: inc risk of CHF, do not use if EF <40%; check LFTs! |
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Acarbose
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α-glucosidase inhbitor
Decreased absorption of carbohydrates GI side effects Weight Neutral A1c drop 0.6-0.8 Dose 25mg -100 mg qac $80/month |
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Incretins
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-intestinal hormones released after meals
-play impt role in normal glucose homeostasis -physiologically help regulate insulin release in a glucose-dependent manner -GLP 1 -GIP |
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slide 42
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slide 42
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Glucagon-like peptide 1 (GLP-1)
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-secreted from L cells of the intestines
-most-well characterized incretin -diminished in type 2 DM -promotes satiety and reduces appetite -short half life -DDP IV inhibition: Could extend endogenous GLP-1 half-life -incretin mimetics: Mimic many of the glucoregulatory effects of GLP-1, Resistant to DPP-IV |
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Exenatide
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-synthetic version of salivary protein found in the Gila monster
-More than 50% amino acid sequence identity with human GLP-1 -Binds to known human GLP-1 receptors on beta cells (in vitro) -Resistant to DPP-IV inactivation -Byetta -give as injection -A1c drop .4-.8 -GI SE very common -wt loss 2-4 lbs -low risk of hypoglcemia |
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Exenatide cont
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-rarely pancreatitis had been noted
-rerely may cause acute renal insuff -Liraglutide is another long-acting GLP-1 analoge -Exenatide-LAR is a once a week SQ formulation which has shown promising results, but is not yet FDA approved |
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Gliptins
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-DPP-4 inhibitors
-Sitagliptin (Januvia) & Saxagliptin (Onglyza) available -raise GLP-1 levels -wt neutral -low risk of hypoglycemia -$$ -dose adjustment in renal failure pts |
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women with DM
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-before menopause, women are generally protected from heart dz
-BUT diabetic women LOSE that protection -most young women who are in the CCU with a heart attack are usually diabetic, esp if they smoke |
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pregnancy in a diabetic woman
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-ALL diabetic women of reproductive age group MUST be counseled to PLAN their pregnancies
-they MUST be in good sugar control BEFORE they get preg -Risk of major malformations in the baby is directly related to the sugar control in the mom, esp in the first trimester, when the baby’s major organs are being formed -IF unplanned pregnancy, before the woman realizes she is pregnant, irreversible damage may have already occured -INSULIN only drug known to be sage in preg -Type 2 diabetic women should be changed from pills to insulin BEFORE they get pregnant |
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diabetic woman planning to get preg..
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-Also, in a diabetic woman planning to get pregnant, STOP ACE-inhibitors, ARBs & statins
-Diabetic women may have progression of their eye disease or kidney disease, esp if they have pre-existing eye or kidney disease, and must be closely monitored by the eye doctor, kidney doctor & diabetes doctor, in addition to a high risk OB MD. |
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Diabetic complications
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-Acute complications:
1. hyperglycemic crisis -Chronic 2. micro-vascular: retinopathy, neuropathy, nephropathy -macro-vascular: CAD, PVD, TIA- MAJOR CAUSE OF MORTALITY |
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DKA
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Usually in uncontrolled Type 1 Diabetics
Due to ABSOLUTE deficiency of insulin Can occur if a type 1 is admitted to the hospital and standing dose of basal insulin is held Pathophysiology: Insulin lack, glucagon excess ---> Hyperglycemia; Keto-acidosis--->Death Dehydration Acidosis (Anion Gap Metabolic Acidosis) Hyperglycemia |
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DKA precipitating factors
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1. omission of insulin
2. intercurrent illness 3. newly recognized DM |
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DKA tx
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1. Iv fluid hydration
2. IV insulin until after Anion gap closes, then transition to SQ insulin 3. watch for hypokalemia, and replete phos 4. treat underlying infx 5. educate pt |
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DM compliations- serious
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1. macrovasular dz: kills 2/3 diabetics
2. kidney disease 3. blindness: leading cause of blindness in adults 20-74 4. amputations 5. co-existent HTN |
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risk of diabetic microvascular complications
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-related to...
1. duration of DM 2. AND degree of -glycemic control -BP control -lipid control 3. Genetic predis |
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Diabetic eye disease
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1. cataracts, glaucoma
2. retinopathy -Background Diabetic Retinopathy (BDR): mico-aneurysm -Proliferative Diabetic Retinopathy (PDR) With or without Macular edema Neovascularisation (NVD or NVE) Leading Cause of Blindness in young adults Prevention: Better glycemic control Treatment: Laser treatment |
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BDR
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1. retinal caps leak lipids, protein, RBCs into retina
2. micro-aneurysms 3. dot hemorrhages 4. exudates |
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PDR
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-Retinal hypoxia--->New vessel growth 'Neo-vascularization'
-New vessels abnormal ---->Vitreous Hemorrhage----- --->Fibrosis--->Traction on retina--->Retinal Detachment--->Blindness -Leading cause of blindness -Neo-vascularization of iris (Rubeosis Irides)----> Neovascular Glaucoma -Treatment: Focal or panretinal Laser Photocoagulation (Decreases retinal hypoxia) |
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recommended screening for DM retinopathy
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-DM1: 5 yrs after dx: annual
-DM2: at dx, and annually after -pregnancy: need close f/u -Intensive Glycemic control in a patient with POOR control, and prevalent severe retinopathy may lead to transient worsening before improvement; go a little slower in these patients, WITH close ophthalmologic follow-up concurrently |
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diabetic nephropathy
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-preclinical phase
1. glomerula hyperfiltration 2. micro-albuminuria -clinical phase 1. overt proteinurea 2. progressive renal failure -pathological findingS: 1. GMD thickening 2. mesangial matrix expansion 3. nodular intercapillary glomerlosclerosis 4. diffuse glomerulosclerosis |
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proteinuria
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1. Micro-albuminuria
NOT picked by routine dipsticks 24 h Urine protein 30-300 mg/24h RANDOM (or SPOT) urine for micro-albumin to creatinine ratio: 30-300 Earliest sign of DM Retinopathy Marker for increased CV risk Start ACE-i EVEN IF Normal BP 2. Overt proteinurea -24 h U protein >300mg; Random U Alb:Cr>300 -Dipstick Positive |
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diabetic nephropathy cont.
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-DM with mirco-albuminuria: risk of macrovascular dz MUCH HIGHER
-most (>90%) diabetics with nephropathy have concomitant retinopathy -without renal transplant, diabetics do VERY POORLY with renal failure -10 yr survival <5% -with renal transplant, diabetics do fairly well |
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diabetic nephropathy-tx
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-aggressive BP, lipid and glycemic control imperative
-ACEI: dec rate of progression -ARBS |
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diabetic foots
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-neuropathy
-PVD -inc risk of ulceration -->infx --> amputation -foot deformities: inc risk of ulceration -screen for HIGH RISK FOOT: 10 site monofilament exam -screen for neuropathy and PVD -FOOT exams (daily by pt) |
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diabetic foot- inc risk for ulceration
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1. neuropathy
2. PVD 3. hx of ulcers or amputation 4. pre-ulcerative callus 5. foot deformities |
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Peripheral vascular dz
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-often asym
-intermittent claudication -rest pain -check pulses -ABI: Ankle Brachial Pressure Index: -Rx: meds: ASA,plavix, pletal; surgery; peripheral angioplasty +/- stents |
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neuropathy in DM
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1. peripheral neuropathy:
-sensory neuropathy: distal symmetric polyneuropathy, large fiber polyneuropathy -motor neuropathy: mononeuritis multiplex, diabetic amyotrophy 2. autonomic neuropathy -cardiac autonomic neuropathy -diabetic gastroparesis 3. cranial neuropathy -diabetic III neve palsy |
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Diabetic Peripheral Sensory Neuropathy
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-Most common form of Diabetic neuropathy
-Increased risk of foot ulceration -Decreased sensation, numbness, tingling -Pain: ache, burning, shooting -'Glove and Stocking' distribution -MUST SCREEN -Treatment 1. Antidepressants: Amitryptiline, Cymbalta 2. Anticonvulsants: Gabapentin, Carbamazepine 3. Lyrica |
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Diabetic Autonomic Neuropathy
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1. CV:
-Orthostatic Hypotension -Resting Tachycardia (Vagal Denervation) -Painless MI -Sudden Cardiac Death (SCD) 2. GI: -Diabetic Gastroparesis -Constipation, Diarrhea 3. GU: -Diabetic Gastroparesis -Constipation, Diarrhea |
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diabetic gastropharesis
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-Impaired gastric propulsive activity, delayed gastric emptying
-Postprandial fullness, nausea and vomiting -Weight Loss -Erratic sugars (Mismatch of insulin and food absorption) -Gastric Emptying Study Tx: Prokinetic agents; erythromycin |
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risk factors for macrovascular disease
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1. genetic
2. FH 3. hyperglycemia 4. HTN 5. dyslipidemia 6. smoking 7. obesity 8. physical inactivity |
