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HHS
- hyperglycemic hyperosmolar syndrome
- -clinical manifestation of T2DM
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hyperglycemic hyperosmolar syndrome
- -blood glucose > 600 mg/dL
- -serum osmolality >320 mOsm/kg
- -absence of ketoacidosis
- -infection
- -dehydration
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HHS symptoms
- -pulyuria
- -polydipsia
- -polyphagia
- -weight loss
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HHS treatment
- -slow rehydration
- -treat underlying conditions
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Metabolic Syndrome
- central obesity
- insulin resistance
- dyslipidemia
- hypertension
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medical treatment for T2DM
- -MNT
- -physical activity
- -medications
- -urine & blood ketone monitoring
- -self-management
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5 finger rule for NIDDM
- -monitor glucose levels (FSBS)
- -maintain/achieve IBW (lower total kcals, total fat, sat. fat)
- -exercise regularly (ACSM, American College of Sports Medicine guidelines)
- -consistent timing of mixed high fiber meals
- -avoid concentrated sweets
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5 finger rule for T1DM
- -monitor glucose levels
- -match insulin to intake
- -maintain weight
- -exercise
- -be prepared for hypoglycemia
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medications for T2DM
- 1.alpha-glucosidase inhibitors (AGIs)
- 2.amylin analogs
- 3.biguanides
- 4.incretin mimetics
- 5.meglitinides
- 6.sulfonylurea agents
- 7.thiazolidinediones
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oral hypoglycemic agents
- -help pancreas to make more insulin
- ex. 1st & 2nd generation sulfonylureas & meglitinide analogs
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oral antihyperglycemic agents
- -targets different organs to help insulin work better
- ex.biguanides, AGIs, thiazoldinedones
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1st generation sulfonulureas
- ex. diabinese
- -oral hypoglycemic agents
- -targets pancreas to increase insulin secretion
- -SE=hyperinsulinemia, hypoglycemia, weight gain
- -avoid alcohol - reactions reported!
- + inexpensive , once a day
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2nd generation sulfonulureas
- ex. Glynase
- -oral hypoglycemic agents
- -targets pancreas to increase insulin secretion
- -SE=hyperinsulinemia, hypoglycemia, weight gain
- -avoid alcohol
- + inexpensive , once a day
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meglintine analogs (secretagogues)
- ex. Prandin
- -oral hypoglycemic agents
- -helps pancreas make more insulin in the presence of glucose
- -acts for only about 4 hours after taken (fast acting, short acting)
- -SE=hyperinsulinemia, hypoglycemia, athralgia (joint pain)
- -more doses, more expensive
- -avoid alcohol
- +less hypoglycemia at night
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AGIs
- -alpha-glucosidase inhibitors
- ex. Glyset
- -oral antihyperglycemic agent
- -inhibits enterocyte disaccharidases thereby delaying CH digestion & absorption
- SE=GI - cramps, flatulence, diarrhea
- -take w/ first bite of meals 3x day
- - less efficacy with frequency of dosing
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thiazoldinedones
- ex. Avandia
- -oral antihyperglycemic agent
- -reduces hepatic glucose production
- -stimulates insulin receptors thereby increasing insulin sensitivity in muscle & adipose cells
- -can use with renal insufficiency
- -dose 1x/d
- -least food & drug interactions
- SE: possible weight gain/edema, but none reported
- - very expensive
- -more effective with insulin deficiency
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GDM
gestational diabetes mellitus
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GDM risk factors
- -overweight
- -physically unfit
- > 25 years
- -family history
- -African American, Hispanic, Native American
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Maternal Risks with GDM
- -HTN (preeclampsia)
- -polyhydramnios (excess amniotic fluid)
- -difficult birth
- -preterm delivery
- -increased rate of C section
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Fetal Risks with GDM
- overproduction of insulin by fetus
- macrosomia (>4500 g)
- birth trauma
- neonatal respiratory distress
- neonatal hypoglycemia
- hypocalcemia
- hyperbilirubinemia
- polycethemia (increase in RBCs)
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Screening for GDM
- done between 24-28 weeks
- 50 g oral glucose challenge test (GCT)
- plasma glucose > 140 mg/dL 1 hour after
- 100 g oral glucose tolerance test (OGTT)
- + if 2 or more result:
- fasting plasma glucose > 95 (prior to oral load)
- 1 hour plasma glucose >180
- 2 hour pm > 155
- 3 hr pg >140
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GTC
glucose challenge test
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OGTT
oral glucose tolerance test
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Why do we focus on consumption of adequate calories in GDM?
- to promote appropriate weight gain
- avoid maternal ketosis
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What discomforts are we trying to decrease when treating GDM?
- hypoglycemia
- nausea
- vomiting
- constipation
- heartburn
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SMBG
self monitoring of blood glucose
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What do we use self monitoring of blood glucose records for?
- (check glucose levels 1 hour after each meal with GDM)
- assess effectiveness of MNT
- guide adjustments to intake
- determine if insulin therapy is needed
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How/why do we adjust CHO intake with GDM?
- -amount & timing
- -avoid highs & lows
- -avoid nausea
- -CHO not well tolerated in a.m. - plan for < 45 g
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Euglycemic Diet
- aka Jovanovic Diet
- reduce caloric intake to just above ketonuric threshold
- restrict CHO to <40% of total calories (>40% from fat & 20% from protein)
- breakfast small & low in CHO to counter effects of high cortisol levels in a.m.
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When should insulin therapy be added for GDM?
- if 1 hour postprandial glucose level is >120 mg/dL more than twice in 2 weeks
- if FBS is >90 mg/dL
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What type of insulin therapy is used with GDM?
- NPH - intermediate-acting before breakfast & at bedtime
- Lispro (Humalog) at lunch and dinner
Don't forget to exercise! This may cure GDM!
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DKA
diabetic ketoacidosis
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Why do we encourage clients with IDDM to rotate injection sites every 2 weeks?
build up of scar tissue surrounding adipose can affect/inhibit absorption (atrophy/hypertrophy)
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too much insulin causes
hypoglycemia
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too little insulin causes
hyperglycemia
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IIT
intensive insulin therapy
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MDI
multiple daily injections
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What is involved with intensive insulin therapy?
- MD, RD and patient work together
- MD adjusts basal insulin to blood sugar (BS) pattern
- Patient must keep records of BS, insulin, & intake
- Bolus insulin bases on FSBS 4 or more times/day
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CSII
continueous subcutaneous insulin infusion
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General Diabetic Diet Guidelines
- kcals to maintain optimal body weight
- CHO = 55-60% but don't increase if they consume less (as long as they have at least 130 g/d)
- protein = 10-20% (usually 15-20, but can be 10% if they have nephropathy)
- fat = 25-30% of total kcalories
- cholesterol <300 mg/d
- Na < 3000 mg/d
- eat carbs with alcohol & be careful
- Be careful about sugar alcohols.
- Sugarfree candy is not carb-free
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Goals when following diabetic diet guidelines
- reduce risk of micro & macrovascular disease by addressing lipoprotein profile
- reduce risk associated with HTN
- address individual nutritional needs accounting for cultur & lifestyle
- enhance health
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What do we teach patients with IDDM in survival mode?
- What's a carb?
- Where is it in your diet?
- Eat at regular intervals.
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When in individualization phase with IDDM, what should we teach?
- alcohol
- exercise
- being sick
- menstrual cycle
- eating & exercise pattern
- morning
- fiber
- sugar alcohol
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dosing insulin
1 unit/10-15 g CHO
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TAG
- total available glucose
- or
- triacylglycerol
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Why do we encourage exercise if someone has DM?
- will decrease blood glucose unless BG > 250-300 (there is insulin deficiency)
- exercise can speed the absorption of insulin in the active limb
- blood lipid control
- blood pressure control
- depression
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What recommendations should we give to someone with IDDM if fasting glucose is <180?
- add 15 g CHO if exercising moderately for 1 hour
- add 30-45 g CHO if 100-180 exercising for 1-2 hours
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What are the rules for counting sugar alcohols & fiber for DM?
if >5 g, subtract half from total carbs
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glycosylated hemoglobin
- HbA1c fraction
- reflects average glucose level over last 4 mo.
- 6-7% are normal values for someone with DM
- 8-9% acceptable
- 11-13% poor
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long term complications of hyperglycemia affect:
- eyes
- kidneys
- nerves
- macrovascular
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long term complications of hyperglycemia on eyes
- retinopathy
- cataract
- glaucoma
- ...blindness
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long term complications of hyperglycemia on kidneys
- nephropathy
- microalbuminuria
- gross albuminuria
- ...kidney failure
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long term complications of hyperglycemia on nerves
- neuropathy
- peripheral
- autonomic
- ...amputation
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long term complications of hyperglycemia & CVD
- coexistence of HTN & dyslipidemia
- underlying metabolic syndrome
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FMH
family medical history
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HEENT
head, eyes, ears, nose, throat
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HPI
history of present illness
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TPR
temperature, pulse, respirations
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body's response to low blood pressure
- renin released from kidney
- angiotensinogen converted to angiotensin I
- angiotensin I converted to angiotensin II
- -decrease of Na+ & H2O excretion
- -vasoconstriction
- -increase in aldosterone...increased blood volume
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EF
- ejection fraction
- end of diastole
- amount of blood ejected
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possible symptoms of HTN
- dizziness
- faintness
- headaches
- vision changes
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etiology of hypertension
- 90% of cases are idiopathic - primary or essential
- secondary - result of another chronic condition
- lifestyle - smoking, exercise, diet, obesity
- sodium intake
- inflammatory response
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ATP III
- adult treatment panel III
- guidelines used for cholesterol management
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hypertension treatments
weight reduction, PA, nutrition therapy, pharmacological
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medication classes for HTN
- "loop" diuretics
- thiazides
- carbonic anhydrase inhibitors
- potassium sparing diuretics
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loop diuretics
- used for HTN
- ex. furosemide
- effective in patients with impaired kidney function
- inhibit sodium & chloride reabsorption in the ascending loope of henle
- potassium depleting
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thiazides
- diuretic treatment for HTN
- ex. hydrochlorothiazide, hydrodiuril
- inhibits sodium-chloride-potassium reabsorption in distal convoluted tubule leading to a retention of water in the urine
- decreases calcium lost
- potassium depleting except for hydrochlorothiazide
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carbonic anhydrase inhibitors
- diuretic treatment for hypertension
- ex. acetazolamide
- prevents exchange of hydrogen, sodium, and water by blocking sodium anhydrase
- inhibit the transport of bicarbonate out of the proximal convoluted tubule, which leads to less sodium reabsorption and therefore greater sodium, bicarbonate and water loss in the urine
- the weakest of the diuretics and seldom used in CVD
- main use is in the treatment of glaucoma
- potassium depleting
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potassium sparing diuretics
Amiloride (Midamor®) Amiloride and Hydrochlorothiazide (Moduretic®) Spironolactone (Aldactone®) Spironolactone and Hydrochlorothiazide (Aldactazide®) Triamterene (Dyrenium®)Triamterene and Hydrochlorothiazide (Dyazide®, Maxzide®)
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What is the Dawn Phenomenon?
- Release of growth hormone, cortisol, glucagon and epinephrine in the early morning causes an increase in blood glucose
- NOT the same as the Samogyi Effect,thought to be a reaction to earlier hypoglycemia (if it occurs at all)
- Can distinguish between the Dawn Phenomenon and the Samogyi Effect by checking 2 am sugar.
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How does Type 1 Diabetes Mellitus present?
- Peak onset age 4-6 and 10-14 (bimodal)
- Weight loss
- Polydipsia and polyuria
- Polyphagia, fatigue and weight loss
- Often with ketoacidosis
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To diagnose diabetes: (type 1)
- Fasting blood glucose >126 mg/dL
- Random blood glucose >200mg/dL
- 2 hour oral glucose tolerance test > 200 mg/dL
- HbA1c 6.5% or higher
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IGT
impaired glucose tolerance
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somatostatin
inhibits secretion of both insulin & glucagon
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To confirm Type 1 DM
- Presence of serum islet-specific pancreatic autoantibodies
- Note: About 10% are idiopathic (antibodies negative), and some patients with Type 2 diabetes DO have antibodies
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Guidelines for being sick with IDDM
- Continue usual dose of insulin when sick
- Monitor blood sugar and urine ketones closely to prevent DKA
- Ingest 45-50 g CHO every 3-4 hours to prevent DKA
- Drink more fluids than normal
- Follow insulin adjustments as per MD's recommendations
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What is recommended when a person with DM drinks alchohol? Why?
Consume CHO when consuming alcohol
- Alcohol -> AcetylCoA(not glucose)
- Alcohol metabolism requires glucose
- Insulin and alchohol both lower blood glucose
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other drugs for HTN
- ace inhibitors - angiotensin converting enzyme, restricts body's production of the chemical that makes vessels constrict ex. lotensin, vasotec, accupril, altase, prinivil, zestril
- beta blockers - reduces HR / lower force with heart s pressure,
- sympathetic nerve inhibitors - prevent certain nerves from constricting blood vessels
- vasodilators - relax muscles in walls of arteries allowing blood vessels to widen
- calcium antagonists - (calcium channel blockers) reduce HR & relax blood vessels, ex. norvasc, vacor, plendil
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digitalis
used for CHF to increase strength of contraction
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PTCA
percutaneous transluminal coronar angioplasty
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CABG
coronary artery bypass graft
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CRP
- C reactive protein
- indicator of inflammation
- good predictor of IHD (ischemic heart disease)
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dietary intake of trans fat should be less than
2 g
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saturated fats
- 4:0-12:0 - SCFA & MCFA
- 14:0 - myristic acid (milk fat)
- 16:0 - palmitic acid (animal fats / palm oil)
- 18:0 - stearic acid (beef tallow, shortening, coconut oil)
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MUF
- 16:1 - palmitoleic acid (macadamia nuts)
- 18:1 - oleic acid (oo, canola oil, avocado, almonds, dark chocolate, most common source in American diet - fr. fries, pizza...)
-does not raise LDL
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omega 6 FA
- 18:2 - linoleic acid - oils in seeds & nuts
- shoudn't exceed 10% or more of total calories
- 11-17 g/day
- polyunsaturated
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omega 3 FA
- a 18:3 - a linonlenic acid (veggies, flax seed)
- 20:5 - eicosapentaeic acid / EPA (fish oil, salmon, sardines)
- lower cholesterol & TAGs, inhibit platelet aggregation & reduce risk of sudden death
- 1.1-1.6 g/d meet needs
- oxidize easily
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How can arachadonic acid be created?
- LA, linoleic acid, can be desaturated & elongated
- conversion of 18:2 to 20:4 omega 6
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arachadonic acid
substrate for eicosanoids, some being proinflammatory (ex. prostaglandin E2 & thromboxane A2) and some being antiinflammatory (ex. prostacyclin)
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viscous fiber
- soluble
- ex. oat bran, dried beans
- lowers blood lipids
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