Home > Preview
The flashcards below were created by user
on FreezingBlue Flashcards.
What is a normal A1c value? What is the American Diabetes Association's goal?
What is a normal blood sugar level?
Why do we need insulin?
- Glucose Regulation (stimulate glucose uptake from blood, suppress gluconeogenesis and gluycolysis)
- Fat storage regulation (prevent ketoacidosis
- Keep eyes, kidneys, nerves form getting glucose toxic
- To make sure glucose can get to other tissues (need insulin to push sugar in)
What are the s/s of metabolic syndrome? When in the clinical course of diabetes development does this happen?
- high TGs
- low HDL
- LDL often normal (but small, dense, atherogenic)
- waist > 40 in
- insulin resistance
This occurs as the pt is becoming insulin resistant
What does glucose toxicity in the tissues cause?
- peripheral neuropathy
What are the glucose levels for "pre-diabetes" for 2 hour post-glucose and fasting glucose?
- 2 hour post glucose: 140-199
- fasting glucose: 101-125
What are the fasting glucose and random glucose levels for diabetes?
- fasting Glc of 126+
- random Glc of 200 or greater with symptoms
What is A1c and what are the normal, pre-diabetes, and diabetes levels for diagnosis?
- Hemoglobin A1c is a subfraction of hgb that is glycosylated by too much glucose - it measures the last 3 months
- normal: < 5
- pre-diabetes: 5.7-6.4
- diabetes: 6.5+
What does A1c tell us about micro and macrovascular disease?
the higher the A1c, the higher the incidence of micro or macro vascular disease
What does incretin do?
- decrease appetitie
- increase gastric emptying
- (doesn't work very well in T2DM)
What does glucagon do?
increases blood sugar
Which meds are GLP-1 receptor agonists? How do they work?
- exenatide and liraglutide
- stimulate insulin release and inhibit glucagon release
Which meds are DPP-4 inhibitors? How do they work?
- sitagliptin and saxagliptin
- inhibit the breakdown of GLP-1 (so keep incretin from being inactivated)
- decrease glucose
Give examples of thiazoladinediones. What is their main activity? Name some of their SEs.
- Actos and Avandia (-glitazones)
- they increase insulin sensitivity
- peripheral edema (leading to CHF) and weight gain
If a pt is experiencing hypoglycemia, how much glucose should be given?
about 15 g (3-4 glucose tabs)
s/s of hypoglycemia
- mood changes - crying
- tingling around the mouth
- difficulty paying attention
After having a hypoglycemic episode, when should a pt recheck their blood sugar?
- 15 to 20 minutes after treatment
- retreat if necessary
s/s of hyperglycemia
- increased thirst
- freq urination
- weight loss
- blood glucose > 180 mg/dL
- vaginal and skin infx
- slow healing cuts and sores
- nerve damage causing painful cold or insensitive feet, hair loss on lower extremities, ED
- chronic constipation or diarrhea
What is the development/time course of Type 2 diabetes?
- Insulin resistance: extra fat, liver makes more glucose, pancreas makes more insulin, BG stays normal
- Pancreas cannot make extra insulin anymore: BG is high sometimes; sx like urinating more, tired, thirsty
- Pancreas no longer makes normal insulin: BG is always high, worse sx, T2DM diagnosed
Physiologic difference in DM between kids and adults
- insulin sensitivity is diff in kids - related to sexual maturity
- physical growth
- ability to provide self-care
- unique neurologic vulnerability to hypoglycemia
- care plans must include family dynamics, developmental stages
Name 3 ways that insulin therapy can be implemented in a child with Type I diabetes
- 1. Split-Mixed (short acting + NPH); 70/30
- 2. Basal Bolus
- 3. Continuous Subcutaneous Insulin Pump (CSII)
Describe how Split-Mixed insulin therapy is given
- 2/3 given in AM, 1/3 in PM.
- In AM, 1/3 is short acting and 2/3 is NPH.
- In PM it is 50/50.
- Not recommended post-honeymoon.
Describe how BB insulin is given
- rapid acting + long acting (glargine or detemir)
- at least 4 injections/day
- Pre-meal rapid acting dose is based on current BG, anticipated carb intake, atnicipated level of physical activity
- Inject with meals and snacks
- Can dose post-prandially in toddlers because it's hard to know how much/what they're going to eat
Describe CSII insulin dosing
- continuous subcutaneous insulin pump
- requires carb counting
- must test 4-6 x/day and bolus
- adult supervision and support needed
- most often in pre-teens and adolescents
Describe the dosing when implementing insulin therapy in a child with Type 1 DM
- 0.5 - 1 units/kg/day or less during honeymoon
- usually 1 unit/kg/day
- during puberty up to 1.5 units/kg/day because of increased insulin resistance, growth hormone, and sex hormones
What is the honeymoon phase in Type I diabetes?
the phase where the disease has been diagnosed and insulin therapy has been started, but not all the beta-cells have been destroyed yet
Plasma BG and A1c goals for T1DM by age group
- < 6 years: before meals 100-180; bedtime/overnight 110-200; A1c < 8..5 and > 7.5; rationale is that they are high risk and vulnerable to hypoglycemia
- 6-12 years: before meals 90-180; bedtime/overnight 100-180; A1c < 8 ; rationale is their risks of hypoglycemia and relatively low risk of complications before puberty
- 13-19 years: before meals 90-130; bedtime/overnight 90-150; A1c <7.5; rationale is their risk of hypoglycemia and developmental and psych issues
What ethnicity is at highest risk for Type2DM?
native american > asian > black > hispanic > white
What are the ADAs screening recommendations for Type 2 DM?
- begin @ puberty or 10 year old, whichever is less
- when BMI is >/= 85th percentile plus two of the following: family hx in 1st or 2nd degree relative, non-white race, signs of insulin resistance (acanthosis nigricans, PCOS, HTN, incr lipids)
Goals of treatment for T2DM in kids
- physical and psychological well-being (prevent ketosis, hyperglycemia, infx)
- glycemic control - euglycemia or A1c < 7%
- prevention of micro and macro vascular disease complications
In treating T2DM, what must be used with severe hyperglycemia or ketosis?
Algorithm for treatment of pediatric T2DM
- after diagnosis of T2DM
- if mild hyperglycemia (FBG < 150; 2h OGTT < 300) do diet and exercise for 3-6 mo then if FBG is < 100 and A1c < 6% consider success, if not then go to metformin x 3-6 mo. If metformin unsuccessful add another agent like sulfonylurea, TZD, glitinide, alpha-glucosidase inhibitor
- if severe hyperglycemis (FBG > 150; 2h OGTT > 300) if the BG is > 350 or diabetic ketoacidosis give insulin until stable. if not then do metformin for 3-6 mo. if unsuccessful add another agent (listed above)
How do biguanides work? Name one.
- inhibit gluconeogenesis
- improve insulin sensitivity
- decrease intestinal absorption of glucose
How do secretagogues work? Name some.
- stimulate insulin secretion from pancreatic beta-cells
- Sulfonylureas - glyburide, glipizide, glimipiride
- Meglitinides - repaglinide, nateglinide
How do DPP-4 inhibitors work? name some.
- inhibit GLP-1 and GIP from inactivating incretin
- increase insulin secr from pancreas
- decrease secretion of glucagon
Which diabetes med classes are PPAR modulators?
- Alpha Glucosidase inhibitors
MOA of thiazolidinediones and name some
- increase insulin sensitivity by modulating PPAR-gamma
- decrease glucose output
MOA of alpha glucosidase inhibitors and name some
- slow the conversion of polysaccharides into glucose
- inhibit carb absorption in intestine
Which diabetes med classes work on the pancreas?
- DPP-4 inhibitors
- they increase insulin secretion
Which diabetes med classes work on the liver?
- DPP-4 inhibitors
- they decrease gluconeogenesis
Which diabetes med classes work on the GIT?
- alpha glucosidase inhibitors
- they decrease glucose absorption
Which diabetes med classes work on muscle and fat?
- they increase glucose uptake
What is metformin's place in diabetes therapy?
it is first line - especially in obesity and hyperlipidemia
Treatment algorithm from ADA for diabetes
- Lifestyle + metformin
- then add either basal insulin or sulfonylurea
- if sulfonylurea was added first, can add the basal insulin next
- then add intensive insulin
What diabetes meds should not be used in pts with renal impairment?
- no metformin if SCr is >/= 1.4 in women or 1.5 in males
- No sulfonylureas in severe renal or hepatic impairment (no glyburide if CrCl < 50; no glipizide if CrCl < 10)
- renal dose adjustment needed with Dpp-4 inhibitors
- no alpha-glucosidase inhibitors if SCr > 2
Which diabetes meds have severe GI SEs?
- metformin (go away in a few weeks)
- alpha glucosidase inhibitors (CI's in IBD)
What must be adjusted if a pt is taking a secretagogue and a DPP-4 inhibitor?
the secretagogue dose should be decreased by 50%
Which oral diabetes meds are CI'd in class III-IV CHF? Which is CI'd with decreased perfusion?
What effect on weight do the various oral diabetes meds have?
- sulfonylureas and TZDs cause gain
- metformin causes loss (or is weight neutral)
- if pt has metabolic syndrome or non-alcoholic fatty liver disease, use TZDs
Which oral diabetes meds are CI'd in T1DM?
How are the oral diabetes meds dosed?
- Metformin is 500 mg bid-tid
- Sulfonylureas 1.25 -10 mg qd -bid
- TZDs 2-45 mg qd-bid
- alpha glucosidase inhibitors 25-100 mg qd, then bid, then tid
What values need to be monitored with which oral diabetes meds?
- FBG and A1c with all
- PPBG with alpha-glucosidase inhibitors
- Renal fxn with metformin, sulfonylureas, DPP-4 inhibitors
- LFTs with TZDs and alpha glucosidase inhibitors
Which oral diabetes med do you need to take a multivitamin with and why?
metformin because it causes malabsorption of B12 and folic acid
Can sulfonylureas be used in patients with sulfa allergies?
What other meds need to be monitored if taken with nateglinide? Why?
- phenytoin, furosemide, metformin
- because of plasma protein binding
What is the MOA of insulin?
- stimulate entry of glucose into cells
- promotes storage of glucose as glycogen in muscle and liver cells
What meds are also known as incretin mimetics? What is their MOA?
- GLP-1 agonists (exenatide, liraglutide)
- stimulate glucose dependent insulin secretion
- inhibit glucagon release
- slow rate of gastric emptying and increase satiety
What is the MOA of pramlintide?
- It is an amylin agonist
- it decreases PPBG and glucagon secretion
- it increases satiety
What is the different onset, peak, and duration of action of the various forms of non-oral diabetes therapies (insulin)?
- rapid acting: onset 5-15 min; peak 30-90 min; duration < 5 hours
- short acting: onset 30-60 min; peak 2-3 h; duration 5-8 hours
- intermediate acting: onset 2-4 h; peak 4-10 h; duration 10-16 h
- long acting: onset 2-4 hours (detemir), 3-8 h (glargine); no peak; duration 12-24 h (detemir), 20-24 h (glargine)
Which insulin products are rapid acting?
Which insulin is short acting?
Which insulin is intermediate acting?
Which insulin products are long acting?
What is the place in therapy of basal insulin?
- used with orals
- can use NPH, glargine, or detemir
- adjust based on fasting BG
What is the place in therapy of intensive (basal-bolus) insulin? Describe this type of dosing.
- always begin with basal - don't start bolus without having basal on board
- usually 50:50
- don't combine with secretagogues (sulfonylureas and meglitinides) d/t risk of hypoglycemia.
- for bolus, use rapid acting insulin (aspart, lispro, glulisine)
- consists of a mealtime dose + a correction factor (can be a set amount or can be an insulin to carb ratio if the pt is carb counting)
Which insulin product should look cloudy?
What is the correction factor for bolus insulin dosing?
- it accounts for pre-meal hyperglycemia
- this is NOT a sliding scale
- since we are adding it to the mealtime dose (before the meal) it is proactive. Sliding scales are reactive.
When do patients need to self monitor their blood glucose when on BB dosing?
- fasting in the AM
- 2 hour post prandial or HS
- usually about 4-6 x/day - depends on control
Can GLP-1 receptor agonists be combined with oral diabetes meds? Why or why not?
- no because increased hypoglycemia risk
- can give with metformin
What is pramlintide's place in therapy?
it is only dosed with bolus insulin
What is the goal for FBG?
How is basal bolus insulin adjusted?
- if fasting BG is high, adjust HS basal dose
- if 2 hr post prandial is high, or the pre-meal pre-prandial is high, adjust the dose at the previous meal
what BG level is considered hypoglycemia? what is the treatment?
Counseling points for GLP-1 agonists
- cause weight loss
- cause hypoglycemia when mixed with orals
- take exenatide 60 min before AM and PM meal to decrease GI SEs
- take liraglutide w/o regard to meals
- BBW on liraglutide - risk of thyroid c-cell tumors
What is the BBW on liraglutide?
risk of thyroid c-cell tumors
what is the BBW on pramlintide?
increased risk of insulin-induced severe hypoglycemia
Explain the normal physiology of erection
- smooth muscle cells in corpora cavernosa relax
- sinusoids engorge with blood
- penis swells
- expanding sinusoids compress subtunical venous plexus
What is the role of ACh in erection physiology?
- increases NO production
- increased guanylate cyclase activity
- increased conversion of cGTP to cGMP
- decreased intracellular calcium conc in penis
- smooth muscle relaxation
- increases adenyl cyclase
- conversion of cATP to cAMP
- decreased intracellular calcium conc in penis
- smooth m relaxation
Explain the pathophys of erectile dysfxn
- insufficient relaxation of sm muscle cells
- decreased sinusoid compliance
- tunical degeneration
- all 3 of the above lead to insufficient compression of the subtunical veins leading to ED
Name 3 organic causes of ED
- vascular (PVD, HTN, ateriosclerosis)
- neurologic (stroke, spinal cord injury, diabetes)
- hormonal (hypogonadism)
Name some oral phosphodiesterase 5 inhibitors (PDE5) and their MOA
- MOA: increased cGMP leading to sm. m. relaxation (PDE usually breaks down cGMP)
What drugs are first line therapy for ED?
What meds are used for intrapenile therapy for ED and what is their MOA?
- intra-urethral - alprostadil
- intercavernous vasoactive injection - alprostadil, papaverine, phentolamine
- They are vasodilators identical to prostaglandin E1 that lead to smooth m. relaxation
Name 2 non-pharmacological therapies for ED
- vacuum constriction devices
- penile prosthesis implantation
What percentage of ED cases are d/t drug related causes? What are some of these drugs?
- H2 antagonists
- recreational drugs - alcohol
What is the indication for testosterone replacement for treatment of ED and what is the MOA?
- correction of hypogonadism in pts with low testosterone levels
- MOA is direct stimulation of androgen receptors (may stimulate NO synthase)
Why is testosterone not given orally?
- extensive 1st pass hepatic metabolism
- alkylated derivatives have improved bioavailability but are assoc with a higher incidence of hepatotoxicity
What are the regimen and counseling points for PDE5 inhibitors?
- CI'd with nitrates
- need sexual stimulation
- take sildenafil on empty stomach
- take sildenafil and vardenafil 30-60 min before intercourse
- take tadalafil 2 h before intercourse
- sildenafil is the only agent studied in severe hepatic impairment
- tadalafil's duration is up to 36 hours
What are some SEs of PDE5 inhibitors?
- facial flushing, nasal congestion, HA, dyspepsia (d/t peripheral vasodilation)
- visual SEs - blue haze (d/t XR with PDE6 - only sildalavil and vardenafil)
- decreased BP
- priapism (highest risk with tadalafil)
- increased MI risk
- QT prolongation (vardenafil)
- myalgias (tadalafil d/t XR with PDE11)
Which drugs have the highest priapism potential of all ED treatments?
intercavernous vasoconstrictive drug injection (alprostadil, papaverine, phentolamine)
What are the 5 characteristics of metabolic syndrome?
- 1. abdominal obesity (men > 40 inch waist; women > 35 inch)
- 2. TG > 150
- 3. HDL < 40 in men; < 50 in women
- 4. increased BP
- 5. insulin resistance
What are 5 risks for CV complications in the diabetes patient?
- 1. smoking
- 2. HTN
- 3. dyslipidemia
- 4. hyperglycemia
- 5. thrombus formation
- and immunization status
What is the BP goal in diabetes pts to decrease CV risk? When should therapy be initiated?
- < 130/80
- 130-139/80-89 do lifestyle modifications x 3 month
- 140+/90+ do lifestyle mods + pharmacotherapy
Which HTN meds have renal protection properties for diabetes pts?
ACEs and ARBs
Which antihypertensives can be used in pregnancy? Which should not?
- methyldopa, labetalol, diltiazem, clonidine, prazosin
- NOT ACEs and ARBs
What are the lipid goals in diabetes pts?
- LDL < 100 (this is the focus in DM pts)
- HDL > 40 for men and > 50 for women
- TG < 150 (high TG often indicates uncontrolled DM)
What is the DOC for dyslipidemia in diabetes pts?
In a diabetes pt when should statin therapy be started regardless of the pt's LDL?
- if they have overt CVD
- if they are over age 40 and have one or more CV risk factor or under 40 with multiple risk factors
- risk factors are HTN, family hx of CVD, smoking, dyslipidemia, albuminuria
When do we use antiplatelet treatment in diabetes pts?
- primary prevention - to prevent 1st CV event
- secondary prevention - to decrease morbidity and mortality in pts with previous CV event
- secondary is more effective b/c there's higher risk of a 2nd event than a 1st
When is ASA indicated for prevention of thrombus formation in diabetes pts?
- for anyone with personal hx of CVD or
- if their 10 year framingham risk is > 10%
- this usually includes med > 50 and women > 60 with one or more of these - HTN, fam hx of CVD, smoking, dyslipidemia, albuminuria
- not recommended for pts < 21 y.o.
- can add clopidogrel for the 1st 12 mo post event, or if pt is ASA intolerant
What are the BP goals for a pregnant diabetes pt?
If CVD is established in a diabetes pt, what meds should the pt be on?
- Post MI - beta blockers for 2 years
- NO thiazolidinediones
- metformin is ok if stable CHF and normal renal fxn
What are the immunization recommendations for diabetes pts?
- influenza for all pts over 6 months of age
- pneumococcal one time once a pt is older than 2 y.o. , then revaccination at age > 64 years (if they were less than 65 when they got the original vaccination and it has been at least 5 years since the original vacc.)
What is the #1 cause of renal failure and dialysis?
Screening for diabetic nephropathy
- random spot test for albumin (albumin:SCr ratio) - once a year
- SCr - get checked yearly - to estimate GFR; normal is < 30, microalbuminuria is 30-299, macroalbuminuria (aka proteinuria) is 300+
Screening for diabetic neuropathy
- Sensory neuropathies - painful or loss of sensation
- monofilament test - tests for loss of sensation (testing for vibration and temperature increases the sensitivity of the monofilament test)
- diabetic foot exams - annually
- autonomic neuropathy d/t loss of vagal stimulation
What is the DOC for diabetic nephropathy?
- ACE inhibitors (they are renoprotective) - should use in all pts with microalbuminuria
- ARBs are good for pts who get the ACE cough
- ACE + ARB is superior to monotreatment in decreasing the progression of renal disease
What meds should be used for diabetic nephropathy?
- ACEs and ARBs
- Non-DHP CCBs (verapamil and diltiazem)
- Do not use DHP CCBs (amlodipine)
What meds can be used for diabetic neuropathy?
- these drugs are to treat painful neuropathies
- TCAs (most data and most effective)
- gabapentin or pregabalin - must do renal adjustments
What meds are used to treat gastroparesis in diabetes pts?
What is used to treat retinopathy in the diabetes pt?
- no vitamin E
- laser photocoagulation is best to prevent blindness
What are SEs of nephropathy meds used in DM?
- ACEs - hyperkalemia, cough
- ARBs - hyperkalemia
What are SEs of drugs used to treat diabetic neuropathy?
- TCAs: decrease nerve conduction speed, anticholinergic, weight gain, QT prolongation
- Carbamazepine: (autoinduction) aplastic anemia, CNS effects
- Valproate: (old fat bald alcoholic) weight gain, tremor, alopecia, increased LFTs, increased ammonia, libido loss
- Gabapentin and Pregabalin: sedation, blurred vision, weight gain
- Duloxetine: dry mouth, fatigue, HA
What are SEs of drugs used for gastroparesis in DM?
- Metoclopramide: facial spasms, EPSEs, depression, BBW for tardive dyskinesia
- Erythromycin: rash, cramps
What is the MOA of erythromycin in diabetic gastroparesis?
Motilin receptor agonist (this receptor is present in about 50% of people)
What are the normal ranges for thyroid lab values?
- TSH 0.5-4.7
- free T4 0.8-1.8
- total T4 4.5-10.9
- total T3 60-181
s/s of hypothyroidism
- pale cool skin, decreased sweating
- cold intolerance
- brittle hair
- facial puffiness
- constipation, lethargy, decreased deep tendon reflexes
- increased TGs and TC
- impaired memory fxn, confusion
- women often infertile
- weight gain
s/s of hyperthyroidism
- warm skin, excess sweating
- heat intolerance
- fine, thin hair
- palpitaitons, tachycardia
- increased appetite and weight loss
- frequent bowel movements
- nervousness, emotional lability
If a pt is hypothyroid, which of their lab values are increased or decreased? Hyperthyroid?
- Hypothyroid: TSH is high and T3 and T4 are low
- Hyperthyroid: TSH is low and T3 and T4 are high
When is therapeutic treatment appropriate for subclinical hypothyroidism and hypothyroidism in pregnancy?
- Subclinical hypothyroid: TSH high, freeT4 normal. Treat if TSH > 10.
- Pregnancy: requires treatment. Goal TSH is < 1 and normal T4
How is levothyroxine therapy initiated?
- 50 mcg x 1 mo then increase to 100 mcg in healthy pt
- 25 mcg x 1 mo then titrate up by 25 mcg in CVD or elderly
- normal maintenance dose is 1.7mcg/kg/d
What is the normal maintenance dose of levothyroxine?
What meds must be adjusted when a pt is being treated with levothyroxine?
What needs to be separated by 4 hours from a levothyroxine dose? Why?
- aluminum hydroxide
- because of absorption issues
What values should be monitored after initiating levothyroxine and when? What is the goal?
- TSH and T4 q 6 weeks after induction
- should be at steady state in about 8 weeks
- goal TSH is 0.5-2.5
How is hyperthyroidism treated?
- radioactive iodine
- antithyroid meds - thioamides (MMI and PTU)
- adjuncts to treat symptoms - propranolol, clonidine, diltiazem
Compare and contrast the thioamides used in treatment of hyperthyroidism
- MMI - methimazole
- PTU - propylthiouracil
- MMI is more potent, but has inconsistent absorption
- PTU has more predictable absorption - preferred in pregnancy
- both are dosed TID
Name 2 meds that contribute to thyroid disorders
How is BMI calculated?
(weight in pounds x 703)/height in inches2
What are the BMI values for underweight, normal weight, overweight, obesity, and extreme obesity?
- underweight < 18.5
- normal weight 18.5-24.9
- overweight 25-29.9
- obesity class I 30-34.9
- obesity class II 35-39.9
- extreme obesity >/= 40
What are some appropriate dietary goals and exercise goals for the treatment of obesity?
- decrease of 10% in 6 mo
- 1-2 lb loss/wk
- decrease 500-1000 cal/d
- increase exercise gradually
- 30 min + of moderate intensity, most all days of the week
When is pharmacologic treatment approved for obesity?
if BMI > 30 or BMI > 27 + risk factors (HTN, dyslipidemia, CHD, T2DM, sleep apnea)
What meds are used for pharmacologic treatment of obesity? What are their MOAs? How are they dosed? How long can they be used?
- orlistat - blocks the absorption of fat - 60-120 mg TID with food - long term use
- phentermine - enhances norepi and dopamine neurotransmission - 8 mg TID with food - short term use (3 mo)
SEs and counseling points for orlistat
- SEs - oily spotting, stool, evacuation; fecal urgency; incontinence; increased defecation, etc.
- SEs may decrease after 1-4 weeks on the med
- Need to take a fat soluble medicine 2 hours before or after dose
- Eat low fat meals to avoid SEs
- don't use if meal has no fat
- use with diet and exercise
SEs of phentermine
insomnia, increased BP, palpitations, arrhythmias
What herbals are commonly used to lose weight? How do they work? Which show efficacy?
- Increase energy expenditure: ephedra, hoodia, caffeine
- Carb metabolism: chromium
- Increase satiety/inhibit digestion: fiber, chitosan, guggul
- Increase fat oxidation or decrease fat synthesis: hydroxycitric acid, camellia sinesis, acai
- Ephedra decreases 0.9 kg/mo
- limited efficacy shown for chitosan
- contradictory evidence for hydroxycitric acid
- no efficacy shown or no data for the rest
Which herbal products are probably the best for losing weight safely?
fiber > hydroxycitric acid > chromium > acai > green tea (camellia) > caffeine > ephedra
When is bariatric surgery approved?
BMI > 40 or > 35 with risk factors
Suggested supplements for after bariatric surgery
- high potency multivitamin with 100% DV of at least 2/3 of needed nutrients (gastric banding pts); 200% for gastric bypass pts
- 50-100 mg elemental iron (ferrous sulfate not well absorbed - use diff salt form)
- 1500-2400 mg calcium + vitamin D
- 350-500 mcg B12
- 20-100 B1
- other fat soluble vitamins - D, A, K
Considerations after bariatric surgery
- don't get pregnant for 18 months post-op
- initially use liquid preps of meds (for 3-8 weeks post-op)
- Monitor meds with narrow TIs
- May need to decrease dose of antihypertensives and antidiabetic meds
What meds should be used with caution or avoided after bariatric surgery?
- NSAIDs, salicylates, corticosteroids
- oral bisphosphonates
- ER or CR products
- Products with sucrose, fructose, maltose, lactose, honey, mannitol, sorbitol
- meds that increase weight gain
- meds assoc with gallstones (e.g. gemfibrozil)
What are some of the risks to mom and baby if good glycemic control is not maintained during pregnancy?
- spontaneous abortion
- fetal malformations
- macrosomia ---> risk for C-section
- risk of neonatal hypoglycemia, jaundice, polycythemia, and hypocalcemia
- risk of future obesity and diabetes
- retinopathy in mom
- decrease in mom's kidney fxn (esp if SCr is > 3)
What percentage of pregnancies in women with DM are unplanned? What 2 counseling points are essential for women with DM of child-bearing age?
- 2/3 are unplanned
- 1. counsel re fetal malformations
- 2. use of effective contraception
What meds should be d/c'd prior to conception in DM pts?
- ACEs, diuretics, beta-blockers
- stop oral hypoglycemic agents and switch to insulin
What are preconception goals for glycemic control? How long should a woman be at these goals prior to stopping contraceptives?
- preprandial: 80-110
- postprandial: < 155
- A1c: < 5%
- want euglycemia!
Monitor A1c q 1-2 months and consider attempting conception when stable - should be at goal for at least 2-4 mo
What complications of DM require special consideration in the woman with DM contemplating pregnancy?
- retinopathy: may increase during preg
- HTN: complicates preg and DM
- nephropathy: pregnancy may exacerbate (esp in SCr > 3)
- neuropathy: gastropariesis, urinary retention, orthostatic hypotension
- CVD: untreated can increase mortality in preg
What is GDM? When a Type 1 pt becomes pregnant do they have GDM? Could a pt with GDM be an undiagnosed T2DM pt?
- GDM is gestational diabetes mellitus. Any degree of Glc intolerance with onset or first recognition during preg.
- Does not include T1DM
- A pt with T2DM could be found out this way and it would be considered GDM
Women @ high risk for GDM should undergo glc testing ASAP. What 4 factors palace a woman at high risk of GDM?
- 1. obesity
- 2. hx of GDM
- 3. strong family hx of GDM
- 4. glycosuria
Women at average risk should undergo testing at how many weeks of gestation?
Women at low risk of GDM require no glc testing in pregnancy. What characteristics put a woman in this category?
- < 25 y.o.
- normal pre-preg weight
- no known DM in 1st degree relatives
- no hx of abnormal Glc tolerance
- no hx of poor OB outcome
For the average or high risk pt who requires screening but has a normal fasting or casual plasma glucose, what are the 2 approaches for glucose tolerance testing?
- 1. Perform OGTT (100 g oral load and fasting 1,2, & 3 hour postprandial Glc checks)
- 2. 50 g GCT with 1 hr post prandial with those who fail going on to take an OGTT to confirm
name 7 obstetric and perinatal complications assoc with GDM
- 1. fetal macrosomia
- 2. post partum neonatal hypoglycemia
- 3. post partum neonatal jaundice
- 4. post partum neonatal polycythemia
- 5. post partum neonatal hypocalcemia
- 6. maternal HTN
- 7. c-section
What are the long-term risks to the mother with GDM and her child after pregnancy?
- risk of obesity and DM in adolescents
- increased risk of T2DM later in the mother
When MNT fails to reach maternal glycemic goals during pregnancy, insulin therapy should be started. What are these glycemic goals?
- FBG </= 105
- 1 hour PP </= 155
- 2 hour PP </= 130
For a pt who had GDM in the post partum period assuming glucose levels are now normal, how often should we recheck the glycemic status? Does that differ from pts with IFG of IGT post partum? What meds should be avoided in pts with a hx of GDM to prevent development of glucose intolerance/DM?
- check glycemic status at least 6 wk post delivery and q 3 years after that
- women with post partum IFG and IFT should be checked annually and be on a diet and exercise regimen
- avoid corticosteroids and high-dose niacin (would tip pt toward Glc intolerance)