DM, Thyroid, Osteoporsis Flashcards
Type 1 diabetes
Insulin deficiency cause by beta cell destruction. Dependency on exogenous insulin for survival
Type II DM
Insulin resistance, linked to obesity. Exogenous insulin not necessary for survival but may be required as the disease progresses
Gestational DM
Glucose intolerance with onset during pregnancy
Pre - diabetic
Intermediate stage in which glucose levels abnormal but does not meet the criteria for official dx. Impaired fasting glucose and glucose intolerance
Type I symptoms
Brief period of profound symptoms : polyuria, polydipsia, polyphagia, weight loss , blurred vision / fatigue
Type II symptoms
Relatively symptom free or only subtle symptoms that may persist fir weeks months or years
Polyuria, polydipsia, blurred vision, slow healing wound, freq infection
Pre-diabetic fasting plasma glucose , oral glucose tolerance test, and HbGAiC
Fasting : 100-125
Oral : 140-199
H1C : 5.7-6.4 %
NORMAL fasting plasma glucose , oral glucose tolerance test, and HbGAiC
Fasting : < 100
Oral : < 140
H1C : < 5.7
DM fasting plasma glucose , oral glucose tolerance test, and HbGAiC
Fasting > 126
Oral > 200
H1C ; > 6.5
Management and proper treaments for DM
Nutritional therapy :
Exercise and physical activity : causes increased glucose uptake in skeletal muscle and improved insulin sensitivity ; in type II also decreases insulin resistance and increases glucose uptake into cells
Current goals : are individualized and are based on what is acceptable to the medical provider and patient while preventing acute complication and progression of chronic complication
insulin
Insulin receptor allow utilization of glucose by cells
Exogenous insulin should closely mimic endogenous insulin ( basal + bolus)
of insulin receptor mitigated by obesity and long standing hyperglycemia
Theory to administer early on in type II may reduce progression
Rapid acting insulin
Novolog , Glulisine, Lispro
Novolog
Onset : 10-20 min Peak : 1-3 hours Duration : 3-5 hours
Meal and correction
Lispro
Onset : 15-30 min
Peak L 1.5-2.5 hours
Duration : 5 hours
Meal and correction
Short acting insulin
Regular
Regular insulin
Onset : 30-60 m in
Peak : 2-4 hours
Duration : 5-8 hours
May mix with NPH, MUST be given 20-30 min before a meal
Long acting
Langues, Levemir, Teresiba
Lantus
Onset: 50-120 min
Peakless
Duration : 24 hours
Do not mix with other insulin’s . Given once daily or 12 hours apart if BID
Individualized A1C targets
A1C < 6.5 % for patient w/o cocurrent serious illness and at low hypoglycemic risk
A1C > 6.5 % for pt with concurrent serious illness and at risk for hypoglycemia
7-7.9 % : in older adults with polypharmacy and other comorbidtities
8-8.9 % - end of life
Metformin
MAO: decreases hepatic glucose production and intestinal glucose absorption : increases insulin sensitivity
Adverse: N/V/D ( take with food ) Vitamin B12 depletion
Serious adverse effects : lactic acidosis, megablastic anemia , hepatotoxicity
Pearls: hold for acute MI, CHF , surgery or CT with contrast , take extended release tablets with evening meals
Exantatide
MOA: stimulates insulin secretion, slows gastric emptying and decrease food intake
Brand name : Byetta
Adverse : n/v/d weight loss
Serious : pancreatitis , nephrotoxicity
Contraindication : IM/IV use
Pearls: use Byetta within 60 min before eating the meal
Liraglutide
MOA: stimulates insulin secretion, decreases glucagon levels
Brand name: Victoza
Pearls: may be taken at anytime of the day ( w/ or w/o meal) .
Only GLP-1 RA approved for cardiac event risk reduction
Dapaglifozin , Canagliflozin Empagliflozin
SGLT2
Oral
MOA: promotes the renal excretion of glucose
Adverse: UTI
Clinical pearls: should be taken before 1 st meal of day
Black box warning for toe and foot amputations with - Canagliflozin
Possible ASCVD risk reduction with Jardiance
Rosiglitazone and Pioglitazone
Oral
Increases insulin sensitivity and decreases hepatic glucose output
contraindication: HF and MI
Not recommended for use with insulin … may cause anovulatory women to resume ovulation
Glipizide, Glyburide and Glimepiride
Sulfonylureas
Oral
MOA: stimulates islet cells to secrete insulin, prolonged administration may reduce hepatic glucose output and improve insulin sensitivity
Clinical pearls : take 30 min before meal . Therapy may fail after 10-15 years
Normal TSH and T4 levels
TSH - .3-.52
T4 .7-1.85
Values in hyperthyroidism
TSH = low t4 = high
Values in hypothyroidism
TSH = high T4 = low
Hypothyroidism effects on the body
Brain fog, thinning hair, goiter, heart attack risk, gallstones, mental health, high blood pressure, heartburn, dry skin, weakness
Diagnosing hypothyroidism
Most times symptoms may not be present
Primary : high TSH and low T4
- after repeat —> replacement therapy with t4 should be initiated
Sub Clinical : high TSH T4 - WNL
— > replacement therapy a case by case
Goals of therapy for hypothyroidism
Amelioration of symptoms
Normalization of serum TSH secretion
Reduction in the side of goiter
Avoidance of over treatment
Treatment - hypothyroidism
Levothyroxine
MOA: de-iodinates in peripheral tissues to form T3, the active thyroid hormone
Clinical pearls: take on empty stomach , ideally 1 hour before breakfast and do not take with other medications
Monitoring: check levels 6 weeks after initial dose and increase by 12-25 mcg/day
Dose increase when : preg, weight gain, diminished absorption , increased rate of metabolism
Dose decrease : normal aging, weight loss
Pediatrics and hypothyroidism
Look for pt with slow growth patterns, decreasing school performance and delayed puberty
Pregnancy and hypothyroidism
They will need a higher dose of T4 during pregnancy to maintain normal TSH secretion
Give levothyroxine dosage should be returned to the pre-pregnancy dose
Treatment for hyperthyroidism
Symptom control : beta-blocker initiation w/ diagnosis to decrease palpitations, tachycardia, tremulousness, anxiety and heat intolerance
Decrease thyroid hormone synthesis : anti thyroid / thionamide drugs , radiodine or surgery
Thionamides
Advantages = chance of permanent remission lower initial cost
Disadvantage : requires frequent monitoring
Radioiodine
Advantage : permanent resolution of hyperthyroidism
Disadvantage : permanent hypothyroidism
Surgery
A: rapid, permanent cure
D: high cost
Treatment for significant treatment of hyperthyroidism ( older age, CV risk )
Thionamide with beta blockers followed by radioiodine or surgery
TD for mild hyperthyroidism , minimal thyroid enlargement an no orbitopathy
Radioiodine w/o thionamide pretreatment or gluccorticoid
Or
1-2 yr course of thionamides
Mild hyperthyroidism minimal thyroid englarment and milt orbitopathy
Radioiodine with glucocorticoid coverage but w/o thionamide pretreatment
Or
1-2 yr course of thionamides
Severe and moderate to severe
Surgery rather than radioiodine w/ glucocorticoid
Pregnancy hyperthyroidism
1 st = PTU
2nd and 3rd = methimazole
Methimazole > PTU with teratogencity
Heptatoxicity ; PTU > methimazole
Gestational weeks 6-10 highest incidence of birth defects
Switch to methimazole at week 16
Major clinical recommendations for osteoporosis
Assure ca .1200 and vit D 800-100 IU intake after age 50+
Weight and muscle strengthening intake
Preforms BMD females 65 + every two years
Initiate tax for BMD Y scores < 2.5
Initiate in postmenopausal with T score -1.0 and -2.5
Osteoporosis risk factors
Decrease calcium intake / vitamin D insufficieny
Immobilization
3 + alcohol drinks
Females
Low BMI
Active or passive smoking
Medication use
Medications that affect bone density
Heparin Anticonvulsants Glucocorticoid Chemo Psychotropics Narcotics Barbiturates PPI
Defining osteoporosis by BMD
Normal T = -1.0
Low bone mass : t score -1.0 and -2.5
Osteoporosis : T score at or below -2.5
Pharmacotherapy for osteoporosis
First line is bisphosphonates
Calcitonin
SERM
Fosamax
Bisphosphonates
Remain upright at least 30 min before eating, drinking or taking any other medication
Consider drug holiday after 3-5 years
Don’t use PO with comorbid GI issues
Calcitonin
Approval for women > post menopausal when alt not suitable
