OME+ - Endocrine Flashcards
Diabetes
Pearls of insulin resistance (IR)
- genetically predetermined and environmentally modified
- results in hyperinsulinemia
- hyperinsulinemia is an independent predictor of ischemic heart disease
- obesity, inactivity, and carbs >60% of the diet
- increase IR related to reduced clearance of uric acid (leads to increased gout)
- polycystic ovarian disease and anovulation
- increased acanthosis nigricans found in the neck and axilla (post-puberty & YA)
- Birthweight low for gestational age contributes
- prothrombotic and proatherogenic state
Who is tested for DM2?
- test asymptomatic adults ≥ 45 every 3 years
What are the risk factors that require Sooner testing? if risk factors: physical inactivity, first degree relative with DM2; high-risk ethnic population; delivery of high birth weight baby; HTN, HDL <35; TG ≥ 250; PCOS; A1c ≥ 5.7%; severe obesity, acanthosis nigricans; CVD
What time period does HgA1c test?
- glucose trends for 90 days; best measures past 28-42 day
What value diagnoses DM?
- ≥ 6.5% is DM2 diagnosis
Prediabetes labs
IFG
- IFG 100-125 mg/dL
IGT?
- iGT 140-199 mg/dL with75 OGTT
A1C?
- A1c = 5.7-6.4%
DM Med Pearls
which medications are insulin secretagogues?
What meds decrease the plasminogen activator inhibitor?
metformin and TZD/Glitazones
When would a provider start treatment with 2 diabetic drugs?
when A1c is 1% above the goal A1c or target not achieved after 3 months
When would a provider start treatment with 3 diabetic drugs?
or target not achieved after 3 months of dual therapy.
When would a provider start basal insulin/injectibles?
- if target not achieved after 3 months of oral therapy
- At the beginning of diagnosis to achieve initial control when BS are > 250-300 mg/dL.
- when 2 insulin secretagogues have failed
What are the two medications most commonly started in a new diabetic?
metformin (biquanide) and sulfonylurea
What conditions should indicate stopping metformin even just temporarily? Why?
radiocontrast, surgery, renal impairment, HF, >80. (all affect renal function or hydration - lactic acidosis).
What medication might be ineffective during periods of hyperglycemia such as an illness?
sulfonylureas;
what diabetic medications have a risk of hypoglycemia?
Sulfonylureas and insulin
Diabetic meds that have weight gain?
Metformin, TZD/glitazones, Insulin
Benefit/MOA/SE of metformin (biguanide)
- 1-2%
- secretagogue; reduced hepatic glucose production increases skeletal muscle receptor sensitivity
- GI symptoms and lactic acidosis
Benefit/MOA/SE/common names of SU
- 1-2%
- secretagogue
- hypoglycemia
- glipizide (glucotrol); glyburide (diaBeta); glimepiride (amaryl)
Benefit/MOA/SE of TZD/glitazones
- benefit?
- MOA?
- edema, HF, fxs
- Examples?
Benefit/MOA/SE of SGLT2
- benefit?
- MOA?
- GU, dehydration
- Examples?
Benefit/MOA/SE of GLP-1
- benefit?
- MOA?
- Examples?
What must be monitored in a diabetic patient?
think physical, labs, and immunizations;
Physical:
BP, eye, feet, dental, lower extremities,
Lab:
A1c, FBG; lipid panel; urine microalbumin/creatinine; serum creatinine, EKG, Thyroid
Immunizations:
Flu, PCV23, Hep B (at time of diagnosis)
misc.
tobacco use,
what is the frequency of necessary monitoring in a diabetic patient?
Physical: BP (3-6m JNC-8 < 140/90), 1 year for all others: eye, feet, lower extremities, dental, tobacco use,
Lab: 3-6 m A1c , annual: FBG; lipid panel; urine microalbumin/creatinine; serum creatinine, initial and as needed: EKG, Thyroid
Immunizations: Flu, PCV23, Hep B (at time of diagnosis)
Heat Stroke
Obesity
What is Class I; Class II; and Class III obesity?
Class 1 30-34.9
Class II 35 -39.9
Class III > 40 BMI
What cancers are associated with obesity?
esophagus, postmeno breast, endometrium, colon, rectum, kidney, pancreas, thyroid, gallbladder
Amount of weight loss for immediate positive effects?
10%
When should a med for weight loss be discontinued?
No loss after 12 weeks.
The function of Orlistat (xenical)? when must be taken?
REduced amount of digested fat; within 1 hour of a meal
/ SE?
anal leakage and loose stool.
Qsymia (phentermine/topiramate): MOA/SE
- phentermine - the release of norepinephrine to reduce appetite and food consumption.
- topiramate-unknown. /
- must have a pregnancy test and use birth control.
Lorcaserin (Belviq) MOA/SE/concerns
- decrease food consumption and increase satiety with 5-HT2c receptors (anorexigenic neurons)
- Do not use with any med that has serotonergic properties
Contrave (naltrexone and bupropion). MOA/SE
- MOA uncertain perhaps dopamine.
- monitor for SI and depression. Do not use with bupropion, opioids or MAOIs.
- Mnt. BP and HR. so watch in pts with CVD and CVAs.
Liraglutide - GLP-1 agonist MOA/SE
- appetite regulation;
- medullary thyroid cancer; no one with family hx.
What are Meds that cause weight gain:
2nd gen antipsychotics - risperidone; olanzapine
- AED: valproate (Depakote); Carbamazepine (Tegretol)*
- Corticosteroids: prednisone, methylprednisolone*
Surgical Interventions in Obesity
indications?:
- BMI 40 or BMI 35 with a comorbid condition.
contraindications?:
- unstable mental health, active drug or alcohol abuse, poor adherence to medical advice;
Which surgery is most effective for weight loss?
gastric bypass
- SE: 5% have long term health consequences. Must have a consultation on micronutrient supplementation.
Thyroid
What does T4 do: movement, mentation, metabolism; excess T4 turns off TSH and TRH. Too little T4
A
Addisons disease
Path?: Main cause? cause not to miss?
Primary adrenal gland deficiency of cortisol and aldosterone (autoimmune- 80% or infection (TB), hemorrhage, tumors, or
Cause not to miss! abrupt discontinuation of steroids
How can you separate primary, secondary, and tertiary?
Addison disease (primary adrenocortical insufficiency) can be differentiated from secondary (pituitary failure) and tertiary (hypothalamic failure) causes because mineralocorticoids are intact in secondary and tertiary.
Presentations Acute Addisons:
- HoTN, n/v and AMS, cyanosis
- hypoglycemia
What is missing?
- cortisol and aldosterone both not being made:
Presentation for Chronic Addison:
- Orthostatic HoTN;
- hypopigmentation (excess ATCH)
- (no aldosterone) low sodium & high potassium
- weakness, fatigue, weight loss, poor appetite
Test?
for sodium, potassium, cortisol and ACTH
What is the treatment?
- 5 S’s: Salt, sugar, steroids, support, and search for a precipitating illness (usually infection, trauma, recent surgery, or not taking prescribed replacement therapy)
- Give hydrocortisone;
- fludrocortisone.)
What creates secondary adrenal insufficiency?
the pituitary gland is diseased or pt has had chronic steroids and has abruptly ended taking them (asthma, OA)
Exercise recommendations for adrenal insufficiency?
replace sodium
Bonus: onlinemeded
Test: am Cortisol. will have NONE Cosyntropin stimulus test:
NO change: adrenal gland problem ( CT adrenal gland) give cortisol and aldosterone
Increase in cortisol: Anterior pituitary problem –MRI
What can cause Cushing syndrome?
Path:
excess cortisol
Presentation/S/Sx of Cushing’s: :
HTN, DM & Obesity, moon facies with acne, truncal obesity, buffalo hump, purple striae on abd., irregular menses, muscle weakness/pain, new diabetes, HA and bone loss
Diagnostics
Low dexamethasone suppression test (failure is cushings)
ACTH is normal then adrenal tumor (CT/MRI)
ACTH is high: The high dose dexamethasone suppression therapy.
What are some endogenous and exogenous causes?
- lung tumor (small cell) that secretes ACTH
- tumor of the anterior pituitary
- taking steroids
- Cushings disease: primary tumor of the adrenal gland
Treatment for exogenous cushings?
taper steroid intake
Treatment for endogenous cushings?
Surgical resection of the ACTH producing tumor.
Treaments for endogenous cushings for individuals that can’t tolerate surgery?
mitotane, metyrapone, mefepristone