|Rapid and Short Acting Insulin: 5-10 minute|| Lispro (humalog) and Aspart (Novolog)|
For quick glucose untilization before a meal
|Intermediate Acting Insulin: 1/4 - 2 hours|| Neutral Protamine Hagedorn (NPH) and Lente|
Usually mixed with a SA insulin, taken at bedtime
|Long Acting Insulin: 4-8 hr onset and lasts 24 hours||Ultralente, Glargine (Lantus), and Detemir (Levemir)|
|Interpret the following labs: Fasting Blood Glucose of 112 on Day 1 and 116 on Day 2.|| Impaired Fasting Glucose = Prediabetes|
|Interpret the following labs: Fasting Blood Glucose of 145 on Day 1 and 152 on Day 2.|| Impaired Glucose Tolerance = Diabetes|
|What are the 4 aspects of Syndrome X/ Metabolic Syndrome?||HTN, Dyslipidemia, DM, and Obesity|
|Metabolic Syndrome Requirements: Abdominal Obesity Waist Circumference|| Men > 40 in|
Women > 35 in
| Metabolic Syndrome Requirements: |
Triglycerides and Cholesterol
| TGs > 150|
HDL Women < 50
HDL Men < 40
| Metabolic Syndrome Requirements: |
| Metabolic Syndrome Requirements: |
|What is a catecholamine-secreting tumor in the medulla of adrenal glands?|| Pheochromocytoma|
* Common with HTN crisis = HALLMARK
|Pt presents with HA, diaphoresis, palpitations, and severe HTN. She also has cafe au lait spots. What dx are you suspecting? What is your next step?|| Pheochromocytoma|
Dx = 24 hour urine for creatinine, total catecholamines, vanillylmandelic acid and metanphrines
|What DM Type II drug class reduces hepatic glucose production and can be used as a first or second line agent? It helps increase weight loss and decrease TGs, and is therefore first line in obese patients. It is CI in renal and hepatic insufficiency, as well as CHF. Insulin must be present (secreted) to work.|| Biguanides|
* Less common hypoglycemia AE
|What hypoglycemic drug class for DM Type II delays absorption of carbohydrate from the intestine, thereby decreasing glucose in the bloodstream?|| Alpha-Glucosidase inhibitors|
Acarbose and Miglitol
|What DM Type II hypoglycemic agents work by stimulating insulin secretion? They are associated with weight gain and increased risk of hypoglycemia, because insulin secretion is stimulated even when glucose uptake is not needed.|| Sulfonyureas|
Glipizide, Glimerpiride, and glyburide
* Glimepiride is safe with Metformin and insulin and Heart Disease
|What DM Type II drug class sensitizes peripheral tissues to insulin and may be used alone or in combination with sulfonylureas, biguanides, and insulin? They reduce glucose without increasing the risk for hypoglycemia but are CI in patients with CHF. Insulin must be present to work.|| Thiazolidinediones|
Glitazones... pioglitazone > rosiglitazone (heart disease/ stroke)
|What diabetic drug class stimulates glucose-dependent insulin release by slowing gastric emptying and preventing glucagon release after meals? Modest weight loss, must be injected. CI in patients with gastroparesis.|| Incretin Mimetics|
Exenatide (Byetta) and Liraglutide (Victoza)
|What diabetic drug class degrades GLP-1 and glucose-dependent insulinotropic peptide (GIP) that destroy incretin (hormone that stimulates insulin secretion)?|| Dipeptidyl Peptidase IV Inhibitors (DPP-4)|
Sitagliptin and Saxagliptin
|What is the TOC for phenochromocytoma?|| Surgical Resection|
ALPHA Blockers before BB prior to surgery!!
|What is the MC pituitary tumor?|| Adenoma... Prolactinoma|
* Sx - Vision changes for any type of tumor since the optic chiasm is so close, prolactin specific =
Women: oligomenorrhea, amenorrhea, galactorrhea, infertility
Men: hypogonadism, decreased libido, gynecomastia, infertility
|What hormones does the Anterior pituitary secrete? Posterior?|| GH, Prolactin, FSH, LH, TSH, ACTH|
|How do you dx a pituitary tumor?||MRI = Study of choice... CT if MRI is CI or unavailable.|
|What 2 drugs can help decrease the sx of a prolactinoma?|| 1) Cabergoline|
Surgery Indications: CSF leak due to tumor, CN deficit, HA, Visual field deficit
|What is the MCC of Cushing's SYNDROME?|| Long exposure to increased levels of exogenous glucocorticoids (steroids)|
* Can also be caused by endogenous glucocorticoid overexposure.
|What is the MCC of Cushing's DISEASE?|| Excess secretion of ACTH by the pituitary|
* ACTH ectopic tumors like Oat Cell Lung tumors also cause Cushing's Disease
|T or F: Cushing's DISEASE is the MCC of ENDOGENOUS Cushing's SYNDROME|| True|
PANCE book pg. 199
| Which of the following is not a sign or symptom of Cushing's Syndrome?|
B) Buffalo Hump
C) Acanthosis Nigricans
D) Central Obesity
E) Purple Striae
| C) Acanthosis Nigricans... Sx of DM|
Thinning skin is also a sign.
* Labs = increased serum and urine cortisol levels and lack of normal dexamethasone depression
|How do you dx Cushing's Syndrome/ Disease?|| Dexamethasone Suppression Test|
* LOW ACTH with NO Cortisol Suppression = Primary Cushing's Syndrome
* Normal to high ACTH with NO Cortisol Suppression = Ectopic ACTH Cushing's Disease
* HIGH ACTH with Cortisol Suppression by HD Dexamethasone = Cushing's Disease
|What is the MCC of an adrenal crisis?||Patients on steroids who stop taking them without weaning off of them.|
|What is a chronic corticosteroid insufficiency?|| Addison's Disease|
* MC is an autoimmune destruction of the adrenal cortex
** Hypotension, acute pain (abdomen, low back), vomiting, diarrhea, dehydration, and altered mental status. Can be fatal.
| Giantism = _______ GH prior to puberty/growth plate closure.|
Acromegaly = excessive GH (IFG-1) ____ puberty.
* Tx = Pituitary tumor removal, Octreotide, Dopamine agonists
|What is the key to dx of acromegally?||IGF-1: An inability to suppress serum GH level during GTT is key dx.|
|What is the best indicator of DM glucose control?|| Hb A1C|
Normal = 4-5.6% for non-DM
Pre-DM/ Risk of = 5.7-6.4%
DM = 6.5%
GOAL for DM patients is < 7%
|2 hour GTT and Random plasma glucose of > _____ on 2 occasions is dx for DM.||200|
|Patho for DM Type 1: ↑ Plasma glucagon, Pancreatic ____ cells fail to respond, Autoimmune dz, Most islet cell antibodies directed against GAD w/in pancreatic B cells, Damage from infectious/Viral/Environmental agent, Vitamin D may prevent.||Beta|
| Dawn Phenomenon: Normal tendency of glucose to rise in early morning due to nocturnal spikes in _ _ causing insulin resistance.|
________ Phenomena: Nocturnal hypoglycemia followed by increase in fasting plasma glucose w/increase in ketones leading to Reactive Hyperglycemia.
|What is amylin?|| A hormone that slows gastric emptying.|
* Pramlintide Acetate (Symlin): Synthetic analogue of human amylin which slows gastric emptying, suppresses postprandial glucagon secretion, Causes less insulin use and leads to reduction in body wt.
|What is the MCC of hyperthyroidism?||Grave's Disease = autoimmune disorder in which autoantibodies attach to TSH receptors and stimulate thyroid hyperfunctioning.|
|What is the cornerstone of DM Type 2 management?||Lifestyle changes with weight loss... sometimes weight loss will reverse DM Type 2.|
|What is the MC complication of DM Type 2?|| Neuropathy (paresthesias, numbness, pain, especially in the feet), + PVD ulcers.|
Retinopathy and nephropathy are also common. Keep BP undercontrol with ACE-I and ARBs.
| Grave's Disease symptoms include all of the following except:|
A) Peripheral Edema
B) Pretibial myxedema
E) All of the above are sx of Grave's Disease.
| A) Peripheral Edema|
Pernicious Anemia and DM are also common with Grave's Disease.
* Tx = Propanolol, Thioureas (Methimazole, Propylthiouracil), Radioactive Iodine
|What mineral is needed for proper thyroid function?|| Iodine|
If Iodine is not present in the diet, then T3 and T4 cannot be produced, causing hypothryroidism and a goiter.
|What is the appearance of a pituitary adenoma after bilateral adrenalectomy for Cushing's Syndrome?|| Nelson's Syndrome|
The (-) feedback of fortisol is eliminated, so ACTH and MSH (melatonin Stimulating Hormone) greatly increase = hyperpigmentation
|A female patient presents with hyperpigmentation of the sun exposed areas. She also has fatigue, hyporeflexia, weight loss, and thin axillary and pubic hair. What is your suspected dx? What labs will you order? How do you definitively dx?|| Addison's Disease|
Labs: ACTH/MSH, aldosterone, cortisol, glucose
Dx = Rapid ACTH stimulation test where no change = Positive
|What electrolyte imbalances will you find with Addison's Disease?|| Hyponatremia and Hyperkalemia from lack of aldosterone.|
Hypoglycemia from decreased cortisol.
|How do you treat Addison's Disease?|| Need glucocorticoid and mineralocorticoid replacement of life, 2x-3x during stressful situations|
Hydrocortisone Sodium Succinate or Phosphate = TOC
|What is the MCC of Conn's Syndrome?|| Aldosteronoma = Primary Hyperaldosteronism|
* MC presentation is a hypertensive crisis
|What labs will be abnormal with Conn's Syndrome?|| Decreased Renin from trying to regulate BP|
Hypokalemia and Hypernatremia from aldosterone stimulating Na+ retention and K+ excretion in Cortical collecting duct of the kidneys.
|What is a familial autosomal dominant multiglandular syndrome that causes endocrine tumors in multiple areas of the body?|| MEN1 - Werner's Syndrome|
MC Tumors are parathyroid (causing hyperparathryoidism), but tumors can be gastrinomas (ZE syndrome), insulinomas (Hypoglycemia), prolactionomas (Hyperprolactinemia), carcinoid tumors (like a cancer).
|What are some sx associated with hyperparathyroidism?|| Hypercalcemia from PTH taking Ca2+ from the bone leads to bone pain, arthralgias, pathologic fractures, and cystic bone lesions (fallen-leaf pattern on X-ray)|
* BONEs, Psychic MOANs, STONEs, Abdominal GROANs, with fatigue OVERTONEs *
|MEN 2A = Whipples Syndrome = _____ Cancer + Pheochromocytoma|| Thyroid|
* Medullary thyroid carcinoma (MTC) (99%), Pheochromocytoma (50%), and Hyperparathyroidism caused by parathyroid gland hyperplasia (20%)
|MEN 2B = Medulary Thyroid Cancer + _________|| Pheochromocytoma|
MEN 2A vs 2B is genetic testing only.
|What is the MC thryoid cancer? What is the most fatal thyroid cancer?|| Pappilary|
|A patient presents with cold intolerance, fatigue, dry skin, 52 bpm HR, 90/65 BP, and weight gain. What do you suspect? What labs will you order?|| Hypothyroidism|
TSH, FT3, FT4, CBC, UA, and BMP
* FT4 (decreased) is the most diagnostic lab.
|What is the TOC for hypothyroidism?|| Levothyroxine (Synthroid): interacts with OCPs, estrogen, insulin|
Take 30 minutes prior to eating!!
|Pt presents with increased sweating, wt loss, diarrhea, heat intolerance, menstrual irregularity, anxiety, 110 bpm HR, goiter, exophthalmos, and BP of 134/89. What is your suspected dx? Labs?|| Hyperthyroidism|
TSH (low), T4/FT4 (high), T3/FT3 (high), CBC, UA
|How do you treat hyperthyroidism?|| Beta Blockers!! + hydrocortisone if in a storm|
|HMG CoA Reductase Inhibitors =|| Statins|
* TOC for hyperlipidemia
* Best at decreasing LDL, and they also increse HDL and decrease TGs
| Which of the following is not a major AE of statins?|
B) Increased LFTs
C) Warfarin interaction
D) All of the above are AE of statins.
| D) All of the above are AE of statins.|
Pravastatin has the least AE because it is on a different P450 enzyme pathway.
|What hyperlipidemia treatment disrupts the enterohepatic circulation of bile acids by binding them and preventing their reabsorption from the gut?|| Bile Acid Sequestrants|
Cholestyramine, Colestipol, Colesevelam
* TOC for hyperlipidiemia is Pregnancy or on Warfarin
* Not the best with hypertriglyceridemia
|What drug is best for lowering TGs? It works by breaking down lipoproteins for excretion, increased HDL production, and decreasing hepatic TG production.|| Fibrates/ Fibric Acid|
Gemfibrozil, Fenofibrate, and Clofibrate
* CI with renal or hepatic disease
|What hyperlipidemia drug class is actually a vitamin? It works by binding to and stimulating a G-protein-coupled receptor, which causes the inhibition of fat breakdown in adipose tissue. Lipids that are liberated from adipose tissue are normally used to build very-low-density lipoproteins (VLDL) in the liver, which are precursors of low-density lipoprotein (LDL) or "bad" cholesterol. By lowering VLDL levels, it also increases the level of high-density lipoprotein (HDL) or "good" cholesterol in blood, and therefore it is sometimes prescribed for people with low HDL, who are also at high risk of a heart attack.|| Nicotinic Acid/ Niacin|
AE = FLUSHING, hyperuricemia, hepatoxicity