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Endocrine 1
Clinical Medicine: Endocrine 1: Intro, Diabetes, Thyroid
| Term | Definition |
|---|---|
| Most abundant precursor of eicosanoids? How long are they active for? | Arachadonic acid; Typically active for only a few seconds. |
| What is omega 3 associated with? Omega 6? | Omega 3: fish oil/vasodilation; Omega 6: vasoconstriction. |
| 5 classifications of hormones and one example | 1) amino acid deriviatives (dopamine) 2) small neuropeptides (ADH/vasopressin) 3) large proteins (insulin) 4) Steroid hormones (cortisol) 5) Vitamin derivatives (vit A, vid D) |
| What is used to detect DM type 2? Can we use it for type 1? Why or why not? | C peptide. Can't use it in type 1 because it is created by proinsulin, which is not producing c peptide or insulin in type 1. |
| Half life of T4? How long should you wait after you initiate or change treatment to re-evaluate TSH? | 7 days; 4-6 weeks. |
| What is PTH useful for monitoring? | Intraoperative PTH levels to confirm removal of adenoma. |
| Where are oxytocin and vasopressin released from and what is their mechanism of transportation? | Released from hypothalamus and travel down magnocellular neurons to be secreted directly into capillaries of posterior pituitary, which enter arterioles. |
| What is mechanism of transportation in anterior pituitary? | Capillary beds stretch from anterior pituitary up to hypothalmus. |
| What does Corticotropin releasing hormone (CRH) do? | Stimulates ACTH secretion |
| Effect of thyrotropin releasing hormone (TRH)? | Stimulates TSH and prolactin |
| Effect of Growth hormone releasing hormone (GHRH)? | Stimulates GH secretion |
| Effect of somatostatin? | Inhibits GH and other secretions |
| Effect of Gonadotropin releasing hormone (GnRH)? | Stimulates LH and FSH |
| Effects of prolactin relasing hormone (PRH) and prolactin inhibiting hormone (dopamine)? | Stimulates and inhibits PRL secretion respectively |
| Other things effect insulin production other than glucose...name a few? (there are 5 others but just know a few) | 1) Glucagon 2) CCK 3) GIP 4) Parasympathetic activity 5) Increased amino acides |
| Is hormone cross-reactivity possible? How does this connected with acanthosis nigricans? Addison's? | Yes. High concentrations of insulin bind to IGF-1 receptor. Melanocyte stimulating hormone and ACTH cross talk also explains hyperpigmentation in Addison's with adrenal insufficiency. |
| Very high level or receptor specificity indicates? Lack of specificity? Why might there be no response to a particular hormone? | response to a single hormoen; cross talk between hormones; no receptors found |
| What actually performs actions of hormones? How? | Protein performs actions of hormones. Hormone -> receptor -> DNA synthesis -> protein synthesis |
| T/F: Changes evoked by actions of second messengers are slow | False: usually rapid. |
| What is the relationship between the neuorlogical system and the endocrine system? | Both respond to same stimulus...neurological system fast, endocrine slower. |
| T/F: Steroid hormones are secondary messengers | F: NO, they work directly with nucleus. |
| Physiologic compensatory response to hypoglycemia? | anxiety, tachycardia, diaphoresis following growth hormone and cortisol secretion raising glycogenolysis and gluconeogenesis |
| Most important acute stress response to severe trauma ? | Activation of renin-angiotensin-aldosterone axis |
| What are the 5 key features of the stimulus response system of hormone secretion/? | 1) Receipt of stimulus 2) Synthesis/secretion of hormone 3) delivery of hormone to target cell 4) evoking target cell response 5) degradation of hormone |
| Characteristics of Addison's? | Autoimmune damage to adrenal glands make it so cortisol can't be produced. Low cortisol production with a high ACTH due to positive feedback, but cortisol can't be produced due to damage. |
| Characteristics of pituitary adenoma? | Creates extra hormones creating constantly creating cortisol despite feedback mechanisms. |
| Characteristics of carcinoma of lung? | Ectiopic production of ACTH creates extra stimulation of the adrenals (leading to ectopic amounts of cortisol), and the pituitary receives negative feedback and turns off but ACTH is still secreted from the carcinoma |
| Characteristics of ectopic tumor? | Creates positive feedback to pituitary which goes into overdrive trumping negative feedback from adrenal glands, creating stimulating adrenals, so high cortisol production. |
| Characteristics of adrenal adenoma/carcinoma? | Loss of response of adrenals to pituitary feedback, so despite positive feedback from adrenals for pituitary to create more ACTH, the adrenals fail to create more cortisol |
| Characteristics of exogenous corticosteroids? | Extra stimulation of negative feedback, reducing pituitary secretions, inhibiting size and function of adrenals, making body exogenous corticosteroid dependant. |
| Circhoral rhythm | one hour |
| Ultradian rhythm | longer than 1 hour but less than 24 hours |
| Circadian rhythm | approximately 24 hours |
| ACTH and cortisol peak when and are low when? | Peak in AM, low during night. |
| T/F: Benign endocrine tumors often retain capacity to produce hormones | True |
| Sx of hyperparathyroidism; hyperthyroidism | para: hypercalcemia, hypophosphatemia; anxiety, tachycardia, tremor, wt. loss |
| Thyrotoxic (hyperthyroid) initially followed by hypothyoid and recovery all following a viral infection | Subacute thyroiditis |
| Thyrotoxicosis with ophthalmopathy; dermopathy over the shins; autoantibodies induce conformational changes that released TSH receptor from constraint | Grave's disease |
| Suppressed thyroglobulin levels without goiter or eye findings | Exogenous hyperthyroidism (iatrogenic) |
| Most common cause of hypothyroidism in industrialized countries? | Hashimoto's thyroiditis |
| Low testosterone and elevated LH | primary gonadal problem |
| Elevated TSH and low T4 | primary thyroid problem |
| Elevated PTH and hypercalcemia | hyperparathyroidism |
| What test can evaluate Cushing's syndrome? | Dexamethasone suppression test |
| Absolute insulin deficiency that can't be treated with oral meds | Type 1 DM |
| Heterogenous group of disorders with a relative insulin deficiency | Type 2 DM |
| Effects of insulin (4) | 1) promotes storage of carbs 2) enhances glucose cellular membrane transport 3) storage of fat 4) protein synthesis |
| 2 things that can up-regulate GLUT receptors | 1) Sustained exercise 2) insulin |
| 2 things you only see in Type 1 Diabetes Mellitus | 1) Positive anti-islet cell antibodies 2) Glutamic acid decarboylase 65 (GAD 65) |
| Other autoimmune disease associated w/ Type 1 DM (3) | Celiac, thyroid, rheumatoid arthritis |
| How would you Tx someone with hyperglycemia, polyuria, polydipsia, wt loss, blurred vision, ketoacidosis? | Insulin (Type 1 DM), self monitoring, lifestyle adaptations |
| 3 things incretin does. When is it decreased? | 1) slow gastric emptying 2) increase insulin response to a meal 3) affect in brain on appetite; DECREASED in DM2 |
| T/F: Normal fasting glucose with a high A1c almost always indicates that insulin is not taking care of glucose after meal | True |
| Generalized pruritis w/o rash, vulvovaginitis, hyperglycemia, retinopathy, neuropathy, truncal obesity, acanthosis nigracans, elevated triglycerides, reduced HDL, increased LDL, increase FFAs | DM type 2 (enough hints????) |
| T/F: Wt loss + diet + exercise = benefits of metformin | FALSE DUH; Wt loss + diet + exercise > benefits of metformin |
| DCCT results | Determined early intensive therapy of type 1 DM made a significant difference in CV events 16 years out, dropping retinopathy and microalbuminuria significantly as well. |
| VADT results | lower calcium scores were more free of CVD (surprise suprise) |
| 4 ways hypoglycemic episodes stimulates the sympathetic nervous system that are harmful | 1) Prolongation of QT interval 2) Cardiac arrhythmias 3) Sudden cardiac death 4) Acute MI |
| T/F: You are not helping the patients if you get their A1c down at the expense of hypoglycemic attacks | TRUE |
| A1c goal for most non-pregnant adults? Who benefits from a more stringent A1c goal? Less stringent? | less than 7%; Short duration of DM, long life expectancy, no significant CVD benefits most. Less stringent: those with severe hypoglycemic Hx, short expectancy, complications, co-morbid conditions, inability to lower A1c long term |
| LDL goal for DM2 pts? | NO GOAL |
| T/F: A1c is a test you can use 1-2 weeks out upon changing med to test for changes? | False: Fructosamine test is used 1-2 weeks out. |
| AACE/ACE T2DM Algorithm | Initial monotherapy for A1C 6.5% to 7.5% Initial dual therapy for A1C 7.6% to 9.0% Initial triple therapy OR insulin for A1C >9.0% |
| Mild postprandial and nonalcoholic fatty liver disease benefit, moderate fasting glucose benefit; wt loss benefit, can't use in renal/liver problems, cautioned in CHF (Lactic acidosis); GI side effects ^as dose does; MOA: decreases hepatic glucose product | Metformin: lower 1.5% |
| Moderate to marked postprandial glucose lowering with wt loss and BP; slows gastric emptying, increased insulin release, decreased glucagon and appetite; GI sx, pancreatitis possible | GLP-1 agonist: lowers .6%-1% |
| Moderate postprandial and fasting glucose lowering but mild wt gain and moderate renal/liver issues; main risk: hypoglycemia MOA: increase basal/postprandial insulin secretion | Sulfonylrea: lowers 1.5% |
| Moderate nonalcoholic fatty liver disease benefit, moderate fasting glucose benefit, mild postprandial lowering benefit, CONTRA in class 3/4 CHF, w/ moderate wt gain; MOA: enhance tissue response to insulin; $$$ | Thiazolidinedione (TZD): lowers 1% |
| Moderate to marked postprandial and fasting glucose benefits but moderate to severe hypoglycemia possible with mild to moderate wt gain, moderate risk of renal insufficiency | Insulin: lowers >2.5% |
| Moderate to marked postprandial and mild fasting glucose benefits, moderate GI Sx, benefit w/ wt loss; MOA: alpha cell function, suppresses glucagon. Main risk: hypoglycemia. Take as shot, but doesn't mix with insulin so 2 shots required around meals :( | Pramlintide |
| When is metformin not choice in monotherapy? | Obviously when A1c is super high...insulin is choice there. Not choice in CKD 3b+ or stage 4/5 CHF |
| Moderate postprandial benefit with moderate GI issues. MOA: delay carb absorption; causes flatulence and rare elevated liver enyzmes | AGI (α-Glucosidase Inhibitors); lowers: 1% |
| What 2 things are degraded by DDP-4 enzyme? | 1) GLP-1 2) GIP |
| MOA: slows gastric emptying and can cause HAs and viral infxs or inhibits enzymatic degradation of GLP-1; long term safety unknown. | DPP-4 Inhibitors; lowers 1% over 104 weeks or .5% over 24 weeks |
| MOA: alters bile acid metabolism and can reduce LDL. GI sx possible and triglyceride elevation. Obstruction main risk. | Bile Acid Sequestrants: lowers .5% |
| MOA: neurotransmitter modulation; main risks: hypotension/syncope, hypoglycemia | Bromocriptine; lowers .5% |
| 3 considerations in choice of combo therapy | 1) Pt characteristics (old, obese etc) 2) Hypoglycemia risk 3) Cost |
| T/F: In type 2 DM, rapid-acting insulin analogues are preferred over regular human insulin | True |
| HPS study | Adding simvastatin had significant effects on every category over placebo with diabetes |
| UKPDS study | Found that adding strict BP control reduced CV and DM adverse effects and death more than tight glucose control. |
| 5 components to diabetes management | 1) Lifestyle intervention 2) glucose management 3) lipid management 4) HTN management 5) comprehensive management (like anti-platelet) |
| Steno-2: Goals of Intensive Pharmacologic Strategy | 1) ACEI 2) Aspirin 3) BP control 4) Glucose control 5) Lipid control; strong evidence for targeting multiple risk factors simultaneously using multiple agents. |
| Adult that becomes diabetic but is not overweight. Tx? | Insulinopenic type 2 diabetes start initially on insulin |
| 3 Criteria for DM Dx | 1) A1c > 6.5 2) Fasting glucose >126 3) random glucose >200 |
| What age should you start testing overweight with one or more risk factors for DM? Follow up? | 45 yo; Should be tested every 3 years |
| What 3 times do you screen for pregnant women for DM? | 1) first prenatal visit 2) 24-28 weeks 3) 6-12 weeks postpartum |
| What is important for women with a history of GDM that have pre-diabetes? | Lifestyle intervention or metformin |
| How long should you wait before you add someone onto a second oral agent? | 3 months |
| What should be prescribed for all individuals at significant risk of severe hypoglycemia? | Glucagon |
| What is key for insulin-treated patients that get hypoglycemia? | Understanding their warning signs. Raise glycemic targets to avoid hypoglycemia for several weeks to restore hypoglycemic awareness |
| At greater than what BMI might you consider bariatric surgery? | 35 |
| T/F: Statin therapy is safe in pregnancy because it doesn't cross into the placenta. | False, Statins are CONTRA in pregnancy |
| T/F: ACEI/ARB not recommended in diabetic patients with normal blood pressure, albumin excretion <30 mg/24 h for primary prevention of diabetic kidney disease | True |
| At what points might you refer to a nephrologist? | Possible referral if possibility for nondiabetic kidney disease exist. Definitely refer if GFR<30 |
| When do you refer to an ophthalmologist? | Type 1: w/in 5 years of onset. Type 2: shortly after Dx |
| Results of NICE-SUGAR study? | Tight glycemic control was not as beneficial as expected in critically ill patients |
| DKA happens more in Type 1 or type 2? What primarily causes mortality? | Type 1; precipitating illness |
| 3 major metabolic effects of insulin deficiency | Elevated free fatty acids (FFAs), ketoacidosis, muscle wasting |
| Magnesium and phosphorus deficits, intravascular fluid deficit of 5-8 liters, potassium and sodium deficits. Presence of acetoacetic acid, beta-hydroxybutyric acid, acetone in urine | DKA |
| Anion Gap formula and what is normal? in DKA? | AG= Na- (Cl + HCO3); Normal <12; DKA >20 |
| Tx for DKA | Intubate, insulin drip to bring down glucose gradually, replace volume, monitor potassium |
| T/F: Start dextrose in DKA therapy when glucose <200 to avoid hypoglycemia | True |
| What differentiates HHS (hyperosmolar hyperglycemic state) from DKA? | Very high blood sugar w/o acidosis; residual insulin insensitivity and secretion minimizes ketotic response; no cognitive impairment. More often caused by type 2 DM. Bicarb might be a little high. MINIMAL amounts of ketones. High serum osmolality. NO a |
| What two main things do T4 and T3 help do in the body? | 1) Maintain thermogenic homeostasis 2) Maintain metabolic homeostasis |
| T3 vs T4: Larger amount in body? More active? | T4; T3 |
| Most sensitive test for hyper or hypothyroidism | TSH |
| Anti-thyroglobulin and anti-thyroperoxidase (TPO) found in? | Hashimoto's thyroiditis |
| Anti-thyroglobulin and Thyroid stimulating immunoglobulin (TSI) found in? | Grave's |
| Abnormal TSH levels lead to the measurement of: | free (unbound or active) T4 hormone levels |
| When would you measure levels of T3? | If TSH was suppressed, but T4 were normal and they were presenting with thyroid Sx |
| High TSH, normal T4 | subclinical hypothyroidism |
| High TSH, elevated T4 | Pituitary adenoma |
| High TSH, low T4 | Hypothyroidism |
| Low TSH, normal T4 | Subclinical hyperthyroidism |
| Low TSH, elevated T4 | Hyperthyroidism |
| Low TSH, low T4 | 2ndary 3rdary hypothyroidism |
| How do you treat someone with: autoimmune; TPO, TBG, females 30-50, PAINLESS thyroid and ASx, high TSH, low T4, most common cause of hypothyroidism | Hashimotos: Tx: Levothyroxine |
| Structurally related to thyroid hormone, strong percentage of iodine | Amiodareone |
| Kind of anemia typically associated with hypothyroidism? Others? | Normocytic, normochromic anemia (occasionally macrocytic non-hypersegmented polys) |
| What is a myxedema crisis? | Life threatening, impaired cognition, hypothermia, hypotension, hyponatremia, hypoglycemia precipitated by infx, anesthetics, cold, trauma, MI/CHF/CVA, amiodarone; SUPER Hypothyroidism essentially |
| Tx for myxedema crisis | Start w/o lab confirmation; supportive care, thyroid replacement (levothyroxine) |
| Tx of hypothyroidism | Levothyroxine; if pt older and more fragile, slower and less dosing |
| Thyrotoxicosis, women>men, high iodine intake, ophthalmopathy, clubbing, pretibial myxedema, homogenous pattern on thyroid scan, low TSH, elevated T4, TPO present | Grave's |
| TSH low, T4/T3 elevated, iodine scan would look patchy with a few intense areas. | Toxic Goiter Multinodular |
| One overproducing nodule and hot spot on iodine scan. Rest of thyroid cold since it is appropriately responding to negative feedback loops, may have elevated T3 | Toxic ademoma |
| Most common Tx for Toxic Goiter Multinodular and Toxic ademoma? | Radioiodine |
| Tender with high sed rate, iodine uptake is low, transient | Subacute thyoriditis |
| Scan low as thyroid has shut down T4...TSH high, wt loss, low thyroglobulin level, can be caused by taking exogenous thyroid hormone for weight loss | Thyrotoxicosis factitia |
| Excessive thyroid hormone. Excessive free iodine can trigger immunologic attack | Type 1 Amiodarone thyrotoxicosis |
| Destructive thyroiditis, low thyroid uptake, may cause hypothyroidism | Type 2 Amiodarone thyrotoxicosis |
| Low or undetectable TSH, normal T4, can result from endogenous overproduction of thyroid (graves, toxic nodules), intentional dosing, unintentional dosing | Subclinical hyperthyroidism |
| RARE presentation of hyperthyroidism usually in the elderly. Features exhaustion, weakness, apathy, depression, wt loss, atrial fibrillation, mimics malignancy | Apathetic thyrotoxicosis |
| 2ndary to acute severe illness, low T3, normal T4, normal TSH, increased rT3 (not clearing adequately in acute illness). Tx? | Sick Euthyroid Syndrome; Avoid routine testing of thyroid function in setting of acute illness altogether..as Tx is generally not recommended. Repeat thyroid test down the road |
| Autoimmune mechanism that occurs w/in one year of delivery. | Silent/Post-partum thyroiditis |
| Often follows a URI/ post-viral. Hyperthyroid: At first T4 is up, TSH is down. TENDER THYROID GLAND, SED RATE HIGH, TSH VERY LOW. Then become hypothyroid: TSH up, T4 down; then it normalizes during recovery. | Subacute thyroiditis |
| Bacterial, fungal, mycobacterial infx cause. More common in HIV. Large and warm thyroid w/ signs of infx. Drain abscess and obtain Cx; high mortality w/o Tx | Acute thyroiditis |
| What does hoarseness with a non-toxic multinodular goiter indicate? | Malignancy and involvement of recurrent laryngeal nerve |
| What are the steps of Dx for a toxic multinodular goiter | 1) U/S to see prominent nodules and TSH at same time. 2) If hyperthyroid: radioactive iodine scan |
| What is essential if you incidentally find a thyroid nodule w/ imaging? | TSH to evaluate thyroid fn |
| Risk Factors for Thyroid cancer (3 big ones) | Lymphadenopathy, hoarseness (vocal cord paralysis), MEN 2 gene. |
| 3 things that rule out malignancy, Several things that rule it in | Out: Hot nodule on scan, FH of goiter, response to thyroid Tx. In: Hoarseness, adenopathy, solid on U/S, Hx head/neck radiation, firm nodule, cold nodule scan, young adults and men, elevated serum calcitonin, microcalcifications, increased vascularity |
| Serum thyroglobulin marker for metastatic disease (overproduce thyroglobulin), grows slow; surgery TOC | Papillary Cancer |
| More aggressive, metastases to local nodes, bones, lungs. Elevated thyroglobulin levels | Follicular Cancer |
| Genetic analysis mandatory if positive an indication for prophylactic thyroidecomy as cancer risk is so high. 1/3 associated with MEN 2. Early local metastasis, elevated calcitonin. | Medullary Thyroid Cancer |
| Older patients w/ rapidly enlarging mass in a multinodular goiter. Most aggresive. 10% 1 year survival | Anaplastic Thyroid Carcinoma |
| T/F: We DON'T back down on hormones to lower TSH as it is part of the Tx. Cancer well differentiated enough to respond to TSH. TSH can be a trigger for recurrence so we trade not getting cancer for hyperthyroidism Sx. | True |
Created by:
crward88
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