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ClinMedWinterFinal
Thyroid, Parathyroid, Adrenal Gland
| Question | Answer |
|---|---|
| Thyroid problems, more common in men or women? | Women |
| MOST common type of hyperthyroidism | Grave's _Autoimminue where ab's attack TSH receptors, INC thyroid gland growth & hormone |
| Most common type of thyroidism in smokers | Hyperthyroid |
| Toxic adenoma & toxic multinodular goiter | Autonomous thyroid tissue |
| Hyperemesis gravidarum & trophoblastic disease | HCG-mediated HYPERthyroidism |
| Excess replacement therapy & intentional suppressive therapy | Exogenous thyroid hormone intake & intentional suppressive therapy |
| Autoimminue where ab's attack TSH receptors, INC thyroid gland growth & hormone release | Grave's Disease _At risk: familial, autoimmune dz |
| Presence of a goiter along with tachy, tremors, increased reflexes (ALL senses heightened), yet weak | Grave's Disease _Autoimmune ab's to TSH receptors |
| Exopthalamus caused by Grave's | Inflammation of extraocular mm & orbital fat & connective tissue Tx=CORTICOSTEROIDS & topical lubes |
| ONLY level decreased when looking at Grave's disease? | TSH is decreased All other levels (T3,T4, Antibodies) are high. |
| Why use a thyroid ultrasound if suspect Grave's | Detects multinodular goiter |
| GOLD standard for making DEFINITIVE dx of Graves | Thyroid radioactive uptake & scan _Will show HOT GLAND-NEVER biopsy a HOT gland! |
| Patient has a HOT gland when perform thyroid radioactive uptake & scan. Should you do a biopsy next? | NEVER biopsy an inflamed HYPERthyroid gland/nodule (Graves & toxic multinodular goiter) |
| How would you treat Grave's hyperthyroidism SYMPTOMS (won't actually cure)? | Beta Blockers (to stop tachy, tremors, etc) NO Strenuous activity |
| When would you use surgery to treat Grave's hyperthyroidism? | If pregant, LARGE goiter, or suspect cancer |
| How would you actually treat Grave's autoimmune HYPERthyroidism? Can be used for 1-2 years until more definitive tx. | Thiourea(Anti-Thyroid) Drugs: Methimazole PTU=propylthyrouracil (DOC if pregnant/breast feeding) |
| When would you use PTU in the treatment of Grave's hyperthyroidism? | If pregnant or breast feeding |
| How would you PERMANENTLY control Grave's hyperthyroidism? | Radioactive Iodine (I-131 ablation) _Preferred over surgery _Destroys thyorid in 6-18wks _FU w/thyroid function tests, once becomes hypothyroid, begin giving replacement drugs |
| Complications of Radioactive Iodine (I-131 ablation)for tx of Graves autoimmune HYPERthyroidism? | THYROID STORM _Afib, CHF, Osteoporosis |
| RARE life-threatening, MOST severe form of HYPERthyroidism. Usually WITH ACUTE EVENT: stressful illness, thyroid surgery, trauma, infection or acute iodine load. | THYROID STORM _Sx: FEVER, tachy, N/V/D, dehydration, weak, confused, restlessness, Abif, CHF _Tx: MORE frequent dosing of beta-blockers and radioactive iodine |
| Autoimmune thyroiditis (Hashimoto's Thyroiditis), previous thyroid surgery or radiation may cause this | HYPOthyroid |
| Primary Hypothyroidism, commonly think of this MOST common cause | Hashimoto's Thyroiditis |
| CENTRAL hypothyroidism (secondary & tertiary) | TSH or TRH deficiency from hypothalmus |
| Chronic autoimmune thyroiditis caused by cell & antibody-mediated thyroid tissue destruction. Occurs after hyper-/euthyroidism is "burning out" from autoimmune dz. Diffusely enlarged, firm thyroid. | Hashimoto's Thyroiditis _Hypothyroidism |
| Weight gain, thick tongue, edema, dry skin, slow speech, HYPOreflexia, depression (everything depressed) | Hashimoto's Thyroiditis _Hypothyroidism |
| Lab values which will decrease with overt hypothyroidism (Hashimoto's) | DEC in free T3 or T4 |
| Lab values which will increase with overt hypothyroidism (Hashimoto's) | INC in ab's |
| Tx for Hashimoto's Thyroiditis _Hypothyroidism | Synthetic T4 (PO Levothyroxine) _Re-check TSH & free T4 in 4-6wks (increase requirement during pg) |
| Would you use T3 or T4 replacement or combo tx when treating hypothyroidism | T4 is standard, can use T3 if not converting well or still have sx (=Cytomel). Dessicated thyroid (combo) is more unstable. |
| Complications of tx for Hashimoto's Thyroiditis _Hypothyroidism | Myxedema Coma _In older patients who had long-standing profound hypothyroidism. |
| Hypothermia, bradycardia, hypoxia, hypoventilation, severe hypotension. Caused by HYPOthyroid & infection, cardiopulm illness, cold exposure, IVDU | Myxedema Coma _IV levothyroxine & tx of underlying cause |
| Granulomatous, de Oquervain's, giant cell thyroiditis | SUBacute thyroiditis _acute sx or silently _Tx: ASPIRIN _associated w/viral illness |
| Even if the patient has no sx, what should you do if you feel a thyroid nodule? | Do workup & get ultrasound (solid=malignant, cystic=benign) |
| See Cold on the thyroid scan when you have LOW TSH levels. Next step? | Cold=Cancer Biopsy |
| What's the next step after you see that a cold thyroid scan is actually cancer (already done biopsy) | Endocrinology & suregeon (ENT, general) |
| Usually presents as a single nodule in older females. At risk if had prior radiation exposure | Thyroid Cancer |
| Painless neck swelling, single firm nodule, hoarseness, hemoptysis | Thyroid Cancer=Cold Nodule _Fine needle biopsy & CXR for metastases |
| Least aggressive but MOST common type of thyroid cancer | Papillary |
| MOST aggressive type of thyroid cancer | Anaplastic |
| Tx of Thyroid Cancer | Surgical resecretion Radioactive I ablation for residual dz T4 replacement for iatrogenic hypothyroidism(Monitor TSH) |
| Female >50 usually dx after findings of HYPERcalcemia | HYPERparathyroidism _INC Ca2+ levels |
| MOST common type of primary hyperparathyroidism | Parathyroid Adenoma |
| RAREST type of primary hyperparathyroidism | Parathyroid Carcinoma |
| Common causes of secondary/tertiary hyperparathyroidism | Chronic renal Failure Renal Osteodystrophy |
| Symptoms if have HYPER-parathyroidism | Bones, stones, ab groans, psychic moans w/fatigue overtones |
| INC Calcium (>10.5 mg/dL), if albumin is decreased you must calculate the corrected calcium. | Can be HYPERparathyroidism OR w/malignancy multiple myeloma |
| How can you confirm dx of HYPER-parathyroidism when see levels of high calcium? | Will also see high PTH and decreased phosphate (unless it's secondary to renal failure) |
| What is the definitive tx of HYPER-parathyroidism | Surgery! Parathyoridectomy |
| Conservative tx of hyper-PTHism | Physical activity, drink fluids, avoid Li/HTCZ, Restrict Ca intake, take Vitamin D |
| What can you do for temporary reduction of hyperparathyroidism which also causes bone pain? | Aredia or Zometa (IV Bisphophates) |
| Tx of secondary/tertoary hyperparathyroidism | Cinacalcet & paricalcitol |
| HYPOcalcemia & DEC PTH. Will see INC phosphate and often DEC Mg | HYPOParathyroidism _Tetany, m cramps, spasms, tingling, convulsion |
| Most common cause of HYPOparathyroidism | Post-Thyroidectomy _HYPOParathyroidism: HYPOcalcemia & DEC PTH _Tetany, m cramps, spasms, tingling, convulsion |
| Positive Chvostek's (facial m contraction when tap facial n) & Trousseau's (carpal spasm after inflate BP cuff) | HYPOParathyroidism _Tetany, m cramps, spasms, tingling, convulsion |
| ER tx for acute tetany caused by HYPO-PTHism | IV Calcium Gluconate & Airway maintenance |
| Maintenace tx for HYPO-PTHism | Calcium & Vit D supplements _Avoid too much Ca & Lasix _May need Mg supplements |
| #1 cause of renal failure, new onset blindness, nontraumatic amputations | Diabetes |
| Destroyed pancreatic b-cells from autoimmune or unknown causes. Prone to "ketosis" (Diabetic ketoacidosis). Usually younger onset. 10% of cases | Type 1 DM (IDDM) _NEED exog Insulin for survival |
| Combined insulin resistance & defective insulin secretion. Usually after age 30. Obesity. 90% cases | Type 2 DM (NIDDM) _Do NOT need exog Insulin for survival |
| Elevated glucose during pregnancy may cause this. Screen ppl >25, obesity, FH | Gestational Diabetes |
| Stages of Type 2 DM | Periph insulin resistance(hyperinsulinemia)--> Impaired Glucose Tolerance--> Early DM--> Late DM (b cell fails) |
| When peripheral tissues are no longer able to secrete insulin what happens? | Liver will inc glucose production Muscle/Fat (Peripheral tissues) will not be able to respond to insulin |
| Greater than normal amts of insulin needed to make a NORMAL bio response (a normal drop in blood glucose) | Insulin Resistance _Can cause Metabolic Syndrome & Type 2 DM |
| KEY Symptoms of INC glucose (3Ps) | Polyphagia, Polydipsia, Polyuria _May also see blurred vision, infections, delayed wound healing |
| ER for DM | HYPOglycemia, DKA, Nonketotic hyperosmolar syndrome (NKHS) |
| 2hr prosprandial glucose of 140-199 after ingesting 75gm of oral glucose | Impaired Glucose Tolerance |
| Fasting glucose between 100-125 | Impaired Fasting Glucose |
| A measurable increase in glycosylation (adding sugar residues) to RBC can be measured in this test | HbA1C _Goes back prev 2-3mos _Monitors effectiveness of DM tx & tests for pt compliance w/tx & differentiate btwn short-term & glucose rise. _Now can use for Dx |
| Normal range for HbA1c | 4-6% |
| Satisfactory DM control is considered to be <1% above top normal | <7% HbA1c |
| How often should you ck HbA1c in stable DM patients? | At least every 6 months |
| How often should you ck HbA1c in less controlled or if therapy has changed? | At least every 3 months |
| Dx of abnormal HbA1c | 6.5% or greater |
| Dx of diabetes with OGTT=Oral Glucose Tolerance Test (2hr postload glucose) | >200 |
| In the absence of symptoms of hypoglycemia, what should you do if see abnormal lab values for DM? | Repeat lab values! |
| During pregnancy, with DM mother, besides an increased risk of fetal death in last 4-8wks of gestation what may be another neonatal prob that may arise? | Macrosomia _LARGE birth-wt infant w/congenital deformities, hypoglycemia, hypocalcemia, polycythemia & jaundice |
| Crucial during the planning of pregnancy with DM mom | SMBG! _Urine glucose monitoring is NOT helpful |
| When should you screen for DM during pregnancy? | 24-28wks gestation _2hr GTT with 75g glucose _Can MAKE DX if ONE blood test meets requirements |
| Fasting Glucose >92, 1hr >180, 2hr >153 may meet requirement for gestational DM if what? | If meet at least ONE requirement _Screen @24-28wks |
| Why is glucosuria NOT a requirement of gestational DM? | Because pregnant women have a lower renal threshold more likely to spill sugar in urine, even if not DM. Therefore NOT a reliable test!! |
| Dx of Pre-Diabetes (IGF or IGT) | HgbA1c btwn 5.7-6.4% |
| Goal for pre-meal glucose in DM pts | 80-120mg/dl |
| Goal for 2hrs post-meal glucose in DM pts | 100-160mg/dl |
| Goal for bedtime glucose in DM pts | 100-140mg/dl |
| Goal for HbA1c in DM pts | <7% |
| Increased urinary albumin is an early sign of this (microalbumineria) | Diabetic nephropathy =30-300mg in 24hr of Albumin |
| BEST quantitative test for microalbuminera to dx diabetic nephropathy | 24hr urine test _Make sure to also get creatinine clearance to test renal function too |
| When should you screen for DM? | At 45 (if normal then every 3yrs after), unless risk factors _Use HbA1c, FPG, 2hr 75gm OGTT |
| High risk patients who need to be screened for DM | Obese First degree relative Blacks, Hispanics, Native Americans Baby >9lb at birth Hx of gestational DM HTN Dyslipidemic pts (HDL<40 or TriG>200) Prev hx of impaired glucose |
| Goal in diabetic dyslipidema (HDL <40 or TriG>200) | LDL <100 (or <70 if CAD) HDL >40 TriG <150 BMI <25 |
| Signs of MICROvascular disease associated with DM | Retinopathy Nephropathy Neuropathy |
| Ketones (building up because cannot utilize glucose metab) in DM may spill into urine causing this | Diabetic Ketoacidosis _MUST admit for aggressive tx! |
| LOW serum bicarb may be a sign of this in DM pts! | Diabetic Ketoacidosis! _THEN ask lab to look for ketones! _Positive: admit for aggressive tx |
| Classic lab findings in DKA | INC glucose (blood/urine) LOW Bicarb + Ketones (urine & serum) |
| Glucose <40 and adrenergic sx related to epi release(sweats, tremors, tachy, weak) & neuroglycopenic sx caused by low glucose (dizzy, HA, clouded vision, blunt mental activity, confusion, seizures, coma) | TRUE hypoglycemia _Take in carbs w/sugar: milk, candy, fruit |
| If pt cannot ingest food, tx of hypoglycemia | 1mg IM of Glucagon (may vom) OR IV Dextrose (bolus followed by continuous infusion) |
| Common causes of FASTING hypoglycemia | SURREPTITIOUS injection of insulin or ingestion of HYPOglycemic meds (Sulfonylureas) Insulinoma (poor secretion) EtOH effects Severe liver/kidney failure Glucocorticoid failure HYPOpituitarism |
| Vague sx after 1-2hr post meal. Caused by too quick of glucose absorption followed by "robust" insulin response causing low blood sugar. | Postprandial Hypoglycemia (Alimentary) _high protein, low carb diet may fix _in ppl w/partial gastrectomy or intestinal resection |
| Postprandial adrenergic sx suggesting hypoglycemia (relieved by giving glucose) BUT ACTUAL blood glucose is normal (some may have IGT) | Postprandial Hypoglycemia (Functional) _Do NOT use the 5hr GTT for dx (too many false +) |
| Insulin >6 with hypoglycemia may suggest | Insulinoma (insulin secreting tumor) Factitious insulin or sulfonylurea use Insulin Ab's or receptor Ab's |
| Insulin ab's made during hypoglycemia may need to be watched, why? | May cause insulin resistance so will need to give a larger dose of insulin to get proper glucose-lowering effect |
| This will ONLY increase if ENDOGENOUS insulin is being made | C-Peptide (cleaved from pro-insulin-->insulin) |
| Would you expect high or low C-peptide with Type 1 DM? | Very LOW, not making insulin |
| Would you expect high or low C-peptide with Type 2 DM? | Very HIGH, making too much insulin |
| Hypoglycemia caused by intentional excess dose of insulin or oral hypoglycemic drugs | Will see LOW C-Peptide levels =Factitious (self-induced) HYPOglycemia |
| Sulfonylurea excess | INC C-Peptide levels |
| Insulinoma (islet cell hyperplasia) | INC C-Peptide, Insulin, Proinsulin |
| Oral agents which stimulate insulin secretion | Insulin secretagogues: Sulfonylureas (Glucotrol & Amaryl) Meglitinides ("glinides") |
| Oral agents which inc sensitivity of liver & mm to insulin. Lowers BOTH glucose & insulin levels | Insulin Sensitizers: _Biguanides: Metformin _Thiazolidinediones: Actos, Avandia |
| Alpha glucosidase inhibitors which block carbohydrates | Acarbose & Miglitol |
| Stimulate insulin secretion by binding specific receptors in pancreatic b cells to increase sensitivity to glucose & thus releasing insulin. Can cause HYPOglycemia & weight gain. | Sulfonylureas (Glucotrol & Amaryl) |
| Stimulates insulin production with rapid onset & clearance. Take 30 mins before meal | Meglitinides "Glinides" |
| Reduces heaptic glucose production & increases glucose uptake by cells. Good if pt is OBESE. No hypoglycemia caused | Biguanides: Metformin |
| Main side effects to worry about when using Metformin | Lactic acidosis (do not use if have Cr >1.4) Mixes with Iodine contrast (do NOT resume until kidney function returns to normal after) |
| "Glitazones" used in the tx of diabetes may take 3-8wks to work, are insulin-sparing but can cause liver toxicity (ALWAYS monitor LFTs). What should you watch for? | EDEMA _Contraindicated in ppl w/CHF |
| Delay carb absorption to control postprandial hyperglycemia. Take ONLY before meals (just before). | Alpha Glucosidase Inhibitors _Causes farts! |
| Combo sulfonylurea & biguanide drugs | Glucovance (Glybiride+Met) Metaglip (Glipizide+Met) |
| Combo biguanide & "glitazone" | Avandament Actoplus Met |
| Combo "glitazone" & sulfonylurea | Avandaryl |
| Process of DM progression | 1)INC insulin resistance 2)DEC insulin secretion by beta cells 3)EXCESS glucagon secretion by alpha cells 4)IMPAIRED incretin effect |
| DM appears when? | 80% of beta cells don't work 50% of patients already have Type2 DM complications |
| Synthesized in gut to stimulate insulin secretion in response to food consumption. Receptors are mainly on beta cells. After eating will be secreted then bind to receptors on beta cells, PROMOTING insulin secretion | Incretins (GLP1 & GIP) |
| First incretin mimetic which helps make more insulin be secreted from beta cells. Synthetic version of GLP1. May INCREASE beta cell mass!!! | Byetta _Will ONLY release insulin if glucose is high. Suppresses glucagon release _Full faster! _Slows gastric emptying to less glucose enters circulation |
| When would you use insulin mimetic (Byetta) in a DM patient? | Type 2 DM who are unable to control glycemia with other drugs. _SE: nausea, WEIGHT LOSS _$$$$ and need subq injections |
| When should you NOT give Byetta? | If suspect pancreatitis or has had pancreatitis |
| Amylin (hormone) made in beta cells will work w/insulin to decrease blood sugar. What's the synthetic form? | Symlin _For Type 1 & Type 2 DM _Injected w/insulin before meal will work together to control glucose released |
| Prevent GLP1 degradation by inhibiting DPP4. Will enhance incretin effects | "Gliptins" |
| ONLY for use in Type 2 DM, this gliptin is used @ 100mg once daily ORAL with or without food (reduce dose if renally insufficient) | Sitagliptin _DPP4 inhibitor |
| DPP4 Inhibitor which works for 24hrs to ENHANCE natural incretin action | Saxagliptin |
| Used for insulin resistance (especially in mm & fat) | Metformin "Glitizones" |
| DOC for ALL Type2 DM | Metformin since reduces weight & insulin resistance _May need to add sulfonylurea or incretin mimetic(Byetta) in order to have addtl glycemic control |
| First stage tx of Type2 DM | Lifestyle changes |
| Second stage tx of Type2 DM | Lifestyle changes+ oral agents |
| Third stage tx of Type2 DM | Lifestyle changes+ oral agents+ Bedtime intermed/long acting Insulin |
| Fourth stage tx of Type2 DM | Lifestyle Change + 1_Once daily long-acting insulin + pre-meal rapid acting insulin OR 2_Twice daily intermed acting+ pre meal short or rapid acting insulin |
| Insulin in Diabetic Use | Necessary for TYPE 1, may be needed in type 2 |
| Would you add oral agents to insulin in Type 1 DM | No! Do not add insulin to Type 1 DM |
| When should you start DM tx to prevent Type 2 progression? | When HbA1c approaches 8% despite optimal oral therapy |
| Goal of FPG(fasting plasma glucose) in diabetics | 80-120 |
| Goal of glucose @2hrs post-meal | 100-180 |
| Goal of bedtime glucose levels | 100-140 |
| Goal of HbA1C | <7% |
| Rapid acting insulin | Lispro, Aspart, Glulisine |
| Short acting insulin | Regular (Humulin R) |
| Intermediate acting insulin | NPH |
| Long acting insulin | Lantus, Levemir (L's are Long) |
| What MUST you know for the safe management of insulin tx | 1)Onset of action 2)Time of peak activity 3)Duration of action *Must know amt of insulin needed to cover one's caloric intake & physical activity* lets ppl self manage |
| What must pt know for self-administering Insulin | Amt insulin needed to cover calorie intake & physical activity |
| How much insulin for Type 1 DM? | Calculate expected final range of total daily insulin dose (.5 unit*wght) _Split btwn bolus(prandial: 50% divided in thirds before each meal) & basal(50% as single dose) |
| Physiologic Regimen | Mimics normal B cell secretion. Typically replace "Basal" insulin & "Prandial" (or bolus) insulin separately |
| NONPhysiologic Insulin replacement | (Basal) Glargine: given once @bedtime NPH or Lente: after breakfast & bedtime |
| Insulin program for Type2 DM | Continue oral agents but DECREASE sulfonylurea to 50% of max dose if using NPH or pre-mixed, or to 25% if using glargine or detemir @bedtime |
| How should you begin an insulin program for Type2 DM | Single dose of .15units/kg as: NPH, glargine, detemir @bedtime OR 70/30 given 30min before dinn Humalog 75/25 before dinn |
| What should you use for 50% of the daily insulin needs? | Basal Insulin _Suppresses glucose production btwn meals & overnight. |
| What should you use for 10-20% of total daily insulin requirements? | Bolus Insulin (Mealtime) |
| Microvascular complications of DM | Retinopathy Nephropathy Neuropathy |
| Macrovascular complications of DM | CAD Cerebrovascular Dz Peripheral Vascular Dz |
| Complications of DM not vascular | HYPOglycemia HYPERglycemia: DKA, NKHS |
| #1 cause of renal failure | DM |
| This microvascular complication of DM may cause proteinuria, HTN and decreased GFR (progressive renal failure) | Nephropathy _ACE Inhibitors may reduce risk |
| Slow progressive dz preferentially affecting the long axons. Numb/tingle, cramps, urinary incontinence, loss of sexual response, gastroparesis, orthostatic HTN | Neuropathy |
| INC generalized atherosclerosis & stroke incidence | Cerebrovascular Dz |
| Rapid, life-threatening can cause death in mins. ER complication of DM | HYPOglycemia |
| ER complication of DM takes longer to devo, more gradual onset. Can be life-threatening (esp if with ketoacidosis) | HYPERglycemia |
| Sweating, tremor, tachy, anxiety, weakness & hunger are this | Adrenergic sx related to epi release in HYPOglycemia |
| Dizzy, HA, clouded vision, blunt mental activity, confusion, abnormal behavior, seizures, coma | Neuroglycopenic Sx due to low CNS glucose |
| Tx of HYPOglycemic rxns | Glucose ASAP and oral carbs |
| Waning of Insulin Action | Possible cause of MORNING HYPERglycemia _pt's prior pm insulin has worn off _Tx: INC insulin dose or change timing |
| Dawn Phenomenon | Possible cause of MORNING HYPERglycemia _increase in Growth Hormone btwn 3-7am which INC blood glucose _Tx: INC insulin dose or change timing |
| Somogyi Phenomenon | Possible cause of MORNING HYPERglycemia _REBOUND hyperglycemia caused by nocturnal hypoglycemia & subsequent release of cortisol, glucagon & GH (counter regulatory hormones) _Tx: Reduce night time dose a/o have bedtime snack |
| Diabetic whose blood sugar bounces from extreme to extreme. Small dose changes will cause disproportionate large changes | "Brittle" Diabetics |
| Almost always in Type 1 DM, caused by insulin insufficiency & infection or MI, PG. | DKA! Life threatening ER |
| INC blood/urine glucose LOW bicarb + ketones in urine, serum | DKA _Usually seen w/Type1 DM |
| Tx of DKA | Correct electrolytes (give K, PO4) Reverse acidosis (with IV bicarb, cautious) _Tx until pH normal and NO ketones! |
| How long should you continue to give fluids in DKA | Until NO more ketones in serum! _Add dectrose to saline to AVOID hypoglycemia |
| N/V, ab pain, HYPERventilation, HYPOtension, shock, DEHYDRATION, metab acidosis, INC ketones | DKA _usually seen with Type 1 DM |
| Sign that DKA has resolved | Blood pH has returned to normal |
| Secondary to severe stress will see w/decreased renal excretion of glucose. Azotemia (INC BUN). See SEVERE HYPERglycemia (glucose >500-600) & DEHYDRATION(Osm>320). There is NOT ketonemia | Nonketotic Hyperosmolar Syndrome _Type 2 DM _Tx: Fluids/electrolytes. IV insulin |
| TSH | negative control=T3, Postive control=TRH |
| Thyroxine (T4) | 80-100mg released/day. Will be deIONIZED to make more T3 and even out |
| Triiodothyronine (T3) | 10x more bio active than T4 with weaker binding properties |
| 75% of T3/T4 is bound to what? | Thyroxine Binding Globulin (TBG). Will increase half-life & give reservoir |
| BEST screening of thyroid function | TSH (low=HYPERfunction), (high=HYPOfunction) |
| High TSH levels may show this in pt being tx for thyroid | UNDER-treatment |
| Low TSH levels may show this in pt being tx for thyroid | OVER-treatment |
| MORE direct measure of hormone activity | FREE T4 levels (not total) since shows hormonal activity (FT4 should be 5-12) |
| FTI(Free Thyroxine Index) & thyroid hormones move in same direction | Likely thyroid prob |
| FTI(Free Thyroxine Index) & thyroid hormones move in OPPOSITE direction | Likely protein binding problem |
| Elevated Thyroglobulin (Tg) | Acute thyroiditis, Grave's, Thyroid cancer |
| Why monitor Tg levels? | Eval for THYROID CANCER tx effectiveness |
| Common ab's seen in Hashimotos (less common in Graves), will also see in post-partum thyroiditis | Microsomal TPO Ab's (Antithyroid peroxidase Ab's) which convert T4 to T3 |
| Commonly seen in Hashimotos aka Antithyroglobulin Abs. Use to evaluate likelihood that a Graves pt will eventually become HYPOthyroid w/o iatrogenic destruction of the gland) | TgAB (Thyroglobulin Ab's) |
| Ab's which prevent TSH from binding cell receptor. Will ONLY be positive in Hashimotos!! Therefore if + & have hyperthyroid must wonder if hyperthyroid episode is in the setting of Hashimotos | (TBAb or TSBAb)Thyrotropin Receptor Blocking Ab |
| Common ab's seen in Grave's (less likely Hashimoto's) | Thyroid Stimulating Immunoglobulins (TSI) & Thyroid-Binding Inhibitory Immunoglobulin (TBII) |
| First step in thyroid eval | test TSH levels |
| Normal TSH levels but suspect thyroid | No further testing |
| High TSH levels, next step? | Eval FT4 & all Ab's |
| Low TSH levels, next step? | Eval FT4, FT3, Tg, TPO Ab's, TgAb's, TSI |
| What should you always check when thyroid probs? | Med lists |
| Typical thyroid Panels | TSH with reflex T4, Thyroid function panel |
| Calcitonin Effects | Will supress calcium resorption in bones by inhibiting osteoclasts, will inhibit reabsorption of Ca in kidneys causing increase loss of Ca and PO4 in urine |
| When should you use Thyroid Ultrasound? | Distinguish solid v cystic nodules, have abnormal function test, following growth patterns |
| Upon imaging of a "cyst" found on ultrasound what should you always do? | Follow Up since not really benign, could be cystic degeneration of solid nodules |
| Complex Nodule is what | Hemorrhage in nodules causes original clot to be hyperechoic after liquefiding hypoechoic |
| See Bright Echogenic densities creating shadows on thyroid US | Calcifications! Investigate further! |
| See homogenous thyroid US, no nodules, next step? | Don't need to repeat testing |
| See homogenous thyroid US w/nodules, next step? | Repeat testing |
| See heterogenous thyroid US, next step? | Shows autoimmune destruction therefore: 1)get TFTs and Repeat US in 6-12mos |
| See nodules on thyroid US >4mm, do what? | Fine needle Biopsy (Follicular cells are malignant till proven otherwise!!) |
| See nodules on thyroid US <4mm, do what? | Repeat US in 3-4mos |
| Need to differentiate btwn Graves, toxic multinodular goiter, thyroiditis, thyroid malignancy | Thyroid Nuclear Med Scan (Must be on low-Iodine diet & off vitamins for at least 4wks leading up). Shows hot/cold lesions |
| See ENTIRE hot gland | Graves |
| See low uptake & patchy hot spots | Hashmitos |
| Hot nodule without clinical sx of Graves | rarely cancer |
| Cold nodule | Cancer |
| What should you NEVER biopsy? | A HOT nodule! _Grave's or Hashimotos |
| When cking for parathyroid disease, measure | PTH & DEXA Scan (for osteoporosis). Also include Ca(serum & ionized), Mg, PO4, VitD |
| Acts on bone to pull calcium (phase 1) & stimulate calcicum & Po4 release, will also keep mineral ion homeostasis in kidney | PTH |
| Gold standard for eval & monitor of Bone Mineral Density | DEXA Scan (use when suspect PTH-ism dz) |
| Bone mineral content/Bone are=? | Bone mineral density |
| T Score | Take's bone mineral density and compares to normal person |
| Z Score | Take's bone mineral density and compares to normal population |
| Estrogen, OCP, amphetamines, prednisone, spironolactone will increase these | Plasma cortisol |
| Androgens, aminoglutethimide, Li, levodopa, phenytoin will decrease this | Plasma cortisol |
| Test Ant Pituitary function) | Plasma ACTH |
| INC effect of ACTH (tests anterior pituitary fcn) | estrogens, ETOH, vasopressin, amphetamines, levodopa, spironolactone |
| DEC effect of ACTH(tests anterior pituitary fcn) | exogenous steroids |
| Tests Adrenal HYPERfunction | 24 hour urinary free cortisol (17-OCHS). Will decrease with estrogen, OCPs, phenothiazines, reserpine |
| Evaluates Adrenal HYPOfunction | Cosynotopin Stimulation Test (shows response to ACTH given) |
| Cortisol levels inc to >19 AND a min of >7 above baseline shows what on Cosynotropin Stimulation test (shows Adrenal HYPOfunction) | Normal resposne |
| Below normal response (<18 of cortisol) in Cosynotropin Stimulation test) | Adrenal HYPOfunction |
| Used to eval hypothalmic, pituitary & adrenal function | Dexamethasone Suppression Test (mostly use rapid). Interfered by STRESS! (Will INC levels of ACTH hiding the results) |
| Bilateral Adrenal Hyperplasia (Cushing's) see what? | 50% decrease in plasma cortisol & urine 17-OCHS levels, no change in cortisol after Dexamethasone Suppression |
| Adrenal Adenoma or Carcinoa, see what? | No change in prolonged dose, rapid test dose after Dexamethasone Suppression |
| Ectopic ACTH-Producing Tumor, see what? | No change in prolonged dose, rapid test dose after Dexamethasone Suppression |
| Used to dx Pheochromocytoma, must do inpatient | Clonidine Suppression Test (If does not suppress Epi, NE then + test) |
| When in excess can stop GnRH & FSH production causing hypogonadism & amenorrhea. Will also overtimulate breasts causing galactorrhea & gynecomastia | Prolactin |
| Uterus probs, HYPOgonad, HYPOthyroid, Adrenal dz, vision loss/HA, epilepsy/seizures test this | Prolactin levels |
| Stimulates IGF1 & released in large pulses or peaks from 10-30mins. | Growth Hormone (largest peak after 1 hr onset) |
| Somatostatin, GH & IGF1 levels, dietary carb & glucocorticoids will do this to GH | Inhibit GH secretion |
| GH deficiency/excess or monitoring replacement best evaluated using this as a screening tool | IGF1 |
| Microadenoma | <1cm in diameter _Must do lab workup! |
| Macroadenoma | >1cm in diameter _Must do lab workup! |
| Adrenal cortex makes 3 major classes of hormones | Glucocorticoids-->Cortisol Mineralcorticoids-->Aldosterone Adrenal Androgens-->DHEA |
| Adrenal medulla secretes this | Catecholamines _Epi, NE |
| Prolonged exposure to glucocorticoids (cortisol). | Cushing's SYNDROME |
| Caused by EXCESS ACTH (usually from pituitary adenoma ~70%). More common in women. Iatrogenic cortisol excess is most common cause of Cushingoid features. | Cushing's DISEASE |
| Fat, thin skin, moon face, HTN, purple stria, hirsutism, menstrual prob, impotence, m weakness, truncal obesity, acne, osteoporosis, Glucose intolerance | Cushing's |
| Screening test for Cushings | 24hr Urinary Free Cortisol (INC) Dexamethasone Suppression Test (cannot suppress) ACTH assay (ACTH INC) |
| Tx of Cushings | TRANSESOPHONOIDAL resection of pituitary adenoma Neoplasms are resected laproscopically |
| If after resection of Cushing's it persistently recurs, next step? | Pituitary Irradiation and/or Steriodogenic Inhibitors. Then can try adrenalectomy |
| Caused by destruction of adrenal tissue (80% autoimmune), can be from surgery, hemorrhage, infect, AIDS | Addison's Disease _JFK had |
| Primary adrenal insufficiency causes not enough production of cortisol, mineralcorticoids & androgens. Causes: weakness, fatigue, HYPERpigment, anorexia, wt loss, HYPOtension | Adrenal Insufficiency in Addison's |
| Secondary adrenal insufficiency is caused by decreased production of ACTH by pituitary. How difft than primary (which JFK had) | NO HYPERpigmented skin or mineralcorticoid deficiency (Na wasting, hypovolemic, orthostatic hypotension, HYPERkalemia, mild metab acidosis) |
| Common from glucorticoid withdrawal after tx associated suppression of HPA axis. May also be caused by surgery for ACTH secreting adenoma. A deficiency can be UNMASKED during acute illness. | Secondary Adrenal Insufficiency: presents like Addison's without hyperpigmentation or decreased mineralcorticoids _Tx: CORTICOSTEROIDS! |
| Addison's Disease: Adrenal Gland Failure. What do you expect of cortisol & ACTH levels | DEC Cortisol HIGH ACTH _Destroying adrenal tissue w/ab's but still producing ACTH in pituitary |
| HYPOpituitarism, what do you expect of cortisol & ACTH levels | DEC Cortisol DEC ACTH |
| Cosyntropin (iv ACTH) Stimulation Test | Will show increase in cortisol if normal. _Tests for adrenal HYPOfunction |
| Workup for Addison's dz | Cosyntropin (iv ACTH) Stimulation Test Adrenal Imaging w/CT or MRI Anti-Adrenal ab's found in 70% of Addison's dz |
| Tx for Addison's dz | Glucocorticoid Replacement with "sone" Mineralcorticoid replacement if Primary Adrenal Insufficiency(Fludrocortisone) Adrenal Androgen Replacement (DHEA) |
| How do you manage Addisons during stressful times? | Give additional glucorticoids knowing its gonna be a stressful time _ie surgery, trauma _These pts are NOT able to increase their own ACTH & corticosteroids in response to stress therefore MUST give supplements or causes HYPOtension & death |
| An emergent situation caused by inadequate cortisol | Adrenal Crisis_Acute Adrenal Insufficiency _Sudden withdrawal of exog steroid _Bilateral adrenalectomy _Extreme stress in pt w/borderline adrenal insufficiency _Injury to adrenal glands _Sudden destruction of pituitary gland |
| HA, N/V, ab pain, HYPOtension, confusion, coma, HYPOnatremia, HYPERkalemia, HYPOglycemia | Signs of adrenal crisis _DRAW BLOOD: to ck cortisol levels _Tx: IV Hydrocortisone STAT & 50-100mg q6hrs & adjust dose later _IV Saline as fluid resuscitation |
| Primary HYPERaldosteoronism usually caused by this. See HTN, HYPOkalemia, m weakness, paresthesias, HA, polyuria, polydipsia | Conn's Syndrome |
| With Conn's what would you expect for lab values? | INC plasma & urine aldosterone LOW plasma renin levels *Do CT to look for adrenal adenoma |
| Tx of Conn's (HYPERAldosteronism) | Surgery to remove unilateral adenoma If bilateral hypertrophy, use spironolactone & anti-HTN drugs |
| Tumor that secretes catecholamines. 90% located in Adrenal medulla. 40-50yo, can be associated with MEN type 2 (medullary thyroid cancer, HYPER-PTHism) | Pheochromocytoma |
| Paroxysmal attacks of HA, sweating, palpitations, profound acute HTN @time of episode. Lasts 30-40mins & may occur bc lifting, bending, deep palpation. INC in frequency, severity over time. | Pheochromocytoma "attacks" |
| If patient has refractory BP to conventional therapy what must you do? | Start workup to look @pheochromocytoma _Look for catecholamines!! _Plasma, urine studies. Localize tumor. |
| Initial evaluation of Pheochromocytoma | Thyroid function tests Plasma Epi & NE Plasma Metanephrines 24hr urine catecholamines, metanephrines, & VMA |
| Tx of pheochromocytoma | Chemical sympathectomy _Stabilizes pt till therapy is complete _Use pure ALPHA BLOCKER (like phenoxybenzamine) followed by BETA BLOCKER |
| Definitive tx of pheochromocytoma | Surgical Excision _ALWAYS REFER to Endo & Surgery |
| Posterior Pituitary Disorders (makes AVP/ADH & oxytocin) | Diabetes Insipidus SIADH |
| Genetically defective GnRH synthesis. Causes LOW LH, FSH & testosterone and/or estradiol w/delay in onset of puberty or lack of devo of secondary sex characteristics. Also anosmia or hyposmia | Kallman Syndrome |
| Chromosomal defect causing HYPOgonadotropic HYPOgonadism. GH defect. See excess weight w/obesity, hypotonia, mental retardation | Prader-Willi Syndrome |
| Sarcoidosis, Amyloidosis, Hemochromatosis, lymphocytic hypophysitis can cause this | Infiltration of hypothalmus & pituitary _will CAUSE: DEC GH, GnRH, AVP(ADH) |
| TB, fungal infections, HIV & tertiary syphilis are examples of this | Infectious disorders that can damage the pituitary |
| Acute intra-pituitary vascular event that damages pituitary gland. Can be caused by hemorrhage, infarction from hypo/hypertension, acute shock, Sheehan's syndrome (post-partum) | Pituitary Apoplexy _Vascular disorder damaging the pituitary |
| After life-threatening blood loss during childbirth the pituitary will become ischemic and cause HYPOpituitarism. Sx devo slowly & common in 3rd world. | Sheehan's Syndrome |
| Slowed mental fcn, weight gain, difficulty staying warm, difficulty breast feeding, amenorrhea, loss of pubic/axillary hair, low BP, fatigue may be sx of this | HYPOpituitary _like Sheehan's |
| Test and Tx for Sheehan's HYPOpituitarism | Test hormone levels, MRI to r/o cancer _Tx: Lifelong hormone replacement (Hydrocortisone, L-thyroxine, Estrogen, GH) |
| Head injuries, surgical resection, radiation damage | Pituitary Trauma |
| MOST common cause of pituitary hormone HYPOsecretion or HYPERsecretion in adults | Pituitary Tumors |
| Genetic mutations which devo tumors in pituitary gland, Parathyroid glands, Pancreatic islet cells | MEN1 (multiple endocrine neoplasia type 1 syndrome) |
| Adenoma which secretes GH & caues acromegaly | Somatotroph Adenoma |
| Adenoma which secretes ACTH & causes Cushing's | Corticotroph Adenoma |
| Adenoma which secretes TSH | Thyrotroph Adenoma |
| Adenoma which secretes Prolactin leading to HYPOgonadism | Lactotroph Adenoma |
| Adenoma which is sometimes NOT functioning | Gonadotroph Adenoma |
| Fatigue, weight gain, depression, DEC libido, impotence, infertility, loss of mens. Vision loss. HA. Apoplexy (tumor bleeding w/rapid onset of vision loss, HA, pituitary failure) | Sx from MACROadenoma |
| Benign cyst within or above pituitary that can result in HYPOpituitarism with HA & occasional vision loss | Rathke's Cleft Cyst _Parasellar Tumor |
| Benign cystic or solid tumor coming from pituitary stalk, gland, hypothalmus. Often adheres to optic nn & blood vessels. | Craniopharyngioma _Pituitary failure, vision loss &/or HA occur with |
| Malignant tumor of skull base that often invades dura & sellar/pituitary area. Typically manifests w/diplopia first. | Clival Chordoma _Parasellar tumor |
| Benign growth on meninges & adherent to dura. Manifests with vision loss first. | Meningioma _Parasellar tumor |
| Stimulates growth & cell reproduction. GH is NOT dx ALONE, therefore MUST measure this for the more accurate marker. | IGF1 _Measure if suspect growth hormone abnormalities |
| Normal aging consequence with possible causes from pituitary dysfunction, hypothalmic dysfunction or Iatrogenic (side effect of uncontrolled DM) | Adult-Onset GH deficiency _Will NOT have GH defic alone |
| Side effect of uncontrolled DM | Adult-Onset GH deficiency |
| Dx workup for GH deficiency | FULL pituitary hormone workup CBC, CMP, fasting insulin, fasting lipid DEXA |
| If see any abnormalities on workup for GH deficiency, what's your next step? | Confirm: **Arginine-GH-releasing hormone** _Insulin-induced hypoglycemia (stimulation test) |
| HYPERlipidemia, cardiovascular dz, low BMD, High BMI, Psych dysfunction, mortality & low quality of life can result if this is NOT treated | Adult onset GH deficiency |
| Childhood GH excess that occurs before epiphyseal plates have fused. See INC levels of GH & IGF1. | Gigantism |
| Caused by excess GH secretion. Most commonly from SOMATOTROPH adenoma of ant pituitary! Clinical features form GH & IGF1 | Acromegaly _Adult GH excess |
| Slow insidious onset of sx (~12yrs). HA, vision sx, LARGE hand/feet, carpal tunnel, coarse skin, macroglossia, voice deepens, hypertophic arthropathy (joint sx), obstructive sleep apnea | Acromegaly (Somatotroph Adenoma typically) _Adult GH excess |
| Screening tests for Acromegaly (Somatotroph Adenoma typically) _Adult GH excess | IGF1 (serum) Oral Glucose Test (GH >1ug/L) MRI Vision field testing |
| MOST common cause of changed hormone secretion in adults of pituitary hormones | Tumors |
| Tx of choice for treating Acromegaly (Somatotroph Adenoma typically) _Adult GH excess | Surgery! (to remove the adenoma) _TRANSPHENOIDAL resection Meds to DEC GH secretion (somatostatin analogs/GH receptor antagonists) Dopamine Agonists (Bromocriptine, Cabergoline) |
| Amenorrhea, Infertility, Galactorrhea (females) Impotence, loss of libido, infertility (men) If occurs outside sella will cause HA & vision changes | Prolactinoma _INC PRL(Prolactin levels) >200 |
| After measuring serum levels and see increased prolactin >200, next step to dx prolactinoma | MRI of sella vision field testing other pituitary hormone testing |
| After measuring serum levels and see increased prolactin >200, you do an MRI & see a Prolactinoma. Tx? | Meds! _Oral Dopamine (Cabergoline & Bromocriptine) Can do surgery, but only if meds not working or side effects too great Radiation is LAST option |
| Dx workup of pituitary adenomas & related tumors | Pituitary Hormone Testing (blood/urine) Vision field/acuity testing MRI, CT, CT angiography |
| Tx of pituitary adenomas & related tumors | Surgery: ENDONASAL approach Radiation: radiosurgery or therapy Meds: Therapy & hormone replacement |
| Pressure on optic chiasm may cause this | Bitemporal Hemianopsia |
| Caused by posterior pituitary disease causing DEC levels of ADH (AVP). Can be from trauma or genetic. Results in EXCESS DILUTE urine & rise in plasma osmolarity. | Diabetes Insipidus _Tx: Desmopressin (DDAVP)=analog of AVP |
| Excess secretion of ADH (AVP) will cause DEC volumes of more highly conc urine & hyponatremia. | Syndrome of Inappropriate ADH (SIADH) _pituitary makes too much ADH _ectopic production by neoplasms |
| Allows for reabsorption of water from CD, allowing for more concentrated urine. | ADH effect on kidneys |
| What happens when a Diabetes Insipidus patient is given desmopressin (DDAVP)? | Patient will make a smaller volume of more concentrated urine |
| Pretibial myxedema, Goiter, HYPERreflexes | Grave's |
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