Clinical medicine textbook, Summaries of Clinical Medicine

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Clark, Clinic Medicine ENDOCRINE CHART Diabetes Mellitus TYPE II DM: PATHOPHYSIO + COMPLICATIONS Diabetes Complication and Pathophysiology of the complication Pathology Type II DM: progressive disorder defined by deficit in insulin secretion & action (insulin resistance) Insulin Organ responsible for making and secreting insulin: pancreas - Pancreatic acinar cells (contain exocrine cells) → releases enzymes for digestion that goes to the small intestine - Islets of Langerhans (cluster of endocrine cells) → where the hormone insulin is secreted into the blood - Insulin targets skeletal muscles, liver, adipose tissue/fat - Main fxn of insulin is to store energy - Alpha cells → produces glucagon (a hormone that does the opposite function of insulin) - Beta cells → produces insulin & amylin - Delta cells → somatostatin S/Sx Can be Asx for some time Common s/sx: infections, fatigue, blurred vision, 4 Ps (paresthesia – aka pins & needles sensation, polydipsia – intense thirstiness, polyuria – abnormally large volumes of dilute urine, polyphagia – excess hunger/increased appetite) RF Older age, obese, FHx diabetes, CVD risk factors, gestational diabetes, polycystic ovary Complications Can be d/t poorly managed/untreated DM what we measure - Ideal is <7.0% 6. What are the consequences of glomerular vascular injury with regards to albumin and the development of chronic kidney disease? - Hyaline arteriosclerosis can occur in vessels of glomeruli and whenever these proteinaceous deposits within the glomeruli, it can damage glomeruli and lead to ⬆ filtration of proteins like albumin - This albumin can enter into the urine → microalbuminuria → over time can lead to CKD - Microalbuminuria MC cause of CKD 7. What portions of the anatomy are unable to make fructose from sorbitol, thereby being at risk for osmotic cell death? - In the lens of the eye, which could lead to cataracts - If it occurs in proximal convoluted tubule cells or other tubular cells it can lead to progression of nephropathy 8. What are some results of the demyelination of autonomic nerves that occurs as a result of Schwann cell damage? - The stomach can’t contract properly, leading to gastroparesis - If in bladder, they have a neurogenic bladder and urine retentive - If no nerves to blood vessels to promote vasoconstriction when they go from seated to standing & they need blood to get to the right side of the heart, they can become lightheaded and dizzy which is called orthostasis 9. What are some results of the demyelination of peripheral nerves that occurs as a result of Schwann cell damage? - MC is CN III (oculomotor), causes eye to move laterally and downward (but pupils are SPARED!) - Somatic sensory nerves supplying distal extremities bilaterally (loss of sensation, burning sensation aka dysesthesias, tingling sensation aka paresthesia) - Over time, sensory deficits may make the individual UNAWARE of their wounds and hyperglycemia impairs wound healing too. It can progress to foot ulcers Clinical Practice [ : Torres Interview] 1. How do you distinguish pre-diabetes from diabetes? a. Based on the A1C b. If A1C is between 5.7-6.4 this is prediabetic. People also do a fasting blood glucose <126 mg/dL. 100-126 is considered impaired fasting glucose & those individuals tend to have a higher propensity for developing diabetes down the road 2. Diabetes is a very complex condition and I imagine can be overwhelming for patients. Once you do diagnose a patient with diabetes, how do you explain it in a way they understand? a. Break things down to them in the simplest form and provide visuals to conceptualize things for them. b. Example given by Torres: imagine that the patient room is a RBC and in order to come into the room, you must open/close the door but you need the key. In the cell, you’d need insulin as the key to allow the sugar outside of the RBC to come in. When you have diabetes, you have too much sugar outside of the room and it cannot come inside of the room, so insulin allows the room door to open and have the sugar come inside the room to be utilized i. DM can become toxic to kidneys, eyes, nerves 3. What is the most important lab value when deciding initial treatment? a. A1C is going to determine the entry treatment; whether they need single or dual therapy b. Ex: If the person is symptomatic (polydipsia, polyphagia, polyuria) + high A1c (>9.0) → they require immediate insulin 4. How does the initial A1c help determine your choice of treatment in general terms? a. A1C <7.5 is a good indicator for monotherapy like Metformin, sulfonylureas (Glimepiride, Glipizide, Pioglitazone) b. One of the distinguishing factors to determine is the cost , compliance, frequency c. A1C 7.5-9 could be candidates for dual therapy like Actos (Pioglitazone) PLUS Glyburide or Glimepiride d. Symptoms can also help decide tx, if someone is Asx with high A1C (>9.0): you can put them on three agents e. If A1C >9.0 with symptoms: go straight to insulin 5. What factors do you consider in choosing the best oral agents(s) for patients? a. Metformin; it’s the least costly b. Consider renal clearance though, remember to discuss s/sx for hypoglycemia and educate pts on how check BS daily 6. What are your 3mo goals for treatment? a. First goal: educate them on what diabetes is and what the problem is & don’t overwhelm patients b. To have compliance, to understand their disease, to educate them on the target/goals of diabetes (e.g. keeping fasting glucose <130), check postprandial glucose (2 hours after meal) c. A1C: as long as the trajectory is going down 7. When do you consider starting basal insulin? a. If their A1C is going up and worry about compliance issue b. If A1C > 9.0 with symptoms → go right away to basal insulin 8. Describe the different types of insulin and their respective utilities. a. Rapid acting (e.g. Lispro, novolog) – lasts 45 min and they peak, good postporandial insulin to give after meals. those meds at dosed 3x a day with meals, check glucose before meals. If glucose <140 then don’t inject additional insulin. If 140-180 then do 2 units. If normal reaction, then 3 units. If high resistance to insulin, do 4 units. A lot of it is trial and error b. Education pt on s/sx on hypoglycemia c. Long acting (Glargine) – Basaglar, Lantus they’re dosed 1x daily and tend to last 24 hr d. Short acting – lasts 6 hours and given 3x daily, good for infusions like people with DKA or hospitalized pts e. Intermediate (NPH) or Long (Determir) – lasts around 12 hours and dosed 2x daily 9. Please briefly explain a sliding scale. a. A sliding scale on how to start rapid acting insulin 10. What health maintenance measures are employed and how often do patients receive them? a. Immediately when dx with DM, go get a retinal eye exam and then do it annually thereafter b. Keep up with dental exams, foot exams (3-6 mo) to check for sensation for monofilaments. See podiatrist if foot ulcers. c. Vaccinations (flu, Shingles) d. Check for renal damage every 3 mo: do CMP, urine microalbumin for nephropathy, hemoglobin A1C, lipid panel 11. When do you involve endocrinology in a patient's care? a. Type 1 diabetics: involve them immediately b/c they’re more complicated to manage b. Type 2 diabetes: after going over 3 oral agent or starting insulin, establish care with an endocrinologist in case things go crazy LMAO 12. When do you send a patient to the ER? a. Glucose >400-500 or spilling ketones in urine → worry for DKA esp for type 1 DM FLUID RESUSCITATION POTASSIUM INSULIN Rehydration improves responsiveness to insulin and use of NS prevents precipitous fall in extracellular osmolarity and resulting transfer of water into CNS - Children in particular can manifest cerebral edema even with correct fluid resuscitation - First 2L over 1-2 hrs, next 2L over 2-6 hrs, next 2L over 2-6 hours (be aware of extenuating circumstance such as acute decompensated HF being the pt’s precipitant for DKA etc.) - Some prefer to start with NS, then switch to .45% NS - When glucose reaches 250, switch to 5% dextrose in 45% NS Patients will almost invariably be total-body K+ deficient regardless of numeric value on CMP. The big risk here is fatal cardiac arrhythmias - K will fall very quickly once insulin is started (this KILLS PEOPLE) - If initial K > 3.3, <5.3 should get 10 mEq KCl/hr in IV fluids for at least 4 hours - If initial K < 3.3, should get 15 mEq/hr and DO NOT start insulin until K > 3.3 - Recheck K every 2 hours - Be aware of hypomagnesemia, this can be repleted orally Use regular insulin via infusion pump at 0.1 unit/kg/hr - Serum glucose generally decreases by 50 mg/dL/hr - Optional 0.1 mg/kg initial bolus in adults - Insulin should continue until serum ketones have cleared and anion gap has normalized - When glucose reaches 250, add 5% dextrose in 45% NS b/c glucose often normalizes before gap/ketones - Bicarbonate has no established role unless pH < 6.9 Hyperosmolar Hyperglycemia State (HHS) Description Hyperglycemia and hyperosmolarity with associated profound dehydration but NOT ketoacidosis b/c these patients do not have a total lack of insulin (why it’s more common in Type II) - In a type II diabetic pt, HHS results from physiologic stress (urine infxn/pneumonia MC) plus inadequate water intake (common in elderly) w/ underlying insulin resistance and/or deficiency - Mortality rate significantly higher than DKA - Can result in total body water losses of 20-25% of total body weight (~12L) - Takes longer than DKA to develop, meaning often more profound diuresis by time of presentation Three factors: 1. Insulin 2. Increased hepatic gluconeogenesis/glycogenolysis – the body 3. Profound osmotic resistance and/or thinks you’re glucose deficient even though you’re not so it’s diuresis → dehydration deficiency going to flip out and make a ton of glucose of liver and → impaired renal exacerbates the whole ordeal : glucose excretion Etiology S/Sx Dx Tx Usually elderly, type II diabetic with comorbid medical conditions that presents for AMS, weakness, anorexia - Limited access to water or means to communicate thirst to caregivers is a major RF - Common rx that predisposes to HHS: beta blockers, diuretics, glucocorticoids, CCB Signs of dehydration (sunken eyes, poor skin turgor, dry membranes, hypotension - Altered mental status - 15% present w/ seizures In general… Half the 8-12L fluid deficit should be replaced with 0.9% NS over first 12 hrs, second half over the next 24 hrs - Potassium repletion at 10-20 mEq/hr (same rationale as DKA) - Insulin at 0.1 unit/kg/hr +/- loading bolus AFTER volume repletion to avoid vascular collapse resulting from glucose going into cells and bringing H2O with it, thereby exacerbating dearth (lack) or intravascular volume So fluids FIRST, then potassium, THEN insulin! Hypoglycemia Etiology / Epidemio 3 components: - Brain needs glucose but is unable to synthesize/store it, accounting for AMS (altered mental status) - Vast majority of cases are iatrogenic (insulin, sulfonylureas most implicated) - Renal clearance of insulin decreases with increasing age and renal failure - Other RF: age, vascular disease, renal failure, decreased food ingestion, EtOH S/Sx AMS (altered mental status), lethargy, agitation, seizures, focal neuro deficits, vomiting, palpitations, tremor, sweating, bradycardia or tachycardia, tremor - Dis is why hypoglycemia is appropriate differential item for many different presenting symptoms Dx Bedside glucometer, then confirm with formal lab value (more accurate) Tx Glucose/dextrose - If AMS, need 50 mL IV bolus dose of 50% Dextrose in water to be repeated until hypoglycemia resolved - Once patient returns to baseline mental status (no longer aspiration risk), add PO carbohydrate. Can also use continuous infusion of D10 - If sulfonylurea induced, also give Octreotide - Check glucose level Ǫ30 min for first 2 hrs to check for rebound hypoglycemia Negative Feedback Loop Concept THYROID DIsORDERs Explanation by Jahn in his lecture video: An example of a negative feedback loop can be alluded to by a thermostat in the house. • Similar to how the body wants to maintain homeostasis, there must be a mechanism to regulate the thermostat ➔ The blue arrows in the image are the negative feedbacks ➔ Think of the pituitary gland like a thermostat and thyroid as the furnace, thyroid hormones as heat ➔ In pathologies, what happens when the thyroid/furnace stops working and does not respond to the thermostat? ◆ The furnace might just continue heating up regardless of what the thermostat reads Hypothyroidism Definition Any structural or functional derangement that interferes with production of adequate levels of thyroid hormones Etiology / Epidemio Approx 0.3% of population; 10x more common in females than males - Primary MC: pathology at the thyroid (leading to low T3 and T4, will show super high TSH) - Secondary: pathology at the pituitary gland - Tertiary: pathology at the hypothalamus S/Sx Effects of decreased metabolic rate: cold intolerance, weight gain, fatigue, increased menstrual flow d/t increased thyrotropin-releasing hormone ➔ Myopathy, dry (decreased sweat gland activity)/thickened/cool (vasoconstriction) skin, ptosis ➔ +/- goiter ➔ Nonpitting edema (myxedema) d/t high TSH leading to high glycosaminoglycans in the interstitum that elevates the osmotic pressure leading to water retention ➔ Hyporeflexia, constipation, decreased appetite (anorexia), depression, bradycardia Dx Initial test: TSH (thyroid stimulating hormone). - After initial: Then free T3/T4 - If primary: high TSH with low T3/T4 - If secondary or tertiary: low TSH with low T3/T4 Graves Disease Definition Autoimmune disease in which thyroid-stimulating autoantibodies (aka thyroid stimulating immunoglobulins) result in increased synthesis and release of thyroid hormones Etiology MC cause of hyperthyroidism in U.S. $ highest incidence in women 20-40 y/o S/sx Hyperthyroidism symptoms – diffusely enlarged, firm, palpable non-tender goiter +/- thyroid bruit PLUS: - Proptosis (bulging eyes ), diplopia (double vision) and pretibial myxedema; swollen red/brown patches on legs with non-pitting edema (all specific to Graves) Dx Decreased TSH, increased T4/T3. Pos thyroid-stimulating immunoglobulins - Radioactive uptake scan: diffuse, increased iodine uptake Tx Radioactive iodine ablation (MC), antithyroid rx (Methimazole/Propylthiouracil), partial or total thyroidectomy - Sx management: beta blockers - After radioactive tx, important to have pt avoid pregnant women and children and contraindicated in preg/lactating - should avoid getting pregnant until at least 4 months AFTER radioactive tx finished - Radioactive tx and smoking may worsen proptosis Thyroid Storm Definition Acute exacerbation; abrupt onset of severe hyperthyroidism Etiology Most commonly, pts suffer underlying Graves & there is an insult to the body that raises catecholamine levels (similar to myxedema coma and DKA/HHS) - Medical emergency; 8-25% mortality rate - 10x more common in females; most typically younger women - Illness can also alter the concentration of binding proteins like thyroid binding globulin and increase thyroid receptor sensitivity Sx Fever, tachycardia, hypertension. Often die of arrhythmias; can cause CHF - CNS: agitation, seizures, delirium, psychosis, coma - GI: n/v/d, jaundice Dx Clinically, can use Burch-Wartofsky Point Scale (BWPS) - Lab derangements: leukocytosis with left shift, hyperglycemia, hypercalcemia, elevated alk phos, elevated liver enzymes - ECG: sinus tach, afib/flutter, PVCs, heart block Tx Methimazole and propylthiouracil first if not pregnant, then Iodone and/or Lithium - If symptomatic: Propranolol - Glucocorticoids to block conversion of T4 to T3 (T3 is active form) Toxic Multinodular Goiter (Plummer Disease) Etiology Autonomous hyperfunctioning thyroid nodules (multiple) that produce thyrotoxicosis (aka hyperthyroidism) - Hyperplasia of thyroid follicular cells such that functionality of the thyroid hormone producing cells is independent of TSH input - Common in older patients and geographic regions of iodine deficiency S/sx Hyperthyroid sx from prev slides PLUS mass effect form goiter: dyspnea/dysphagia/stridor from tracheal/esophageal compression - Hoarseness from recurrent laryngeal nerve compression (innervates vocal cords) - NO SKIN OR EYE CHANGES as these are specific to Graves Disease Dx Increased T3/T4 and decreased TSH - Ultrasound: to assess nodules - Radioactive iodine scan: >1 focal areas of increased uptake Toxic Thyroid Gland Adenoma Etiology Single hyperfunctioning autonomous thyroid nodule. Most are follicular and benign - RF: iodine deficiency (rare in US). Certain genetic mutations. More common in females S/sx Many Asx with only a small palpable nodule - When symptomatic, same hyperthyroid & mass effect sx as MNG (multinodular goiter) Dx Increased T3/T4, decreased TSH Radioactive uptake: single “hot nodule” with decreased uptake in surrounding tissue Tx Surgery, ablation, thioamides - If symptomatic: beta blockers De Quervain Thyroiditis (Subacute/Granulomatous Thyroid Gland) Etiology Transient thyrotoxicosis from inflamed thyroid gland often occurring after viral infection S/sx Follows pattern of hyperthyroid → euthyroid → hypothyroid → resolution - Painful, tender thyroid gland, sore throat, neck pain exacerbated with head movement, coughing, swallowing. Diffusely tender goiter - Viral sx: low-grade fever, myalgias, malaise, fatigue, anorexia Dx Inflammatory markers: High ESR/CRP; and negative thyroid antibodies. TSH/T3/T4 pattern mirrors stage of presentation Radioactive uptake: diffuse, decreased iodine uptake Biopsy: granulomatous inflammation with multinucleated giant cells Tx Self-limiting; you can tx symptomatically - Neck discomfort: salicylates or NSAIDs - Severe/refractory: steroids Suppurative Thyroiditis Definition A rare bacterial infection of the thyroid gland Etiology Most commonly staph aureus, but can be other gram positives, gram negatives, and in the immunocompromised, coccidioidomycosis has been reported - Usually occurs in children S/sx Sudden onset of pain/tenderness to thyroid gland that worsens with extension and improves with flexion - Erythema, fevers/chills, dysphagia, dysphonia, hoarse voice Dx Thyroid function testing usually normal. May be a leukocytosis on CBC and elevated ESR (both nonspecific) - FNA: culture/gram stain to identify specific causative pathogen Tx Antibiotics (use broader spectrum that includes staph coverage and then pair down based on C&S) - Incision and drainage if amenable Postpartum Thyroiditis Etiology Autoimmune, occurs in approx. 7% of mothers. Self-limiting but 70% chance of reoccurrence in subsequent pregnancies - More common in women with pre-existing type 1 diabetes S/sx Starts with thyrotoxicosis followed by hypothyroidism Dx TSH/T3&T4 dependent on when they present (hypo vs hyper); positive thyroid antibodies - Radioactive iodine uptake: decreased Tx Self-limiting in 12-18 months - ASA/NSAIDs - NO anti-thyroid rx (not worth since self-limiting) Malignant Thyroid Nodules Benign Thyroid Nodules MC Diagnostic Algorithm Etiology/ RF Male gender, age <30 or >60, hx of radiation to neck, smoking, obesity, EtOH Comprise 90% of nodules (MC nodules are benign!), MC are follicular adenomas S/sx Rapid growth, fixed position, does not move with swallowing, obstructive sx from mass effect Smooth, firm, irregular, discrete and painless - Vast majority do not cause thyroid hormone derangements so are asymptomatic beyond mass effect Dx TSH then ultrasound - US: solid hypoechoic nodule, irregular margins, central vascularity, microcalcifications, abnormal lymphadenopathy - If TSH is high → hypofunctioning “cold nodule” on uptake scan → higher malignant potential → FNA TSH, then ultrasound - US: partially cystic with eccentric solid areas - If TSH is low → hyperfunctioning “hot” nodule on uptake scan → lower malignant potential so FNA NOT needed Tx If FNA inconclusive → thyroid scintigraphy (radioiodine uptake scan) If FNA suspicious for malignancy → surgical excision Observative and follow-up US Secondary Hyperparathyroidism Etiology / Epidemiology Any condition that results in chronic hypocalcemia, which then leads to compensatory overactivity of the parathyroid glands - Most common is renal failure: renal failure → decreased phosphate excretion → hyperphosphatemia → serum calcium suppression - Tertiary hyperparathyroidism: if PTH activity becomes autonomous/excessive, resulting in hyperCa - Also decreased ability to synthesize vit D in renal failure S/sx hypoPTH sx, while present, are generally not as severe as in primary and renal failure sx dominate more Hypoparathyroidism Etiology / Epidemiology If acquired, almost always inadvertent consequence of surgery (thyroidectomy) - Can also be autoimmune, genetic (i.e. DiGeorge syndrome) S/sx Consequences of hypocalcemia – tetany and increased DTRs aka hyperreflexia (neuromuscular irritability), circumoral/extremity paresthesias, laryngospasm, seizures, hallucinations/confusion/psychosis, increased ICP - If in early development, dental hypoplasia, defective enamel → abraded carious teeth - Chvostek sign: examiner taps on the course of the facial nerve, which induces contractions of the muscles in the eye, mouth, or nose - Trousseau sign: carpal spasms produced by occlusion of the circulation to the forearm and hand with a blood pressure cuff for several min Dx Triad: 1. hypoCa 2. Decreased PTH 3. Increased phosphate ECG: prolonged ǪT Tx Calcium and Vit D supplementation If symptomatic: IV Calcium gluconate + oral Calcitriol (Vit D) PITUITARY DIsORDERs Prolactinoma Etiology / Epidemiology Expansion of pituitary lactotroph cells on anterior pituitary that secrete prolactin - MC form of pituitary adenoma - Most are benign - Can be part of MEN 1 - Prolactin’s physiologic function is lactation, suppression of GNRH → decreased FHS/LG → suppression of pregnancy (during lactation) - Distinct from other pituitary hormones in that it receives hypothalamic inhibition through dopamine Sx oligomenorrhea/amenorrhea, decreased libido, decreased vaginal librucation, galactorrhea, erectile dysfunction, oligozoospermia (low sperm), osteopenia - HA/visual changes from mass effect - If optic chiasm compressed: bitemporal hemianopsia (vision loss on lateral vision field, bilaterally) Dx Increased prolactin decreased FHS/LH, MRI to visualize the tumor itself - TSH, GH, ACTH b/c often occur with hypersecretion of other pituitary hormones Tx First line: dopamine agonists (Bromocriptine) b/c dopamine inhibits prolactin release - If refractory to med tx or >3cm: transsphenoidal surgery Corticotroph Adenoma (or ACTH Cell Adenoma or Cushing’s Disease) Etiology / Epidemiology Adrenocorticotropic hormone (ACTH) releasing pituitary adenoma that results in too much cortisol (Cushing Syndrome) - When Cushing syndrome is caused by adenoma specifically, it’s called Cushing Disease Sx Weight giant (truncal obesity), HA, ED, oligomenorrhea, osteoporosis, mental disturbances (from mild to psychosis), limb muscle wasting/weakness, HTN, poor wound healing, pigmented striae - Think all the corticosteroid side effects/risk we’ve discussed Dx Overnight dexamethasone suppression (1mg), 24-hr urinary free cortisol and creatinine tests confirm hypercortisolism. Then need: - Increased ACTH but also cortisol suppression (at least 50%) with high dose (8 mg Dexamethasone) Tx Transsphenoidal resection of tumor - Need postop hydrocortisone - Need to be screened for hyponatremia, hypothyroidism afterwards (other cell types may be damaged in surgical process) Somatotroph Adenoma Etiology / Epidemiology Growth hormones secreting pituitary adenoma. GH increases glucose and insulin-like growth factor (IGF-1) - Children: Gigantism - Adults: Acromegaly Sx Both can have DM or glucose intolerance, CHF, HTN, gonadal dysfunction - Children (growth plates not closed): generalized increase in body size with disproportionately long arms and legs - Adults: large jaw with broadening of lower face (prognathism), enlarged forehead/tongue, large hands/feet with “sausage fingers”, increased bone density, deep voice, “doughy” skin Dx Elevated IGF-1. Then oral glucose suppression test to confirm MRI: to look at adenoma itself Tx Transsphenoidal surgery preferred - Meds: Octreotide, Dopamine agonists, Pegnisomant - If refractory to both surgery and meds: radiation rx SIADH (Syndrome of Inappropriate ADH) Etiology / Epidemiology Posterior pituitary hypersecretion of antidiuretic hormones (ADH aka Vasopressin) that results in excessive resorption of H2O and hyponatremia - Most common cause: CNS pathology (SAH, CVA, trauma, infection, tumors, iatrogenic from surgery - Can also be small-cell lung cancer, legionella pna, HIV, Rx (HCTZ, NSAIDs, TCA/SSRIs), elicit drugs (MDMA) Sx Hyponatremia → cerebral edema sx (from mild HA to death), will NOT have edema Dx Decreased serum osmolality & increased urine osmolarity (too much of NOT peeing, and NOT losing water) - Normovolemic hyponatremia, increased urine sodium Tx Remember risk of central pontine myelinolysis if correct hypoNa too quickly, so 3% NS reserved for obtunded or comatose patients - Mild: water restriction +/- salt tablets - Moderate: above measures PLUS ADH receptor antagonist SIADH Definition A condition where the body makes way too much ADH (as opposed to DI where there isn’t any ADH or kidneys don’t respond to ADH) - Aka syndrome of inappropriate antidiuretic hormone secretion Etiology Ectopic ADH secretion (tumor outside the hypothalamus or pituitary) → paraneoplastic syndrome (associated with small lung cell carcinoma) Other causes: central nervous system surgery or head trauma (could cause ADH released from damaged pituitary gland), pulmonary diseases (pneumonia, COPD), meds like Cyclophosphamide (⬆ ADH receptors on principal cells) S/sx Hyponatremia sx: could be Asx; anorexia, nausea, malaise are early sx - Later sx: headache, muscle cramps, irritability, drowsiness, confusion, weakness, seizures, coma PE : (may be seen only in severe/rapid-onset hyponatremia) → confusion, disorientation, delirium, generalized muscle weakness, myoclonus, tremor, asterixis, hyporeflexia, ataxia, dysarthria, Cheyne-Stokes respiration, pathologic reflexes, generalized seizures, coma - Euvolemic hyponatremia on PE aka no edema Complications: cerebral edema & seizures Dx Lab findings: hyponatremia, ⬇ serum osmolality, ⬆ urine osmolality Tx Fluid restriction! Correct hyponatremia: salt tablets, IV hypertonic saline; diuretics to excrete extra water Meds to antagonize Vasopressin receptor: Tolvaptan, Conivaptan, Demeclocycline If hyponatremia corrected too quickly → osmotic demyelination syndrome w/ severe neurological consequences Pheochromocytoma Definition Rare adrenal gland tumor where the cells darken when they form tumors Etiology Most arise sporadically; some are associated with an inherited syndrome Associated conditions: - Multiple endocrine neoplasias (type 2A and 2B → mutation in RET oncogene that causes cells to divide constantly) - Von Hippel-Lindau disease (mutation in VHL tumor suppresor protein → uncontrolled proliferation → tumors) - Neurofibromatosis (type 1 - mutation in NF1 gene, similar mechanism to VHL disease) Once developed, they cause problems by releasing too many catecholamines into the blood (unregulated) - Things that could trigger release: stress, physical exercise, wine, cheese, chocolate Sx Catecholamine release sx: HTN (>180/120 – hypertensive urgency) & could lead to hypertensive emergency and other conditions (CHF, ischemic/hemorrhagic stroke, retinal hemorrhage, kidney failure) - Common sites of mets: lymph nodes, liver, bone, lungs Sx: high blood pressure MC, anxiety, headaches, sweating, palpitations Dx Labs: testing for high levels of catecholamines (in blood or urine), metanephrine in urine Ultrasound/CT: can be used to identify location Multiple Endocrine Neoplasia (MEN) Definition Group of inherited diseases which cause tumors to grow in the endocrine glands of the body - Endocrine glands affected: pituitary gland, thyroid gland, parathyroid glands, adrenal glands, and the pancreas - There are tumors that form in these glands that leads to overproduction of hormones Etiology Genetic mutations in one of two genes (MEN1 or RET aka receptor tyrosine kinase) - Both of these genes have a dominant inheritance pattern Types: *know which endocrine organs are affected !* MEN TYPE 1 MEN TYPE 2A MEN TYPE 2B MUTATIONS in MENI GENE = “SHUTATIONS in RET GENES MUTATIONS in RET GENE PARATHYROID ADENOMAS PHEOCHROMOCYTOMA = PHEOCHROMOCYTOMA PANCREATIC TUMORS ~ MEDULLARY “Miponas HUCOSAL NEUROMAS = GLUCAGONOMAS ~ = MOUTH - GASTRINOMAS ~ INTESTINE (Osmosis.org