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ENDOCRINOLOGY - Coggle Diagram

- - - - most common
      - progressive gland destruction
      - usually presents in hypothyroid phase & TFTs like that of hypothyroidism
    - - self-limiting; usually preceded by viral illness
      - painful thyroid gland
      - triphasic clinical course; over months
      - labs: elevated ESR, radioactive iodine uptake low
      - tx: NSAIDs for symptoms
    - - mild alteration in TFTs requiring no treatment
      - diffuse lymphocytic infiltration of thyroid gland
      - triphasic clinical course
    - - usually within 6 months of childbirth
      - 20% will have permanent hypothyroidism
- - - - adrenocorticotropic hormone (ACTH)
      - thyroid stimulating hormone (TSH)
      - follicular stimulating hormone (FSH)
      - luteinizing hormone (LH)
      - prolactin (PRL)
      - growth hormone (GH)
    - - antidiuretic hormone (ADH) aka vasopressin
      - oxytocin
  - - - size:
        
        macroadenoma = >1cm
        
        microadenoma = <1cm
      - cell type:
        
        gonadotroph --> NFPA
        
        thyrotroph --> NFPA or hyperthyroidism
        
        corticotroph --> Cushing's disease
        
        lactotroph --> hyperprolactinemia --> hypogonadism
        
        somatotroph --> acromegaly
    - - the only pituitary tumor that has non-surgical first line treatment
      - treatment: dopamine agonists
    - - surgical intervention indicated for pituitary hormone deficiency, optic nerve compression, sellar or bone invasion
- - - - mobilize calcium from skeletal stores
      - increase osteoclast activity & bone resorption
      - stimulates calcium reabsorption & inhibits phosphate reabsorption in the kidneys
      - stimulates vitamin D to active form
    - - DECREASES calcium
      - suppresses bone resorption (inhibits osteoclasts)
      - inhibits renal resorption of calcium & phosphorus
    - - stimulates intestinal absorption of calcium & phophate
      - helps calcium efflux out of bone in concert with PTH
      - deficiency:
        
        Rickets (children) or Osteomalacia (adults)
        
        impaired mineralization of new bone matrix
        
        causes: inadequate exposure to sunlight, decreased dietary intake, liver/kidney disease, malabsorption, genetic defects
  - - - [N]eoplasm (SCC, RCC, ovarian, breast, MM, mets)
      - [D]rugs (thiazides, theophylline, lithium)
      - [I]nfection (TB, coccidiomycosis, histoplasmosis)
      - [T]PN
      - [M]ilk alkali/milk of magnesia
      - [R]enal failure (tertiary hyperparathyroidism)
      - [A]ddison's (adrenal insufficiency)
      - vitamin [A] excess
      - [T]hyrotoxicosis
      - [P]rimary hyperparathyroidism (#1 cause)
      - [I]mmobilization
      - [P]aget's of bone
      - [V]itamin D excess
      - [S]arcoid
  - - - adenoma, hyperplasia, carcinoma
      - labs: high calcium, low phosphorus, inappropriately high PTH
      - management: surgery, bisphosphonates, calcimimetics
    - - renal insufficiency, vitamin D deficiency
      - labs: low calcium, high/low phosphorus, high PTH
      - Osteitis Fibrosa Cystica - increased bone turnover; defective mineralization, cysts/nodules
    - - autonomous PTH secretion from long standing history of secondary hyperparathyroidism; CKD or kidney transplant
      - treatment: 3 gland parathyroidectomy
      - labs: high calcium, variable phosphorus, high PTH
  - - - low PTH states - surgical hypoparathyroidectomy or extensive neck dissections, autoimmune, abnormal parathyroid gland development (DiGeorge Syndrome)
      - high PTH states - sepsis, pancreatitis, vitamin D deficiency, large volume transfusions
- - - - ~5%
      - absolute insulin deficiency caused by autoimmune destruction of pancreatic beta cells
      - younger age of onset, higher risk of ketosis, less insulin resistance, presence of islet cell antibodies
      - thin/losing weight, rapid progression, polyuria, polydipsia, polyphagia, weakness/fatigue, DKA
    - - 90-95%
      - insulin resistance AND relative insulin deficiency
      - genetic predisposition + excess body weight
      - obese, slow progression, may be asymptomatic, blurry vision, recurrent vaginal yeast infections, peripheral neuropathy, acanthosis nigricans
    - - diagnosis of DM during pregnancy
      - the insulin resistance of pregnancy is thought to be due to the effects of increased production of human placental lactogen & placental growth hormone
      - asymptomatic, macrosomic infant
      - OGTT test:
        
        performed at 24-28 weeks gestation
        
        fasting >= 92 mg/dL
        
        1 hr >=180 mg/dL
        
        2 hr >= 153 mg/dL
    - - looks like type 2 but pt may be "skinny", have a strong FHx of T2DM in early adulthood, had a known predisposing condition
  - - - impaired glucose tolerance: 2 hr plasma glucose 140-199 mg/dL
      - HbA1c 5.7-6.4%
      - impaired fasting glucose: 100-125 mg/dl
    - - fasting plasma glucose >= 126 mg/dL
      - 2 hr plasma glucose >=200 mg/dL
      - in a pt with classic symptoms of hyperglycemia or hyperglycemic crisis PLUS a random plasma glucose >= 200 mg/dL
      - HbA1c >= 6.5%
  - - - DKA -- triad of hyperglycemia, anion gap metabolic acidosis, and ketonemia
      - HHS -- little/no ketoacid accumulation, plasma glucose frequently exceeds 1000 mg/dL, serum osmolality is elevated, neurologic abnormalities (i.e. coma)
    - - macrovascular -- CVD, stroke, PAD
      - microvascular -- retinopathy, nephropathy, peripheral neuropathy, autonomic neuropathy (gastroparesis, BP instability, sexual dysfunction)
    - - infant -- macrosomia, shoulder dystocia, structural anomalies, cardiac septal hypertrophy, neonatal respiratory distress syndrome, hypoglycemia, hypocalcemia, hyperbilirubinemia, polycythemia
      - mother -- labor & delivery complications, higher rate of c-section delivery, pre-ecclampsia, HTN, progression of microvascular complications
  - - - biguanides
        
        Metformin
        
        decrease hepatic glucose production and increased insulin-mediated peripheral glucose uptake
        
        other effects: diarrhea & abdominal discomfort, lactic acidosis, no weight gain to modest weight gain
        
        cheap
        
        contraindications: eGFR <30
      - sulfonylureas
        
        glyburide, glipizide, glimepiride
        
        increase endogenous insulin secretion
        
        other effects: hypoglycemia, weight gain, pancreatic exhaustion
        
        generally least expensive class of medication
        
        avoid in renal & liver failure, elderly, & pts at risk for hypoglycemia
        
        indications: contraindications to metformin, severe hyperglycemia, MODY
      - meglitinides
        
        stimulate insulin secretion in the presence of glucose
        
        other effects: hypoglycemia, weight gain, safe at higher levels of serum Cr than sulfonylureas
        
        repaglinide, nateglinide
        
        must be taken with meals; shorter-acting
      - thiazolidinediones (TZD)
        
        decrease insulin resistance by making muscle and adipose cells more sensitive to insulin; also suppresses hepatic glucose production
        
        other effects: weight gain, edema, increased risk for osteoporosis & osteoporotic fractures, improves HDL cholesterol & plasma triglycerides, can help treat early stage fatty liver disease
        
        most expensive
        
        contraindications: pts with CHF
        
        pioglitazone
        
        black box warning for increased risk of bladder cancer
      - alpha-glucosidase inhibitors
        
        block the enzymes that digest starches in the small intestine
        
        other effects: flatulence or abdominal discomfort, no weight gain
        
        contraindicated in pts with IBD or cirrhosis
        
        acarbose, miglitol
      - GLP-1 mimetics
        
        increases insulin secretion in a meal-dependent manner
        
        now available in weekly formulations and in single injections premixed w/ long-acting insulin
        
        other effects: significant N/V, slows gastric emptying/reduces appetite, promotes weight loss, CV protective, potentially preserves beta-cell mass
        
        contraindications: pts with hx of medullary thyroid carcinoma, MEN-2 or pancreatitis
        
        exenatide, liraglutide, lixisenatide
      - DPP4 inhibitors
        
        increased GLP-1 levels which increases insulin secretion in response to a meal
        
        other effects: oral but weaker version of GLP-1
        
        sitagliptin, saxagliptin, linagliptin
      - SGLT2 inhibitors
        
        inhibits the sodium-glucose cotransporter 2 which prevents the reabsorption of glucose in the kidneys
        
        other effects: atherosclerotic CVD, reduce progression of diabetic kidney disease, reduce CV death/hospitalization for HF, decreased weight, decreased bp, increased GU infections, euglycemic DKA
        
        black box warning for increased risk of amputations for canagliflozin
        
        canagliflozin, dapagliflozin, empagliflozin
    - - basal:
        
        NPH
        
        onset: 1-2 hrs
        
        peak: 4-6 hrs
        
        duration: 12-16 hrs
        
        Glargine
        
        onset: 2-3 hrs
        
        peak: "peakless"
        
        duration: 24 hrs
        
        Detemir
        
        onset: 1-2 hrs
        
        peak: 3-9 hrs
        
        duration: 6-24 hrs
      - bolus/prandial
        
        Regular
        
        onset: 30min-1hr
        
        peak: 1.5-3.5 hrs
        
        duration: 6-8 hrs
        
        Aspart Lispro Glulisine
        
        onset: 5-15 min
        
        peak: 30min-1hr
        
        duration: 3-5 hrs
  - - - primarily seen in T1DM
      - complex disordered metabolic state characterized by hyperglycemia, metabolic acidosis, and ketonuria
      - common precipitating factors: infection, intoxication, ischemia, iatrogenic (corticosteroids), impregnation, insulin (lack of)
      - polyuria, polydipsia, polyphagia, fatigue, N/V, abdominal pain, weight loss, dehydration, Kussmaul respirations, fruity odor to breath, altered mentation
      - labs: fingerstick blood glucose, BMP, serum ketones, UA, blood gas, serum osmolarity, HbA1c
      - diagnosis: pH <7.3, serum bicarbonate <18, anion gap >12 in the setting of elevated ketones, glucose >350
      - pseudohyponatremia, K+ levels normal/high but total body K+ stores severely depleted
      - management: IV fluid resuscitation, potassium replacement, IV insulin, serial laboratory & clinical monitoring, assess for underlying causes, add dextrose to fluids when BG <250
      - complication of DKA treatment: cerebral edema --> due to very rapid correction of blood glucose (headache, AMS, lethargy); treat with mannitol & dexamethasone
    - - a syndrome of decompensated diabetes with severe hyperglycemia & dehydration with hyperosmolarity
      - usually a state of severe T2DM
      - unlike DKA, the body is producing enough insulin to prevent ketosis, so anion gap & ketones are generally normal
      - higher mortality rate than DKA, but far less common
      - pts more often have altered mental status
      - provoking factors: infection, new-onset diabetes, acute illness, non-compliance
      - severe dehydration w/o acidosis
      - prolonged course of polydipsia, polyuria, fatigue, weight loss; severe signs of clinical dehydration, signs of infection/sepsis, AMS (confusion up to coma)
      - diagnosis: BG >600 mg/dL, serum osmolality >320mOsm/kg, pH >7.3, bicarbonate >15 mEq/L
      - treatment: ABCs, O2, monitor, large volume IV fluids, IV insulin, potassium, identification & treatment of underlying cause
    - - etiologies: iatrogenic, severe malnutrition, factitious insulin intake, weight loss, increased exercise, gastroparesis, N/V, CKD, sulfonylureas, chronic liver disease, medications (beta blockers)
      - diaphoresis, tremors, palpitations/tachycardia, anxiety, dizziness, headache, cloudy/blurry vision, confusion, seizures, LOC
      - RF: tight control of diabetes, T1DM, inexperience w/ insulin, pts with CKD, liver disease, elderly & malnourished
      - treatment: 15 g oral carbohydrate
- - - - aldosteronism producing adenoma, bilateral adrenal hyperplasia
      - symptoms: hypertension, hypokalemia, hypernatremia, hypervolemia without peripheral edema, metabolic alkalosis
      - screening tests: plasma aldosterone concentration (PAC) >15ng/dL, plasma renin level ratio (PRA) >20
      - confirmatory tests: oral sodium suppression, supine IV saline suppression, Fludrocortisone suppression, Captopril challenge
      - gold standard: adrenal vein sampling (AVS)
      - treatment: for adenoma adrenalectomy or mineralocorticoid receptor antagonists; for bilateral adrenal hyperplasia mineralocorticoid receptor antagonists
    - - any condition which reduces renal blood flow therefore stimulating the renin-angiotensin system, renin secreting tumors (rare)
      - diagnostic criteria: 1. structural abnormality 2. functional abnormality (evidence of excess renin secretion by the affected kidney)
  - - - Cushing's syndrome
      - adrenal carcinoma (very rare)
      - congenital adrenal hyperplasia
        
        autosomal recessive
        
        most common mutation is 21-hydroxylase
  - - - aldosterone --> Aldosteronism
      - glucocorticoids --> Cushing's
      - androgens --> virilization syndromes
      - catecholamines --> Pheochromocytomas
- - - - causes: corticosteroid treatment, autoimmune lymphocytic hypophysitis, tumor of hypothalamic-pituitary region
      - no hyperpigmentation, severe hyponatremia, severe dehydration, or hyperkalemia
    - - Addison's disease
      - causes: autoimmune adrenalitis, infectious adrenalitis, bilateral adrenal hemorrhage, adrenal infiltration
      - in addition to glucocorticoids, also need to treat mineralocorticoid deficiency with mineralocorticoids (fluodrocortisone) and liberal access to salt
    - - dehydration, hypotension, shock out of proportion to severity of current illness, N/V with history of weight loss & anorexia, abdominal pain, unexplained hypoglycemia, unexplained fever, hyponatremia, hyperkalemia, azotemia, hypercalcemia, eosinophilia, hyperpigmentation or vitiligo, hypothyroidism and gonadal failure
      - treatment: IV fluid replacement, reversal of electrolyte abnormalities, IV dexamethasone or hydrocortisone
- - - - primary (thyroid failure):
        
        most common
        
        MOA: Hashimoto thyroiditis, radioactive iodine therapy, subtotal thyroidectomy, excessive iodide intake, subacute thyroiditis, iodide deficiency, inborn errors of thyroid hormone synthesis, drugs
        
        Hashimoto thyroiditis:
        
        transient "hashitoxicosis" period of hyperthyroidism (usually unrecognized) followed by euthyroid period, then permanent hypothyroidism
        
        lymphocytes become sensitized to thyroidal antigens --> infiltration --> destruction of thyroid gland
        
        painless
        
        antibodies: TPO ab, Tg Ab, TRAb
        
        treatment: levothyroxine therapy
      - secondary (pituitary TSH deficiency)
        
        MOA: hypopituitarism due to pituitary adenoma, pituitary ablative therapy, or pituitary destruction
      - tertiary (hypothalamic deficiency of TRH)
        
        MOA: hypothalamic dysfunction (rare)
      - Peripheral resistance to the action of thyroid hormones
    - - endocrine emergency requiring hospitalization and possibly ICU level care
      - end stage of untreated hypothyroidism
      - progressive weakness & stupor, hypothermia, bradycardia, hypercapnea & hypoxia, hyponatremia
  - - - 3) Is it causing significant enough compression on structures in the neck to cause problems with speaking, swallowing, or breathing?
      - 2) Is it thyroid cancer?
      - 1) Is it causing hyperthyroidism? aka a toxic nodule or toxic multinodular goiter
    - - enlarged thyroid gland with many nodules
      - "non-toxic" if it is not associated with hyperthyroidism
      - worldwide MCC = iodine deficiency
      - developed countries MCC = Hashimoto's thyroiditis
      - impaired hormone synthesis drives TSH secretion which induces thyroid hyperplasia, including areas of focal hyperplasia w/ necrosis
      - usually euthyroid; but if TSH is low --> toxic multinodular goiter
    - - includes papillary (most common type) & follicular thyroid cancer
      - slow growing neck mass, often discovered incidentally
      - excellent prognosis, esp. if pt <55yo
      - treatment: surgery followed by radioiodine therapy and thyroid hormone suppression therapy (levothyroxine to suppress TSH)
      - advanced differentiated -- systemic chemotherapy, external radiotherapy, percutaneous ethanol injection of cervical nodal metastases
    - - arises from parafollicular c-cells of thyroid gland
      - occurs in MEN 2a, MEN 2b, and familial MTC syndromes
      - produce calcitonin & CEA (can serve as serum tumor markers)
      - survival is very good typically
      - may metastasize to nodes, bone, brain, liver
      - treatment: total thyroidectomy +/- cervical node dissection
    - - least common
      - almost always rapidly fatal (distal metastases common)
      - should be evaluated for the presence of a BRAF mutation ASAP
      - treatment depends on staging and may include: surgical resection, BRAF/MEK inhibitor therapy, cytotoxic chemotherapy, eternal beam radiation
      - palliative/comfort care should be part of treatment plan up front