Endocrine System
Adrenal Crisis
Definition: Mineralocorticoid and glucocorticoid deficiency can lead to adrenal crisis. It is a life-threatening emergency requiring immediate treatment.
Presentation: shock with cardiovascular collapse, abdominal tenderness, fever, weight loss; may have hyperpigmentation from chronic corticotropin (ACTH) stimulation; serum electrolyte abnormalities.
Diagnosis and urgency: Endocrine emergency; requires rapid recognition and treatment.
Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic State (HHS)
Description: Serious acute diabetes complications characterized by uncontrolled hyperglycemia.
DKA specifics:
Classic triad: ext{anion gap metabolic acidosis}, ext{ ketonemia}, ext{hyperglycemia}
Serum glucose usually <800\ ext{mg/dL}, often 350-500\ \text{mg/dL}
Signs of dehydration: decreased skin turgor, dry axillae/oral mucosa, low JVP, tachycardia, hypotension if severe
DKA may present abdominal pain, fruity breath, and Kussmaul respirations
HHS specifics: Neurologic symptoms are more common than in DKA; often marked dehydration; often in type 2 DM or elderly with precipitating illness
Refer to ED for emergencies
Hyperprolactinemia
Potential sign of a pituitary adenoma; slow onset
Female presentation: amenorrhea; galactorrhea in both genders
Physiologic causes include pregnancy, lactation, stress
Serum prolactin elevated
Mass effect if tumor large: headaches and vision changes
Hypoglycemia
Definition: blood glucose < 70\ ext{mg/dL}
Symptoms: weakness, hand tremors, anxiety, sensation of impending syncope, difficulty concentrating
Epidemiology: more common in type 1 DM (about 5 ext{–}10 ext{0%} of diabetics experience episodes; average ~2 episodes/week)
ADA levels for diabetics:
Level 1 (glucose alert): ext{FBS} <70\text{ mg/dL but} >54\text{ mg/dL}
Level 2: <54\text{ mg/dL}
Level 3: severe event requiring assistance
Nondiabetic hypoglycemia: rare; reactive (diet-related) or fasting (disease-related)
Myxedema Coma
Medical emergency from severe hypothyroidism with mental status decline, hypothermia, bradycardia, hypoglycemia, hypotension, hypoventilation
Early recognition and treatment essential
Check labs: serum T4 (usually low), TSH (may be high), and cortisol
Pheochromocytoma
Rare adrenal tumor; age range ~20–50 but can occur at any age
Symptoms: random episodes of headache, diaphoresis, tachycardia with HTN; episodes resolve spontaneously; between attacks vitals normal
Triggers include: physical exertion, anxiety, stress, surgery, anesthesia, posture changes, labor/delivery
Dietary/Drug triggers: tyramine-rich foods (certain cheeses, beers, wines, chocolates, cured meats), MAOIs, stimulant drugs
Thyroid Cancer
Presentation: single thyroid nodule often in upper half of one lobe; may have cervical lymphadenopathy, swelling, or pain; hoarseness; dysphagia/dyspnea/cough
Risk factors: Childhood radiation exposure (Wilms’ tumor, lymphoma, neuroblastoma); low-iodine diet; higher prevalence in women; peak incidence 20–55 years; positive family history
Metastasis: via lymphatics
Type 1 Diabetes Mellitus (T1DM)
Common in childhood but can occur at any age
Classic presenting symptoms: polydipsia, polyuria, weight loss; polyphagia; blurred vision; fruity breath; ketonuria
DKA presentation possible; neurologic symptoms (drowsiness, lethargy) may progress to coma
Age distribution: peaks at ages 4–6 and 10–14
Normal Findings (Endocrine Feedback) and Target Organs
Endocrine system operates via negative feedback: low hormone → increased production; high hormone → production inhibited
Hypothalamus stimulates anterior pituitary to release stimulating hormones (FSH, LH, TSH)
Target organs respond by producing active hormones (e.g., estrogen, T3/T4, cortisol, etc.)
High levels of active hormones feedback to suppress stimulating hormones
Key target organs and hormones:
Thyroid (TSH → T3, T4)
Ovaries/Testes (FSH/LH → estrogen, progesterone, androgens, testosterone)
Adrenal cortex (ACTH → glucocorticoids, mineralocorticoids)
GH body-wide growth
Uterus (oxytocin) – contractions, bonding
Kidneys (vasopressin) – blood volume
Pineal (melatonin) – circadian rhythm
Breast (prolactin) – milk production
Abbreviations: ACTH, FSH, GH, LH, TSH
Endocrine Glands and HPA Axis
Hypothalamus: coordinates nervous and endocrine systems; sends neurohormones to stimulate or inhibit pituitary hormones
Pituitary Gland: located at the sella turcica; two lobes (anterior and posterior); stimulated by hypothalamus to release key hormones (FSH, LH, TSH, ACTH, GH, prolactin, MSH)
Anterior Pituitary (Adenohypophysis): secretes hormones that regulate target organs: FSH, LH, TSH, GH, ACTH, Prolactin, MSH
Posterior Pituitary: stores and secretes vasopressin (antidiuretic hormone) and oxytocin (made by hypothalamus)
Thyroid Gland: two lobes connected by isthmus; uses iodine to produce T3 and T4
Parathyroid Glands: regulate calcium balance via PTH
Pineal Gland: produces melatonin; regulates sleep-wake cycle
Addison’s Disease (Primary Adrenal Insufficiency)
Definition: autoimmune destruction commonly causing deficient mineralocorticoids and glucocorticoids
Risk: untreated → adrenal crisis under stress (infections, illness, injury)
Classic case findings: fatigue, weight loss, GI symptoms (nausea/vomiting/diarrhea/constipation), amenorrhea, myalgia, psychiatric changes (depression, psychosis); postural hypotension, salt craving, hyperpigmentation; presents in vasodilatory shock when crisis occurs
Labs in crisis:
Electrolytes: hyponatremia, hyperkalemia, hypercalcemia (rare)
Blood glucose: hypoglycemia may occur after fasting
CBC: normocytic anemia, eosinophilia
Diagnostic tests:
Serum ACTH, renin, cortisol, and aldosterone concentrations
High-dose ACTH stimulation test (250 μg) to exclude primary adrenal insufficiency and most secondary adrenal insufficiency
Primary AI: low cortisol with very high ACTH
Secondary (pituitary) and tertiary (hypothalamic) AI: both cortisol and ACTH inappropriately low
CRH stimulation to differentiate secondary vs tertiary AI
Secondary AI: little/no ACTH response
Tertiary AI: exaggerated/prolonged ACTH response due to CRH deficiency
Treatment plan:
Chronic primary AI: glucocorticoid replacement (e.g., hydrocortisone, dexamethasone, prednisone) and mineralocorticoid (fludrocortisone); DHEA may be considered in some women
Monitoring: use the lowest effective dose; monitor ACTH levels
Adrenal crisis: immediate IV fluids (normal saline or dextrose-containing if hypoglycemic) and IV hydrocortisone; intensive supportive care
Until crisis resolves: possible intubation, mechanical ventilation, vasopressors as needed
Special considerations:
Minor illness: 3x3 rule (double or triple maintenance glucocorticoid dose for 2–3 days)
Surgical procedures or severe illness: additional coverage may be needed (graded hydrocortisone dosing)
Emergency preparedness: medical alert bracelet; supplies for emergency glucocorticoid injections
Cushing’s Disease and Cushing’s Syndrome
Definition: Cushing’s syndrome from hypercortisolism; can be ACTH-dependent (most common) or ACTH-independent; most common cause is iatrogenic from exogenous glucocorticoids; Cushing’s disease is pituitary ACTH excess
Phenotype: moon face, buffalo hump, supra-clavicular fat, easy bruising, striae, skin atrophy, infections, edema, weight gain, menstrual changes, hirsutism, HTN, osteoporosis risk, venous thromboembolism, EKG abnormalities; symptoms vary by cause/duration/androgen excess/adrenal tumors
Labs/evaluation:
Electrolytes: hypokalemia, hypernatremia
Hyperglycemia from glucose intolerance
CBC: leukocytosis possible
Tests: serum ACTH, cortisol, aldosterone; first-line tests can include late-night salivary cortisol (2 measurements), 24-hour urinary free cortisol (2 measurements), overnight dexamethasone suppression test (1 mg)
Low suspicion: start with one first-line test
High suspicion: start with two or three first-line tests
Treatment plan:
Goal: reverse signs/symptoms and comorbidities; normalize cortisol secretion; eradicate tumor; avoid permanent dependence on glucocorticoids or hormone deficiency
Acute management: electrolyte stabilization and symptom control
Exogenous Cushing’s: taper glucocorticoids
Cushing’s disease: may require pituitary surgery or irradiation; medical therapy if not surgical candidate
Adrenalectomy for ACTH-secreting pituitary/ectopic tumors
Symptoms resolve gradually over 2–12 months after cure; HTN, osteoporosis, and glucose intolerance may improve but may require ongoing therapy
Tips:
Classic Cushingoid features: moon face, buffalo hump, acne, poor wound healing, purple striae, hirsutism, HTN, edema, menstrual disturbance
Addisonian features differ (see Addison’s section)
Diabetes Mellitus (DM)
Overview: Chronic metabolic disorder affecting carbohydrate metabolism; untreated can cause microvascular and macrovascular damage and immune effects
Microvascular complications: retinopathy, nephropathy, neuropathy
Macrovascular complications: atherosclerotic heart disease, MI, stroke
Type 1 Diabetes Mellitus (T1DM):
Autoimmune destruction of pancreatic beta cells → insulin deficiency
Presentation: polydipsia, polyuria, weight loss; may have DKA; fruity breath; most common in childhood; adults comprise ~5–10%
Pathophysiology: acute onset with ketosis; insulin deficiency with counterregulatory hormonal response to triggers
Type 2 Diabetes Mellitus (T2DM):
Progressive beta-cell dysfunction with insulin resistance; chronic hyperglycemia
Most common type (>90% of U.S. cases); many patients asymptomatic at diagnosis
Can present with HHS (hyperosmolar hyperglycemic state) without ketoacidosis
Metabolic Syndrome (MetS):
Alternative names: insulin-resistance syndrome, syndrome X
Increased risk for type 2 DM and cardiovascular disease
Criteria (any 3 of 5):
Male waist > 102\ ext{cm}; female waist > 88\ ext{cm}
HTN: ext{BP} \ge 130/85\ \text{mmHg} or treatment for HTN
Triglycerides \ge 150\ \text{mg/dL} or treatment
HDL: < 40\ \text{mg/dL} in men; < 50\ \text{mg/dL} in women or treatment
Hyperglycemia: FPG \ge 100\ \text{mg/dL} or treatment
Risk factors for T2DM (screening): BMI \ge 25\ \text{kg/m}^2 (or \ge 23\ \text{kg/m}^2 in Asian Americans) plus one or more risk factors (family history, central obesity, CVD, dyslipidemia, HTN, etc.)
Prediabetes and abnormal glucose tolerance:
Prediabetes criteria: A1C between 5.7\%\text{ and }6.4\%; fasting glucose 100-125\ \text{mg/dL}; 2-hour OGTT between 140-199\text{ mg/dL}
Diagnostic criteria for diabetes:
A1C \ge 6.5\%
FPG \ge 126\ \text{mg/dL} (8-hour fast)
Classic hyperglycemia symptoms + random plasma glucose \ge 200\ \text{mg/dL}
2-hour plasma glucose \ge 200\ \text{mg/dL} during an OGTT (75 g load)
Laboratory monitoring and tests:
A1C is used to estimate mean glucose, diagnose DM, and monitor treatment efficacy
Point-of-care blood glucose testing
Lipid profile at diagnosis and periodically (every 5 years if <40, more often if indicated)
Urine albumin-to-creatinine ratio for nephropathy progression monitoring
Check electrolytes (K+, Mg2+, Na+), creatinine, LFTs, TSH
Treatment plan (overview):
Lifestyle changes are first-line (preventive care recommendations)
Vital signs, weight, BMI, and blood glucose monitored at every visit; assess pulses, skin, acanthosis nigricans, injection sites, lipodystrophy
Blood pressure control is crucial to prevent CVD and renal progression; use ACE inhibitors, ARBs, or ARNI as appropriate
Pharmacotherapy to achieve glycemic targets; aim for A1C ≤ 7\% for most adults; consider individualized goals (less stringent in frail or high hypoglycemia risk; pregnancy requires tighter control)
Glycemic targets: FBG 80-130\text{ mg/dL}; postprandial < 180\text{ mg/dL} (2 hours after meals)
Medications for Diabetes (Drug Classes and Key Points)
Biguanides
Metformin (Glucophage): first-line for T2DM; decreases hepatic gluconeogenesis and intestinal glucose absorption; improves insulin sensitivity
Advantages: glycemic efficacy, modest weight loss, low hypoglycemia risk, tolerability, cost
Side effects: GI upset (diarrhea, nausea); B12 deficiency with long-term use
Monitoring: renal function (creatinine, eGFR), LFTs; risk of lactic acidosis in hypoxia/hypoperfusion/renal failure
IV contrast caution: hold for day of procedure and 48 hours after; baseline creatinine, reassess
Dosing tips: escalate if A1C remains >7%; if maximum dose (1 g BID) insufficient, consider add-ons
Sulfonylureas
Stimulate pancreatic beta cells to secrete insulin; decrease hepatic glucose output; increase insulin sensitivity
Generations: first-gen (chlorpropamide) less used due to hypoglycemia risk; second-gen (glipizide, glyburide, glimepiride)
Adverse effects: hypoglycemia, weight gain, photosensitivity, rash; monitor hepatic/renal function
Cautions: use with caution in hepatic/renal impairment
Thiazolidinediones (TZDs)
Pioglitazone (Actos) and Rosiglitazone (Avandia): increase insulin sensitivity in adipose/muscle/liver; often second/third-line
Not for NYHA III/IV HF; boxed warning for fluid retention; increased fracture risk; monitor LFTs
Meglitinides (Glinides)
Repaglinide (Prandin) and Nateglinide (Starlix): rapid-acting, pre-meal dosing; short half-life (<1 h)
Side effects: GI symptoms; hypoglycemia less risk than sulfonylureas; caution with liver disease
Bile-Acid Sequestrants
Colesevelam (Welchol): lowers LDL; modest glucose-lowering effect; not routinely recommended due to limited efficacy/cost
Take with meals; GI side effects; monitor renal/LFTs
Alpha-Glucosidase Inhibitors
Slow carbohydrate digestion/absorption; modest postprandial glucose reduction; no hypoglycemia risk
GI side effects: flatulence, diarrhea
GLP-1 Receptor Agonists (GLP-1 RAs)
Exenatide (Byetta), Liraglutide (Victoza): stimulate insulin, inhibit postprandial glucagon, slow gastric emptying; promote weight loss; CV and kidney benefits
Low hypoglycemia risk; GI side effects common; pancreatitis risk; contraindicated with personal/family history of medullary thyroid carcinoma or MEN2A/2B
SGLT2 Inhibitors
Canagliflozin (Invokana), Dapagliflozin (Farxiga), Empagliflozin (Jardiance): promote glucosuria; effective across DM stages; generally do not cause hypoglycemia
Benefits: CV risk reduction, CKD progression slowing
Side effects: polyuria, weight loss, dehydration, vulvovaginal candidiasis; caution with frequent UTIs, low bone density, fracture risk; monitor Cr
Cautions: risk of DKA in predisposed patients
DPP-4 Inhibitors
Sitagliptin (Januvia), Saxagliptin (Onglyza), Linagliptin (Tradjenta), Alogliptin (Nesina)
Mechanism: inhibit DPP-4 to enhance glucose-dependent insulin secretion; moderate glucose lowering; not typically first-line; possible joint pain, angioedema, pancreatitis risk; caution in CKD
Avoid combination therapy with GLP-1 RAs (no additive effect)
Amylin Analog
Pramlintide (SymlinPen): amylin analog; slows gastric emptying, suppresses glucagon, promotes satiety, weight loss
Used with prandial insulin; boxed warning for severe hypoglycemia when used with insulin; requires patient training
Insulin Therapy (Overview)
Prandial (rapid-acting): Lispro (Humalog), Aspart, Glulisine; onset 15–30 min; peak 1–3 h; duration 4–6 h; can be used IV in DKA/HHS
Regular (short-acting): Regular insulin; onset ~30 min; peak ~1.5–3.5 h; duration ~8 h; IV in hospital settings
Basal (intermediate-acting): NPH; onset/acting; dosing at least twice daily; mixing rules: draw Regular first, then NPH
Premixed: Humulin 70/30 (70% NPH, 30% Regular); often for noncompliance; not ideal for all patients
Basal analogs: Glargine (Lantus), Detemir (Levemir); longer-acting; once daily at fixed time
Concentrations: U-100 and U-300 insulin glargine; note half-life and duration variations
Insulin pumps: intensive training; expensive; suitable for T1DM and some T2DM; remove during swimming/showering
Injection sites: abdomen, leg, arm, buttock; absorption fastest in the abdomen; rotate sites
Practical tips (Pearls)
All patients with T1DM require insulin
Many T2DM patients start with metformin; insulin may be added if symptomatic or severe hyperglycemia or persistent hyperglycemia despite lifestyle changes and metformin
If diagnostic uncertainty or diabetes due to pancreatic insufficiency (e.g., CF), insulin is often indicated
Most T2DM patients eventually require exogenous insulin due to progressive beta-cell decline
For patients with CV/CKD/HFpEF, consider SGLT2 inhibitors and/or GLP-1 RA
If persistent hyperglycemia after metformin+other oral agents, consider insulin
Pharmacokinetics of commonly used insulin (prandial vs basal)
Rapid-acting analogs: Lispro, Aspart, Glulisine
Onset: [15, 30]\text{ min}
Peak: [1, 3]\text{ h}
Duration: [4, 6]\text{ h}
Regular insulin: onset \approx 30\text{ min}; peak 1.5-3.5\text{ h}; duration \approx 8\text{ h}
NPH (intermediate): half-life \approx 4.4\text{ h}; peak 4-6\text{ h}; duration \approx 12\text{ h}
Glargine (Lantus): half-life \approx 12\text{ h}; peak none; duration 20-24\text{ h} (U-100)
U-100 vs U-300 glargine: differences in onset/peak/duration; specify device/brand dosing
Detemir (Levemir): half-life 5-7\text{ h}; peak 3-9\text{ h}; duration 6-24\text{ h}
General Management of Diabetes and Preventive Care
Preventive care recommendations:
Lifestyle: weight loss (~7\% of body weight), physical activity 150 min/week, smoking cessation
Vaccinations: influenza, pneumococcal, Tdap, hepatitis B, zoster, COVID-19
PPSV23: one dose (age 19–64); after age 65, second dose per guidelines; revaccinate every 10 years
PCV13: one dose (age 19–64); after age 65, give PCV13 once after prior PCV23
Aspirin 81 mg: for high-risk MI/stroke; generally not recommended <30 years
Ophthalmology: yearly dilated eye exam; type 2 at diagnosis; type 1 after 5 years
Podiatry: refer yearly or more
BP target: < 130/80\text{ mmHg}
Dental care: important due to link between oral health and heart disease
Lipids: lipid management to improve/maintain profile
Glycemic targets and monitoring:
A1C target: ≤ 7\% for most adults; individualized based on risk/age/comorbidity; A1C goals may be as low as <6% or as high as <8% in certain patients
Fasting glucose target: 80-130\text{ mg/dL}
Postprandial target: < 180\text{ mg/dL} (2 hours after meals)
Illness and surgery management:
Self-monitoring during illness; do not stop antidiabetic meds unless advised; maintain fluids and electrolytes
Eat small frequent meals; do not fast excessively
Exercise considerations:
Exercise increases glucose utilization; monitor more frequently; have simple carbs before activity and complex carbs after to prevent post-exercise hypoglycemia
If hypoglycemia occurs after exercise, adjust insulin and/or intake to prevent nocturnal hypoglycemia if exercise occurs in afternoon
Dawn phenomenon and Diabetic Retinopathy/Foot care:
Dawn phenomenon: nocturnal GH spikes → morning hyperglycemia; adjust nighttime insulin/basal dosing
Diabetic retinopathy: screen with ophthalmology
Diabetic foot care: protective footwear; foot checks; podiatrist visits; inspect for ulcers; monofilament and vibration sense testing
Charcot’s foot (neuropathic arthropathy): foot deformity from neuropathy; may involve midfoot collapse
Complications of DM summary:
Eyes: retinopathy, cataracts, glaucoma, blindness
Dental: periodontal disease
Cardiovascular: hyperlipidemia, CAD, MI, HTN
Kidney: nephropathy
Feet: ulcers, infections, neuropathy, amputation
Gynecologic/genitourinary: candidal infections
Thyroid Disorders and Gland Tests
Primary hyperthyroidism (thyrotoxicosis)
Classic labs: very low TSH with elevated free T4 and T3
Most common cause: Graves’ disease (autoimmune) with higher prevalence in women; risk factors include family history and other autoimmune disease (RA, type 1 DM)
Classic presentation: weight loss with anxiety/insomnia, palpitations, HTN, tachyarrhythmias (AF/PAC), warm moist skin, ophthalmopathy with lid lag, frequent bowel movements, amenorrhea, heat intolerance, goiter, possible pretibial myxedema; signs in skin, eyes, thyroid, heart, GI, GU, extremities, neurologic, and psychiatric domains
Graves’ disease specifics
Labs: suppressed TSH (< 0.05\ \,\mathrm{mU/L}) with elevated free T4 and T3; TRAb/TSI positive; TPO antibodies may be positive in Graves' and Hashimoto’s
Diagnostics: thyroid ultrasound for palpable single mass; RAIU/thyroid scan to differentiate Graves' from toxic multinodular goiter/toxic adenoma; pregnancy is a contraindication for certain scans
First-line medications (thionamides):
Methimazole (Tapazole) – inhibits thyroid hormone synthesis
Propylthiouracil (PTU) – inhibits synthesis; preferred in the first trimester of pregnancy or in moderate-severe disease
Side effects: rash, granulocytopenia/aplastic anemia, thrombocytopenia, hepatic necrosis; monitor CBC and LFTs
Adjunctive treatment: beta-blockers (propranolol, metoprolol, atenolol) for symptom relief
Radioactive iodine (RAI): contraindicated in pregnancy/lactation; ablates thyroid leading to lifelong hypothyroidism
Complication: thyroid storm (thyrotoxicosis) – sudden, life-threatening elevation of HR, BP, and temperature; requires urgent hospitalization
Thyroid nodules and cancer diagnostics
Thyroid ultrasound for goiter, multinodular goiter, nodules; fine-needle biopsy for cancer
Thyroid scans and RAIU to categorize hot vs cold nodules; hot usually benign; cold spots raise concern
Primary hypothyroidism and Hashimoto’s thyroiditis
Primary hypothyroidism: high TSH with low free T4; most common cause worldwide is Hashimoto’s thyroiditis
Hashimoto’s: autoimmune destruction of thyroid; TPO antibodies present in ~90% of cases; goiter common in Hashimoto’s
Subclinical hypothyroidism: TSH > 5.0\ mU/L with normal free T4
Subclinical hyperthyroidism: low TSH with normal free T4 and T3
Treatments:
Levothyroxine (Synthroid) replacement; typical full replacement dose ~1.6\ \mu g/kg/day; dosing ranges from 50-200+\ \mu g/day depending on patient factors
Start low in older adults or those with heart disease (e.g., 25-50\ \mu g/day); titrate every few weeks to normalize TSH
Monitor TSH every 6-8\ weeks until normal; then every 6-12\ months when stable
Pearls:
Subclinical hypothyroidism can progress to overt hypothyroidism
Some patients prefer Armour thyroid (desiccated pig thyroid) containing T3 and T4; evidence mixed
All hyperthyroid patients should be managed with an endocrinologist
Diagnostic labs and test interpretation (thyroid)
TSH ranges: normal roughly 0.5-5.0\ \,\mathrm{mU/L} (third-generation assay)
Free T4 and T3 used to corroborate diagnosis
If a goiter or nodules: thyroid ultrasound; if nodules, consider fine-needle aspiration biopsy
Antibody testing: TPO antibodies; TRAb/TSI support Graves' diagnosis
Test interpretations
Hyperthyroidism: TSH < 0.05\ \,\mathrm{mU/L}; Free T4/T3 elevated; TRAb positive in Graves’
Subclinical hyperthyroidism: TSH < 0.05\ \,\mathrm{mU/L}; Free T4/T3 normal
Hypothyroidism (overt): TSH > 5.0\ \,\mathrm{mU/L}; Free T4 low
Subclinical hypothyroidism: TSH > 5.0\ \,\mathrm{mU/L}; Free T4 normal
Practical treatment notes and reminders
In hyperthyroid patients, monitor for osteoporosis; supplement calcium and vitamin D if indicated
Crush levothyroxine tablets before swallowing to improve absorption
Avoid Armour thyroid unless specifically indicated or preferred by patient; ensure monitoring
Case Scenarios and Exam Pearls
General exam tips (insights from case scenarios):
Images of funduscopic exams in diabetic retinopathy are common on exams; review common findings including cotton-wool spots, microaneurysms, neovascularization
Charcot’s foot is more common in diabetes and should be recognized clinically
In insulin adjustment cases, understand the concept of meal-time bolus versus basal needs; e.g., lispro covers meals; basal glargine provides overnight coverage
Insulin-related problem solving example:
If lunch glucose is high in a patient using lispro before meals and glargine once daily, consider increasing lispro dose to cover lunch; basal dose might require adjustment if morning and afternoon readings remain high
Quick Reference: Key Numeric Thresholds and Targets
Hypoglycemia (diabetics):
Level 1: <70\ \text{and} \ >54\ \text{mg/dL}
Level 2: <54\ \text{mg/dL}
Level 3: severe event requiring assistance
DKA features: anion gap metabolic acidosis, ketonemia, hyperglycemia; glucose often 350-500\ \text{mg/dL}; can be <800 mg/dL
HHS: severe hyperglycemia with marked dehydration and altered mental status; often in type 2 DM
Metabolic syndrome cutoffs (any three):
Waist: men > 102\ \text{cm}, women > 88\ \text{cm}
BP: \ge 130/85\text{ mmHg} or treatment
Triglycerides: \ge 150\ \text{mg/dL}
HDL: men < 40\ \text{mg/dL}, women < 50\ \text{mg/dL} or treatment
Fasting glucose: \ge 100\ \text{mg/dL} or treatment
Diabetes diagnostic cutoffs:
A1C \ge 6.5\%
FPG \ge 126\ \text{mg/dL}
2-hr OGTT \ge 200\ \text{mg/dL}
Symptoms + random glucose \ge 200\ \text{mg/dL}
Thyroid lab reference points:
TSH: normal roughly 0.5-5.0\ \mathrm{mU/L} (third-gen assay)
Hypothyroidism: high TSH with low free T4
Hyperthyroidism: low TSH with high free T4 and T3
Graves’ antibodies: TRAb/TSI positive; TPO commonly positive in Graves’ and Hashimoto’s
Notes
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