Course: Pathophysiology · Professor: E. Schaumberg, PT, MS, DPT, PhD Sources: Endocrine System and Disorders Part 1 (2025-26) + Part 2 Student (2025-2026)
The endocrine system is the body’s slow, long-acting control system: glands release hormones that travel through the blood and act only on cells with matching receptors. Almost every disorder in this module is one of two things — hypofunction or hyperfunction of a gland — and the professor wants you to reason from that: if a hormone is missing or excessive, what happens to the tissues it normally controls?
The lecture moves gland by gland: Part I covers general principles, the hypothalamus–pituitary, thyroid, and parathyroid; Part II covers the adrenal gland, the endocrine pancreas (diabetes — the biggest chunk), metabolic syndrome, and aging. For PT, the recurring questions are always: How does this affect muscle, bone, nerve, and exercise tolerance — and what should I monitor or avoid?
Note on objectives: The Part II objective slides are images with no extractable text. Part I ends with “Next up… Adrenal gland,” so these notes treat the six Part I objectives as covering the whole two-part lecture. Check the Part II deck to confirm.
Image-only slides: Several Part II slides had no text (e.g., insulin actions summary, hormonal glucose management summary, cardinal signs of DM, T2DM pathogenesis figure, “After Exercise”). Where I filled in standard content for those, it’s marked [image slide — verify against deck].
| # | Objective | Can I speak to it? |
|---|---|---|
| 1 | Review and describe the anatomy, histology, and physiology of the endocrine system | ☐ |
| 2 | Describe positive and negative feedback loops and how endocrine function is regulated | ☐ |
| 3 | Identify the endocrine glands, their hormones, and the primary actions of those hormones | ☐ |
| 4 | Describe the effects of aging, physical (including exercise) and psychological stressors on the endocrine system | ☐ |
| 5 | Explain how endocrine dysfunction (hypo/hyperfunction) affects the neuromusculoskeletal system | ☐ |
| 6 | Outline specific endocrine diseases: pathophysiology, signs & symptoms, medical management, PT considerations | ☐ |
Can I speak to it? ☐
5 general functions 1. Maintain an optimal internal environment across the life span 2. Initiate corrective/adaptive responses to emergency demands 3. Differentiate the reproductive and central nervous systems of the developing fetus 4. Stimulate sequential growth and development in childhood/adolescence 5. Coordinate male and female reproductive systems
By what they target - Effector hormones → act directly on target tissue (e.g., GH, prolactin, ADH, oxytocin) - Tropic hormones → act on other glands (e.g., TSH, ACTH, FSH, LH)
By chemical structure
| Type | Made from | Solubility | Examples |
|---|---|---|---|
| Peptide | Proteins | Water-soluble | GH, insulin, leptin, PTH, prolactin |
| Amine | Amino acids | Water-soluble | Catecholamines from adrenal medulla: epinephrine, norepinephrine, dopamine |
| Steroid | Cholesterol | Lipid-soluble | Estrogens, glucocorticoids (cortisol), mineralocorticoids (aldosterone), progesterone, testosterone |
Contrast: water-soluble peptide/amine hormones can’t cross the membrane — they bind surface receptors and act through second-messenger pathways (faster).
Can I speak to it? ☐
🔗 This is the core of Type 2 diabetes: insulin is present, but receptor sensitivity is impaired. Receptor sensitivity is affected by age, weight***, abdominal fat, and physical activity*** (starred on the slide).
Can I speak to it? ☐
| Hormone | Type | Target | Action |
|---|---|---|---|
| GH | Effector | Bone, muscle, organs | ↑ growth & cell reproduction; nitrogen retention; ↑ protein synthesis |
| Prolactin | Effector | Mammary glands | Lactation |
| TSH | Tropic | Thyroid | ↑ T3/T4 secretion |
| ACTH | Tropic | Adrenal cortex | Cortisol synthesis (also stimulates aldosterone) |
| LH | Tropic | Gonads | Ovulation (estrogen/progesterone from corpus luteum); testosterone in males |
| FSH | Tropic | Gonads | Follicle development/estrogen (F); spermatogenesis (M) |
| Lipotropin | — | — | Fat lysis; ↑ melanin production |
The pituitary also secretes endorphins.
| Hormone | Target | Action | Released by |
|---|---|---|---|
| ADH (vasopressin) | Kidney DCT & collecting duct | Water conservation (↑ reabsorption); ↑ BP via arteriolar vasoconstriction | ↓ water content (↑ plasma osmolality / ↓ volume); shock, hemorrhage, pain, emotional stress, trauma, positive-pressure breathing |
| Oxytocin | Uterus, breast | Contraction; milk release; social bonding, well-being; circadian rhythm | Hypothalamic impulses; cervical/nipple stretch; hugging/cuddling |
| Hormone | Target | Actions | Regulated by |
|---|---|---|---|
| T3, T4 | All tissues | ↑ basal metabolic rate; regulates oxidation, growth, gluconeogenesis, fat mobilization, protein synthesis; heat production; cardiac rate/force/output; muscle tone; GI secretion; RBC production; CNS development; insulin antagonist in liver/agonist in muscle | TRH → TSH (negative feedback) |
| Calcitonin | Bone, plasma | ↑ Ca²⁺ storage in bone; ↓ blood Ca²⁺; phosphorus metabolism | ↑ blood Ca²⁺ (hypercalcemia) |
Glucocorticoids — cortisol (steroid) - Released under stress: hypoglycemia, hypoxia, exercise. - Primary role: mobilize blood glucose for the fight/flight/freeze response → gluconeogenesis, glycogenolysis, ↓ glucose uptake in muscle → more glucose for the brain. - Other effects: protein catabolism, mood, anti-inflammatory, immunosuppressive, growth-suppressing. - Long-term immune effects: inhibits antigen-presenting cells; ↓ T-cell proliferation; ↓ NK cell response; ↓ inflammatory (barrier) response; ↓ wound healing.
🔗 Immune module: cortisol blunts both innate (NK cells, inflammation) and adaptive (APCs, T-cell proliferation) immunity — this is why patients on chronic steroids heal poorly and get infections.
Mineralocorticoids — aldosterone (steroid) - Acts on Na⁺ channels/pumps in the DCT and collecting duct. - Primary function: ↑ Na⁺ reabsorption and secretion of K⁺ and H⁺ into urine. Water follows sodium (indirectly ↑ fluid volume). - Activated by: ACTH, angiotensin II, ↑ K⁺ (hyperkalemia). - ACTH and ANG II release are triggered by ↓ blood volume and by ↑ osmolality sensed at the macula densa. - Renal effect takes 90 min–6 h. - Major regulator of plasma Na⁺ and K⁺; participates in acid–base balance; target of antihypertensives.
🔗 Fluid Dynamics: aldosterone (Na⁺ → water) and ADH (water directly) are the two hormonal levers on extracellular volume and blood pressure.
Glucagon (alpha cells) — catabolic; insulin antagonist - ↑ blood glucose during fasting, exercise, hypoglycemia - Stimulates hepatic glycogenolysis and adipose lipolysis - Released by ↓ glucose and sympathetic stimulation; inhibited by ↑ glucose
Insulin (beta cells) — anabolic - ↓ blood glucose by moving glucose into cells - ↓ plasma K⁺ (drives K⁺ into cells) - ↓ glycogenolysis, ↓ lipolysis, ↑ protein synthesis [insulin actions summary is an image slide — verify] - Mechanism: insulin binds receptor → GLUT transporters move to the cell surface → facilitated diffusion of glucose into cells; 10–21× ↑ GLUT in skeletal muscle, cardiac muscle, liver, adipose.
Regulation of insulin release
| ↑ Insulin | ↓ Insulin |
|---|---|
| Parasympathetic stimulation before meals (pulsatile) | ↓ blood glucose |
| ↑ blood glucose, amino acids (leucine, arginine, lysine), K⁺ | Sympathetic stimulation |
| GI hormones (gastrin, CCK, secretin, glucagon) | ↑ insulin itself (negative feedback) |
| ↑ prostaglandins |
Slide asks “Sympathetic stimulation ↓ insulin — why?” → In fight-or-flight you want glucose kept in the blood for the brain and working muscle, not stored away.
Somatostatin (delta cells) — regulates insulin and glucagon release.
Can I speak to it? ☐
Can I speak to it? ☐
Muscle weakness/atrophy/pain · fatigue · carpal tunnel syndrome · periarthritis · adhesive capsulitis · chondrocalcinosis · pseudogout · DISH · OA · osteonecrosis · arthralgia · RA-like arthritis · synovial fluid change · spondyloarthropathy · hand stiffness
Excessive/delayed growth · polydipsia · polyuria · dehydration or water retention · mental changes · hair and skin pigment changes · fat redistribution · vital-sign changes · palpitations · ↑ perspiration · Kussmaul respirations
| Disorder | Key NMSK effects |
|---|---|
| Acromegaly / gigantism | Overgrowth of bone & cartilage; arthritis, spinal OA; CTS in 50% with acromegaly; thoracic/lumbar pain; myopathy with weakness |
| Hypothyroidism | Proximal weakness ± pain; CTS (myxedematous tissue — may appear before diagnosis, often resolves with thyroid replacement); flexor tenosynovitis; RA-like small-joint arthritis; trigger points, myalgia; delayed DTR relaxation (esp. Achilles); paresthesia; rhabdomyolysis risk |
| Hyperthyroidism | Proximal weakness, fatigue, atrophy; chronic periarthritis/tendon calcification; tremor; ↑ DTRs |
| Hypoparathyroidism (↓Ca²⁺) | Neuromuscular hyperexcitability → tetany; carpopedal spasm; laryngeal/diaphragm spasm; short 4th–5th metacarpals |
| Hyperparathyroidism (↑Ca²⁺) | ↓ neuromuscular excitability — weakness, low tone, sluggish reflexes; osteitis fibrosa, osteoporosis, fractures, gout, chondrocalcinosis, periarthritis (Achilles, triceps, obturator tendons) |
| Cushing syndrome | Progressive proximal muscle wasting; marked osteoporosis → vertebral wedging, kyphosis, pathologic fractures; femoral head osteonecrosis; bone and back pain |
| Secondary adrenal insufficiency | Arthralgias, myalgias, tendon calcification |
| Conn syndrome | Hypokalemia → hyperpolarization → flaccid weakness; paresthesia; tetany risk |
| Diabetes mellitus | 30% have hand/shoulder disease: CTS, Dupuytren, trigger finger, adhesive capsulitis; DISH; arthritis (50%); limited joint mobility; osteoporosis within 5 yrs; peripheral/motor/autonomic neuropathy; skin stiffening (peau d’orange) |
Can I speak to it? ☐
For each disorder: Patho → S&S → Medical management → PT considerations.
Hypothalamic dysfunction — usually from pituitary stalk disruption (lesion, head injury, surgery, tumor) → hypothalamic hormones can’t reach the pituitary → ↓ FSH, LH, ACTH, TSH, GH.
| Gigantism | Acromegaly | |
|---|---|---|
| Timing | Before epiphyseal closure (children) | After epiphyseal closure (30–50 y) |
| Features | Long-bone overgrowth, ↑ bone thickness, cartilage/CT hypertrophy, visual change (optic nerve compression) | Enlarged face, jaw, hands, feet, tongue, ears, nose; slow onset; headache, diplopia, blindness, lethargy (brain compression); myopathy |
| Diabetes insipidus (DI) — hypo | SIADH — hyper | |
|---|---|---|
| Problem | ↓ ADH → can’t conserve water | Excess ADH → water retention |
| Urine | Large volume, dilute, no glucose (unlike DM) | Concentrated, low volume |
| Blood | Dehydration, ↑ Na⁺ concentration | Water intoxication + hyponatremia |
| S&S | Polydipsia, nocturia, dehydration (poor turgor, dry mucous membranes, weakness, dizziness), fatigue; can be fatal | Severe (Na⁺ <115): lethargy, weakness, nausea, anorexia. Mild (125–130): thirst, muscle cramps, lethargy |
| Causes | Hypothalamic/neurohypophyseal/posterior pituitary damage — neoplasm, metastasis, vascular lesion, autoimmune | Pituitary damage (infection, trauma); malignancy — oat-cell (small-cell) lung, pancreatic, brain, prostate CA, Hodgkin’s |
| Treatment | ADH replacement; tumor resection | Correct Na⁺; tumor removal; fluid restriction |
🔗 Oncology: SIADH is a classic paraneoplastic syndrome of small-cell lung cancer.
Epidemiology: 27 million Americans have low thyroid function. Risk factors: women, ↑ age, family history. Underdiagnosed after 60. Responds well to treatment.
Systemic manifestations (Table 11-6)
| System | Manifestations |
|---|---|
| CNS | Depression/anxiety, lethargy, fatigue, HA, slowed speech & mentation, poor short-term memory |
| MSK | Proximal weakness, CTS, trigger points, myalgia, ↑ bone density, cold intolerance, paresthesia |
| CV/pulm | Dyspnea, bradycardia, ↑ diastolic BP (↑ TPR compensating for ↓ CO), CHF, respiratory muscle weakness, ↓ peripheral circulation, angina, ↑ cholesterol, anemia |
| GI | Anorexia, constipation, weight gain, achlorhydria |
| GU | Infertility, irregular/heavy menses |
| Skin | Thick cool skin, carotenosis, non-pitting edema of hands/feet, poor wound healing |
Myxedema — severe, life-threatening hypothyroidism: confusion, edema, hypothermia, hypotension, bradycardia, ↓ CO, slow breathing.
🔗 Fluid Dynamics / Lymphatics: myxedema edema is non-pitting (mucopolysaccharide deposition in tissue) — contrast with the pitting edema of ↓ oncotic pressure/↑ hydrostatic pressure.
Exercise & PT - Start after medical management begins; expect poor initial tolerance/lethargy. - Monitor for rhabdomyolysis, CV/pulmonary response, pseudogout. - Benefits: MSK, CV, digestion, lipid profile.
Rhabdomyolysis — rapid muscle breakdown → myoglobin in blood → kidneys try to clear it → renal failure risk. Watch for muscle pain (shoulders, thighs, low back), weakness, dark red/brown urine, ↓ urination. Half of patients have no muscle symptoms.
Systemic manifestations (Table 11-4)
| System | Manifestations |
|---|---|
| CNS | Tremor, hyperkinesis, nervousness, irritability, emotional lability, weakness/atrophy, ↑ DTRs, fatigue |
| CV/pulm | Tachycardia/palpitations, ↑ CO, ↑ blood volume, arrhythmias (esp. A-fib), ↑ systolic BP, HF; respiratory muscle weakness, ↑ RR |
| MSK | Weakness, fatigue, atrophy, chronic periarthritis |
| Skin | Warm, flushed, moist skin; heat intolerance; onycholysis; brittle hair/hair loss; pretibial lesion (hard, purple, itchy) |
| Eyes | Exophthalmos, extraocular weakness, photosensitivity, lid retraction/tremor |
| GI | ↑ appetite with weight loss, ↑ bowel frequency, diarrhea, dysphagia |
| GU | Polyuria, amenorrhea, infertility, ↑ first-trimester miscarriage, gynecomastia |
Medical: no prevention; radioactive iodine uptake test; ↑T3/T4 on blood test; antithyroid meds, radioactive iodine, surgery. PT not indicated until medically managed (then often treated as hypothyroid).
Exercise & PT - Exercise intolerance, proximal weakness, fatigue. - Monitor vitals more often if HR > 100 or age > 60. - Dyspnea → high Fowler position, knees elevated. - Heat intolerance — avoid heated pools. - Tendon calcification/periarthritis. - After thyroid surgery: watch for twitching around the mouth (parathyroid damage → ↓Ca²⁺).
Hashimoto’s disease - Women:men 10:1; 30–50 y; autoimmune; genetic predisposition (HLA-DR3). - May start hyperthyroid, then become hypothyroid. - Treatment: suppress TSH, give T4.
Postpartum thyroiditis (≈3 in 100 deliveries; painless) - Phase 1 (1–4 mo): hyperthyroid — tachycardia, weight loss, fatigue, heat sensitivity, irritability — often missed as “just postpartum.” - Phase 2 (4–8 mo): hypothyroid — hoarse voice, depression, cold sensitivity, dry skin, poor exercise tolerance.
🔗 Lymphatic System & Oncology: post-thyroidectomy/neck dissection lymphedema.
Expect ↓ exercise capacity and fatigue · avoid hot aquatic/gym settings (Graves) · avoid CV stress · monitor vitals closely · know radioiodine effects · watch for rhabdomyolysis (hypo) · skin breakdown risk.
| Hypoparathyroidism | Hyperparathyroidism | |
|---|---|---|
| Cause | Iatrogenic (most common — e.g., thyroid surgery), idiopathic | Primary, secondary, tertiary; women:men 2:1; > 60 y |
| PTH | ↓ | ↑ |
| Bone | ↓ resorption, poor Ca²⁺ retention | ↑ resorption (bone broken down for Ca²⁺) |
| Serum Ca²⁺ | ↓ (hypocalcemia) | ↑ (hypercalcemia) |
| Serum phosphate | ↑ | ↓ |
| Neuromuscular | ↑ excitability → tetany | ↓ excitability |
| Other | Short 4th/5th metacarpals; laryngeal/intercostal/diaphragm spasm (breathing compromise); arrhythmias, HF | Osteitis fibrosa (bone replaced by fibrous tissue → “brown tumors”), subperiosteal resorption, osteoporosis, deformity; nephrocalcinosis, renal HTN; gout |
| Medical | Severe = emergency (laryngospasm); raise Ca²⁺ pharmacologically; good prognosis if early; calcifications (cataracts, basal ganglia) irreversible; lifelong meds, Ca²⁺ checks 3×/yr; high-Ca, low-phosphorus diet | Labs: ↑Ca²⁺, ↑PTH, phosphorus low/normal; X-ray for skeletal damage; parathyroidectomy |
| PT | Watch for acute tetany; breathing exercises; vitals | Fracture/compression fracture risk; erosive polyarthritis; chondrocalcinosis; periarthritis (Achilles, triceps, obturator) |
Post-op/acute care PT (parathyroid): auscultate for pulmonary edema (large IV saline volumes) · watch for tetany/perioral tingling · semi-Fowler to reduce tracheal pressure · early ambulation to promote bone recalcification · home health: fluids (acidic fluids help prevent Ca²⁺ stones), environment, impairments.
S&S - Hallmark: low serum cortisol. - Weakness (asthenia), exhaustion, hypotension, anorexia, weight loss, N/V, emotional changes, salt craving, poor stress tolerance. - Hyperpigmentation — ↑ ACTH (no cortisol negative feedback) stimulates melanocytes → bronzed skin, darkened scars (slate-gray in darker skin). - Vitiligo — autoimmune melanocyte destruction.
Lab complications — reason them out:
| Missing hormone | Consequence |
|---|---|
| ↓ Cortisol | Hypoglycemia |
| ↓ Aldosterone → can’t reabsorb Na⁺ | Hyponatremia, dehydration, low BP (+ hypercalcemia per slide) |
| ↓ Aldosterone → can’t excrete K⁺ and H⁺ | Hyperkalemia, metabolic acidosis |
Addisonian crisis: severe hypotension + hypoglycemia + hyperkalemia → volume depletion + loss of cortisol-dependent vasomotor tone → shock and death.
Medical: lifelong glucocorticoid + mineralocorticoid replacement, ↑ doses during stress; ↑ dietary sodium (especially with sweating/diarrhea).
PT considerations - Closely monitor physical stress — can’t make enough cortisol to meet exercise demand. - Aquatic therapy contraindicated — can’t produce enough aldosterone to raise BP and cool the body. - Watch for impending crisis: dizziness, nausea, profuse sweating, ↑ HR, tremors — especially with medication changes. - Illness may require a medication increase; monitor vitals; coordinate with ortho/endocrinology after surgery.
| Cushing syndrome | Cushing disease | |
|---|---|---|
| Definition | Clinical picture of chronic ↑ cortisol (hypercortisolism) | ↑ ACTH from a pituitary adenoma → ↑ cortisol |
| Level | Primary (adrenal) or exogenous | Secondary (~70% of cases) |
| Causes | Long-term corticosteroids (exogenous), adrenocortical tumors (endogenous) | Pituitary tumor |
Definition: chronic, systemic metabolic disease from defects in insulin secretion, insulin action, or both → hyperglycemia + disrupted carbohydrate, fat, and protein metabolism.
Core concept: in either type, glucose can’t get into cells → high blood glucose but no intracellular glucose for glycolysis → ↓ ATP. - Type 1: impaired insulin production - Type 2: impaired receptor sensitivity (insulin resistance)
Epidemiology - Most common endocrine disorder; leading cause of adult blindness and renal failure; T1DM = most common pediatric chronic disease. - ~¼ of US adults have prediabetes; projected up to 1 in 3 Americans with DM by 2050.
Cardinal signs at diagnosis [image slide — verify]: polyuria, polydipsia, polyphagia, unexplained weight loss, fatigue.
T1DM is associated with other autoimmune disorders: Graves, Hashimoto, Addison’s, vitiligo, autoimmune gastritis, pernicious anemia.
🔗 Immune module (autoimmunity, T-cell mediated destruction) · Hematology (pernicious anemia) · Genetics (HLA-DR3/DR4).
| Feature | Type 1 (ketosis-prone) | Type 2 (not ketosis-prone) |
|---|---|---|
| Onset age | < 20 (peak 11–13) | > 40, ↑ in children |
| % of cases | 10% | 90% |
| Onset | Abrupt | Gradual |
| Etiology | Viral/autoimmune | Obesity-associated insulin resistance |
| HLA | Yes (DR3, DR4) | No |
| Insulin antibodies | Yes | No |
| Body weight | Normal/thin | Obese (80%) |
| Endogenous insulin | Little/none | Variable |
| Ketoacidosis | May occur | Rare |
| Treatment | Insulin, diet, exercise | Diet, exercise, weight loss, oral hypoglycemics, ± insulin |
I can’t see which values are highlighted from the slide text — the bolded numbers above are the most likely candidates. Check slide 65.
| Complication | Mechanism / key points |
|---|---|
| Atherosclerosis (macrovascular) | ↑ fat metabolism + hyperglycemia → mitochondrial free radicals → vessel damage → lipid accumulation, wall thickening → ↓ lumen, ischemia. CV/cerebrovascular disease, skin/nail changes, absent pedal pulses, poor healing. ↑ especially in T1 |
| Microvascular | Hyperglycemia → microvascular inflammation → thickened capillary basement membrane → endothelial hyperplasia → hypoxia/ischemia → thrombosis risk. Severity tracks duration + control |
| Retinopathy | Retinal microvascular occlusion → progressive ischemia, tissue death |
| Nephropathy / CKD / ESRD | DM = leading cause of CKD/ESRD; thickened glomerular basement membrane → poor filtration; microalbuminuria = early sign (1 in 4 with T2); control glucose and HTN |
| Diabetic cardiomyopathy | 1.5–4× ↑ CAD/MI risk; ↓ renal blood flow → ↑ renin → ↑ BP → LVH |
| Impaired wound healing / infection | Poor distal perfusion (feet); ↑ glucose feeds bacterial growth |
| Musculoskeletal | See Objective 5 table |
| Neuropathies | Painful hyperalgesia/allodynia; insulin neuritis (feet > hands); motor (weakness, atrophy); autonomic (BP, temperature, sweating control → dry cracked skin, callus; limb blood flow) |
| Psychosocial | Self-esteem, family dynamics, support, adherence, motivation, eating disorders, QOL |
🔗 Fluid Dynamics / Hematology thread: microalbuminuria = albumin leaking through damaged glomeruli — the same albumin → oncotic pressure → edema thread. Progressive protein loss lowers plasma oncotic pressure. 🔗 Clot spectrum: endothelial damage in DM microvasculature → thrombosis risk → feeds into thrombus → embolus → infarction.
Causes - Hyperglycemia: too little insulin or poor T2 management; illness/infection; stress; poor medication or diet adherence. - Hypoglycemia: insulin “overdose”/poor dosing; skipped or late meals; overexertion; ↑ activity without insulin adjustment.
Hypoglycemia S&S
| Sympathetic (↑ epinephrine) | CNS (↓ glucose to brain) |
|---|---|
| Pallor, sweating, piloerection, tachycardia, palpitations, nervousness/irritability, weakness, shakiness, hunger | Headache, blurred vision, thickened speech, numb lips/tongue, confusion, emotional lability, convulsion, coma |
→ Immediately give fast-acting carbohydrate: juice, honey, hard candy, glucose tablets.
Hospital admission if: glucose < 50 mg/dL or treatment doesn’t promptly restore mental status · seizures or unconsciousness · no responsible adult available for the next 12 h.
Diabetic ketoacidosis (DKA) — most common in T1 - Causes: too little insulin, omitted doses, unmet ↑ need (surgery, trauma, pregnancy, stress); infection = most common precipitant. Progresses to coma. - S&S: polyuria, thirst, acetone (fruity) breath, dehydration, weak rapid pulse, Kussmaul respirations (deep, rapid — compensating for low pH), dry mouth, hot dry skin, weakness, confusion → coma. - Treatment: insulin, fluids, electrolyte monitoring.
Side-by-side
| Factor | Hypoglycemia | Hyperglycemia |
|---|---|---|
| Onset | Rapid (minutes) | Gradual (days) |
| Mood | Labile, irritable, nervous, weepy | Lethargic |
| Mental status | Difficulty concentrating, speech | Dulled, confused |
| Feels | Shaky, hungry, HA, dizzy | Thirsty, weak, N/V, abdominal pain |
| Skin | Pale, sweaty | Flushed, dehydrated |
| Mucous membranes | Normal | Dry |
| Respiration | Shallow | Kussmaul |
| Pulse | Tachycardia | Less rapid, weak |
| Breath | Normal | Fruity/acetone |
| Neuro | Tremor, dilated pupils, seizure | ↓ reflexes, paresthesia |
| Blood glucose | < 50 mg/dL | > 250 mg/dL |
| Ketones | Negative | High |
| pH | Normal | Low (< 7.25) |
| Urine | Normal output; glucose & ketones negative | Polyuria → oliguria; glucose & ketones high |
Tests & measures: arousal/attention/cognition · community/work integration · environmental barriers · gait, locomotion, balance · integumentary integrity · motor function · muscle performance · posture · ROM · self-care/home management.
PT considerations - Recognize risk of peripheral neuropathy, small-vessel disease, ischemia, ulceration, poor healing, necrosis, amputation. - Recognize acute metabolic changes and sudden hypoglycemia — and treat it. - Support consistent management of insulin, diet, activity. - Educate on skin care, shoe evaluation, footwear.
Benefits of exercise: ↑ muscle glucose transport and whole-body glucose homeostasis · ↑ insulin binding/sensitivity · better glucose control · improved CV function and lipid profile · ↓ insulin requirements · ↓ HTN · weight reduction · well-being/QOL · promotes other healthy behaviors.
Absolute contraindications to exercise ⭐ - Poorly controlled blood glucose - Unevaluated/poorly controlled retinopathy, HTN, neuropathy (autonomic or peripheral), nephropathy - Recent photocoagulation or retinal surgery - Dehydration - Extreme environmental temperatures
Before exercise - ~17 oz fluid (≈ two 8-oz glasses) - Check glucose immediately before - Carbohydrate snack - Avoid peak insulin activity (2–4 h after injection) - T1 may need ↓ insulin or ↑ food - Watch clients on beta-blockers (mask tachycardia warning sign), diuretics, estrogen — ↑ exercise-induced hypoglycemia risk
During exercise - 5×/week or every other day; start at 20–30 min (not 40–50) - Same time each day - T1DM: 50–60% predicted HR - Carbohydrate on hand; ingest and check glucose every 30 min - Replace fluids
After exercise [image slide — verify]: typically recheck glucose, rehydrate, and watch for delayed hypoglycemia (↑ insulin sensitivity persists up to 48 h).
Potential risks: hypoglycemia · CV complications · microvascular disease · DJD · orthopedic injury related to neuropathy.
3 or more of the following → ↑ risk of stroke, heart disease, DM: - Central obesity: waist > 40 in (men), > 35 in (women) - Triglycerides > 150 mg/dL - HDL < 40 mg/dL - BP: systolic > 130 and/or diastolic ≥ 85 mmHg - Fasting glucose > 100 mg/dL
→ PT role: encourage lifestyle change to reduce risk factors.
Rule: if the thyroid is the problem, TSH moves opposite to T3/T4 (the pituitary is trying to compensate). If TSH moves the same direction as T3/T4 — or stays “normal” when it shouldn’t — suspect the pituitary/hypothalamus.
| TSH | T3/T4 | Interpretation |
|---|---|---|
| ↑ | ↓ | Primary hypothyroidism (thyroid failing; pituitary pushing harder) |
| ↓ | ↑ | Primary hyperthyroidism (e.g., Graves; pituitary backing off) |
| ↓ | ↓ | Secondary (pituitary) hypothyroidism |
| ↑ | ↑ | Secondary (pituitary-driven) hyperthyroidism |
| Normal | ↓ | TSH should be high → inappropriately normal → points to pituitary/hypothalamus (central hypofunction) |
| Normal | ↑ | TSH should be suppressed → points to pituitary-driven hyperfunction |
(Slide’s reference values say “not on the exam,” but this reasoning is — “Know this for the Exam!” Think-Pair-Share.)
| Cortisol | Na⁺ | K⁺ | BP | Acid–base | Glucose | Skin | |
|---|---|---|---|---|---|---|---|
| Addison’s | ↓ | ↓ | ↑ | ↓↓ | Acidosis | ↓ | Hyperpigmented |
| Secondary insufficiency | ↓ | ± | Usually normal | Less ↓ | — | ↓ | No hyperpigmentation |
| Cushing’s | ↑ | — | — | ↑ | — | ↑ | Purple striae, thin |
| Conn’s | Normal | ↑ | ↓ | ↑↑ | Alkalosis | — | — |
Memory hook: aldosterone keeps Na⁺, dumps K⁺ and H⁺. Too much (Conn) → high Na, low K, alkalosis, HTN. Too little (Addison) → low Na, high K, acidosis, hypotension.
| DM | DI | SIADH | |
|---|---|---|---|
| Hormone | Insulin ↓/resistance | ADH ↓ | ADH ↑ |
| Urine | Glucose +, high volume | Dilute, glucose –, high volume | Low volume, concentrated |
| Serum Na⁺ | Variable | ↑ (dehydration) | ↓↓ |
| Value | Number | Notes |
|---|---|---|
| Fasting plasma glucose (DM dx) | > 126 mg/dL | Diagnostic |
| 2-h OGTT (DM dx) | > 200 mg/dL | Diagnostic |
| A1c | < 5.7% normal · 5.7–6.4% prediabetes · ≥ 6.5% DM | Target ≤ 7% |
| Hypoglycemia (slide) | < 50 mg/dL | Hospital admission threshold |
| Hyperglycemia (DKA table) | > 250 mg/dL, pH < 7.25 | |
| Fasting glucose (metabolic syndrome) | > 100 mg/dL | |
| Triglycerides | > 150 mg/dL | Metabolic syndrome |
| HDL | < 40 mg/dL | Metabolic syndrome |
| Serum Ca²⁺ | 8.6–10.3 mg/dL | |
| Serum osmolality | 280–300 mOsm/kg | |
| SIADH Na⁺ | Severe < 115 · mild 125–130 mEq/L | |
| Hyperthyroid exercise | Monitor more if HR > 100 or age > 60 | |
| Exercise in T1DM | 50–60% predicted HR, start 20–30 min | |
| Pre-exercise fluid | 17 oz | |
| Avoid exercise | 2–4 h after insulin injection (peak) |
⚠️ Not on the exam (preserved for context): thyroid reference values — T4 4.5–11.5 μg/dL; T3 80–200 ng/dL; TSH 0.3–3.0 U/mL.
| Endocrine concept | Links to |
|---|---|
| Aldosterone (Na⁺ → water) and ADH (water) control ECF volume and BP | Fluid Dynamics |
| Myxedema = non-pitting edema vs. pitting edema from ↓ oncotic/↑ hydrostatic pressure | Fluid Dynamics / Lymphatics |
| Diabetic nephropathy → microalbuminuria → albumin loss → ↓ oncotic pressure | Oncotic pressure → albumin → edema thread |
| DM microvascular endothelial damage → thrombosis | Clot spectrum (Hematology) |
| Cortisol suppresses APCs, T cells, NK cells, inflammation, wound healing | Immune System |
| Autoimmune endocrine disease: T1DM, Graves, Hashimoto’s, Addison’s, vitiligo | Immune System |
| T1DM ↔︎ pernicious anemia; hypothyroidism → anemia | Hematology |
| HLA-DR3/DR4 (T1DM), HLA-DR3 (Hashimoto’s) | Genetics |
| SIADH from small-cell lung CA; thyroid CA; pituitary adenomas | Oncology |
| Post-thyroidectomy lymphedema | Lymphatic System |
Likely explanation: acute (secondary) adrenal insufficiency from abrupt discontinuation of corticosteroids (e.g., an oral steroid course or steroid injections for radicular pain). Exogenous steroids suppressed ACTH → adrenals atrophied → when the drug stopped, he can’t make enough cortisol. Hypotension + tachycardia + weakness + salt craving fit.
Questions to ask: What was the medication, dose, and how long was he on it? Did he stop abruptly or taper — and did his physician approve? Dizziness/lightheadedness on standing? Nausea, vomiting, abdominal pain, appetite/weight change? Recent illness or infection? Confusion? Skin changes? Other steroid use (injections, inhalers)?
Action: this is a potential Addisonian-type crisis → do not exercise; urgent communication with/referral to his physician.Concerns: hypoglycemia during/after exercise (and delayed, up to 48 h); DKA with illness/missed insulin; neuropathy (falls, foot injury, ulcers); retinopathy (avoid high-intensity/Valsalva if unevaluated); nephropathy; CV disease; autonomic dysfunction (abnormal HR/BP response, thermoregulation); poor wound healing; MSK issues (adhesive capsulitis, CTS, limited joint mobility).
Program: check glucose before/during/after; time exercise away from insulin peak; carb snack and fast-acting glucose on hand; hydration; consistent daily timing; 50–60% predicted HR, start 20–30 min; daily foot inspection, skin care, proper footwear; aerobic + resistance work; education on recognizing hypo/hyperglycemia.