Endocrine

Endocrinology Quiz Study Guide

Chapters 21 22 and 23

Quiz due Sunday October 11 2026

Use this guide to explain each mechanism in simple steps. For every disorder, connect the hormone change to the body response, laboratory findings, symptoms, and possible complications.

Study chain: What changed → what the hormone does → body changes → laboratory results → symptoms.

Read one section, cover the answers, and explain the chain aloud. The final review provides short memory prompts.

Part 1 Endocrine regulation and feedback

Completed blanks

• Overall purpose: maintain an optimal INTERNAL environment.

• Negative feedback: the response DECREASES or INHIBITS further hormone synthesis or secretion.

• Positive feedback: the response INCREASES or STIMULATES hormone synthesis or secretion.

What hormones do

Hormones are chemical messages. They help coordinate metabolism, growth, reproduction, water balance, glucose, calcium, and responses to changing conditions. The internal environment means conditions inside the body. Homeostasis means keeping these conditions stable.

Negative feedback step by step

1. The hypothalamus releases TRH, thyrotropin-releasing hormone.
2. TRH stimulates the anterior pituitary to release TSH, thyroid-stimulating hormone.
3. TSH stimulates the thyroid to produce T3 and T4.
4. As T3 and T4 rise, they inhibit TRH and TSH.
5. Less upstream stimulation reduces further thyroid hormone production.

T3 means triiodothyronine. T4 means thyroxine, also called tetraiodothyronine. The sequence is TRH → TSH → T3/T4; rising thyroid hormone then turns down TRH and TSH.

Why negative feedback matters: it prevents continued production after the body has enough hormone. Failed feedback can lead to excessive or insufficient hormone effects.

MEMORY: Negative feedback means “we have enough; slow down.”

Positive feedback

The chapter defines positive feedback as a response that increases hormone synthesis or secretion. In its thyroid example, TRH stimulates TSH, and TSH stimulates thyroid hormone production.

MEMORY: Positive increases; negative decreases.

Part 2 Transport receptors and cell response

Completed blanks

• Only FREE or UNBOUND hormone is available to signal a target cell.

• Only cells with the appropriate RECEPTORS are target cells.

• Low hormone concentration may cause receptor UP-REGULATION; high concentration may cause DOWN-REGULATION.

Free hormone and receptors

Some hormones travel attached to carrier proteins. Bound hormone must separate from its carrier to become available to signal a target cell. MEMORY: Free hormone is free to act.

A receptor recognizes and binds a hormone. Imagine the hormone as a key and the receptor as its matching lock. A target cell has the correct lock. Hormone concentration alone does not guarantee a normal response.

Up regulation and down regulation

Up-regulation: low hormone levels can increase receptor number or affinity, making cells more sensitive. Affinity means how strongly the receptor binds the hormone. MEMORY: Less hormone → more listening.

Down-regulation: high hormone levels can decrease receptor number or affinity, making cells less sensitive. MEMORY: More hormone → less listening.

Water-soluble hormones bind outside and use an internal messenger. Lipid-soluble hormones can enter and influence genetic instructions. Some lipid-soluble hormones also have membrane-associated receptors with rapid effects. MEMORY: Water waits outside; lipid enters.

Part 3 Major endocrine relationships

HPA axis and cortisol

HPA means hypothalamic–pituitary–adrenal. CRH is corticotropin-releasing hormone from the hypothalamus. ACTH is adrenocorticotropic hormone from the anterior pituitary. ACTH stimulates the adrenal cortex to release cortisol. Rising cortisol reduces upstream stimulation through negative feedback.

ADH and water

ADH means antidiuretic hormone, also called arginine vasopressin. Diuresis means urine production. Antidiuretic means opposing water loss in urine. ADH tells kidneys to reabsorb water into the body. MEMORY: ADH adds water back.

PTH and calcium

Low serum calcium stimulates PTH. PTH mobilizes calcium from bone, increases renal calcium reabsorption, and helps activate vitamin D to increase intestinal calcium absorption. It reduces phosphate reabsorption so more phosphate leaves in urine. MEMORY: Calcium into blood; phosphate into urine.

Pancreas and adrenal glands

Beta cells produce insulin. Alpha cells produce glucagon. Glucagon stimulates glycogenolysis, breaking stored glycogen into glucose, and gluconeogenesis, making new glucose.

Adrenal cortex is the outer portion and produces cortisol and aldosterone. Medulla is the inner portion and produces catecholamines such as epinephrine and norepinephrine. MEMORY: Cortisol = stress/glucose; aldosterone = sodium/potassium; catecholamines = fight or flight.

Part 4 Direction of hormone change

Completed blank and mechanism

Adequate hormone production with too few functional receptors is a TARGET-CELL RESPONSE problem, specifically a receptor-associated disorder.

Endocrine disease can result from abnormal production, failed feedback, abnormal delivery through blood or carrier proteins, or a failure of receptors or intracellular processes to respond. A normal hormone level does not guarantee normal action.

GI = gastrointestinal or digestive system. Tachycardia = fast heart rate. Lethargy = reduced energy/alertness. Hypernatremia = high serum sodium; hyponatremia = low serum sodium. Tetany = sustained involuntary muscle contractions.

STUDY METHOD: First name the hormone’s normal action. Then ask what happens if that action becomes excessive or insufficient.

Part 5 SIADH and diabetes insipidus

SIADH step by step

SIADH means syndrome of inappropriate antidiuretic hormone secretion. Excess ADH activity inserts water channels into renal tubule membranes and increases water reabsorption. More water stays in the body, diluting serum sodium. Serum sodium and osmolality fall. Urine is inappropriately concentrated because water that should leave is retained.

Why hyponatremia? The main problem is retained water. Adding water to salty liquid makes the salt less concentrated. MEMORY: Water stays; sodium concentration sinks.

The chapter describes euvolemic hyponatremia and absence of peripheral edema. Retaining water does not automatically mean visible swelling. Symptoms include nausea, fatigue and mental changes; severe hyponatremia can cause seizures and neurologic injury.

DI step by step

DI means diabetes insipidus. Central DI results from insufficient ADH secretion. Nephrogenic DI results from an inadequate kidney response to ADH. The kidneys cannot conserve water appropriately, so large amounts of dilute urine are lost. Thirst increases. If replacement cannot keep up, dehydration, hypernatremia and high serum osmolality develop.

Why hypernatremia? Free-water loss concentrates the remaining blood. High sodium is especially likely when drinking cannot replace the loss. MEMORY: DI = dilute urine and dry body.

Osmolality = concentration of dissolved particles. Polyuria = excessive urine output. Polydipsia = excessive thirst/drinking. QUIZ: Dilute blood + concentrated urine → SIADH. Concentrated blood + dilute urine → DI.

Part 6 Thyroid parathyroid and growth hormone

Primary versus secondary thyroid disease

Primary means the problem starts in the thyroid. Secondary or central disease means inadequate pituitary or hypothalamic stimulation.

MEMORY: In primary thyroid disease, thyroid hormone and TSH generally move in opposite directions. Hyperthyroidism is hot and fast; hypothyroidism is cold and slow.

Graves disease

Autoimmune antibodies stimulate TSH receptors, causing excess thyroid hormone. Increased metabolism produces heat intolerance, weight loss and tachycardia. The two distinguishing blanks are OPHTHALMOPATHY and DERMOPATHY, particularly pretibial myxedema. Ophthalmopathy means eye involvement, which may include protruding eyes. Dermopathy means skin involvement. Pretibial means over the front of the shin. MEMORY: Graves stimulates.

Hashimoto disease

Autoimmune inflammation gradually destroys thyroid tissue, producing progressive LOSS of thyroid function. Thyroid hormone falls and TSH rises. MEMORY: Hashimoto harms.

Parathyroid disorders

Primary hyperparathyroidism: excess PTH → high calcium and low phosphate. Bone resorption causes osteoporosis/fractures. Calcium and phosphate in urine promote stones. Symptoms can include muscle weakness, fatigue, memory or mood changes, constipation, nausea and vomiting.

Important exception: secondary hyperparathyroidism from kidney disease can have high PTH with LOW calcium and HIGH phosphate. Do not apply the primary pattern to every form.

Hypoparathyroidism: low PTH → low calcium → neuromuscular excitability, spasms and tetany. MEMORY: Low calcium makes muscles excitable.

Why an upstream disorder affects several organs

The hypothalamus and pituitary regulate several pathways. TSH affects thyroid hormone; ACTH affects cortisol; FSH and LH affect reproduction; GH affects growth/metabolism. FSH = follicle-stimulating hormone; LH = luteinizing hormone; GH = growth hormone. One control-center problem can affect multiple organs.

Excess GH in children and adults

With open epiphyseal growth plates, excess GH causes excessive lengthwise bone growth: GIGANTISM. With closed adult growth plates, GH and IGF-1 cause bony and soft-tissue proliferation: ACROMEGALY. IGF-1 = insulin-like growth factor 1. MEMORY: Open plates → taller; closed plates → enlargement.

Part 7 Diabetes mellitus and acute complications

Type 1: beta cells are destroyed → insulin falls → glucose uptake/storage are impaired and glucagon is less suppressed → liver glucose production increases → hyperglycemia. Fat and protein breakdown also increase.

Type 2: cells respond poorly to insulin → pancreas initially produces more insulin → beta-cell function declines over time → insulin becomes inadequate → hyperglycemia. MEMORY: Type 1 = deficient supply; type 2 = resistance plus declining supply.

Why glucose causes polyuria and thirst

High blood glucose → glucose appears in urine → osmotic diuresis → water loss → polyuria → dehydration and thirst. Osmotic diuresis means dissolved substances such as glucose promote water loss in urine.

Completed DKA pathway

Decreased insulin → increased GLUCAGON/counterregulatory hormone effects → increased lipolysis → free fatty acids → increased KETONE production → acid accumulation → METABOLIC ACIDOSIS.

DKA = diabetic ketoacidosis. Lipolysis = fat breakdown. Ketonuria = ketones in urine. Metabolic acidosis = acid accumulation lowers blood pH.

Why both glucose and ketones? Less insulin reduces glucose uptake and permits more liver glucose production. At the same time, reduced inhibition of lipolysis sends fatty acids to the liver for ketone production. MEMORY: Glucose rises and fat breakdown rises.

Ketone accumulation causes acidosis. Kussmaul respirations are deep, increased breathing that attempts to compensate. Clues include hyperglycemia, ketonuria, abdominal pain, nausea and Kussmaul respirations.

HHS = hyperosmolar hyperglycemic state. The chapter calls it HHNKS, hyperosmolar hyperglycemic nonketotic syndrome. Some insulin effect remains sufficient to prevent major lipolysis/ketosis but not severe glucose elevation. MEMORY: DKA = ketones and acid; HHS = very high glucose and concentration.

Chronic injury and hypoglycemia

Persistent hyperglycemia changes cell metabolism and communication and causes glycation, attachment of glucose to molecules. Small-vessel injury affects eyes, kidneys and nerves; larger-vessel disease affects heart, peripheral circulation and brain. Immunity and wound healing can be impaired.

Treatment can cause hypoglycemia. Autonomic signs include sweating, tremor, palpitations, tachycardia, anxiety and hunger. Neurologic signs include confusion, impaired concentration, visual changes, seizures and coma. MEMORY: Shaky/sweaty body, then impaired thinking.

Part 8 Adrenal disorders

Cushing syndrome

Excess cortisol increases liver glucose production and insulin resistance → hyperglycemia. Protein breakdown → muscle weakness/wasting. Collagen loss → thin skin, bruising and purple striae. Bone effects → osteoporosis/fractures. Increased vascular sensitivity to catecholamines → hypertension. Immune suppression → infection risk. Fat distribution can produce truncal obesity, moon face and buffalo hump. MEMORY: Glucose rises; protein breaks down.

Hyperaldosteronism

Excess aldosterone increases sodium/water reabsorption → volume and blood pressure rise. Potassium and hydrogen excretion increase → hypokalemia and possible metabolic alkalosis. Low potassium can cause weakness and altered cardiac conduction. MEMORY: Save sodium; send potassium out.

Primary adrenal insufficiency and adrenal crisis

Addison disease is primary adrenal insufficiency. Low cortisol impairs energy/stress responses. Low aldosterone reduces sodium/water conservation and potassium excretion. Findings include weakness, GI symptoms, hypotension, dehydration and hyperkalemia. Cortisol is low and ACTH rises because negative feedback is lost, but the damaged gland cannot respond adequately.

Why crisis is dangerous: severe deficiency during physiologic stress can cause profound hypotension → vascular collapse → SHOCK. Hyperkalemia = high potassium; hypokalemia = low potassium.

Secondary adrenal insufficiency

Exogenous means supplied from outside the body. Prolonged glucocorticoid use suppresses ACTH → reduced adrenal stimulation → adrenal atrophy. After withdrawal, endogenous cortisol production may be insufficient. Aldosterone and potassium often remain normal because the renin–angiotensin system is usually intact. MEMORY: Primary = gland fails; secondary = stimulation fails.

Pheochromocytoma

A catecholamine-secreting tumor causes excess sympathetic effects. Increased peripheral vascular resistance → hypertension. Sympathetic activation → tachycardia, palpitations and sweating. Inhibition of pancreatic insulin release can cause glucose intolerance. MEMORY: High pressure, fast pulse, sweating.

Part 9 Obesity and metabolic risk

Completed mechanism and inflammation

Excess adipose tissue → altered adipokines + increased inflammatory-cell infiltration/cytokine production → chronic low-grade INFLAMMATION → metabolic complications. Increased lipolysis also contributes.

Fat is an endocrine organ. Adipokines are signaling proteins that influence appetite, energy expenditure, insulin sensitivity, immune responses and vascular function. Enlarged fat cells can outgrow their supporting blood supply → hypoxia/stress → immune-cell infiltration → inflammatory mediators → insulin resistance.

TNF-alpha = tumor necrosis factor-alpha. IL-6 = interleukin-6. These are examples of inflammatory mediators. MEMORY: Excess fat can become stressed and inflamed, not just stored.

Lipotoxicity

Completed blanks: FREE FATTY acids; cellular DEATH. Excess storage and impaired insulin suppression of lipolysis increase fatty acid delivery to nonadipose organs. When use capacity is exceeded, cells malfunction or die. Organs include liver, kidney, heart and skeletal muscle. MEMORY: Excess fat delivery can harm cells.

Why visceral fat is riskier: it is more hormonally active, lipolytic and inflammatory. Its venous blood drains into the portal vein, contributing to liver lipid synthesis and fatty liver risk. MEMORY: Location matters as well as amount.

BMI and normal weight obesity

BMI = body mass index. It describes BODY MASS relative to height but does not directly measure the amount or LOCATION/DISTRIBUTION of body fat. Normal-weight obesity means normal weight/BMI with EXCESSIVE body fat and possible metabolic abnormalities. A normal BMI does not guarantee normal metabolic health.

Part 10 Appetite starvation and eating disorders

Completed starvation sequence

GLYCOGENOLYSIS → GLUCONEOGENESIS → LIPOLYSIS/KETONE UTILIZATION → PROTEOLYSIS. Processes overlap rather than switching on/off perfectly.

1. Glycogenolysis: break stored glycogen into glucose. First use the liver’s stored carbohydrate.
2. Gluconeogenesis: make new glucose from lactate, pyruvate, amino acids and glycerol. “Neo” means new.
3. Lipolysis/ketones: low insulin and counterregulatory hormones promote fat breakdown. Fatty acids fuel tissues; ketones help sustain the brain.
4. Severe proteolysis: after fat is depleted, muscle and visceral protein become the final major energy source. Electrolyte abnormalities and organ dysfunction can become fatal.

Prolonged starvation increases ketone use, reducing dependence on GLUCONEOGENESIS/glucose production and helping preserve PROTEIN, especially muscle protein. Some glucose is still needed, including for red blood cells. MEMORY: Fat fuel helps save protein.

Cachexia often involves systemic inflammation and abnormal metabolism in chronic disease. It is not simply another name for poor appetite.

Severe anorexia nervosa and bulimia

Final system blank: NEUROLOGIC. Anorexia nervosa can cause cardiac bradycardia/dysrhythmias, endocrine changes such as amenorrhea and low sex hormones, GI constipation/gastroparesis, anemia and low white cells/platelets, electrolyte abnormalities, osteoporosis/fractures, and brain atrophy/cognitive impairment.

Bulimia vomiting blank: METABOLIC alkalosis. Recurrent vomiting can cause hypokalemia, metabolic alkalosis, dental erosion and parotid enlargement. MEMORY: Vomiting/purging → potassium and acid–base problems.

Part 11 Refeeding syndrome high priority

All completed blanks

• Starvation: phosphate, magnesium and potassium move OUT OF CELLS INTO PLASMA.

• Nutrition restarts: carbohydrate intake increases → insulin INCREASES.

• Glucose, phosphate, magnesium and potassium move BACK INTO CELLS.

• Serum abnormalities include hypophosphatemia, hypomagnesemia, hypokalemia, hyponatremia and HYPOCALCEMIA.

• Vitamin deficiency particularly associated with refeeding: THIAMIN.

• Low phosphate → altered RBC function → tissue HYPOXIA → increased respiratory DRIVE.

Mechanism explained simply

During starvation the body loses minerals, and phosphate, magnesium and potassium move out of cells. When carbohydrate feeding restarts, insulin rises. Glucose and these electrolytes move into cells. Their blood concentrations can drop dangerously. MEMORY: Refeeding raises insulin; insulin moves them IN.

Why low phosphate and rapid refeeding are dangerous

RBC means red blood cell. Low phosphate alters RBC shape/function → tissue hypoxia, or inadequate oxygen → increased respiratory drive. Refeeding can also cause respiratory muscle weakness. Carbohydrate refeeding may rapidly expand extracellular fluid, causing fluid overload.

Consequences include life-threatening dysrhythmias, congestive heart failure, weakness including respiratory muscle weakness, and death. The chapter states changes usually occur within 72 hours after nutritional therapy starts.

Clinical application answers

A malnourished patient with falling phosphate, potassium and magnesium after feeding has insulin-mediated intracellular electrolyte shifts characteristic of REFEEDING SYNDROME.

Close monitoring is necessary because electrolyte and fluid changes can damage cardiac and respiratory function. The chapter emphasizes identifying risk, restarting nutrition slowly, and monitoring phosphate, potassium, magnesium and calcium during the change from catabolism to anabolism.

Catabolism = breaking down stored materials. Anabolism = building and storing materials. QUIZ CLUE: Starvation + feeding begins + electrolytes fall → refeeding syndrome.

Part 12 Anorexia of aging

Completed pathway

Age-related decreased intake → MALNUTRITION/UNDERNUTRITION → physical frailty → reduced functional reserve. Functional reserve means the ability to cope with extra demands, stress or illness.

Poor dentition means problems with teeth. Dysphagia means difficulty swallowing. Polypharmacy means use of multiple medications. These factors can reduce intake even if food is available.

Clinical application answer

Three contributors: poor teeth make chewing difficult; reduced taste makes food less appealing; difficulty preparing meals limits access to food. Multiple medications and social isolation are additional contributors.

Major downstream concern: malnutrition → frailty → reduced ability to function and tolerate illness. The chapter also lists reduced regenerative capacity, mitochondrial dysfunction, increased oxidative stress and hormone imbalance.

The chapter states anorexia of aging should not simply be accepted as a normal consequence of aging. Supportive approaches described include exercise, nutrition, improved food access, dental/eye care and social stimulation.

Memory tip

Older adult eating less → look for sensory, functional, social and medical barriers → watch for malnutrition and frailty.

Final clinical integration and concept map

Completed one minute concept map

Disorder: SIADH.
Hormone abnormality: Excess ADH activity.
Primary physiologic change: Increased renal free-water reabsorption.
Laboratory changes: Low serum sodium, low serum osmolality, inappropriately concentrated urine.
Manifestations: Low urine output, water-related weight gain, nausea, fatigue and mental changes.
Potential complication: Severe neurologic dysfunction and seizures.

Whole chain: Too much ADH → water retained → sodium diluted → serum sodium falls → neurologic symptoms can develop.

Practice without looking

For each disorder, say: “The hormone change is ____. This causes ____. Therefore, the lab result is ____ and the patient develops ____.” If you can explain the “because,” you understand the mechanism.

Quick review before the quiz

• Negative feedback: enough hormone turns down production.

• Free hormone is available to act.

• Low hormone: receptors may increase. High hormone: receptors may decrease.

• Water-soluble hormones usually bind membrane receptors. Lipid-soluble hormones mainly act at internal receptors.

• SIADH: water stays; serum sodium falls; urine is concentrated.

• DI: water leaves; urine is dilute; sodium rises if water replacement is inadequate.

• Hyperthyroidism: hot and fast. Hypothyroidism: cold and slow.

• Primary thyroid disease: TSH and thyroid hormone usually move in opposite directions.

• Graves stimulates the thyroid. Hashimoto destroys thyroid tissue.

• Primary hyperparathyroidism: calcium up, phosphate down.

• Low PTH: low calcium, muscle excitability/tetany.

• Open growth plates: gigantism. Closed plates: acromegaly.

• Type 1 diabetes: severe insulin deficiency. Type 2: resistance plus declining beta-cell function.

• DKA: ketones and acidosis. HHS: severe glucose elevation and dehydration without significant ketosis in the classic chapter pattern.

• Cortisol excess: glucose rises; protein breaks down.

• Aldosterone: sodium retained; potassium excreted.

• Primary adrenal insufficiency: gland fails. Secondary: stimulation fails.

• Visceral fat has greater inflammatory and metabolic risk.

• Ghrelin promotes hunger. Leptin, GLP-1, PYY and CCK contribute to fullness signals.

• Starvation: stored glucose → new glucose → fat/ketones → severe protein breakdown.

• Anorexia = low appetite. Anorexia nervosa = eating disorder causing starvation. Cachexia = involuntary weight loss and muscle wasting.

• Refeeding: insulin rises; phosphate, potassium and magnesium move into cells.

• Anorexia of aging: reduced intake can cause malnutrition and frailty.

Source chapters

Chapter 21 Mechanisms of Hormonal Regulation
Chapter 22 Alterations of Hormonal Regulation
Chapter 23 Obesity Starvation and Anorexia of Aging
Question structure follows the Module 5 Endocrine Interactive Reading Guide.

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