Hormones – Physiology · FCPS Part 1

Cell Type	Secretion / Hormone	Primary Function
Delta Cells	Somatostatin	Inhibits secretion of both insulin and glucagon (paracrine action)
Alpha Cells	Glucagon	Increases blood glucose levels by stimulating glycogenolysis & gluconeogenesis
Beta Cells	Insulin	Decreases blood glucose levels by promoting tissue uptake & storage
Acinar Cells	Digestive Enzymes	Exocrine function; secretes enzymes into the pancreatic duct for digestion

Cortisol

Aspect	High-Yield MCQ Details
Chemical Nature & Origin	Steroid hormone (lipid-soluble, synthesized from cholesterol). Produced in the Zona Fasciculata of the adrenal cortex.
Secretory Stimuli	ACTH (from anterior pituitary) Stress (physical, emotional, surgical) Hypoglycemia Circadian rhythm (peaks early morning ~8 AM, lowest around midnight).
Inhibitors & Regulation	Inhibited by elevated Cortisol levels via negative feedback on both CRH (hypothalamus) and ACTH (anterior pituitary).
Mechanism of Action	Intracellular/Nuclear steroid receptors - alters gene transcription. Increases synthesis of Lipocortin (annexin A1).
Metabolic Actions	• Glucose: Increases blood glucose via gluconeogenesis, decreases peripheral glucose utilization (diabetogenic). • Proteins: Promotes protein catabolism in muscle and skin (causes muscle wasting and thin skin). • Lipids: Promotes lipolysis (creates glycerol for gluconeogenesis) and redistributes fat (truncal obesity, buffalo hump, moon face).
Vascular Actions	Up-regulates alpha_1 adrenergic receptors on arterioles - maintains vascular tone and responsiveness to catecholamines (permissive effect to maintain blood pressure).
Anti-Inflammatory Actions	• Stimulates Lipocortin synthesis - inhibits Phospholipase A_2 - blocks Arachidonic acid production. • Inhibits Interleukin-2 (IL-2) and T-lymphocyte proliferation. • Inhibits histamine and serotonin release from mast cells/platelets.
Other Actions	• Bone: Inhibits osteoblasts, decreases intestinal Ca2+absorption - leads to osteoporosis. • GI: Increases gastric acid secretion. • Blood: Causes eosinopenia, lymphopenia, but increases neutrophils, RBCs, and platelets.
Classic MCQ Trap Answers	• Cortisol INCREASES (not decreases) Lipocortin synthesis. • Cortisol INHIBITS (does not stimulate) Arachidonic acid synthesis. • Anti-inflammatory & immunosuppressive effects require large/pharmacological doses.

Aldosterone

Aspect	High-Yield MCQ Details
Chemical Nature & Origin	Steroid hormone (lipid-soluble, synthesized from cholesterol). Produced in the Zona Glomerulosa (outermost layer) of the adrenal cortex.
Secretory Stimuli	High extracellular potassium level (most potent direct stimulator) Angiotensin II (activated via renin release) ACTH (permissive effect, minor role in long-term control).
Inhibitors & Regulation	Inhibited by Atrial Natriuretic Peptide (ANP) Decreased plasma potassium levels E levated blood pressure or high sodium intake
Mechanism of Action	Binds to intracellular mineralocorticoid receptors in principal cells of late distal tubules and cortical collecting ducts, leading to gene expression of sodium-potassium ATPase pumps and epithelial sodium channels (ENaC).
Electrolyte Actions	Promotes sodium reabsorption and potassium excretion in renal collecting tubules Also promotes hydrogen ion excretion via intercalated cells.
Fluid & Pressure Actions	Water follows reabsorbed sodium passively by osmosis Causes volume expansion and increases blood pressure without changing plasma sodium concentration significantly.
Acid-Base Effect	Promotes hydrogen ion secretion in renal tubules, leading to metabolic alkalosis.
Clinical MCQ Effects	• Hyperaldosteronism (Conn's Syndrome): Causes hypertension, hypokalemia, and metabolic alkalosis. • Hypoaldosteronism (Addison's Disease): Causes hypotension, hyperkalemia, hyponatremia, and metabolic acidosis.
Classic MCQ Trap Answers	• Aldosterone DOES NOT directly control plasma sodium concentration; it controls extracellular fluid volume. • High potassium (not high sodium) directly stimulates aldosterone secretion. • Primary target organ is the cortical collecting duct of the nephron.

Inuslin

Aspect	High-Yield MCQ Details
Chemical Nature & Origin	Peptide hormone (consists of two peptide chains linked by disulfide bonds). Synthesized and secreted by Beta cells of the pancreatic islets of Langerhans.
Secretory Stimuli	Increased blood glucose (primary trigger), increased amino acids (arginine, leucine), gastrointestinal hormones (GLP-1, GIP / incretins), glucagon, and parasympathetic stimulation (vagus nerve / acetylcholine).
Inhibitors & Regulation	Inhibited by Somatostatin, fasting/hypoglycemia, exercise, and sympathetic stimulation (alpha_2 adrenergic receptors).
Mechanism of Action	Binds to a transmembrane Tyrosine Kinase receptor - autophosphorylation inserts GLUT-4 transporters into cell membranes of skeletal muscle and adipose tissue.
Carbohydrate Actions	• Decreases blood glucose (major anabolic/hypoglycemic hormone). • Promotes glycogenesis (glycogen storage in liver and muscle). • Inhibits gluconeogenesis and glycogenolysis.
Lipid Actions	• Promotes lipogenesis and fatty acid synthesis in liver and adipose tissue. • Inhibits lipolysis (inhibits hormone-sensitive lipase). • Inhibits ketone body formation (ketogenesis).
Protein & Growth Actions	• Increases amino acid uptake and protein synthesis. • Inhibits protein breakdown/catabolism.
Electrolyte Actions	Promotes potassium K+ movement into cells by stimulating the Na+/K+ ATPase pump (used clinically to treat acute hyperkalemia).
Clinical MCQ Effects	• Insulin Deficiency (Diabetes Mellitus): Causes hyperglycemia, glucosuria, polyuria, polydipsia, ketoacidosis, and muscle wasting. • Insulin Overdose: Causes rapid hypoglycemia, neuroglycopenia, and sympathetic discharge (sweating, tremors).
Classic MCQ Trap Answers	• Insulin INHIBITS (does not stimulate) Hormone-Sensitive Lipase. • Brain and RBC glucose uptake is independent of insulin (uses GLUT-1 / GLUT-3, not GLUT-4). • Primary driver of insulin release is increased glucose entering Beta cells via GLUT-2.

Glucagon

Aspect	High-Yield MCQ Details
Chemical Nature & Origin	Single-chain peptide hormone (29 amino acids). Synthesized and secreted by Alpha cells of the pancreatic islets of Langerhans.
Secretory Stimuli	Decreased blood glucose (hypoglycemia, primary trigger), increased blood amino acids (arginine, alanine), exercise, stress, and sympathetic stimulation (beta 2adrenergic receptors).
Inhibitors & Regulation	Inhibited by Somatostatin, high blood glucose (hyperglycemia), Insulin (via local paracrine action), free fatty acids, and ketones.
Mechanism of Action	Binds to G-protein coupled receptors Gs on target cells - activates Adenylate Cyclase - increases intracellular cAMP - activates Protein Kinase A.
Carbohydrate Actions	• Increases blood glucose (major catabolic/hyperglycemic hormone). • Stimulates glycogenolysis (glycogen breakdown) in the liver. • Stimulates gluconeogenesis (glucose synthesis from lactic acid and amino acids) in the liver.
Lipid Actions	• Promotes lipolysis (breaks down triglycerides in adipose tissue to yield fatty acids). • Promotes ketogenesis (formation of ketone bodies in the liver from fatty acid oxidation).
Protein Actions	Promotes amino acid uptake by the liver to serve as substrates for gluconeogenesis, reducing plasma amino acid levels.
Other Actions	At high/pharmacological doses, increases heart rate and cardiac contractility (via cAMP, independent of beta-receptors) and relaxes GI smooth muscle.
Classic MCQ Trap Answers	• Glucagon stimulates glycogenolysis in the LIVER, but NOT in skeletal muscle (muscle lacks glucagon receptors and glucose-6-phosphatase). • Glucagon and Insulin are stimulated by the SAME trigger regarding amino acids (both increase after a protein-rich meal), but opposed by glucose. • Glucagon works via cAMP, whereas insulin works via Tyrosine Kinase.

Growth Hormone

Aspect	High-Yield MCQ Details
Chemical Nature & Origin	Single-chain peptide hormone (191 amino acids). Synthesized and secreted by Somatotropes (acidophilic cells) in the anterior pituitary gland.
Secretory Stimuli	GHRH (from hypothalamus), hypoglycemia (low blood glucose), starvation/fasting, exercise, deep sleep (stages 3 and 4), stress, thyroid hormones, and ghrelin.
Inhibitors & Regulation	Inhibited by Somatostatin (GHIH from hypothalamus), high blood glucose (hyperglycemia), elevated free fatty acids, aging, obesity, and negative feedback from IGF-1 and GH itself.
Mechanism of Action	Binds to cell surface cytokine/growth hormone receptors - activates JAK-STAT pathway. Indirect effects (on bone and muscle) are mediated via IGF-1 (Insulin-like Growth Factor 1 / Somatomedin C), which is primarily produced by the liver.
Growth Actions	• Bone: Increases linear bone growth at the epiphyseal plates (promotes chondrocyte proliferation) before epiphyseal closure. • Soft Tissue: Increases organ size, protein synthesis, and lean body mass.
Metabolic Actions	• Carbohydrate: Diabetogenic effect—decreases glucose uptake/utilization in muscle and fat, increases hepatic gluconeogenesis - leads to hyperglycemia and insulin resistance. • Lipids: Promotes lipolysis (breaks down triglycerides in adipose tissue) -increases free fatty acids in blood. • Protein: Anabolic effect—increases amino acid transport into cells and increases protein synthesis.
Clinical MCQ Effects	• Excess in children (pre-puberty): Gigantism (excess linear bone growth). • Excess in adults (post-puberty): Acromegaly (coarsening of facial features, enlargement of hands, feet, tongue, and membranous bones like jaw and skull). • Deficiency in children: Dwarfism (proportional short stature with delayed bone age).
Classic MCQ Trap Answers	• GH DECREASES (does not increase) glucose uptake in peripheral tissues (causes insulin resistance). • GH acts on bones indirectly through IGF-1 peptide produced by the LIVER (not directly by the brain or kidney). • Secretion occurs in pulsatile bursts, with the largest surge during deep sleep.

Prolactin - Oxytocin - GnRH

Feature	Prolactin	Oxytocin	GnRH (Gonadotropin-Releasing Hormone)
Site of Synthesis	Anterior Pituitary (Lactotrophs)	Hypothalamus (Paraventricular & Supraoptic nuclei)	Hypothalamus (Arcuate & Preoptic areas)
Release Site	Anterior Pituitary	Posterior Pituitary (via axonal transport)	Hypothalamus into Hypophyseal Portal System
Primary Target	Mammary glands	Myoepithelial cells (breast) & Myometrium (uterus)	Anterior Pituitary (Gonadotrophs)
Main Functions	• Stimulates milk production (lactogenesis) • Inhibits GnRH (causes lactational amenorrhea)	• Stimulates milk ejection/let-down reflex • Causes uterine contractions during labor	• Stimulates secretion of FSH and LH • Controls reproductive axis and ovulation
Regulation / Stimulus	• Inhibited by Dopamine (prolactin-inhibiting factor) • Stimulated by suckling and TRH	• Stimulated by suckling and uterine/cervical stretch (Ferguson reflex)	• Released in pulsatile fashion • Regulated by sex steroid feedback (estrogen, progesterone, testosterone)

Substance P - Kallikrein - Lactoperoxidase

Substance P: A neuropeptide that acts as a potent sialagogue (saliva stimulator). It binds to NK-1 receptors on salivary acinar cells, triggering a (G-alpha q)/IP-3/DAG signaling pathway that increases intracellular calcium (Ca^2+). This stimulates fluid and electrolyte secretion.
Kallikrein: An enzyme secreted in saliva that converts kininogen to bradykinin (a potent vasodilator that increases blood flow to the glands), facilitating high salivary secretion rather than directly stimulating the acinar cells itself.
Lactoperoxidase: An antibacterial enzyme present in saliva that plays a role in innate immunity, not in regulating secretion flow.

GH disorder	Typical pattern	Dental relevance / treatment in source
Deficiency in childhood	Poor growth/short stature, mild obesity, delayed puberty	May reflect pituitary, hypothalamic, IGF production or receptor problem
Excess before epiphyseal closure	Gigantism; increased linear growth	Excess GH before puberty
Excess after epiphyseal closure	Acromegaly; periosteal bone growth, enlarged organs, glucose intolerance	Mandibular prognathism/Class III tendency, interdental spacing, macroglossia, enlarged lips/gingiva; somatostatin analog such as octreotide

Endocrine pancreas: insulin, glucagon and diabetes

Islets of Langerhans

Cell	Hormone	Main role
β (beta)	Insulin	Lowers blood glucose; anabolic
α (alpha)	Glucagon	Raises blood glucose; catabolic/fasting response
δ (delta)	Somatostatin	Inhibits insulin, glucagon and gastrin
PP cells	Pancreatic polypeptide	Pancreatic polypeptide secretion

GLUT transporter	Typical location / role	Insulin-dependent?
GLUT1	RBCs, brain, placenta	No
GLUT2	Liver, pancreatic β-cells, kidney; glucose sensor/high Km	No
GLUT3	Neurons; high affinity	No
GLUT4	Skeletal muscle and adipose tissue	YES — principal insulin-dependent transporter
GLUT5	Small intestine; fructose transport	No

MCQ tip: If asked for the insulin-dependent glucose transporter, choose GLUT4.

Diabetes mellitus: Type 1 vs Type 2

Feature	Type 1 DM	Type 2 DM
Pathology	Autoimmune β-cell destruction (e.g., anti-GAD/islet-cell antibodies)	Insulin resistance with relative β-cell failure
Insulin	Absolute deficiency; insulin always required	Initially present but ineffective; may decline over time
Typical onset/body habitus	Often younger; may be lean	Usually adult onset but increasingly seen in youth; often associated with obesity/metabolic syndrome
DKA	More common; unopposed glucagon promotes ketogenesis	Less common because residual insulin often suppresses ketogenesis
HHS	Less common	More common

DKA mechanism and clinical cues

Insulin deficiency → reduced glucose uptake/storage and increased gluconeogenesis → hyperglycemia.
Glucose exceeding renal tubular reabsorptive capacity causes glycosuria and osmotic diuresis → dehydration/hypotension.
Increased lipolysis produces ketoacids (β-hydroxybutyrate and acetoacetate) → metabolic acidosis; Kussmaul breathing compensates for acidosis.
Reduced insulin-mediated cellular K⁺ uptake shifts K⁺ out of cells; serum K⁺ may be high despite total-body potassium depletion.

Fruity breath is due to acetone. DKA/HHS require emergency hospital treatment, not dental-office management.

Dental management of diabetes

Prefer morning appointments after the patient has eaten normally and taken usual medication as directed; avoid prolonged fasting.

Ask about last meal and medication; check glucose before long procedures when appropriate. Keep fast-acting oral glucose available for a conscious patient with hypoglycemia.

Diabetes is associated with infection risk and delayed healing; use strict asepsis, minimize trauma and arrange follow-up.

Periodontitis and diabetes have a bidirectional relationship. AGEs increase inflammation and impair collagen quality; neutrophil dysfunction increases infection risk. HbA1c >7% is associated with worse periodontal outcomes.

Dental emergencies

Emergency	Recognition	Immediate action
Hypoglycemia — conscious	Sweating, tremor, confusion, tachycardia; often rapid onset	Stop treatment; give 15 g fast-acting oral glucose (e.g., juice/glucose tablets), recheck after 15 minutes and repeat/seek help as needed.
Hypoglycemia — unconscious	Altered consciousness/unresponsive	Do NOT give anything orally because of aspiration risk. Call emergency services; recovery position and trained-provider IM glucagon or IV dextrose per protocol.
DKA/HHS	Gradual deterioration, thirst/polyuria, altered consciousness; fruity breath/Kussmaul breathing may indicate DKA	Stop procedure, call emergency services, monitor and transfer to hospital; do not try to manage in the dental chair.