Renal
On this page 6 sections
Adrenal cortex and medulla
Cortex zones: GFR
| Layer (outside → inside) | Product | Main regulator | Main action |
| Zona glomerulosa — Salt | Aldosterone; mineralocorticoid | Angiotensin II and extracellular K⁺; ACTH permissive | Retains Na⁺/water; secretes K⁺ and H⁺ |
| Zona fasciculata — Sugar/stress | Cortisol; glucocorticoid | ACTH; circadian rhythm | Stress response, gluconeogenesis, anti-inflammatory effects, vascular responsiveness |
| Zona reticularis — Sex | DHEA and androstenedione | ACTH | Androgenic activity |
Memory cue — GFR: Glomerulosa = Salt (aldosterone); Fasciculata = Sugar (cortisol); Reticularis = Sex (androgens). All cortical steroids derive from cholesterol.
Steroid synthesis and cortisol rhythm
- ACTH stimulates cholesterol desmolase and conversion of cholesterol to pregnenolone.
- 21-carbon steroids include progesterone, deoxycorticosterone, aldosterone and cortisol; 19-carbon steroids include DHEA and androstenedione.
- Cortisol follows a circadian rhythm: highest around 6–8 AM (before waking) and lowest around midnight.
HPA axis: hypothalamic CRH → anterior pituitary ACTH → adrenal cortex cortisol. Cortisol inhibits CRH and ACTH by negative feedback.
Dexamethasone suppression: normal physiology suppresses cortisol; ACTH-secreting tumour may suppress only with high-dose testing; adrenal tumour generally suppresses with neither dose.
Cortisol actions
| Cue | Effect |
| A — Appetite | Increases appetite and central adiposity |
| B — Blood pressure | Permits catecholamine action; increases α1-receptor sensitivity |
| I — Insulin resistance | Antagonizes insulin; diabetogenic |
| G — Gluconeogenesis | Increases hepatic glucose production; muscle protein and fat provide substrates |
| F — Fibroblasts | Inhibits fibroblast activity and wound healing; thin skin/striae |
| I — Inflammation/immune suppression | Induces lipocortin, inhibits PLA2, reduces prostaglandins/leukotrienes and IL-2/T-cell activity |
| B — Bone | Reduces osteoblast activity and supports bone loss/osteoporosis |
Aldosterone
- Acts mainly on principal cells of late distal tubule/collecting duct: increases ENaC and Na⁺/K⁺-ATPase → Na⁺ reabsorption, water retention, ECF expansion and increased BP; increases K⁺ secretion.
- Acts on α-intercalated cells to increase H⁺ secretion; excess may cause metabolic alkalosis.
Regulation: renin–angiotensin–aldosterone system (RAAS) and serum K⁺ are key controls; ACTH has a permissive role.
Adrenal medulla and catecholamines
Adrenal medulla is a modified sympathetic ganglion derived from neural crest; chromaffin cells secrete catecholamines.
Synthesis: tyrosine → DOPA → dopamine → norepinephrine → epinephrine. PNMT converts norepinephrine to epinephrine and is induced by high local cortisol from the cortex.
Approximate secretion: 80% epinephrine and 20% norepinephrine. Release increases with stress, hypoglycemia, exercise, hemorrhage and hypoxia.
| Receptor | Coupling | Major effects |
| α1 | Gq → IP3/DAG/Ca²⁺ | Vasoconstriction, mydriasis, increased glycogenolysis |
| α2 | Gi → ↓ cAMP | Inhibits presynaptic norepinephrine release; reduces insulin secretion; promotes platelet aggregation |
| β1 | Gs → ↑ cAMP | Increased heart rate, contractility and renin release |
| β2 | Gs → ↑ cAMP | Bronchodilation, vasodilation in skeletal muscle, glycogenolysis/gluconeogenesis |
| β3 | Gs → ↑ cAMP | Lipolysis in adipose tissue |
| Feature | Norepinephrine | Epinephrine |
| Dominant effects | α1 and β1 | α1, β1 and β2 |
| Vascular effect | Predominantly vasoconstriction; increased TPR/MAP | Mixed effects; β2-mediated skeletal-muscle vasodilation |
| Heart-rate pattern | May cause reflex bradycardia | Usually increases heart rate and cardiac output |
| Bronchi | Little bronchodilation | Stronger bronchodilation |
Adrenal disorders
| Condition | Core pattern | Exam clues |
| Addison disease (primary adrenal insufficiency) | Low cortisol and aldosterone; ACTH rises | Hypoglycemia, hypotension, hyperpigmentation, hyponatremia, hyperkalemia, weight loss and weakness |
| Secondary/tertiary adrenal insufficiency | Low ACTH/CRH drive; aldosterone relatively preserved compared with primary disease | Hyperpigmentation generally absent; distinguish using ACTH and aldosterone pattern |
| Cushing syndrome | Excess cortisol from exogenous steroids, adrenal disease or ACTH-driven disease | Central obesity, moon face/buffalo hump, muscle wasting, osteoporosis, hypertension, hyperglycemia, poor wound healing; ACTH often low in adrenal cortisol excess but high in ACTH-driven Cushing disease |
| Conn syndrome (primary hyperaldosteronism) | Aldosterone-producing adrenal tumour/hyperplasia | Hypertension, hypokalemia, metabolic alkalosis and suppressed renin |
| 21-hydroxylase deficiency | Congenital adrenal hyperplasia; reduced cortisol and often aldosterone with increased androgen pathway activity | Androgen excess/virilization; salt wasting may occur |
| 17α-hydroxylase deficiency | Reduced sex steroids and cortisol pathway; mineralocorticoid effects increased | Hypertension and hypokalemia with impaired sexual development |
Pheochromocytoma
Chromaffin-cell catecholamine-secreting tumour of adrenal medulla or sympathetic ganglia.
Classic triad: episodic hypertension, headache and diaphoresis. Palpitations, pallor, anxiety, weight loss and hyperglycemia may also occur.
Plasma metanephrines or 24-hour urinary catecholamines/metanephrines for diagnosis, with CT/MRI for localization.
Dental considerations: adrenal disease
Identify patients with adrenal insufficiency and those using long-term corticosteroids; assess risk of adrenal suppression before significant stress/invasive care.
Known Addison disease: avoid withholding prescribed steroid; consider appropriate stress-dose/steroid-cover plan for invasive procedures or significant stress in consultation with the treating clinician.
Suspected adrenal crisis: severe weakness, hypotension, vomiting, confusion or collapse in an at-risk patient is an emergency. Stop procedure, call emergency services, support airway/breathing/circulation and arrange immediate transfer.