Endo Physiology Flashcards
What is the main function of the endocrine system?
Regulate homeostasis, growth, metabolism, and reproduction.
What is the difference between autocrine, paracrine, and juxtacrine signalling?
- Autocrine: Acts on the same cell.
- Paracrine: Acts on neighboring cells.
- Juxtacrine: Requires direct cell-to-cell contact.
What are the main chemical classes of hormones?
- Amino acids (e.g., adrenaline).
- Peptides/proteins (e.g., insulin).
- Steroids (e.g., cortisol).
How do lipid-soluble hormones exert their effects?
Bind intracellular receptors, affecting DNA transcription.
What are the primary mechanisms controlling hormone secretion?
Nervous system signals, other hormones, and metabolite levels.
Which hormones regulate metabolic fuel use?
Insulin, glucagon, cortisol, adrenaline, and growth hormone.
What happens during the anabolic state?
- Increased insulin.
- Glucose and FFAs (free fatty acids) taken up.
- Activation of anabolic enzymes.
What happens during the catabolic state?
- Increased glucagon.
- Release of glucose and FFAs.
- Activation of catabolic enzymes.
What are the consequences of insulin failure?
Hyperglycemia, ketoacidosis, coma, and death.
What are the consequences of excess insulin?
Hypoglycemia, coma, and death.
Where is insulin secreted?
Pancreatic β-cells.
What stimulates insulin release?
Increased plasma glucose, parasympathetic activity, and secretin.
Where is glucagon secreted?
Pancreatic α-cells.
What are glucagon’s effects?
Opposes insulin by promoting gluconeogenesis and glycogenolysis.
How does glucagon ensure basal insulin levels?
Stimulates insulin release.
What percentage of the UK population is diabetic?
~4-5%.
What are the two main types of diabetes?
Type 1 (autoimmune) and Type 2 (insulin resistance).
What percentage of diabetes cases are Type 2?
~90%.
What is the main pathophysiology of Type 1 DM?
Autoimmune destruction of β-cells.
What is the significance of GAD antibodies in Type 1 DM?
Marker of autoimmune β-cell destruction.
What are the plasma glucose thresholds for diabetes diagnosis?
- Random: >11.1 mmol/L.
- Fasting: >7.0 mmol/L.
- OGTT: >11.1 mmol/L (2 hours post-test).
What does HbA1c measure?
Glycated hemoglobin, reflecting long-term glucose control.
What is the diagnostic HbA1c threshold?
48 mmol/mol (6.5%).
What is the role of C-peptide in DM diagnosis?
Differentiates Type 1 (low) from Type 2 (normal/high).
What are the three hallmark features of DKA?
Hyperglycemia, ketosis, and acidosis.
What causes DKA?
Insulin deficiency and uncontrolled catabolic state.
What are common triggers for DKA?
Infection, missed insulin doses, stress, and drug/alcohol use.
What are the key symptoms of DKA?
Polyuria, polydipsia, weight loss, and abdominal pain.
What are Kussmaul respirations?
Deep, labored breathing due to acidosis.
What metabolic abnormalities are seen in DKA?
- Hyperkalemia (plasma).
- Total body potassium deficit.
What is the anion gap in DKA?
Elevated (>12).
What is the primary goal of DKA treatment?
Correct dehydration, acidosis, and electrolyte imbalance.
What distinguishes HHS from DKA?
Extreme hyperglycemia without significant ketosis.
What is the plasma glucose level in HHS?
30 mmol/L.
What is the typical osmolality in HHS?
320 mOsm/kg.
What complications are associated with HHS?
Stroke, MI, DVT, cerebral edema.
What is the primary treatment for HHS?
Gradual normalization of osmolality, fluids, and glucose.
What are the two divisions of the pituitary gland?
- Anterior (adenohypophysis).
- Posterior (neurohypophysis).
How is the anterior pituitary controlled?
Via hypothalamic releasing and inhibiting hormones.
What hormones are stored in the posterior pituitary?
Oxytocin and vasopressin (ADH).
What hormones are secreted by the thyroid?
T3, T4, and calcitonin.
What is the primary action of thyroid hormones?
Increase metabolic rate via Na-K ATPase production.
Which thyroid hormone is more potent?
T3 (10x more than T4).
What percentage of T4 is bound in the blood?
~99.98%.
What is the main transport protein for T4?
Thyroid-binding globulin (TBG).
What is sick euthyroid syndrome?
Low T3 levels with normal/low TSH in critical illness.
What causes thyrotoxic storm?
Poorly controlled hyperthyroidism with a precipitating event.
What are the features of myxedema coma?
Decreased consciousness, hypothermia, and cardiovascular collapse.
What is the primary treatment for thyrotoxic storm?
Carbimazole, propranolol, and iodine (post-blocking).
What is the primary treatment for myxedema coma?
Gradual thyroid hormone replacement and supportive care.
What are the three zones of the adrenal cortex?
- Zona glomerulosa: Aldosterone.
- Zona fasciculata: Cortisol.
- Zona reticularis: Androgens.
What hormones are secreted by the adrenal medulla?
Adrenaline and noradrenaline.
What triggers cortisol release?
ACTH from the anterior pituitary.
What is the diurnal pattern of cortisol release?
Peak in the morning, trough at night.
What are the primary causes of adrenal insufficiency?
Autoimmune Addison’s, infections (TB, sepsis), malignancy.
What are secondary causes of adrenal insufficiency?
Pituitary or hypothalamic dysfunction (e.g., Sheehan’s syndrome).
What electrolyte abnormalities are seen in adrenal insufficiency?
Hyperkalemia, hyponatremia, and metabolic acidosis.
What is the definitive test for adrenal insufficiency?
Short Synacthen Test.
What is the emergency treatment for adrenal crisis?
Hydrocortisone 100 mg QDS.
What distinguishes endocrine signaling from nervous signaling?
Endocrine signaling is slower, uses hormones in the bloodstream, and has widespread effects.
What are the key features of peptide hormones?
- Water-soluble.
- Act on cell-surface receptors.
- Quick onset but short duration.
What are the key features of steroid hormones?
- Lipid-soluble.
- Act on intracellular receptors.
- Slow onset but long-lasting effects.
What role do G-protein-coupled receptors play in hormone signaling?
Activate intracellular signaling cascades (e.g., cAMP, IP3 pathways).
How does negative feedback maintain hormonal balance?
A rise in hormone levels inhibits its further release.
What secondary messenger system does glucagon primarily use?
cAMP signaling pathway.
How does insulin affect glycogen synthesis?
Activates glycogen synthase in liver and muscle cells.
What effect does insulin have on fat metabolism?
Promotes triglyceride formation and inhibits lipolysis.
How does glucagon affect protein metabolism?
Stimulates amino acid mobilization for gluconeogenesis.
What is the “basal state” in glucose regulation?
Resting condition where glucagon maintains blood glucose levels.
What is the role of genetics in Type 1 DM?
HLA-DR3 and HLA-DR4 are genetic markers associated with increased risk.
Why is Type 2 DM often associated with obesity?
Increased fat mass promotes insulin resistance through inflammatory cytokines.
What is MODY (Maturity-Onset Diabetes of the Young)?
A monogenic form of diabetes caused by a single gene mutation.
What is the significance of ketones in diabetes?
Indicate a shift to fat metabolism due to glucose unavailability.
What are the vascular complications of DM?
- Microvascular: Retinopathy, nephropathy, neuropathy.
- Macrovascular: Stroke, MI, peripheral artery disease.
What is euglycemic DKA?
DKA with normal glucose levels, often seen in SGLT2 inhibitor use.
What distinguishes HHS from DKA?
HHS has higher glucose levels, no significant ketosis, and more severe dehydration.
What is the role of sodium correction in DKA?
Accounts for pseudo-hyponatremia caused by hyperglycemia.
Why is cerebral edema a complication of DKA treatment?
Rapid fluid shifts during treatment disrupt osmotic balance in the brain.
What is the role of potassium in DKA management?
Replace potassium to prevent hypokalemia as insulin therapy lowers serum K+.
What are tropic hormones?
Hormones that regulate the secretion of other hormones (e.g., TSH, ACTH).
What is the role of the hypothalamic-pituitary portal system?
Transports releasing and inhibiting hormones directly to the anterior pituitary.
What is Sheehan’s syndrome?
Postpartum pituitary necrosis due to ischemia from severe blood loss.
Which hypothalamic hormone inhibits prolactin secretion?
Dopamine.
What is the feedback loop for cortisol release?
Hypothalamus → CRH → Anterior pituitary → ACTH → Adrenal cortex → Cortisol.
How is iodine used in thyroid hormone synthesis?
Iodine is incorporated into tyrosine residues to form T3 and T4.
What is the Wolff-Chaikoff effect?
Excess iodine temporarily inhibits thyroid hormone synthesis.
How does thyroid hormone influence cardiovascular function?
Increases heart rate and cardiac output by enhancing β-adrenergic sensitivity
What is the most sensitive test for thyroid dysfunction?
TSH levels.
What is the role of reverse T3 (rT3)?
An inactive form of T3 that competes for receptor binding.
What is a toxic multinodular goiter?
Thyroid nodules that autonomously secrete thyroid hormones, leading to hyperthyroidism.
What is a common cause of hypothyroidism worldwide?
Iodine deficiency.
What is the pathophysiology of Graves’ disease?
Autoantibodies stimulate TSH receptors, causing excessive thyroid hormone production.
How does subacute thyroiditis present?
Painful, tender thyroid with transient hyperthyroidism followed by hypothyroidism.
What is the typical TFT pattern in sick euthyroid syndrome?
Low T3, normal/low TSH, and normal/low T4.
How does cortisol affect blood glucose?
Increases gluconeogenesis and decreases glucose uptake in tissues.
What is the primary action of aldosterone?
Increases Na+ reabsorption and K+ excretion in the kidney.
What are the three stages of the stress response?
- Alarm: Catecholamine release.
- Resistance: Cortisol release.
- Exhaustion: Prolonged stress leading to system failure.
What is the role of DHEA (Dehydroepiandrosterone)?
A precursor to sex steroids, with minor androgenic effects.
What is Cushing’s syndrome?
Chronic excess cortisol due to endogenous or exogenous causes.
How does Addison’s disease present?
Fatigue, weight loss, hyperpigmentation, hypotension, and salt craving.
What is the hallmark electrolyte abnormality in Addison’s?
Hyponatremia and hyperkalemia.
What is adrenal crisis?
Life-threatening exacerbation of adrenal insufficiency with refractory hypotension.
What causes secondary adrenal insufficiency?
Pituitary or hypothalamic dysfunction reducing ACTH production.
What is the treatment for chronic adrenal insufficiency?
Hydrocortisone and, if necessary, fludrocortisone for aldosterone replacement.
What is pheochromocytoma?
A catecholamine-secreting tumor of the adrenal medulla.
What are the clinical features of pheochromocytoma?
Episodic headache, sweating, tachycardia, and hypertension.
How is hyperaldosteronism diagnosed?
Elevated aldosterone-to-renin ratio.
What is the function of growth hormone?
Stimulates growth and metabolism via IGF-1 from the liver.
What is the role of somatostatin?
Inhibits the release of growth hormone, TSH, insulin, and glucagon.
