Endocrine Anatomy & Physiology and Clinical Conditions Flashcards

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Vocabulary practice flashcards covering endocrine anatomy, physiology, hormonal pathways, pancreatic, adrenal, and thyroid pathologies.

Last updated 11:17 AM on 9/18/26
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18 Terms

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Cortisol

A lipophilic glucocorticoid synthesized from cholesterol that stimulates glycogenolysis and gluconeogenesis, decreases serum glucose uptake during stress, sensitizes arteriolar endothelium to catecholamines, and exerts anti-inflammatory effects via the arachidonic acid pathway.

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Aldosterone

A mineralocorticoid synthesized from cholesterol that serves as the primary hormone in the RAAS to increase blood volume and blood pressure by reabsorbing sodium in exchange for potassium and hydrogen ions.

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Primary Adrenal Insufficiency

Adrenal insufficiency caused by direct destruction of the adrenal cortex, resulting in a deficient production of glucocorticoids, mineralocorticoids, and adrenal androgens despite compensatory increases in CRH and ACTH.

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Secondary Adrenal Insufficiency

Adrenal insufficiency caused by insufficient pituitary ACTH secretion, leading to reduced cortisol production while leaving aldosterone levels normal.

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Tertiary Adrenal Insufficiency

Adrenal insufficiency caused by disrupted hypothalamic secretion of CRH, which leads to inadequate pituitary ACTH production and subsequent adrenal gland atrophy.

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Addison's Disease

An autoimmune condition targeting the adrenal cortex, leading to hormone deficiencies corresponding to affected zones, such as loss of aldosterone from the zona glomerulosa and loss of cortisol from the zona fasciculata.

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Cushing's Syndrome

A broad clinical spectrum of symptoms resulting from long-term exposure to excessively high levels of glucocorticoids (hypercortisolism) from endogenous or exogenous sources.

<p>A broad clinical spectrum of symptoms resulting from long-term exposure to excessively high levels of glucocorticoids (hypercortisolism) from endogenous or exogenous sources.</p>
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Cushing's Disease

A specific form of secondary hypercortisolism caused by an ACTH-secreting pituitary tumor.

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Hypothalamic-Pituitary-Thyroid Axis

A neuroendocrine feedback loop where the hypothalamus secretes TRH to stimulate the anterior pituitary gland to release TSH, which in turn acts on the thyroid gland to release T3 and T4 hormones.

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Graves' Disease

An autoimmune thyroid disorder characterized by autoantibodies that continuously stimulate the thyroid gland to overproduce thyroid hormones, leading to hyperthyroidism.

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Thyroid Storm

An acute, life-threatening severe hyperthyroid state (thyrotoxicosis) in Graves' disease patients, often triggered by stress or infection, presenting with fever, tachycardia, hypertension, delirium, and diaphoresis.

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Myxoedema Coma

A severe, life-threatening state of decompensated hypothyroidism characterized by diminished level of consciousness, hypothermia, hypotension, hypoglycaemia, and lactic acidosis.

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Diabetic Ketoacidosis (DKA)

An acute metabolic emergency driven by severe insulin deficiency, resulting in severe hyperglycaemia, ketosis from increased fatty acid breakdown, and metabolic acidosis.

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Type 1 Diabetes

An autoimmune disease characterized by the destructive immune attack on pancreatic beta cells, leading to an absolute lack of insulin.

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Type 2 Diabetes

A metabolic disorder involving peripheral insulin resistance and defective insulin secretion, eventually leading to pancreatic beta-cell exhaustion and elevated blood glucose levels.

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GLUT4 Transporter

A glucose transport protein vesicle that translocates to the cell plasma membrane in response to insulin receptor signaling to allow glucose influx into target cells.

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Atrial Natriuretic Peptide (ANP)

A cardiac hormone produced by atrial cells that opposes the renin-angiotensin-aldosterone system by increasing GFR, decreasing renal sodium reabsorption, and suppressing renin, aldosterone, and ADH release.

<p>A cardiac hormone produced by atrial cells that opposes the renin-angiotensin-aldosterone system by increasing GFR, decreasing renal sodium reabsorption, and suppressing renin, aldosterone, and ADH release.</p>
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Rapid-acting Insulin

A formulation of insulin that begins working within 510 minutes5\text{--}10\text{ minutes} and reaches peak effect at 3090 minutes30\text{--}90\text{ minutes}.

<p>A formulation of insulin that begins working within $$5\text{--}10\text{ minutes}$$ and reaches peak effect at $$30\text{--}90\text{ minutes}$$.</p>