Physiology - Block 1 - Part 5

davidwurbel7's version from 2015-06-07 22:05


Question Answer
Secretes Mineralocorticoids (Aldosterone & Deoxycorticosterone) - Mineralocorticoids play a role in mineral metabolism. Regulated by angiotension II and stimulated by hyperkalemiaZona Glomerulosa
Secretes Glucocorticoids - Glucocorticoids (Cortisol/Hydrocortisone). These play role in carbohydrate & protein metabolism. Regulated by ACTHZona Fasciculate
Secretes Sex steroids (Androgens -mainly DHEA and Androstenedione). Minor effect on reproductive functions because gonads secrete most of sex hormones. Regulated by ACTHZona Reticularis
Aldosterone low, Corisol low, Androgens low, ACTH high, CRH highAddison's Disease (Primary Adrenal Insuffiency)
Aldosterone normal, Corisol low, Androgens low, ACTH low, CRH high. Responds to administration of ACTHSecondary Adrenal Insuffiency
Increases blood sugar levels (Hyperglycemia) by two mechanisms - Decrease glucose uptake in muscle, Adipose and lymphoid, thereby - Anti Insulin action and acts synergistly with glucagon to induce gluconeogenesis by liverCortisol
Without this hormone, fasting hypoglycemia rapidly developsCortisol
Enhances the capacity of glucagon and catecholamines. Promotes glycogenolysis, gluconeogenesis and lipolysisCortisol
Inhibits phospholipase A2 by inducing synthesis of lipocortin reducing inflammationGlucocorticoids
Inhibits release of histamine & serotonin from mast cells & platelets to treat allergiesGlucocorticoids
Inhibits collagen synthesis, thereby prevents tissue adhesions. Therefore given therapeutically after abdominal surgeriesGlucocorticoids
Suppress the immune response by inhibiting production of Interleukins IL-2 & T-lymphocytes to prevent rejection of transplanted organsGlucocorticoids
Act synergistly with norepinephrine to increase blood pressureGlucocorticoids
If in excess, increases bone resorption by increasing osteoclastic activity & decreases bone formation. Breakdowns collagen and inhibits synthesis of collagenGlucocorticoids
Glucocorticoids are contraindicated in patients with this because it increases electrical activity in the brainEpilepsy
Reabsorption of Sodium & water, excretion of Potassium & Secretion of H+Aldosterone
Mechanism of action on principal cells of late distal tubule & collecting ducts by increasing renal Na+ reabsorption by increasing epithelial Na+ channelsAldosterone
Patient presents with hypertension, hypokalemia, and metabolic alkalosis. Serum show elevated aldosteroneConn's Syndrome
Most commonly occurs due to administration of high pharmacological doses of GlucocorticoidsCushing's Syndrome
Pituitary adenoma secreting ACTH, leading to high cortisol and androgensCushing's Disease
Bilateral hyperplasia of Adrenal glands (GC and Androgens). Adrenal adenoma (GC and Androgens). Adrenal carcinoma (GC and Androgens)Cushing's Syndrome
Ectopic ACTH secretion by oat cell or small cell carcinomaCushing's Syndrome
To differentiate between a Primary & Secondary cause, this test is doneDexamethasone Suppression Test
Low dose dexamethasone given, ACTH levels will go down and cortisol levels will go down the following the dayNegative Low Dose Dexamethasone Suppression Test (Obese)
Low dose dexamethasone given, ACTH levels will go down and cortisol levels with stay the samePositive Suppression Low Dose Dexamethasone Test (Cushing's Syndrome)
High dose dexamethasone given, ACTH levels will go down and cortisol levels will go downPositive High Dose Dexamethasone Suppression Test (Cushing's Disease)
High dose dexamethasone given, ACTH levels will remain the same and cortisol levels will remain the sameNegative High Dose Dexamethasone Suppression Test (Ectopic ACTH)
Inhibitor of steroid hormone synthesis can be used to treat Cushing’s SyndromeKetoconazole
Most commonly due to autoimmune destruction of Adrenal cortex leading to adrenal crisis. Second most common cause is TB infection of the adrenal glands. There is decreased GC, MC & Androgen secretion. Increased ACTH because low Cortisol levels stimulate ACTH secretion. Since ACTH has MSH-like activity, this disease is characterized by Hyperpigmentation.Primary Adrenocortical Insufficiency (Addison’s Disease)
Caused by deficiency of ACTH. This in turn leads to decreased Adrenocortical hormones. No hypertension and hyperpigmentation. Serum aldosterone and K+ levels are normal. Hypoglycemia seen between mealsSecondary Adrenocortical Insufficiency
Patients exhibits hypertension - increased ECF & blood volume. This increased ECF volume & BP in turn decreases Renin secretion, Hypokalemia, Metabolic AlkalosisHyperaldosteronism (Conn's Syndrome)

Biosynthesis of Adenocortical Hormone

Question Answer
Conversion of cholesterol to pregnenoloneCholesterol Desmolase
Rate limiting enzyme of biosynthesis of adrenocortical hormonesCholesterol Desmolase
Converts pregnenolone to 17-hydroxypregnenolone and progesterone to 17-hydropregesterone17a-Hydroxylase
Converts 17-hydroxypregnenolone to dehydroepiandrosterone and 17-hydropregesterone to androstenedione17, 20 Lyase
Converts pregnenolone to progesterone and 17-hydropregesterone to 17-hydropregesterone3b-Hydroxysteriod Dehydrogenase
Coverts progesterone to 11-deoxycorticosterone and 17-hydropregesterone to 11-deoxycortisol21b-Hydroxylase
Converts 11-deoxycorticosterone to corticosterone and 11-deoxycortisol to cortisol11b-Hydroxylase
Converts corticosterone to aldosteroneAldosterone Synthase
Aldosterone synthase is positively regulated byAngiotensin II