ADVANCED PATHOPHYSIOLOGY - EXAM 4 (ENDOCRINE) LATEST UPDATE 2024/2025 (ACTUAL QUESTIONS AN, Exams of Nursing

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Adrenal cortex (zona glomerulosa) secretes: Mineralcor7coids (aldosterone) Adrenal cortex (zona fasciculate) secretes: Glucocor7coids (cor7sol, cor7costerone) Adrenal medulla - contains _______ cells and secretes ________: Chromaffin cells secretes epi and norepi Glucocor7coid func7ons *gluconeogenesis (to maintain blood glucose levels) *catabolic effects (promotes liver uptake of amino/faGy acids for gluconeogenesis)(degreda7on of muscle and adipose 7ssue) *suppression of immune system and inflammatory response (inhibits il-2, decreases wbcs, intereferen with an7body produc7on and clearance) *increase co & peripheral vascular tone

ADVANCED

PATHOPHYSIOLOGY - EXAM 4

(ENDOCRINE) LATEST UPDATE

2024/2025 (ACTUAL QUESTIONS

AND ANSWERS)

*increased gfr *mediate adapta7on to stress *suppresses normal growth and development Regula7on of cor7sol secre7on is controlled primary though _________ released from the __________ *acth (adrenal cor7cothrophin hormone) *anterior pituitary Acth secre7on is regulated by ________ from the __________ Crh (cor7cotrophin releasing hormone hypothalamus Secre7on of acth (adrenal cor7cotrophin hormone) is released in a __________ *diurnal rhythm with a peak level between 6-8 am *also in response to stress. Prolonged stress may abolish the normal diurnal rhythm of acth and cor7sol Nega7ve feedback of cor7sol secre7on: decreased serum level of cor7sol _______ acth

increased serum level of cor7sol ______acth *increased acth *decreased acth The primary mineralcor7coid Aldosterone Regula7on of aldosterone secre7on *raas (angiotensin ii binds to zona glomerulosa cell membrane receptors to increase synthesis and secre7on of aldosterone) *acth can s7mulate secre7on of aldosterone (transient) *increased k+ and/or decreased na+ concentra7on can s7mulate secre7on of aldosterone Diabetes insipidus is a syndrome due to a lack of ac7on of ________ leading to the inability of the ____________ Adh (vasopressin) kidney to reabsorb water in the collec7ng tubule E7ology of central diabetes insipidus *loss of 85% of cells that secrete adh in the hypothalamus *head trauma, tumor, autoimmune disorders, post-surgery E7ology of nephrogenic diabetes insipidus

*loss of the kidney's ability to respond to circula7ng adh *hypokalemia, hypocalcemia, postrenal obstruc7on, drugs, amyloidosis Clinical manifesta7ons of diabetes insipidus *polyuria (10-20 l/day) of dilute urine *hypernatremia (can cause neurologic abnormali7es) *polydipsia (due to hypertonicity) Central diabetes insipidus (different from nephrogenic because) *is responsive to injected vasopressin causing a decrease in uo and increase in urine osmolality *low level of vasopressin Nephrogenic diabetes insipidus (different from central because) *unresponsive to injected vasopressin that causes no change in uo or urine osmolality *high level of vasopressin The parathyroid glands are the key regulators of ____________ homeostasis Calcium Decreased levels of free calcium _______ the synthesis and secre7on of

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*s7mulate *pth Effects of pth

*increased renal reabsorp7on of calcium *increased urinary excre7on of phosphate (it binds to ionized calcium) *increased conversion of vitamin d that augments gi calcium absorp7on *enhanced osteoclast ac7vity which releases calcium from the bone, freeing it up Primary hyperparathyroidism is characterized by ______ secre7on of _______ leading to __________ *excess *pth (hypercalcemia) E7ology of primary hyperparathyroidism *parathyroid adenomas (most common) *primary hyperplasia *parathyroid neoplasia or carcinoma - rare Clinical manifesta7ons of hyperparathyroidism *increased serum level of ionized calcium (most common) *elevated serum pth level *constella7on of symptoms: painful bones, renal stones, abdominal groans (cons7pa7on, nausea), psychic moans (depression, lethargy, seizures) *neuromuscular abnormali7es (weakness, hypotonia)

*polyuria and secondary polydipsia Secondary hyperparathyroidism is characterized by ___________ and overproduc7on of ________ associated with ___________ *glandular hyperplasia *pth *chronic condi7ons that depress serum calcium levels leading to compensatory overac7vity of the parathyroid gland E7ology of secondary hyperparathyroidism Renal failure (most common) vitamin d deficiency Clinical manifesta7ons of secondary hyperparathyroidism *s/s of renal failure *bone abnormali7es *near normal serum calcium level (because its related to gland hyperplasia and increased pth) *metasta7c calcifica7on of blood vessels leading to ischemic damage (calciphylaxis) Hypoparathyroidism is characterized by __________ Pth deficiency E7ology of hypoparathyroidism *parathyroid damage from thyroid surgery *gene7c muta7ons *autoimmune loss Clinical manifesta7ons of hypoparathyroidism *secondary to hypocalcemia (muscle spasms and cardiac arrhythmias) Osteoporosis risk factors

*sex steroid deficiency *use of cor7costeroids or endogenous cor7sol excess *meds (thyroid hormone, an7convulsants, chronic heparin therapy) *immobiliza7on *alcohol abuse *smoking *inadequate intake of calcium and vitamin d Osteoporosis patho: increased ac7vity of ______ and decreased ac7vity of

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*increased osteoclast (increased bone reabsorp7on) *decreased osteoblast (decreased bone forma7on) leads to bone loss Osteoporosis patho: the site of ac7ve bone remodeling: Trabecular bone. Therefore, is the site of bone loss in osteoporosis. Common sites of bone fracture due to osteoporosis *wrist, hip, & spine (due to the high level of trabecular bone in these areas) How does aging relate to osteoporosis? *decreased osteoblast replica7on *decreased response to bone reabsorp7on

*slower manufacture of vitamin d in skin *decreased renal mass so decreased vitamin d ac7va7on *decreased calcium reabsorp7on by gi Osteoporosis patho: decreased dietary intake of _______ & ________ s7mulates bone ________ Calcium & vitamin d reabsorp7on Clinical manifesta7ons of osteoporosis *bone density mass > 2.5 sd below peak bone mass *fx of vertebral column, hip, and wrist *kyphosis r/t small fx in the vertebral column due to bone loss that heals and causes forward curvature of the spine Secre7on of thyroid hormones is s7mulated by __________ Thyrotropin (tsh) Thyroid hormones include __________ and require ________for synthesis T3, t iodine Secre7on of t3 & t4: *the majority of t3 and t4 are reversibly bound to plasma protein for transport *t4 serves as a pro-hormone for t *t3 has a greater affinity for target cell receptor sites than t

Secre7on of thyroid hormones is inhibited by: A nega7ve feedback loop High circula7ng levels of t3 and t4 ___________ the secre7on of __________ from the ______________ *inhibit *tsh (thyrotropin) *anterior pituitary High circula7ng levels of t3 and t4 ____________secre7on of ____________ from the _________ (thus indirectly inhibi7ng secre7on of tsh) *inhibit *trh (thyrotropin releasing hormone) *hypothalamus Effects of thyroid hormone: *increases basal metabolic rate, heat produc7on, and s7mulates o consump7on *promotes bone and brain growth *increases rate of carb absorp7on, protein synthesis, and lipid catabolism *s7mulates the nervous system *s7mulates cardiac rate and contrac7lity

Goiter: defini7on Diffuse enlargement of the thyroid gland due to prolonged s7mula7on of thyroid s7mula7ng hormone (tsh) or tsh-like agent may be associated with hypo or hyperthyroidism Goiter - associated with hypothyroidism. The most common cause in developing countries? Dietary iodine deficiency Goiter - associated with hypothyroidism. Other causes? *hashimoto's thyroidi7s *inges7on of goitrogenic medica7ons (block synthesis of thyroid hormones) *congenital disorders Goiter - associated with hyperthyroidism. E7ology *graves disease (tsh receptor s7mula7ng an7body) *pituitary adenoma - tsh overproduc7on *germ cell tumor - hcg s7mula7on *toxic mul7nodular goiter (autonomous hyperfunc7oning) Goiter - associated with hypothyroidism. Pathogenesis. *decreased serum t3 and t4 causes increased secre7on of tsh from the anterior pituitary that is constantly s7mula7ng the thyroid leading to hyperplasia, enlargement, and then a goiter.

*nontoxic goiter *prolonged tsh s7mula7on --> forma7on of nodule --> autonomous nodules --> mul7nodular goiter (tsh-independent) Goiter - clinical manifesta7ons *large neck mass with enlarged thyroid gland *airway obstruc7on, dysphagia *superior vena cava syndrome - due to compression of large vessels in the neck and upper thorax *hypo or hyperthyroidism depending on the cause Graves' disease is an _________disorder characterized by

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*autoimmune *hyperthyroidism, thyrotoxicosis, infiltra7ve ophthalmopathy, and dermopathy Graves' disease - pathogenesis (ini7a7ng event) *immune system responds to microbe proteins that have the same amino acid sequence as "self" proteins *breakdown in helper t cell tolerance Graves' disease - pathogenesis (development of autoan7bodies) *thyroid receptor-s7mula7ng an7body (tsh-r[s7m]ab) is developed towards the tsh receptor

*the autoan7body binds to and ac7vates tsh receptors to produce excess amounts of t3 and t *increased number and size of follicles *scanty colloid *infiltra7on of lymphocytes Graves' disease - clinical manifesta7ons *increased metabolic rate (heat intolerance, increased appe7te and weight loss) *overac7vity of the sympathe7c nervous system (increased co, tachy, palpita7ons, nervous, insomnia, muscle weakness) *altered skeletal system (increased bone reabsorp7on) *exopthalmos (due to infiltra7on of the retro-orbital space by leukocytes, edema, and extracellular matrix) from reac7on to the tsh-r[s7m]ab *thyroid storm - untreated thyrotoxicosis (abrupt onset of tachy, fever, agita7on, n/v/d, restlessness, psychosis) *lab findings (increased t3 and t4, decreased tsh, presence of tsh-r[s7m]ab Hypothyroidism - most common e7ology Hashimoto thyroidi7s Hypothyroidism - other primary e7ologies

Surgery autoimmune iodine deficiency drugs radioiodine therapy or external radia7on Hypothyroidism - clinical manifesta7ons in adults *decreased basal metabolic rate (weight gain, cold intolerance, hypothermia) *neurologic abnormali7es (slow thinking, depression, forgeiulness, sluggish dtrs) *abnormal bioenerge7cs in mitochondria (muscle weakness, cramps, and s7ffness) *cardiovascular: bradycardia, cardiomyopathy *decreased gi mo7lity --> cons7pa7on *dry, cool, skin *myxedema (nonpijng puffiness of the skin due to accumula7on of sodium and water, proteins, etc)

*briGle hair *lab findings (low serum t3 and t4, elevated tsh level) ----elevated tsh level is most sensi7ve test for early hypothyroidism---- *decreased iodine uptake Hypothyroidism - clinical manifesta7ons in infants and young children *cre7nism. *impaired development of the nervous system leading to severe mental retarda7on *impaired development of the skeletal system with short stature and course facial features Hashimoto thyroidi7s: defini7on An autoimmune disease that is characterized by gradual thyroid failure secondary to autoimmune destruc7on of the thyroid gland. Most common cause of hypothyroidism Hashimoto thyroidi7s - patho *ini7a7ng event (breakdown in helper t cell tolerance) *development of autoan7bodies against the thyroid follicular cell membrane (tsh receptor blocking an7body) --tsh-r block ab-- *tsh-r block ab blocks the s7mula7on of t3 and t4 produc7on

*cd8+ (cytotoxic t cell) mediated destruc7on and loss of thyroid cells *produc7on of proinflammatory cytokines that injure thyroid cells *leukocyte infiltra7on leads to atrophy and fibrosis of the thyroid gland Hashimoto thyroidi7s - clinical manifesta7ons (early phase) *painless enlargement of the thyroid associated with some degree of hypothyroidism. May be preceded by transient thyrotoxicosis due to release of thyroid hormones from damaged follicles increased t3 and t4, decreased tsh level Hashimoto thyroidi7s - clinical manifesta7ons (later phase) S/s of hypothyroidism high levels of an7body 7ters Subclinical thyroid dysfunc7on: defini7on Low or high tsh levels associated with normal circula7ng t3 and t4 levels Subclinical thyroid dysfunc7on - clinical manifesta7ons *s/s are not consistent with overt hypothyroidism *increased risk of cardiovascular complica7ons (atherosclero7c heart disease and heart failure) Thyroid neoplasms - risk factors that a nodule is a neoplasm *solitary nodule > mul7ple *young adults > older

*males > females *hx of radia7on tx to the head and neck *cold nodule > hot nodule (takes up radioac7ve iodine) Thyroid neoplasms - types *follicular adenoma (benign) - most common. Solitary nodule surrounded by a fibrous capsule. *thyroid carcinoma (papillary 85%, follicular) *medullary carcinoma - less common. (neoplasms of the c cells --> increased produc7on of calcitonin) Thyroid neoplasm - pathogenesis *papillary carcinomas: ac7va7on of the mitogen-ac7vated kinase pathway (map) *follicular thyroid carcinomas: gene7c muta7ons in the pi-3k/akt signaling pathway *medullary thyroid carcinomas: ret proto-oncogene muta7ons. *environmental: ionizing radia7on and deficiency of dietary iodine. Thyroid neoplasms - clinical manifesta7ons A. Papillary carcinoma: painless neck mass, 10-year survival rate > 95% b. Follicular carcinoma: solitary cold thyroid nodules, tend to metastasize to the lungs, bone, and liver via bloodstream

c. Medullary carcinoma: mass in the neck, associated with dysphagia, hoarseness Cushing's syndrome - defini7on A clinical condi7on that results from chronic exposure to excessive glucocor7coids Cushing's - iatrogenic e7ology Secondary to exogenous glucocor7coid administra7on increased cor7sol levels leads to cushing's increased cor7sol levels lead to decreased acth along with hyposecre7on, adrenal atrophy, and loss of normal response to stress Cushing's - noniatrogenic e7ology (hypothalamic crh hypersecre7on) *uncommon *increased crh secre7on from the hypothalamus --> hyperplasia of pituitary cor7cotroph cells --> increased acth hypersecre7on Cushing's - noniatrogenic e7ology (pituitary cushing's disease) *the most common *anterior pituitary adenoma --> hypersecre7on of acth *high levels of acth and cor7sol Cushing's - noniatrogenic e7ology (adrenal cushing syndrome) *adrenocor7col adenomas/carcinomas/hyperplasia --> hypersecre7on of cor7sol (independent of acth)

*high level of cor7sol but low level of acth (nega7ve feedback) Cushing's - noniatrogenic e7ology (ectopic cushing syndrome) *secre7on of acth by nonpituitary tumor (small cell carcinomas of the lungs and bronchial carcinoid tumors) *ectopic crh secre7on by bronchial carcinoid tumors --> secre7on of acth Cushing's - clinical manifesta7ons *excess protein catabolism and decreased muscle protein synthesis (muscle weakness and was7ng) *redistribu7on of body fat (buffalo hump, moon face) *inhibi7on of fibroblasts (thin skin, abd striaie, easy bruising, poor wound healing) *acanthosis nigricans - dark, son, skin in fine folds and papillae *hirsu7sm and menstrual abnormali7es *osteoporosis *increased risk for infec7on *neuropsychiatric abnormali7es (mood swings, depression) Cushing's - lab findings

*increased 24 hour urine cor7sol level (>100) *loss of diurnal cor7cal secre7on *hyperglycemia *increased (hypothalamic origins) or decreased (adrenal origins) acth levels depending on e7ology Adrenocor7cal insufficiency - types Primary: *acute (adrenal crisis) *chronic (addison's) secondary: hypofunc7on of the hypothalamus and/or pituitary E7ology of acute adrenocor7cal insufficiency (adrenal crisis) *rapid withdrawal of long term cor7costeroid therapy *massive adrenal hemorrhage *stress in pts with underlying chronic adrenocor7cal insufficiency E7ology of chronic adrenocor7cal insufficiency (addison's disease) *autoimmune destruc7on of the adrenal cortex *infec7ons (tb, hiv, fungus)

*infiltra7ve diseases (amyloidosis, cancer) Clinical manifesta7ons - primary adrenocor7cal insufficiency *hyperpigmenta7on of skin (due to increased acth) *salt cravings, hyponatremia, hyperkalemia (due to aldosterone deficiency) *lab findings (decreased cor7sol level and increased acth) Clinical manifesta7ons - secondary adrenocor7cal insufficiency *secre7on of aldosterone is usually preserved *no hyperpigmenta7on (since acth is low) *altera7on in male sex characteris7cs, decreased libido (due to androgen deficiency) *lab findings (decreased acth, decreased cor7sol) Hyperaldosteronism Excessive secre7on of aldosterone by the adrenal cortex Causes of primary hyperaldosteronism *aldosterone-secre7ng adenoma (autonomous overproduc7on of aldosterone) such as: bilateral adrenal hyperplasia unilateral adrenal hyperplasia adrenocor7cal carcinomas gene7c altera7ons

Causes of secondary hyperaldosteronism (common) *excessive renin produc7on leads to overac7va7on of raas and increased secre7on of aldosterone Hyperaldosteronism - clinical manifesta7ons *hypernatremia, hypokalemia *htn *muscle weakness, cardiac dysrhythmias, visual disturbances *lab findings (increased level of aldosterone and decreased level of renin - primary) (increased aldosterone and renin - secondary) Hypoaldosteronism Characterized by a deficiency in aldosterone secre7on or ac7on. May be primary or secondary. Hypoaldosteronism - primary. Causes *destruc7on of adrenocor7cal 7ssue *defects in adrenal synthesis of aldosterone Hypoaldosteronism - secondary. Causes *low renin produc7on leading to decreased s7mula7on of aldosterone secre7on *hypopituitarism leading to inadequate s7mula7on of aldosterone secre7on Hypoaldosteronism - clinical manifesta7ons

*hyponatremia, hypovolemia, hypotension *impaired secre7on of k+ in the tubules leading to hyperkalemia *increased renin level in primary hypoaldosteronism Pheochromocytoma - defini7on A neoplasm of the chromaffin cells of the adrenal medulla that synthesizes and secretes excessive catecholamines Pheochromocytoma - e7ology *adrenal medulla neoplasm (the majority)(10% are malignant) *familial gene7c syndromes like neurofibromatosis, von hippel-lindau, men2 *neoplasms composed of chromaffin cells in extramedullary sites (10%) Pheochromocytoma - clinical manifesta7ons *htn, tachycardia, palpita7ons *ha, swea7ng, tremor, anxiety *weight loss, n/v *increased urinary excre7on of free catecholamines Pheochromocytoma - complica7ons *cardiac disease states (cardiomyopathy, ischemia, arrhythmias) *pulmonary edema

*renal artery stenosis Post-transla7onal processing of proglucagon *glucagon is secreted by alpha cells of pancreas. *alpha cells produce pancrea7c glucagon --> opposes effects of insulin *proglucagon is also expressed in the intes7ne and brain *produced glucagon-link pep7de (glp-1 and glp-2) --> enhances glucose- s7mulated insulin secre7on and s7mulate beta cell prolifera7on and mass. Diagnosis of diabetes mellitus A. A random blood glucose level > or equal to 200 mg/dl with clinical s/s of diabetes b. A fas7ng blood glucose level > or equal to 126 on more than one occasion c. A blood glucose level > 200 mg/dl 2 hours aner a standard oral glucose load (75 g). D. A1c level of > 6.5% (dependent on ethnicity) Prediabetes A fas7ng glucose level between 100- 125 Type i diabetes - defini7on

An autoimmune disease caused by selec7ve destruc7on of beta cells of the pancreas by t lymphocytes targe7ng beta cell an7gens, leading to severe deficiency in insulin Type 1 diabetes - patho *autoimmune destruc7on of beta cells results from th1 cells s7mula7ng cytokines, cd8+, autoan7bodies against the beta cells and insulin *inflammatory response --> release of macrophage, cytokines resul7ng in more beta cell injury and necrosis (insuli7s). Beta cell apoptosis. *ongoing process of islet atrophy and fibrosis leading to insulin deficiency *clinical manifesta7ons appear aner loss of 90% of b cells Type 2 diabetes - defini7on Caused by a combina7on of peripheral resistance to insulin ac7on and inadequate compensatory response of insulin secre7on by pancrea7c beta cells Type 2 diabetes - insulin resistance *failure of target 7ssue to respond to insulin ac7on --> decreased glucose uptake in muscle and fat, insulin does not inhibit gluconeogenesis --> increased glucose level *func7onal defects in insulin signaling pathway: abnormal insulin molecule, decreased insulin receptors on cell surface, abnormali7es in glut-4 transporter *central obesity induces insulin resistance: increased fat and triglycerides inhibit insulin signaling, increased secre7on of inflammatory cytokines, and dysregula7on of adipokines (lep7n, adiponec7n)

Type 2 diabetes - inadequate insulin secre7on *beta cell dysfunc7on leading to insulin hypersecre7on ini7ally. Causes beta cell hyperplasia to support *then eventually beta cells become exhausted and lose pulsa7le effect and hyposecrete insulin *then beta cells fail Type 2 diabetes - beta cell loss from lipotoxicity *increased faGy acids lead to apoptosis, glucotoxicity, increased ros produc7on and oxida7ve stress Diabetes mellitus - clinical manifesta7ons *polyuria, polydipsia, polyphagia *glycouria *increased level of glucagon *ketosis - from lipolysis of fat *increased lipid levels Diabe7c ketoacidosis (dka) - e7ology Occurs due to profound loss of insulin ac7vity causing lipolysis with significant hyperglycemia and ketosis. Primarily in type 1. May be brought on by stress, failure to take meds Dka - patho