Pathophysiology: Hormones and Endocrine Disorders - Key Concepts and Review Questions, Exams of Pathophysiology

A concise overview of hormone actions, hormone structures, and the regulation of homeostasis by the hypothalamus. It covers the sources of hormones in the body, including the pituitary, adrenal glands, thyroid, parathyroid, pancreas, ovaries, testes, and kidneys. The document also details the causes, clinical manifestations, diagnosis, and treatment of endocrine disorders such as hypothyroidism, hyperthyroidism, cushing's syndrome, and addison's disease. It includes review questions to test understanding of key concepts.

Typology: Exams

2025/2026

Available from 11/12/2025

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Portage Learning Pathophysiology Module 9
3 ways that hormones act on the body -
1. endocrine๎˜โ˜‘๏ธ๎˜‚
2. paracrine
3. autocrine
3 categories for hormone structure -
1. amines/amino acidsโ˜‘๏ธ๎˜‚
2. peptides, polypeptides & proteins (freely floating in bloodstream)
3. steroids (transported in blood by carrier protein
what does the hypothalamus regulate? -
homeostasisโ˜‘๏ธ๎˜‚
body temp
hunger
behavior
emotion
pain
how do the hypothalamus and pituitary interact? -
hormones released from the hypothalamus stimulate hormone release from the โ˜‘๏ธ๎˜‚
pituitary
what are the 11 sources of hormones in the body -
hypothalamusโ˜‘๏ธ๎˜‚
anterior pituitary
posterior pituitary
ovaries
testes
kidneys
thyroid
parathyroid
pancreas
adrenal cortex
adrenal medulla
What is CRH and what does CRH do to the anterior pituitary? -
corticotropin releasing hormone; stimulates pituitary to release acthโ˜‘๏ธ๎˜‚
what is acth and what does it do -
Adrenocorticotropic hormoneโ˜‘๏ธ๎˜‚
- stimulate adrenal cortex to secrete corticosteroids
which hormones are released by the posterior pituitary and what do they do? -
ADH (increases reabsorption of H2O in kidney) and oxytocin (stimulates breast milk โ˜‘๏ธ๎˜‚
ejection and contractions)
which hormones are released by the anterior pituitary -
pf3
pf4
pf5
pf8
pf9
pfa

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Portage Learning Pathophysiology Module 9

3 ways that hormones act on the body -  โ˜‘๏ธ 1. endocrine

  1. paracrine
  2. autocrine 3 categories for hormone structure - โ˜‘๏ธ 1. amines/amino acids
  3. peptides, polypeptides & proteins (freely floating in bloodstream)
  4. steroids (transported in blood by carrier protein what does the hypothalamus regulate? - โ˜‘๏ธ homeostasis body temp hunger behavior emotion pain how do the hypothalamus and pituitary interact? - โ˜‘๏ธ hormones released from the hypothalamus stimulate hormone release from the pituitary what are the 11 sources of hormones in the body - โ˜‘๏ธ hypothalamus anterior pituitary posterior pituitary ovaries testes kidneys thyroid parathyroid pancreas adrenal cortex adrenal medulla What is CRH and what does CRH do to the anterior pituitary? - โ˜‘๏ธ corticotropin releasing hormone; stimulates pituitary to release acth what is acth and what does it do - โ˜‘๏ธ Adrenocorticotropic hormone
  • stimulate adrenal cortex to secrete corticosteroids which hormones are released by the posterior pituitary and what do they do? - โ˜‘๏ธ ADH (increases reabsorption of H2O in kidney) and oxytocin (stimulates breast milk ejection and contractions) which hormones are released by the anterior pituitary -

โ˜‘๏ธ GH

ACTH

FSH

LH

TSH

Prolactin Which hormones are released by adrenal cortex and what do they do? - โ˜‘๏ธ aldosterone (increases Na absorption and K loss by kidney), cortisol (regulates metabolism, blood glucose levels, anti-inflammatory, and decreases effects of stress), DHEA/androstenedione (converted to DHT and testosterone for minimal androgenic activity) which hormones are released from adrenal medulla and what do they do? - โ˜‘๏ธ norepinephrine/epinephrine; neurotransmitters for SNS which hormones are released by the thyroid and what do they do? - โ˜‘๏ธ thyroid hormone (TH) T3 and T4 ( increase metabolic rate, protein/bone turnover; fetal/infant growth & development) & calcitonin (decreases blood calcium and phosphate levels) which hormone is released by the parathyroid? - โ˜‘๏ธ PTH - regulates serum calcium levels which hormone is secreted by the pancreas and what do they do? - โ˜‘๏ธ insulin (decreases blood glucose), glucagon (increases blood glucose), somatostatin (delays intestinal absorption) what two site release the hormone somatostatin - โ˜‘๏ธ hypothalamus & pancreas what hormone is released by the kidney - โ˜‘๏ธ 1,25 dihydroxyvitamin D - stimulates Ca absorption from intestine what hormones are released from the ovaries and testes - โ˜‘๏ธ respectively - estrogen (female sex organ development and characteristics) & progesterone (menstrual cycle), and testosterone (male organ development and characteristics) what are the 2 disease states of an endocrine disorder - โ˜‘๏ธ 1. hyper states (increased hormone secretion)

  1. hypo states (decreased hormone secretion) what are the 4 causes of hyper states - โ˜‘๏ธ 1. target gland oversecretes
  2. pituitary or hypothalamus over stimulate
  3. additional hormones being produced from different site
  4. target receptor becomes hyper active what are the 5 causes of hypo states - โ˜‘๏ธ 1. congenital/acquired disorder of target gland
  5. pituitary not secreting enough stimulating hormone
  6. hypothalamus not secreting enough releasing hormone
  7. defective hormone

primary hyperthyroidism - โ˜‘๏ธ thyroid is secreting too much T4 and T3 regardless of pituitary stimulation secondary hyperthyroidism - โ˜‘๏ธ thyroid is secreting too much T4 and T3 because of overstimulation by pituitary what are the 2 primary causes of primary hyperthyroidism - โ˜‘๏ธ 1. grave's disease

  1. toxic nodule what are the 2 causes of secondary hyperthyroidism - โ˜‘๏ธ 1. pituitary tumor
  2. ectopic source (ovarian tumor) what are some clinical manifestations of hyperthyroidism - โ˜‘๏ธ weight loss/ increased appetite tacycardia dyspnea heat intolerance Grave's Disease/ hyperthyroidism - โ˜‘๏ธ autoimmune disease that attacks thyroid and causes it to produce more hormone opthalmopathy exopthalmos pretrial myxedema thyroid bruit - rushing sound over thyroid upon auscultation how is primary hyperthyroidism diagnosed - โ˜‘๏ธ low TSH (no stimulus from pituitary) and elevated T4 and T3 because thyroid is oversecreting w/o stimulus how is secondary hyperthyroidism diagnosed - โ˜‘๏ธ TSH high because of over secretion by pituitary and subsequent elevated T4 and T levels what is the main difference between hypothyroidism and hyperthyroidism - โ˜‘๏ธ T4 and T3 levels are ELEVATED in hyperthyroidism which autoantibodies would be present for a patient to be diagnosed with grave's disease primary hyperthyroidism? - โ˜‘๏ธ anti-TSH receptor antibodies which diagnostic scans can be done to detect toxic nodules for primary hyperthyroidism? - โ˜‘๏ธ 1. radioiodine uptake (thyroid function)
  3. thyroid scans (nodule detection)
  4. ultrasound (cystic vs solid)
  5. fine-needle aspiration biopsy (malignant vs. benign) what are the main treatments for hyperthyroidism -

โ˜‘๏ธ 1. beta-blockers - treat tachycardia and anxiety

  1. methimazole & propylthiouricil - reduce T4 and T3 levels by decreasing synthesis
  2. thyroidectomy/radioactive iodine therapy - long term treatment to destroy thyroid (can lead to hypothyroidism) where are the adrenal glands located - โ˜‘๏ธ on top of the kidneys what is the adrenal medulla and what does it secrete? - โ˜‘๏ธ inner part of the adrenal gland; secretes norepinephrine and epinephrine why is the adrenal cortex important and what are it's 3 layers - โ˜‘๏ธ it is necessary to sustain life; zona glomerulosa, zona fasciculata, zona reticularis zona glomerulosa - โ˜‘๏ธ secretes aldosterone (mineralocorticoid) - triggers reabsorption of Na/H2O to increase BP and secretion of K into filtrate what triggers the secretion of aldosterone - โ˜‘๏ธ RAAS - renin-angiotensin-aldosterone system zona fasciculata - โ˜‘๏ธ secretes mainly cortisol (glucocorticoids) triggered by secretion of ACTH from pituitary; reduces inflammation, increases BP and Blood Sugar, and aids in stress response & metabolism zona reticularis - โ˜‘๏ธ secretes androgens (sex hormones) what is Cushing's syndrome and what are the 4 main causes? - โ˜‘๏ธ over-production of cortisol;
  3. iatrogenic (meaning due to long term treatment w/ steroids)
  4. over secretion from adrenal glands (one or both)
  5. over stimulation of adrenal glands by ACTH-secreting tumor in pituitary Cushing's Disease
  6. over stimulation of adrenal glands by ectopic ACTH producing tumor what are some clinical manifestations of Cushing's syndrome - โ˜‘๏ธ buffalo hump (fat pads) abdominal obesity muscle weakness easy bruising thin skin/purple striae edema hirsutism how to diagnose cushing's syndrome - โ˜‘๏ธ 1. check cortisol levels w/ urine, saliva, or dexamethasone suppression test
  7. low acth levels due to increased negative feedback on pituitary because adrenals are hyper secreting w/o stimulus
  8. hypokalemia (too much K lost in urine) & hypertension (retaining too much Na in blood)

where are the islets of Langerhans located and what do they do? - โ˜‘๏ธ they are cells located in the pancreas and are responsible for the secretion of insulin and glucose what is insulin and where is it released from? - โ˜‘๏ธ beta cells in the pancreas; stimulates cells to uptake glucose and store it as glycogen through a process called glycogenesis what is glycogen - โ˜‘๏ธ stored form of glucose in the cell what is glycogenesis - โ˜‘๏ธ the process of storing glucose as glycogen in the cell what is glucagon and where is it excreted from? - โ˜‘๏ธ alpha cells in the pancreas; causes cells to release stored glucose to raise blood glucose levels -decreases glycolysis and increases gluconeogenesis/glycogenolysis what is glycolysis - โ˜‘๏ธ breakdown of glucose what is gluconeogenesis - โ˜‘๏ธ formation of glucose what is glycogenolysis - โ˜‘๏ธ glycogen breakdown to release glucose what are the 2 types of diabetes? - โ˜‘๏ธ Type 1 and 2 type 1 diabetes - โ˜‘๏ธ no insulin production at all -autoimmune process that destroys beta cells in pancreas -usually diagnosed at young age -DKA may occur abruptly type 2 diabetes - โ˜‘๏ธ insulin does not work effectively and fails to stimulate glucose uptake into the cell -obesity leads to a decreased # of insulin receptors -over type, pancreas may become exhausted and insulin injections may be needed -diagnosed later in life -symptoms more gradual what are some clinical manifestations of diabetes - โ˜‘๏ธ polydipsia, polyuria, polyphagia, weight loss fatigue, blurred vision, skin infections, UTI GI motility disorders Ketosis (type 1) HHS/NKHS (type 2)

what does HHS/NKHHS stand for? - โ˜‘๏ธ Hyperosmolar Hyperglycemic State/Non-Ketotic Hyperosmolar Hyperglycemic Syndrome HHS/NKHHS - โ˜‘๏ธ occurs w/ dehydration &/or infection -manifest: confusion or disorientation -diagnosed: hyperglycemia >500mg/dL; hyperosmolarity; dehydration -treatment: correcting hyperglycemia, electrolyte imbalances, and dehydration ketosis/ DKA - โ˜‘๏ธ fat broken down and forms ketones/ketoacids usually brought on by extreme stress (pregnancy, infection, anxiety) and causes epinephrine to stimulate glucagon increases lipolysis leading to increased free fatty acids that are converted to ketones -manifest: weight loss, tachycardia, hypotension, nausea/vomiting, fruity smell on breath (ketoacids) -diagnosed: hyperglycemia >250mg/dL, low serum bicarbonate <15mmol/L, low pH, ketonemia& ketonuria, hyperkalemia -treatment: iv insulin, fluids, electrolyte replacement what 3 things can chronic hyperglycemia cause? - โ˜‘๏ธ 1. diabetic retinopathy - microvascular complication in retina that can lead to blindness

  1. diabetic nephropathy - damage to small vessels in kidney that lead to renal failure
  2. diabetic neuropathy - nerve damage leading to pain/numbness, and weakness in hands and feet what is the leading cause of CKD and high risk of cardiac disease? - โ˜‘๏ธ diabetic nephropathy diabetic retinopathy - โ˜‘๏ธ -pathology: microaneurysm formation, abnormal retinal vascular permeability, scarring, retinal detachment -control: blood glucose, pressure and cholesterol annual dilated eye exams recommended diabetic nephropathy - โ˜‘๏ธ -pathology: basement membrane of glomeruli thickens and forms sclerosis and nodular lesions; plasma proteins can enter filtrate leading to proteinuria and edema; kidney enlargement; nephron hypertrophy b/c of increased workload -diagnosis: urine microalbumin test to test for excessive protein loss; normal range 30-300mg/day -control: tight glycemic control, BP control, hyperlipidemia treatment, smoking cessation, limit proteinuria through ARBs/ACE inhibitors diabetic neuropathy - โ˜‘๏ธ -pathology: (2) - vessel ischemia due to nutrient vessel wall thickening and slow nerve conduction from demyelinated Schwann cells -manifest: loss of feeling, sensation, touch, position sense, sometimes pain -diagnosed: annual monofilament test to assess sensation, vascular status, and skin integrity what are some things macrovascular complications are a major risk for - โ˜‘๏ธ 1. peripheral vascular disease

โ˜‘๏ธ activate GLP-1 receptor and increase insulin secretion, decrease glucagon secretion, and delay gastric emptying -taken by injection, watch for nausea and weight loss what are the 4 types of action for insulin - โ˜‘๏ธ 1. rapid-acting

  1. short-acting
  2. intermediate acting
  3. long-acting what are the 2 ways insulin can be administered daily? - โ˜‘๏ธ 1. MDI - multiple daily injections
  4. CSII - cont sub-q insulin infusion (pump); still need to bolus around mealtimes Hypoglycemia - โ˜‘๏ธ side effect of insulin therapy <60mg/dL -caused by: change in dosage, lack of adherence, not eating, increased exercise -treatment: 15-20g of glucose then complex carbs, IV, IM or SubQ glucose can be given in life- threatening emergencies what are some symptoms of hypoglycemia - โ˜‘๏ธ headache, anxiety, tachycardia, cool/clammy skin, confusion what the regular screenings/monitoring that diabetics have to undergo - โ˜‘๏ธ weight checks bp checks FPG and A1C lipid profile serum creatinine microalbumin foot exams dilated eye exams dental exams