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Portage Learning Pathophysiology Module 9
3 ways that hormones act on the body - โ๏ธ 1. endocrine
- paracrine
- autocrine 3 categories for hormone structure - โ๏ธ 1. amines/amino acids
- peptides, polypeptides & proteins (freely floating in bloodstream)
- 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)
- hypo states (decreased hormone secretion) what are the 4 causes of hyper states - โ๏ธ 1. target gland oversecretes
- pituitary or hypothalamus over stimulate
- additional hormones being produced from different site
- target receptor becomes hyper active what are the 5 causes of hypo states - โ๏ธ 1. congenital/acquired disorder of target gland
- pituitary not secreting enough stimulating hormone
- hypothalamus not secreting enough releasing hormone
- defective hormone
- target receptors are unresponsive what are the 2 types of thyroid disorders -
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
- toxic nodule what are the 2 causes of secondary hyperthyroidism - โ๏ธ 1. pituitary tumor
- 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)
- thyroid scans (nodule detection)
- ultrasound (cystic vs solid)
- fine-needle aspiration biopsy (malignant vs. benign) what are the main treatments for hyperthyroidism - โ๏ธ 1. beta-blockers - treat tachycardia and anxiety
- methimazole & propylthiouricil - reduce T4 and T3 levels by decreasing synthesis
- 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;
- iatrogenic (meaning due to long term treatment w/ steroids)
- over secretion from adrenal glands (one or both)
- over stimulation of adrenal glands by ACTH-secreting tumor in pituitary Cushing's Disease
- 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
- low acth levels due to increased negative feedback on pituitary because adrenals are hyper secreting w/o stimulus
- hypokalemia (too much K lost in urine) & hypertension (retaining too much Na in blood) how to treat Cushing's syndrome - โ๏ธ if iatrogenic is the cause: tapper off glucocorticoid therapy other causes: surgical removal of tumor that is causing over secretion what are the 3 categories of Addison's disease -
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
- diabetic nephropathy - damage to small vessels in kidney that lead to renal failure
- 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
- CAD
- Heart attack
- stroke what are some risk factors FOR macrovascular complications - โ๏ธ -hyperglycemia/tension/lipidemia -obesity -altered platelet function
what are the 2 ways insulin can be administered daily? - โ๏ธ 1. MDI - multiple daily injections
- 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
