Exam 2 Anatomy and Phys

Lecture 6 Objectives: 

1. What is the definition of a hormone? 

Chemical substance released into extracellular fluids that regulate metabolic function 

Hormones are classified by their chemical structure: 

1. Amino acid-based hormone: most hormones are peptide hormones 

2. Steroid hormone: come from cholesterol, gonadal hormones such as estrogen and testosterone, as well as adrenocortical hormones

3. Eicosanoids: bioactive lipids, have a more localized effect (does not circulate around the whole body) 

   1. Ex. prostaglandins → inflammation, BP increase, uterine contraction during labor, and enhancing blood clotting 

Hormones stimulate changes in cells: 

1. Change membrane permeability 

2. Stimulate protein synthesis or enzymes 

3. activates/deactivates enzymes 

4. Induces secretion 

5. Stimulates mitosis (cell division, growth) 

2. What intracellular mechanism do peptide hormones use to influence cell function? 

G proteins activate intracellular messengers → amino acid- based hormones 

Amino acid hormones – second messengers 

cAMP 

1. Hormone binds to receptors outside of the cell - changing the shape of the cell activating a G protein 

2. G protein binds to GTP (therefore removing GDP). Activating G protein.  

3. G protein binds to effector caller adenylate cyclase 

4. Adenylate cyclase produces cAMP - uses ATP 

5. cAMP activates different enzymes, usually activates or deactivates proteins 

   1. Usually activated Kinases - adds a phosphate group to protein 

6. Alters cell function   

** these changes don’t last long and are “brief” since cAMP phosphodiesterase (PDE) degrades cAMP. 

Amplification - changes in cAMP only short lived to change cell function 

Calcium signal mechanism - 

1. Hormone binds to receptor, leads to the activation of G protein (as it binds to GTP) 

2. G protein (active) binds to “phospholipase C” (PC) enzyme 

3. PC splits - PIP2 

4. PIP2 produces 2 secondary messengers: 1. Diacylglycerol (DAG) 2. Inositol triphosphate (IP3) 

5. DAG activates a kinase (adds a phosphate group to the protein) 

6. IP3 releases intracellular calcium from ER (causing the calcium in the cell to increase) 

7. There are now 3 messengers present: 1. DAG 2. IP3 3. Calcium 

8. Calcium alters specific enzymes, calcium channels open, calcium binds to calmodulin (calcium-binding protein) and enzymes are activated and amplification occurs 

3. How do steroid hormones activate genes? 

1. Steroids cross the cell membrane easily 

2. Bind to “intracellular” receptor (found inside the cell) 

3. Activates the receptor 

4. Receptor/hormone binds to DNA associates receptor complex 

5. Binds to DNA → turning on genes and making RNA 

1. Turns on genes 

2. Makes RNA 

3. Production of mRNA 

4. Produces a specific protein: enzymes, structural proteins, and protein exported out of cell 

• Without the hormone, specific genes are not activated (no mRNA is produced) because chaperone proteins bind/inactivate receptors and block gene activation 

• With hormones. Chaperone falls off of receptors, receptor is then phosphorylated, and receptor and steroid bind to DNA (deactivating mRNA and produce steroids) 

6. How does the parathyroid gland work as a humoral release system? 

Endocrine gladns stimulate the production of or release hormones by three mechanisms: 

1. Humoral → secretes hormone in response to changes in blood concentration of ions or nutrients 

2. Neural - NS can cause release of hormones. 

3. Hormonal 

Example of humoral stimuli: 

Parathyroid hormone (PTH) 

1. Parathyroid gland detects low calcium 

2. Release PTH from parathyroid 

3. PTH - functions at many cells and increases blood calcium concentration 

4. Increases calcium preventing PTH from releasing more from the parathyroid gland 

Neural stimuli - nerve fibers stimulate the release of hormone 

• Sympathetic NS stims release of catecholamines from adrenal medulla (during stress) → epinephrine and norepinephrine

Hormonal stimuli - endocrine gland release hormone in response to another hormone

• Hormones for hypothalamus regulate release of many hormones from a. pituitary

Major endocrine glands: 

• Pituitary gland 

• Thyroid gland 

• Adrenal gland 

• Pineal 

• Thymus 

Endocrine tissues secrete hormones

• Ex. pancreas and gonads 

Neuroendocrine organ - hypothalamus (neuronal and endocrine function) 

Target cell activation is dependent on: 

1. Blood levels of hormone 

2. Number of receptors on cell 

3. Affinity of receptor for hormone - can receptor bind to hormone tightly (is it sensitive0 

Changes in these can enhance or ablate hormone function 

Lecture 7 Objectives: 

1. Describe the pathway of the “hypophyseal portal system”  (look at paper drawing) 

ADH produced in hypothalamus, stored in p. pituitary gland and released (specific ADH sources found in hypothalamus are supraoptic nuclei and paraventricular nuclei that lead to the p. pituitary) 

2. Where is “growth hormone” produced and how does it function? 

The growth hormone is produced from somatotropic cells. They stimulate cells to divide and increase in size, which is very active in children. Their major target is bone and muscle cells (promoting long bone growth, and increased muscle mass) 

• Long bone growth

• Increased muscle mass: increases protein synthesis (telling cells to divide and grow) and increased use of fats to maintain glucose levels elevated for energy and growth 

  Important thing to remember about GH is that it works via another homeone called IGF “insulin-like growth factor” which is synthesized in liver cells, muscle, bone, and other tissues 

IGF function: stims the uptake of amino acids and uptake of sulfur for cartilage matrix 

Direct effects of GH: 

1. Mobilizes fat stores - increases fatty acid levels in the blood 

2. Glucose spared “diabetogenic effect” - higher glucose (makes sure glucose is high) 

   1. Decreases glucose uptake 

   2. At liver - tells it to breakdown glycogen (increasing blood glucose levels) 

Regulation of GH Release: 

1. Hypothalamic hormones (from the hypothalamus) 

   1. GHRH causes the release of GH 

   2. GHIH inhibits GH 

3. Where is GnRH produced and what does it do? 

Hypothalamus release GnRH “gonadotropin-releasing hormone” during puberty 

• Stims a. Pituitary to produce FSH/LH (activation of testes and ovaries) 

• Negative feedback inhibition 

4. How does prolactin function? 

At the hypothalamus, PRH (prolactin-releasing hormone) is released which then causes the release of prolactin from a. Pituitary (PIH, released from the hypothalamus, prolactin inhibiting hormone regulates the secretion of prolactinsa) 

In females: 

• High estrogen: PRH release PRL 

• Low estrogen: PIH lower PRL 

• During ovulation: there is a brief pulse pf PRL (sligh increase which declines after) that cause breast tenderness 

5. After drinking alcohol, would blood ADH levels be high or low? Would rblood volume be high or low? 

Drinking alcohol inhibits ADH from rescuing water from urine 

1. Increases urine output (peeing out all water from urine) 

2. Leads to “dehydration-like” response → dry mouth w alcohol ingestion 

After drinking alcohol, ADH levels in the blood would be low 

Usually, when dehydrated ADH levels would be high, rescuing water from renal tubules (more water in blood) and forming urine. Not only that, but blood volume would increase. 

High ADH - urine dark since water in urine is so little 

Lecture 8 Objectives: 

1. Describe how thyroid hormone is synthesized 

TSH released by a. Pituitary 

TSH binds to thyroid cells (follicular cells) 

1. All is stimulated by TSH 

2. Thyroid cells pulls in iodide (stimulated by TSH) - occurs at the same as thyroglobulin production 

3. Thyroglobulin pulled in colloid 

4. Iodide oxidized into iodine 

5. Iodine pulled into colloid (thyroglobulin and iodine are found in colloid) 

6. One iodine hooks onto a thyroglobulin (T1)

7. Two iodine hook into a thyroglobulin (T2) 

**this entire process occurs in the colloid 

8. T1 and T2 come together to form = T3

9. T2 and T2 come together to form = T4 

10. Thyroid cells pulls into cell, combine with lysosome → forming mature T3 and T4 

11. Thyroid hormone is made and increases in blood 

2. Name 3 sites of action of PTH 

Parathyroid hormone (PTH) 

1. Sitms osteoclasts → responsible for the breakdown of bone and releases calcium 

2. Stimulates the reabsorption of calcium at the renal tubules in the kidney 

   1. From urine to blood - calcium is rescued 

   2. Excretion of phosphates from the blood into urine 

This is an exchange* 

3. Increases absorption of calcium at intestines 

3. How does the renin-angiotensin system influence aldosterone? 

• Kidney - “juxtaglomerular apparatus” JG 

• Low BP (=low blood volume) 

1. Release of “renin” 

2. Cleaves “angiotensinogen” 

3. Enzymatic cascade produces angiotensin II 

4. Aldosterone release (pulls sodium from urine to blood - blood volume goes up since water follows sodium → causing BP to go up) 

5. Stimulates other systems 

4. Describe the difference between long term and short-term stress at the adrenal gland 

Short-term stress – “fight or flight” 

1. At the hypothalamus, nerve impulses are sent and activate the sympathetic nervous system 

2. Adrenal cortex secretes catecholamines (epinephrine and norepinephrine) 

3. Epinephrine and norepinephrine cause a short-term stress response: 

   1. Increased HR

   2. Increased BP 

   3. Increased blood glucose 

   4. Blood diverted to brain, heart, and skeletal muscle → leading to increased alertness, decreased digestive system activity, and reduced urine output

   5. Increased metabolic rate 

Long term stress - 

1. External or internal stress causes hypothalamus to release CRH 

2. Anterior pituitary releases ACTH that goes in the blood and targets the adrenal cortex 

3. Adrenal cortex releases mineralocorticoids (primary: aldosterone) and glucocorticoids (primary: cortisol) 

4. Increased cortisol in the body causes: 

   1. Increased glucose (via gluconeogenesis from fats and proteins), amino acids (for metabolic proteins), and fatty acids 

   2. Increased BP → causes vasoconstriction 

   3. Enhances circulation of nutrients and respiratory gases to get around the body quicker 

5. Where is glucagon produced and how does it function 

Glucagon is produced in the pancreas by alpha cells. 

Glucagon is a hyperglycemic agent - in other words, causes glucose to increase in blood. 

Glucagon is released when glucose levels are low 

Targets liver and releases glucose from liver via two ways: 

1. Glycogenolysis: making more glucose by breaking down glycogen 

2. Gluconeogenesis - glucose (made from other stuff like lactic acid, glycerol and amino acids) - increasing glucose levels 

6. How is blood glucose regulated? 

High blood sugar → causes insulin to be released from the pancreas → insulin stims. The uptake of glucose from blood via tissue cells → decreasing blood glucose OR insulin from the pancreas stimulates glycogen formation → glucose converts into glycogen in liver → decreasing blood glucose 

Low blood sugar promotes the release of glucagon in the pancreas → glucagon stimulates glycogen breakdown in the liver → increasing blood glucose 

Vitamin D is required when absorbing calcium in the intestines. 

PTH converts vitamin D to vitamin D3 

Vitamin D from skin and diet is inactive 

At the kidney, PTH activates conversion of Vitamin D (inactive form) to vitamin D3 (active form - known as “calcitriol ”) which allows calcium to go from the gut to the blood 

Lecture 9 Objectives: 

1. Understand diabetes insipidus (DI) 

There are two types of diabetes insipidus (DI) 

1. Neurogenic (central form) - insufficient amounts of ADH from p. pituitary, can’t make ADH (the most common form) 

   1. Inability to form concentrated urine - losing water from production of dilute water. 

      1. Reduced ADH secretion (can’t make ADH) 

      2. Producing huge amounts of urine 

      3. Dehydrated - water is decreasing and lots of sodium and electrolytes in blood 

** blood becomes more concentrated, increasing thirst (losing water, ADH increases) - thirst mechanism is turned on along the way - pt’s have a big drive to replace fluid (since they are dehydrated) 

2. Nephrogenic (renal form) - inadequate response to ADH (can make ADH but doesn’t work at the collecting ducts in kidney) —> no known cause 

   1. insensitivity to ADH at the collecting ducts 

      1. This can be caused by drugs or toxins (ex. Lithium or some anesthetic ) 

      2. Can inhibit cAMP production → will not activate aquaporins 

• Diabetes insipidus, pt’s with diabetes have excessive thirst and polyuria 

  • Polyuria results in loss of water, hypernatremia, and dehydration 

    •  Where does the water go from the cells? → high sodium, cells are dehydrating (water is going out, pt experiences dizziness, nausea, etc.) 

• Idiopathic Neurogenic Diabetes Mellitus 

  • Rapid onset: three phase syndrome 

1. Increased diuresis → due to hypothalamic damage at ADH centers 

2. Antidiuresis (concentrated urine) 

   1. Necrosis of posterior pituitary that leads to a pulse of ADH to be released (using the last bit of ADH it has) 

3. Polyuria (elevated urine output) and polydipsia 

   1. Loss of ADH secretion 

Testing: Water restriction test - other disorders will cause a decrease in urine 

• Caution - those w/ insipidus experience extreme loss of water 

Urine concentration and serum ADH are monitored 

Treatment: neurogenic insipidus can’t make ADH - ADH replacement if 

• They produce dilute water during water restriction test 

• Excessive urine output/production - extremely dehydrated 

ADH replacement: 

• Synthetic vasopressin = “desmopressin” 

• Chlorpropamide 

  • Enhances endogenous ADH production w/ pt’s that produce some ADH 

  • Thiazide and anti-inflammatory drugs to reduce urine production - tx for nephrogenic insipidus 

1. Know how ADH works at the renal tubule and its role in DI 

ADH (antidiuretic hormone) 

• Retention of water - kidney takes water from forming urine and pulls into blood - prevents dehydration 

• Increases permeability at the collecting ducts 

• Urine concentrated - volume decreases 

  • Water retained in blood 

  • Regulates aquaporins in collecting ducts 

** volume of urine decreases in presence of ADH → water retained in blood (regulated by aquaporins in collecting ducts) 

• Usually water can’t go from forming urine into the blood (low water permeability from tubule lumen to interstitium) unless ADH binds to a receptor, produces cAMP, aquaporins inserts itself into membrane, and water can be rescued from forming urine (water can go from urine to blood) 

• When dehydrating ADH goes up causing this to happen 

2. Understand hypopituitarism - “Sheehan Syndrome” 

• During pregnancy, the pituitary is at risk 

  • pituitary gland increases in vasculature and size 

  • Hypophyseal system reduced in oxygen → increased risk of ischemia to a. Pituitary (this is normally the case) 

• Sequence of postpartum pituitary infarction: 

1. Vasospasms - pituitary artery 

2. Extended vasospasms that leads to necrosis 

3. Necrosis leads to edema 

4. Pituitary expands and blood flow is reduced 

• Symptoms of hypofunction of anterior pituitary: hormone producing cells are damaged

Hormone producing cells that are damaged are: 

• ACTH : cortisol and stress will be the issue 

• TSH : hyperthyroidism will be the issue 

• FSH/LH : infertility will be the issue 

3. Know the mechanisms involved in hypersecretion of GH 

• Acromegaly: adults are exposed to high levels of GH → often produced by a tumor that produces GH 

  • Normally GH peaks during sleep. However, with acromegaly, GH is continuously released (always active and secreting GH) 

  • Unlike with children, adults already have epyphyseal closure meaning that no additional long bone growth occurs. However, instead: 

    • Connective tissue growth occurs 

    • Bony proliferation 

    • Renal tubules: increased carbohydrate tolerance 

    • Hyperglycemia: reduced glucose uptake

      • Cells can’t pull glucose in and will have high levels of blood glucose 

      • Increased hepatic glucose production → liver producing lots of glucose and will just have high levels of insulin. Over time, the body becomes insulin resistant (diabetes mellitus) 

    • Clinical manifestations: enlarged tongues, edema, increase activity of sebaceous/sweat glands, thick hair/skin, enlarged body proliferations (face, hands, and feet) 

    • Clinically: 

      • IGF-1 stimulates cartilaginous growth

      • Elongation of ribs - barrel chest 

      • Increase in cartilage at joints (increased risk of onset arthritis) 

    • Treatment: 

      • Monitor GH levels 

      • Limit tumor expansion 

      • Reduce GH → 

        • Surgical removal of adenoma (tumor) 

        • Radiation therapy 

        • Drug therapy: somatostatin, growth hormone inhibitory hormone → limit GH release or cause a slower production of GH 

• Gigantism: high GH in children, causing growth of long bones 

4. Understand GH as a possible anti-aging hormone 

• No data showing GH alone slows aging 

• Patient without GH secretions (as adults) experience accelerated aging 

• Decreased protein deposition and increased fat deposition. Which results in: 

  • Increased skin wrinkling 

  • Decreased function in some organs 

  • Decreased muscle mass 

BASICALLY normal aging symptoms 

• GH in geriatric pt’s is low naturally, some processes during normal aging result from GH decreasing 

GH replacement: 

1. Increased protein deposition (increased muscle mass) 

2. Decreases fat deposition 

3. Increased energy 

Lecture 10 Objectives: 

1. Be able to define different classes of diabetes mellitus

Types of diabetes mellitus: 

Type I: insulin dependant diabetes, pt cannot produce insulin 

• There are two types of Type I diabetes 

  • Immune-mediated: immunologically mediated destruction of beta cells 

  • Environmental-genetic factors 

    • Results: cell mediated destruction of beta cells (which are the insulin producing cell in the pancreas) 

• Common markers of immune destruction: 

  • Autoantibodies (antibodies against their body) identified: 

    • Pancreatic islet cells 

    • Insulin 

    • GAD - glutamic acid decarboxylase (those w/ type 1 diabetes produce antibodies against this)

    • HLA-DR3 markers (human leukocyte antigen) 

• GAD → enzyme that produces GABA (inhibitory neurotransmitter) 

  • GAD in synaptic-like vesicles in beta cells 

  • GABA paracrine factor in pancreatic islets → w/o GABA there is less support for pancreatic islet cells 

  • Most autoantibodies in diabetes target GAD 

Type II: non insulin dependant diabetes, pt can produce insulin but it does not work 

General symptoms: 

• Polydipsia 

• Polyphagia 

• Polyuria 

2. Know the sequence of symptoms of type 1 diabetes 

• Polyuria 

• Polydipsia 

• Polyphagia 

• Weight loss 

• Wide changes in blood glucose (when they eat, blood glucose levels rise dangerously high) 

• Glucose accumulates in the blood, appearing in urine (glucose cannot be reabsorbed into blood) resulting in osmotic diuresis (loss of water) → diuresis leads to polyuria and excessive thirst, weight loss due to breakdown of fats/proteins 

General sequence of events in disease:

1. General susceptibility (genetic susceptibility) 

2. Long  preclinical period (asymptomatic) - ongoing diabetes and experience no symptoms 

3. Immune-mediated destruction of beta cells - still asymptomatic. Immune system is destroying beta islet cells 

4. Insulin deficiency - so many beta islet cells are destroyed that not enough insulin is being produced - still asymptomatic 

5. Hyperglycemia - increase blood sugar (begin to experience symptoms) 

3. Understand the mechanism of ketoacidosis as related to type 1 diabetes

A common symptom of type I diabetes 

• Mobilized fat particles cannot be metabolized - they build up in the blood and form “ketone bodies” due to excessive ketones in the blood 

• Decreases in blood pH - acidosis (blood becomes acidic) 

• To remove ketones, production of “acetone” → causing breath to smell sweat or have a fruity smell (SEVERE) 

• Coma induced ketoacidosis can also occur 

4. Understand the profession of type II diabetes 

Type II is the most common, the cause is unknown

• Mostly seen in pt’s who are older than 40 yrs. old and/or obese individuals 

• Insulin resistance (type II diabetic can produce insulin but their cells aren’t responding to insulin) → lower response of insulin-sensitive tissues: 

  • Tissues do not take up glucose: Liver, muscles, and adipose tissue 

  • Hyperglycemia 

  • During the progression of the disease, Beta cells become unresponsive to glucose changes in the blood (can usually detect changes in glycose levels), meaning no insulin is secreted to decreased glucose levels → leading to hyperglycemia 

  • Theories of what causes type II diabetes: 

    • Increases in insulin levels due to obesity

    • Pancreas can’t sustain high insulin (makes less and less) which leads to peripheral insulin resistance (overexposed to insulin and don’t respond - causing hyperglycemia) 

5. Be able to describe diabetic neuropathy as a complication of type II diabetes 

Diabetic neuropathies: 

• “Dying back” neuropathy

• Distal neurons affects 

• Later in diseases - severely damaged 

• *loss of sensation 

• *cause pain 

Suggest metabolic changes, not completely responsible for neuropathies 

Major point: good glucose control improves complications, reverse neuropathies 

Lecture 11 Objectives: 

1. Know the general anatomy of the adrenal gland 

There are two regions of adrenal gland: 

• Adrenal medulla - inner 

  • Part of sympathetic nervous NS, wired up to the nervous system 

• Adrenal cortex - outer 

2. Know the general types of adrenal hormones produced by distinct regions of adrenal 

Three categories of adrenal steroids: 

1. Glucocorticoids → cortisol 

2. Mineralocorticoids → aldosterone 

3. Androgens 

3. Understand different levels of Cushing’s syndrome 

Cushing’s - excessive glucocorticoids - high levels of cortisol 

• There are different levels of Cushing’s (where is dysfunction located, what level)

Primary Cushing’s → at adrenal, producing too much cortisol

• Adrenal tumor produces cortisol (high cortisol levels are suppressing ACTH causing low ACTH)

  • High cortisol 

  • Low CRH and low ACTH 

Secondary Cushing’s → at pituitary there is a tumor or tumor outside of pituitary

• High ACTH and high cortisol

• Because tumor does not respond to cortisol, tumor keeps producing ACTH (not part of negative inhibition cycle) 

• Getting too much ACTH from tumor → as a result, adrenal is producing too much cortisol → cortisol goes back and suppresses pituitary gland, the pituitary suppressed for a long time → tumor is removed → all ACTH disappears, and cortisol levels go back down → cortisol crashes and ACTH (since pituitary gland has been suppressed for so long that it doesn’t produce these anymore) - pt’s need to take cortisol 

• Causes hyperpigmentation due to to high ACTH, caused by high levels of MSH (melanocyte stimulating hormone) which darkens the skin and hair 

Hypothalamic origin → excessive CRH, stimulating expensive ACTH = excessive cortisol (high level of cortisol and CRH) 

4. Explain microadenomas as ectopic sources of hormones 

5. Know symptoms of hypercortisolism and the physiology of why they occur 

Symptoms of hypercortisolism: 

• Weight gain 

• Accumulation of adipose tissue  → trunk, face, and cervical area 

• Glucose intolerance = diabetes mellitus (20% of cases) 

• Cortisol stimulates glucose release → insulin resistance → tissue not responsive to insulin → high levels of glucose and cortisol, high levels of insulin produced (tissue become unresponsive to insulin, at more risk of type II diabetes

• Polyuria due to hyperglycemia w/ glycosuria

• Protein wasting - muscle wasting (muscle weakness accompanied) 

• Increased bone resorption, inhibition of bone formation (bone being broken down by the catabolic effect of cortisol) 

• Hypocalcemia *renal calcium excretion → loss of calcium (dumping calcium via urine) 

1. More at risk of kidney stone formation and osteoporosis

• Loss of collagen - weakened skin support - adipose deposition stretched skin causing striae (purple)   

• Increased sensitivity to catecholamines due to high cortisol

  •  results in hypertension

  • Dysfunction at the CNS: deficit learning/memory, depression, schizophrenia 

6. What are the implications of Cushing’s to women relating to secondary sex characteristics 

• High cortisol in females causes high adrenal androgens → converted into testosterone → causing abnormal menstrual cycle, increased hair growth 

7. Why is the dexamethasone test used to diagnose Cushing’s 

• Dexamethasone: synthetic steroid that suppresses cortisol 

• If cortisol levels fail to drop → cushing’s 

Negative inhibition cycle 

Hypothalamus sits on top of everything → hypothalamus produces CRH → CRH goes up → CRH goes to a. Pituitary → a. Pituitary releases ACTH → ACTH in blood increases → ACTH targets/stimulates adrenal, causing it to produce cortisol → blood levels of cortisol go up → goes back and suppresses production of CRH and ACTH (negative feedback inhibition) 

Lecture 12 Objectives: 

1. Know the causes and different levels of hypoadrenal dysfunction (low levels of cortisol) 

• Primary adrenal insufficiency → inability of adrenals to produce cortisol

  • “Addison’s disease” - autoimmune addison’s disease is the most common form (autoimmune destruction of the adrenal cortex) 

  • Infections of the adrenal cortex 

  • Adrenal hemorrhage 

• Secondary adrenal insufficiency → inadequate ACTH, the problem most likely at the pituitary

2. Define the different types of addison disease 

Autoimmune Addison’s Disease → most common form 

• High ACTH with low cortisol 

• Symptoms appear after 90% of the cortex has been destroyed, until then asymptomatic 

Idiopathic Addison’s Disease - organ-specific autoimmune adrenalitis 

3. Describe the symptoms of addison’s disease 

• Weakness and fatigue 

• Anorexia 

• Weight loss 

• Nausea 

• Diarrhea 

• Possible hyperpigmentation (most often seen in primary addison’s disease since cortisol levels are low, causing ACTH to be high which turns on melanocytes) 

4. Be able to explain the cortrosyn stimulation test 

• Cortrosyn: synthetic ACTH 

• Idea is to stimulate the adrenal to produce cortisol

• Normal result: w/o addison’s disease → cortisol will increase in 30 min 

• Abnormal result: no increase in cortisol, adrenal in insensitive to ACTH (pituitary Addison’s)