150 questions and answers patho study quide 100% score

Module VII (Renal) 1. Where organ produces urine? ● in your kidneys 2. Where are kidneys? ● retroperitoneal space (pts can present with back pain due to renal issues) 3. What is the hilum of the kidney? ● central portion of kidney where the entrance and blood vessels come together ● *note: hilum is general term for an organ 4. Describe the flow of urine from the kidneys. ● kidney → ureter (binds to bladder posteriorly) → bladder → urethra 5. How do the IVC and abdominal aorta play a role in blood supply for the kidneys? ● they are the major blood vessels near the kidneys that branch out to supply a renal artery and vein to each kidney 6. How do the IVC and abdominal aorta play a role in blood supply to the lower extremities? ● the IVC and the abd aorta branch out to become iliac vessels that supply lower extremities 7. Where do the adrenal glands sit? ● on top of the kidney 8. Where is the spleen? ● LUQ usually in association with the L kidney 9. What are the parts of the kidney? ● cortex = outermost portion of the kidney ● capsule = fibrous layer on top of the kidney ● medulla = innermost part of the kidney; consists of pyramids ● minor calyx (apexes of pyramids project here) → renal pelvis will join the major calyces → join together to become the ureter 10.Why is the rugae of the bladder important? ● similar to the stomach, kind of convoluted to help with expansion 11. What is the functional unit of the kidney? ● the nephron 12.Where does concentration of urine usually occur in the nephron? ● medulla, specifically loop of Henle 13.Where do the various portions of the nephron sit in the medulla or cortex? ● glomeruli, most of proximal convoluted tubule, some of distal tubule → sits in the cortex ● loop of Henle → medulla 14.How many nephrons do we have? ● millions in our kidneys 15.Identify the structures of the nephron. ● corpuscle, glomerulus, bowman’s capsule ● proximal convoluted tubule (PCT) ● loop of Henle (descending and ascending) ● DCT = reabsorption of some ions (isotonic or hypotonic) ● collecting duct = reabsorption of water when in the presence of ADH → final concentration 16.Define tubular reabsorption. ● movement of fluid, electrolytes, water from tubular lumen to peritubular capillary plasma (back into the blood) 17.Describe where in the nephron reabsorption occurs ● PCT , loop of Henle, DCT and collecting ducts ● most water reabsorbed in PCT , loop of Henle and DCT 18.Define tubular secretion. ● movement from capillary to tubular lumen (from the blood to the interstitium into urine) 19.What is the corpuscle? ● region of the nephron where the glomerulus sits ● glomerulus = tuft of capillaries that loops into Bowman’s capsule ● mesangial cells that support the capillaries ● VASCULAR COMPONENT → will be filtering blood here 20.Why is the proximal convoluted tubule so important in reabsorption? ● reabsorbs MOST of the ions (Na+, Cl-, K+, glucose; active transport) ● isotonic with the blood 21.What is the function of the loop of henle? ● create a concentration gradient to reabsorb water and concentrate urine 22.Describe the osmolarity throughout the loop of Henle. ● osmolarity changes as you travel through the loop (isotonic → hypertonic → hypotonic) 23.What is important about the descending limb? ● thin, no active transport (osmosis only; H2O reabsorbed), urine becomes very concentrated (hypertonic) ● impermeable to ions 24.What is important about the ascending limb? ● active transport for ion reabsorption into the blood ● urine will become less concentrated and urine will continue into DCT 25.What is important about the DCT? ● more active transport for reabsorption 26.What types of cells are found in the collecting duct and what are their functions? ● principal cells = reabsorb Na+ and H2O, secrete K+ ● intercalated cells = secrete H+ and reabsorb K+ 27.Where does ADH work? ● in the collecting duct and DCT 28.What don’t we want filtered? ● RBCs ● albumin ● other larger plasma proteins 29.What can we see in our urine if our glomeruli were dysfunctional? ● blood in urine; hematuria (i.e., RBCs escaping) ● albumin found in urine 30.What is the role of nitric oxide in vessels? ● vasodilation 31.What molecules function to vasoconstrict or vasodilate in the glomerulus? ● NO → dilation ● endothelin-I → constriction 32.Why do our kidneys go through fluctuations of vasodilation or vasoconstriction? ● dilation → we are well-hydrated; don’t need to hold onto as much ● constriction → we are dehydrated; need to reabsorb more 33.If we are really sick, would we observe vasodilation or vasoconstriction in the kidneys? ● vasoconstriction to restrict blood flow to major organs (i.e. heart, brain) 34.What is the function of podocytes in the glomerulus? ● they adhere to the basement membrane of the glomerulus and form the filtration sites/slits → abnormalities can lead to filtration of large proteins 35.What does the afferent arteriole do? ● brings blood INTO the glomerulus 36.What does the efferent arteriole do? ● brings blood AWAY from the glomerulus 37.Where are juxtaglomerular cells located? ● next to (juxta) the glomerulus; found near the afferent/efferent arterioles 38.What is a major function of the juxtaglomerular cells? ● production of RENIN 39.What structure can be found between the afferent and efferent arterioles? ● portion of the distal convoluted tubules that have specialized macula densa cells 40.In what ways are macula densa cells specialized? ● they can sense Na+ and Cl41.Which two structures make up the juxtaglomerular apparatus? ● JG cells and macula densa cells 42.What important processes are occuring in the JGA? ● renin production ● control of renal blood flow = can SENSE renal perfusion ● glomerular filtration 43.How do we assess the function of the kidneys? ● GFR = glomerular filtration rate ● can tell us about how well the kidneys are functioning 44.What is autoregulation in reference to the kidneys? ● the kidneys are able to maintain a fairly constant GFR over a wide range of BP values (80-180 mm Hg) ● can become compromised if you’re really sick 45.How are resistance and pressure related in GFR? ● they are affected in the SAME direction (i.e., increased resistance → increased pressure) 46.How can neural regulation affect your GFR? ● aortic baroreceptors sense low BP → will stimulate SNS → production of epinephrine → vasoconstriction → decreased GFR 47.What occurs when GFR decreases as a response to activation of SNS? ● decreased GFR → decreased excretion of Na+ and H2O → increased blood volume → increase BP 48.How does the carotid body affect GFR? ● chemoreceptor senses hypoxia → also releases hormones to activate SNS → decreased GFR 49.Define excretion in the renal system. ● elimination of substance in the final urine; whatever comes out of our body 50. What hormones play a role in reabsorption? ● aldosterone ● antidiuretic hormone 51.What are the nml functions of a kidney? ● solute and H2O transport ● excretion of waste via urine ● regulation of acid and bases ● secretion of hormones (renin, EPO, vitamin D3) ● control of BP regulation, RBC production and calcium metabolism ● gluconeogenesis 52.Describe the RAAS system. ● liver produces angiotensinogen ● liver produces renin in response to decreased BP, decreased renal perfusion, etc., → activates angiotensin I ● lungs produces ACE and activates angiotensin II ● angiotensin II stimulates adrenal cortex to produce aldosterone and causes vasoconstriction = potent vasoconstrictor ● aldosterone encourages Na+ and H2O reabsorption by acting on DCT and collecting duct ● reabsorption increases ECF and BP 53.When does Na+ and H2O reabsorption make sense? ● when someone is hypotensive, dehydrated or hyponatremic 54.When does Na+ and H2O reabsorption not make sense in response to aldosterone? ● when someone has decreased renal perfusion or has CHF and already has so much fluid overload, reabsorption will be counterproductive 55.How much blood per day is passing through the nephrons of the kidney? ● 180 L per day → most of it being reabsorbed! 56.What regulates the amount of H2O that is reabsorbed or lost? ● ADH, aldosterone and indirectly via renin 57.How much fluid/H2O makes it to the collecting duct? ● 10% or 18 L ● dehydration → can reabsorb almost all water under the influence of ADH ● in cases of fluid overload → will not reabsorb water 58.How do the kidneys help with maintaining pH? ● kidneys can sense what your nml should be and as a result will either release bicarb or H+ 59.What is nml body pH? ● 7.35-7.45 60.What is nml urine pH? ● ~6 61.How much does a person normally urinate in a day? ● about 1 L 62.What are things you consider when you see glucose in urine? ● kidney dysfunction OR too much blood glucose (DM) 63.How are the kidneys able to concentrate urine? ● there is a concentration gradient present due to the descending and ascending limbs of the loop of Henle ● descending only permeable to H2O; ascending limb permeable to ions ● final urine concentration is determined in collecting duct and the influence of ADH; ADH will open channels for H2O to flow via osmosis ● H2O will be drawn out according to the salt gradient 64.What is the vasa recta? ● capillaries that lie parallel to the nephron (embedded) 65.What is the countercurrent multiplier that occurs in the kidneys? ● the concentration in the descending loop of Henle is very different from the concentration in the ascending loop of Henle ● it is also under the influence of the vasa recta, where blood is flowing in the opposite direction of loop of Henle 66.Describe the concentrations of the urine when under the influence of ADH and when not. ● ADH = more concentrated urine, because of water reabsorption ● no ADH = more dilute, because of water excretion 67.What is diabetes insipidus? ● condition that leads to large volumes of dilute urine due to lack of ADH 68.How do diuretics affect the active transport going on in the nephron? ● loop diuretic → acting on ascending loop of Henle and blocking the Na+/K+/2Cl- symport → no reabsorption → these will be excreted; also inhibits Mg and Ca reabsorption in the ascending loop ○ hyponatremic, hypokalemic, hypochloremic, hypocalcemia ● thiazide diuretics → work on DCT; block Na+/Cl- symport → less Na+ in the cell; indirect effect = more Ca2+ in blood due to Na+/Ca2+ antiport compensating ● potassium-sparing diuretics (i.e., Triamterene, Spironolactone) → works on DCT; helps prevent loss of K+; not a great diuretic on its own but can be combined with other types of diuretics 69.What are some examples of loop diuretics? ● Lasix, Furosemide 70.What can be a consequence of someone being on too much loop diuretics? ● low amounts of Na+, K+, Cl- in the blood (hyponatremia, hypokalemia, hypochloremia) ● hypocalcemic as a result of Na+/Ca2+ antiport being ineffective in response to low Na+ 71.Why are renal stones formed? ● due to calcium build up in the urine, which is a result of an indirect effect of loop diuretics on Na+/Ca2+ antiport 72.What are some conditions that can occur in someone with renal failure? ● anemia (lack of EPO) ● hypercalcemia (lack of vitamin D3) ● overproduction of renin → HTN ● edema in extremities; may also have pulmonary edema ● vitamin D deficiency ● hyperphosphatemia ● sometimes hypoglycemia (remember the gluconeogenesis function) 73.What is the general function of diuretics? ● enhance urine flow ● interfere with Na+ reabsorption and decrease ECF 74.Which type of diuretics are not usually used with pt who are chronically on diuretics? ● osmotic diuretics = act most predominantly on the beginning portion of PCT to help us urinate quickly (i.e., someone with brain trauma) 75.What is an example of an osmotic diuretic? ● Mannitol 76.Where is Ca2+ generally reabsorbed? ● mostly in the PCT, somewhat in the DCT ● PTH and vit D in DCT are responsible for this reabsorption ● PTH also decreases phosphorus reabsorption ● lost with loop diuretics and maintained with thiazide diuretics 77.What is the formula for GFR? ● ([urine] x urine volume)/plasma concentration 78.What is the relationship of a substance that is supposed to be filtered and GFR? ● when something is supposed to be filtered, the plasma concentration should be inversely proportional to the GFR ● i.e., Inulin, creatinine, BUN, plasma Cystatin C 79.What are some things a urine dipstick can tell us and what are the norms? ● glucose - normally entire reabsorbed, should be negative ● leukocyte esterase - enzyme in WBCs that should not normally be present in urine, should be negative ● nitrates - should be negative, positive with some bacteria ● ketones - byproduct of fat breakdown; positive in starvation and DKA ● albumin - normally does not make it past glomerulus; positive in glomerular failure ● Hgb - normally not free; positive in RBC breakdown ● Myoglobin - normally not free; positive in muscle breakdown 80.What are the different tests that can indicate renal function? ● urine dipstick ● urine sediment/urine cytology 81.What is urine sediment? ● holistic microscopy analysis 82.What are the different aspects to consider for renal dysfunction? ● vascular dysfunction (less common) ● pre-renal dysfunction → a result of dehydration or CHF ● renal dysfunction itself → nephrotic or nephritic syndromes, acute tubular necrosis or interstitial nephritis ● post-renal (obstructive) - external obstruction of flow (i.e., pregnancy) 83.What can lots of obstruction for renal flow lead to? ● hydronephrosis (renal pelvis expands → increase in intra-renal pressure → renal pyramids infarct → nephrons are destroyed → dysfunction 84.What is the different compositions of mineral salts in renal stones? ● calcium oxalate, calcium phosphate (70 to 80%) → precipitate is formed between calcium and oxalate; not recommended to decrease dietary Ca as it usually binds the precipitate and can be taken to gut ○ can be caused by being on loop diuretics ● struvite (15%) → Magnesium, ammonium and phosphate ○ Proteus mirabilis, as well as other infections → alkaline urine → big struvite, staghorn stones ● uric acid (7%) → largely found in the urine, sometimes in the blood; will crystalize in the blood and cause deposits in small joints (like gout); influenced by diet ● genetic disorders of AA metabolism (excess urine can cause cystinuric or xanthine → stone formation in the presence of a low urine pH 85.What is a UTI? ● urinary tract infection → inflammation of the urinary epithelium after invasion and colonization by some pathogens in the urinary tract ● retrograde movement of bacteria into the urethra and bladder due to sex or poor hygiene or just females having shorter urethras in general 86.How are UTIs classified? ● complicated vs uncomplicated ● cystitis - bladder inflammation (acute or chronic) ● pyelonephritis - inflammation of upper urinary tract, can be a result of cystitis moving up 87.What are common pathogens for UTIs? ● E. coli which can happen in the very young and the very old ● Staphylococcus saprophyticus (nml vaginal flora) → cystitis 88.Where will pts present with pain for cystitis vs pyelonephritis? ● cystitis = abd region where bladder is ● pyelonephritis = retroperitoneal area → back pain 89.What are some protective urinary mechanisms? ● during micturition → washing out of the urethra ● low pH and high osmolality of urea ● secretions from the uroepithelium → bactericidal effect ● women → mucus-secreting glands ● men → long urethra 90.What are some sx of UTI? ● often asymptomatic; however, you can have frequency, dysuria, urgency, low back and/or suprapubic pain 91.How is cystitis evaluated? ● urine culture with counts of 10000/mL or more 92.How is cystitis tx? ● antimicrobial therapy 93.What are glomerulopathies? ● disorders that directly affect the glomerulus 94.How are nephrotic and nephritic glomerulopathies different? ● nephrotic = massive loss of protein → hypoalbuminemia ○ frothy urine ○ anasarca ○ urine contacts >3g protein/day and lipids ○ microscopic amount of blood or none at all ○ pt will look swollen ● nephritic = usually also extra renal syndromes (i.e., lupus, hx of strep, goodpasture's also affects lung) ○ urine will contain massive amounts of blood and less protein (300 mg to <3 g/day) 95.What are the clinical manifestations of nephrotic syndrome? ● hypoalbuminemia ● peripheral edema ● prone to infection due to loss of Ab 96.Why is nephrotic syndrome often associated with an increased risk for blood clots? ● proteins C and S, AT III can be lost 97.What causes nephritic syndrome? ● increased permeability of the glomerular filtration membrane ● pore sizes enlarge → RBC and proteins pass through 98.What occurs with advanced stages of nephritic syndrome? ● HTN, uremia, oliguria 99.What is the pathophysiology of acute glomerulonephritis? ● formation of Ag/Ab complexes in circulation with subsequent deposition in glomerulus ● Ab produced against the organism that cross-react with the glomerular endothelial cells ● complement system activate ● immune cells and mediators activated or recruited ● decreased GFR due to inflammation, scarring or thickening of the basement membrane (still show increased permeability to RBC and proteins) 100. Is acute glomerulonephritis nephrotic or nephritic? ● NEPHRITIC 101. What is chronic glomerulonephritis? ● glomerular diseases with a progressive course leading to chronic renal failure 102. What are some secondary causes of glomerulonephritis? ● diabetic nephropathy (injury of podocytes → thickening and fibrosis of glomerular basement membrane → expansion of mesangial matrix) ● lupus nephritis (inflammatory complication of chronic autoimmune syndrome SLE) ● formation of auto-Ab against DNA and nucleosomes with glomerular deposition of the immune complexes 103. Describe the cycle of chronic kidney disease. 104. Describe acute renal necrosis or acute tubular injury. 105. How can you tell if renal dysfunction is due to a prerenal or intrarenal issue? ● BUN/creatinine ratios ● urine sodium 106. What is a nml BUN/creatinine ratio? ● 10-15:1 107. What is a BUN/creatinine ratio for someone with pre-renal dysfunction? ● >20: 1 108. What is a BUN/creatinine ratio for someone with intrarenal dysfunction? ● 30:3 → 10:1; nml ratio but higher values 109. What urine sodium value do you usually see with pre-renal dysfunction? ● <20 110. What urine sodium value do you usually see with intrarenal dysfunction? ● >40 111. What is clear cell renal carcinoma? ● very invasive type of renal CA that has fat invading the large vessels 112. What is urothelial carcinoma? ● type of renal CA; multifocal ● unpredictable clinical course and grade will be more indicative of prognosis ● can metastasize via lymph nodes 113. Why are diuretics used in CHF? ● kidneys sense renal perfusion is too low → RAAS activated → Na+ and H2O retention which contributes to CHF → diuretics to remove 114. Mechanisms that protect urinary tract from infection include: ● Monocytes in the urine ● Acidic urine ● Decreased urine osmolarity ● Short urethra of males 115. Nephrotic syndrome produces which of the following: ● Sodium loss ● Protein retention ● Susceptibility to infection ● IgA nephropathy 116. What is the main hormone responsible for urine concentration? ● Aldosterone ● Renin ● ADH ● EPO 117. In the nephron, where does the reabsorption of MOST ions occur? ● Distal convoluted tubule ● Proximal convoluted tubule ● Collecting Duct ● Glomerulus 118. The Juxtoglomerular apparatus is important as this is where _____________ is made in response to decreased renal perfusion ● Glucose ● Aldosterone ● Proteins ● Renin 119. Loop diuretics such as furosemide (brand name Lasix) will block sodium from getting reabsorbed via active transport in the ___________________ loop of Henle. ● Ascending ● Descending ● Proximal ● Distal 120. Hypocalcemia is often seen in patients who are on _____________ diuretics. ● Osmotic ● Loop ● Thiazide ● Potassium-sparing 121. Your patient is on a loop diuretic for their congestive heart failure. They presented to the ED with flank pain, nausea, and hematuria. You suspect renal stones. What is the most likely composition of these stones? ● Magnesium ● Calcium ● Uric acid ● Phosphate 122. Common protective mechanisms against urinary tract infections include all of the following EXCEPT: ● Long ureter length ● Mucous-secreting cells ● Acidic urine ● Alkalotic urine 123. Those with nephrotic syndrome often present with peripheral edema. What mechanism of action is most likely the cause of this? ● The loss of proteins to the urine is increasing capillary oncotic pressure, causing fluid to leak into the interstitial space ● The loss of proteins to the urine is decreasing capillary hydrostatic pressure, causing fluid to leak into the interstitial space ● The loss of proteins to the urine is decreasing capillary oncotic pressure, causing fluid to leak into the interstitial space ● The loss of proteins to the urine is increasing capillary hydrostatic pressure, causing fluid to leak into the interstitial space 124. Your patient presents with hematuria, hypertension, and blood work indicates a decreased glomerular filtration rate. The most likely diagnosis for this person will be: ● Nephrotic syndrome ● Nephritic syndrome ● Renal stones ● Urinary tract infection Module VIII (Endocrine) 1. What are the five functions of the endocrine system? (SDMIC) ● Differentiation of the reproductive and CNS in the developing fetus ● Stimulation of sequential growth and development during childhood and adolescence (helps us grow into adults) ● Coordination of the male and female reproductive systems ● Maintenance of an optimal internal environment (homeostasis) ● Initiation of corrective and adaptive responses when emergency demands occur (stress response internally to what is going on externally) 2. What is responsible for signaling a gland when a hormone is high or low? ● CNS in response to environment 3. What are hormones? ● Chemical messengers/communicators 4. What are the different classes of hormones? ● autocrine - cells that can self-stimulate (i.e., T cells, cytokine receptors) ● paracrine - between cells locally (i.e., growth signaling pathways) ● endocrine - between remote cells 5. What are the general characteristics of hormones? ● specific rates & rhythms of secretion ● operate within feedback systems ● affect target cells (they have appropriate receptors) ● can be inactivated by the liver or directly excreted via kidneys 6. Why are hormones released? ● in response to change in the cellular environment ● to maintain a regulated level of certain substances or other hormones 7. What influences hormone release? ● internal chemical environment ● current growth or metabolic needs (maintain, slow down or speed up) ● neural factors (a lot of these hormones are considered neurotransmitters) 8. What type of feedback system do hormones operate in? ● typically negative feedback loops, but positive loops exist too 9. What are the different types of hormones when it comes to solubility? ● water-soluble ● lipid-soluble 10.What are water-soluble hormones? ● hormones that circulate freely ● they will attach to cell membrane receptors due to high MW 11. What are lipid-soluble hormones? ● hormones that typically require some sort of transporter or carrier protein to travel through the bloodstream ● can easily diffuse across the cell membrane ● will attach to intracellular receptors (either cytosolic or nuclear) 12.What’s another name for lipid-soluble hormones? ● steroids 13.What are lipid-soluble hormones made from? ● made from cholesterol 14.What are some examples of steroids? ● androgens, estrogens, progestins, glucocorticoids, mineralocorticoids, vitamin D, retinoid 15.What can lipid-soluble hormones activate? ● RNA polymerase ● DNA txn 16.Where are hormone receptors founds? ● in or on a target cell 17.What are target cells? ● cells that we want the hormones to act upon that is often distant from the gland that released the first hormone 18.What increases a target cell’s sensitivity? ● more receptors 19.Hormone receptors have a high affinity for _____. ● hormones 20.What occurs when a hormone binds to its target cell? ● target cell initiates a signal 21.What is the difference between downregulation and upregulation? ● upregulation - low concentrations of hormones increase the number of receptors per cell (trying to increase the chances of “catching” hormone) ● downregulation - high concentrations of hormones decrease the number of receptors per cell 22.Describe a general feedback loop and how target cells will up or downregulate. ● Gland A (usually hypothalamus) will release hormone A. ● Hormone A will stimulate Gland B to make more Hormone B. ● Gland B releases more Hormone B into the bloodstream. ● Target cells receive Hormone B. ● Gland A senses high levels of Hormone B. ● Gland A will stop releasing Hormone A and system will stop or slow down. ● Gland A senses low Hormone B levels and REPEAT. ● upregulation: target cells will upregulate Hormone B receptors to catch more hormone, in response to low concentrations of Hormone B ● downregulation: target cells with downregulate Hormone B receptors in response to increased concentrations of Hormone B 23.Which organs are part of the endocrine system? ● pineal gland ● hypothalamus ● pituitary ● parathyroid ● thyroid ● thymus ● adrenal gland ● pancreas ● ovaries/testes 24.Where is the pineal gland? ● deep in the center of the brain (up above palate, behind the nose) 25.Describe the structure of the pineal gland. ● pea-shaped, photo-receptive cells 26.What are the functions of the pineal gland? ● secrete melatonin ● regulates circadian rhythms ● regulates secretion of GnRH ● plays a role in immunity and aging 27.Where are the hypothalamus and the pituitary gland located? ● at the base of the brain 28.Which systems are integrated through the hypothalamus and pituitary? ● neuro and endo = neuroendocrine 29.What general types of hormones are produced by the hypothalamus and pituitary? ● releasing, inhibitory and tropic (growth) hormones 30.Which organ is “in charge”? ● hypothalamus 31.When we spike a fever, which structure in our body is likely responsible for telling us to have this response? ● hypothalamus 32.What are the functions of the hypothalamus? ● monitors hormones via neuro signaling ● produces and releases hormones that tell other organs to either stop or produce hormones (i.e., TRH) ● regulates body cycles ● maintains daily physiological cycles ● helps with controlling appetite, sexual behavior and emotional responses 33.Which exact hormones are released by the hypothalamus? ● prolactin releasing hormone (PRH) ● prolactin-inhibiting factor (PIF) → milk production ● thyrotropin-releasing hormone (TRH) ● gonadotropin-releasing hormone (GnRH) → gonads, sex organs ● growth hormone-releasing factor (GRF) ● somatostatin (growth hormone-inhibiting hormone) ● corticotropin-releasing hormone (CRH) ● substance P (don’t really need to know) 34.Which corticotropin-related hormones are produced by the ANTERIOR pituitary? ● adrenocorticotropic hormone (ACTH) ● melanocyte-stimulating hormone (MSH) 35.What types of glycoproteins are produced by the ANTERIOR pituitary? ● thyroid-stimulating hormone (TSH) ● follicle-stimulating hormone (FSH) ● luteinizing hormone (LH) 36.What types of somatomammotropins are produced by the ANTERIOR pituitary? ● growth hormone (GH) ● prolactin 37.What types of minor corticotropins are produced by the ANTERIOR pituitary? ● beta lipoprotein for fat catabolism ● beta endorphins for pain perception 38.Where are hormones of the posterior pituitary synthesized? ● nuclei of the hypothalamus and then stored/secreted by posterior pituitary 39.What are some examples of hormones of the posterior pituitary? ● ADH = arginine vasopressin (same things!) ● oxytocin → cuddle hormones 40.What are the adrenal glands and where are they located? ● two pyramid shaped organs that sit above the kidneys 41.What are the parts of the adrenal gland? ● cortex and medulla (inner portion) 42.What class of hormones does the adrenal cortex produce? ● glucocorticoids, androgenic 43.What do glucocorticoids do? ● controls use of fats, proteins and carbohydrates ● suppresses inflammation (similar to oral prednisone) ● regulates BP ● increases blood sugar ● decreases bone formation ● controls sleep/wake cycle: diurnal rhythms 44.What are the names of some glucocorticoids produced by the adrenal gland? ● cortisol ● cortisone ● corticosterone ● these are ALL produced and have the same function; however, our focus will be cortisol 45.Which hormone is known as the “stress” hormone? ● cortisol 46.Describe the HPA axis. (hypothalamus-pituitary-adrenal) ● hypothalamus releases CRH as a response to stress ● CRH acts on the anterior pituitary ● anterior pituitary produces ACTH ● ACTH acts on the adrenal cortex ● adrenal cortex produces cortisol ● NEGATIVE feedback loop! 47.What is the target gland or organ for the HPA axis? ● adrenal cortex 48.Which systems interact to respond to stressors? ● endocrine system interacts with nervous system ● immune system is also involved 49.What is aldosterone? ● mineralocorticoid that causes Na+ retention and K+ loss 50.What system regulates the production of aldosterone? ● RAAS; specifically angiotensin II 51.What activates the RAAS? ● Na+ and H2O depletion ● increased K+ levels ● low blood volume 52.What type of pressure is meant to be increased in response to RAAS? ● hydrostatic pressure 53. What are the effects of angiotensin II? ● stimulates production of aldosterone ● stimulates ADH secretion → water reabsorption and thirst 54.What happens to the precursor sex hormones produced by the adrenal cortex? ● converted to estrogen in the ovaries ● converted to testosterone in the testes 55.When are precursor sex hormones released? ● in response to ACTH from the anterior pituitary 56.What types of hormones are produced by the adrenal medulla? ● catecholamines (i.e., epinephrine, norepinephrine) 57.Epinephrine is also known as ____. ● adrenalin 58.What does epinephrine do? ● stimulates SNS for fight-or-flight response for a physical and emotional response to stress 59.Where does epinephrine bind at the cellular level? ● Alpha receptors found in the arteries (think A and A) ● Beta receptors found in the lungs, heart and arteries of skeletal muscles 60.What are the general effects of catecholamines? ● increased blood sugar → for energy ● increased heart rate ● increased contractility → to increase HR and more blood circulating ● relaxation of smooth muscle; bronchodilation → allows us to take in more air so that we are equipped to do what we need to do ● breakdown of fat in cells → ready source of energy ● increased metabolic rate ● pupil dilation ● vasoconstriction 61.What controls the thyroid gland? ● the pituitary gland (but remember, it’s informed by the hypothalamus) 62.Describe the pathway for the production of thyroid hormone 3 (T3) and T4. ● hypothalamus produces TRH ● TRH acts on anterior pituitary ● anterior pituitary produces TSH ● TSH stimulates the thyroid gland ● thyroid gland produces T3 and T4 63.Which structure produces calcitonin? ● thyroid gland 64.What are the effects of calcitonin? ● inhibits osteoclast activity; decreases Ca+ resorption in kidneys → lowers serum calcium levels 65.What vital body functions do T3 and T4 regulate? ● metabolism ● cardiac output/heart rate ● ventilation rate ● increase SNS activity (via adrenal-based catecholamines) ● brain development ● endometrial thickening 66.What does the parathyroid hormone do? ● regulates serum calcium levels ○ stimulates osteoclasts to enhance bone resorption ○ influences reabsorption of Ca+ in distal tubules and renal collecting ducts ○ cofactor with Vitamin D to increase Ca+ absorption from intestines ● regulate serum phosphate levels ○ reduces reabsorption of phosphate from proximal tubule increases phosphate excretion 67.What do osteoclasts do? ● break up bones 68.What counters the parathyroid glands? ● calcitonin which is produced the thyroid 69.Where are the parathyroid glands located? ● 4 tiny bean-structured glands that sit within the thyroid 70.Describe the T3/T4 and negative feedback loop. ● hypothalamus will release TRH in response to low levels of T3 and T4 hormones circulating in the blood ● TRH acts on the anterior pituitary ● anterior pituitary releases TSH ● TSH will act on thyroid ● thyroid will produce T3 and T4 ● when T3 and T4 levels increase, the hypothalamus will shut down TRH production 71.Which structure works to increase Ca+ levels? Decrease? ● parathyroid vs thyroid 72.What does the pancreas produce? ● digestive enzymes and hormones 73.Which pancreatic cells produce glucagon? ● Alpha cells 74.What does glucagon do? ● acts in liver to increase glycogenolysis and gluconeogenesis 75.What do beta pancreatic cells (islets of Langerhans) produce? ● insulin ● amylin 76.What do amylin do? ● increases satiety (feeling full) and suppresses glucagon 77. What do delta pancreatic cells produce? ● somatostatin ● gastrin 78.What do F pancreatic cells produce? ● pancreatic polyps 79.Which organ secretes insulin? ● pancreas (endocrine function) - specifically beta cells 80.How is insulin regulated? ● chemical, hormonal and neural mechanisms 81.What promotes the secretion of insulin? ● increased BG levels; circulating glucose will stimulate the pancreas 82.What does insulin facilitate? ● rate of glucose uptake in the body’s cells (acts as a key) ● intracellular transport of K+ ● storage of glucose in liver as glycogen 83.What is insulin resistance? ● when the sensitivity of the insulin receptor is dysfunctional and can therefore no longer maintain nml cellular function 84.What do incretins do? ● from GI tract in response to food to increase sensitivity of beta cells to glucose 85.What are the different mechanisms for hormone alterations? ● feedback system is broken ○ communication is hindered to stop or start production of hormone ○ may respond inappropriately to a signal ● dysfunction of a gland (i.e., tumor) ○ inability to produce hormone or acquire hormone precursors ○ inability to convert precursor into active hormone ○ excessive or inadequate hormone production ● altered hormone ● ectopic hormone release ○ autonomous production = when there are cells somewhere in the body that make hormones, while bypassing feedback loops ● target cell dysfunction ○ hormone insensitivity (i.e., insulin resistance) ○ receptor-associated disorders ● decrease in receptors ● impaired function ● autoimmune condition → Ab act against receptors or mimic hormone action ● unusual expression of receptor function ○ intracellular disorders ● inadequate synthesis of second messenger ● failure of target cell to produce anticipated response ● don’t need to know specifics 86.What are some disorders of the hypothalamus? ● none r/t overproduction ● underproduction → leads to hypopituitarism; often caused by radiation damage, CA, infections or traumatic brain injury 87.What is the consequence of a disorder of the hypothalamus? ● all target organs/glands will not have a stimulus to produce products 88.What are the most common disorders we see in the endocrine system? ● hyperfunction of anterior pituitary due to Adenoma ● 3rd most common after meningiomas and gliomas 89.True or false: most pituitary adenomas are malignant. ● False: most are benign. 90.What are the most common types of pituitary adenomas? ● Prolactinomas or Lactotroph adenomas; ~40% ○ making milk out of nowhere, can affect men too ● Growth hormone secreting tumors → Acromegaly; ~20% ● ACTH secreting tumors → Cushing’s disease; ~10% ○ note: this is a pituitary adenoma; however, this condition is also grouped in with disorders of the adrenal cortex 91.What are the sx of a pituitary adenoma? ● dependent on what hormones are being produced ● dependent on the size of the tumor: HA, vision issues, bleeding 92.What is acromegaly? ● a condition in which excessive amounts of growth hormone (GH - somatotropin) even after nml bone growth has stopped (after puberty) 93.Which gland is affected by acromegaly? ● anterior pituitary 94.At what age does acromegaly normally occur? ● 30-50 years of age ● can also occur in childhood which would be classified as gigantism 95.What are the tx options for acromegaly? ● surgical removal of the adenoma ● medications that block GH ● radiation 96.What are the s/s of acromegaly? ● exaggerated chin, coarser features 97.What are the different disorders of the anterior pituitary? ● adenoma or tumor that can impair function ● hypofunction 98.What causes hypofunction of the anterior pituitary? ● congenital conditions (very rare, so this was not discussed) ● acquired: ○ tumors pressing on the gland and impairing function ○ infections (i.e., TB meningitis, syphilis) ● TB can also deposit granulomas in the pituitary and make the surrounding tissue nonfunctional ○ surgery ○ skull or brain injury ○ radiation damage burns out gland ○ chemotherapy 99.What are the s/s of anterior pituitary hypofunction? ● fatigue ● weight loss OR weight gain ● generalized weakness ● low mood ● difficulty concentrating ● reduced appetite ● postural hypotension ● dizziness ● sexual dysfunction ● largely dependent on the missing hormones 100. What occurs with hyperfunction of the posterior pituitary? ● syndrome of inappropriate antidiuretic hormone (SIADH) ● excessive amounts are produced → water retention → low Na+ levels → hyponatremia; low UO → high urine osmolality (concentrated urine) 101. What does ADH do? ● tells our body not to produce urine 102. In SIADH, describe the levels for blood volume, BP and electrolytes? ● BV is nml or high ● BP is nml or high ● [electrolytes] = low ● important takeaway = ADH is not being released because of abnml levels → they are being released in inappropriate situations; not compensatory 103. How are aldosterone and ADH different in terms of functions? ● aldosterone retains salt ● ADH works on the DCT to not allow H2O out 104. What can cause SIADH? ● certain medications (i.e., seizure drugs, diabetes drugs, antidepressants, cardiac or BP drugs, CA drugs ● General anesthesia ● Brain disorders (i.e., stroke, injury, infection) ● lung disease or lung cancer (could be drugs or tumor itself secreting ADH) ● pituitary disorder 105. What are some tx options for SIADH? ● always remember to treat the underlying causes ● fluid restriction (most common), salt intake (combat hyponatremia), vasopressin receptor antagonists 106. At what point does hyponatremia become potentially life-threatening? ● when Na < 125 mEq/L ● reminder: nml levels = 135-145 mEq/L 107. What are the s/s of hyponatremia? (SALTLOSS) ● S tupor/confusion/coma ● A norexia ● L ethargy (due to cerebral edema) ● T endon reflexes decreased ● L imp muscles (weakness) ● O rthostatic hypotension ● S eizures/headaches ● S tomach issues: nausea/vomiting 108. What occurs with specific gravity in SIADH? ● SG will be very high 109. What occurs with hypofunction of the posterior pituitary? ● diabetes insipidus which can be a result of any of the three below ○ low ADH ○ central (damage to pituitary; head trauma; surgery; idiopathic; tumors; infections; toxin (snake venom, puffer fish) ○ nephrogenic (kidney resistance to ADH as a result of renal disease or medication) → not a disorder of the pituitary but really the kidney 110. What are the s/s of diabetes insipidus? ● polydipsia (excessive thirst) ● polyuria (urinating too much) – 4-18 L/day ● low urine specific gravity ● very dilute urine ● weight loss ● insomnia ● change in mentation or mental activity ● tachycardia ● signs of dehydration 111. Compare DI and SIADH. DI SIADH - posterior pituitary HYPO function - low ADH; low H2O in body - high UO; polyuria - high Na+; hypernatremia - high H&H and serum osmolality from dehydration - risk for hypovolemic shock - tx: DDAVP (ADH) - posterior pituitary HYPER function - high ADH; high water in body - low UO; oliguria - low Na+ due to dilution; hyponatremia - low serum osmolality - weight gain - risk for seizures - tx: hypertonic saline 112. Describe the pathway for nml thyroid function in terms of T3/T4 production. ● hypothalamus produces TRH ● TRH acts on anterior pituitary ● anterior pituitary produces TSH ● TSH stimulates the thyroid gland ● thyroid gland produces T3 and T4 113. What are alterations that can occur to the thyroid gland? ● dysfunction of the thyroid gland which alters T3/T4 production ● primary hypothyroidism (not making enough) ○ goiter, hashimoto disease, thyroiditis ● primary hyperthyroidism (making more than it should) ○ graves’ disease, thyrotoxicosis, nodular thyroid disease, thyrotoxic crisis ● secondary alterations ○ hypothalamus or pituitary issues ○ exogenous thyroid hormone taken in excess (taking more thyroid hormone they should) 114. Pts with primary hypo thyroidism would have what types of T3/T4/TSH levels? ● low levels of T3/T4 because there is a problem with the gland itself ● high levels of TSH; trying to encourage the thyroid to make more 115. Pts with secondary hypo thyroidism would have what types of T3/T4/TSH levels? ● low levels of T3/T4 because it lacks the stimulus to produce more ● low levels of TSH; there is an issue with the pituitary or hypothalamus 116. Pts with primary hyperthyroidism would have what types of T3/T4/TSH levels? ● high levels of T3/T4; excessive production by thyroid gland ● low levels of TSH to try and stop or slow production of T3/T4 117. Pts with secondary hyperthyroidism would have what types of T3/T4/TSH levels? ● high levels of T3/T4 in response to high levels of TSH ● high levels of TSH due to dysfunction of the pituitary or hypothalamus ● low levels of TSH due to excess thyroid medications 118. What are the s/s of hyperthyroidism? ● intolerance to heat ● fine, straight hair ● bulging eyes ● facial flushing ● enlarged thyroid ● tachycardia ● increased systolic BP ● breast enlargement ● weight loss ● muscle wasting ● localized edema ● amenorrhea ● increased diarrhea ● tremors ● finger clubbing 119. What is Grave’s disease? ● primary hyperthyroid condition ● autoimmune disease the exhibits type II hypersensitivity ● TSH receptor Abs will bind to TSH receptors in thyroid → increased production of T3/T4 120. What are the RF for grave’s disease? ● family history, stress, infection, giving birth, other autoimmune disease (Type 1 diabetes, rheumatoid arthritis), smoking 121. What are the sx of Grave’s disease? ● all the same sx as hyperthyroidism INCLUDING… ● pretibial myxedema: thickening/edema of skin on shins; “orange peel skin” ● Graves’ ophthalmopathy: exophthalmos, periorbital edema, orbital fat accumulation, upper eyelid retraction, lid lag, redness, conjunctivitis, diplopia 122. How is Grave’s disease dx? ● thyroid levels, radioactive iodine and uptake scan 123. How is Grave’s disease tx/managed? ● antithyroid agents, beta blockers, thyroid removal, radiation therapy 124. What is nodular thyroid disease? ● a condition that is generally associated with hyperthyroidism (not always) ● these nodules can be palpated on a PE while being nonfunctional ● in cases of hyperthyroidism, it can be 2 different things ● toxic multinodular goiter - several nodules hypersecrete T3/T4 ● solitary toxic adenoma - only one nodule hypersecretes T3/T4 125. What causes nodular thyroid disease? ● cause is largely unknown 126. What condition puts people at a higher risk for thyroid CA? ● nodular thyroid disease 127. What is thyrotoxic crisis aka thyroid storm? ● rare, acute, life-threatening complication of hyperthyroidism (30% mortality rate) that has a sudden, multi-system involvement 128. What causes a thyroid storm? ● the pathogenesis is unclear; however, there needs to be some sort of precipitating factor (i.e., abrupt stopping of anti-thyroid meds, thyroid surgery, trauma, stress, acute illness, parturition/childbirth, recent iodine contrast use ● can possibly be due to rapid increase in T3/T4 OR increase in cell sensitivity to T3/T4 with hyperactivity of SNS 129. What are the s/s associated with thyroid storms? ● fever (>104 °F) with diaphoresis, HR > 140 bpm, HF, delirium, nausea, vomiting, acute liver failure, death 130. What are the s/s of hypothyroidism? ● intolerance to cold ● receding hairline ● facial and eyelid edema ● dull-blank expression ● extreme fatigue ● thick tongue - slow speech ● anorexia ● brittle nails and hair ● menstrual disturbances ● constipation ● muscle aches and weakness ● dry skin (coarse and scaley) ● lethargy ● apathy ● hair loss ● late clinical manifestations: subnormal temp, bradycardia, weight gain, decreased loss of consciousness, thickened skin, cardiac complications 131. What is Hashimoto’s disease? ● HYPO thyroidism ● type IV hypersensitivity rxn; most common cause of hypothyroidism in US ● cellular-mediated immunity (lymphocytes, especially CD8+) 132. Who is more affected by Hashimoto’s disease? ● women; 30-60 y/o; family hx; autoimmune disease; radiation exposure 133. What is endemic goiter? ● most common cause of hypothyroidism worldwide → largely preventable ● iodine deficiencies due to diet lead to T3/T4 deficiencies ● TSH will constantly stimulate thyroid causing hyperplasia ● hyperplasia can be reversed with iodine and replacement thyroid hormones ONLY IF TREATED EARLY (<5 years) ● endemic when it affects greater than 5% of population; currently at 2.7% 134. What is required to produce T3/T4? ● iodine 135. What is congenital hypothyroidism? ● lack of or dysfunction of the thyroid gland present at birth 136. How is congenital hypothyroidism discovered? ● at 2-6 months of age, these s/s will present ● hoarse cry ● distended abdomen ● dry skin and hair ● macroglossia (unusually large tongue) ● slow responses ● poor growth and development ● mental deficits 137. What is a fatal fallout of hypothyroidism when missed? ● cretinism → permanently cognitively impaired 138. What are the most common thyroid cancers? ● papillary thyroid cancer ○ usually affects those 30-50 y/o ● follicular thyroid cancer ○ usually affects those >50 y/o ● medullary thyroid cancer ○ c-cells = calcitonin production ● anaplastic thyroid cancer ○ very rare and aggressive with poor prognosis 139. How are thyroid CA treated? ● lobectomy or thyroidectomy ● radioactive iodine ● chemo 140. What is the survival rate for those dx with thyroid CA? ● 5 years (follicular, papillary and medullary = 100 %; anaplastic = 30%) 141. How is the parathyroid gland stimulated? ● NOT mediated by the pituitary like most glands we’ve seen ● this is mediated by Ca2+ levels 142. Describe the pathway that occurs when the parathyroid gland is stimulated. ● low blood Ca2+ levels will lead to a signaling pathway that stimulates the parathyroid glands to secrete PTH ● PTH will encourage bone breakdown; Ca2+ reabsorption by the kidneys and increased vitamin D; intestines absorb more Ca2+ ● blood Ca2+ levels will increase and do a feedback loop 143. What is hyperparathyroidism? ● condition that results in hypercalcemia typically because of a benign adenoma; common cause of 80% of hypercalcemia cases 144. What are the RF for hyperparathyroidism? ● women are 3x more likely than men, >50 y/o, ionizing radiation, lithium ingestion (bipolar pts), family hx 145. What systems does hyperparathyroidism affect? S/S? ● digestive system → loss of appetite, N/V, constipation ● nervous system → fatigue, depression, confusion ● musculoskeletal system → muscle weakness, aches/pain in bones/joints ● urinary system → kidney stones, increased thirst and urination 146. What is hypoparathyroidism? ● abnormally low levels of PTH ● low serum Ca2+ levels → confusion, muscle spasms/cramps, numbness in hands, feet and face ● increased serum phosphate levels → mainly asymptomatic; however, it can present same as Ca2+ with pruritic rash 147. What are the typical causes of hypoparathyroidism? ● thyroid surgery (hard to preserve parathyroid), autoimmune, genetics 148. What are disorders of the adrenal medulla? ● no known conditions of hypofunction ● hyperfunction → pheochromocytoma → rare tumor on gland that secretes Catecholamines → HTN, tachycardia, diaphoresis and HA (think of rage!) 149. What are the different hyperfunction diseases of the adrenal cortex? ● Cushing disease : this is a disease that results in high cortisol levels in response to ACTH (anterior pituitary adenoma, ectopic ACTH); the cortisol levels will be chronically elevated; lose the ability to produce cortisol in response to stressors ● Cushing syndrome : increased cortisol because of adrenal cortex adenoma ● Cushing- like syndrome: exogenous glucocorticoids (i.e., oral prednisone and giving too much of it to a pt) ● hyperaldosteronism → excessive aldosterone → high BP 150. What are the s/s of all the Cushing related disorders? ● personality changes ● moon face ● increased susceptibility to infection ● gynecomastia in males ● fat deposits on face and back of shoulders ● osteoporosis ● hyperglycemia ● CNS irritability ● Na+ and fluid retention → edema ● thin extremities ● GI distress due to increased acid ● amenorrhea and hirsutism in females ● thin skin ● purple striae ● bruises and petechiae 151. What are the primary and secondary causes of hyperaldosteronism? ● primary → adrenal adenoma, CA, hyperplasia (overgrowth of gland) ● secondary → diet, other disorders r/t heart, liver and kidneys 152. What are the S/S of hyperaldosteronism? ● HA, blurred vision, dizziness, hypokalemia 153. What are the adrenal medulla hypofunction diseases? ● Addison’s disease aka primary adrenal insufficiency ● secondary adrenal insufficiency 154. What are the characteristics of Addison’s disease? ● low or lacking in cortisol or sometimes aldosterone ● caused by damage to the adrenal gland (autoimmune ~75%, infection such as TB, CA metastasis, injury that causes hemorrhage into adrenal) 155. What are the sx of Addison’s disease? ● weakness ● nausea and loss of appetite ● weight loss ● hyperpigmentation ● vitiligo ● hyperkalemia and hyponatremia ● hypotension 156. How is Addison’s disease treated? ● treated with replacement hormones 157. What are the characteristics of secondary adrenal insufficiency? ● failure of the pituitary to stimulate adrenal cortex hormone production (i.e., lack of ACTH) ● exogenous corticosteroids (i.e., glucocorticoids, steroids) ○ when we give people steroids, the adrenal gland loses its drive to make more cortisol; the pituitary senses that steroid levels are fine, it won’t make ATCH; no signal to adrenal cortex; no cortisol; adrenal gland can shrink and stop working 158. Describe adrenal crisis. ● a life-threatening condition in which there is a severe acute adrenal insufficiency of cortisol (sometimes aldosterone) 159. What causes adrenal crisis? ● trauma ● Addison’s disease ● pituitary injury ● severe dehydration ● physiological stress (e.g. infection), emotional stress, or strenuous physical activity ● sudden discontinuation from glucocorticoids – most common cause; usually want to gradually decrease the pt’s dosage 160. What are the s/s of adrenal crisis? ● acute shock that doesn’t respond to fluids or medications ● hypotension ● tachycardia ● weakness ● fatigue ● decreased appetite/weight ● orthostatic hypotension ● electrolyte imbalances 161. What is the origin of the name for DM? ● Greek origin (diabetes = siphon, pass through; mellitus = honey, sweet) 162. Diabetes mellitus is characterized by…. ● sugar in the blood and urine ● elevated BG levels over a prolonged period of time 163. What are the most common types of DM? ● I and II 164. How are DM type I and type II different? ● type I = inability to produce insulin because of destroyed beta cells (due to an autoimmune response); also known as juvenile DM but can affect anyone; common causes are family hx and viral exposure ○ younger onset (preteen to adolescence) ○ little insulin resistance ● type II = visceral fat and fatty liver will cause the liver to release increased levels of glucose and triglycerides; skeletal muscle will develop insulin resistance; beta cells will wear out = decrease insulin production ○ modifiable RF ○ insulin resistance → declining insulin production; will look like type I 165. How long does it usually take someone with DM type 2 to destroy beta cells? ● about 12 years 166. Who is at risk for DM type 2? ● 45+ y/o ● physically active < 3x a week ● family hx ● HTN ● hx of gestational diabetes ● overweight 167. What is the dx criteria for DM type 2? ● fasting BG is normally < 100 mg/dL; DM ≥ 126 mg/dl; in between is considered prediabetes ● HgbA1C is normally < 5.7%; DM ≥ 6.5%; in between is considered prediabetes; will tell us how much sugar the Hgb was exposed to ● oral glucose tolerance test is normally ≤ 140 mg/dL; DM ≥ 200 mg/dL; in between is considered prediabetes ● random plasma glucose test → DM ≥ 200 mg/dL 168. Compare and contrast the clinical manifestations of DM type I and II. ● type I = weight loss, fatigue ● type II = frequent infections, paresthesias ● in both = polys (uria, dipsia, phagia) and blurred vision ● polyuria = trying to pee out glucose ● polydipsia = trying to dilute BG levels ● polyphagia = cells are starving because glucose can’t get in, body is getting signal to keep eating!!! 169. What is a common complication of diabetes? ● DKA = diabetic ketoacidosis 170. What occurs with DKA? ● lack of insulin → increasing BG levels → starving cells → fats broken down for fuel → ketone production (acid) → ketones in urine 171. What are the S/S of DKA? ● fruity-scented breath, N/V, polyuria/polydipsia, fatigue, confusion → coma or death 172. What increases the risk for DKA? ● Type 1 or insulin-dependent diabetes (missed insulin dose, clog in pump, etc.) ● BG > 250 mg/dl x 2 in people who usually have well-controlled BG ● Ketones in urine ● Infection, stress, etc. 173. What are the macrovascular complications of DM? ● brain, heart and extremities are affected 174. What are the microvascular complications of DM? ● eyes and kidneys are affected, neuropathy 175. Sensitivity of a target cell is down-regulated when the: ● Level of hormone that binds with the receptor is high ● Number of receptors for the hormone is high ● Direct effects of the hormone are detected ● Permissive effects of the hormone are detected 176. True or false: The target organ or cells are responsible for signaling a gland when circulating levels of that hormone are low. ● False: CNS signals hormone release 177. The adrenal cortex produces _____________ in response to _____________ release from the anterior pituitary? ● cortisol, corticotropin-releasing hormone (CRH) ● Thyroid stimulating hormone (TSH), cortisol ● Cortisol, adrenocorticotropic hormone (ACTH) ● Insulin, T3/T4 178. The parathyroid hormone increases serum calcium by stimulating _________________ and _______________ calcium resorption in the kidneys. ● Osteoblasts; decreasing ● Osteoclasts; increasing ● Osteoclasts; decreasing ● Osteoblasts; increasing 179. Excessive antidiuretic hormone production will elevate the blood pressure through which mechanism? ● activation of the RAAS by the liver (this is RENIN) ● decreasing urine output ● increasing Na+ retention (this is ALDOSTERONE) ● activation of cortisol (this is ACTH) 180. Hyponatremia is a potentially life-threatening condition and can cause (SELECT ALL THAT APPLY): ○ Confusion ○ Seizures ○ Fever ○ Dyspnea 181. You are working on a rehab unit for patients with head injuries. You notice your patient is always at the water fountain and seems to go to the bathroom a lot. You suspect ______________ due to ________________. ● diabetes insipidus; antidiuretic hyposecretion ● acute nephron damage; hypercalcemia ● diabetes mellitus; aldosterone hypersecretion ● syndrome of inappropriate ADH; antidiuretic hypersecretion 182. You received blood results from the lab on a person newly diagnosed with Hashimoto’s disease who has not yet started treatment. You would expect their TSH levels to be ________________ and their T3/T4 levels to be ___________. ● Elevated, Elevated ● Elevated, Decreased ● Decreased, Decreased ● Decreased, Elevated 183. Your patient with Hashimoto’s has been on thyroid hormone replacement therapy for a few months now but wants their levels to be checked as they are still having symptoms. Which of the following is NOT a symptom of hypothyroidism? ● tachycardia this is seen in hyperthyroidism ● fatigue ● weight gain ● hair loss 184. Cushing’s disease and Cushing’s syndrome both involve elevated levels of cortisol. Cushing’s disease however, is due to a(n) ____________ gland issue, whereas Cushing’s syndrome is due to a(n) ______________ gland issue. ● Adrenal, Hypothalamus ● Hypothalamus, Pituitary ● Pituitary, Adrenal ● Adrenal, Pituitary 185. The signs and symptoms of adrenal crisis can be subtle, but include (SELECT ALL THAT APPLY): ● Weakness ● Fatigue ● Hypertension ● Electrolyte imbalance 186. Aldosterone helps to maintain blood pressure by: ● Increasing potassium reabsorption ● Increasing hydrogen reabsorption ● Increasing sodium reabsorption ● Increasing glucose reabsorption 187. When there is destruction of the beta cells of the pancreas, you would expect the loss of which hormone? ● Glucagon ● Insulin ● Cortisol ● Norepinephrine 188. Which of the following lab values is worrisome for diabetes? ● Random blood glucose: 150 mg/dl ● Fasting blood glucose: 89 mg/dl ● Hemoglobin A1C: 6.9% ● Oral glucose tolerance test: 139 mg/dl 189. Insulin resistance means that cells have _______________ sensitivity to insulin and thus, ___________________ cannot enter the cells ● Increased, calcium ● Increased, glucose ● Decreased, ketones ● Decreased, glucose Module IX (Skin, Reproduction SKIN 1. What is the largest organ of our body? ● skin 2. What are the six functions of skin? ● physical barrier between the inside of the body and outside world ● body temperature regulation ● production of vitamin D ● involved in immune surveillance ● sensory functions for pain and pleasure ● appearance - integral part in human mating 3. Why is the physical barrier function of the skin considered multifaceted? ● protection from biological agents (bacteria, fungi, viruses, etc.) ● protection from the sun’s UV radiation (our organs cannot handle it) ● keeps our fluid inside by preventing evaporation ● protection of sensitive inner structures (could not handle the pressure) 4. How is vitamin D synthesized? ● from UV light 5. What occurs if you don’t have vitamin D supplementation or in your diet? ● you need to compensate by being in the sun for at least 15-20 mins/day 6. Why is vitamin D important? ● increased intestinal absorption of Ca2+ ● increased bone resorption ● decreased Ca2+ and phosphate excretion 7. Describe the epidermal skin layer. ● the layer that shows on the outside ● a bunch of keratinocytes that sits atop a basement membrane 8. Describe the dermal skin layer. ● layer that contains hair follicles, sebaceous glands, sweat glands and nerve endings 9. Which two nerve endings are found in the dermis? ● meissner corpuscle = light touch ● pacinian corpuscle = vibration, rough vs. smooth 10.Which muscle in the dermis is the basis for goosebumps? ● arrector pili muscles 11. Which cells produce brown pigment in the epidermis? ● melanocytes → melanin 12.What layer is found under the dermal layer? ● subcutaneous fat layer 13.Describe the basement membrane of the epidermis. ● very bottom layer of the epidermis with a single layer of keratinocytes and melanocytes (also known as stratum basale) 14.Describe the layers of the epidermis, excluding the basement membrane. ● stratum spinosum = keratinocytes get pushed up and get bigger ● stratum granulosum = keratinocytes start to condense ● stratum corneum = anucleated, keratin cells; layer that sheds 15.Why is melanin important? ● can absorb UV light; people with more melanin have an advantage 16.Describe the four stages of a pressure ulcer. ● stage I = non blanchable redness of intact skin ● stage II = partial-thickness skin loss of the epidermis or dermis ● stage III = full-thickness skin loss, involving damage or loss of the subcutaneous tissue ● stage IV = full-thickness skin loss with damage to muscle, bone, or supporting structures 17.How are folliculitis, furuncle and carbuncle different? ● folliculitis = inflammation of a follicle ● furuncle = abscess caused by a consolidation of numerous inflamed follicles ● carbuncle = consolidation of numerous furuncles 18.What is the most common cause of folliculitis? ● S. aureus 19.Which types of lesions do HPV genotypes 1 and 2 cause? ● skin warts 20.Which types of lesions do HPV genotypes 6 and 11 cause? ● genital warts 21.What can HPV genotypes 16 and 18 cause? ● squamous cell carcinoma of the cervix, anus, and oropharynx 22.How are HSV-1 and HSV-2 different? ● HSV-1 is not an STD and it is passed via contact with infected saliva ○ presents as cold sores or fever blisters ● HSV-2 is an STD that is passed via skin-to-skin mucous membrane contact during viral shedding ○ presents as vesicular rashes on genitalia ○ can be transferred from mother to neonate 23.What is pemphigus? ● a type II hypersensitivity reaction that involves Abs attacking protein in the skin → causes a split between epidermis or between epidermis/dermis → fluid accumulation in the split → bulla 24.What are the different pemphigus conditions? ● pemphigus vulgaris → most common ● pemphigus foliaceus → milder form ● pemphigus erythematosus → subset of pemphigus foliaceus ● paraneoplastic pemphigus → most severe form ● IgA pemphigus → most benign form 25.While pemphigus can be caused by several different Abs, what is the fixed antigen that is attacked? ● keratin 26.What is erythematous multiforme? ● also known as “bull’s eye” or target lesion ● characterized by regions that are erythematous an