Physio Lab Exam 4 (22-26)

Q2: Inwhat tubes did digestion NOT occur? Explain why in each case

1- boiled too hot solution denatured protein 4- no starch present 5- no digestive enzyme 6- no starch present

Protein digestion Q4: In what tubes did digestion NOT occur? Explain why in each case.

1- solution boiled, denatured enzyme pepsin 3- no protein BPNA 4- lack necessary enzyme to break down BPNA 6- not at optimal pH for digestion

Lab 25: Endocrine Physio 1 - focuses on how thyroid hormone influences metabolism, and how insulin influencesblood glucose level

1. Thyroid Hormone - Metabolic rate(MR): is the amount of energy required for necessary body functions. There are several factors that control MR, including gender (males have a higher MR) and age (MR decreaseswith age). - There is also a hormone made by our thyroid gland that increases MR; this hormone is called Thyroxine(TH). - Thyroxine's release is a multi-step process. The hypothalamus first secretes a hormone called Thyrotropin Releasing Hormone(TRH). Thisin turn stimulates the anterior pituitary (adenohypophysis) to secrete a hormone called Thyroid Stimulating Hormone(TSH). TSH then heads down to the thyroid gland where itstimulates the follicular cells to secrete Thyroxine. Therefore, several organs are necessary for the proper release of Thyroxine: the hypothalamus, the pituitary gland and the thyroid gland. - thyroidectomy: which is the surgical removal of the thyroid gland - hypophysectomy: which is the surgical removal of the pituitary gland - propylthiouracil: which is a drug that blocks the formation of thyroxine by preventing the binding of iodine to tyrosin - goiter: is an overgrowth of the thyroid gland, which can result from excess TSH secretion or reduced TH secretion. 2. Insulin - Insulin: is secreted by the beta (β) cells of the Islets of Langerhans of the pancreas in response to an increased blood glucose level. Its target tissues are all cells inthe body, except red blood cells and neurons. It tells its target cells to insert a GLUT-4 glucose carrier into their cell membrane so that they may take glucose out of the blood for metabolism. - Glucagon: on the other hand, is secreted by the alpha (α) cells of the Islets of Langerhans in response to a decreased blood glucose level. Its target tissues are the liver and adipose tissue. It tells the adipocytes to release fat from their cells as an alternate energy source for our body's cells. It also tells the liver to break down glycogen into glucose and release that glucose into the bloodstream and to convert non-carbohydrate chemicals such as fat into glucose. These two hormones are antagonistic: insulin acts to lower blood glucose level after a meal and glucagon acts to raise it during starvation. - Type I Diabetes Mellitus is a condition wherein the body does not produce insulin. It is usually caused by an autoimmune disorder that destroys the β cells of the pancreas. The result is that blood sugar increases to a dangerously high level as there is no way of getting glucose into the body's cells. Patients diagnosed with Type I DM are put on insulin therapy, where they have daily injections of recombinant insulin to replace the insulin that would otherwise naturally control their glucose level. - Type II Diabetes Mellitus is a condition wherein the body's cells begin to develop insulin insensitivity and ignore the insulin being secreted naturally by the body. This is usually due to chronic over-section of insulin in people who are obese or inactive. Patients diagnosed with Type II DM are advised to lose weight, eat a low carbohydrate diet and exercise. They can also be put on medication to increase insulin sensitivity, and some even go on insulin injections. > A fasting blood glucose level below 110 mg/dl is considered normal > a fasting glucose level between 110-126 mg/dl is considered pre-diabetic > a fasting blood glucose level over 126 is considered diabetes

Lab 26: Endocrine Physio II

1. estrogen- inhibits bone resorption by osteoclast cells, thereby stimulating bone growth by osteoblast cells. During menopause, or after an ovariectomy(removal of the ovaries), estrogen production drops significantly and bone thinning can result, which can lead to osteoporosis - calcitonin- it inhibits osteoclast activity and stimulates osteoblast activity. - Bone density- can be measured by doing a bone density scan > A T score of +1.00 to -0.99 is considered normal > from -1.00 to -2.49 is indicative of bone thinning, called osteopenia > anything below -2.50 is indicative of osteoporosis. > hormone replacement therapycan improve bone density 2. Cortisolis- a hormone that is part of the stress pathway. In response to stress, the hypothalamus secretes a hormone called Corticotropin Releasing Hormone(CRH), which in turn stimulates the anterior pituitary to secrete another hormone called Adrenocorticotropic Hormone(ACTH). ACTH then stimulates the adrenal cortex to produce a glucocorticoid called Cortisol. Cortisol is involved in preparing the body for fighting its stressors. Cortisol, through negative feedback, then inhibits the secretion of both CRH and AC a. Hypersecretion of cortisol can be caused by either Cushing's Syndrome or Cushing's Disease. In Cushing's Syndromeblood cortisol levels are increased. The increased cortisol then causes ACTH levels to drop due to negative feedback. There are two forms of Cushing's Syndrome. Iatrogenic Cushing's Syndromeresults when patients are given medications such as prednisone (an anti-inflammatory corticosteroid), which causes increased blood levels of cortisol. The second form, Primary Cushing's Syndrome, is caused by a tumor in the adrenal gland, which results in increased cortisol b. Cushing's Disease is caused by a tumor in the pituitary which leads to high cortisol and ACTH levels. - Hyposecretion of cortisol can be caused by either a. Primary Adrenal Insufficiency or Second Adrenal Insufficiency. Primary Adrenal Insufficiency, called Addison's Disease, is caused by destruction of adrenal cortexthrough an autoimmune disease, which results in low cortisol levels. To compensate ACTH secretion increases. b. Secondary Adrenal Insufficiency is caused by damage to the pituitary gland and hypothalamus (usually by steroid use or tumors); both cortisol and ACTH levels would be low as a result.

Q16: Are any of your patients pre-diabetic? What advice would you give them

2+4; low carb diet, exercise, lose weight, monitor glucose levels

Q7: In what tubes did digestion NOT occur? Explain why in each case.

2- no bile 3- no fats to break down 4- no lipase enzyme 5- pH too low 6. no pH change

Q17: Are any of your patients diabetic? What advice would you give them? What course of treatment should they follow?

3+5; exercise more, limit sugar and carb intake, glucose lowering drugs, go on insulin therapy

Q2: What happens when you decrease afferent arteriole diameter? Explain your results.

A decrease in afferent arteriole diameter will cause decrease in GFR, glomerular capillary pressure and urine production (increased resistance)

Q3: What effect does decreasing efferent arteriole diameter have on GFR and urine production? Explain your results.

A decrease in efferent arteriole diameter (more resistance) causes increase in GFR and urine production

Q16: Which hormone, aldosterone or ADH, has a greater impact on urine concentration? Why?

ADH has greater effect because less H2O in filtrate and leave Na giving higher concentration

Q15: Which hormone, aldosterone or ADH, has a greater impact on urine output? Why?

ADH has greater effect. Its responsible for fluid retention and binds receptors on cells into collecting duct of kidneys which then promotes reabsorption of water back into circulation

Q1: What effect does increasing afferent arteriole diameter have on GFR and urine production? Explain your results.

An increase in afferent arteriole diameter (less resistance) causes increase in GFR, glomerular capillary pressure and bring production

Q1: How do the baseline metabolic rates of the thyroidectomized and hypophysectomized rats compare with the normal rat? Explain any difference

Both have lower MR than normal rat. thyroidectomized rat has no thyroid, no T3 and T4 will lower metabolic rate. hypophysectomized rat have no pituitary, no TSH, no thyroxine lower MR.

Q8: What effect does closing the valve have on GFR/urine output? What condition(s) might this simulate?

Closing valve will lower GFR and no urine output - an obstruction of the flow of urine mimics condition of kidney damage

Lab 24: Chemical Digestion

Digestion is the act of breaking food down into smaller components that can ultimately be absorbed into your blood and used for energy 1. Mechanical digestion: involves the physical breakdown of food from large pieces into small pieces. Examples of mechanical digestion include chewing and mixi 2. Chemical digestion: involves enzymes, which break chemical bonds into order to break food down into its building blocks: monosaccharides, amino acids and glycerol and fatty acids. A. Carbohydrate digestion: in the mouth by an enzyme found in saliva called salivary amylase. This enzyme breaks starches down into a reducing sugar called maltose. B. Protein digestion: in the stomach by an enzyme called pepsin. This enzyme cleaves large proteins into smaller polypeptides. C. Fat digestion: in the small intestine is accomplished by an enzyme called pancreatic lipase. In this lab we will be using a synthetic enzyme called pancreatin. Pancreatin breaks down dietary fats (triglycerides) into fatty acids and glycerol. The enzymes is assisted by an emulsifier called bile, which is secreted by the liver and acts to break down large drops of fat into smaller drops of fat, without breaking any chemical bon

Q7: Describe the relationship between blood pressure and GFR/urine output. Explain.

Direct relationship - afferent arterioles bring more blood., increase pressure, increase GFR/ urine output

Fat digestion Q6: Why does the digestion of fat cause the pH of the solution to decrease

Fats have a neutral pH and when digested by lipase they are converted into fatty acids. Their presence can decrease the pH (increase acidity) of solution

Q13: What happens to the concentration of glucose in urine as you add glucose carriers? Why? At what point does the glucose concentration in the urine become zero?

The concentration of glucose in urine decreases as you add glucose carriers. This is necessary for secondary active transport; facilitated diffusion along basolateral membrane. 300-400 carriers will reabsorb the glucose

Q3: Which of the rats developed a goiter after injection with TSH? Explai

The normal and hypophysectomized rat developed goiters. Need thyroid gland, increase THS will cause thyroid gland to grow

Q8: Explain the difference in results between tubes 1 and 2 in the fat digestion experiment. In which tube did more digestion occur? How do you know? Why did more digestion occur?

There is more digestion in test tube b/c there is lipase enzyme and bile salts as well as lowered pH. Tube 2 only has enzyme lipase and no pH change

Lab 22: Renal System Physiology

Urine formation occurs in three steps: 1. glomerular filtration - removal of plasma substances from the blood into a fluid in Bowman's capsule called filtrate. - Glomerular filtration rate (GFR): is a measurement of the volume of filtrate formed per minute. GFR is highly regulated by the kidneys to ensure that blood volume and blood pressure are stable > The afferent arteriole is a vessel that feeds blood into the glomerulus. The efferent arteriole is a vessel that drains blood from the glomerulus. > Blood pressure is the force that drives filtrate into Bowman's capsule during glomerular filtration. > If there is a sudden change in GFR, the afferent and/or the efferent arteriole radius can be altered to restore GFR to normal. You will be testing this homeostatic mechanism 2. tubular reabsorption - Reabsorption occurs when filtered substances are returned back to the blood. This process returns "good" solutes, such as glucose, ions, hormones, etc., back to the blood. Some substances are reabsorbed through simple diffusion, while others, such as glucose, require secondary active transport carriers. > One factor is the concentration of solutes found in the interstitial fluid surrounding the nephron. Antidiuretic Hormone (ADH) has been added to the tubule so that water reabsorption can occur. > Glucose is filtered through the glomerulus during filtration. To prevent excretion there are glucose carriers in the proximal convoluted tubule of the nephron which actively transport glucose back into our blood. There is a maximum amount of glucose reabsorption that can be accomplished; this is referred to as the Transport Maximum, or Tm. > Antidiuretic hormone, is secreted in response to changes in blood osmolarity. ADH causes water reabsorption in the collecting duct. The other, called Aldosterone, is secreted in response to changes in blood pressure. Aldosterone causes sodium and water reabsorption in the distal convoluted tubule and collecting duct. 3. tubular secretion.

Q6: In the normal rat was there any change in metabolic rate when you injected TSH? Expla

Yes, MR increases and T3 + T4 increase. TSH stimulates secretion of TH

Q5: In the normal rat was there any change in metabolic rate when you injected thyroxine? Explain.

Yes, MR increases and T3 + T4 increase. Thyroxine should increase MR b/c goes directly to target cells

Q5: Explain any changes in wave amplitude that you observed during rebreathing.

amplitude slowly increasing then maintain levels; CO2 levels increase

Q4: Predict the effect of increasing efferent arteriole diameter.

an increase in efferent arteriole diameter (decrease resistance) causes decrease in GFR and urine production

Q9: When blood pressure drops, what must the afferent arteriole do to compensate?

as blood pressure drops, afferent arteriole will dilate, increase amount of filtrate in the glomerulus

Q10: What can the efferent arteriole do to compensate for a drop in BP?

as blood pressure drops, efferent arterioles will constrict, reduce amount going out glomerulus and increase pressure inside

Q1: What effect did estrogen and calcitonin have on bone density? Explain the effects of these hormones on bone.

both estrogen and calcitonin will increase rats vertebral bone density (indicated by a less negative t-score) - estrogen, inhibits reabsorption by osteoclast cells, to stimulate bone growth by osteoblast cells - calcitonin inhibits osteoclast activity and stimulates osteoblast activity

Q6: How does respiratory alkalosis affect urine? Explain.

decrease in urine, more HCO3- (bicarbonate) and decrease H+ because pCO2 levels are low. Reabsorb less HCO3- and release more in urine, less H+ secreted

Q14: What is the purpose of barium hydroxide?

dissolves proteins and cell membranes, so glucose readings can be read better

Q9: What is the optimal condition for fat digestion in the small intestine? Include enzyme, temp., and pH. Is anything else needed for optimal digestion

enzyme pancreatic lipase (chemically digests) and bile (mechanically digests), optimally in 37C and pH 7.0

Q5: What is the optimal condition for protein digestion in the stomach? Include enzyme, temp., and pH.

enzyme pepsin breaks down protein into small peptides, optimal temp 37C and pH 2.0

Q2: Did either hormone work more effectively? If so, which one?

estrogen

Q5: Diagnose Patient 3. Explain your logic.

high cortisol, high ACTH - Cushings disease (secondary hypercortisolism) a tumor in pituitary

Q4: Diagnose Patients2and 5. Explain your logic.

high cortisol, low ACTH - Iatrogenic cushings syndrome, when given an anti-inflammatory corticosteroid, which causes high cortisol then causes ACTH levels to drop due to negative feedback

Q9: How does metabolic acidosis affect respiration? Explain.

if pH is down, H+ levels are high. Breathing rate should increase to release more CO2 - example kidneys not remove enough acid, diabetics when ketone bodies build up; diarrhea

Q8: How does metabolic alkalosis affect respiration? Explain.

if pH is up, H+ levels are low and CO2 levels low. So, retain more CO2 by slowing BPM - example vomiting

Q7: How does respiratory acidosis affect urine? Explain.

increasing H+ and decreasing HCO3- in urine. Increased H+ because pCO2 is high. Reabsorb more HCO3- in blood and release less in urine. More H+ in urine

Q5: What condition(s) might result if GFR is too high?

kidney damage (high albumin levels in urine); diabetes incifidus (excessive H2O) causes dehydration; hypokalemia high blood pressure/ hypotension - absorption capacity of Na and H2O will lead to renal tubules be overwhelmed electrolyte imbalance, excess salt

Q6: What condition(s) might result if GFR is too low?

kidney failure, chronic kidney disease, build up of waste, dilute electrolytes

Q6: Diagnose Patient 4. Explain your logic.

low cortisol, high ACTH - Addisons disease (primary adrenal insufficiency) destruction of adrenal cortex through an autoimmune disease, which will lower cortisol and higher ACTH to compensate

Q3: Diagnose Patient 1. Explain your logic.

low cortisol, low ACTH - secondary adrenal insufficiency (hypopituitarism) damage pituitary gland and hypothalamus

Carbohydrate digestion Q1: Why is the incubator's temperature set at 37ºC

mimics human body temp

Q1: Did you observe any change in pH or PCO2 with normal breathing?

no change

Q9: In the thryoidectomized rat was there any change in metabolic rate when you injected TSH? Explain.

no change in MR, no thyroid gland to release T3 + T4, no thyroid gland to stimulate and no thyroxine

Q10: In the thryoidectomizedrat was there any change in metabolic rate when you injected propylthiouracil? Explain

no change in MR, no thyroid gland, to thyroxine production, nothing for PTU to block

Q13: In the hypophysectomized rat was there any change in metabolic rate when you injected propylthiouracil? Explain

no change, no pituitary gland, no TSH. Thyroid does not produce TH, nothing for PTU to block

Q2: Which of the rats developed a goiter after injection with thyroxine? Expla

none, Thyroxine does not effect hypothalamus and anterior pituitary gland. TSH is what causes goiter not thyroid hormone (TH)

Q4: Which of the rats developed a goiter after injection with propylthiouracil? Expl

normal rat, both thyroid and pituitary gland present. PTU block thyroxine formation and negative feedback does not occur (TSH increases)

Q3: What is the optimal condition for starch digestion in the mouth? Include enzyme, temp., and pH.

optimum temp 37C, salivary amylase enzyme, most active at optimal pH 7.0

Q2: Did you observe any change in pH or PCO2 with hyperventilation? Explain.

pCO2 decrease and pH increase. Hyperventilation is excessive exhalation therefore decreases CO2 levels in blood to cause pH levels to dip to the point of acidosis

Q4: Did you observe any change in pH or PCO2 with rebreathing? Explain.

pCO2 increase in blood resulting in more H+ which causes pH levels to rise into alkalosis

Q15: What is the purpose of heparin

prevent blood clots, which would interfere with cleat glucose readings

Q14: A person with diabetes is unable to absorb glucose into most of their body's cells. What would you expect to find in the urine of a diabetic person? Why?

since a diabetic has insufficient insulin to transport glucose from the blood into the cell, there is increased glucose in the blood therefore increased glucose in filtrate and urine

What happened to the amplitude of the waves during rebreathing?

small wave, big wave - amplitude increased slowly. pCO2 leaves rise

In the hyperventilation/normal run, describe the tracing after hyperventilation stopped.

small wave, big waves, flat, small wave - after hyperventilating treating stopped to restore pCO2 levels

Lab 23: Acid/ Base Balance

ur body's proteins can only function within a strict range of pH so there are several homeostatic mechanisms to ensure that we remain within that range. Our blood has a normal pH range of 7.35-7.45, which is slightly alkaline due to an abundance of bicarbonate ions circulating through our blood. - pH below 7.35 is acidotic - pH above 7.45 is alkalotic. 1. Respiratory Acidosis/Alkalosis: change in pH is caused by a change in respiration (e.g. hyper- or hypo-ventilation) - Hyperventilation: is characterized by an increase in respiratory rate and tidal volume, which are not matched by an increase in metabolism. - Rebreathing: involves inhaling the air that was previously exhaled into a closed system (e.g. a bag). 2. Renal Compensation: Abnormal breathing can change blood pH. the urinary system - can jump into action to help restore pH. It does so by altering the consistency of the urine that it creates. Recall that the intercalated cells of the distal convoluted tubule and collecting duct are able to secrete either H+ or HCO3- into the urine, 3. Metabolic Acidosis/Alkalosis. If the change is caused by a change in metabolism: during metabolism, CO2 is created. So if you increase metabolic rate, for example, CO2 levels rise. how the respiratory system compensates for this by changing respiratory rate.

Q12: What would have happened to urine volume and concentration if you did not add ADH? Explain.

urine volume will increase in the absence of ADH in collecting duct

Q11: What happened to urine volume and concentration as you increased ISF concentration? Explain.

when the solute concentration gradient in ISF is increased, the urine volume will decrease

Q11: In the hypophysectomized rat was there any change in metabolic rate when you injected thyroxine? Explain.

yes increased MR, more thyroxine will increase MR regardless of condition of the rat

Q12: In the hypophysectomizedrat was there any change in metabolic rate when you injected TSH? Explain.

yes increased MR. TSH makes thyroid gland to grow and release TH

Q3: During the Hyperventilation/Normal run, why was there a pause in breathing?

yes the pause was to retain CO2 and restore normal levels (apnea vera)

Q8: In the thryoidectomizedrat was there any change in metabolic rate when you injected thyroxine? Explain.

yes, MR increases. Thyroxine goes to target cells and increase MR. Result in hyperthyroidism b/c hypothalamus and pituitary cannot regulate the increase of thyroxine, no negative feedback

Q7: In the normal rat was there any change in metabolic rate when you injected propylthiouracil? Explain

yes, decreased MR. PTU blocks formation of TH, not producing as much thyroxine reduces MR