front 1 ACTIVITY 1:
| back 1 THE NORMAL RAT HAD THE FASTEST BASELINE METABOLIC RATE. |
front 2 ACTIVITY 1:
| back 2 THE THYROIDECTOMIZED RATS BMR WAS SLOWER THEN THE NORMAL RAT. THE HORMONE OF THE THYROID GLAND HELPS MAINTAIN METABOLISM AND BODY HEAT SINCE THE THYROID GLAND IS REMOVED THE RAT COULDNT DO THAT AND ITS BMR WAS SLOWER. |
front 3 ACTIVITY 1:
| back 3 THE HYPOPHYSECTOMIZED RATS BMR WAS SLOWER THEN THE NORMAL RAT. THIS SI BECAUSE THE PITUITARY GLAND HAS BEEN REMOVED. PITUITARY GLAND SECRETES TSH THAT CONTROLS PRODUCTION AND RELEASE OF THYROXINE, WITHOUT IT THE METABOLIC RATE IS EFFECTED AND IS SLOWER. |
front 4 ACTIVITY 2:
| back 4 THE THYROXINE MADE THE RATS METABOLIC RATES VERY CLOSELY SIMILIAR. THE EFFECTS OF THE THYROXINE INCREASED THE METABOLIC RATES OF EACH RAT COMPARED TO ACTIVITY 1. |
front 5 Ok, so you’re using my notecards which is great. I am glad I could help you out cause I wish I had someone to help me out when I took this course. I know Anatomy is super hard. | back 5 I only ask that if you find these notecards helpful, you join Easy Notecards and create at least one notecard set to help others out. It can be for any subject or class. Thanks and don’t forget to rate my helpfulness! |
front 6 ACTIVITY 2:
| back 6 THYROXINE IS THE MOST IMPORTANT HORMONE IN MAINTAINING METABOLISM AND BODY HEAT. |
front 7 ACTIVITY 3:
| back 7 IT INCREASED BUT HARDLY AT ALL. IF THE RAT HAS NO THYROID THE TSH IS NOT GOING TO STIMULATE ANYTHING, SO THYROXINE WONT BE RELEASED AND THERE WAS HARDLY NO CHANGE. |
front 8 ACTIVITY 3:
| back 8 IT INDICATED HYPOTHYROIDISM |
front 9 ACTIVITY 4:
| back 9 THE EFFECT OF PROPYLTHIOURACIL ON THE RATS MADE THE METABOLIC RATES REMAIN LOW. THIS IS BECAUSE PROPYLTHIOURACIL INHIBITS THYROXINE. SO THYROXINE IS NOT STIMULATED IN ANY RAT AND THE RATS THEREFORE CAN NOT MAINTAIN METABOLISM AND BODY HEAT MAKING NO CHANGE IN THE RATES. |
front 10 ACTIVITY 4:
| back 10 IT IS USED TO TREAT HYPERTHYROIDISM. SINCE IT INHIBITS THYROXINE IT CAN BE USED TO CONTROL THYROID PRODUCTION OF THYROXINE, AND FURTHER CONTROL HYPERTHYROIDISM. |
front 11 ACTIVITY 5:
| back 11 THREE OVARIECTOMIZED RATS WERE USED BECASUE THEY ARE NO LONGER PRODUCING ESTROGEN DUE TO THE REMOVAL OF THEIR OVARIES. BECAUSE ESTROGEN IS NOT BEING PRODUCED MENOPAUSE STARTED AND THE RESULT WAS OSTEOPOROSIS WITH THE BASELINE T SCORE AT -2.6 |
front 12 ACTIVITY 5:
| back 12 I PREDICTED THAT THEY WOULD BOTH IMPROVE THE BONE DENSITY. BECAUSE ADMINISTRATING ESTROGEN OR CALCITONIN ARE FORMS OF HORMONE REPLACEMENT THERAPY. ESTROGEN WILL INCREASE BONE DENSITY AND CALCITONIN WILL INHIBIT OSTEOCLAST ACTIVITY AND STIMULATE CALCIUM UPTAKE FOR DEPOSIT IN BONE. |
front 13 ACTIVITY 5:
| back 13 THIS IS THE CONTROLLED PORTION OF THE EXPERIMENT SINCE SALINE IS JUST SALT AND WATER IT WOULDN'T CASE ANY AFFECT ON THE RAT. |
front 14 ACTIVITY 5:
| back 14 IT IMPROVED BONE DENSITY FROM -2.6 OSTEOPOROSIS TO -1.9 OSTEOPENIA. |
front 15 ACTIVITY 5:
| back 15 IT IMPROVED BONE DENSITY FROM -2.6 OSTEOPOROSIS TO -2.47 OSTEOPENIA; ALTHOUGH IT WAS NOT A BIG DIFFERENCE THE LEVELS IN CLASSIFICATION ARE DIFFERENT. |
front 16 ACTIVITY 5:
| back 16 MY PREDICTIONS WERE RIGHT, ALTHOUGH I THOUGHT THERE WOULD BE A GREATER IMPROVEMENT. |
front 17 ACTIVITY 6:
| back 17 THE GLUCOSE STANDARD CURVE GIVES THE POINT OF REFERENCE FOR CONVERTING OPTICAL DENSITY READINGS. YOU CAN USE THIS TOOL TO DETERMINE THE CONCENTRATION OF GLUCOSE BY USING A SPECTROPHOTOMETER TO DETERMINE HOW MUCH GLUCOSE IS PRESENT IN A BLOOD SAMPLE. |
front 18 ACTIVITY 7:
| back 18 PATIENT 1 (TUBE 1) HAD A READING OF 101MG/DL, WAY BELOW 110 MG/DL SO IT FALLS IN THE NORMAL RANGE. |
front 19 ACTIVITY 7:
| back 19 PATIENTS 3 AND 5 HAD GLUCOSE READING IN THE DIABETIC RANGE. |
front 20 ACTIVITY 7:
| back 20 PATIENTS 2 AND 4 HAD GLUCOSE READINGS IN THE IMPAIRED OR BORDERLINE IMPARIMENT RANGE. |
front 21 ACTIVITY 7:
| back 21 TYPE 2 DIABETES MELLITUS - GLUCOSE REMAINS IN BLOODSTREAM UNABLE TO BE TAKEN UP BY THE BODY'S CELLS TO SERVE AS THE PRIMARY FUEL FOR METABOLISM. |
front 22 ACTIVITY 8:
| back 22 PATIENT 3; BECAUSE HYPERCORTISOLISM CAUSED BY A PITUITARY TUMOR ALSO CAUSES LEVELS OF ACTH TO INCREASE, THIS PATIENT HAS BOTH THESE LEVELS HIGH SO IS MORE THEN LIKELY TO HAVE CUSHING'S DISEASE. |
front 23 ACTIVITY 8:
| back 23 PATIENT 2 AND 5 HAVE HORMONE LEVELS THAT ARE SIMILAR TO THOSE OF CUSHING'S SYNDROME. |
front 24 ACTIVITY 8:
| back 24 ITS NOT CUSHING'S SYNDROME IF ITS IATROGENIC (PHYSICIAN INDUCED). THE PATIENT DOES NOT NORMALLY HAVE CUSHING'S SYNDROME AND ITS PURPOSELY POSSIBLY A TEMPORARY TREATMENT THAT WHEN IT STOPS BEING INDUCED MIGHT BE CORRECTED AGAIN. |
front 25 ACTIVITY 8:
| back 25 PATIENT 4 WOULD MOST LIKELY BE DIAGNOSED WITH ADDISON'S DISEASE. THE PATIENT HAS LOW CORTISOL BUT ACTH LEVELS WERE HIGH. IN THIS DISEASE THE LOW CORTISOL IS DIRECTLY DUE TO GRADUAL DESTRUCTION OF THE ADRENAL CORTEX, AND ACTH LEVELS ARE TYPICALLY ELEVATED AS A COMPENSATORY EFFECT. |