THE NORMAL RAT HAD THE FASTEST BASELINE METABOLIC RATE.

ACTIVITY 1:
WHICH RAT HAD THE HASTEST BASELINE METABOLIC RATE?

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.

ACTIVITY 1:
COMPARE THE BASELINE METABOLIC RATES FOR THE THYROIDECTOMIZED RAT AND THE MORNAL RAT AND EXPLAIN YOUR RESULTS.

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.

ACTIVITY 1:
COMPARE THE BASELINE METABOLIC RATES FOR THE HYPOPHYSECTOMIZED RAT AND THE NORMAL RATAND EXPLAIN YOUR RESULTS.

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.

ACTIVITY 2:
WHAT EFFECT DID ADMINISTERING THYROXINE HAVE ON EACH OF THE RATS?

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THYROXINE IS THE MOST IMPORTANT HORMONE IN MAINTAINING METABOLISM AND BODY HEAT.

ACTIVITY 2:
EXPLAIN WHY THYROXINE HAD THESE EFFECTS.

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.

ACTIVITY 3:
WAS THERE A CHANGE IN THE METABOLIC RATE OF THE THYROIDECTOMIZED RAT WITH THE ADMINISTRATION OF TSH? EXPLAIN YOUR RESULTS.

IT INDICATED HYPOTHYROIDISM

ACTIVITY 3:
DID THE RESULTS OR THE THYROIDECTOMIZED RAT INDICATE HYPERTHYROIDISM OR HYPOTHYROIDISM?

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.

ACTIVITY 4:
DESCRIBE THE EFFECT OF ADMINISTERING PROPYLTHIOURACIL ON EACH OF THE RATS, AND EXPLAIN WHY IT HAD THIS EFFECT.

IT IS USED TO TREAT HYPERTHYROIDISM. SINCE IT INHIBITS THYROXINE IT CAN BE USED TO CONTROL THYROID PRODUCTION OF THYROXINE, AND FURTHER CONTROL HYPERTHYROIDISM.

ACTIVITY 4:
DO YOU THINK THE DRUG PROPYLTHIOURACIL IS USED TO TREAT HYPOTHYROIDISM OR HYPERTHYROIDISM? EXPLAIN YOUR ANSWER.

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

ACTIVITY 5:
EXPLAIN WHY OVARIECTOMIZED RATS WERE USED IN THIS EXPERIMENT AND CORRELATE THIS TO THEIR BASELINE T SCORE.

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.

ACTIVITY 5:
RECAP YOUR PREDICTIONS REGARDING THE EFFECTS OF CALCITONIN AND ESTROGEN ON BONE DENSITY AND EXPLAIN WHY YOU MADE THOSE PREDICTIONS.

THIS IS THE CONTROLLED PORTION OF THE EXPERIMENT SINCE SALINE IS JUST SALT AND WATER IT WOULDN'T CASE ANY AFFECT ON THE RAT.

ACTIVITY 5:
WHY WAS ONE OF THE OVERIECTOMIZED RATS INJECTED WITH SALINE?

IT IMPROVED BONE DENSITY FROM -2.6 OSTEOPOROSIS TO -1.9 OSTEOPENIA.

ACTIVITY 5:
WHAT EFFECT DID THE ADMINISTRATION OF ESTROGEN INJECTIONS HAVE ON THE ESTROGEN-TREATED RAT?

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.

ACTIVITY 5:
WHAT EFFECT DID THE ADMINISTRATION OF CALCITONIN INJECTIONS HAVE ON THE CALCITONIN-TREATED RATS?

MY PREDICTIONS WERE RIGHT, ALTHOUGH I THOUGHT THERE WOULD BE A GREATER IMPROVEMENT.

ACTIVITY 5:
HOW DID YOUR RESULTS COMPARE TO YOUR PREDICTIONS?

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.

ACTIVITY 6:
WHAT IS A GLUCOSE STANDARD CURVE AND HOW CAN YOU USE THIS TOOL TO DETERMINE A CONCENTRATION OF GLUCOSE?

PATIENT 1 (TUBE 1) HAD A READING OF 101MG/DL, WAY BELOW 110 MG/DL SO IT FALLS IN THE NORMAL RANGE.

ACTIVITY 7:
WHICH PATIENT(S) HAD GLUCOSE READING(S) IN THE NORMAL RANGE?

PATIENTS 3 AND 5 HAD GLUCOSE READING IN THE DIABETIC RANGE.

ACTIVITY 7:
WHICH PATIENT(S) HAD GLUCOSE READING(S) IN THE DIABETIC RANGE?

PATIENTS 2 AND 4 HAD GLUCOSE READINGS IN THE IMPAIRED OR BORDERLINE IMPARIMENT RANGE.

ACTIVITY 7:
WHICH PATIENT(S) HAD GLUCOSE READING(S) IN THE IMPAIRED RANGE?

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.

ACTIVITY 7:
DESCRIBE THE DIAGNOSIS FOR PATIENT 3.

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.

ACTIVITY 8:
WHICH PATIENT WOULD MOST LIKELY BE DIAGNOSED WITH CUSHING'S DISEASE? WHY?

PATIENT 2 AND 5 HAVE HORMONE LEVELS THAT ARE SIMILAR TO THOSE OF CUSHING'S SYNDROME.

ACTIVITY 8:
WHICH TWO PATIENT'S HAVE HORMONE LEVELS CHARACTERISTIC OF CUSHING'S SYNDROME?

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.

ACTIVITY 8:
PATIENT 2 IS BEING TREATED FOR RHEUMATOID ARTHRITIS WITH PREDNISONE. HOW DOES THIS CHANGE THE DIAGNOSIS?

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.

ACTIVITY 8:
WHICH PATIENT WOULD MOST LIKELY BE DIAGNOSED WITH ADDISON'S DISEASE? WHY?