chapter 22.docx

5 Pages
119 Views
Unlock Document

Department
Biochem. and Medical Genetics
Course
BGEN 3020
Professor
Jason Leboe- Mcgowan
Semester
Fall

Description
Chapter 22 Fat soluble vitamins: 1. Vitamin A a. Function: Is very imp in children for growth and can have failure to thrive in vit A def. Very important in iodopsin/rhodopsin within the eye and the first sign of vit A def is night blindness which is called nictolopia. Vit A also prevents sq metaplasia. b. Example of Vit A def: eye with sq metaplasia, goose bumps on back of arm called follicular hyperkeratois. Eye is lined with cuboidal epithelium; when you get sq metaplasia, will get white spots on the eye. If become extensive, grow over eye, and can lead to softening of the cornea (keratomalacia), and leads to blindness. 2 MCC blindness globally = vit A def. MCC blindness globally = trachoma; MCC blindness in USA = diabetes. Therefore, vit A will prevent sq metaplasia, if you are Vit A deficient and a nonsmoker, a person can end up with sq metaplasia in mainstem bronchus and bronchogenic carcinoma. c. Toxicity: Hypervitaminosis A – ex. big game hunter that eats bear liver and has headaches. Increased vit A causes cerebral edema, also get papilloedema (which causes the headache), can alsp lead to herniation and death. There is also an increase of retinoic acid (used from treating acne and acute progranulocytic anemia). The retinoic acid toxicity can lead to severe liver toxicity. Therefore, hypervitaminosis of vit A affects 2 areas: 1) cerebral edema (brain) 2) liver. Example: if have young lady pt on retinoic acid for acne, need to check liver enzymes and ask for headaches (can be developing papilloedema or cerebral edema related to vit A toxicity). Massive amount of vit A in bear livers, and hunter dies with massive headaches or liver failure Vitamin D = VERY imp on the boards; MC source of vit D is from sunlight. a. Cholesterol is the 1. Main component of our cell membranes 2. Starting point for making bile salts and bile acids 3. First compound that starts the synthesis of steroid hormones in the adrenal cortex 4. And the 7-dehydrocholesterol in the skin is photoconverted to vitamin D. Therefore we need cholesterol! (makes bile salts, hormones, cell membranes, and vit D). b. Source: Sun is the most imp source of vit D. take baby out to expose to sunlight (no vit D or vit K in breast milk, therefore must be supplemented – expose to sun for vit D). c. Synthesis of Vitamin D: Reabsorbed in the jejunum. Undergoes 2 hydroxylation steps; first is in the liver, where it is 25 hydroxylated and the 2 is in the kidney and its 1 alpha hydroxylase. What hormone puts 1-alpha hydroxylase in the proximal tubule? PTH. PTH is responsible for synthesis of 1-a-hydroxylase and is synthesized in the proximal tubule. (ACE is from the endothelial cells of the pulmonary capillary, EPO is from the endothelial cells of the peritubular capillary). 1-a-hydroxylase is the 2 hydroxylation step, and now it is active (the first was in the kidney). d. Vit D function: reabsorb Ca and phosphorus from the jejunum. It HAS to reabsorb both of these, b/c its main job is mineralizing bone and cartilage. Have to have appropriate solubility product to be able to do that; Ca and phosphorus are necessary to mineralize cartilage and bone (like the osteoid making bone). Therefore, it makes sense to reabsorb Ca and phosphorus b/c it needs to make sure that both of them are present in adequate amounts to have an adequate solubility product to mineralize bone. e. Parathyroid Hormone (PTH) – Functions: (1)is somewhat related to Vitamin D metabolism, it helps last step for hydroxylation of vit D syn. (2) PTH will lead to reabsorption of Ca in the early distal tubule (this is also where Na is reabsorbed, and thiazides block this channel). At that location, there is a Ca channel; PTH helps reabsorption of the Ca in this location. Ca has to ‘take turns’ with Na, usually more Na, reabsorbed; therefore Ca has to sneak through channel, with help of PTH. Therefore, with thiazides, Na is blocked, leaving the Ca channel completely open, and the thiazides will lead to hypercalcemia. Therefore, use in Ca stone formers – most of stone formers have hypercalciurea; these pts have too much Ca in their urine; when they are on thiazides, the drug takes Ca OUT of the urine, so they do not form stones. (3) PTH will decrease reabsorption of phosphorus in the prox tubule, and (4) decrease the reaccumulation of bicarb, too. f. Vitamin D and PTH and how they work together: Vit D’s main function is mineralizing bone, and osteoblasts (bone builders) are involved with this process, therefore the receptor for Vit D is located on the osteoblast. When vit D hooks into the receptor, it causes the release of alkaline phosphatase. So, when you are growing bone or rehealing of a fracture, you expect to see an increase in alkaline phosphatase, which makes the appropriate solubility product to mineralized cartilage and bone. Knowing that PTH breaks down bone (maintains Ca levels in the blood stream) you would think that its receptor would be on the osteoclast (cell normally breaks bone down). However, only one hormone has a receptor on ostoeclasts and that is calcitonin. When calcitonin hooks into the osteoclast receptor, it inhibits the osteoclast, and therefore is used to treat hypercalcemia. Calcitonin also used in treating osteoporosis. The receptor for PTH is on the osteoblast, but not sharing the same one as vit D. When PTH hooks on the osteoblast, it releases IL-1. Another name for IL-1 is osteoclast activating factor (other functions of IL-1 are also involved in fever, stimulates Ab synthesis, and B cell stimulation). So, IL-1 (released from the osteoblast) activates osteoclasts via IL-1 release from osteoblast, and osteoclast is signaled to break down bone to maintain Ca levels in our bloodstream. Sex hormones keep IL-1 in check; in women, estrogen levels keep a check on IL-1 (do not want too much osteoclast activation); in men, it is testosterone that keeps IL-1 in check (puts inhibitory effect on IL-1 release from the osteoblast after PTH hooks in). Therefore, in women, can see why they get osteoporosis – lack of estrogen = IL-1 not in check and breaking more bone down than making (this is the mechanism of postmenopausal osteoporosis). PTH is more involved in maintaining Ca levels in our blood, while Vit D is more involved in mineralizing our bones and cartilage. g. Vitamin D deficiency: Many reasons: lack of sun, poor diet, liver dz, renal dz. Example: Pt on phenytoin and pt has hypocalcemia, why? Phenytoin, alcohol, barb’s, rifampin all induce the cyt p450 system located in the SER. Therefore, get SER hyperplasia; therefore, you metabolize drugs and other things made in the liver, including 25- hydroxyvitamin D. Therefore, anything that rev’s up the p450 enzymes will cause a decrease in vit D, and any other drugs being taken. Example: woman on birth control pills and taking phenytoin, and she got pregnant, why? The phenytoin rev’ed up the p450 system, which i
More Less

Related notes for BGEN 3020

Log In


OR

Join OneClass

Access over 10 million pages of study
documents for 1.3 million courses.

Sign up

Join to view


OR

By registering, I agree to the Terms and Privacy Policies
Already have an account?
Just a few more details

So we can recommend you notes for your school.

Reset Password

Please enter below the email address you registered with and we will send you a link to reset your password.

Add your courses

Get notes from the top students in your class.


Submit