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310 Midterm 3

Pharmacology science that deals with the fate of drugs in the body and their actions on the body
drug any substance, other than what's found in the body or required by the body, that changes a physiological response
controlled by DEA, schedule I to IV
therapeutic prescription
problem with herbal extracts extracts are uncontrolled, but as soon as the active chemical is isolated, it is classified as a drug and becomes controlled
pharmacodynamics study of actions of drugs on the body
pharmacokinetics quantitative description of drug disposition
drug disposition absorption, distribution, elimination
drug disposition curve graph to show drug disposition
fate of a drug absorbed, distributed, eliminated
routes of drug administration enteral, parenteral
enteral vs. parenteral enteral: through alimentary canal parenteral: everywhere else
venous samplings/vein sticks sample of blood to see drug disposition
extra label drug use using a drug other than how it is indicated on the label
capillary barriers continuous, fenestrated, or discontinuous
blood brain barrier layer of lipophilic cells surrounding capillaries
fat stores of the body store drugs
hydrophilic vs. lipophilic water-loving vs. fat-loving
free vs. bound in blood bound to albumin, free drugs get absorbed quicker
biotransformed way in which drug gets eliminated
specific receptors/target cells some drugs have specific cells that they target
site of action where the drug takes effect
receptor pull/affinity receptors have affinity to drug, pull out even if bound in blood
drug eliminated in general, 10 half lives and a drug is considered eliminated
first pass effect first time the blood passes through the liver, 100% of it is broken down
therapeutic objective how quickly you want the drug to work vs. route of administration
drug conjugation bound to a sugar molecule
half-life amount of time it takes for 1/2 the drug to be broken down
quality assurance issues in food animals, quality of meat
quantitative vs. qualitative dose-response curves quantitative: numerical measurements qualitative: yes/no response
potency how much of a drug is needed to get the desired response
equipotent doses amounts of drugs needed to achieve same response
effective dose 50 effective dose in which 50% of the population responds
TD50 toxic dose, 50% of population gets sick
therapeutic index TD50/ED50
LD50 lethal dose, 50% of population dies
AD50 anesthetic dose, 50% of population goes under anesthesia
choice of route therapeutic objective, physical properties of drug, lipophilic/hydrophilic, quality assurance issues, cost
kidney excretion, regulation, endocrine
adrenal gland/supra adrenals secrete hormones
hilus ureter/renal artery/renal vein enter into kidney
micturition urination
sphincter holds bladder closed
metanephric nephron anatomy tubular part, blood vessels
glomerulus first capillary bed
PTC peritubular capillary/second capillary bed
descending limb thin walled
ascending limb thick walled upper portion, thin walled lower portion
loop of Henle allows last 20-40% of water to not be lost in urine
DCT where aldosterone works, can pump so much sodium that osmotically it can become more dilute than normal interstitium
collecting duct receives the urine from many distal tubules
Bowman's capsule filters/cleans the plasma
blood supply 20-25% goes to kidney
vasa recta 1-2% of PTC bed that forms a loop around the loop of Henle
portal system high filtration rate, high absorptive/reabsorptive pressure in PTC bed
renal corpuscle glomerulus + Bowman's capsule
glomerulus and filtration filters and cleans plasma, 20-25% filtered out into Bowman's capsule
proximal tubule active transport of toxins directly into urine from PTC, reabsorption
aldosterone steroid hormone from adrenal cortex, mineral corticoid
osmolarity/milliosmole saltiness of blood
cortical vs. juxtamedullary nephrons cortical: short loop of Henle, completely within cortex juxtamedullary: long loop of Henle
ammonia/urea/uric acid waste products
salt gland concentration of salt out of it is greater than sea water, found in sea birds
control of blood volume if blood volume is too high, urine volume increases to compensate and vice versa
juxtaglomerular apparatus source of renin
juxtaglomerular cells macula densa cells
macula densa monitor monitor if kidney isn't filtering enough blood and if the osmolarity of blood is correct
glomerular filtration rate how much fluid is filtered out of glomerulus into Bowman's capsule
renin-angiotensin system renin converts angiotensinogen into angiotensin
ACE angiotensin converting enzyme
angiotensinogen always in blood, made by liver
angiotensin circulation, vasoconstriction, renal blood flow increases, constriction of efferent artery, increase in glomerular filtration
angiotensin activator activates angiotensin
systemic vasoconstriction entire body experiences vasoconstriction
GFR homeostasis/disturbance/recovery disturbance: GFR goes down, renin released, angiotensin activated, BP and BV increase recovery: restored homeostasis, GFR increases
aldosterone/mineral corticoid steroid hormone from adrenal cortex
adrenal cortex outer portion of adrenal gland
zona glomerulosa outer layer of adrenal cortex, makes aldosterone
sodium reabsorption reabsorbed in proximal tubule
blood-born enters into circulatory system from endocrine system
diuresis excessive urination
high blood pressure vasoconstriction
ADH decreases urine volume, affects collecting duct of nephrons, allows for very concentrated urine
hypothalamus/posterior pituitary hormones made in the hypothalamus travel down and are released from the posterior pituitary
range of urine osmolarities dependent upon thirst and water intake
hypovolemic vs. osmotic thirst hypovolemic: loss of blood volume osmotic: high osmolarity
body water balance drinking and eating provide water, kidney conserves water so output=intake
endocrine functions maintain homeostasis, support cell growth, coordinate development/reproduction, facilitate responses to external stimuli
paracrine stimulates neighboring cells
autocrine stimulates self only
exocrine stimulates cells far away
endocrine/ductless glands invading epithelia become a deep gland or get isolated/pinched off
hormone a chemical made in one part of the body that becomes blood born, travels to another part of the body to affect a target cell
receptor/target cell has receptors for hormone
hypothalamus controls pituitary gland
stalk connects hypothalamus and pituitary
Rathke's pouch outgrowth of base of brain, forms posterior pituitary
posterior pituitary/neurohypophysis releases hormones made in hypothalamus
anterior pituitary/adenohypophysis outgrowth of roof of mouth, portal system between it and hypothalamus, produces hormones to be released into body
growth hormone releasing hormone stimulates release of growth hormone
growth hormone/GH/somatotrophin causes fat to be broken down
IGF-1/somatomedin bone growth, muscle development
somatostatin polypeptide
bST vs. hGH bovine vs. human growth hormone
gigantism too much growth hormone released
controlling hormones/factors control amount of initial stimulant produced
thyroid composed of epithelial cells, 2 lobes, made of fluid filled follicles, releases T3 and T4
isthmus connects two lobes of thyroid
left and right lobe located on either side of trachea
thyroglobulin huge protein that stores MIT and DIT and when epithelia lining follicle get stimulated, thyroglobulin gets internalized and then metabolizes into T3 and T4
colloid fluid filling follicles
follicle small sac or vesicle, filled with fluid
MIT monoiodotyrosine
DIT diiodotyrosine
triiodothyronine T3, MIT + DIT
tetraiodothyronine T4, DIT + DIT
TRH thyrotropin releasing hormone, released by hypothalamus, stimulates release of TSH by anterior pituitary
TSH thyroid stimulating hormone, released by ant. pit., stimulates thyroid to release T3 and T4
metabolic hormones T3, T4
hypothalamo-pituitary-organ axis step-by-step process, end product = feedback
effect of T3 and T4 negative feedback on hypothalamus (causes it to release less TRH)
hypo/hyperthyroidism hypo: underactive thyroid hyper: overactive thyroid
Grave's disease autoimmune disorder, most common cause of hyperthyroidism
myxedema swelling of the skin, caused by hypothyroidism
goiter hypothyroidism, swelling of thyroid and neck, low iodine in diet
goitrogens drugs or feed that interferes with thyroxin production
exopthalamos hyperthyroidism
feedback negative causes less activity, positive causes more
parathyroid/PTH released when calcium in blood is low
effect of PTH calcium is reabsorbed into kidney, calcium comes out of bone and into blood, kidney activates vitamin D
vitamin D activation caused by parathyroid hormone when Ca in blood is too low to help absorb Ca from intestine
kidney concentrates urine
C-cells/parafollicular cells make calcitonin, controlled by Ca in blood, oppose PTH, released when Ca in blood is too high
calcitonin released from C-cells
CRH corticotrophic releasing hormone made by hypothalamus, causes production of ACTH
ACTH released by anterior pituitary, goes to adrenal cortex and stimulates production of cortisol
glucocorticoid steroid from adrenal cortex affecting glucose
cortisol most common adrenal steroid, anti-inflammatory, stress hormone, inhibits fertility, stimulates fetal lung maturation, increase glucose levels in blood, induces parturition
corticosterone/cortisone adrenal steroids
pancreatic islets/Islets of Langerhans endocrine portion of pancreas, secrete alpha and beta cells
alpha/beta cells alpha: secrete glucagon beta: secrete insulin work opposite each other
glucagon acts on liver to stimulate glucose production and release, causes fat breakdown, rises when glucose falls
insulin necessary for sugar to get inside a cell, allows body cells to take in circulating glucose, works opposite glucagon
control of insulin released in response to high blood glucose levels
diabetes inability to bind glucose
hypo/hyperglycemia hypo: lack of glucose hyper: too much glucose, leads to hyperosmolarity
ketotic/ketosis decreased blood pH
peripheral circulation/capillary health diabetics have decreased peripheral circulation because endothelial cells surrounding capillaries cannot function
A1C glycosylated hemoglobin (hemoglobin with sugar molecules attached)
Created by: hbrandt



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