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GNUR 294 FINAL EXAM- Pharmacotherapy of Edocrine System / GNUR294 FINAL EXAM- Pharmacotherapy of Edocrine System:NEWEST-2022

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GNUR 294 FINAL EXAM- Pharmacotherapy of Edocrine System / GNUR294 FINAL EXAM- Pharmacotherapy of Edocrine System:NEWEST-2022GNUR 294 FINAL EXAM- Pharmacotherapy of Edocrine System / GNUR294 FINAL EXAM- Pharmacotherapy of Edocrine System:NEWEST-2022GNUR 294 FINAL EXAM- Pharmacotherapy of Edocrine System / GNUR294 FINAL EXAM- Pharmacotherapy of Edocrine System:NEWEST-2022

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GNUR 294 FINAL EXAM

Pharmacotherapy of the Endocrine System: Diabetes & Thyroid Disorders
 In terms of a patient with diabetes we know that it’s a disorder of normal carbohydrate
metabolism
 Cells rely on glucose for ATP and energy production
 Two organs that keep glucose levels within normal range
 Pancreas and liver
 Beta cell produces-insulin
 Alpha- glucagon
 Drives the glucose from the bloodstream into the cells to use and then rest goes to liver to be
stored as glycogen
 60-100 mg/dL
 If there’s an issue we may see some abnormalities
 Pancreas has impaired insulin secretion, too much glucose absorbed
 The cells decrease their uptake of glucose because they become resistant
 Type I diabetes is an absolute lack of insulin
 Problem organ is pancreas
 Beta cells become destroyed
 Not 100% sure why this happens
 Probably a combination of genetics, some autoimmune process, and maybe environmental
exposure, all together in destruction
 Glucose cannot get into cells for metabolism, the cells use fatty acids and proteins break
those down, and use that instead of energy and results in substance called a ketone which is
acidotic, the patient also has to have exogenous insulin administered to them
 5-10% of the population
 Type II much more common 90-95% population
 Completely preventable
 More chronic process, chronic increase of glucose in the bloodstream from increased
carbohydrates in diet and decreased activity to reduce those glucose levels, the pancreas is
consistently stimulated to release insulin in order to get that glucose crossing through the
cell membrane to be used for cell metabolism
 After awhile, the cells become used to it and do not respond (insulin resistance)
 If goes untreated the beta cells of the pancreas being to become exhausted and stop
producing as much insulin as they should
 Two Problems:
o 1. Insulin resistance
o 2. Decrease insulin production
 Will result in cells not getting enough glucose
 Aimed at reducing chronic elevated glucose levels
 Have to reduce glucose levels
 Elevated glucose levels >250 to 300, when you have those levels elevated acutely, it acts as
an osmotic diuretic, causes a massive diuresis- becomes dehydrated
 Dehydration is going to cause a problem with perfusion to the tissues
 Long term causes damage to many organs: macro and micro vascular disease, damage to the
nephrons, kidney failure, problems with tissue perfusion (poor wound healing, visions
abnormalities
 Need to have those glucoses in control
 Type 1- just need exogenous insulin, they don’t have endogenous insulin
 Type 2- lifestyle changes (most important initially), exercise, if that fails than oral drug
therapy would be the next level of treatment. When insulin is no longer produced when
needed then insulin will be needed
 DKA
o Disorder that only happens with Type I

, o If there’s not enough insulin and not enough glucose getting into cell then break
down of fatty acids and then produces ketones. Also diuresis
o Become hypovolemic, and acidotic
o Ketones have fruity smell to them, smells like juicy fruit gum
o RR- become deeper and frequent because trying to adjust acid balance by getting rid
of CO2
o Tachycardia- becomes BP dropped, HR stimulated to increases CO
o Lots of urine, white looking
o Treatment: IV fluids and IV insulin, cannot give them sucrose because not sure of the
absorption on the SQ
 Hypoglycemia
o Situation where patient who is being treat by hyperglycemia is over treated
o 3 different perspectives: taking medication to lower glucose but don’t enough food
that day to keep glucose in normal range, too much insulin, or exercising too much.
One or all three can occur
o Anxious, sweaty, hungry, tachycardia, cool, clammy skin, glucose levels need to be
increased
 Antihpyoglcemia Agent
o Patient who for some reason becomes hypoglycemia
o Comes in an injectable format (IM,IV, SQ)
o Glucagon will be fast acting
o If in the hospital, they will get D50W hanging in an IV
o D50W- giving IV don’t give glucagon because way more expensive
o Glucagon- will already be drawn up in the exact amount, and can given an
emergency
 Insulin Therapy
o When we think about insulin therapy, have to think about keeping glucose levels at
60-100 range in our bloodstream, our bodies normally do that having basal levels
secreted by the pancreas all the time, very low level always in bloodstream, also a
bolus form every time we eat something
o A basal bolus process is what we normally in our body
o If they require insulin they will be prescribed the body the same way
o Short, rapid, long constant long (basal), intermediate acting
o Based on what is going on with that patient acutely in the hospital and chronically
when they get discharged
o We know that cortisol is released when we are stressed, also increased glucose
levels.
o When in the hospital they may be under some type of stress, glucose levels are going
to be higher when they are hospitalized versus when they are at home when they
have chronic insulin therapy
o Should know: about when they start to act, and there duration of action because also
worried about hypoglycemia, person system is in some type of uproar and don’t
want to give them something that will lower their glucose levels too low
o Insulin can only be given through parenteral route
o Destroyed by the acidity in the GI tract
o All forms of insulin can be given SQ but only regular insulin can be given IV
o i.e. in DKA can only get regular insulin
o BE AWARE OF ONSET AND DOA
o Rapid acting going to see hypoglycemia way sooner
o Type I- has the potential for DKA when there isn’t enough insulin in the bloodstream
o Type II- the patient may have a situation called hyperglycemic hyperosmolar
syndrome, no acidosis, just treated with IV insulin and IV fluids
o Injection site- must rotate the site because it might get irritated
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