GNUR 294 EXAM 3 REVIEW (M14-18)
MODULE 14
PHARMACOTHERAPY OF ENDOCRINE SYSTEM
Diabetes Mellitus
Diabetes – disorder of CHO metabolism
Cells prefer glucose for energy metabolism
Normal BG level 60-100 mg/dL
If high BG (hyperglycemic) pancreas releases insulin cells take up glucose from
blood and liver produces glycogen (remainder of insulin not used is brought to liver,
converted to glycogen and stored) BG falls
If low BG (hypoglycemic) pancreas releases glucagon liver breaks down glycogen
(glycogenolysis) BG rises
Type 1 DM
Autoimmune response triggered by viral infection
Cause – destruction of beta cells with lack of insulin
Symptom onset is rapid (acute) – immune system attacks beta cells of pancreas
o Polyuria
o Polydipsia
o Polyphagia
BG >350
o Acts as osmotic diuretic – very hypertonic
o Pulls fluid from other tissues
o Pt has significant profound diuresis
o Pt becomes hypovolemic
Cells convert metabolism from using glucose for energy to breaking down fatty acids
o Ketones are by-product – highly acidic
o Leads to metabolic acidosis
Treatment – IV insulin, IV fluids
Type 2 DM
Completely preventable
Cause – insulin resistance or insulin deficiency
Intake of too much simple CHO that body does not need for energy metabolism – extra
glucose in blood stream
Pancreas continuously forced to secrete insulin every time person takes in simple CHO
o Causes hyperglycemia
Cells become resistant to insulin constantly trying to push glucose into cell membrane
when it doesn’t need it
Beta cells become exhausted
o Don’t secrete as much insulin as they should
Symptom onset is gradual (chronic)
, o 3 P’s
o Blurred vision
o Fatigue
o Recurrent infections
If BG spikes – presents with hypovolemia and metabolic acidosis BUT no ketones
Treatment – PO (up to 3)
o May also need insulin if not changing lifestyle
Treatment for DM
Type 1 – not preventable, unusual response of immune system
Pt does not really need lifestyle change
Insulin therapy
Type 2 – preventable
Lifestyle changes – diet control, exercise
Oral drug therapy
Insulin – if TLC and drug therapy does not provide glycemic control
Antihypoglycemic Agent
glucagon
Synthetic form of glucagon – released from pancreas in response to hypoglycemia
Hypoglycemia – dangerous because no steady glucose is being supplied to brain
Pen delivery system
Use depends on whether pt is A&O
Insulin Therapy
Exogenous insulin needed due to no endogenous insulin
Drawing insulin in same syringe – “clear before cloudy” to prevent cross contamination
Pt can receive one or combination of insulin
Short-acting:
o human regular insulin
Rapid-acting: “LAG”
o Insulin lispro
o Insulin aspart
o Insulin glulisine
Intermediate-acting:
o isophane insulin
Long-acting:
o Insulin detemir
o Insulin glargine
Endogenous insulin release in the body:
Basal level of insulin – constant low level of insulin in bloodstream released by pancreas
o Takes care of random glucose elevation that occurs
, Bolus insulin – when we eat a meal and food is digested and absorbed into bloodstream,
BG level rises
o Pancreas releases bolus of insulin to drive glucose into cells and send remainder
of unused insulin to liver for storage in form of glycogen
Basal-Bolus – normal insulin production and release
Physical stress situations to our system:
Cortisol (stress hormone) released in response to stress
o Stimulates liver to release glucose into bloodstream for “fight or flight” response
to stress
o BG rises (pt can become hyperglycemic)
For pt with DM who comes into hospital – give short-acting or rapid-acting insulin every
few hours because BG can fluctuate
Insulin Therapy
human regular insulin
Route: SQ, IV (only regular insulin can be given IV)
Onset: SQ: 30-60 min, IV: 15 min
Duration of action: 6-10 hr
Indications:
Monotherapy for Type 1 DM
Combination therapy for Type 2 DM
DKA
HHS
Gestational DM
Mechanism of action: increases cellular uptake of glucose and stimulates storage of glucose as
glycogen
Adverse effects:
Hypoglycemia
Injection site irritation – site should be rotated so scar tissue does not form and cause
problem with absorption
Lipohypertrophy
Weight gain
Hypokalemia
Somogyi phenomenon
Contraindications:
Hypersensitivity to beef or pork
Hypoglycemia
Pregnancy: Category B
Insulin Administration
SQ injection
o Syringe and needle – most common in hospitals
o Pen injectors – easier for at home use
, o Jet injectors – needless burst of build up pressure to push insulin through skin
Inhalation
o Afrezza – increases sore throat and cough
SQ infusion
o Portable insulin pump
o Implanted insulin pump
IV infusion
Insulin Storage
Unopened insulin should be stored in refrigerator
After opening, insulin can be kept up to 1 mos at room temp
Keep out of direct sunlight and extreme heat – makes molecules ineffective
Cannot be frozen
Insulin Adjunct
pramlintide
Synthetic analog of amylin – hormone from beta cells
Used for Type 1 and Type 2 DM who are not controlled by insulin
Acts synergistically with insulin
Reduces gastric emptying
Decrease glucagon
Increase satiety
Cannot be mixed with insulin – administer in different site
PO DM Medications
Works effectively to affect 1 of 3 prongs of DM control:
1) Glucose from diet absorbed into bloodstream
2) Decreased insulin release from pancreas
3) Resistance at cell site to insulin
Sulfonylureas
glyburide
Route: PO
Onset: 15-60 min
Duration of action: up to 24 hr
Indications:
Lower glucose in Type 2 DM
Only after diet and exercise have proven ineffective
Mechanism of action: stimulates release of insulin from pancreas and increases sensitivity of
peripheral tissues to insulin
Adverse effects:
Hypoglycemia
Skin effects – non-allergenic
Blood dyscrasias
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