ANTIHYPERGLYCEMICS o Insulin can also be given

 GDM
 Insulin – by beta cells o During pregnancy only
o Lowers blood glucose o To be discussed in maternal
 Glucagon – by alpha cells
o Increases blood glucose Hyperglycemia
 When do we need glucose?  Increased blood glucose
 Postprandial hyperglycemia – term used for the  s/sx:
increase of blood glucose after eating o fatigue – glucose is in the blood and
 During stressful times: cant be used by the cells
o For production of energy o 3 P’s
o One of the reasons why stress can o Glycosuria = polyuria
induce hyperglycemia / DM.
Tests:
INSULIN  FBS
 Glucose in the blood needs to go inside the cells o Fasting is supposed to lower sugar
to be used as an ingredient to produce energy o Prediabetes can still be corrected
in the form of ATP. through lifestyle change
 Insulin is needed to allow glucose to enter the  Glycated hemoglobin test
cell = decrease of blood glucose o Aka HbA1C
 Insulin stimulates glycogen formation in the o Shows blood sugar control in the past 3-
liver 4 months (saunders)
 Glycogen – stored form of glucose; excess  OGTT
glucose o Oral glucose solution is given to patient
(usually pregnant women to confirm
GLUCAGON GDM)
 Produced by kidney that breaks down glycogen o Usually done as 3-hour glucose
back to glucose. tolerance test
If left unchecked…
Incretin – support ng insulin, increases insulin release  DKA – can occur
Catecholamines – released during stress o Excessive fat breakdown as a source of
 Increases conversion of fats to free fatty acids energy due to lack of cellular glucose
as a source of energy o Ketones are the byproduct of this
 Induces conversion of glycogen to glucose mechanism
Corticosteroids o Too much ketones make blood acidic
 increased glucose output
(ketones are acid)
 Decreased insulin sensitivity
 Symptoms:
o Fruity breath
Diabetes Mellitus
o Kussmaul breathing / respiration – deep
 Type 1:
rapid breathing
o Common in younger
o Coma
o Destruction of beta cells (produces
insulin)
o “juvenile diabetes”
Hypoglycemia
o Insulin is the DOC
 Low blood sugar >40 mg/dl
o Oral drugs are less preferred  Occurs in starvation or overtreatment (insulin
 Type 2: overdose) of hyperglycemia
o Adult onset
o Not enough insulin/ insulin resistance AGENTS:
o Lifestyle induced or acquired type
o OHA are the DOC – stimulates pancreas INSULIN
to produce more insulin  Transports glucose into the cells
  Only given via parenteral route (IV and SQ)
 Non-human source are from pork and beef
pancreas
 Indication
o Type 1 DM
o Type 2 for failed OHA treatment
o For stress – increases blood glucose;
short term
o DKA
o Hyperkalemia – yes po.
 SKL: insulin also transports
potassium inside the cells
 Usually incorporated in glucose
solutions
o no contraindications
 insulin does not cross placenta
 gets destroyed in stomach
when ingested
o adverse effects
 hypoglycemia or DKA
 lipodystrophy – loss of fats on
the injection site
 site in admin is SQ for slow
absorption of insulin
o nursing considerations
 nutrition – health teaching PRN
 gently rotate vial
 keep refrigerated, avoid
sunlight
 rotate sites with distancing
 if IV – use Regular ONLY
 warm insulin before giving
o monitor:
o proper administration:
 measure by units using insulin
syringe
o mixing insulin:
 short acting + long acting
 cloudy and clear insulin
 RN-NR
o health teaching:
 warning signs in relation to its
onset, peak, and duration of
effect
 Types:
o Give importance on peak hours – WOF
hypoglycemia
 Insulin pen
SULFONYLUEREAS
 Stimulates insulin release
 Creates more insulin receptors
 Only for functioning beta cells
 Indications:
o Used with diet and exercise
o Type 2 DM
st
 1 GEN:
o Declining in use
o Causes CV death
nd
 2 GEN:
o Safer for renal dysfunction
o Excreted in urine and bile
o Less interaction and longer duration
Other OHA:
 Unrelated to sulfonylureas
 Effective when combined with insulin or sulfas
Alpha-Glucosidase Inhibitors
 Enzyme that breaks down glucose for
absorption – in the intestine
 Inhibition delays absorption of glucose
 Mild effect
 Causes severe hepatic toxicity and GI distress
Biguanides
 Metformin
 Decreases production, absorption, and uptake
of glucose
 Does not cause hypogly
 Associated with Lactic Acidosis and GI distress
Meglitinides
 Nateglinide & Repaglinide
 Act like sulfonylureas
 Increases insulin release
Synthetic Human Amylin
 Pramlitinide
 By pancreas
o Decreases gastric emptying
o Stops Postprandial glucagon = NO
elevation of blood glucose after meals
o Increased satiety
 Minimal effect in lowering sugar
 Not used for pt unable to eat – eating problems
 In combi with insulin
Incretin Mimetics
 Exenatide & Liraglutide
 Mimics incretin (GLP1) – increases insulin
release
DPP4 inhibitors
 Lina-, saxa-, sitagliptine
 DPP4 – inhibits GLP1 to avoid hypogly by
inhibiting insulin release