PHARM WEEK 7 - DIABETES

type I diabetes

autoimmune destruction of beta cells so little to no insulin is being produced

REQUIRES INSULIN TO SURVIVE

type II diabetes

insulin resistance, beta cells are working overtime to compensate

• overtime, insulin production declines

beta cells produce

insulin

alpha cells produce

glucagon

what are the main cell types of the pancreas

alpha cells and beta cells

blood sugar is too high —>

insulin brings it down

blood sugar is too low —>

glucagon brings it up

what is the paradox in diabetes

there is lots of glucose in the blood BUT the body acts like its starving

why? the glucose cannot get into the cells by themselves, they need insulin as the key to unlock the door and so no insulin = no key = cells cant open the door → glucose sits in the bloodstream → cells get zero fuel and starve

how does the liver come into play with making hyperglycemia in diabetic patients worse

the liver panics and thinks the body is starving → liver produces more glucose → dumps it into the bloodstream → hyperglycemia gets even worse

signs of hyperglycemia

• polydipsia (triggered from the polyuria, fluid loss triggers thirst signal)

• polyphagia (the starving cells trigger hunger signal)

• polyuria (so much glucose is in the bloodstream it “spills” into the urine, glucose in the urine pulls water with it → too much glucose overwhelming the kidney)

effect of chronic hyperglycemia

glycation → vessel walls thicken and stiffen → blood cant flow properly → tissue ischemia

glycation

the sugar coats and damages blood vessel walls

what are the two types of vessel damage with chronic hyperglycemia

1. microvascular disease

2. macrovascular disease

microvascular disease

SMALL PIPES (the capillaries)

• these tiny vessels are what supply blood to delicate structures like the eyes, kidneys, and nerves

→ when small vessels are damaged, those specific organs lose blood supply

results of microvascular disease

• retinopathy

• nephropathy

• neuropathy

macrovascular disease

LARGE PIPES/ ATHEROSCLEROSIS (the arteries)

• the big highways of the body: heart arteries, brain arteries, leg arteries

→ when large vessels are damaged, major organs lose blood supply

results of macrovascular disease

• coronary artery disease

• stroke

• peripheral artery disease

examples of rapid acting insulin

• lispro

• aspart

• glulisine

onset, peak, and duration of rapid acting insulin

onset: 15 min

peak: 1-2 hours

duration: 3-5 hours

onset, peak, and duration of short acting insulin

onset: 30-60 min

peak: 2-4 hours

duration: 5-8 hours

examples of short acting insulin

regular insulin

what insulin is the only type of insulin that can be administered IV

regular insulin

onset, peak, and duration of intermediate acting insulin

onset: 1-2 hours

peak: 4-12 hours

duration: 14-24 hours

example of intermediate acting insulin

NPH

examples of long acting insulin

• glargine

• detemir

onset, peak, and duration of long- acting insulin

onset: 1-2 hours

peak: none (steady release)

duration: up to 24 hours

key note for rapid acting insulin

give right before meals

key note for short acting insulin

it can be mixed with NPH

key note for intermediate acting insulin

it has a cloudy appearance and must be rolled

key note for long acting insulin

do not mix it with other insulins

insulin nursing safety

• rotate injection sites appropriately

• follow proper mixing protocols

• monitor continuously for hypoglycemia

what med class can mask the adrenergic symptoms of hypoglycemia

beta blockers

what med is biguanide

metformin

what is metformin

• medication that targets the liver

• it tells the liver to make less glucose

• it tells the cells to listen to insulin better

GI side effects of metformin

• nausea

• diarrhea

• upset stomach

metformin has a low or high hypoglycemia risk?

low

what med is sulfonylurea

glyburide

what suffix is sulfonylurea

starts with gl- ends with -uride or -amide

what is glyburide

• targets the pancreas

• tells the beta cells to produce more insulin

glyburide has a low or high hypoglycemia risk

high because it forces insulin regardless of sugar levels

metformin nursing cautions

• renal function matters

• serious risk of lactic acidosis

• hold for iodinated contrast

glyburide nursing action

• major risk for hypoglycemia

• associated with weight gain

what med is GLP-1 receptor agonist

liraglutide

what is the suffix for GLP-1 receptor agonist

-glutide

what does liraglutide do

• decreases glucagon secretion → liver stops dumping extra glucose

• increases glucose- dependent insulin secretion → only releases insulin when blood sugar is actually high

• increases satiety

• slows gastric emptying

clinical effects of GLP-1 receptor agonist

• weight loss

• nausea/ vomiting

• decreased appetite

safety precautions with GLP-1 receptor agonist

• risk of pancreatitis

• thyroid tumor

• MEN2 precautions

** patients with family history of thyroid cancer = CONTRAINDICATED

what med is DDP-4 inhibitors

sitagliptin

what does sitagliptin do

blocks DDP-4 → incretins survive longer → increases glucose- dependent insulin and decreased glucagon → blood glucose goes down

what is DDP-4

an enzyme that breaks down GLP-1 naturally

what is GLP-1

a naturally occurring hormone tour body releases after you eat

what is the suffix for DDP-4 inhibitors

-gliptin

clinical profile of DDP-4 inhibitors

• oral administration

• type 2 diabetes only

• generally weight neutral

• low hypoglycemia risk when used alone

sitagliptin safety and cautions

• monitor for pancreatitis

• severe joint pain

• hypersensitivity reactions

• renal dose considerations

what is SGLT2 inhibitor med

canagliflozin

what is SGLT2

sodium- glucose cotransporter 2

• transporter in the kidneys that normally reabsorbs glucose back into the blood after filtering

what do SGLT2 inhibitors do

blocks the glucose reabsorption in the kidneys → glucose stays in the urine and gets excreted out

side effects of SGLT2 inhibitors

• with more sugar in the urine → genital fungal infections/ UTI

• with osmotic water loss → polyuria → dehydration → dizziness/ hypotension

SGLT2 inhibitors serious warnings

• risk of euglycemic DKA (when DKA is happening but blood sugar levels look normal)

• requires strict kidney monitoring

how does steroids cause hyperglycemia

steroids cause insulin resistance → AND tells the liver to make more glucose (gluconeogenesis) → AND breaks down fat and protein in the glucose → blood sugar rises = steroid induced hyperglycemia

what are the nursing actions when a patient is on steroids

• check blood glucose more frequently

• report persistent hyperglycemia

• educate patient about steroid effects

clinical effects of steroids

• elevated blood glucose

• increased thirst and urination

• fatigue

• blurred vision

what are the signs of hypoglycemia

• confusion

• hungry

• anxious/ irritable

• tachycardic

• shaky

• sweaty

treatment for hypoglycemic patient who is awake and able to swallow

• rapid acting oral carbohydrate

• reassess

treatment for hypoglycemix patient who is unable to swallow/ unconscious + has no IV

and what is the caution for it

• glucagon via IM or SQ

CAUTION: nausea and vomiting so protect airway

what is the treatment plan for a hypoglycemic patient who is unable to swallow/ unconscious + has IV

• IV dextrose

treatment triad for DKA

• fluids (IV): restore circulating volume

• insulin (IV regular): stops ketone production, lowers glucose

• potassium: monitor and replace

normal blood glucose

70-99 mg/dL