Diabetes Mellitus
NCLEX Girl
Key Players: all work together to help body deal with glucose
 Glucose
o w/o insulin you can’t use glucose and bring it into cells, so glucose just stays in
blood  hyperglycemia
 Insulin: regulates amount of glucose in blood
o Secreted by beta cells of the inlets of Langerhans of pancreas
 Glucagon: helps us increase our blood sugar
o Causes glycolysis to breakdown glycogen and release glucose stores to increase
blood sugar
 Liver
o Very sensitive to insulin levels
o High glucose  promotes storage
o Low glucose  promotes using stores for fuel
Feedback Loop in Normal Person w/o DM:
 High blood sugar  pancreas releases insulin that pulls glucose into cells and extra into
liver
 Low blood sugar  pancreas releases glucagon that pulls glycogen out of storage and
breaks it down into glucose for body to use as fuel
Feedback Loop in DM:
 Body can’t get to glucose you are eating for 2 reasons:
o Beta cells are damaged – no insulin present (T1DM)
o Body is resistant to insulin (T2DM)
 Result is hyperglycemia that starts to impact major organs negatively because body
needs energy so…
o T1DM: body begins to burn fats and ketones (acids)  causes acid/base
imbalances
o T2DM: there is enough insulin so body doesn’t burn fats, but it doesn’t use the
carbs (issues with CHO metabolism)
Causes of DM:
 T1DM
o Pt doesn’t have any insulin b/c beta cells in inlet of Langerhans have been
destroyed and don’t function properly to make insulin
o Tx: HAVE to take insulin
o Not related to lifestyle; genetic, autoimmune
o S/S: Pts are thin (b/c they are burning all their fats and ketones), young, happens
suddenly, ketones present in the urine
 T2DM
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o Cells have quit responding to insulin  insulin resistant
o Hyperglycemic
o Pancreas oversecretes insulin b/c it senses the high levels of glucose in the
blood, but the levels won’t ever go down b/c insulin resistance 
hyperinsulinemia  leads to metabolic syndrome
o Tx: diet and exercise, but if that doesn’t work oral medications will be
prescribed; usually don’t take insulin, but if stress/infection present, they might
get insulin injections
o Related to lifestyle  obesity, poor diet, poor physical activity levels, genetic
o S/S: overweight, happens slowly overtime, older age, rare to have ketones in the
urine (they don’t have issue with metabolizing fats)
GDM
o Similar to T2DM  insulin resistant
o Develops during pregnancy
Complications of DM:
 Hypoglycemia: <60 mg/dL
o Usually, a side effect of too much insulin or too much oral diabetic medication
o S/S: sweaty, clammy, confused, lightheaded, dizzy, and double vision
o Tx: “Im sweaty, cold, and clammy gimme some candy”  need some simple
carbs
 Organ problems
o Too much glucose in the blood causes atherosclerotic issues (hardening of the
blood vessels) b/c glucose sticks to the proteins of the vessels becoming hard
and forming plaques
 Heart disease b/c narrow flow  MI, strokes (weakening of BV),
hypertension, neuropathy, decreased wound healing (b/c compromised
circulation with hardened vessels makes it hard for blood to carry healing
components to the impacted area; happens especially with feet), eye
trouble, and infections
 Diabetic Ketoacidosis (DKA)
o Occurs in T1DM (rare in T2DM)
o Burning ketones from fat stores in the liver  causes acid in blood  acid/base
imbalances that are life threatening
o S/S: extremely high glucose levels in blood, very thirsty, kussmaul breathing
(from acid buildup in blood), acetone breath (fruity smell from ketones breaking
down)
 Hyperglycemic hyperosmotic nonketogenic syndrome (HHNS)
o Occurs typically in T2DM
o No breakdown of ketones here b/c T2 has enough insulin where they don’t break
down fat
o S/S: thirsty, dehydrated, mental status changes, high blood sugar
Assessment:
 3 P’s (mainly seen in T1DM)
o Polyuria: frequent urination
 Poly = many; uria = urine
 Happens b/c osmosis  higher concentration of glucose in blood than in
cells so water leaves the cells and goes into the blood stream so the
kidneys start removing all the extra fluids you have but it also reabsorbs
the glucose but there is too much, so you start seeing glycosuria
o Polydipsia: very thirsty
 Poly = many; dipsia = thirst
 Happens b/c of polyuria
o Polyphagia: very hungry
 Poly = many; phagia = eating
 Happens b/c burning fats/ketones. Body needs energy so it tells you to
keep eating more food because you need fuel
 SUGAR pneumonic
o S: slow wound healing
 Sticky, hard vessels so you have decreased profusion to help heal wounds
o U: blurry vision
 Damage to eyes with all glucose
o G: glycosuria
 Kidneys can’t cope with all the blood glucose, so it begins to leak in urine
o A: acetone breath (T1DM)
 Burning ketones so sweet breath smell
o R: rashes on the skin and repeated yeast infections in women
 Yeast loves glucose so too many causes repeated yeast infections in
women
DM Management
 Triangle of DM Management
o Diet, Meds, and Exercise on outside and monitor on the inside (b/c lifestyle will
impact what meds they need)
Diet
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Individualized based on the pts lifestyle
Good to follow the ADA diet
o Carbs 45-60%
o Fats <20% - limit this the most, especially saturated fats, trans fats, and
cholesterol  encourage mono- and polysaturated fats instead
o Proteins 15-20% - meat doesn’t increase the glycemic index  try to avoid red
meats
Exercise
 Best for DM is aerobic b/c it helps them use their insulin
 Education prior to exercise:
o Check your BG before exercising, if its <100 mg/dL eat a small snack
 b/c you could risk hypoglycemia (“I’m sweaty, cold, and clammy, gimme
some candy”)
 carry simple carbs with them
o If exercising for a long time, check BG before, during, and after the exercise
o If glucose is >250 mg/dL before exercise with ketones in urine, they need to
avoid exercising
 b/c body is already burning the ketones because it can’t utilize the
glucose, so they don’t want to use up more ketones and develop
acid/base imbalances and go into DKA
 S/S of hyperglycemia: 3 Ps  “I’m hot and dry, I must be on a sugar high”
Drug$$$
 Oral Meds – typically for T2DM when they can’t manage their BG with diet and exercise
o Sulfonylureas – most common types
 Glyburide, Glipizide, Diabinese, Amaryl
 Generic name ends with “ides: zides, mides, rides”
 Fxn: stimulate the beta cells to make insulin
 Complications/Education:
 can cause hypoglycemia
 no alcohol consumption at all (b/c EtOH causes hypoglycemia on
its own and drug causes hypoglycemia so very bad)
o Meglitinides
 Generic name ends with: glinide like Repaglinide
 Fxn: stimulate the beta cells to produce insulin
 Complications/Educations:
 Taken with the first bite of food
o Biguanides
 Metformin (Glucophage)
 Fxn: decreases the liver stores of glucose
 Complications/Education:
 Patient needs to stop medication for 48 hours with
surgery/procedure and watch renal function
 Can cause diarrhea
o Alpha-glucoside inhibitors
 Precose, Glyset (starch blockers)
 Fxn: lowers BG by breaking down starches in the gut
 Complications/Educations:
 Taken with first bite of food b/c drug is acting on the food you
ingest
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o Thiazolidinedione (TZDs)
 Glitazone, Actos, Avandia
 Fxn: decreases glucose production in the liver
 Complications/Education:
 Monitor lung and heart function (increased risk of Mis)
Meds that cause Hypoglycemia:
o Beta blockers
 Metoprolol
 -olol
 Can make the symptoms of hypo and cause it
o EtOH
o ASA - aspirin
o Sulfonylureas
 Oral diabetic meds
o MAO inhibitors (depression meds)
o Bactrim – popular antibiotic
Meds that cause Hyperglycemia:
o Thiazides
 Like HCTZ which is a diuretic
o Glucocorticoids
 Hydrocortisone, prednisone
o Estrogen Therapy
 Oral contraceptives
Insulin - given subcutaneously
o Dawn Phenomenon:
 Pt has hyperglycemia during the waking hours (5-8am)
 Happens because the body shoots extra glucose as you wake up, but
diabetics can’t handle this extra glucose  develop hyperglycemia in the
morning
o Somogyi Effect:
 Hyperglycemia during sleeping hours (2-3am)
 Blood sugar drops and body responds by secreting glucagon, cortisol,
catecholamines to raise blood sugar but diabetic can’t cope so they get
hyperglycemia
o Types of Insulin
 Ready: rapid-acting
 Humalog and NovoLog
 Set: short-acting
 Humulin-R, Novolin-R
 Inject: intermediate-acting
 NPH
 Love: long acting
 Levemir, Lantus
o Peak and Duration of Insulins (peak times are when the patients are most at risk
for hypoglycemia)
 Rapid-Acting
 Onset: 15 min
 Peak: 1 hr
 Duration: 3 hrs
 Short-Acting
 Onset: 30 min
 Peak: 2 hrs
 Duration: 8 hrs
 Intermediate Acting
 Onset: 2 hrs
 Peak: 8 hrs
 Duration: 16 hrs
 Long Acting
 Onset: 2 hrs
 Peak: NONE
 Duration: 24 hrs
Diabetic Ketoacidosis (DKA)
 Definition: life threatening complication of DM  no insulin so breaking down fats into
ketones for energy  (S/S) causes hyperglycemia, ketosis, and acidosis from the fat
breakdown
 Mainly occurs in T1DM, but it is possible in T2DM patients with severe illness
 Key Players:
o Glucose
 Glucose stays in blood b/c no insulin so BG >300 mg/dL
o Insulin
 No insulin with T1DM or resistant in T2DM
o Liver and Glucagon
 Low glucose entering cells stimulates the liver to release glucagon to
breakdown glycogen via glycolysis into glucose b/c it thinks that there
isn’t enough glucose/energy in the body which elevates the BG even
more
o Ketones
 Break down fat b/c cells aren’t getting energy (b/c no insulin to bring
glucose into cells)
 Ketones are a byproduct of fat metabolism  breakdown of ketones
causes acid to be produced in the body b/c ketones are very acidic
 Body uses ketones, but DM patients can’t tolerate excess ketones so
blood pH drops causing metabolic acidosis (pH < 7.35)
o Kidneys
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Play a role in reabsorbing glucose in the renal tubules, but in DKA we
have super high glucose that kidneys can’t help with
BG gets so high that renal tubules can’t take anymore so it begins to leak
out of body in the urine (glucosuria)  osmotic diuresis  polyuria
develops, and electrolytes are excreted with causes electrolyte
imbalances
Causes of DKA
o Undetected DM – usually the first sign of DM in undiagnosed T1DM patients
 Excessive thirst, urination  high BG and ketones in urine
o Body needs more insulin than normal b/c of illness, stress, or meds like
corticosteroids and thiazide diuretics
o Not eating or skipping meals – body enters starvation mode and burns ketones
as fuel
o Not taking insulin as scheduled – glucose not controlled
S/S of DKA  happen suddenly
o Hyperglycemia  intracellular to extracellular shifting b/c higher concentration
in blood causing dehydration and electrolyte imbalances
o Ketones in blood  causes blood pH to drop, weight loss, electrolyte shifting,
metabolic acidosis, and fruity acetone breath
o Metabolic acidosis  pH <7.35, HCO3 <15, Kussmall breathing
o Occurs suddenly  patient BG >300 mg/dL
o Polyuria  due to osmotic diuresis; too much glucose for kidney tubules so it
leaks into the urine and dehydration and excretion of electrolytes occurs
o Polydipsia  frequent drinking b/c of extreme thirst caused by polyuria and
osmotic diuresis
o Dehydrated  dry mucous membranes and decreased skin turgor
o N/V, abdominal pain  present in peds, caused by high BG and ketones In body
o Kussmall Breathing  rapid, deep breathing caused by the respiratory system
trying to compensate for metabolic acidosis
o Acetone Breath  fruity breath caused by breakdown of ketones
o Ketones present in urine
o Tachycardia b/c of dehydration
o Hypotension b/c of dehydration
o Fatigue
o Confusion
Pharmacological:
o Goal: hydrate, decrease blood glucose, monitor hydration level for cerebral
edema, correct acid-base imbalance
o Monitor K+ level and renal fxn
Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS)
 Definition: life threatening complication of DM where extreme hyperglycemia (>600
mg/dL) causes very concentrated hyperosmolar blood without the breakdown of fat
o So, you have hyperglycemia and dehydration but no ketones (look at name)
 Occurs mainly in T2DM, rare in T1DM
 Key Players:
o Glucose
 Body is resistant to using glucose through insulin so BG increases causing
hyperosmolarity b/c concentration shift, hyperglycemia,
o Insulin
 There is some insulin present, so the body doesn’t have to turn to fat
breakdown for ketones
o Ketones – not present
o Kidneys
 Osmotic diuresis b/c BG too concentrated  polyuria 
polydipsia/dehydration
 Causes:
o Main cause: illness or infection (especially in older adults)
o HHNS occurs gradually (warning signs: extreme increase in BS, polyuria, and
polydipsia)
o S/S:
 Super high hyperglycemia >600 mg/dL
 Polyuria (b/c osmotic diuresis)
 Polydipsia (b/c polyuria)
 Majorly dehydrated  dry mucous membranes
 Fever
 Fatigue and mental status altered
 Interventions:
o Goal: hydration and decrease BS
Gestational DM (GDM)
 Definition: development/form of DM during pregnancy
 Occurs usually during the 2nd or 3rd trimester
 Risk Factors:
o M: maternal age over 25
o O: overweight or obese (BMI >25 or >30)
o M: macrosomia (previous large baby for GA, >9 lbs.)
o M: multiple pregnancies
o A: history (previous diagnosis or family history of DM)
 Pathophysiology (why it occurs):
o Key Players
 Pregnancy itself and the hormones produced to maintain pregnancy
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Changes in mom’s body and metabolic system that make her less
sensitive to insulin
 Baby’s growth needs at different stages in pregnancy
o What is Diabetes?
 Overall: issue with insulin produced by beta cells in the pancreas. Insulin
is a hormone that brings glucose into your cells for energy
 T1DM: autoimmune condition where beta cells don’t work or
aren’t there
 T2DM: cells are insulin resistant
 GDM: similar to T2DM with insulin resistance that occurs during
pregnancy but tends to disappear after pregnancy.
o However, ~50% of women who develop GDM will end up
developing T2DM later
o What is insulin?
 During pregnancy metabolic system is altered and changes insulin
sensitivity
 In early pregnancy, cells have high insulin sensitivity for growth of
adipose tissue needed to support mom and baby
 High insulin sensitivity in cells can impact mom b/c she may
experience insulin shifts towards hypoglycemia (s/s: nausea,
weak, tired)
 As pregnancy progresses, baby needs more nutrients as they grow bigger
and baby’s demands for glucose increase in 2nd to 3rd trimester
 So, the placenta lowers mom’s insulin sensitivity to leave more
glucose in mom’s blood to make it more available to baby
 Hormones that cause this shift of lowering insulin sensitivity are
human placental lactogen, estrogen, cortisol, and progesterone
 Normally moms body can compensate for low insulin sensitivity because
higher blood glucose level causes metabolic system to compensate by
keeping euglycemia (glycemic balance)
 Metabolic system increases the size and number of beta cells
 Patients with GDM don’t get this compensatory mechanism so
they get hyperglycemia causing glucosuria
o Risks of this occurring are:
 Preeclampsia (b/c hypertension with increased BV)
 UTIs, yeast infections
 T2DM
 Increased risk of c-section (b/c more glucose going
to baby causes its growth to increase and you get a
big ole baby)
 Complications with baby
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o S/S:
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Baby is getting tons of glucose and they make more insulin to deal
with this but they grow a lot and end up macrosomia (big ole
baby)
When baby is born, baby can become hypoglycemic b/c high
glucose feeding them through placenta is gone)
Extra glucose can impact lung development (especially surfactant)
so at birth they are at risk for respiratory problems
Similar to hyperglycemia
3 P’s
 Polyphagia
 Polydipsia
 Polyuria
Sugar in urine
Dry mouth
Fruity breath
UTIs, yeast infections
NCP
o SUGAR BABE
o Screening for GDM
 1 hr Oral Glucose Tolerance Test (fasting not required)
 24-28 weeks
 >140 mg/dL is abnormal
 3 hr ORTT
 Administered if 1 hr. OGTT abnormal
 Blood drawn at fasting, 1 hr, 2 hr, and 3 hr
 Looking for two or more abnormal BG results (below results are
abnormal)
o Fasting >95 mg/dL
o 1 hr >180 mg/dL
o 2 hr >155 mg/dL
o 3 hr >140 mg/dL
o Use diet and exercise to manage blood glucose
 Some patients may need insulin or oral meds like Glyburide
o Glucose monitoring (daily basis at home)
 Fasting: 70-95 mg/dL
 1 hr post-meal: >70, <140 mg/dL
o Assess urine for glucose and ask about UTIs
o Risk factors for MOMMA
o Blood glucose swings during and after labor
 Monitor BG levels during and after labor b/c we want to maintain
euglycemic levels (70-130 mg/dL0
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Monitor for hypoglycemia in baby and mom after birth (GDM tends to go
away after birth)
o Adverse effects of GDM
 Preeclampsia (HTN and proteinuria)
 UTIs, yeast infections
 Risk for C-section (large baby) and pre-term labor
 Hypoglycemia and respiratory distress in baby
o Blood glucose monitoring postpartum
 6-12 weeks after delivery have mom take a 2 hr OGTT
o Educate about importance of regular diabetic testing due to risk of developing
T2DM (even if GDM disappears)
 Recommend being tested every 1-3 years.