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Diabetes Mellitus

Problem of carbohydrate metabolism; problem of not having enough insulin

Islets of Langerhans (pancreas) – secrete protein substances, thus adequate protein in diet
important

Secretions/Functions
1. Insulin
• Secreted from the pancreas
• Facilitator of glucose. Hormone secreted by the Beta cells to in response to high
glucose levels.
• Take glucose out of the vascular system and into the cells. (K goes in with insulin
into the cell)
• Lowers blood sugar

2. Glucagon
• Also secreted by pancreas
• Polypeptide hormone that is secreted by the Alpha cells in response to low
glucose levels.
• Causes the liver to release stored glucose for cellular energy, decreasing the
movement of glucose into the cells.
• Raises blood sugar

Health Deviations of Pancreas

• Hypofunction of the Pancreas- chronic disorder of carbohydrate metabolism

marked by hyperglycemia and glycouria resulting from the inadequate production or
use of insulin.
• Hyperfunction- Body produces too much insulin resulting in hypoglycemia.

1. Hypofunction of Pancreas – Diabetes Mellitus

Types of DM – stopped using those terms b/c Type II do better in the long run if they take
insulin
1. Type I ( formerly Insulin-dependent diabetes mellitus – IDDM )
• Destruction of pancreatic B cells; so they make no insulin or they make so
little that it doesn’t even show up
• W/o insulin pt will develop Ketoacidosis (life threatening)  metabolic
acidosis
• Need insulin
• Something goes wrong with pancreases that’s why we give them exogenous
insulin
• Typically smaller people
• Juvenile diabetes
o Occurs in young individuals
o Usually younger than age 30, some as young as 3 yrs old.
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• Exogenous insulin needed b/c endogenous insulin is not enough

• Not genetic, but tends to run in families

S&S of Type I DM
• Polyuria (↑ urination)
• Polydipsia (↑ thirst)
• Polyphagia (↑ hunger)
• Weight-loss (IDDM) (energy comes from fats and proteins)
• Fatigue
• Frequent infections (Blood, urine are sweet causing bacteria to grow)
• rapid, early onset (early in life)

2. Type II ( formerly Non-insulin-dependent diabetes mellitus – NIDDM)

• There are more cells than insulin
• As you gain weight there are more cells (that need energy) and there must
be enough insulin to get the glucose into the cells
• Stress raises blood sugar
• Promote eating healthy, lose weight, exercise, maintain stress (may not
have to take medicine)
• Weight maintenance (wt loss) is very important
• Sometimes are put on insulin, but have to take large doses b/c they are
insulin resistant

S&S of Type II DM
• Weight gain (NIDDM)
• Older people, comes later in life (after 30s)
• Significantly overweight
• Sedentary lifestyle
• Familial tendency
• Avg. age 50 yrs.
• Hx of ↑ BP
• Fatigue; ↓ energy
• Recurrent infections

DX Procedures for Hypofunction of Pancreas

1. Fasting Blood Sugar
• Fasting Blood Sugar: NPO before bed; labs drawn 1st thing in the morning before
breakfast
• Normal FBS is around 120
• Can brush teeth and have water before test
• If >126 for more than two occasions, NPO for at least 4 hrs.

2. Postprandial Blood Glucose (PPG)

• Have them eat prescribed calories then check blood sugar afterwards
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• People without diabetes blood sugar is high then lowers as times progresses;
doesn’t happen with diabetes (it stays high)

3. Glucose Tolerance Test (GTT)

• Pt comes in NPO and is given a large glucose load and then you check sugar 1, 2,
3, 4 hrs later
• If no sugar, levels would remain to be high; not used much anymore

4. Capillary blood glucose monitoring (CBGM) or also called self monitoring of blood
glucose (SMBG)
• Finger sticks; stick on sides b/c of nerves on finger pads

5. Glycosylated Hemoglobin (Ghb or HbA1c) – normal 4-8%; poor control 13-20%

• Glucose attaches to hemoglobin and b/c of that we can find the avg. for the last 2-
3 months.
• Normal: 4-8 (means pt glucose is within control)/
• Less than 10  Poor control

6. Urine Ketone Levels

• If they have been breaking down fats and proteins they will have ketoacidosis and
ketones will spill in urine

DM CONTROL CRITERIA
1. Optimal weight
2. Glycosylated HBG WNL
3. FBS < 140
4. BS < 180 1-2 hours after meal

Hypoglycemia < 60 – 120 < Hyperglycemia (without eating)

Medical Management of DM
1. Diet
• Special diets based on amount of activity
• Diet Exchange System: x number of carbs, proteins, starches everyday
• i.e. “I won’t eat meat today so I’ll eat 2 doughnuts”; same calories, but not healthy
• Stop eating simple CHO (powdered doughnuts)
o 50-60 CHO (complex, whole grain)  cellular energy
o 20-30 Fat
o < 10 Protein
• You can do it every now and then, but not every day and be ok
• Calorie Count: people take meds based on the number of calorie intake; not right
for all patients

2. Medications (Cross Sheet)

Oral hypoglycemic agents (OHAs) also called oral antidiabetic agents
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• Some given before, with, or after meals; know when appropriate to give meds
• used to stimulate pancreas to make more insulin and used to reduce resistance to
insulin

b. Insulin Therapy
• can come from pigs, cows, and humans
• elderly are the only people taking beef and pork because they are doing well with it
• less reactions to human insulin b/c we don’t have to worry about bodies rejecting it

Types of Insulin
a. Rapid Acting (humalog or insulin lispro)
• Clear
• Given SQ only
• Onset 10-15 min
• Eat within 10-15 minute interval or they will become hypoglycemic
• Peaks in 1 hr.
• Lasts 3 hrs.

b. Short acting (clear)

• Regular
• IV (the only one given in either fluids of IVP, SQ, IM (rare))
• Onset 30-60 minutes
• Peaks in 2-3 hrs.
• Lasts 4-6 hrs.
• Given based on sliding scale

c. Intermediate acting (cloudy)

• NPH
• Given SQ
• Onset 2 hrs.
• Peaks 6-8 hrs
• Lasts 12-16 hrs.

d. Long acting (cloudy) – ultralente

• Protamine Zinc (PZI) or
Ultralente • Lantus (used w/lispro)
• Given SQ • Given SQ (usually hs)
• Onset 2hrs. • Onset 1-2 hrs.
• Peaks 6-20 hrs. • No pronounced peak
• Lasts 20-30 hrs. • Lasts 24 hrs
Pre-mixed
• Mixture of NPH and regular (70/30)
• Given SQ
• 70% NPH
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• 30% Regular
• i.e. if dr. asks for 100U of 70/30 there are 70U NPH and 30 regular

Mixing Regular and NPH

• You can’t mix NPH in regular because it’ll slow it down
• Put air in NPH, then air in regular and draw regular, then draw NPH
• If regular gets into NPH it’s ok
• You need a licensed witness to draw insulin

Types of Insulin Administration

SQ
Injections
Insulin Pens
IV
Regular only one given IV
Insulin Pump

Insulin Complications
1. Allergic Reaction
a. Local (itchy)
b. Systemic (anaphylaxis reaction)

2. Lipodystrophy
• Tissue damage from injections
• Hard, lumpy, sclorosed, cratered skin
• Rotate within sites every week to prevent hypertrophy
• Doesn’t happen as often with human insulin
• If you keep injecting in the same site the blood sugar will remain high
because insulin will stick in hard skin
• Tissue atrophy (usually occurs with beef or pork)

3. Insulin Resistance

4. Morning Hyperglycemia
a. Somogyi Phenomenon
• Diabetic wakes up every morning with blood sugar elevated; the
doctor increases insulin to keep sugar under control
• Blood sugar bottoms out between 1-3am. and stress response
(fight or flight) secretes glucocorticoid (cortisol) released from adrenal
gland; makes your liver release stored glucose; causing it to raise in the middle of the night.
• Must have a bedtime snack before bed; important that they receive
all calories to help
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b. Dawn Phenomenon
• Occurs with NPH patients who receive their insulin 2x/day (7A,
5P) peaks 4-5A and growth hormone is secreted right before you
wake up
• Usually in type I children
• NPH is peaking when growth hormone is secreted
• Growth hormone secreted around 4-6am and antagonizes the
afternoon dose of NPH.
• Blocks the effects of insulin; so blood sugar is elevated first thing
in the morning.
• Tx: Alter evening dose; give it at 6 or 7P and it’ll peak later than
growth hormone

c. Honeymoon Phase
• Occurs on a diabetic right after they get diagnosed
• They go home and follow directions and blood sugar is normal
• Pancreas starts to put out enough to satisfy needs, but then that fizzles
out
• Diabetic can become non-compliant and get into severe complications
b/c they think that they are not diabetic; causing ketoacidosis
3. Exercise
• Lowers blood sugar
• Lowers weight
• Stress-buster
• Don’t exercise if BS is elevated/ low or if ketones are present in urine.
• If pt levels are normal needs to have an extra 15g snack (fruit, cheese & crackers,
fruit & cracker)
• Make sure someone is aware of their plans or take a partner in case they pass out

Nursing Mgt of DM
• Chart on pg.1299 about foot care KNOW
• They have foot problems b/c elevated glucose damages nerves and blood vessels
• You won’t know if something is irritating your foot because circulation is messed up the
blood can’t get to it adequately for healing

Acute Complications of DM
When in doubt of pt condition, Tx as if hypoglycemia b/c its more fatal.

1. Hypoglycemia
• Causes
o Taken too much insulin or OHA
o Too little food
o Exercised too much; carbohydrate stores weren’t there to supply cellular
need
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• If you suspect somebody is hypoglycemic give a glass or orange juice, ½ glass of

coke, sugar package, 3-5 m&m’s until normal (check q15-20 min)
• If they are unconscious or sleeping, give glucagon. If in hospital, give 50%
glucose
• If in doubt get the sugar up; hyperglycemia causes problems after a long amount
of time; hypoglycemia causes problems very quickly (too low causes brain damage and death)
• If they maintain a high blood sugar and come to the hospital and it’s lowered from
400-500 to 140; they will show signs of hypoglycemia because they are not used to levels that
low; takes a while to get used to it

• Clinical Manifestations of Hypoglycemia

o Headache o Slurred speech
o Weakness o Alterations in gait
o Irritability o Decreasing LOC
o Apprehension o Pallor
o Hunger o Cold, clammy skin
o Visual disturbances o Diaphoresis
o Tremor o Tachycardia

Untreated:
o LOC, seizure, coma, and
death

o Hot & Dry = Sugar High (serum osmolality increased causing polyuria –
dehydration)
o Cold and Clammy = Need Some Candy

2. DKA (Diabetic Ketoacidosis)

• Type I diabetics
• Very high blood glucose because it’s not getting into cells; cells are starving so they
breakdown fats and proteins releasing ketones = ketoacidosis
• Metabolic Acidosis (respiratory compensated by breathing deeper and faster;
releasing CO2)
• Fluid Volume Deficit

• Clinical Manifestations of Hypoglycemia

o Increased BP
o Increased serum osmolality  Polyuria
o Dehydrated, dry mucous membrane
o Unresponsive/ Lethargic
o Fruity (ketone) breath
o Ketones are spilled in urine
o Increased respirations (blowing off CO2)
o Poor skin turgor
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o Abdominal pain (anorexia, nausea)

• DKA:
Diabetic KetoAcidosis occurs in type I

Inadequate insulin
↓
Hyperglycemia
↓
Breakdown of proteins and fats for energy
↓
Release of ketones in serum and urine
↓
Osmotic diuresis (Polyuria) to flush out glucose and ketones
↓
Metabolic acidosis ( ↑ H & K) (hyperkalemia)
(watch very carefully for hypokalemia b/c K will follow insulin & glucose into cell)
↓
Kussmaul respiratory with fruity breath
↓
Altered level of consiousness (acidosis causes CNS deoression)
↓
Dehydration
↓
Shock

• Treatment:
o Insulin (to get glucose into cells)
o Hydration NS 1000 cc/hr
o B/c there is not cellular dehydration yet and we need to get vascular volume
back up) (numerous L); check blood sugar every 30 minutes; insulin in IV; IV
bolus(IVP regular insulin)…eventually wakes up after sugar is down and
volume is replaced (quickly); very good teaching to prevent
o When blood sugar gets to 250 stop insulin and hang an IV fluid with glucose
in it (D5N or D5 ½ N)
o B/c sugar will continue to come down and if they stay on insulin until about
60 they will become hypoglycemic

3. HHNK (also called HHNS) (Hyperglycemic Hypertonic Non-Ketotic)

• Type II diabetics
• High blood sugar and dehydration
• Sugar levels worse than DKA b/c there is some glucose in cells and they’re not
getting acidotic so sugar continues to climb
• Higher sugar you will have osmotic diuresis (dehydration)
• There is some insulin so fats and proteins are not broken down and no ketoacidosis
• Treatment:
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o Hydration
o Insulin
o When they get to 250 stop insulin and hang sugar IV

Chronic Complications of DM
1. Macrovascular
• Damage to larger vessels (heart, brain, and peripheral vascular (veins in
extremities))
• Pulses, edema, sores, discoloration, wounds that won’t heal
• Stroke, cardiovascular disease (diabetics have frequent cases of cardiovascular
disease because heart vessels are damaged)
• Will have angina from heart attack and won’t feel pain (i.e. foot problems)
causing more damage b/c they take a long time to get to the doctor
(asymptomatic)

2. Microvascular
• Eyes (diabetic retinopathy = go blind), kidneys (diabetic nephropathy = renal failure),
skin
• Result from thickening of the vessel membrane in the capillaries and arterioles in
response to chronic hyperglycemia

a. Diabetic retinopathy
• Microvascular damage to the retina as a result from chronic hyperglycemia
• Funduscopic - dilated eye exam

b. Diabetic nephropathy
• Microvascular complication associated with damage to the small blood
vessels that supply the glomerli of the kidney. Leading cause of end-stage
renal disease

c. Diabetic neuropathy
• Nerve damage that occurs because of metabolic derangements
• Loss of protective sensation in lower extremities
• Sensory neuropathy: hands / feet
• Autonomic neuropathy: bowels incontinence, diarrhea, and urinary retention