X Diabetes Mellitus - Burke Ch 36 Flashcards
Definition of Diabetes Mellitus
a group of systemic metabolic disorders characterized by hyperglycemia
How much of US population is Diabetic?
- 1 mil, 9.3% of population
- 21 mil Dx
- 8.1 mil Un Dx
Diabetes interferes w ability to use?
Glucose
What is Glucose?
Simple sugar, monosaccharide
What is glucose used for and by
Used by cells for energy
Does brain need insulin?
No, brain only uses glucose. When none available, brain cells die
Glucose comes from ?
Carbs broken down into sugar.
End products of digestion?
Protein, fats, carbs
Carbs break down to….
Glucose, fructose, lactose
Fats (lipids) break down to….
Fatty acids, glycerol
Protein breaks down to…..
Amino acids
Pathway of glucose from intestines…..
Intestines absorb water And nutrients……glucose to blood……from blood to cells……
Where is excess glucose stored?
Liver and adipose and muscles
Explain lock and key method
Insulin attached to insulin receptor, opens door, allows glucose in.
Stimulus for insulin release?
Body senses UP glucose and stimulates pancreas to release insulin
Excess glucose converted to ? Stored where?
Converted to glycogen and stored in liver
Organs involved in BG regulation?
Pancreas and liver
What is glucagon?
Pancreas releases glucagon when senses LO BG, glucagon stimulates liver to break down glycogen into glucose.
Glycogen bs Glucagon
Glycogen lowers BG
Glucagon raises BG
Some fictions of liver
- Regulate BG
- Synthesis and storage of amino acids, proteins, vits, fat
- detox
- blood circulation and filtration
- bile drainage
What other sources of energy can the body use other than carbs
fat
what are complications of metabolizing fat for energy?
ketones are released. Too many ketones in body give off fruity breath. (acetone)
what does buildup of ketones do to body’s pH
acidotic
3 Ketone bodies?
AHH….
Acetone, Acetoacetic Acid, Hydroxybutyric Acid
normal body pH
7.35 - 7.45 pH
Ketosis
presence of ketone bodies in blood
Ketonuria
ketones eliminated in urine
common people ketones found in?
starving, fasting, diabetic
Glycogen
storage form of glucose. stored in liver
Glucagon
Hormone secreated by pancreas in response to LO BG, stimulating liver to breakdown glycogen into glucose
Insulin
Hormone secreted by Pancreas to LOWER BL levels
DM risk factors
- Diet/Lifestyle (diet hi in fried, carbs and sweets)
- Aging
- Obesity
- Genetic pre-disposition
- virus
- T-lymph/autoimmune
- race
Non-Modifiable risk factors for NIDDM
- Family Hx
- Race/Ethnicity
- Age
- Hx of gestational diabetes. chance of devoping later in life.
- Gave birth to large UP 9lb baby.
Races at risk of NIDDM
Af-Am Latino Asian Am Native Am Pacific Islanders
Modifiable risk factors for NIDDM
- overweight/obese (50% men, 70% women w diabetes are obese)
- Physical inactivity
- Hypertension
- UP alchohol consumption
- smoking (18-24 cigs per day)
How much of US population is pre-diabetic
86 mil
1/3 adults are pre-diabetic
9/1 adults don’t know they are
Definition of Pre-Diabetics
BG levels are abnormal (80 - 100mg/dL) but don’t meet criteria for being diabetic
11% of PD develop DM within 1 year
common Dx tests
- Hb A1C (glycosylated Hemoglobin)
- FBG, Fasting Blood Glucose
- OGTT, Oral Glucose Tolerance Test (drink bottle fast, test BG in 1 hr)
- serum Insulin
- C-Peptide test
- Post Prandial Blood Sugar (2 hr after meal)
What does it mean if glucose is in the urine?
Body is not absorbing it, causing build up and spill over
Insulin made in what part of Pancreas? by what cells?
Islets of Langerhorn by B cells
Types of DM
- Type 1, IDDM (Juvenile)
- Type II, NIDDM
- Gestational
- Other: Meds (long term steroid use, Chemo), Organ Transplant Recipients, Trauma to Pancreas, Cancer of Pancreas)
How common is Type I
5-10% of cases
IDDM, Pathos, Cause
- Insulin Dependent Diabetes Mellitus
- Progressive destruction of B cell function (lose ability to secrete Insulin)
- Cause unknown
How does blood work show Type I?
Islet cell antibodies. Means body is attacking the Islet cells
upon Dx, how many B cells are destroyed?
80-90%
within 5 years, 100% will be destroyed
How does Type I lead to Hyperglycemia?
No insulin. Body BG UP, body can’t use glucose for energy, blood becomes Hyperglycemic.
How are symptoms displayed in IDDM?
Sudden Onset. Usually discover when body goes into DKA. Diabetic Keto Acidosis
DKA
Diabetic Keto Acidosis
when body starts metabolizing fat, creating ketones in the body. Ketones make body acidotic.
NIDDM
- Non-Insulin Dependent DM
- Type II
- Gradual onset of symptoms. Body always making some insulin, but insufficient amounts
- Insulin RESISTANT rather than LACK of insulin
Insulin Resistance
cells become resistant to effect of Insulin. More insulin needed for same effect.
Causes of Insulin Resistance
- Obesity
- Metabolic Syndrome
- Pregnancy
- Infection
- Stress
- Long term steroid use
Rx for Type I vs Type II
Insulin vs Diet, exercise, meds
Incidence of complications for Type 1 v Type II
both frequent
High BG complications for Type 1 v Type II
DKA (metabolize fat) vs Hyperglycemic, hyperosmolar, nonketotic syndrome
Usual age onset Type 1 vs Type II
40 and below vs 40 and up
Body weight of Type 1 vs Type II
lean vs Obese
Onset of SS for Type I vs Type II
sudden vs gradual
When do mothers usually find out about Gestational Diabetes
- ~ 28wks at time of OGTT
- 2-10% of US pregnancies
- Rx, Glucose control, diet, excercise
- Risk of dev DM later in life
Macrosomomia
Big Baby, over 9lbs. due to uncontrolled insulin production and UP BG in mom and baby during gestation
Women w Gestational DM have 30-65% chance of
developing DM in 10-15yrs
Glycosuria
glucose in urine
Gluycosuria –> Polyuria –> Polydipsia
Hyperclycemia –> Polyphagia
Difference between Glycogen and Glucagon?
Glycogen - stored in liver
Gloucagon - Hormone that breaks down Glycogen to Glucose.
3 Ps?
Polyuria - frequent urination
Polydipsia - frequent drinking
Polyphagia - frequent eating
Other S/S of DM
- Nausea
- Cold extremities
- blurred vision
- halos (vision)
- Neuropathy (nerve pain)
- LO sensation to pain/temp in feet
- Impotence (ED)
- Slow wound healing
Hirsutism
in Type I, male pattern hair growth in women (beard)
Dx test for PreDiabetes (only need 1 out of 3 to be diagnosed)
- Fasting BG (100 - 125 mg/dL)
- Elevated Hba1c (5.7 - 6.4)
- 2hr Oral Glucose Tolerance (140-199mg/dL)
DM Dx tests (only need 1 out of 4 to be diagnosed)
- Elevated fasting BG on 2 occassions (>126mf/dL)
- Casual BG level (>200mg/dL w 3 classic Ps)
- OGTT w 2hr BG (>200mg/dL)
- Hba1c (>6.5%)
Fasting BG test steps
1) Fast for 8 hrs
2) obtain blood sample
3) normal = 99mg/dL or less
Normal BG Ranges for Adults
-Preprandial glucose (before meal) =
What does OGTT measure and recomendations
this test involves drawing a fasting blood test, followed by having a person drink a 75-gram glucose drink and then drawing another sample two hours after consuming the glucose.
- ability to use glucose
- NPO for 8-12hrs before test
- no smoking, caffeing
- drink glucose drink
- test 2 hrs later (pregnant women only wait 1 hr)
- ptn can drink water during test
Normal Insulin levels
5-24mcU/mL
Serum Insulin test steps
used to dx ?
1) NPO for 8 hrs
2) obtain blood sample
diagnose IDDM
abnormal: no insulin present. in NIDDM, level will be normal to High
Post Prandial Blood Sugar test steps
- 12hr fasting. BG done before meal
- eat entire meal (75g of CHO)
- rest and no smoking after meal
- Blood sample obtained 2 hrs after meal
if result >200mg/dL = DM
if result 140 - 160 = Pre DM
if result
Glocosylated Hemoglobin (HbA1c) test steps
- monitors Rx, Dx DM, How well controlled DM is
- 2-3 mos blood sugar average
- shows Hgb to which glucose is bound
- no fasting required
- results
A1c Level
Normal - or equal 6.5%
C-Peptide Test steps
- Determines insulin production. (for every insulin produced, 1 c-peptide made)
- identify’s pts who secretly seld administer insulin = Facticious Hypoglycemia
- C-Peptide levels corrolate 1:1
- NPO 8 hrs prior
- obtain blood sample
- Normal fasting level = .78mg/ml
Can distiguish btwn Type I and II. NO insulin produced = no cpeptide produced.
Facticious Hypoglycemia
when patients deliberately administer insulin to create hypoglycemia (suicide?)
DISEASE
Fasting Sugar >120
OG TT > or equal 200
HbA1c >6.5
PRE-DISEASE
Fasting Sugar 100-125
OGTT 140-199
HbA1c = 5.7-6.4
NORMAL
Fasting Sugar 99 or less
OGTT
.
People w Diabetes are at higher risk of developing …..?
heart disease & stroke
DM is the ? leading cause of ? in the US
6, death
What virus’ trigger Type 1 DM?
Mumps/Rubella, Coxsackie 4
Lantus is a type of ?
long acting insulin
Name of Intermediate acting Insulin?
NPH, NovolinkR, HumalinR
Table 36-2 Action of Insulin Preps
see pic in phone
Short Term Complications
- DKA
- Hyperglycemic Hyperosmolar Noketotic Syndrome (HHNS)
- Hyperglycemia
- Hypoglycemia
You can NOT live with these conditions chronically. They are acute.
Normal body pH?
7.35-7.45
How does glucose end up in the urine?
Blood going into nephron is so concentrated that re absorption in the tubules can’t remove everything. Excess is excreted in urine.
Osmotic diuretic
Substance that attracts water and takes it along into the Urine
Glucose, Na, Asparagus
How does body compensate for acidosis?
Kussmal breathing to breath off acetone, a Ketone
Ketonuria
Ketones in the urine
Metabolism of fat creates ?
Ketones. Acids
Ketones excreted in what ways?
Via lungs- fruity breath
Via urine- acetonuria or Ketonuria
What complication does Ketonuria cause ?
Dehydration, E imbalance
DKA causes
- Type 1 - no insulin production
- problem w insulin therapy (missed doses, not enough etc)
DKA triggers
Infection- UP BG PNA (pneumonia) UTI Stress ETOH abuse Drug abuse MI (myocardial infarction) heart attack CVA (cerebro vascular accident) stroke
???learn level
Na, K, creatinine, BUN, hematocrit, platelets etc
.
Hyperglycemia leads to ?
Polyuria –> dehydration –> tachycardia–> hypotension–>hypovolemic shock
Acidosis leads to ?
K+ leaving cellS and accumulate in blood –> hyperkalemia –> UP K can lead to heart attack
Hyperglycemia and Acidosis can both lead to loss of consciousness and ?
Death
DKA symptoms
3Ps Glucosuria Ketonuria Acetone breath Kussmaul respirations Drowsiness BG 250-800 mg/dL Loss consciousness
DKA tests
BG, Ketone levels
Urine glucose , ketone levels
Blood pH (acidosis) - ABG arterial blood gas
DKA Treatment
- IV Fluids
- Drip: IV Insulin (REGULAR insulin ONLY)
- Monitor qH BG (finger prick, side less painful than center fingertip)
- Monitor Elecrolytes (E)
- ABG for acidosis
DKA patient education
- Teach PREVENTION
- careful SELF/HOME monitoring of BG
- if BG >250 then check for Ketones
- If KETONES present, drink H20 and recheck Ketones again w next urination
- If KETONES present, call MD
- Never stop Insulin w/out MD supervision
STEROIDS increase
UP BG levels
about HHNS (Hyperosmolar, Hyperglycemic Nonketotic Syndrome)
Occurs Primarily in: Type II, Meds (steroids)
Cause: Stress, Illness, Infection, MI, CVA
DKA vs HHNS
DKA
No insulin
metabolizes fat
HHNK
severe hypoglycemia but no Acidotic state (DKA). No DKA because there is always at least a little insulin present
HHNK Pathophisiology. How fast develops?
- Hyperglycemia —> Polyuria —> Dehydration –> a hyperosmolar state (concentrated urine) –> E imbalance
- Develops slowly
HHNK BG levels?
> 600-1500 mg/dL
HHNK Symptoms
- Extreme Polydypsia
- Glucosuria
- 3 Ps
- Lethargy
- Confusion
- Shock
- coma
- death
No ketones (no ketonuria)
HHNK Treatment
- IV fluids
- DRIP: IV REGULAR insulin
- Monitor: qH BG (finger prick)
- Monitor: E
- Teach prevention
All DM patients should have an Endocrinologist
.
HHNK Long Term complications
- Cardiovascular Disease
- Neuropathy
- Nephropathy
- Retinopathy
- Foot damage: blisters, cuts
- Osteoporosis
Hyperglycemia Definition, Cause
Def: calories in excess of insulin available for glucose used
Cause: over-eating, stress, illness, LO DM meds (need to be adjusted)
Stress = release of counter regulatory hormones (epi, cortisol, GH, Glucagon)
S/S Hyperglycemia
- 3Ps
- Fatigue
- Blurred vision
- Headache
- Abdominal Pain
Hyperglycemia Rx
- BG meter monitoring
- BG >250 check urine for Ketones
- sliding insulin scale, oral agents
Hypoglycemia Def.
- not enough glucose in relations to Insulin
- BG
cause of Hypoglcemia?
- meds
- malnutrition
- fasting
- excercise
What’s the danger of repeated hypoglycemic episodes
- Diabetic Coma
- Brain cells deprived of enegy (neuro damage)
Hypoglycemic S/S
- hunger
- sweating
- palor
- tremors
- palpitation
- headache (h/a)
- weakness
- blurred vision
as Hypoglycemia progresses…..s/s
- irritability
- confusion
- seizures
- coma
Hypoclycemia Rx
- if pt AOO (awake, alert, oriented), NON ACUTE
- confirm hypoglycemia w Glucometer
- administer a Fast Sugar, recheck in 15min, if not BG not high enough (~80-120), more fast sugar. End w long acting sugar.
Fast Sugar
- 4oz OJ
- 1 Glucose Tab
- 6-8 lifesavers
- 6oz reg soda
Long Acting Sugar (complex carb)
- crackers
- milk
- peanut butter
- 1/2 sandwich
Hypoglycemia Treatment: If pt not alert or unable to swallow
admin SC, IB, IM
- IVP 50% Dextrose (D50) (admin by RN)
- recheck BG in 15 min
- repeat steps until hypoglycemia subsides
If hypoglycemic exhibit neuro S/S, administer STAT?
D50 (IV)
Glucagon (SubQ)
Treat asap because brain cells dying. If it turns out to NOT be hypoglycemia, you can always correct the condition by administering insulin.
Fasting BG Levels (8-12hrs NPO)
- 70 to 99 mg/dL - Normal
- 100 to 125 mg/dL - Pre DM
- > 126 mg/dL on more than 1 test occasion - DM
Long Term Complications of DM
- Macrovascular
- Microvascular
- Nerves
- Infection
- Foot Complications
MACROvascular Complications
Involve circulatory system
- Atherosclerosis (plaque/narrowing of arteries)
- Arterioosclerosis (Hardening of arteries)
- HTN (UP press in vessels, risk for heart attack)
- UP LDL/Triglycerides
- Platelet fx - MI/CVA
- Poor circulation in feet/legs
- DM alters clotting ability (clotting when not necessary)
MICROvascular Complications
Eyes
- Retinopathy (disease of retina. dmg tiny blood vess that supply eye)
- Cataracts (clouding of lens)
- Glaucoma (UP press in eyes)
Kidneys
-Nephropathy
What % of DM develop cataracts? Glaucoma?
60%, Cataracts
40%, Glaucoma
Leading cause of blindness
Glaucoma
Types of Retinopathy
Nonproliferative
Proliferative
Non Proliferative Retinopathy
capillaries in back of eye balloon, form pouches that inhibit passage of substances btwn blood and retina
Proliferative Retinopathy
blood vessels so damaged they close off. new weak vessels grow in retina, leak blood
Nephropathy
Disease of kidneys. Blood vessels damaged due to hyperglycemia. Result in ESRD - Dialysis. affect filtering ability
Leading cause of ESRD?
DM
what % of DM px develop nephropathy?
40% develop some degree of kidney problems
Neuropathy
nerve damage from Chronic Hyperglycemia
- numbness/pain in extremities
- Gastroparesis
Gastroparesis?
delayed gastric emptying (paralyzed stomach)
MED: REGLAN, 2 uses?
Nausea and Gastroparesis
-Increase speed in which contents empty from stomach
Complications of INFECTION
DM px prone to infection
- UP BG
- lead to DKA in Type 1
- slow healing, impaired circulation. not enough blood getting to would
- Hyperglycemia -> WBCs sluggish/ineffective. can’t fight infection
- ulcers/infections -> gangrene, necrosis, death
- Abx given, but not effective due to poor circulation
- use TOPICAL Abx
what 3 factors lead to Foot Complications?
- poor circulation (vascular disease)
- prone to infection (poor would healing)
- neuropathy (limits sensation)
leading cause of Amputation?
DM
Foot Care Steps
- wash and dry feet DAILY
- Inspect for cracks, sores, foreign objects
- clip toe nails across, not angle, to avoid ingrown
Teaching Footcare. What to AVOID?
- pantyhose, garters, tight socks
- crossing legs
- foot soaks/powders
- lotion btwn toes –> fungal infec.
- never barefoot
- hot H2O bottles, heating pads on feet
Teaching Footcare. What to DO?
- use alcohol free lotion, NONE btwn toes
- wear proper shoes, wide, sturdy
- see podiatrist
- annual checkups
- notify MD of abnormalities
DM Rx
- education w monitoring
- diet
- excercise
- oral agents
- Insulin (last resort)
Goals of Diet
1) achieve/maintain BG and Lipids to near normal (CONTROL to avoid complications)
2) weight loss and BP control / Meal planning
3 Methods of Meal planning
-Plate method
-carb counting
-glycemic index
(refer pt to nutritionist/dietitian)
Benefits/Risk of Excercise
UP Muscular activity -> glucose utilization, insulin receptors become more sensitive to insulin
Risk for HYPOglycemia (supervised exercise recommended)
Exercise Concerns
- monitor BG before, during, after (to see how BG affected)
- Gradually UP level of activity
- Avoid extremes -> Hypoglycemia
- Excercise SAME time daily. easier to monitor
- BG 90andUP before exercise (if on oral meds)
- BG 110andUP before exercise (if on insulin)
When Exercise make sure to:
- carry Fast Sugars
- eat carb snacks before and at intervals during strenuous workouts.
If on INT acting Insulin, DO NOT exercise during
PEAK hours (when BG is lowest)
Type1, if BG is 250andUP, what to do before excercise? why?
-check for Ketones. If present, DON’T excercise because Ketones will increase. Body will start metabolizing fat after all glucose is done.
- Drink H2O, check urine again
- H2O to prevent dehydration because Glucose and Ketones in urine are Osmolor diuretics.
Excercise - pre-workout list
- Med alert ID
- Comfy shoes (prevent blisters)
- bring glucometer
- carry fast sugar
- bring emerg glucagon kit
If BG is 300andBLO, no ketones present, can you exercise?
yes
Exercise if Type II, if BG 400andBLO?
YES
Exercise if Type II, if BG 400andUP?
NO
BG monitoring
- self monitoring
- take daily log w times, #s
- Tight glucose control - qac and qhs (b4 meals and bedtime)
??? Glucosuria when BG is ?
> 80 mg/dL
Test urine for ketones when ?
> 250 mg/dL
Type II don’t check for ketones because they always make insulin
MEDS: 6 class of Oran HYPOglycemics
1) Sulfonylureas
2) Meglitinides
3) Alpha-glucosidase inhibitors
4) Thiazolidinediones
5) Biguanide
6) DPP-4 Inhibitors
Ca and K for?
Ca - relieves contracting Muscles
K - relaxing muscles (too much, risk for MI)
MEDS: Sulfonylureas - how do they work?
Type II DM
- stimulate pancreas to release more insulin
- NOT dependent on BG
- can –> HYPOglycemia (monitor BG because of this)
- NEVER use on Type 1 (IDDM)
MEDS: Sulfonylureas - examples
1st gen:
Diavinese
2nd gen:
Glipizide (Glucotrol)
Glyburide (Diabeta, Micronase, Glynase)
3rd gen:
Glimepiride (Amaryl)
SIDE EFFECTS: Nausea, Diarrhea, Constipation
MED: Diavinese
- 1st Gen Sulfonylurea
- not used often. stress on kidney. Renal function can be altered
MED: Glipizide (Glucotrol)
- 2nd gen Sulfonylurea
- given 30 min B4 1st meal, breakfast
SE: Nausea, Diar, Constip
MED: Glyburide (Diabeta, Micronase, Glynase)
- 2nd gen Sulfonylurea
- given 1x day w 1st meal
SE: Nausea, Diar, Constip
MED: Glimepiride (Amaryl)
- 3rd gen Sulfonylurea
- 1x day w 1st meal
SE: Nausea, Diar, Constip
MEDS: Meglitinides - how do they work?
- stim pancreas to release insulin
- Glucose DEPENDENT
- Taken 30min B4 meal
once pt eats, UP BG, then pancreas w stim insulin. absorption happens in sm intestines. Med will already be working
MED: Meglitinides - examples
- Prandin (Repaglinide)
- Starlix (Nateglinide)
- stim pancreas to release insulin
- Glucose DEPENDENT
- Taken 30min B4 meal
MED: Alpha-glucosidase Inhibitors - how do they work?
- prolong absorption of carbs in stomach & intestines. BLOCKS enzyme needed to digest starch.
- slows post prandial, UP BG
- given w EACH meal on 1st bite, not convenient
MED: Alpha-glucosidase Inhibitors - i.e.
Precose (Acarbose)
not convenient because have to remember for each meal.
MED: Precose (Acarbose)
w EACH meal on 1st bite.
MED: Thiazolidinediones - how do they work? (like Biguanides)
-UP insulin sensitivity at insulin receptors
-LO amount of glucose released by liver
-taken daily w NO regard to meals
-similar to Biguanide’s
UP risk/rate of bladder CA. Contraindicated in pts w Hx of Bladder CA
MED: Thiazolidinediones - i.e.
Avandia (risk for MI) not used anymore
Actos (Pioglitizone)
- UP insulin sensitivity at insulin receptors
- LO amount of glucose released by liver
- taken daily w NO regard to meals
MED: Actos (Pioglitizone) class
Thiazolidinedione
- UP insulin sensitivity at insulin receptors
- LO amount of glucose released by liver
- taken daily w NO regard to meals
MED: Biguanide -(2 uses, Bi) how does it work?
- used in combo w Sulfonylureas
- LO hepatic glucose output
- UP insulin sensitivity at cell. so don’t need as much
- taken w 1st meal, 1x day
- DOES NOT cause HYPOglycemia because it doesn’t raise insulin. only makes insulin already there more effective.
- RISK hepatotoxicity. don’t use on pts using contrast mediums because dyes are nephrotoxic. drug already hard on kidneys
MED: Metformin (Glucophage) class
Biguanide
- taken w 1st meal, 1x day
- DOES NOT cause HYPOglycemia because it doesn’t raise insulin. only makes insulin already there more effective.
- used in combo w Sulfonylureas
- LO hepatic glucose output
- UP insulin sensitivity at cell. so don’t need as much
MED: DPP-4 Inhibitors aka (Gliptins) - how do they work?
- hormone in GI tract sign pancreas to produce insulin
- glucagon like polypeptide 1 (GLP-1)
- DPP-4 is protein found in blood. it stops breakdown of diff hormones to UP insulin to LOWER BG.
- short acting in blood
- taken w/out regard to food
- Only for Type II, dependent on insulin releasing cells
i.e. Januvia
MED: Januvia class
Gliptin (DPP-4 Inhibitor)
-taken w/out regard to food. anytime
MED: Glucagon
- converts Glycogen to Glucose
- Emergency med
- UP BG levels
- Rx for unconsios pt (subQ, IV, IM, parenteral)
- must be constituted STAT before injection
- RISK for bleeding with pts on Cumadin
Evidence of internal bleeding?
- urine in blood
- bruising
- bleeding mouth
Insulin pump
- CSII - Continuous SubQ Insulin infusion (mimics pancreas)
- Batter powered computer device
- Admin a BASAL rate or a BOLUS rate
GOAL: keep BG steady btwn meals and at night
Insulin made of
Human or Pork
-if you don’t know what type of insulin pnt uses, use Human
Types of Insulin
Rapid, short, inter, long acting
What type of Insulin can you mix?
All but Lantus (Long Acting)
Where to store insulin?
in fridge. Avoid Extreme temp and agitation.
Discard after 1 mos. and if has precipitate, lumpy, frosted.
Safe use of pump requires?
- committed to checking BG at lease qID (4x day)
- CHO counting method
- adjust Insulin based on BG levels, CHO and physical activity
Pump Advantages
- flexibility in lifestyle
- predictable insulin delivery
- precise insulin deliver
- accurate deliver (up to 1/10th unit) human eye can only see 1u.
- LO episodes of HYPOglycemia
- LO fluctuations in BG
- helps manage Dawn Phenomenon
Pump Disadvantages
- risk of skin infections
- risk of DKA from pump malfunction
- cost
- lets other know you have DM (?)
Good sites for Insulin inj.
fleshy parts
- Abdomen
- back of arm where you can bunch skin
- 45* subq, if can bunch more than 1”, 90*
- needle bevel up
- only RN can administer
Somogyi effect
rebounding high blood sugar that is a response to low blood sugar.
Dawn Phenomenon/Dawn Effect,
abnormal early-morning increase in blood sugar (glucose) — usually between 2 and 8 a.m. — in people with diabetes.
