Diabetes Mellitus
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| What are the 3 types of cells in the pancreas? | Alpha, Beta, Delta
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| Alpha Cells secrete... | Glucagon, and are located in the peripheral portion of the islet
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| Beta Cells secrete.... | Insulin & Mylin, and are located in the central portion of the islet
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| Delta Cells secrete | Gastrin & Somatostatin
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| Insulin is secreted in response to | elevated blood glucose levels
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| 2 Problems associated with DM | Chronic Insulin Dependency (Type I)
Insulin Resistance (Type II)
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| What does insulin Do? | -Blood Glucose levels
+uptake & use of glucose by adipose and muscle cells
+ phosphorylation of glucose by liver
+lipogenesis
+Amino Acid incorporation into proteins
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| Why do we need insulin? | -transport of glucose, amino acid, potassium, & phosphorous across the membrane
-to activate enzymes that promote metabolism
-fixed receptor model-combines with receptor on cell
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| Insulin Deficit causes | -hypoglycemia
+increased fat metabolism
-protein synthesis
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| If insulin is present... | glucose intake is excess of caloric need is stored as glycogen in liver, and muscle or fat , when it is absent or not used.
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| If insulin is deficit there is decreased.... | -transport of glucose across the cell membrane
-glycogenesis & excess glucose remains in the blood
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| If insulin is deficit there is increased... | -glycolysis: glycogen stores are reduced and liver glucose added to blood
-glucogenesis and more liver glucose is added to the blood
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| What happens to the brain when there is an insulin deficit? | Brain cells are not insulin dependent & must have a constant supply of glucose.
-the brain can get glucose out of the blood without insulin
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| What happens to the metabolism when there is an insulin deficit? | fatigue, weakness, and weight loss
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| If a person is hypoglycemic what happens? | They could go into a coma
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| What is hyperosmolarity? | Excess sugar in the blood
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| Glycosuria and osmotic diuresis occurs when... | -Blood Glucose conc. exceeds renal threshold
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| Glycosuria causes.... | -Sugar detected in urine
-lrg amts. of water, electrolytes, and calories may be lost
-polyphagia
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| Osmotic diuresis causes... | -fluid shifts from intracellular to extracellular resulting in a deficit
-body tries to dilute sugar & throws all intracellular water into the blood
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| Glycagon | -counter regulatory hormone to insulin
-promotes use of stored fuels during fasting
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| Glycogenolysis | breakdown of glycogen
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| Glyconeogenesis | Creation of glucose
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| Ketogenesis | Creation of Ketones
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| Lipolysis | breakdown of fat-->results in weight loss
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| Diabetes Risk Factors | -Obesity
-Family Hx
-Race (AA, Latin, Asian, N. Americans)
-HTN
-Triglycerides
-Hx of Fast Glucose btwn 110 & 125
-Delivery of a bby > 9lbs
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| Diabetes Screening | -@ least q yr beginning at age 45 (A1C)
-@ risk ethnic groups (AA, Latin, Asian, N. Americans)
-Bp > 140/90
-Hx of impaired glucose tolerance
-Delivered bby > 9lbs
-Obesity: > 120% of desired weight
-DM in 1st degree relative
-HDL (good) < 35
-Tri
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| Type I Diabetes Facts | -beta cells
-pancreatic failure
-needs insulin replacement
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| Type II Diabetes Facts | -Insulin Resistance
-Deficit
-Have some pancreas function
-These pts take pills
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| Diabetes #1s | -#1 cause of non-traumatic amputations
-#1 reason for dialysis
-#1 cause of blindness in US (diabetic retinopathy)
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| Type I DM info | -Affects 5-10% of all diabetics
-Juvenile onset
-Ketosis prone (DKA)
-Rapid onset
-Viral mediated (abnormal immune response)
-Mostly thin at Dx
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| Type I: Patho | -Cellular destruction, IgG antibodies
-Viral disease or inherited and combined with environment factors
-destruction associated with hla-dr3 or hla-dr4
-lack of insulin, excess glucagon
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| Type I Signs and Symptoms | -polyuria
-polydypsia
-polyphagia
-hyperglycemia
-weight loss
-weakness
-ketosis-->DKA-->Coma
(Ketones pickle the brain causing coma)
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| Type 2: DM Info | -Affects 90-95% of all diabetics
-adult onsdet, ketosis resistent
-usually >40
-Genetic or obesity induced
-no islet cell antibodies
-40% will eventually need insulin
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| Type 2: Patho | -genetic susceptibility unmasked by environmental factors
-pancreas may produce too little insulin
-body can't use insulin that's produced
-resistance
-decreased weight
-decreased # of beta cells
-normal ration of alpha to beta cells
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| Insulin Resistance | Glucose can't move from blood into cells and builds up in the blood
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| The body's insulin responses include.... | -normal: peak at zero then levels out
-Type 2: no significant spike then levels out
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| Type 1.5 Diabetes | -Form of Type 1
-affects people over 30
-produce islet cell antibodies & Glutamic acid decarboylases antibodies that destroy insulin producing cells
-may respond to diet, exercise, and oral agents
-over time insulin production drops and insulin needed
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| Type 1.5 Diabetes continued | -lower lipid & total cholesterol levels
-less HTN
-Less Insulin resistance than Type 2
-Hepatitis
-drug induced toxicity
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| Diabetes Blood Tests | -Glycosylated hbg (A1C <6.5)
-3 hr glucose tolerance test
-self monitoring of blood glucose
-Fastic blood sugar < 100
-2 hr after meal <180
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| A1C test | -if blood sugar is elevated, glucose attaches to hbg for life of the red blood cell (60 to 90 days)
-Shows pattern of blood glucose levels over 2-3 months
-normal values 5-6%
-Prediabetes 6-6.5%
-Diabetes > 6.5%
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| Normal Glucose Values | Fasting < 100
After meal <180
A1C <6
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| Diabetes Diagnosis Criteria | -Fasting BS > 126
-Random BS > 200
-Polyuria
-Polydipsia
-Polyphagia
-Glucose Tolerance Test > 200 after drinking beverage with 75g of carbs
-A1C > 6.3
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| Diabetes Management | -Reducing A1C by 1% to reduce (eye problems, nerve damage, & kidney problems (25%))
-Controlled HTN: BP < 130/80
-Controlled Lipids: LDL, HDL, triglycerides
-Exercise
-Weight Control
-Minimize risk factors
-medications
-prevent complications
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| DIabetes Goals | -Blood glucose: individual goals
-Fasting 80 to 120
-after meal <180
-A1C < 6.5%
-HS BS 100-140
-Urine: negative ketones (if BS > 250)
-Avoid hypoglycemia
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| Blood sugar and the Elderly | Keep it higher than lower to prevent falls
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| To Avoiding Complications | -BP < 130/80
-LDLs < 130
-HDLs > 35
-Daily aspirin for prophylaxis
-Statins every day to reduce risk of coronary artery disease
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| What can a diabetic do to avoid kidney disease? | Take an Ace Inhibitor (prils)
Slows decline in GFR
protect kidneys
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| Adverse reaction of Ace Inhibitors | Dry Cough
Angioedemia
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| What can be used instead of ace inhibitors to protect the kidneys? | Calcium Channel Blockers
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| Monitoring pts with Diabetes | -quarterly dr. visits
-A1C 3 to 6 months
-Lipids annually
-Urinalysis, micoralbumin yearly
-yearly dilated eye exam
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| How does exercise help diabetic patients? | -need for insulin and other meds
+insulin sensitivity in muslces
enhances fibrinolysis
-platelet adhesiveness
-progression from IGT to Type 2
-BS by + uptake of glucose by body muscles
regular exercise 20 to 45 minute aerobics 3x week
if bs <100 ea
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| Weight | -80 to 90% of TYpe 2 are overweight
-establish ideal body weight
-Overweight: loss of 10 to 20 lbs
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| Diet | -medical nutrition therapy
-keep glucose, lipids, & weight as close to normal as possible
-1600, 1800 cal ADA diet
-Carb Counting: (60g limit meals, 30g limit snacks)
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| Oral Drug Therapy | -If A1C > 8, start lifestyle changes
-Avoid clinical inertia
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| What are some Insulin Stimulators (squeeze pancreas)? | sulfonylureas
-glimipride
-glipizide
-glyburide
-meglitimide
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| What are some Insulin sensitizers? | Thiazolidinediones (actos)
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| What are some liver blockers? | Biguanide (metformin)
DPP4s: "gliptins"
(keeps BS down without side effects of sulfa-drugs)
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| Sulfonylureas | -stimulating pancreas to release insulin
-hypoglycemia most common side effect
-First generation no longer used
-2nd generation: (-ide)1/2 hr ac
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| Biguanides | 1st drug of choice (metformin)
used alone or in combo.
--suppresses glucose production in liver
-increases tissue sensitivity to insulin
-doesn't stimulate insulin secreation (no hypoglycemia)
-Enhances weight loss
-GI Upset, diarrhea, take with mea
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| Meglitinides | -Helps pancrease make more insulin
-Take w/ meals
-Very expensive
-Causes gas
-Nateglinide (starlix)
-Repaglinide (prandin)
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| Alpha-glucosidase inhibitors | -Take with 1st bite of food
-work in digestive tract
-excreted by kidneys
-blocks action of enzyme that breaks down carbs
-no hypoglycemia
-SE: flatuence
-Acarbose (precose) & miglitol (glyset)
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| Thiazolidinediones (TZDs) | -decrease insulin resistence
-wt gain
-swelling (may indicate CHF)
-may preserve beta cell function
-class effect + CHF
-risk of osteoporosis in post menopausal women
-Avandia (rosiglitazone) (off market)
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| Dipeptidyl peptidase-4 (DPP IV) inhibitors | -latest class
-reduces blood glucose
-"Gliptins"
-inhibits degredation of GLP-1
-doses based on creatinine clearance
-once daily w/ or w/o meal
-no hypoglycemia
-no GI SE with metformin
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| Combo Drugs | -Glycovance (glyburide & Metoformin)
-Metaglip (glipizide & Metformin)
-Janumet (Januvia & Metformin)
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| Combo Treatment | -insulin +sulfonylurea
-insulin + Metformin
-insulin + alpha-glycosidase inhibitor
-insulin + thiazolidinedione
minimizes cost
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| Injectable Meds | Amylin analog: pramlintide (symlin)
Incretin mimetics: exenatide (Byetta)
Incretin mimetics: liraglitude (Victoza)
Insulin
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| Insulins | All are hypoglycemics
Differ in
a) speed of onset
b) time of peak action
c) duration
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| Types of insulin | Rapid, Short, intermediate, & long-acting
Basal: controls fasting blood sugar (once per day)
Bolus: controls meal time insulin
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| Rapid Insulin | Onset: < 15 min
Peak: 0.5 to 1.5 hrs
Duration: 4 to 6 houris
Out of system after meal is digested
Ex. Lispro (Humalog), Aspart (Novolog)
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| Short Insulin | Onset: 30 to 60 minutes (already finished meal)
Peak: 2 to 4 hours (meal had digested)
Duration: 6 to 8 hours (risk for hypoglycemia before nxt meal)
Ex. Novolin R, Humulin R, regular insulin
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| Intermediate Insulin (bid insulins) | Onset: 1 to 4 hours
Peak: 6 to 12 hours
Duration 12 to 18 hours
these are being phased out
Ex. NpH, Novolin, Humalin
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| Long acting Insulin | Onset: 6 to 14 hours
Peak: many small peaks
Duration: 18 to 36 hours
Ex. Glargine (Lantas), Detemir (Levemir)
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| Mixed Insulin (bid dosing) | Novolin 70/30=Novolin & Regular
Humalin 70/30=Humalin & Regular
Novolog 70/30=Novolog 12 hr & Novolog Short acting
Humalog 75/25=Humalog 12 hour & Humalog Short Acting
Humalog 50/50=Humalog 12 hour & Humalog short acting
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| Insulin strength | u-100 or 100 units/ml (most common)
u-500 or 500 units/ml
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| How is insulin made? | Past: beef and pork pancreata
Now: all human or analog insulin
(human insulin being phased out)
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| Can log insulins be mixed? Ex. Humalog + Novolog | No.
Lantas, Levemir, Novolog, and humalog cannot be mixed with each other. However you can mix Humalog long acting, with humalog short acting
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| What are the rules of injecting insulin? | -store syringes at room temp.
-Don't clean needle with etoh
-store open insulin and pens at room temp
-warm cold insulin
-store pre-filled syringes with needle up
-Draw up regular then nph
-Rotate injection sites
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| What are the preferred insulin injection sites? | Abdomen (fastest absorption)
Arms
thighs
Buttocks
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| IV Insulin | ICU: infusions/drips: Regular
-Regular is cheaper and consistent with no peaks
In 2006: IV approved
-Aspart (recombinant)
-Human insulin (recombinant)-Novolog & Novolin-R
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| Insulin Problems | -allergic reac. (not w/human)
-Lipodystrophy-irreg. absorption
-Lipoatrophy < of sq fat, dimpling
-lipohyperthrophy-dev. of fibrofatty masses
-insulin edema
-insulin resistence- requires > 200 u for more than 2 d w/ no infection. Tx. Diff combo of in
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| Insulin Pens | -Virtually Painless
-3 indicators to verify accuracy of dose (visual, aud, tactile)--safer
-lacks stigma of needle, better adherence
-> cost, shorter storage life 7 to 30 d
-don't carry with needle attached
-Ex. Novolog, Humalog, Levemir, Lantis, Aph
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| Insulin pumps are good for... | -pts who have fluctuating BS levels despite diet & insulin (A1C >7)
-pregnant women
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| What are drawbacks of insulin pumps? | -infection at the site
-catheter clogging
-insulin loss for loose connection
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| Insulin pumps are not good for... | -pts who don't comply with standard diet, insulin, or self monitoring
-pts who miss scheduled appointments
-those who can't recognize hypoglycemia
-pts w/ microvascular diabetic complications
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| Continuous glucose monitoring systems | -several on the market
-sensor implanted under skin in abd, changed q3d
-con't glucose readings sent from transmitter to monitor clipped on belt
-waterproof
-costs $1000, sensor $35
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| Complications of DM | -hypoglycemia
-insulin shock (coma)
-Lipodystrophies
-Hyperglycemia
-DKA
-HHNK
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| Characteristics of hypoglycemia | -BS < 70
-too little food, too much med
-tremors, weakness, cold, clammy, unconscious sudden onset
-Treatment: 15gm carbs prn, retest BS, repeat q 15 min
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| Characteristics of Hyperglycemia | -BS >350
-too much food, too little med, infection
-polyuria, polydypsia, polyphagia
-blurred vision, dry skin, slow onset
-Treatment: insulin
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| Hypoglycemia | -may not proceed from mild to severe
-Beta Blockers (-olol) may mask adrenergic s/s of low BS
- >1/2 episodes occur at night
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| Risk factors of hypoglycemia | -Insulin
-wt loss
-onset of menses
-intense exercise
-etoh
-drugs
-low cal meal
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| Which factors differentiate DKA from HHNKS | -Level of hyperglycemia
-amt of ketones produced
-potassium levels
-amt of vol. depletion
-dosage of insulin needed
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| Mild hypoglycemia | -adrenergic & cholinergic s/s
-sweating, tremor, pallor
-tachycardia, palpitations, anxiety, weakness, hunger, cold, clammy, paresthesia
-Treatment: 15gm of carbs
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| Moderate Hypoglycemia | -neuroglycopenia, impaired function of the brain & CNS
-H/A, irritability, confusion, behavior change, drowsy
-decreased concentration, blurred vision
-Treatment: 15gm carbs
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| Severe Hypoglycemia | -Neuroglycopia: unable to swallow
-disoriented, unresponsive, stupor, sz, coma
-Treatment: glucogon 1 mg sc/IM
-IV-50% Dextrose: check BS 15min
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| What do fast acting carbs do (15gm)? | -Raise BS within 15 min
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| Examples of 15 gm carbs | -4-6 oz OJ
-3 glucose tabs
-4-6 oz reg. soda
-piece of fruit
-8 oz milk
-2 T raisins
-3-4 packets of sugar
-1 tube glucose gel
-1 tube cake icing
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| Characteristics of HHNK | -Usually Type 2
-BS >1000
-Azotemia, hct
+ plasma osmolarity
+pH >7.45
+bicarb >15
+BUN & creatinine
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| S/s of HHNK | Dehydration
hypotension
- CVP
dry mucus membranes
-skin turgor
neurologic impairment
seizures
confusion
tremor
hallucinations
coma
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| Characteristics of DKA | Usually Type 1
BS >500 but <1000
+Plasma osmolarity
-pH < 7.3
-Bicarb <15
+BUN
hyperkalemia (initially)
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| S/s of DKA | dehydration (thirst)
hypotension
tachycardia
dry skin
dry mucus membranes
Kussmaul respirations
Acetone breath (fruity)
polyuria
nocturia
visual disturbances
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| Treatment for HHNKS | FLUIDS
insulin to a lesser degree
assess for & treat cause
monitor neuro and cv status
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| Treatment for DKA | INSULIN
fluids to a lesser degree
D5NS if BS <250
correct BG first then lytes
monitor K levels
if pH <7 may give bicarb
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| Etiology of HHNKS | Type 2 diabetes
concurrent illness
elderly & institutionalized
drugs, enteral feedings, peritoneal dialysis
mortality up to 70%
Preventive ED: call provider if 2 consecutive BS > 300, tired w/o cause, frequent urination
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| Etiology of DKA | Type 1 diabetic
young pt
missed or reduced insulin dose
stress, growth spurts, pregnancy, infection, surgery
meds-thiazie, phenytoin, glucocorticoids, sympathomimetics
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| DKA Pathology | -stimulates counterreg. hormones, causes incr. in BS severe circulating insulin ineffective
-can't burn glucose w/o insulin-->fat metab.-->Inc. ketones-->overloads metabolic sys. & resp. buffering begins
-glucose in urine, diuresis-->dehyd & lyte imbal.
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| Macrovascular complications | -atherosclerotic changes
-cerebrovascular disease
-coronary artery disease
-renal artery stenosis
-peripherovascular disease
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| Microvascular complications | -neuropathies
retinopathies
nephropathies
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| Retinopathy | -DM leading cause of blindness
-Types: Background & proliferative
-vision not affected w/ background
-can become blind w/proliferative
-Type 1: visit opthamologist w/in 5 yr of dx & yrly therafter
-Type 2: examined @ dx & yearly
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| Nephropathy | -proteinuria 1st sign
-low protein diet
-ace inhibitors, calcium antagonist decreased protein excretion
-diabetic nephrology is the number one leading dx of new dialysis
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| Autonomic neuropathy | -affects cardiovascular, GI, & urogenital
-GI: gastroparesis--stomach empties slowly, fills up quickly, bloated, retain food for 12 hrs, BS fluctuates
-RX: frequent sm. meals, low fat & fiber, reglan
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| Peripheral neuropathy | -numbness, tingling, burning pain in fet
-sy usually initially worse @ nite
-relieved by walking progressing to constant w/ greater intensity
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| Peripheral Vascular Disease | -DM #1 cause of amputations in US
-aggravated by activity
-relieved by rest
-cold, loss of hair
-shiny skin, toenail hypertrophy, decreased pulses, pallor on elevation, prolonged cap refill
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| Diabetic food care | -never barefoot, well fitting shoes, clean stockings
-don't self treat corns, ingrown toenails, etc.
-avoid smoking (decr. circul.) & cold exposure
-check temp of h20 before bathing
-don't use heating pad or hot h20 bottles
-don't cross legs when sit
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| What is Regranex? | -topical gel
-stimulates collagen growth
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