NUR 239 Study Guide - Final Guide: Diabetic Neuropathy, Adipose Tissue, Diabetes Mellitus Type 2
21 May 2018
School
Department
Course
Professor
Mennonite College of Nursing at Illinois State University
NUR 239 – PathoPharm 1
Book/ Chapter
Topic/Pages
# of ?’s
Porth Chapter
33 - Diabetes
Mellitus and
the Metabolic
Syndrome
Glucose-Regulating Hormones/794 – 799
1. Insulin
1) Promotes glucose uptake by target cells and allows glucose to be stored as
glycogen
2) Prevents fat and glycogen breakdown
o Inhibits gluconeogenesis & increases protein synthesis
2. Glucocorticoid Hormones- How does stress effect cortisol levels?
o Increase in ATCH, which causes an increase ion cortisol secretion;
Hypoglycemia is major stimulus for cortisol release.
3. Diagnostic Criteria for metabolic syndrome?
o 3+ of the following: Intra-abd. obesity, elevated TG (triglycerides) > 150
mg/dL, low High-density lipoproteins (<50 mg women or <40 men), blood
pressure > 130/85 mm Hg, & fasting glucose >100
4. What are the risks for Type 1 DM?
- Hypoglycemia due to ability to maintain glucose levels hampered because
failure to suppress absorption of injected insulin, insulin absorption
increases, even after exercise, insulin’s lower effect continues 3 hours, liver
& skeletal muscles increase uptake of glucose for stores
5. Diabetic Management- How would multiple day injections of insulin work?
- Basal insulin requirements are met by intermediate/long-acting insulin 1-2
day by bolus or injection devices.
6. What times of the day would a patient give intermediate and rapid acting types
of insulin?
- Intermediate acting → Taken in the morning but have slower onsets, takes
more hours to reach therapeutic levels so their use in Type 1 requires
supplementation with rapid/short-acting insulin. With MDIs (multiple day
injections), the base insulin requirements are met by an intermediate or long-
acting insulin administered 1-2x daily. Boluses of rapid or short acting
insulin are used before meals.
- Rapid acting → given 30 minutes before meals
- Long acting → May need rapid supplements
- Short acting → Works within 30 minutes, lasts 5-8 hours
Acute Complications
7. DKA: hyperglycemia & dehydration (electrolyte loss) lead to this; develops
when individual has no insulin reserve (Type 1). It is the result of fatty acids
from adipose tissue.
- Treatment: Improve circulatory volume & tissue perfusion, decrease blood
glucose, and correct the acidosis & electrolyte imbalances. You do this by
administering insulin and IV fluids/electrolyte imbalances.
8. Hypoglycemia: Reaction from excess of insulin, low blood sugar
- Treatment: Immediate administration of 15g of glucose carbs; IV
dextrose/glucagon, juice. If a patient is unconscious or unable to swallow,
glucagon may be IM or 50% glucose solution may be given IV.
Chronic Complications:
9. Diabetic Neuropathies aka peripheral neuropathies: Impaired and delayed
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healing is a complication of chronic neuropathies; kidneys is one of the first
manifestations of diabetic neuropathy is an increase in urinary albumin
excretion (microalbuminuria).
o HTN accelerates the progression of diabetic nephropathy, even a moderate
lower of the BP can decrease the risk of Chronic Kidney Disease
(CKD)
10. Foot Ulcers: Most common complication in DM leading to hospitalization,
distal symmetric neuropathy is a major risk factor for foot ulcers. Results
from neuropathy, can’t feel breakdown of skin, impaired pain sensation.
Caused by constant trauma, poor fitting shoes, improper weight bearing,
gait. Self-check every day.
11. Infections: Soft tissue infections of extremities, osteomyelitis, UTI’s, more
serious for them, may not feel it, suboptimal response.
Overview of Diabetes
12. Type 1- absolute deficiency of insulin because of destruction of pancreatic beta
cells (mostly seen in children),
o Insulin promotes glucose uptake by the target cells & requires
exogenous insulin for life because they don’t make any of their own
o Type 1a is caused by an auto-immune destruction of the pancreatic
beta cells.
o Exercise Risks: Symptoms of hypoglycemia occur several hours after
cessation of exercise because subsequent insulin doses are not adjusted to
accommodate the exercise-induced decrease in blood glucose. Not only is
there an inability to suppress insulin levels, but insulin absorption may also
increase.
13. Type 2- insulin resistance, increased glucose production by the liver, impaired
secretion by the pancreas
o Insulin resistance – the failure of the target cells to respond to insulin.
Often because of pancreatic beta cell hyper-function (so they get worn out
& stop working) and hyperinsulinemia (keep secreting insulin to try to
lower blood glucose but the insulin doesn’t work because of resistance)
o Type 2 DM is the result of beta cell exhaustion due to long standing
insulin resistance.
14. Which type needs exogenous insulin for life?
- Type 1
15. What are the long-term complications of DM?
- DKE: Severe insulin insufficiency, life-threatening, glucose can’t be used by
the body cells for energy, fat used instead & fat starts floating in the
bloodstream, kidneys try to excrete.
- S&S: Blurred vision, anorexia, vomiting, thirst, polyuria, treatment is
insulin, IV fluids, K+ supplements.
- Hyperosmolar hyperglycemia non-ketotic coma: Rare but excessive amount
of glucose, high mortality, osmotic diuresis, leads to extreme thirst, polyuria,
dehydration treat same.
16. Do type 2 DM patients have to take insulin?
- Not unless it advances.
Insulin
17. What type of insulin is administered IV?
- NPH/Regular insulin
18. How is the type of insulin used determined?
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- The type of insulin prescribed is based on onsets & durations of actions.
Before administering insulin in the hospital, the nurse must have a colleague
confirm the dosage. Endogenous insulin is produced by the pancreas,
exogenous insulin is given by injection.
19. How can you prevent hypoglycemia?
- Maintain glucose level 100-200, spread snacks throughout the day.
20. Onset of action & Peaks of Types of Insulin
- Regular insulin is the insulin of choice for DKA. It is also the most common
insulin regimen, but doesn’t give as tight of blood glucose control as other
regimens. Two daily doses of NPH regular or insulin analog. First dose is
given before breakfast- covers breakfast and lunch, peaks in afternoon.
Second dose is before dinner, covers dinner and through the night.
➢ Long Acting Insulin (insulin glargine and insulin detemir) to mimic the basal
metabolic rate
o Lantus and Levemir- steady state, never really peaks just lasts the
whole 24 hours
➢ Short acting for meals and bedtime (insulin lispro/humalog, insulin
aspart/novolog, insulin glulisine/apidra
o Regular insulin (Humulin R, Novolin R)- spikes quickly and is gone
quickly
o Intermediate (isophane/NPH)- doesn’t spike as high and lasts a little
longer
o Short acting insulin: (Humulin R, Novolin R (regular insulin): Only
Insulin given IV; Used for DKA/HHNC, acute/emergency
situations
▪ Onset short-acting insulin: 30-60 minutes
▪ Peak short acting insulin: 2-3 hours
Sulfonylureas/730-733 - glipizide (Glucotrol), glyburide (DiaBeta)- enhance insulin
secretion
21. It is effective only when there are functioning beta cells in the pancreas (so
doesn’t work in type 1 or type 2 bad enough to almost have non-functioning
beta cells).
22. Contraindicated with allergy to sulfonamides
Alpha-Glucosidase Inhibitors: Acarbose (Precose)- delay absorption of carbs
23. Improves the A1C, Works best used with a sulfonylurea
- Action: Delays the digestion of carbohydrates
Biguanides/734-735 – suppress glucose production, enhance insulin in peripheral
tissues
24. Metformin contraindicated in diabetes complicated by fever, pregnancy, Severe
infections, trauma, major surgery, severe liver or kidney impairment
(decreases glomerular filtration rate), cardiac or respiratory insufficiency
Dipeptidyl-Peptidase-4 (DPP-4) Inhibitors - Sitagliptin (Januvia)
25. Action: Incretin hormones stimulate insulin release in response to meals, which
normalizes glucose levels. Sitagliptin minimizes (slows) the rate of
inactivation of the incretin hormones and prolongs their activity. This drug
increases and lengthens the release of insulin and decreases hepatic glucose
production, promoting glycemic control. Only used for Type 2 DM
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Document Summary
Mennonite college of nursing at illinois state university. Glucose-regulating hormones/794 799: insulin, promotes glucose uptake by target cells and allows glucose to be stored as glycogen, prevents fat and glycogen breakdown. # of ?"s: inhibits gluconeogenesis & increases protein synthesis, glucocorticoid hormones- how does stress effect cortisol levels, increase in atch, which causes an increase ion cortisol secretion; Hypoglycemia due to ability to maintain glucose levels hampered because failure to suppress absorption of injected insulin, insulin absorption increases, even after exercise, insulin"s lower effect continues 3 hours, liver. Intermediate acting taken in the morning but have slower onsets, takes more hours to reach therapeutic levels so their use in type 1 requires supplementation with rapid/short-acting insulin. With mdis (multiple day injections), the base insulin requirements are met by an intermediate or long- acting insulin administered 1-2x daily. Boluses of rapid or short acting insulin are used before meals. Rapid acting given 30 minutes before meals.
