Exam #2 Diabetes Flashcards

1
Q

Glucose

A

“Sugar” the body needs to survive fuels the cells of your body so they can work properly but it can not enter the cell without the help of INSULIN.

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2
Q

Insulin

A

Deals with high blood sugar levels; lowering!
- It regulates amount of glucose in the blood, it allows your body to use glucose by allowing it to enter the cells
- Secreted by the BETA cells of the pancreas from the islets of Langerhans.

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3
Q

Glucagon

A

Deals with low blood sugar levels; bringing it up
- a peptide hormone that causes the liver to turn glycogen into glucose
- secreted by pancreas

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4
Q

Pancreas

A

Releases insulin and glucagon

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5
Q

Glycolysis

A

The breakdown of carbohydrates
- Central to all the metabolic pathways of carb metabolism
- All body tissues use the glycolytic pathway for the breakdown of glucose to provide energy.

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6
Q

Glycogen

A

The storage form of glucose
- Located in skeletal muscle and liver
- In SM, glycogen acts as a fuel reserve for use in the synthesis of ATP during muscle contraction
- In the liver, glycogen acts as a fuel reserve to maintain blood glucose concentrations

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7
Q

Glycogenolysis

A

The process through which liver and muscle glycogen are converted to glucose

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8
Q

Gluconeogenesis

A

The formation of glucose or glycogen from non-carbohydrate sources.

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9
Q

Ketogenesis

A

Production of ketones
= BAD

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10
Q

When do blood glucose levels rise?

A

After a meal

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11
Q

When blood sugar rises cells in the pancreas release what?

A

Insulin, causing the body to absorb glucose from the blood and lowering the blood sugar level to normal.

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12
Q

When blood sugar drops to low…

A

The level of insulin declines and other cells in the pancreas release glucagon, which causes the liver to turn stored glycogen back into glucose and release it into blood.
- Brining blood sugar levels back up to normal.

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13
Q

Diabetes Mellitus

A

Complex disorder of impaired nutrient metabolism, especially glucose, that can affect the function of every body system.
- The body is unable to make insulin either the absence of it or resistance. So patients suffers from hyperglycemia.

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14
Q

Type 1 Diabetes

A

An autoimmune condition in which the pancreas being unable to make insulin at all.
- The beta cells don’t work, so the body doesn’t release anymore insulin.

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15
Q

T1DM Risk Factors

A

Genetics, virus, not related to lifestyle!

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16
Q

Type 2 Diabetes

A

Progressive disorder in which the person initially has insulin resistance that progresses t decreased beta cell secretion.
- Cells stop responding to insulin
- INSULIN RESISTANT
- The patients experiences hyperinsulinemia

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17
Q

T2DM Risk Factors

A

Lifestyle, being obese, sedentary lifestyle, poor diet, stress, genetic

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18
Q

TDDM Treatment

A

Diet and exercise when that does not work medications are started.
- May need insulin during stress, surgery or infection.

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19
Q

Gestational Diabetes Mellitus ( GDM )

A

Glucose intolerance with onset in or first recognition during pregnancy.

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20
Q

Metabolic Syndrome
( Pre-Diabetes )

A

Presence of metabolic factors that increase the risk for developing type 2 DM and cardio disease.
1. Abdominal Obesity: WC of 40 inches, 35 inches for women
2. Hyperglycemia: 100 mg
3. Hypertension
4. Hyperlipidemia

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21
Q

Diabetes Mellitus: Life w/o Insulin

A

Absence of insulin = Glucose build up resulting in hyperglycemia
- Polyuria: Peeing
- Polydipsia: Thirst
- Polyphagia: Hunger

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22
Q

Without enough insulin the body turns to stored fat for energy…

A

Small ketone bodies, abnormal acidic breakdown results in acid breakdown - metabolic acidosis.
- Krebs cycle becomes blocked
= Kussmaul Respiration: Increased rate and depth of breathing. Acetone gives the breath a “rotting citrus fruit” odor.

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23
Q

Diabetes is considered at any age in adults with a BMI greater than 25 kg/m with one or more of these factors

A
  • Have a first degree relative w Diabetes
  • Are physically inactive
  • Hypertensive
  • A1C greater than 6.5%
  • History of vascular disease
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24
Q

Health promotion and maintenance

A

Nutrition: Meal plan, education, consistency
Carbohydrate intake- focus on veggies, fruits, whole grains and dairy products. 25g of fiber daily.
Counting Carbs: 1 unit of rapid acting insulin for each 15 grams of CHO.
Exercise: Increased physical activity. Can cause hypoglycemia.
- If ketones are present do not exercise.
- Insulin levels are not adequate and that exercise would continue to increase glucose levels

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25
Q

Fasting Plasma Glucose

A

Normal: Less than 100
Pre: 100-125
Diabetes: 126

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26
Q

Oral Glucose Tolerance Test

A

Normal: Less than 140
Pre: 140-199
Diabetes: 200 higher

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27
Q

Random Glucose Test

A

Greater than 200

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28
Q

Four glucose emergencies can occur in pts with DM

A
  1. Hyperglycemia
  2. Hypoglycemia
  3. Diabetic Ketoacidosis
  4. Hyperglycemic Hyperosmolar State
    - Emergency treatment
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29
Q

Hyperglycemia

A

Over 140 mg/dl
- Caused by
- Physical stress
- Infection
- Steroids
- Nutriton
S/S
: polyuria, polydipsia, polyphagia

30
Q

Hypoglycemia

A

Blood glucose levels below 70.
- Brain needs constant supply of glucose because it cannot store it.
- When BG reaches 67 mg, hormones increase.
- Main balancing hormone is Glucagon.

31
Q

Problem with Long-Term Hypoglycemia
( T1DM )

A

Hypoglycemic unawareness
- Patients no longer have the warning symptoms.
Loses ability to secrete glucagon in response to hypoglycemia as well!

32
Q

Hypoglycemia Assessment

A

Causes:
- Too much insulin
- Wrong injected time
- Wrong type of insulin
- Decreased food intake
- Delayed gastric emptying

Signs:
- Sweating, tremors, anxiety, tachycardia, hunger, confusion, paralysis, seizure, coma

33
Q

Hypoglycemia Intervention

A

Administer glucose- 15 g
Apple juice, milk, glucose tablets

If unconscious: Dextrose IV, Glucagon SQ, IM

Monitor VS every 15 mins until BG stabilizes

34
Q

DKA

A

State of absolute or relative insulin deficiency with hyperglycemia, metabolic acidosis, ketonemia
- Happens when blood sugar is too high for too long.
- Infection is most common cause
- T1DM
- 10% result in death

35
Q

DKA Assessment

A

Polydipsia
Polyuria
Polyphagia
Rotting Citrus Fruit odor
*Kassmaul Respirations
Vomiting
Abdominal pain
Weakness
Confusion
Shock
Coma

36
Q

DKA Intervention

A

Check vitals Q15 mins
Fluid therapy: Perfusion to organs
0.9 NS, 15-20 ml
When BG reaches 250 mg give 5% dextrose in 0.45 saline

Drug:
Regular insulin by cont IV infusion
Change to SQ when ketosis has stopped
Bicarb used for severe acidosis
- Considered resolved when BG is lower than 200, Bicarb is higher than 18, pH is higher than 7.30 and CAG is less than 12.

37
Q

DKA vs Hyperglycemic Solar State

A

DKA: Serum Glucose- 300 mg, Osmolarity- Variable
HHS: 600 mg, 320

38
Q

HHS

A

Severe hyperglycemia and coma w/o ketosis
Risk: T2DM
***Metabolic acidosis does not devolep:
Blood Glucose: 600 mg/dl
Blood osmolarity: 320 mOsm/l

S/S: Seizures, coma, hemiparesis

39
Q

HHS Intervention

A

Rehydration + restore normal BG in first 36-72 hrs
Normal saline 1L/hour
Reduce 100-200 ml/hr w half fluid replaced within first 12 hrs.
Continue IV until
- BG of 250 mg/dl
- Goal BG reduction 50-70 mg/dl per hour
- Monitor for hypokalemia
- Check VS every 1-2 hrs
- Cardiac monitoring

40
Q

Chronic complications of DM

A

Blood vessel changes that lead to complications from poor tissue perfusion and tissue ischemia

41
Q

Microvascular Diseases

A

Diseases of smaller vasculature

42
Q

Macrovascular Diseases

A

Diseases of larger vasculature

43
Q

Microvascular Diseases

A

Retinopathy: Damage to blood vessels in the tissue target of the back of the eye.
S/S: floaters, blurriness, dark areas of vision, color blind

Nephropathy: Kidney damage causes high blood pressure.

44
Q

Neuropathy ( Micro )

A

Nerve disfunction
- Peripheral: Loss of sensory perception
- Contributes to diabetic foot ulcers

Cardiac Autonomic: Sympatheitc and parasympathetic nerves of heart and blood vessels
- Contributes to left ventricular dysfunction, painless MI, orthostatic hypotension, syncope, exercise intolerence

45
Q

Macrovascular Complications

A

Cerebovascular Disease: diabetes contributes to likelihood of severe cartoid atherscleorosis.
- HTN, Hyperlipidemia, neuropathy and PVD increase stroke
- ETOH and tobacco use further risk of stroke
- 2-4 times higher in adults w DM

Cardiovascular Disease: Diabetic patients have all the CVD risk factors of obesity, high blood lipid levels, hypertension and sedentary lifestyle.

Focus on… Smoking cessation, diet, exercise, blood pressure control

46
Q

Insulin

A

Promote cellular uptake of glucose, converts glucose into glycogen, moves K+ into cells.

Therapeutic uses: Glycemic control of DM, T2D can require insulin when…
- Oral meds, diet, exercise not working
- Severe liver disease
- Painful neuropathy
- Surgery
- DKA / HHS treatment
- Hyperkalemia

47
Q

Insulin complications / Interactions

A

Hypokalemia
- Insulin can decrease K+ levels
Lipohyperthrophy: Rotate injection sites!

Interactions: Sulfonylureas, meglitnides, beta blockers, thiazide, glucocosteroids

  • Do not administer rapid acting insulin then skip meal then exercise!
  • Beta blockers mask hypoglycemia!
48
Q

Insulin Nursing Admin

A

Adjust insulin to meet needs: Meal times
Short acting drawn first
NPH + premixed should appear cloudy
* Glargine and Determir are clear and should not be given IV or mixed!
* Lispro, Aspart, Regular: SQ, IV

49
Q

Storage of Insulin

A

Premixed vials: 3 months
Premixed syringes: 1-2 weeks
- Neede UP

50
Q

IV Admin for Insulin

A

Regular 100 units/100 ml of 0.9%
Aspart, glulisine, lispro= Short acting

51
Q

Rapid Acting Insulin

A

Lispro, Aspart, Glulisin
Onset: 15-30 min
Peak: 0.5-2.5 hr
Duration: 3-6 hrs

52
Q

Short Acting Insulin

A

Regular, Novolin R
Onset: 0.5-1 hr
Peak: 1-5 hr
Duration: 6-10 hrs

53
Q

Intermediate Acting Insulin

A

NPH, Detemir
Onset: 1-2 hr
Peak: 6-14 hrs
Duration: 16-24 hrs

54
Q

Long acting insulin

A

Glargine
Onset: 70 mins
Peak: None
Duration: 18-24 hrs

55
Q

Sulfonylureas: Chlorpropamide, Glipizide, Glyburide, Glimepiride

A

Stimulates pancreas to release insulin
For Hyperglycemia
- End in ides, zide, mide, ride
Complications: Hypoglycemia, weight gain, photosensitivty
Contradictions: Patients w sulfa allergy
Interactions: ETOH can cause disulfiram reaction, NSAIDS, sulfa, ABX ( hypoglycemia )
Beta blockers- Mask hypoglycemia
Admin: 30 min prior to breakfast, needs to be taken w meals

56
Q

Meglitinides: Repaglinide, Nateglinide

A

Insulin release from pancreas
For hyperglycemia
- Ends in glinide
Complications: Hypoglycemia, weight gain
Interactions: Gemfibrozil= Increased hypoglycemia
Admin: 30 mins before mealtime

57
Q

Biguanides: Metformin

A

Reduce liver glucose production
For hyperglycemia
Complications: GU, Vit B12 and Folic acid Def, Lactic acidosis
DO NOT GIVE TO RENAL FAILURE PATIENTS!
BEFORE surgery Metformin is stopped at least 1 day prior and restarted once kidney function has returned to normal or baseline

58
Q

Alpha Glucosides Inhibitors: Acarbose, Miglitol

A

Lowers blood sugar by slowing down the breakdown of starchy foods in GI
For Hyperglycemia
Complications: GI, anemia, hepatoxicity, impaired breakdown of sucrose
Interactions: Insulin, Sulfonylureas- Increased hypoglycemia
* Do not give if GI disorder
- Take w first bite of food, do not double up

59
Q

Thiazolidinediones: Pioglitazone, Rosiglitazone

A

Increases cellular response to insulin by decreasing insulin resistance
- Complications: Fluid retention, increased LDL, hepatoxicity
- ***Contradicitons: Heart failure, CHF, bladder ca
- Interactions: Insulin- Increased fluid retention

60
Q

Amylin Mimetics: Pramlintide

A

Decrease gastric emptying, inhibit secretion of glucagon
- N/V reaction at injection sites.
- Contradicted: Preg C, Kidney failure, Thyroid disease, osteoprosis, etoh
- Interactions: Insulin: Hypoglycemia, opiods
- Take 1-2 hrs prior before injected ( oral )
- Use thigh, abdomen, keep at least 5 cm from insulin injection, keep refridgerated for 28 days

61
Q

GLP-1 ( Exenatide, Liraglutide, Albigliutide )

A

Mimics glucagon like peptide 1 hormone. Increases insulin in response to a meal, decrease secretion of glucagon, slows gastric emptying.
Contradictions: Preg C, Kidney Failure, Crohns, Pancreatis, Older adult
Comp: GI, pancreatitis
Admin: Use thigh or abdomen or upper arm, give within 60 mins before morning or evening meal.

62
Q

Hyperglycemic Agent

A

Glucagon
- Increase blood glucose by increasing the breakdown of glycogen into glucose.
- ***Emergency management for hypoglycemic reaction
- Administer glucagon SQ,IM or IV
- Provide oral glucose

63
Q

Surgical Recovery in Diabetics

A
  • High risk of complications
  • Anesthesia can cause increase of counterregulatory hormones that elevate blood glucose.
  • HHS is present and increases mortality
  • AKI can happen from diuresis from hyperglycemia
64
Q

Diabetes at high risk for?

A

Surgical problems
MI, Stroke, HTN, Cardiomyopathy
Urinary retention
Delayed gastric emptying

65
Q

Surg Recovery
Pre OP

A

Blood glucose checks = Reduce risk for complications!
- Metformin + Sulfonylureas stopped 1 day prior to surgery.
- All other orals stopped day of surgery
- Long acting may need to be changed to intermediate acting 1-2 days before surgery.
- BG= <200

66
Q

Surg Recovery
Intra Op

A

Hourly glucose checks!
- BG: 140-180
- Blood sugars may be higher during surgery because stress releases glucagon and epi.
- Pts recieve 5 g of glucose per hour during surgery! *

67
Q

Surg Recovery
Post Op

A

Insulin Dosing
- BG: 140-180 mg/dl
- Monitor Opiod Use
–> beta blockers mask hypoglycemia, hyperglycemia occurs before a fever
- Hyperglycemia = High mortality level
- Monitor tube feeding, NPO= Low BG

68
Q

In what patients situation would you use glucagon?

A

Emergency management!
- Unconscious

69
Q

Why do diabetics have a higher risk of complication in surgery?

A

Ketoacidosis, higher stress levels = Releasing Epi and glucagon which raises levels

70
Q

Why do we have insulin dosing to maintain BG of 140-180 mg/dl in diabetics post op?

A

Hyperglycemia = High Mortality
Monitor tube feeding, NPO = Low BG