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
Fasting Plasma Glucose
Normal: Less than 100 Pre: 100-125 Diabetes: 126
26
Oral Glucose Tolerance Test
Normal: Less than 140 Pre: 140-199 Diabetes: 200 higher
27
Random Glucose Test
Greater than 200
28
Four glucose emergencies can occur in pts with DM
1. Hyperglycemia 2. Hypoglycemia 3. Diabetic Ketoacidosis 4. Hyperglycemic Hyperosmolar State - Emergency treatment
29
Hyperglycemia
Over 140 mg/dl - Caused by - Physical stress - Infection - Steroids - Nutriton S/S : polyuria, polydipsia, polyphagia
30
Hypoglycemia
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
Problem with Long-Term Hypoglycemia ( T1DM )
Hypoglycemic unawareness - Patients no longer have the warning symptoms. Loses ability to secrete glucagon in response to hypoglycemia as well!
32
Hypoglycemia Assessment
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
Hypoglycemia Intervention
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
DKA
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
DKA Assessment
Polydipsia Polyuria Polyphagia Rotting Citrus Fruit odor *Kassmaul Respirations Vomiting Abdominal pain Weakness Confusion Shock Coma
36
DKA Intervention
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
DKA vs Hyperglycemic Solar State
DKA: Serum Glucose- 300 mg, Osmolarity- Variable HHS: 600 mg, 320
38
HHS
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
HHS Intervention
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
Chronic complications of DM
Blood vessel changes that lead to complications from poor tissue perfusion and tissue ischemia
41
Microvascular Diseases
Diseases of smaller vasculature
42
Macrovascular Diseases
Diseases of larger vasculature
43
Microvascular Diseases
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
Neuropathy ( Micro )
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
Macrovascular Complications
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
Insulin
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
Insulin complications / Interactions
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
Insulin Nursing Admin
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
Storage of Insulin
Premixed vials: 3 months Premixed syringes: 1-2 weeks - Neede UP
50
IV Admin for Insulin
Regular 100 units/100 ml of 0.9% Aspart, glulisine, lispro= Short acting
51
Rapid Acting Insulin
Lispro, Aspart, Glulisin Onset: 15-30 min Peak: 0.5-2.5 hr Duration: 3-6 hrs
52
Short Acting Insulin
Regular, Novolin R Onset: 0.5-1 hr Peak: 1-5 hr Duration: 6-10 hrs
53
Intermediate Acting Insulin
NPH, Detemir Onset: 1-2 hr Peak: 6-14 hrs Duration: 16-24 hrs
54
Long acting insulin
Glargine Onset: 70 mins Peak: None Duration: 18-24 hrs
55
Sulfonylureas: Chlorpropamide, Glipizide, Glyburide, Glimepiride
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
Meglitinides: Repaglinide, Nateglinide
Insulin release from pancreas For hyperglycemia - Ends in glinide Complications: Hypoglycemia, weight gain Interactions: Gemfibrozil= Increased hypoglycemia Admin: 30 mins before mealtime
57
Biguanides: Metformin
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
Alpha Glucosides Inhibitors: Acarbose, Miglitol
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
Thiazolidinediones: Pioglitazone, Rosiglitazone
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
Amylin Mimetics: Pramlintide
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
GLP-1 ( Exenatide, Liraglutide, Albigliutide )
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
Hyperglycemic Agent
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
Surgical Recovery in Diabetics
* 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
Diabetes at high risk for?
Surgical problems MI, Stroke, HTN, Cardiomyopathy Urinary retention Delayed gastric emptying
65
Surg Recovery Pre OP
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
Surg Recovery Intra Op
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
Surg Recovery Post Op
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
In what patients situation would you use glucagon?
Emergency management! - Unconscious
69
Why do diabetics have a higher risk of complication in surgery?
Ketoacidosis, higher stress levels = Releasing Epi and glucagon which raises levels
70
Why do we have insulin dosing to maintain BG of 140-180 mg/dl in diabetics post op?
Hyperglycemia = High Mortality Monitor tube feeding, NPO = Low BG