Exam 3: Diabetes Flashcards
1
Q
Percentage of the US population affected by diabetes
A
8.3% (25.8 million people
2
Q
Risk factors for getting DM (8)
A
- Parent, brother, sister with diabetes
- Race
- Gestational diabetes / gave birth to baby with high birth weight
- Pre-diabetes (FBC of 100-126)
- Overweight
- Inactivity
- High BP
- Abnormal Cholesterol levels
3
Q
Abnormal cholesterol levels that put a person at risk for DM (3)
- LDL
- HDL
- Triglyceride
A
LDL > 100
HDL 250
4
Q
Function of the pancreas as an exocrine gland
A
Releases digestive enzymes
5
Q
Function of the pancreas as an endocrine gland
A
Beta cells secrete insulin
6
Q
How does glucose enter the bloodstream? (3 ways)
A
- Intestinal absorption
- Glycogenolysis in the liver
- Gluconeogenesis (Protein catabolism)
7
Q
What is glucose used for… in tissues?
A
Oxidation
• CO2 + H20 + E
8
Q
What is glucose used for… in the liver?
A
Glycogenesis (glycogen formed)
9
Q
What is glucose used for… in energy storage? (2)
A
- Converted to fat
- Stored as glycogen in muscles
10
Q
When is glucose excreted in urine?
A
BS level exceeds 200
11
Q
Roles of insulin (5)
A
o Transports and metabolizes glucose for energy
o Stimulates the storage of glucose in the liver (Glycogenesis)
o Enhances the storage of fat in adipose tissue
o Transports amino acids and glucose into the cells
o Inhibits the breakdown of stored glucose, protein and fat
12
Q
Constant level of blood sugars occurs in fasting state due to what two factors?
A
- Pancreas releases insulin
* Pancreas releases small amounts of glucagon (Glycogenolysis)
13
Q
When does glyconeogenesis occur?
A
After 8-12 hours without food
14
Q
Pathophysiology of DM Type 1
- MAIN THING
- Three physiological results
- MAIN RESULT
A
- MAIN THING: Destruction of Beta cells
1) Means that glucose is not stored as glycogen
2) Glycogenolysis and gluconeogenesis occur unrestrained
3) Fat breakdown occurs
- MAIN RESULT: Hyperglycemia
15
Q
Pathophysiology of DM Type 2
- Main thing (2)
- Main result
A
- MAIN THING: Insulin resistance and / or decreased production of insulin
- MAIN RESULT: Hyperglycemia
16
Q
Usually a DM2 patient would be started on lifestyle changes before any medication is introduced.
What patient would have lifestyle changes AND medication started right away?
A
A patient who also has cardiac problems
17
Q
Length of onset: DM1 vs DM2
A
DM1: Rapid onset
DM2: Slow onset
18
Q
What does “insulin resistance” mean?
A
- Insulin resistance: Cells are not responsive to stimulating glucose uptake
19
Q
What is the body’s initial response to insulin resistance?
What eventually occurs?
A
Insulin levels will rise to compensate
Eventually, body can’t produce enough insulin: Glucose rises.
20
Q
DM Diagnosis: Fasting Blood Glucose #
A
126mg/dL or higher
21
Q
DM Diagnosis: Random glucose level #
A
200 mg/dL or higher on more than one occasion
22
Q
DM Diagnosis: Hemoglobin A1C #
A
> 6.5 or 7
23
Q
Cause of hyperglycemia (4)
A
- Too much food
- Too little insulin or DM med
- Illness
- Stress
24
Q
Onset of hyperglycemia
A
- Gradual
- May progress to diabetic coma
25
Sxs of hyperglycemia
- Extreme thirst
- Frequent urination
- Hunger
- Dry skin
- Frequent urination
- Blurred vision
- Drowsiness
- Decreased healing
26
Why does a hyperglycemic patient experience hunger?
Becasue not enough glucose actually gets into cells - extreme hunger
27
How often should you check blood sugar for Type 1 DM?
2-4x per day
28
How often should you check blood sugar for Type 2 DM?
2-3x per week, with one two hours post prandial
29
What type of insulin is used for fractionals
Regular insulin always
30
What type of fluids should you use with hyperglycemic patients?
Hypotonic or Isotonic
31
CHO - PROTEIN - FAT
| percentages for diabetic patients
CHO 50%
FAT 25%
Protein 25%
32
Why would you advise a DM patient to increase fibers?
Soluble fibers help control glucose because they slow absorption between the intestines
33
Oral meds for type 2 DM: For insulin resistance (general category)
ANTIHYPERGLYCEMIC AGENTS
34
Oral meds for type 2 DM: For decreased insulin production
| general category
HYPOGLYCEMIC AGENTS
35
Examples of antihyperglycemic agents (5)
```
Glucophage
Precose
Glycet
Actos
Ayandia
```
36
Examples of hypoglycemic agents (4)
Diabinase
Glucotrol
Micronase
Prandin
37
Goals of DM drug therapy - insulins
- Blood sugar at 70-110
- Px complications
- Px hypoglycemia
38
Contraindication of Insulin
Hypoglycemia
39
Humalog
- TIME
- ONSET
- PEAK
- DURATION
- TIME: Rapid acting (clear)
- ONSET: 10-15 minutes
- PEAK: 1 hour
- DURATION: 3 hours
40
Regular (R) Insulin
- TIME
- ONSET
- PEAK
- DURATION
- TIME: Immediate acting (cloudy)
- ONSET: half hour to hour
- PEAK: 2-3 hours
- DURATION: 4-6 hours
41
NPH
(Humulin "N" or "L" (Lente))
- TIME
- ONSET
- PEAK
- DURATION
- TIME: Intermediate acting
- ONSET: 3-4 hours
- PEAK: 4-12 hours
- DURATION: 16-20 hours
42
Glargine (Lantus)
- TIME
- ONSET
- PEAK
- DURATION
- TIME: Long-acting (clear)
- ONSET: 1 hour
- PEAK No peak
- DURATION: 24 hours
43
Humalog: Indication
Rapid reduction of blood sugar
44
R Insulin indication
Works on the immediate meal: Administer 20-30 minutes before a meal
45
NPH Indication
Give after meals helps replace basal insulin
46
Ultralente Indication
Controls FPG (Fasting Plasma Glucose)
47
Ultralente (UL)
- TIME:
- ONSET
- PEAK
- DURATION
- TIME: Long acting (cloudy)
- ONSET 6-8 hours
- PEAK: 12-16 hours
- DURATION: 20-30 hours
48
Glargine indication
Enables LT baseline insulin levels; still need to add insulin at mealtimes with separate needle.
49
Which insulin should you NOT mix with other insulins?
GLARGINE (Lantus)
50
Insulin percentage breakdown
70/30 insuiln: 70% NPH and 30% regular
51
What type of insulin can be given IV?
ONLY regular insulin
52
How is most of the insulin administered?
SUB Q
53
Why should you rotate sites with subQ insulin injections
Lipo-atrophy can develop (gets hard, doesn't absorb well)
54
Mixing types of insulin:
Clear to cloudy
| Regular first, then NPH in syringe
55
Cause of hypoglycemia (3)
- Too little food
- Too much insulin or DM meds
- Extra activity
56
Onset of hypoglycemia
- Sudden; may progress to insulin shock
57
Sxs of hypoglycemia (10)
**MOSTLY NERVOUS SYSTEM
- Shaking
- Fast heartbeat
- Sweating
- Dizziness
- Anxiety
- Hunger
- Imapired vision
- Weakness / fatigue
- Headache
- Irritability
58
Old saying for DM - hyper vs hypoglycemia
Cold and clammy, you need candy
| Hot and dry, blood sugar is high
59
If your DM pt is comatose, what is your priority?
To maintain an airway
60
If you can't tell if a pt is hypo- or hyperglycemic...
ERR ON THE SIDE OF HYPOGLYCEMIC
61
Clinical picture of a patient with mild hypoglycemia (6)
```
Conscious
Hungry
Sweaty
Tremors
Anxiety or drowsiness
Weakness
```
62
Clinical picture of a patient with moderate hypoglycemia (6)
```
Conscious
Headache
Behavioral change
Blurred, impaired or double vision
Irritation / confusion
Difficulty talking
```
63
Clinical picture of a patient with severe hypoglycemia (4)
Unconscious
Unresponsive
Unable to take oral feeding
Seizure activity
64
What do you give a hypoglycemic patient
15 grams of CHO
65
DIabetic ketoacidosis is secondary to...
Inadequate insulin
66
Clinical picture of diabetic ketoacidosis
- Hyperglycemia
- FVD
- Acidosis
- Hypokalemia
67
Why is a ketoacidosis patient at risk for hypokalemia
- K+ can move from intracellular to extracellular to compensate for acidity
- Can get worse as treatment progresses
68
Blood sugar of a ketoacidotic patient
300-800
69
Respirations of a ketoacidotic patient
Rapid, deep
70
Fluid and electrolytes in a ketoacidotic patient
Loss of both
71
Medical management of DKA
- Insulin IV
| - NS or 0.45 NS for dehydration (as much as 500-1000mL over an hour)
72
Mortality rate from ketoacidosis
5-30%
73
Clinical picture of HHNS (4)
* Hyperglycemia
* FVD
* Tachycardia
* Altered senses, decreasd LOC
74
What does HHNS stand for?
Hyperglycemic Hyperosmolar Nonketotic Syndrome
75
Cause of HHNS
Usually non-compliance with treatment
76
Nursing assessment of HHNS: Blood sugar
>1000
77
Nursing assessment of HHNS: RR, pH, ketones
All WNL
78
How do you prevent HHNS?
Sick Day Rules
79
Six Sick Day Rules
1. Take insulin / oral medications as usual
2. Test your blood sugar q 3-4 hours (if more than 200, test for ketones)
3. Report a blood sugar reading greater than 300
4. Eat small, frequent meals
5. If you are vomiting or have diarrhea, have a half of a can of cola, juice or broth every half hour
6. Report nausea, vomiting or diarrhea to your health care provider.
80
DM Complications (7)
1) Complications with insulin therapy
2) DKA
3) HHNS
4) Macrovascular issues
5) Microvascular issues
6) Neuropathies
81
Macrovascular issues with DM (3)
- CAD
- CVD
- PVD
82
What is unique with CAD in DM patients?
Typical ischemic symptoms (early warning sxs) might be absent, because these patients develop an autonomic neuropathy
83
MIs and DM patients
Higher incidence / more complications / higher mortality with diabetic patients
84
Correlation of HTN and DM
60% od DM patients have high BP
85
DM patients and CVD
Higher incidence of strokes, CVAs
| 3x more likely to have a stroke than a non-DM patient
86
PVD and DM: Amputations
600,000 amputations with DM patients
87
Prophylactic meds for Macrovascular issues in DM patients (5)
o An aspirin a day
o beta blocker
o ACE inhibitor or Ca channel blocker
o and a statin
88
Microvascular issues with DM (2)
o Retinopathy
| o Nephropathy
89
What can retinopathy lead to?
Blindness
90
Who is at risk for neuropathies?
Patients with longstanding DM (25+ years)
91
What is a big risk with neuropathies?
Peripheral sensorimotor nephropathy -- affects distal portions of the nerves in the lower extremities
92
Autonomic neuropathy: Systems affected (4)
o CV
o GI
o Urinary
o Adrenal
93
DKA versus HHNK: Caused by which type of diabetes?
DKA: Type 1
HHNK: Type 2
94
DKA versus HHNK: Serum glucose
DKA: 300-800
HHNK: Often >1,000
95
DKA versus HHNK: Arterial pH
DKA: Acidic
HHNK: Normal
96
DKA versus HHNK: Serum and urine ketones
DKA: Positive for both
HHNK: Negative for both
97
DKA versus HHNK: Onset
DKA: Quick
HHNK: Slow
98
DKA versus HHNK: Cause
DKA: Lack of insulin --> Breakdown of fats
HHNK: Inadequate insulin, but enough to prevent the breakdown of fats
99
DKA AND HHNK: Clinical assessment
- Dry skin and mucous membranes
- Decreased skin turgor
- Tachycardia
- Hypotension
- Altered LOC
100
DKA versus HHNK: Breathing
DKA: Kussmaul's respirations
HHNK: Regular and shallow
101
DKA versus HHNK: Mortality
DKA: 5-30%
HHNK: Near 50%
102
Diabetes insipidis is caused by a disorder of the ______
Pituitary gland
103
What causes diabetes insipidus?
Head trauma or neurosurgery -- damage to insipidus
104
Sxs of Diabetes insipidus
Polyuria, Polydipsia
| Can urinate 4-16 L per day
105
Treatment for Diabetes Insipidus (3)
o Replace fluids
o Is & Os
o Diet: High sodium, high potassium
106
Cluster of risk factors involved with syndrome X
* High triglycerides (>150)
* Low HDLs (130/85)
* Insulin-resistance Blood sugar 110-125
* Waist >35" (females) or 40" (males)
