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Med surg 2 Sofia > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is Diabetes Mellitus

A

A chronic multisystem disease related to abnormal insulin production, impaired insulin utilization, or both
Affects 25.8 million people
Seventh leading cause of death

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2
Q

Contributing factors?

A

It is also a major factor contributing to heart disease and stroke.
Adults with diabetes have heart disease death rates two to four times higher than adults without diabetes.
The risk for stroke is also two to four times higher among people with diabetes.
In addition, it is estimated that 67% of adults with diabetes have hypertension.

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3
Q

Leading cause of?

A 
Leading cause of 
Adult blindness
End-stage kidney disease
Nontraumatic lower limb amputations
 Major contributing factor
Heart disease
Stroke
Hypertension
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4
Q

Etiology and Pathophysiology

A 
Combination of causative factors
Genetic
Strong association between DM 2, and to a lesser extent of DM 1 
Autoimmune
Environmental
Cold climate (DM 1)
Viruses (DM1)
Solid food early versus breast fed (DM1)
Obesity (DM2)
Absent/insufficient insulin and/or poor utilization of insulin
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5
Q

Etiology and Pathophysiology

Normal insulin metabolism

A

Produced by B-cells in islets of Langerhans
Released continuously into bloodstream in small increments with larger amounts released after food
Stabilizes glucose level in range of 70 to 120 mg/dL

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6
Q

Insulin is a hormone produced by the β-cells in the

A

islets of Langerhans of the pancreas.
Under normal conditions, insulin is continuously released into the bloodstream in small pulsatile increments, with increased release when food is ingested.
Insulin lowers blood glucose and facilitates a stable, normal glucose range of approximately 70 to 120 mg/dL (3.9 to 6.66 mmol/L).
The average amount of insulin secreted daily by an adult is approximately 40 to 50 U

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7
Q

Altered mechanism in Type 1 and Type 2 diabetes

A

Basically the cells are not receptive to the insulin as pts who do not have diabetes therefore the glucose stays outside of the cell instead of being transferred into the cell to give us energy

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8
Q

Other causes of alterations

A

having excessive adipose tissue

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9
Q

What does insulin do?

A

Insulin
Promotes glucose transport in skeletal muscle and adipose tissue
Storage of glucose as glycogen
Inhibits gluconeogenesis (mostly occurs in liver)
Enhances fat deposition
Increases protein synthesis

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10
Q

Which other organs or tissues require an adequate glucose supply for normal function?

A

Other tissues (e.g., brain, liver, blood cells)

do not directly depend on insulin for glucose transport but require an adequate glucose supply for normal function.
Although liver cells are not considered insulin-dependent tissue, insulin receptor sites on the liver facilitate the hepatic uptake of glucose and its conversion to glycogen.

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11
Q

Type 1 Diabetes Mellitus

A 
Formerly known as juvenile-onset or insulin-dependent diabetes
Accounts for 5% of all cases of diabetes
Onset in people younger than 40 years
Incidence increasing
More frequently in younger children
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12
Q

Type 1 Diabetes MellitusEtiology and Pathophysiology

A

Autoimmune destruction of β-cells = total lack of insulin
Genetic predisposition and viral exposure
HLA-DR3 and HLA-DR4 (remember this is type 1 only)
When a person has certain human leukocyte antigens and is exposed to a virus, the B-cells of the pancreas can be destroyed by the autoimmune procress.
Autoantibodies are present for months to years before symptoms occur
Manifestations develop when pancreas can no longer produce insulin—then rapid onset with ketoacidosis
Idiopathic diabetes
No evidence of autoimmunity, found mostly in Africa and Asia
Latent autoimmune diabetes in adults (LADA)
Longer onset, often mistaken for DM2

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13
Q

Clinical ManifestationsType 1 Diabetes Mellitus

Know the 3 P’s!!

A

Polyuria, peeing a lot!! (losing fluids, important electrolytes)

Polydipsia (very thirsty)

Polyphasia
Hunger bc glucose is not getting into the cells so our body thinks it’s always hungry

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14
Q

Other manifestations

A

Weight loss may occur because the body cannot get glucose and turns to other energy sources, such as fat and protein.
Weakness and fatigue may result because body cells lack needed energy from glucose.
Infections, UTI, skin, vaginal (candidia), familial tendency
10 - 15 years when they get it usually

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15
Q

Type 2 Diabetes Mellitus

A

Lack of exercise
Unhealthy eating
Family history
Overweight

Type 2 diabetes mellitus was formerly known as adult-onset diabetes (AODM) or non–insulin-dependent diabetes (NIDDM).
Type 2 diabetes mellitus is, by far, the most prevalent type of diabetes, accounting for over approximately 90% to 95% of cases of diabetes.
Overweight, obesity, advancing age, and a family history of type 2 diabetes are risk factors for developing the disease.
Although the disease is seen less frequently in children, the incidence in children is increasing as a result of the increase in prevalence of childhood obesity.

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16
Q

Who is most affected?

A

Prevalence of type 2 diabetes is greater in some ethnic populations. African Americans, Asian Americans, Hispanics, Native Hawaiians or other Pacific Islanders, and Native Americans have a higher rate of type 2 diabetes than do white people.

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17
Q

Type 2 Diabetes MellitusEtiology and Pathophysiology

A

Pancreas continues to produce some endogenous insulin
Insulin insufficient or poorly utilized
Multiple etiologic factors
***Obesity is greatest risk factor
Genetic component increases insulin resistance and obesity

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18
Q

Type 2 Diabetes Mellitus: Metabolic Syndrome a Risk

A

What are the 5 characteristics?
elevated glucose levels, abdominal obesity, elevated blood pressure, high levels of triglycerides, and decreased levels of high-density lipoproteins (HDLs).

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19
Q

An individual with 3 of 5 components is

A

considered to have metabolic syndrome.

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20
Q

Clinical ManifestationsType 2 Diabetes Mellitus

A

3 Ps and weight loss are possible

Usually more nonspecific symptoms 
Fatigue
Recurrent infection 
Recurrent vaginal yeast or candidal infection
Prolonged wound healing
Visual changes
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21
Q

Will prediabetic patients go on to develop DM?

A

Unfortunately Yes

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22
Q

Gold standard lab test
Diagnostics

and prediabetic % levels

A

A1C if >6.5% pt has DM

% of glucose that is attached to Hgb molecule
in PRE they ate going to have >5.7-6.4

Fasting plasma glucose level of 126 mg/dL (7.0 mmol/L or greater.

A 2-hr plasma glucose level of 200mg/dL or greater

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23
Q

Gestational Diabetes

A

Develops during pregnancy
Increases risk of need for cesarean delivery and of perinatal complications
Screen high-risk patients first visit; others at 24 to 28 weeks of gestation
Usually glucose levels normal 6 weeks post partum

Fact: about 50% of women with gestational diabetes go on to develop type 2 DM

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24
Q

Diagnostic Studies

A

Hemoglobin A1C test
Glycosylated hemoglobin: reflects glucose levels over past 2 to 3 months
Used to diagnose, monitor response to therapy, and screen patients with prediabetes
Goal: less than 6.5% to 7%
Fructosamine
Reflects glucose levels past 1-3 weeks
Autoantibodies

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25
Q

Patient’s might present with the following:

A

Urine: positive for glucose and negative for protein
Wet preparation of smear from rash: consistent with Candida albicans
ECG: evidence of early ventricular hypertrophy

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26
Q

What three treatment modalities will you expect to teach your patient?

A

Diet, exercise, medications

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27
Q

Collaborative Care

Patient teaching……

A 
Patient teaching
Nutritional therapy
Drug therapy
Exercise
Self-monitoring of blood glucose

Foot care (amputations are primarily caused by pts with infections due to neuropathy, encourage to always wear sturdy shoes, no open toes) Inspect feet!

Do not put a lot of lotions or wet ointments on feet because that can be a breeding ground for bacteria.

KEY: Diet, exercise, and weight loss may be sufficient for patients with type 2 diabetes
All patients with type 1 require insulin

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28
Q

For some people with type 2 diabetes, a regimen of proper nutrition, regular physical activity, and maintenance of desirable body weight is sufficient to

A

attain an optimal level of blood glucose control. However, for the majority, drug therapy is necessary.

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29
Q

Commercially Available Insulin. (know the peak times)

A

Rapid acting Peak: 30 minutes

Short acting (taken before meals) - Peak 2-5 hrs.

Intermediate acting- Peak 4-12 hour

Long acting - no pronounced peak (athletes or activities that require a lot of caloric expenditure)

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30
Q

The insulin regimen that most closely mimics endogenous insulin production is the

A

Basal-bolus regimen
Most closely mimics endogenous insulin production
Rapid- or short-acting (bolus) insulin before meals
Intermediate- or long-acting (basal) background insulin once or twice a day
Less intense regimens can also be used (commonly mixed with short or rapid)

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31
Q

Can the kidneys be injured by any type of DM? if so, what condition will you see?

A

The kidneys can be damaged.

Clinical manifestation for chronic DM is proteinuria (too much protein in urine.)

Also, the left ventricle of the heart can become enlarged ( lack of perfusion in coronary arteries due to CHF, other cardio)

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32
Q

Why is it important to know the peak time of when these insulins begin working?

A

Because as a nurse we want to know when the patient is most likely to be HYPOGLYCEMIC! low blood sugar <70

Monitor patient within 10-

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33
Q

After administering rapid acting insulin when should you check up on your patient?

A

Monitor patient within 10-30 minutes up to 3 hours for S/S of hypoglycemia.

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34
Q

Why do you want to act quickly when you find your patient in a hypoglycemic state?

A

Remember that our brain needs oxygen and glucose and this needs to be addressed right away.
Only 5 minutes to react.

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35
Q

Does long acting insulin have a pronounced peak?

If no, then what does this mean?

A

No

It means that it is not going to throw the patient into a hypoglycemic state at all.

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36
Q

Signs and Symptoms of hypoglycemia

A 
Confusion
Diaphoresis
Extreme hunger
Irritability
Seizure!! if very deprived of glucose
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37
Q

What are the 3

RAPID acting insulin preparations?

A

lispro (humaLOG)
aspart (NovoLOG)
glulisine (Apidra)

Onset 10-30 minutes
Peak: 30 min -3 hr
Duration: 3-5 hr

Typically taken before meals

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38
Q

Short acting
REGULAR
HINT: ends in “lin”

A

Humulin R, and Novolin R
Onset 30 minutes
Peak: 32-5 hr
Duration: 5-8 hr

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39
Q

Independent acting

NPH (Humulin R, and Novolin R)

A

Onset 1.5-4 hour
Peak: 4-12 hr
Duration: 12-18hr

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40
Q

Is Metformin part of the Basal-bolus regimen?

A

Yes. Patients who typically are on a basal bolus regimen take metformin

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41
Q

How do you mix and draw up insulin?
Use sequence of RN
Regular, then NPH

A

Inject air into NPH, then
Air into Regular that’s clear,
Draw up Regular then draw NPH

So we don’t accidentally mix regular with NPH.

42
Q

Insulin biles storage

A

Storage of insulin
Do not heat/freeze
In-use vials may be left at room temperature up to 4 weeks
Extra insulin should be refrigerated
Avoid exposure to direct sunlight, extreme heat or cold
Store prefilled syringes upright for 1 week if two insulin types; 30 days for one

43
Q 
Intermediate-acting insulin
NPH
Duration 12 to 18 hours
Peak 4 to 12 hours
Can mix with short- and rapid-acting insulins
Cloudy; must agitate to mix
A

Intermediate-acting insulin (NPH) is also used as a basal insulin. Its action has a duration of 12 to 18 hours. The disadvantage of NPH is that its peak of action ranges from 4 to 12 hours, which can result in hypoglycemia. NPH is the only basal insulin that can be mixed with short- and rapid-acting insulins.
NPH is a cloudy insulin that must be gently agitated before administration.

44
Q

Combination Insulin Therapy

A

Can mix short- or rapid-acting insulin with intermediate-acting insulin in same syringe
Provides mealtime and basal coverage in one injection
Commercially premixed or self-mix

For patients who want to use only one or two injections per day, a short- or rapid-acting insulin is mixed with intermediate-acting insulin in the same syringe.
This allows patients to have both mealtime and basal coverage without having to administer two separate injections.
Although this may be more appealing to the patient, most patients achieve better control with basal-bolus therapy.

45
Q

Administration of insulin

A

Absorption is fastest from abdomen, followed by arm, thigh, and buttock
Abdomen is preferred site
Do not inject in site to be exercised
Rotate injections within one particular site

46
Q

Insulin Pen

A

An insulin pen is a compact portable device loaded with an insulin cartridge that serves the same function as a needle and syringe.
Pen needles are available in various lengths and sizes.
Many patients prefer using insulin pens because of greater convenience and flexibility.
They are portable and compact, their use is more discreet than using a vial and syringe, and they provide consistent and accurate dosing.
For patients with poor vision, the pen is a better option as they can hear the clicks of the pen as the dose is selected.
Insulin pens come packaged with printed instructions including pictures of the steps to take when using the pen. These instructions are helpful to use in teaching new users and in reviewing technique with current users of a pen.

47
Q

Insulin pump

Program basal and bolus doses that can vary throughout the day
Potential for tight glucose (diabetes) control

A

Continuous subcutaneous infusion
Battery-operated device
Connected to a catheter inserted into subcutaneous tissue in abdominal wall

48
Q

What type of complications may arise with the use of the insulin pump?

A

Problems and complications of insulin pump therapy are infection at the insertion site, an increased risk for DKA if the insulin infusion is disrupted by a problem at the infusion site, and the increased cost of the pump and supplies.

Kinks -

49
Q

1 problem with insulin therapy

and other problems

A

Hypoglycemia

Problems with insulin therapy
Hypoglycemia
Allergic reaction
Lipodystrophy

50
Q

Somogyi effect

Manifested by a patient waking up in the morning and having high blood sugar

A

Somogyi effect
Rebound effect in which an overdose of insulin causes hypoglycemia
Release of counterregulatory hormones causes rebound hyperglycemia

51
Q

What happens in Somogyi effect?

A

Hyperglycemia in the morning may be due to the Somogyi effect.
A high dose of insulin produces a decline in blood glucose levels during the night.
As a result, counterregulatory hormones (e.g., glucagon, epinephrine, growth hormone, cortisol) are released, stimulating lipolysis, gluconeogenesis, and glycogenolysis, which in turn produce rebound hyperglycemia.
The danger of this effect is that when blood glucose levels are measured in the morning, hyperglycemia is apparent and the patient (or the health care professional) may increase the insulin dose.
If a patient is experiencing morning hyperglycemia, checking blood glucose levels between 2:00 AM and 4:00 AM for hypoglycemia will help determine if the cause is the Somogyi effect.
The patient may report headaches on awakening and may recall having night sweats or nightmares.
A bedtime snack, a reduction in the dose of insulin, or both can help to prevent the Somogyi effect.

52
Q

What should the nurse teach the patient to do if they awake with high blood sugar each morning?

REduce insulin

A

If the Somogyi effect is causing the patient’s increased morning glucose level, the patient will experience hypoglycemia between 2:00 and 4:00 AM. The patient should be instructed to check their blood sugars then. The dose of insulin will be reduced..

53
Q

Dawn Phenomenon

decrease insulin, snack, or exercise

A

Dawn phenomenon
Morning hyperglycemia present on awakening
Due to release of counterregulatory hormones in predawn hours

54
Q

What would the glucose reading be at 2-4 am for dawn phenomenon? Treatment?

A

If the predawn levels are less than 60 mg/dL (3.3 mmol/L) and signs and symptoms of hypoglycemia are present, the insulin dosage should be reduced.
If the 2:00 to 4:00 AM blood glucose level is high, the insulin dosage should be increased. In addition, counsel the patient on appropriate bedtime snacks.

55
Q

What is metformin? A biguanide

trade name is Glucophage

What is the mechanism of action of metformin?

A

First line med that pts are typically put on with diabetes.

Work on three defects of type 2 diabetes
Insulin resistance

Decreased insulin production

Increased hepatic glucose production (med will decrease this)

Can be used in combination

56
Q

Biguanides

A

Metformin (Glucophage)
Reduce glucose production by liver
Enhance insulin sensitivity
Improve glucose transport

May cause weight loss

Used in prevention of type 2 diabetes

Withhold if contrast medium is used

57
Q

Can prediabetic patient be prescribed metformin prophylactically?

A

Yes

58
Q

BiGuanides Metformin nursing interventions

Sx

Monitor what?
Contraindications

A

Withhold if patient is undergoing surgery or radiologic procedure with contrast medium
Day or two before and at least 48 hours after!

Monitor serum creatinine

Contraindications
Renal, liver, cardiac disease
Excessive alcohol intake

59
Q

Sulfonylureas

Monitor for what?

A 
↑ Insulin production from pancreas
Major side effect: hypoglycemia
diaphoresis, confusion, hungry, irritable.
Examples	
Glipizide (Glucotrol)
Glyburide (Micronase,

DiaBeta, Glynase)
Glimepiride (Amaryl)

60
Q

Does Metformin increase hypoglycemia?

A

No. Why?

Because it doesn’t increase insulin it only reduces amount of glucose that the liver makes.

Can irritate stomach nausea, take with food

61
Q

When will a patient be most at risk for hypoglycemia while taking NovaLOG? (rapid acting)

A

Onset 10-30 minutes
Peak: 30 min -3 hr
Duration: 3-5 hr

Typically taken before meals

62
Q

DiabetesNutritional Therapy: Type 2 DM

Very important!
Weight loss

A

Emphasis on achieving glucose, lipid, and blood pressure goals
Weight loss
Nutritionally adequate meal plan with ↓ fat and CHO
Spacing meals
Regular exercise
Carbohydrate counting
Serving size is 15 g of CHO
Typically 45 to 60 g per meal
Insulin dose based on number of CHOs consumed
Patient teaching essential

63
Q

What is a consequence of not managing diabetes?

A

Cardiovascular disease, can have MI

64
Q

What should the nurse instruct a patient to do in relation to their medication when exercising, etc…?

Taking Novolog and Metformin

When expending energy/calories

Blood sugar can drop dramatically

Take a less insulin, OR have a bigger meal than normal

What else can you tell athletes? Check their blood sugar throughout exercise

A 
Type/amount
Minimum 150 minutes/week aerobic
Resistance training three times/week
Benefits
↓ Insulin resistance and blood glucose 
Weight loss
↓ Triglycerides and LDL , ↑ HDL
Improve BP and circulation

Monitor blood glucose

Glucose-lowering effect up to 48 hours after exercise

Exercise 1 hour after a meal

Snack to prevent hypoglycemia

Do not exercise if blood glucose level exceeds 300 mg/dL and if ketones are present in urine

65
Q

Blood Glucose Monitors

A

Enables decisions regarding diet, exercise, and medication
Accurate record of glucose fluctuations
Helps identify hyperglycemia and hypoglycemia
Helps maintain glycemic goals
A must for insulin users
Frequency of testing varies

66
Q

Continuous Glucose Monitor

A

The MiniMed Paradigm insulin pump (A) delivers insulin into a cannula (B) that sits under the skin. Continuous glucose monitoring occurs through a tiny sensor (C) inserted under the skin. Sensor data are sent continuously to the insulin pump transmitter (D). The transmitter sends data to the insulin pump through wireless technology.

67
Q

Self-Monitoring of Blood Glucose (SMBG)

A 
Patient teaching 
How to use, calibrate
When to test
Before meals
Two hours after meals
When hypoglycemia is suspected
During illness
Before, during, and after exercise
68
Q

Organ complications
For type 1 diabetes with
Kidney and pancreas transplantation

A 
kidney transplant
Eliminates need for exogenous insulin, SMBG, dietary restrictions
Can also eliminate acute complications
Long-term complications may persist
Lifelong immunosuppression
Islet cell transplantation experimental
69
Q

Never exercise when?

A

When the patient is hyperglycemic >300

70
Q

What are ketones?

A

Ketones occur in the urine, when the body starts burning fat for energy. When there is no more glucose to go into the cell.

71
Q

What is the criteria as recommended by the ADA to be considered for transplantation?

A

Kidney and pancreas transplantations are often performed together, or a pancreas may be transplanted after kidney transplantation. Pancreas transplantation alone is rare.
If renal failure is not present, the ADA recommends that pancreas transplantation be considered only for patients who exhibit the following three criteria: (1) a history of frequent, acute, and severe metabolic complications (e.g., hypoglycemia, hyperglycemia, ketoacidosis) necessitating medical attention; (2) clinical and emotional problems with exogenous insulin therapy that are so severe as to be incapacitating; and (3) consistent failure of insulin-based management to prevent acute complications.

72
Q

If a patient gets their labs drawn four months from now and the a1c is now 7.1%. What does this mean in the progression of her disease?

A

From 9 range to 7.1%.
Progression of disease, improving!

Diabetics get a higher value that is considered normal (A1C)

73
Q

Why would chronic pancreatitis make a difference in a patient with diabetes?

A

BC Isles of langerhans could be damaged and affect insulin excretion

74
Q

Subjective: Nursing Assessment

A

History:
Trauma, infection, stress, pregnancy, chronic pancreatitis, Cushing syndrome, acromegaly, family history of diabetes, baby > 9 lbs
Medications: Insulin, OAs,

corticosteroids-these can increase blood sugar) , diuretics, phenytoin (can impact blood sugar as well)
this is an (anticonvulsant/antiarrhythmics)
Recent surgery
Malaise
Obesity, weight loss or gain
Thirst, hunger, nausea/vomiting
Poor healing

75
Q

Subjective: Nursing Assessment

A 
Constipation/diarrhea
Frequent urination, bladder infections
Nocturia, urinary incontinence
Muscle weakness, fatigue
Abdominal pain, headache, blurred vision
Numbness/tingling, pruritus
Impotence, frequent vaginal infections
Decreased libido
Depression, irritability, apathy
Commitment to lifestyle changes
76
Q

Objective: Nursing Assessment

A 
DEHYDRATION: Sunken eyeballs 
vitreal hemorrhages
cataracts
Dry, warm, inelastic skin
Pigmented skin lesions
ulcers, loss of hair on toes, acanthosis nigricans
Kussmaul respirations
Hypotension
Weak, rapid pulse
Dry mouth
Vomiting
Fruity breath
Altered reflexes, restlessness
Confusion, stupor, coma
Muscle wasting
77
Q

What type of respirations are common to see in patients with DKA?
What happens when there is an acid base imbalance in a patient with diabetes?

What type of breath will you smell?

A

When there is an acid base imbalance and patient have DKA the blood sugar is so HIGH and the patient has NO INSULIN, in order to compensate the respiratory system kicks in first, pretty quickly
resulting in
Kussmaul respirations
which are very deep respirations, and fast. In an effort to blow off CO2.

Fruity breath.

78
Q

Audience Response Question

a. Make all patients responsible for the management of their disease.
b. Involve the family and significant others in the care of these patients.
c. Enable the patients to become active participants in the management of their disease.
4. Provide the patients with as much information as soon as possible to prevent complications.

A

Answer: c
Rationale: The goal of diabetes education is to enable the patient to become the most active participant in his or her own care.

79
Q

Nursing Assessment: LABS

A 
Serum electrolyte abnormalities
Fasting blood glucose level of 126 mg/dL or higher
Oral glucose tolerance test and/or random glucose level exceeding 200 mg/dL
Leukocytosis
↑ Blood urea nitrogen >20, creatinine >1.3
↑ Triglycerides, cholesterol, LDL, VLDL
↓ HDL
Hemoglobin A1C value higher than 6.5%
Glycosuria
Ketonuria
Albuminuria (due to kidney damage)
Acidosis
↑ Triglycerides, cholesterol, LDL, VLDL
↓ HDL
Hemoglobin A1C value higher than 6.5%
Glycosuria
Ketonuria
Albuminuria (due to kidney damage)
Acidosis
Possible diagnostic findings:
 Serum electrolyte abnormalities; fasting blood glucose level of126 mg/dL or higher; oral glucose tolerance test result exceeding 200 mg/dL; random glucose test result of 200 mg/dL or higher; leukocytosis; ↑ blood urea nitrogen, creatinine levels
80
Q

Nursing Implementation

A 
Ambulatory and home care
Frequent oral care
Foot care
Inspect daily
Avoid going barefoot
Proper footwear  closed toe, leather, comfortable 
How to treat cuts
81
Q

Acute Complications

A

Diabetic ketoacidosis (DKA)
Hyperosmolar hyperglycemic syndrome (HHS)
Hypoglycemia

82
Q

Diabetic Ketoacidosis (DKA)

A 
Caused by profound deficiency of insulin
Characterized by 
Hyperglycemia
Ketosis
Acidosis
Dehydration
Most likely to occur in type 1 diabetes
83
Q

Diabetic Ketoacidosis (DKA)

A 
Precipitating factors
Illness
Infection
Inadequate insulin dosage
Undiagnosed type 1 diabetes
Poor self-management
Neglect
Clinical manifestations
Dehydration
Lethargy and weakness early
Skin dry and loose; eyes soft and sunken
Abdominal pain, anorexia, nausea/vomiting
Kussmaul respirations
Sweet, fruity breath odor
Blood glucose level of 250 mg/dL or higher
Blood pH lower than 7.30
Serum bicarbonate level lower than 16 mEq/L
Moderate to high ketone levels in urine or serum
84
Q

DKA

A

When the circulating supply of insulin is insufficient, glucose cannot be properly used for energy. The body compensates by breaking down fat stores as a secondary source of fuel.
Ketones are acidic by-products of fat metabolism that can cause serious problems when they become excessive in the blood. Ketosis alters the pH balance, causing metabolic acidosis to develop.
Ketonuria is a process that occurs when ketone bodies are excreted in the urine. During this process, electrolytes become depleted as cations are eliminated along with the anionic ketones in an attempt to maintain electrical neutrality.
Insulin deficiency impairs protein synthesis and causes excessive protein degradation. This results in nitrogen losses from the tissues.
Insulin deficiency also stimulates the production of glucose from amino acids (from proteins) in the liver and leads to further hyperglycemia.
Because there is a deficiency of insulin, the additional glucose cannot be used and the blood glucose level rises further, adding to the osmotic diuresis.
If not treated, the patient will develop severe depletion of sodium, potassium, chloride, magnesium, and phosphate.
Vomiting caused by the acidosis results in more fluid and electrolyte losses.
Eventually, hypovolemia will ensue and be followed by shock.
Renal failure, which may eventually occur from hypovolemic shock, causes the retention of ketones and glucose, and the acidosis progresses.
Untreated, the patient becomes comatose as a result of dehydration, electrolyte imbalance, and acidosis. If the condition is not treated, death is inevitable.

85
Q

Diabetic Ketoacidosis (DKA)

A

Ensure patent airway; administer O2
Establish IV access; begin fluid resuscitation
NaCl, 0.45% or 0.9%
Add 5% to 10% dextrose when blood glucose level approaches 250 mg/dL
Continuous regular insulin drip, 0.1 U/kg/hr.
Potassium replacement as needed

86
Q

Hyperosmolar Hyperglycemic Syndrome (HHS)

A

Life-threatening syndrome
Occurs with type 2 diabetes
Precipitating factors
UTIs, pneumonia, sepsis
Acute illness
Newly diagnosed type 2 diabetes
Impaired thirst sensation and/or inability to replace fluids
Enough circulating insulin to prevent ketoacidosis
Fewer symptoms lead to higher glucose levels (>600 mg/dL)
More severe neurologic manifestations because of ↑ serum osmolality
Ketones absent or minimal in blood and urine

87
Q

Hyperosmolar Hyperglycemic Syndrome (HHS)

A 
Medical emergency
High mortality rate
Therapy similar to that for DKA
IV insulin and NaCl infusions
More fluid replacement needed
Monitor serum potassium and replace as needed
Correct underlying precipitating cause
88
Q

DKA/HHSNursing Management

A 
Monitor
 IV fluids
Insulin therapy
Electrolytes
Assess
Renal status
Cardiopulmonary status
Level of consciousness
89
Q

Audience Response Question

A

The nurse is caring for a patient with type 1 diabetes mellitus who is admitted for diabetic ketoacidosis. The nurse would expect which laboratory test result?

Hypokalemia
Fluid overload
Hypoglycemia
Hyperphosphatemia

90
Q

Hypoglycemia

A

Too much insulin in proportion to glucose in the blood
Blood glucose level less than 70 mg/dL
Neuroendocrine hormones released
Autonomic nervous system activated

91
Q

Hypoglycemia

Epinephrine release causes manifestations that include shakiness, palpitations, nervousness, diaphoresis, anxiety, hunger, and pallor.

A 
Headache
Ringing in the ears
Trembling
Irritability
Sweatiness
blurry vision
Increase heart rate
Hunger
Feeling anxious
92
Q

Hypoglycemia

Altered mental function

A 
Altered mental functioning
Difficulty speaking
Visual disturbances
Stupor
Confusion
Coma 
Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death
93
Q

Hypoglycemia - altered mental function

A

Because the brain requires a constant supply of glucose in sufficient quantities to function properly, hypoglycemia can affect mental functioning.
The manifestations are speaking difficulties, visual disturbances, stupor, confusion, and coma.
Manifestations of hypoglycemia can mimic those of alcohol intoxication.
Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death.

94
Q

Hypoglycemia

A

Causes
Too much insulin or oral hypoglycemic agents
Too little food
Delaying time of eating
Too much exercise
Symptoms can also occur when high glucose level falls too rapidly

95
Q

Hypoglycemia

Treatment of 15

A 
Treatment: rule of 15
Consume 15 g of a simple carbohydrate
Fruit juice or regular soft drink, 4 to 6 oz 
Recheck glucose level in 15 minutes
Repeat if still less than 70 gm/dL
Avoid foods with fat
Decrease absorption of sugar
Avoid overtreatment
Give complex CHO after recovery
96
Q

Hypoglycemia

A 
Treatment
In acute care settings
Fifty percent dextrose, 20 to 50 mL, IV push 
Patient not alert enough to swallow
Glucagon, 1 mg, IM or subcutaneously
Explore reason why occurred
97
Q

Chronic complications

A 
Stroke
Hypertension
Demopathy
Neuropathy
Gangrene
Neutrogenic bladder
Retinopathy
Cataracts
Glaucoma
Blindness
Atherosclerosis
98
Q

Chronic ComplicationsDiabetic Neuropathy

A 
Autonomic neuropathy
Can affect nearly all body systems
Gastroparesis
Delayed gastric emptying
Cardiovascular abnormalities
Postural hypotension, resting tachycardia, painless myocardial infarction
Sexual function
Erectile dysfunction
Decreased libido
Vaginal infections
Neurogenic bladder → urinary retention
Empty frequently, use Credé’s maneuver
Medications
Self-catheterization
99
Q

Foot

A

Gangrene
Amputations
Neuropathy

100
Q

Chronic ComplicationsDiabetic Neuropathy

A

Diabetic dermopathy is most common

101
Q

Gerontologic Considerations

A 
Increased prevalence and mortality
Glycemic control challenging
Increased hypoglycemic unawareness
Functional limitations
Renal insufficiency
Diet and exercise: main treatment
Patient teaching must be adapted to needs
102
Q

You would expect to see which pH in a patient with DKA?

A

Lower than 7.3

Med surg 2 Sofia (12 decks)

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