Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MedSurg - 341 > MedSurg 3 - Diabetes Mellitus (Chap 67) > Flashcards

MedSurg 3 - Diabetes Mellitus (Chap 67) Flashcards

1
Q

Pancreas

- Anatomy

A
  • Lies behind the stomach

- has exocrine and endocrine functions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pancreas

-Function

A

Exocrine Function:
== secretion of digestive enzymes through ducts that empty into the duodenum

Endocrine Function:
== the cells in the Islets of Langerhans perform the pancreatic endocrine functions. (abt 1 million islets are found throughout the pancreas)
== the islets have 3 distinct cell types:
** ALPHA Cells, secrete Glucagon
** BETA Cells, secrete Insulin
*** DELTA Cells, secrete Somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Glucagon and Insulin

A

Glucagon and Insulin affect the metabolism of:

    • Carbohydrate
    • Protein
    • Fat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Somatostatin

A

Somatostatin is secreted NOT only in the pancreas but also in the intestinal tract and the brain.

Functions:
== Inhibits the release of glucagon and insulin from the pancreas.
== Inhibits the release of gastrin, secretin, and other GI peptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Glucagon

A

Glucagon is a hormone that increases blood glucose levels. It is triggered by decreased blood glucose levels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Insulin

A
    • Insulin promotes the movement and storage of carbohydrate (CHO), protein, and fat.
    • It lowers blood glucose levels by transporting the glucose from blood stream to cells
    • Basal levels of insulin are continuously secreted to control metabolism
    • Insulin secretion increases in response to an increase in blood glucose levels.
    • Stimulates storage of glucose as glycogen in the liver
    • Inhibits gluconeogenesis
    • Enhances fat deposition
    • Increased protein synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Diabetes

A

A chronic multi-system disease related to:

    • Abnormal insulin production
    • Impaired insulin utilization
    • Or Both of the above

Leading cause of:

    • End stage renal disease
    • Adult Blindness
    • Non-traumatic lower-extremity amputation

Major contributing factor:

    • Heart Disease
    • Stroke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Types of Diabetes

A

Type 1 Diabetes Mellitus
– Insulin-Dependent Diabetes Mellitus, which means no or very little production of insulin

Type 2 Diabetes Mellitus
– Non-insulin Dependent Diabetes Mellitus, which means patient produces insulin but not enough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cardinal Signs of Diabetes Mellitus == 3 P’s

A
  • POLYURIA
    • Frequent urination
    • From osmotic effect of glucose
  • POLYDIPSIA
    • Excessive thirst
    • From osmotic effect of glucose
  • POLYPHAGIA
    • Excessive hunger
    • A consequence of cellular malnourishment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Type 1 Diabetes Mellitus

A
    • There is a virtual absence of endogenous insulin
    • Dependent on exogenous insulin
  • if insulin is withdrawn, ketosis and eventually ketoacidosis develops.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

PreDiabetes

IFG: Fasting Glucose Level = 100 to 125 mg/dL
IGT: 2-Hr. Plasma Glucose = 140 to 199 mg/dL
A1C: = 5.7% to 6.4%

A 
Individuals already at risk for diabetes
Blood glucose high but not high enough to be diagnosed as having diabetes
Characterized by:
-- Impaired fasting glucose (IFG) 
-- Impaired glucose tolerance (IGT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Counterregulatory Hormones (CRH)

A
  • Glucagon, Epinephrine, Growth Hormone, & Cortisol

- - works together as Opposite effect of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Type 2 Diabetes Mellitus

A

Four Major Metabolic Abnormalities:

  1. Insulin resistance
  2. Pancreas ↓ ability to produce insulin
  3. Inappropriate glucose production from liver
  4. Alteration in production of hormones and adipokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Secondary Diabetes

A

Caused by other illnesses or treatment of medical condition that causes ↑ BG:
– Cushing Syndrome
– Hyperthyroidism**
– Total Parenteral Nutrition (TPN)**
– Pancreatitis
– Cystic fibrosis
Caused by Rx of medical conditions cause ↑ BG:
– Corticosteroids (Prednisone) **
– Phenytoin (Dilantin)
– Thiazides
– Atypical antipsychotics (clozapine [clozapril])
* Usually resolves when underlying condition is treated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Type 1 DM - Signs & Symptoms

A

Type 1 – Rapid Onset

    • Polyuria
    • Polydipsia
    • Polyphagia
    • Weight loss
    • Weakness
    • Fatigue
    • Ketoacidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Type 2 DM - Signs & Symptoms

A

Type 2 – gradual onset

    • Nonspecific
    • May have classic s & s of Type 1
    • Fatigue
    • Recurrent infections (vaginal yeast & monilia)
    • Prolonged wound healing
    • Visual changes (blurred vision)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Major Risk Factors: Type 2 Diabetes

A
    • Family History
    • Obesity
    • Age > 35 years
    • HTN
    • HDL < 35mg/dl
    • Triglycerides >250 mg/dl
    • Hx of gestational diabetes or delivery of infants weighing > 9 lbs
    • Origin: African-American, Hispanic, Native American, or Asian-American
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Diabetes Mellitus – Methods of Diagnosis

A

Four methods of diagnosis

    • AIC ≥ 6.5% (for diagnosis)
    • Fasting plasma glucose level >126 mg/dL (in 2 separate tests)
    • Random or casual plasma glucose measurement ≥200 mg/dL plus symptoms
    • Two-hour OGTT level ≥200 mg/dL when a glucose load of 75 g is used
    • Ideal A1C goal for patient diagnosed with DM is 7%
    • Normal A1C reduces risks of retinopathy, nephropathy, and neuropathy !!
19
Q

Drug Therapy: Insulin

A
  • Rapid-acting:
    Lispro (Humalog); Aspart (Novolog); Glulisine (Apidra)
  • Short-acting:
    Regular (Humulin R; Novolin R)
  • Intermediate-acting:
    NPH (Humulin N, Novolin N);
    Lente human insulin (Humulin L)
  • Long Acting
    Ultralente (Humulin U)
    Glargine (Lantus)
    Detemir (Levemir)
20
Q

Rapid-acting Insulin:

Lispro (Humalog);
Aspart (Novolog);
Glulisine (Apidra)

A

Inject 0 to 15 minutes before meal

Onset = 15 minutes

21
Q

Short-acting Insulin:

Regular (Humulin R; Novolin R)

A

Regular
Inject 30 to 45 minutes before meal
Onset = 30 to 60 minutes

22
Q

Intermediate-acting:

NPH (Humulin N, Novolin N);
Lente human insulin (Humulin L)

A

Cloudy

23
Q
  • Long Acting

Ultralente (Humulin U)
Glargine (Lantus)
Detemir (Levemir)

A

Injected once a day at bedtime or in the morning
Released steadily and continuously
No peak action
Cannot be mixed with any other insulin or solution
glargine (Lantus); detemir (Levemir)

24
Q

Storage of insulin

A

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.

25
Q

Administration of insulin

Given Subcut
Regular can be given IV

A

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

26
Q

Accepted Insulin Treatment Plans

A

NPH and Regular Insulin
In AM and PM (dinner time)
Coverage during day with Regular insulin

Glargine at HS
Coverage during day with Lispro or Aspart
Split Dosing of Glargine
Glargine in AM and PM

Coverage with Lispro or Aspart

Insulin Pump – using Lispro, Aspart, or Apidra (may use Regular)

27
Q

Problems with Insulin

A

Allergic reactions - rare
Somogyi Effect – overdose of insulin – results in ↓ BG (undetected ↓ BG during sleep)
– then counterregulatory hormones cause ↑ BG; Rx- give less insulin
Dawn Phenomenon –predawn release of counterregulatory hormones – results in ↑ BG in AM; Rx – change timing of insulin or ↑ insulin
Lipodystrophy – atrophy of SQ tissues; due to lack of rotation of sites; rare today

28
Q

Beta Blockers and Diabetes

A

Beta adrenergic blockers may Mask symptoms of hypoglycemia

Prolong hypoglycemic effects of insulin

29
Q

Thiazide/loop diuretics and Diabetes

A

Thiazide/loop diuretics
Can potentiate hyperglycemia
By inducing potassium loss

30
Q

Diabetes: Nutritional Therapy

A
  • Carbohydrates
    Sugars, starches, and fiber
    Carbohydrate allowance is a minimum of 130 g/day.
  • Fats
    Less than 200 mg/day of cholesterol and trans fats
    <7% from saturated fats
  • Protein
    Contribute 15% to 20% of total energy consumed
    Intake should be significantly less than in the general population.
31
Q

Diabetes: Nutritional Therapy

A 
* Alcohol:
High in calories
No nutritive value
Promotes hypertriglyceridemia
Detrimental effects on liver
Can cause severe hypoglycemia
32
Q

Diabetes: Nutritional Therapy

A
  • Diet teaching
    Dietitian initially provides instruction.
    Carbohydrate counting – given a maximum limit per day
  • Plate method
    Helps patient visualize the amounts of vegetable, starch, and meat that should fill a 9-inch plate
33
Q

Diabetes Mellitus: Exercise

A

Essential part of DM management
*Increases insulin sensitivity; increases insulin receptor sites → can lower BG
*Lowers BG levels
*Contributes to weight loss – decreases insulin resistance
May result in decreased need for diabetes meds
May reduce triglyceride and LDL cholesterol levels

34
Q

Diabetes Mellitus: Exercise

A

Several small carbohydrate snacks can be taken every 30 minutes during exercise to prevent hypoglycemia.
Exercise is best done after meals
Exercise plans should be started
After medical clearance
Slowly with gradual progression
Should be individualized
Monitor blood glucose levels before, during, and after exercise.

35
Q

Diabetes Mellitus: Pancreas Transplantation

A

– Used for patients with Type 1 Diabetes who also
Have end-stage renal disease
Had, or plan to have, a kidney transplant
– Pancreas transplants alone are rare.
Usually kidney and pancreas transplants done together
– Eliminates need for exogenous insulin
– Can also eliminate hypoglycemia and hyperglycemia

36
Q

Diabetes Mellitus: Nursing Management

A
    • Overall goals
    • Active patient participation
    • Few or no episodes of acute hyperglycemic emergencies or hypoglycemia
    • Maintain normal blood glucose levels.
    • Prevent or delay chronic complications.
    • Lifestyle adjustments with minimal stress
37
Q

Acute Complications: Diabetes Mellitus

- Diabetic Ketoacidosis (DKA)

A 
* Diabetic Ketoacidosis (DKA)
Diabetic acidosis or diabetic coma
Profound deficiency of insulin
Characterized by 
Hyperglycemia
Ketosis
Acidosis 
Dehydration
Usually in Type 1 DM 
May occur in Type 2 if extreme severe illness/stress
38
Q

Assessment Findings: DKA

A 
Lethargy; weakness
Early symptom
Poor skin turgor
Dry mucous membranes
Rapid, weak pulse
Orthostatic hypotension
Flushed, dry skin
Thirst
Abdominal pain
Anorexia, N, & V
Sunken eyes
Restlessness, confusion
Kussmaul respirations
Breath: ketones - fruity
Fever
Urinary frequency
Serum glucose >250 mg/dl; pH <7.35
Glycosuria & ketonuria
39
Q

DKA - Intervention

A

Airway management
Oxygen administration
Oxygen via nasal cannula/non-rebreather mask
Correct fluid/electrolyte imbalance
IV access – large bore catheter
IV infusion 0.45% or 0.9% NaCl
Restore urine output.
Raise blood pressure.
When blood glucose levels approach 250 mg/dL
5% dextrose added to regimen
Prevent hypoglycemia.
Potassium replacement - Administer K to correct  hypokalemia
Sodium bicarbonate
Administer Na Bicarb if severe acidoisis (pH < 7.0)

40
Q

Acute Complications:

- Hyperosmolar Hyperglycemic Syndrome (HHS)

A

Life threatening syndrome
Less common than DKA
Patient has enough circulating insulin so that ketoacidosis does NOT occur, but….
not enough insulin to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion
See Figure 67-13 page 1457
Few symptoms early
Neurologic symptoms due to  osmolality (somnolence, coma, seizures, hemiparesis)

41
Q

Acute Complications:

- Hyperosmolar Hyperglycemic Syndrome (HHS) – con’t

A 
Common causes
Infections –pneumonia, UTI, sepsis
Newly diagnosed Type 2 DM
Usually history of 
Inadequate fluid intake
Increasing mental depression
Polyuria
Laboratory values
Blood glucose >400 mg/dL
Increase in serum osmolality
Absent/minimal ketone bodies
Glucose & ketones closely monitored!

Medical emergency
**High mortality rate
Therapy similar to DKA
Except HHS requires greater fluid replacement

42
Q

Acute Complications:

- Hyperosmolar Hyperglycemic Syndrome (HHS) – Intervention

A

Patient closely monitored
Administration
IV fluids - correct dehydration
0.9% or 0.45% NaCl – rate depends on cardiac status
IV with glucose given when BS ~ 250 mg/dl
Insulin therapy – to reduce blood glucose; Regular insulin IV after fluid replacement
Electrolytes – correct imbalances; K may be low
Assessment
Renal status – check urinary output; I & O
Cardiopulmonary status – ECG monitoring; monitor vital signs; avoid fluid overload; check lung sounds; CVP;
Level of consciousness – assess mental status

43
Q

Acute Complications: Hypoglycemia

A

*

MedSurg - 341 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions