Nurs 306 Exam 3 [Diabetes Pathophysiology]

Front 1

Identify the action of insulin on blood glucose.

Back 1

Insulin decreases blood glucose levels.

Front 2

Identify the action of glucagon on blood glucose.

Back 2

Glucagon increases blood glucose levels.

Front 3

What happens when insulin binds to its receptors on target cells?

Back 3

results in ↑ facilitated diffusion of glucose into cells

Front 4

TRUE/FALSE

Glucose cannot readily go into cells without the help of insulin.

Back 4

TRUE

Front 5

What is insulin and where is it produced?

Back 5

A hormone that helps glucose go into cells and is produced in the beta cells of pancreas

Front 6

What is the normal serum glucose level?

Back 6

70-100 mg/dL

Front 7

A person has a serum glucose level of 109, identify their diabetes classification.

Back 7

Prediabetes

Front 8

Why does a person's blood sugar tend to increase as they get older?

Back 8

With age, pancreas does not function a well as it used to.

Note: This effect is more intense in people who are already sick.

Front 9

Can a person with pancreatic cancer develop diabetes?

Back 9

Yes. They can develop secondary diabetes.

Front 10

Describe endogenous and exogenous insulin.

Back 10

• Endogenous = insulin produced by the body

• Exogenous = insulin introduced to the body from the outside

Front 11

_________ glucose in blood/plasma means that pt will have high levels of serum blood glucose in blood draw.

Back 11

Increased

Front 12

Identify the role of the liver when the body detects high blood glucose.

Back 12

Liver produces glycogen

Front 13

Identify the role of the liver when the body detects low blood glucose.

Back 13

Liver breaks down glycogen

Front 14

_______ is caused by too much insulin or oral hypoglycemic agents, too little food, or excessive activity.

Back 14

hypoglycemia

Front 15

A patient has severe hypoglycemia, is unconscious, and cannot swallow. How do you treat this patient?

Back 15

Glucagon administered subcutaneously or IM; a second dose is administered in 10 mins if client remains unconscious

Front 16

___% of individuals with DM have Type 1.

Back 16

5%

Front 17

___% of individuals with DM have Type 2.

Back 17

90-95%

Front 18

Type 1 DM occurs in the following type of individuals: __________.

Back 18

Children and young adults

Front 19

Type 1 DM

Back 19

destruction of pancreatic beta cells that results in absolute insulin deficiency

Front 20

Identify 2 reasons as to why pancreatic beta cells could be destroyed.

Back 20

Individual is genetically susceptible

Caused by autoantibodies

Front 21

Weight loss is common in Type ___ DM and rare in Type ____ DM.

Back 21

Weight loss is common in Type 1 DM and rare in Type 2 DM.

Front 22

Identify the 3 P's.

Back 22

Polyuria, polydipsia, polyphagia (more common in type 1
diabetes mellitus)

Front 23

polyuria

Back 23

excessive secretion of urine

Front 24

polydipsia

Back 24

excessive or abnormal thirst

Front 25

polyphagia

Back 25

excessive appetite or eating

Front 26

Why would a person with Type 1 DM be fatigued?

Back 26

Because cells do NOT have glucose to use for energy

Front 27

Identify the clinical manifestations for Type 1 DM.

Back 27

3 P's
Weight loss
Fatigue/Tiredness
Diabetic ketoacidosis (DKA)

Front 28

Why does a person with Type 1 DM experience the polyphagia?

Back 28

Pt is hungry b/c cells are hungry, since they are NOT getting blood glucose

Front 29

Why does a person with Type 1 DM experience the polydipsia?

Back 29

Body is telling pt to drink more b/c blood/plasma is concentrated with too much glucose

Front 30

Why does a person with Type 1 DM experience the polyuria?

Back 30

Body wants to get rid of fluid to get rid of all the extra glucose in the blood

Front 31

diabetic ketoacidosis (DKA)

Back 31

↑ metabolism of Fats and proteins resulting in ↑ levels of circulating ketones

Front 32

Why does a person with DKA have "fruity breath"?

Back 32

↑ levels of circulating ketones. → pH drops → triggers buffering system of metabolic acidosis → ACETONE is blown off, which result in a “fruity breath”

Front 33

What does the body metabolize when it does NOT have glucose to use?

What is the result of this?

Back 33

Body metabolizes fat in the absence of glucose, which causes increased circulating ketones

Front 34

glycosuria

Back 34

the presence in the urine of abnormal amounts of sugar

Front 35

proteinuria

Back 35

the presence of excess protein in the urine

Front 36

Exercise _______ the blood glucose level.

increases/decreases

Back 36

decreases

Front 37

DKA is most common in patients with Type ___ DM, but it can sometimes be seen in patients with Type ____ DM.

Back 37

common in Type 1 DM

rare in Type 2 DM

Front 38

What are treatment options for a patient with DKA?

Back 38

Normal saline IV (prepare to administer first)
Regular insulin (IV)

Front 39

Of the following IV fluids, which would you administer to a patient with DKA: isotonic, hypotonic, or hypertonic?

Back 39

Isotonic

Front 40

Is normal saline (0.9% sodium chloride) isotonic, hypotonic, or hypertonic?

Back 40

Isotonic

Front 41

______ is the only insulin that can be administered intravenously.

Back 41

Regular insulin

Front 42

Identify signs & symptoms of DKA. (6)

Back 42

3 P's
Shortness of breath (fast breathing)
Confusion
Clammy and sweaty
Vomiting
Fruity breath

Front 43

DKA may result from _______. (5)

Back 43

illness, stress, extreme anxiety, vigorous exercise, omission of insulin doses

Front 44

Why do you use an isotonic solution to treat DKA?

Back 44

Isotonic solution has same osmolality as our blood

Front 45

Type 2 DM is common in what age group?

Back 45

Traditionally > 40 year old, but is now being seen in younger people

Front 46

Identify the etiology of Type 2 DM. (2)

Back 46

Relative insulin deficiency, where pancreas does not produce enough insulin

Insulin produced is either insufficient to body needs or poorly utilized by tissues (insulin resistance

Front 47

Type 2 DM is highly related to _______. (2)

Back 47

obesity and lack of exercise

Front 48

What is insulin resistance?

Back 48

Buy tissues do not respond to insulin; Resistance to the actions of insulin in muscle, fat, and liver

Front 49

What is impaired fasting glucose (IFG)?

Back 49

Mild alteration in beta cell function

Fasting plasma glucose ≥100 and < 126 mg/dL

Front 50

What is the treatment for impaired fasting glucose (IFG)?

Back 50

Lifestyle modification

Front 51

What is impaired glucose tolerance (IGT)?

Back 51

Progression from impaired fasting glucose (IFG)

Front 52

What percent of individuals with IGT will convert to Type 2 DM within 10 years?

Back 52

10-25%

Front 53

What is insulin resistance syndrome? (5)

Back 53

– Hypertension
– Obesity
– Hyperlipidemia
– Insulin resistance, Type 2
– Abdominal obesity

Note: Combo of all these conditions; AKA metabolic syndrome X

Front 54

Identify the clinical manifestations for Type 2 DM. (5)

Back 54

– Asymptomatic at early onset
– Obesity --> weight loss
– Patients may complain of other symptoms (e.g. delayed healing)
– HHNKS (hyperglycemic hyperosmolar non ketotic state)
– 3 P's MAY be seen

Front 55

Identify possible physical findings in patients with Type 2 DM. (9)

Back 55

Obesity, central
HTN
Eye problems
Skin-acanthosis nigricans
Candida infections
Decrease neurologic
Dry feet
Ulcers
Muscle atrophy

Front 56

Why do patients with type II DM begin to lose weight when their glucose is out of control?

Back 56

Lose weight due to...
– Not eating
– Body breaking down fat for energy instead of using glucose

Front 57

Why would you see DKA in patients with type II DM?

Back 57

Over time, in patients with type II DM, pancreas is going to fail so that there is ZERO insulin production

Front 58

Which type of diabetes will you see HHNKS?

Back 58

Type II DM only

Front 59

Identify the causes for the following acute complications: DKA and HHNKS.

Back 59

DKA - illness, not taking insulin

HHNKS - high carbohydrate diet

Front 60

Identify the S/S for the following acute complications: DKA and HHNKS.

Back 60

DKA - N/V, malaise,
dehydration, acetone breath

HHNKS - polyuria,
polydipsia,dehydration

Front 61

Identify the blood glucose for the following acute complications: DKA and HHNKS.

Back 61

DKA - 300 + mg/dL

HHNKS - 600 + mg/dL

Front 62

Is the following related to DKA or HHNKS?

More severe dehydration and
electrolyte imbalance

Back 62

HHNKS

Front 63

Is the following related to DKA or HHNKS?

No ketosis

Back 63

HHNKS

Front 64

Is the following related to DKA or HHNKS?

Presence of ketones in
urine, glucosuria, dehydration

Back 64

DKA

Front 65

Is the following related to DKA or HHNKS?

Acetone or fruity breath

Back 65

DKA

Front 66

Is the following related to DKA or HHNKS?

High carbohydrate diet

Back 66

HHNKS

Front 67

fast-acting simple carbohydrate

Back 67

form of carbohydrate that will raise blood glucose levels relatively quickly when ingested

Front 68

Is the following related to DKA or HHNKS?

Gradual onset

Back 68

HHNKS

Front 69

Is the following related to DKA or HHNKS?

Kussmaul respirations

Back 69

DKA

Front 70

Is the following related to DKA or HHNKS?

Sudden onset

Back 70

DKA

Front 71

What is gestational diabetes?

Back 71

High blood sugar (diabetes) that starts or is first diagnosed during pregnancy

Front 72

When is gestational diabetes detected?

Back 72

24 to 28 weeks of gestation

Front 73

Identify the increase risks in gestational diabetes. (3)

Back 73

Increased risk for cesarean delivery, perinatal death, and neonatal complications

Front 74

Identify the cause(s) of gestational diabetes. (3)

Back 74

Mom and baby require more glucose/sugar, but there is only 1 pancreas

Pregnant moms do NOT exercise as much

Hormonal changes in the body

Front 75

macrosomia

Back 75

newborn with an excessive birth weight

Front 76

polycythemia

Back 76

abnormally increased concentration of hemoglobin in the blood

Front 77

hyperbilirubinemia

Back 77

abnormally high amounts of bile pigment (bilirubin) in the blood

Front 78

Identify fetal abnormalities common in babies born to women with gestational diabetes. (5)

Back 78

Macrosomia
Hypoglycemia
Hypocalcemia
Polycythemia
Hyperbilirubinemia

Front 79

Identify the treatment options for gestational diabetes.

Back 79

Diet
Insulin, sulfonylureas (if necessary)

Front 80

secondary diabetes

Back 80

type of diabetes caused by another disease or certain drugs or chemicals

Front 81

Identify possible causes for secondary diabetes. (7)

Back 81

o chronic use of steroids
o TPN (total parenteral nutrition)
o overload of glucose (Crohns)
o severe malnourished pts
o Cushing’s disease (endocrine)
o Pancreatic disease
o organ transplant patients

Front 82

What lab value is the most comprehensive evaluation of glucose control?

Back 82

HgB A1C

Front 83

Identify the normal value for HbG A1C. How does this relate to blood glucose?

Back 83

Goal is < 7.0
Reflects blood glucose less than 100

Front 84

How often is HgB A1C taken? What is the reason for this?

Back 84

Every 3-4 months b/c RBC life is ~120 days

Front 85

How does HgB A1C relate to a patient's DM?

Back 85

It shows how well-controlled DM is.

When pt has uncontrolled DM, the floating glucose in blood/plasma attach to RBC, which is the value for HgB A1C.

Front 86

Identify the 3 acute complications of DM.

Back 86

DKA
HHNKS
Hypoglycemia

Front 87

Identify the 3 chronic complications of DM and their related conditions.

Back 87

Macrovascular (PVD, CAD, CVA)

Microvascular (retinopathy, nephropathy, dermopathy)

Neuropathy

Infection

Front 88

TRUE/FALSE

DM is the number one reason for non-traumatic limb amputation.

Back 88

TRUE

Front 89

Identify the goals of DM management. (4)

Back 89

• Reduce symptoms
• Promote well-being
• Prevent acute complications
• Delay onset and progression of long-term complications

Front 90

Identify the treatment plan for patients with DM.

Back 90

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