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Complex care final > Diabetes > Flashcards

Diabetes Flashcards

1
Q

what cells make and secrete insulin

A

beta cells

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2
Q

what do pancreatic alpha cells do

A

increase production of glucagon

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3
Q

Under normal conditions, what does insulin do?

A

Normally, insulin is continuously released into the bloodstream in small amounts, with increased release when food is ingested.

helps blood sugar enter the body’s cells so it can be used for energy.

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4
Q

What happens when insulin isn’t properly used?

A

glucose cannot enter cells and hyperglycemia occurs

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5
Q

Where are most insulin receptors located?

A

skeletal muscle, fat, and liver cells

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6
Q

What hormones work against the effects of insulin or are “counter-regulatory hormones”? (inverse)

A
  • glucagon
  • epinephrine
  • growth hormone
  • cortisol

These increase blood glucose levels by:

1: stimulating glucose production and release by the liver
2: decreasing the movement of glucose into cells

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7
Q

What does the body do normally when there is a decline in blood glucose levels?

A

The pancreas releases glucagon, which is sent to the liver and stimulates glycogen breakdown. Here, glycogen is broken down to glucose. Blood glucose then rises to a normal range (90mg/100ml).

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8
Q

How frequently should BG be checked in times of acute illness?

A

every four hours

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9
Q

What does the body do normally when there is rise in blood glucose levels?

A

The pancreas secretes insulin. Insulin does:
- stimulates glucose uptake by cells (tissue cells)
- stimulates glycogen formation (glucose is sent to the liver and is converted to glycogen).
Then, blood glucose will fall to a normal range.

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10
Q

What is diabetes mellitus?

A
  • chronic multi-system disease characterized by hyperglycemia from abnormal insulin production, impaired insulin use, or both.
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11
Q

What is the importance of insulin?

A
  • allows the cells in the muscles, fat and liver to absorb glucose that is in the blood
  • the glucose serves as energy to these cells, or it can be converted into fat when needed
  • insulin also affects other metabolic processes, such as the breakdown of fat or protein.
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12
Q

Diagnostics: What is the diagnostic level for the fasting blood glucose (FPG)?

A

FPG greater than or equal to 126mg/dl

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13
Q

What is fasting defined as?

A

Fasting is defined as no caloric intake for at least 8 hours.

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14
Q

What is the oral glucose tolerance test (OGTT)?

A
  • A nurse or doctor will take a blood sample from a vein in your arm to test your starting blood sugar level. You’ll then drink a mixture of glucose dissolved in water. You’ll get another blood glucose test 2 hours later.
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15
Q

Diagnostic: What is the diagnostic blood glucose level for an OGTT after 2 hours?

A

The blood glucose is greater than 200

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16
Q

Diagnostic: What is a normal, pre-diabetes, and diabetes diagnostic level for an A1C?

A

Normal: less than or equal to 5.6%

Pre-diabetes: 5.7-6.4%

Diabetes: greater than or equal to 6.5%

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17
Q

In a pt w/ classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose is_______.

A

Greater than or equal to 200mg/dl

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18
Q

What is the A1C?

A
  • the A1C test measures what percentage of hemoglobin proteins in your blood are coated with sugar (glycated).
  • Hemoglobin proteins in red blood cells transport oxygen. The higher your A1C level is, the poorer your blood sugar control and the higher your risk of diabetes complications.
  • the higher the A1C, the higher the blood sugar
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19
Q

What is the pathology of type 1 diabetes?

A
  • autoimmune mechanism in addition to environmental triggers in genetically susceptible individuals (genetic predisposition and exposure to virus)
  • T-cell mediated destruction of pancreatic beta cells
  • beta cell function will be reduced by 80-90% before hyperglycemia and other symptoms will occur
  • genetic predisposition
    > women: (2.1%)
    > med: (6.1%)
  • onset occurs at any age
  • these patients REQUIRE insulin from outside source to stay alive, otherwise they will develop keto-acidosis
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20
Q

What is the pathology of type 2 diabetes?

A
  • accounts for 90-95% of people with diabetes
  • characterized by a combination of inadequate insulin secretion and insulin resistance
  • the pancreas usually makes some endogenous insulin; however, the body either does not make enough insulin or does not use it effectively or both
  • Beta cell dysfunction + insulin resistance
  • d/t genetic and environmental factors
  • pre-diabetes and diabetes
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21
Q

Genetics: If one parent of an individual has diabetes, what is the percentage that their offspring will get it?

A

40% lifetime risk

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22
Q

Genetics: If both parents of an individual have diabetes, what is the percentage that their offspring will get it?

A

70% lifetime

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23
Q

Genetics: if a first degree relative has diabetes, what is the percentage that you will get diabetes?

A

3 times as likely

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24
Q

Genetics: TCF7L

A

affects insulin secretion and glucose production

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25
Q

Genetics: ABCC8

A

helps regulate insulin

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26
Q

Genetics: CAPN10

A

associated w/ type 2 diabetes risk in mexican americans

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27
Q

genetics: GLUT2

A

helps move glucose into the pancreas

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28
Q

genetics: GCGR

A

glucagon hormone involved in glucose regulation

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29
Q

What is the pathological effect of type 2 diabetes on the GI tract?

A

Decreased incretin effect

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30
Q

decreased incretin effect

A
  • Incretins are gut hormones that are secreted after eating. they regulate the amount of insulin that is secreted after eating.
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31
Q

What is the pathological effect of type 2 diabetes on the adipose tissue?

A

increased lipolysis
- the breakdown of fats and other lipids by hydrolysis to release fatty acids.

results in altered glucose and fat metabolism (type 2 pts are typically overweight)

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32
Q

What is the pathological effect of type 2 diabetes on the kidneys?

A

increased glucose absorption

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33
Q

What is the pathological effect of type 2 diabetes on the MSK system?

A
  • decreased glucose uptake = hyperglycemia
  • defective insulin receptors
  • insulin resistance
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34
Q

What is the pathological effect of type 2 diabetes on the brain?

A

Neurotransmitter dysfunction

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35
Q

What is the pathological effect of type 2 diabetes on the liver?

A
  • increased hepatic glucose production

- Body releases glucagon which turns into glycogen = increased glucose

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36
Q

What is the pathological effect of type 2 diabetes on the islet alpha cell?

A

increase glucagon secretion

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37
Q

What is the pathological effect of type 2 diabetes on the islet beta cell?

A

impaired insulin secretion

  • insulin resistance stimulates increased insulin secretion
  • eventual exhaustion of Beta cells in many people
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38
Q

What are causes of diabetes mellitus?

A
  • pancreatic disorders
  • hormonal disorders
  • drug induced
  • infection/trauma
  • other (down syndrome, cystic fibrosis, hemochromatosis)
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39
Q

What hormonal disorders can lead to DM?

A
  • cushings disorder
  • pheocromocytoma
  • acromegaly
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40
Q

how does cushings disorder lead to DM

A

excess corticosteroids=impairment of glucose metabolism, which leads to hyperglycemia

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41
Q

how does pheocromocytoma lead to DM

A

excess catecholamines=suppress insulin secretion and induce glycogenolysis in the liver = hyperglycemia

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42
Q

how does acromegaly lead to DM

A

excess growth hormone=stimulates gluconeogenesis and lipolysis, causing hyperglycemia and elevated free fatty acid levels

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43
Q

What are the drug-induced causes lead to DM?

A
  • nicotinic acid
  • GCS-steroids
  • anti-rejection meds
  • HIV/AIDs meds
  • chemotherapy
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44
Q

What medications are used to treat type 2 diabetes?

A
  • metformin
  • GLP-1 receptor agonist
  • SGLT-2 inhibitor
  • dipeptidyl peptidase 4 inhibitor (DPP4I)
  • sulfonylureas
  • thiazolidinedione
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45
Q

What is the MOA of Metformin?

A
  • reduce insulin resistance (liver > muscle)

- reduce hepatic glucose production

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46
Q

ADRS of metformin

A
  • GI (big one-the coating of the medication is often rough and hard to digest, therefore, causing irritation to the lining of GI tract)
  • vitamin B12 deficiency (watch for neuropathy s/s)
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47
Q

contraindications of metformin

A

-pts w/ a GFR less than 30ml/min

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48
Q

Why is metformin often held in hospital settings?

A
  • it can cause lactic acidosis in pts w/ renal impairment (less than 30 GFR) also bc pts are more likely to get CT scans w/ contrast dye and that combo can lead to lactic acidosis
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49
Q

GLP-1 Receptor agonist MOA:

A
  • stimulates release of insulin
  • decreases glucagon secretion
  • slow gastric emptying
  • increases satiety (decreases appetite)
  • increase cardioprotection and function

ex. dulaglutide, liraglutide, semaglutide

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50
Q

GLP-1 receptor agonist ADRs to monitor for:

A

GI side effects

  • n/v
  • hypoglycemia
  • diarrhea
  • h/a
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51
Q

Contraindications for GLP-1 receptor agonists

A

some have renal adjustments

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52
Q

SGLT-2 inhibitor MOA:

A
  • decrease renal reabsorption
  • increase urinary glucose excretion
  • approved for HF and reduces kidney damage for pts w/ diabetes
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53
Q

SGLT-2 inhibitor ADRS to monitor for:

A
  • GU infections: increased risk for genital infections and UTIs (fourneirs gangrene)
  • dehydration, hypotension, euglycemic DKA, NPO, bone fracture (canagliflozin)
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54
Q

contraindications of SLGT-2 inhibators

A

renal dosing considerations

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55
Q

Sulfonyrueas: “Gly/Gli”

A

Stimulate functional beta cells

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56
Q

ADR for sulfonyrueas

A

Hypoglycemia

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57
Q

contraindications for sulfonyrueas

A

caution w/ renal or liver disease

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58
Q

Thiazolidinedione: “glitazone”

A

Decrease insulin resistance at peripheral sites and in the liver

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59
Q

Thiazolidinedione ADR

A

Edema, weight increase, bone loss, bladder cancer, +NASH

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60
Q

Thiazolidinedione contraindications

A

NYHA class III or IV

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61
Q

What is basal insulin?

A
  • intermediate (NPH) or long-acting insulin

- basal insulin manages the hepatic and renal glucose output (so the endogenous glucose the body creates)

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62
Q

what is bolus insulin

A
  • short or rapid acting insulin

- manages glucose excursions following meals or snacks

63
Q

what are the basal insulins

A
  • NPH
  • Glargine (lantus)
  • Glargine U-300 (toujeo)
  • Detemir (levemir)
  • Degludec (tresiba)
64
Q

NPH

A

Can purchase OTC-no prescription; dosed twice daily; cloudy and mix before giving
Ex. Humulin N, Novolin N

o: 2-4 hours
p: 8-12 hrs
d: 12-2- hrs

65
Q

Glargine or Basaglar: Lantus

A

Long acting

O: 1-2 hours
P: minimal
D: 20-24 hours

66
Q

Glargine U-300 (toujeo)

A

Long acting

O: 1-2 hours
P: none
D: 24-26hrs

67
Q

Detemir (levemir)

A

Long acting

O: 1-2hrs
P: minimal
D: 18-24hrs

68
Q

Degludec (Tresiba)

A

Long acting

O: 1-2hrs
P: none
D: 36hrs

69
Q

Fast acting Aspart (Fiasp) and Fast acting Lispro (Lyumjev):

A

O: 2-5min
P: 1-2hrs
D: 3-5hrs

70
Q

Lispro (humolog)

A

Rapid-acting insulin

O: less than 15 min
P: 1-2hrs
D: 3-5hrs

71
Q

Aspart (Novolog)

A

O: less than 15 min
P: 1-2hrs
D: 3-5hrs

72
Q

Glulisine (apidra)

A

O: less than 15min
P: 1-2hrs
D: 3-5hrs

73
Q

Regular:

A

Can purchase over the counter, no prescription needed

O: 30-60min
P: 3-4 hrs
D: 6-8hrs

74
Q

Premixed Insulin: Novolin 70/30 and Humulin 70/30

A

NPH and Regular 50/30; Usually given to pts on tube feeds

O: 30-60min
P: 2-10hrs
D: 10-18hrs

75
Q

Premixed insulin: Humalog 75/25 and Novolog 70/30

A

O: 10-30min
P: 1-6hrs
D: 10-24hrs

76
Q

What are nursing considerations for insulin injection sites and insulin?

A
  • training pts on proper injections
  • timing of injection
  • rotations sites
  • cloudy insulins needs to be mixed
77
Q

Quick summary of Diabetic Ketoacidosis and the stressors associated with DKA:

A
  • non-compliance w/ medical treatment or monitoring
  • Other stressor that can be associated w/ DKA:
    Alcohol/cocaine
    CV event
    trauma
    Corticosteroids, antipsychotic medications
    Acute GI disease (pancreatitis) `
78
Q

What is the most common precipitating factor for DKA?

A

infection

79
Q

Is DM a hypoglycemic or hyperglycemic emergency?

A

DM Hyperglycemic Emergency

80
Q

Quick summary of Hyperosmolar Hyperglycemic State (HHS):

A
  • non-compliance w/ medical treatment or monitoring
81
Q

What is the most common precipitating factor of HHS?

A

Infection is the mot common precipitating factor (DM ulcer/Sepsis)

82
Q

Stressors associated w/ HHS:

A 
CHF
Renal dysfunction
Alcohol/cocaine
CV event
Trauma
corticosteroids, antipsychotic meds
Acute GI disease (gastroenteritis)
83
Q

What is the normal lab value range for glucose?

DKA:

HHS:

A

Normal: 75-115

DKA: greater than 250

HHS: greater than 600

84
Q

What is the normal lab value range for arterial pH?

DKA:

HHS:

A

N: 7.35-7.45

DKA: less than 7.3

HHS: greater than 7.3

85
Q

What is the normal lab range for bicarb?

DKA:

HHS:

A

N: 22-28 (26)

DKA: less than 15

HHS: greater than 15

86
Q

What is the normal lab value for Serum Osmo?

DKA:

HHS:

A

N: 275-295

DKA: less than 320

HHS: greater than 320

87
Q

What is the normal lab value for anion gap?

DKA:

HHS:

A

N: less than 12

DKA: greater than 12

HHS: varies

88
Q

What is the normal lab value range for serum ketones:

DKA:

HHS:

A

N: negative

DKA: mod-high

HHS: none-trace

89
Q

What is the normal lab value range for urine ketones?

DKA:

HHS:

A

N: negative

DKA: mod-high

HHS: none-trace

90
Q

For a pt with MILD DKA, what will their pH, bicarb, urine/serum ketones, anion gap, glucose, and mental status be?

A 
pH: 7.25-7.35
Serum bicarb: 15-18
Urine/serum ketones: positive
anion gap: greater than 10
Blood glucose: greater than 250
Mental status: alert
91
Q

For a pt w/ MODERATE DKA, what will their pH, bicarb, urine/serum ketones, anion gap, glucose, and mental status be?

A 
pH: 7.00-7.24
Bicarb: 10-15
U/S ketones: positive
anion gap: greater than 12
Glucose: greater than 250
Mental status: alert/drowsy
92
Q

For a pt with SEVERE DKA, what will their pH, bicarb, urine/serum ketones, anion gap, glucose, and mental status be?

A 
pH: less than 7.00
Bicarb: less than 10
U/S ketones: positive
Anion gap: greater than 12
glucose: greater than 250
mental status: stupor/coma
93
Q

For a pt with DKA, what will their glucose, pH, bicarb, serum osmo, anion gap, serum/urine ketones be?

A 
Glucose: greater than 250
pH: less than 7.3
bicarb: less than 15
serum osmo: less than 320
anion gap: greater than 12
Serum/urine ketones: mod-high
94
Q

What is DKA?

A
  • Caused by a profound deficiency of insulin = glucose cannot be properly used for energy (HYPERGLYCEMIA)
  • mostly in type one
  • the body compensates by breaking down fat stores in liver for fuel = release of glucagon = increase in glycogen = increase glucose even more
  • ketones are acidic by-products of fat metabolism that can cause serious problems = ketosis alters the pH causing metabolic acidosis to develop
  • kidneys try to reabsorb glucose (but there is too much for them to do it) = glucose leaking into the urine = osmotic diuresis = polyuria and excretion of Na+, K+, and Cl-
95
Q

what is DKA characterized by

A

hyperglycemia, ketosis, acidosis, and dehydration

96
Q

precipitating factors of DKA

A

infection, inadequate insulin dosage, undiagnosed type 1 diabetes, lack of education, understanding or resources, neglect

97
Q

What are causes or triggers of DKA?

A
  • absolute insulin deficiency
  • stress, infection or insufficient insulin intake
  • Counter-regulatory hormones
    > increase glucagon
    > increase catecholamines
    > increase cortisol
    > increase growth hormone
98
Q

What will those DKA causes lead to?

A
  • increased lipolysis
  • decrease glucose utilization
  • increased proteolysis
  • decrease protein synthesis
  • increased glycogenolysis
99
Q

What will increased lipolysis lead to?

A

Increased free fatty acid to liver, which leads to:

  • increased gluconeogenesis (glucose is formed from noncarbohydrate sources such as proteins, fatty acids)
  • increased ketogenesis (increased ketones can poison the body)
  • decreased alkali reserve (blood becomes more acidic)
  • ketoacidosis
  • lactic acidosis

The body breaks down fatty acids into ketones, which causes the blood to become more acidic.

100
Q

What will decreased glucose utilization lead to?

A
  • hyperglycemia
101
Q

What will increased proteolysis and decreased protein synthesis lead to?

A
  • increased gluconeogenesis
  • hyperglycemia
  • glucosuria (osmotic diuresis-body is trying to compensate for the increased glucose in the body and it’s trying to excrete it through urine)
  • loss of water and electrolytes (bc of the body’s compensation)
  • dehydration
  • impaired renal function
102
Q

What will increased glycogenolysis lead to the body?

A

hyperglycemia

103
Q

What are the CO2 levels for a patient in DKA

A

21-31

104
Q

What are the symptoms of DKA?

A
  • n/v
  • thirst (polydipsia)
  • increased urination (polyuria)
  • abdominal pain (greater than 50% of pts), anorexia, n/v
  • SOB
  • AMS (altered mental status)
  • acetone is noted on the breath as sweet, fruity odor
105
Q

Defining characteristics of DKA?

A

hyperglycemia, ketosis, acidosis, dehydration

106
Q

What are the physical findings of DKA?

A

orthostatic BP and pulse changes

  • tachycardia, hypotension
  • kussmaul respirations (deep and more rapid breathing in response to metabolic acidosis)
  • poor skin turgor (bc the pt will become severely dehydrated, the skin becomes dry and loose, and the eyes become soft and sunken; dry mucus membranes)
107
Q

Which electrolytes will be severely depleted with DKA?

A

Na, K, chloride, Mg, phosphate

108
Q

What are immediate lab tests that would be done for DKA?

A
  • basic metabolic panel
  • Mg
  • CBC
  • routine urine analysis
  • serum ketones
  • ABGs (acidotic)
109
Q

Treatment: What should you be monitoring for w/ a pt that has DKA?

A
  • vital signs every hour
  • I/Os
  • cardiac or telemetry monitoring (bc is becoming acidotic, there are increases in K [k follows glucose] and high levels of K cause cardiac issues)
110
Q

What is the treatment for DKA?

A

Bolus fluids: 2-4 L of 0.9% NS IV

Maintenance fluids: 0.9% NS or 0.45% NS

DKA: when blood glucose is less than or equal to 250mg/dl, replace IV infusion w/ D5 (dextrose) (replace lost fluids and provide carbohydrates to the body)

Insulin: bolus 10 units regular insulin IVx1 and start IV infusion

Additional: treat underlying patho (infection)

111
Q

What electrolyte dictates when insulin is given to treat DKA?

A

potassium (K+)

112
Q

What should you do with insulin with a potassium level less than 3.3mEq/L?

A

Hold the insulin!!

Give 20-30mEq/hr of K IV

When K is greater than 3.3, add insulin gtt (drip)

113
Q

What should you do with a K =3.3-5.1?

A

Give 20-30mEq/L of K IVF to keep K+ between 4-5mEq/L

114
Q

What should you do with K+ greater than 5.2?

A

Do not give K+ yet!!

Check serum K+ every two hours until it is less than 5.2mEq/L, then add K+.

115
Q

When do you know that DKA has resolved?

A
  • mental status has recovered
  • Blood glucose is less than or equal to 250mg/dL
  • AG less than 12
  • serum bicarb greater than or equal to 18mEq/L
  • venous pH greater than 7.30
116
Q

What is hyperglycemic hyperosmolar syndrome (HHS)?

A

life-threatening syndrome that can occur in the pt w/ diabetes who is able to make enough insulin to prevent DKA, but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion

  • less common than DKA
  • often occurs in pts over 60 years of age w/ type 2 diabetes
117
Q

common causes of HHS

A

UTIs, PNA, sepsis, any acute illness, newly diagnosed w/ type 2 diabetes

  • often related to impaired thirst sensation and/or a functional inability to replace fluids
  • there is usually a hx of inadequate fluid intake, increasing mental depression, or cognitive impairment and polyuria
118
Q

main difference between HHS and DKA

A

-pt w/ HHS usually has enough circulating insulin so that ketoacidosis does not occur
- bc HHS has fewer symptoms in the earlier stages, BG levels can climb quite high before the problem is recognized
the higher the BG levels increase serum osmolality and cause more severe neurologic manifestations, such as somnolence, coma, seizures, hemiparesis, and aphasia
- since these manifestations resemble a stroke, immediate determination of the glucose level is critical for correct diagnosis and treatment

119
Q

What is the pathophysiology of hyperglycemic HHS?

A

hyperglycemia: BG greater than 600mg/dL

120
Q

What is the pathophysiology of hyperosmolar HHS

A

increased BG= an osmotic diuresis that leads to intravascular volume depletion, which is exacerbated by inadequate fluid replacement

121
Q

what is the patho of non ketotic HHS

A

still producing some insulin

122
Q

What are the physical findings of HHS?

A
  • profound dehydration and hyperosmolality
  • hypotension
  • tachycardia
  • altered mental status (effective serum osmolality greater than 320-330 mOsm/kg)
  • poor skin turgor
123
Q

What are the causes of HHS?

A
  • serious, concurrent illness such as MI or stroke
  • sepsis
  • PNA
  • debilitating condition (prior stroke or dementia)
124
Q

What are symptoms of HHS?

A
  • n/v
  • thirst (polydipsia)
  • increased urination (polyuria)
  • AMS (altered mental status)
125
Q

What are the Lab values for HHS? Glucose, arterial pH, bicarb, serum osmolality, anion gap, serum ketones, urine ketons?

A 
Glucose: greater than 600
Arterial pH: greater than 7.3 
Bicarrb: greater than 15
Serum osmolality: greater than 320
Anion gap: variable 
serum/urine ketones: none-trace
126
Q

For HHS, when blood glucose is less than or equal to _______, replace ________.

A

300

IV infusion w/ D5 0.45% NS

127
Q

What is the treatment for HHS?

A

Same as DKA:

Bolus fluids: 2-4 L of 0.9% NS IV infused over one hour

Maintenance fluids: 0.45% NS IV infused at 150-250ml/hr

128
Q

Immediate treatment of HHS

A
  1. 9% or 0.45% NS IV (large volumes of fluid replacement-slowly!)
    - When BG gets to 250 give pt IV dextrose to prevent hypoglycemia
129
Q

What are the medications for HHS?

A

Insulin bolus: 10units regular insulin IV x1

Insulin infusion

Treat any underlying patho

SQ insulin if appropriate

130
Q

Levels of hypoglycemia:

A

Level 1: glucose is less than 70mg/dl and glucose is greater than or equal to 54 mg/dl

Level 2: glucose is less than 54

Level 3: a severe event characterized by altered mental and/or physical status requiring assistance

131
Q

Hypoglycemia:

A

Release of epinephrine and glucagon

Glucagon: glycogenolysis, which leads to gluconeogenesis, which leads to incresaed hepatic glucose release

Epinephrine: reducing glucose up-take, enhances production of hepatic glucose, occurs around 68mg/dl
- epinephrine creates s/s like shakiness, palpitations, nervousness, diaphoresis, anxiety, hunger, pallor

132
Q

What are the neurogenic symptoms of hypoglycemia?

A
  • diaphoresis
  • palpitations
  • apprehension/anxiety
  • tremor
  • hypertension
133
Q

What are the neuroglycopenic symptoms of hypoglycemia?

A
  • cog impairment
  • fatigue
  • dizziness
  • visual changes
  • seizures
  • hunger
  • inappropriate behavior
  • abnormal behavior
  • convulsions
134
Q

What are the risk factors for hypoglycemia? (5)

A
  • hypoglycemia unawareness (has hypoglycemic episodes often, and body gets used to it, so when it’s low, the body stops presenting until it’s super emergent)
  • advanced age
  • chronic renal failure
  • liver disease
  • AMS (altered mental status)
135
Q

What are 7 triggering events for hypoglycemia?

A
  • emesis/ reduced oral intake
  • new NPO status
  • sudden reduction of steroid dose
  • medication errors
  • severe illness
  • alcohol/drugs
  • exercise

*blood sugar is usually a sign that a patient is in sepsis

136
Q

What is a diagnostic level of glucose for a pt w/ hypoglycemia?

A

less than 70

recheck BG and repeat treatment every 15 min until glucose is at least 70

137
Q

What is the treatment for a patient with hypoglycemia that is less than 70 and alert and able to eat and drink?

A

Administer 15-20 g of rapid-acting carbohydrate

138
Q

What is the treatment for a pt w/ hypoglycemia less than 70 that is alert and awake, NPO or unable to swallow?

A

Administer 25mL dextrose 50% solution IV and start IV dextrose 5% in water at 100mL/h

139
Q

What is the treatment for a pt w/ hypoglycemia less than 70 w/ altered levels of consciousness?

A

IV access: administer 25ml dextrose 50% (1/2amp) and start IV dextrose 5% in water at 100ml/h

No IV access: give glucagon 1mg IM limit, two times

140
Q

What is syndrome of inappropriate antidiuretic hormone (SIADH)?

A

Excess ADH, resulting in physiologic imbalance of water

  1. increased ADH
  2. increased water reabsorption in the renal tubules
  3. increased intravascular fluid volume
  4. dilutional hyponatremia and decreased serum osmolality
141
Q

What is the etiology of SIADH? (4 categories)

A

CNS disturbances: stroke, hemorrhage, infection, trauma, psychosis

Malignancies: ectopic production of ADH by a tumor in a small cell carcinoma of the lung; head and neck cancer, olfactory neuroblastoma

Drugs: carbamazepine, high-dose cyclophosphamide, SSRIs

Surgery: transphenoidal pituitary surgery; head injur

142
Q

What are the clinical manifestations of SIADH with a serum sodium less than 125mEq/L?

A
  • thirst
  • DOE (dyspnea on exertion)
  • fatigue
  • HA
  • muscle cramps
143
Q

What are the clinical manifestations of SIADH with a serum sodium level less than 120mEq/L?

A

GI: vomiting, abdominal cramps

MS: muscle twitching

Neuro: cerebral edema, confusion, seizures, coma

144
Q

What are the physical exam findings for SIADH?

A

No edema

Dry mucous membranes

Decreased skin turgor

Dehydrated-water is in the veins, but not in the cells!

145
Q

What is the diagnostic criteria for SIADH? (6)

A

Decreased serum osmolality (less than 275 mOsm/kg)

Urine osmolality greater than 100 mOsm/kg in the setting of serum hypotonicity

Euvolemic clinical examination

in the setting of normal dietary sodium intake, urine sodium is greater than 40mmol/L

Normal thyroid, adrenal, renal, cardiac function

No recent use of diuretics

146
Q

What is the SIADH management?

A
  • treat underlying disease
  • Fluid restriction-intake of less than 800ml/day (except SAH)
  • Correct Na+ deficit (3% NaCl-hypertonic solution; NaCl tabs-2-3grms TID)
  • loop diuretic or a vasopressin receptor antagonist
  • Demeclocycline-acts on the collecting tubule cell to diminish its responsiveness to ADH, thereby increasing water excretion
147
Q

What are the nursing considerations for SIADH?

A

Carefully monitor I/O

Daily weights

Fall precautions

Lower head of bed (flat or less than 10degrees)

148
Q

What is diabetes insipidus?

A

Deficiency of ADH resulting in a physiologic imbalance of water either by:

  • neurogenic: insufficient production of ADH
  • nephrogenic: unresponsiveness of the renal tubules to ADh
149
Q

What is the patho of DI?

A

Decreased ADH

decreased water reabsorption in renal tubules

decreased intravascular fluid volume

excessive urine output and increased serum osmolality

150
Q

What are the diagnostics for DI?

A

Goal: show that polyuria is caused by the inability to concentrate urine

water deprivation test:

  • pt drinks fluids overnight and then deprived of fluids for 8hrs
  • hourly monitoring of plasma osmolality and every 2 hour urine osmolality
  • after 8 hrs, pt is given desmopressin (DDAVP)

Confirmed to have DI if serum Osm is greater than 305mmol/kg

151
Q

Neurogenic DI (central) cause:

Water Deprivation Test result:

management:

A
  • Brain tumor, head injury, brain surgery, CNS infection
  • Urine Osm greater than 800
  • desmopressin (DDAVP) 20-40mcg intranasally qd-tid
152
Q

Nephrogenic DI cause:

Water deprivation test result:

Management:

A

Drug therapy, renal damage, hereditary renal disease

urine osm less than 300

Management: removal of underlying cause (lithium therapy)

  • amiloride 5mg/day for lithium related disease
  • low sodium diet and chlorothiazide to induce mild Na depletion
153
Q

Nursing considerations for DI:

A
  • carefully monitor I/O
  • daily weights
  • hypotonic IV solution
154
Q

Differences between SIADH:

DI:

A

SIADH: low UO, high levels of ADH, hyponatremia, over hydrated, retain too much fluid

DI: High UO, low ADH, hypernatremia, dehydrated, lose too much fluid

Both will have excessive thirst

Complex care final (8 decks)

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