Diabetes Flashcards
(154 cards)
1
Q
what cells make and secrete insulin
A
beta cells
2
Q
what do pancreatic alpha cells do
A
increase production of glucagon
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.
4
Q
What happens when insulin isn’t properly used?
A
glucose cannot enter cells and hyperglycemia occurs
5
Q
Where are most insulin receptors located?
A
skeletal muscle, fat, and liver cells
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
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).
8
Q
How frequently should BG be checked in times of acute illness?
A
every four hours
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.
10
Q
What is diabetes mellitus?
A
- chronic multi-system disease characterized by hyperglycemia from abnormal insulin production, impaired insulin use, or both.
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.
12
Q
Diagnostics: What is the diagnostic level for the fasting blood glucose (FPG)?
A
FPG greater than or equal to 126mg/dl
13
Q
What is fasting defined as?
A
Fasting is defined as no caloric intake for at least 8 hours.
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.
15
Q
Diagnostic: What is the diagnostic blood glucose level for an OGTT after 2 hours?
A
The blood glucose is greater than 200
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%
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
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
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
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
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
22
Q
Genetics: If both parents of an individual have diabetes, what is the percentage that their offspring will get it?
A
70% lifetime
23
Q
Genetics: if a first degree relative has diabetes, what is the percentage that you will get diabetes?
A
3 times as likely
24
Q
Genetics: TCF7L
A
affects insulin secretion and glucose production
25
Genetics: ABCC8
helps regulate insulin
26
Genetics: CAPN10
associated w/ type 2 diabetes risk in mexican americans
27
genetics: GLUT2
helps move glucose into the pancreas
28
genetics: GCGR
glucagon hormone involved in glucose regulation
29
What is the pathological effect of type 2 diabetes on the GI tract?
Decreased incretin effect
30
decreased incretin effect
- Incretins are gut hormones that are secreted after eating. they regulate the amount of insulin that is secreted after eating.
31
What is the pathological effect of type 2 diabetes on the adipose tissue?
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)
32
What is the pathological effect of type 2 diabetes on the kidneys?
increased glucose absorption
33
What is the pathological effect of type 2 diabetes on the MSK system?
- decreased glucose uptake = hyperglycemia
- defective insulin receptors
- insulin resistance
34
What is the pathological effect of type 2 diabetes on the brain?
Neurotransmitter dysfunction
35
What is the pathological effect of type 2 diabetes on the liver?
- increased hepatic glucose production
| - Body releases glucagon which turns into glycogen = increased glucose
36
What is the pathological effect of type 2 diabetes on the islet alpha cell?
increase glucagon secretion
37
What is the pathological effect of type 2 diabetes on the islet beta cell?
impaired insulin secretion
- insulin resistance stimulates increased insulin secretion
- eventual exhaustion of Beta cells in many people
38
What are causes of diabetes mellitus?
- pancreatic disorders
- hormonal disorders
- drug induced
- infection/trauma
- other (down syndrome, cystic fibrosis, hemochromatosis)
39
What hormonal disorders can lead to DM?
- cushings disorder
- pheocromocytoma
- acromegaly
40
how does cushings disorder lead to DM
excess corticosteroids=impairment of glucose metabolism, which leads to hyperglycemia
41
how does pheocromocytoma lead to DM
excess catecholamines=suppress insulin secretion and induce glycogenolysis in the liver = hyperglycemia
42
how does acromegaly lead to DM
excess growth hormone=stimulates gluconeogenesis and lipolysis, causing hyperglycemia and elevated free fatty acid levels
43
What are the drug-induced causes lead to DM?
- nicotinic acid
- GCS-steroids
- anti-rejection meds
- HIV/AIDs meds
- chemotherapy
44
What medications are used to treat type 2 diabetes?
- metformin
- GLP-1 receptor agonist
- SGLT-2 inhibitor
- dipeptidyl peptidase 4 inhibitor (DPP4I)
- sulfonylureas
- thiazolidinedione
45
What is the MOA of Metformin?
- reduce insulin resistance (liver > muscle)
| - reduce hepatic glucose production
46
ADRS of metformin
- 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)
47
contraindications of metformin
-pts w/ a GFR less than 30ml/min
48
Why is metformin often held in hospital settings?
- 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
49
GLP-1 Receptor agonist MOA:
- stimulates release of insulin
- decreases glucagon secretion
- slow gastric emptying
- increases satiety (decreases appetite)
- increase cardioprotection and function
ex. dulaglutide, liraglutide, semaglutide
50
GLP-1 receptor agonist ADRs to monitor for:
GI side effects
- n/v
- hypoglycemia
- diarrhea
- h/a
51
Contraindications for GLP-1 receptor agonists
some have renal adjustments
52
SGLT-2 inhibitor MOA:
- decrease renal reabsorption
- increase urinary glucose excretion
- approved for HF and reduces kidney damage for pts w/ diabetes
53
SGLT-2 inhibitor ADRS to monitor for:
- GU infections: increased risk for genital infections and UTIs (fourneirs gangrene)
- dehydration, hypotension, euglycemic DKA, NPO, bone fracture (canagliflozin)
54
contraindications of SLGT-2 inhibators
renal dosing considerations
55
Sulfonyrueas: "Gly/Gli"
Stimulate functional beta cells
56
ADR for sulfonyrueas
Hypoglycemia
57
contraindications for sulfonyrueas
caution w/ renal or liver disease
58
Thiazolidinedione: "glitazone"
Decrease insulin resistance at peripheral sites and in the liver
59
Thiazolidinedione ADR
Edema, weight increase, bone loss, bladder cancer, +NASH
60
Thiazolidinedione contraindications
NYHA class III or IV
61
What is basal insulin?
- intermediate (NPH) or long-acting insulin
| - basal insulin manages the hepatic and renal glucose output (so the endogenous glucose the body creates)
62
what is bolus insulin
- short or rapid acting insulin
| - manages glucose excursions following meals or snacks
63
what are the basal insulins
- NPH
- Glargine (lantus)
- Glargine U-300 (toujeo)
- Detemir (levemir)
- Degludec (tresiba)
64
NPH
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
Glargine or Basaglar: Lantus
Long acting
O: 1-2 hours
P: minimal
D: 20-24 hours
66
Glargine U-300 (toujeo)
Long acting
O: 1-2 hours
P: none
D: 24-26hrs
67
Detemir (levemir)
Long acting
O: 1-2hrs
P: minimal
D: 18-24hrs
68
Degludec (Tresiba)
Long acting
O: 1-2hrs
P: none
D: 36hrs
69
Fast acting Aspart (Fiasp) and Fast acting Lispro (Lyumjev):
O: 2-5min
P: 1-2hrs
D: 3-5hrs
70
Lispro (humolog)
Rapid-acting insulin
O: less than 15 min
P: 1-2hrs
D: 3-5hrs
71
Aspart (Novolog)
O: less than 15 min
P: 1-2hrs
D: 3-5hrs
72
Glulisine (apidra)
O: less than 15min
P: 1-2hrs
D: 3-5hrs
73
Regular:
Can purchase over the counter, no prescription needed
O: 30-60min
P: 3-4 hrs
D: 6-8hrs
74
Premixed Insulin: Novolin 70/30 and Humulin 70/30
NPH and Regular 50/30; Usually given to pts on tube feeds
O: 30-60min
P: 2-10hrs
D: 10-18hrs
75
Premixed insulin: Humalog 75/25 and Novolog 70/30
O: 10-30min
P: 1-6hrs
D: 10-24hrs
76
What are nursing considerations for insulin injection sites and insulin?
- training pts on proper injections
- timing of injection
- rotations sites
- cloudy insulins needs to be mixed
77
Quick summary of Diabetic Ketoacidosis and the stressors associated with DKA:
- 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
What is the most common precipitating factor for DKA?
infection
79
Is DM a hypoglycemic or hyperglycemic emergency?
DM Hyperglycemic Emergency
80
Quick summary of Hyperosmolar Hyperglycemic State (HHS):
- non-compliance w/ medical treatment or monitoring
81
What is the most common precipitating factor of HHS?
Infection is the mot common precipitating factor (DM ulcer/Sepsis)
82
Stressors associated w/ HHS:
```
CHF
Renal dysfunction
Alcohol/cocaine
CV event
Trauma
corticosteroids, antipsychotic meds
Acute GI disease (gastroenteritis)
```
83
What is the normal lab value range for glucose?
DKA:
HHS:
Normal: 75-115
DKA: greater than 250
HHS: greater than 600
84
What is the normal lab value range for arterial pH?
DKA:
HHS:
N: 7.35-7.45
DKA: less than 7.3
HHS: greater than 7.3
85
What is the normal lab range for bicarb?
DKA:
HHS:
N: 22-28 (26)
DKA: less than 15
HHS: greater than 15
86
What is the normal lab value for Serum Osmo?
DKA:
HHS:
N: 275-295
DKA: less than 320
HHS: greater than 320
87
What is the normal lab value for anion gap?
DKA:
HHS:
N: less than 12
DKA: greater than 12
HHS: varies
88
What is the normal lab value range for serum ketones:
DKA:
HHS:
N: negative
DKA: mod-high
HHS: none-trace
89
What is the normal lab value range for urine ketones?
DKA:
HHS:
N: negative
DKA: mod-high
HHS: none-trace
90
For a pt with MILD DKA, what will their pH, bicarb, urine/serum ketones, anion gap, glucose, and mental status be?
```
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
For a pt w/ MODERATE DKA, what will their pH, bicarb, urine/serum ketones, anion gap, glucose, and mental status be?
```
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
For a pt with SEVERE DKA, what will their pH, bicarb, urine/serum ketones, anion gap, glucose, and mental status be?
```
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
For a pt with DKA, what will their glucose, pH, bicarb, serum osmo, anion gap, serum/urine ketones be?
```
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
What is DKA?
- 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
what is DKA characterized by
hyperglycemia, ketosis, acidosis, and dehydration
96
precipitating factors of DKA
infection, inadequate insulin dosage, undiagnosed type 1 diabetes, lack of education, understanding or resources, neglect
97
What are causes or triggers of DKA?
- absolute insulin deficiency
- stress, infection or insufficient insulin intake
- Counter-regulatory hormones
> increase glucagon
> increase catecholamines
> increase cortisol
> increase growth hormone
98
What will those DKA causes lead to?
- increased lipolysis
- decrease glucose utilization
- increased proteolysis
- decrease protein synthesis
- increased glycogenolysis
99
What will increased lipolysis lead to?
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
What will decreased glucose utilization lead to?
- hyperglycemia
101
What will increased proteolysis and decreased protein synthesis lead to?
- 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
What will increased glycogenolysis lead to the body?
hyperglycemia
103
What are the CO2 levels for a patient in DKA
21-31
104
What are the symptoms of DKA?
- 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
Defining characteristics of DKA?
hyperglycemia, ketosis, acidosis, dehydration
106
What are the physical findings of DKA?
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
Which electrolytes will be severely depleted with DKA?
Na, K, chloride, Mg, phosphate
108
What are immediate lab tests that would be done for DKA?
- basic metabolic panel
- Mg
- CBC
- routine urine analysis
- serum ketones
- ABGs (acidotic)
109
Treatment: What should you be monitoring for w/ a pt that has DKA?
- 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
What is the treatment for DKA?
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
What electrolyte dictates when insulin is given to treat DKA?
potassium (K+)
112
What should you do with insulin with a potassium level less than 3.3mEq/L?
Hold the insulin!!
Give 20-30mEq/hr of K IV
When K is greater than 3.3, add insulin gtt (drip)
113
What should you do with a K =3.3-5.1?
Give 20-30mEq/L of K IVF to keep K+ between 4-5mEq/L
114
What should you do with K+ greater than 5.2?
Do not give K+ yet!!
Check serum K+ every two hours until it is less than 5.2mEq/L, then add K+.
115
When do you know that DKA has resolved?
- 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
What is hyperglycemic hyperosmolar syndrome (HHS)?
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
common causes of HHS
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
main difference between HHS and DKA
-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
What is the pathophysiology of hyperglycemic HHS?
hyperglycemia: BG greater than 600mg/dL
120
What is the pathophysiology of hyperosmolar HHS
increased BG= an osmotic diuresis that leads to intravascular volume depletion, which is exacerbated by inadequate fluid replacement
121
what is the patho of non ketotic HHS
still producing some insulin
122
What are the physical findings of HHS?
- profound dehydration and hyperosmolality
- hypotension
- tachycardia
- altered mental status (effective serum osmolality greater than 320-330 mOsm/kg)
- poor skin turgor
123
What are the causes of HHS?
- serious, concurrent illness such as MI or stroke
- sepsis
- PNA
- debilitating condition (prior stroke or dementia)
124
What are symptoms of HHS?
- n/v
- thirst (polydipsia)
- increased urination (polyuria)
- AMS (altered mental status)
125
What are the Lab values for HHS? Glucose, arterial pH, bicarb, serum osmolality, anion gap, serum ketones, urine ketons?
```
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
For HHS, when blood glucose is less than or equal to _______, replace ________.
300
IV infusion w/ D5 0.45% NS
127
What is the treatment for HHS?
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
Immediate treatment of HHS
0. 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
What are the medications for HHS?
Insulin bolus: 10units regular insulin IV x1
Insulin infusion
Treat any underlying patho
SQ insulin if appropriate
130
Levels of hypoglycemia:
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
Hypoglycemia:
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
What are the neurogenic symptoms of hypoglycemia?
- diaphoresis
- palpitations
- apprehension/anxiety
- tremor
- hypertension
133
What are the neuroglycopenic symptoms of hypoglycemia?
- cog impairment
- fatigue
- dizziness
- visual changes
- seizures
- hunger
- inappropriate behavior
- abnormal behavior
- convulsions
134
What are the risk factors for hypoglycemia? (5)
- 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
What are 7 triggering events for hypoglycemia?
- 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
What is a diagnostic level of glucose for a pt w/ hypoglycemia?
less than 70
recheck BG and repeat treatment every 15 min until glucose is at least 70
137
What is the treatment for a patient with hypoglycemia that is less than 70 and alert and able to eat and drink?
Administer 15-20 g of rapid-acting carbohydrate
138
What is the treatment for a pt w/ hypoglycemia less than 70 that is alert and awake, NPO or unable to swallow?
Administer 25mL dextrose 50% solution IV and start IV dextrose 5% in water at 100mL/h
139
What is the treatment for a pt w/ hypoglycemia less than 70 w/ altered levels of consciousness?
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
What is syndrome of inappropriate antidiuretic hormone (SIADH)?
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
What is the etiology of SIADH? (4 categories)
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
What are the clinical manifestations of SIADH with a serum sodium less than 125mEq/L?
- thirst
- DOE (dyspnea on exertion)
- fatigue
- HA
- muscle cramps
143
What are the clinical manifestations of SIADH with a serum sodium level less than 120mEq/L?
GI: vomiting, abdominal cramps
MS: muscle twitching
Neuro: cerebral edema, confusion, seizures, coma
144
What are the physical exam findings for SIADH?
No edema
Dry mucous membranes
Decreased skin turgor
Dehydrated-water is in the veins, but not in the cells!
145
What is the diagnostic criteria for SIADH? (6)
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
What is the SIADH management?
- 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
What are the nursing considerations for SIADH?
Carefully monitor I/O
Daily weights
Fall precautions
Lower head of bed (flat or less than 10degrees)
148
What is diabetes insipidus?
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
What is the patho of DI?
Decreased ADH
decreased water reabsorption in renal tubules
decreased intravascular fluid volume
excessive urine output and increased serum osmolality
150
What are the diagnostics for DI?
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
Neurogenic DI (central) cause:
Water Deprivation Test result:
management:
- Brain tumor, head injury, brain surgery, CNS infection
- Urine Osm greater than 800
- desmopressin (DDAVP) 20-40mcg intranasally qd-tid
152
Nephrogenic DI cause:
Water deprivation test result:
Management:
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
Nursing considerations for DI:
- carefully monitor I/O
- daily weights
- hypotonic IV solution
154
Differences between SIADH:
DI:
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
