T2: DKA, HHS, SIADH, DI Flashcards
What is DKA caused by
profound deficiency of insulin
what is DKA characterized by
Hyperglycemia
Ketosis
Acidosis
Dehydration
DKA is more likely to develop in why type of diabetic
type 1
pH normal range
7.35-7.45
PaCO2 normal range
35-45 mm Hg
HCO3 normal range
22-26
blood glucose in DKA
≥ 250 mg/dL
main s/s of hyperglycemia
polyuria
polydipsia
polyphagia
“hot and dry, sugar high”
precipitating factors of DKA
-Illness
-Infection
-Inadequate insulin dosage
-Undiagnosed type 1 diabetes
-Poor self-management
-Neglect
clinical manifestations of DKA
-Dehydration (poor skin turgor, dry mucus membranes, tachycardia, orthostatic hypotension)
-Lethargy and weakness early
-skin is dry and loose, eyes become soft and sunken
-Abdominal pain/ anorexia, nausea, vomiting
-Kussmaul Respirations
-Acetone breath
blood pH in DKA
lower than 7.30
serum bicarb in DKA
< 16 mEq/L
UA in DKA
Moderate to high ketone levels in urine or serum
fluids for DKA
start on 0.9% NS
when BG reaches 250mg/dL, add 5-10% dextrose to 1/2 NS
when the BG reaches 250 mg/dL
add 5-10% dextrose to 1/2 NS, turn off insulin drip, then begin sub-q insulin, and take off NPO
HINT HINT: what is the rate for continuous regular insulin
0.1 U/kg/hr
what are the IV/Lines needed in a patient in DKA?
A line: to get ABGs
2 IV access: one for fluids and one for insulin
what is the rate we want to restore the UO to in DKA
30-60 mL/hr
measuring potassium in patient with DKA:
If the patient is hypokalemic, insulin administration will further decrease the potassium levels since insulin drives potassium into the cells, may need to give potassium replacement
what do we do if the patient becomes hypoglycemic
push D50
Hyperosmolar hyperglycemic syndrome (HHS)
a life-threatening syndrome that can occur in the patient with diabetes who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion
what type of diabetes does HHS occur more in
type 2
precipitating factors of HHS
*UTIs, pneumonia, sepsis
*Acute illness
*Newly diagnosed type 2 diabetes
*Impaired thirst sensation and/or inability to replace fluids
glucose levels in HHS
> 600 mg/dL
UA in HHS
Ketone bodies are absent or minimal in both blood and urine
management for HHS
includes immediate IV administration insulin and either 0.9% or 0.45% NaCl,
When blood glucose levels fall to approximately 250 mg/dL, IV fluids containing dextrose are administered to prevent hypoglycemia.
what is a useful aid in detecting hyperkalemia and hypokalemia
cardiac monitoring
rapid insulin onset
rapid insulin peak
Rapid insulin duration
10-30min
30min-3hr
3-5 hrs
Short acting insulin onset
short acting insulin peak
short acting insulin duration
30min-1hr
2-5 hr
5-8 hours
intermediate acting insulin onset
intermediate acting insulin peak
intermediate acting insulin duration
1.5-4 hours
4-12 hours
12-18 hours
long acting insulin onset
long acting insulin peak
long acting insulin duration
0.8-4 hours
none
24 hours
Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is characterized by
*fluid retention,
*dilutional hyponatremia
*Concentrated urine
clinical manifestations of SIADH
-Low urine output
Increased weight
-Initially, thirst
-Dyspnea on exertion
-Fatigue
diagnosis of SIADH
get blood and urine samples at SAME TIME
serum sodium in SIADH
<135 (dilutional hyponatremia from excess fluid)
urine specific gravity in SIADH
> 1.025 (amber urine)
Pathophysiology Map of SIADH
-Increased Antidiuretic Hormone
-Increased water reabsorption in renal tubules
-Increased intravascular fluid volume
-Dilutional hyponatremia and decreased serum osmolality
Causes of SIADH
-Malignant Tumors; cancers
-CNS Disorders; head injuries, stroke, infection, Guillain-Barre, SLE (SWELLING IN BRAIN PUSHING ON PITUITARY)
-Drug Therapy; Tegretol, general anesthesia, opiods, thiazides, SSRI, Chemotherapy
-Miscellaneous; hypothyroid, COPD, HIV, and Adrenal insufficiency
management for SIADH
-loop diuretics
-Monitor urine output and urine specific gravity
-Daily weights, I&O, vital signs, monitor Lab values
-Monitor for seizures, headache, vomiting, and decreased neurological function
-fluid restrictions: Provide frequent oral care
In extreme dilutional hyponatremia give
3% fluid
Medications to treat SIADH
-Demeclocycline
-Vassopressor receptor antagonists
-loop diuretics
-sodium and potassium replacement
Demeclocycline action
blocks the effect of antidiuretic hormone on renal tubules resulting in more dilute urine.
Vasopressor Receptor Antagonists action
block the activity of antidiuretic hormone to treat hyponatremia
loop diruetic action
promotes diuresis
diabetes insipidus (DI)
antidiuretic hormone (ADH) is not secreted, or there is a resistance of the kidney to ADH
“PEE THEIR BRAINS OUT”
Central DI causes
Head injury, surgery, CNS infections
clinical manifestations of DI
polyuria, polydipsia (2 to 20 L/day)
urine specific gravity in DI
< 1.005 (dilute urine)
serum sodium in DI
> 145mg/dl
HINT HINT: DDAVP (desmopressin) is used for
diagnosis of DI
Water deprivation test
for diagnosis of DI
no water intake 2-3 hours followed by hourly measurements of urine vol/oslmolarity and plasma Na+ conc. and osmolarity
important things to know about a hypophysectomy
biopsy of pituitary
-check “mustache dressing” for CSF making sure it is not saturated with fluid
-keep HOB up
what can be given if a lot of CSF is present after a hypophysectomy
caffiene or vasoconstrictors
management for DI
-Maintain adequate hydration, IV or PO
-Maintain electrolyte balance
-Monitor BP, HR, LOC, I&O
-Monitor specific gravity-urine or serum
Hypokalemia EKG changes
ST depression
T inversion
U wave
Hyperkalemia EKG changes
Tall T wave
Flat P wave
Wide QRS
Prolonged PR
DDAVP for central DI is a
hormone replacement
what is important when a client is on DDAVP
monitor pulse
diet considerations for DI
LOW sodium diet
HINT HINT: indocine (NSAID) and DI
helps increase renal responsiveness to ADH (watch for bleeding in the gut)
