Module 5 - Viral AGE, DKA, Acid-base Flashcards
Gastroenteritis
inflammation of stomach/small/large intestine s/t infection
Common viruses causing AGE
rotavirus
norovirus
adenovirus
Rotavirus pathophysiology
virus binds to enterocytes
virus produces enterotoxin NSP4
alters villi function (blocks transport of glucose/Na+ & flattens cell –> lack of ATP/changed shape = decreased absorption)
decreased absorption = osmotic diarrhea
S/S of AGE
fever
nausea
vomiting
abdominal cramping/pain
++ diarrhea
dehydration s/t to fluid losses
anorexia –> hypoglycemia
S/S of mild dehydration
dry mucous membranes
increased thirst
asymptomatic
S/S of moderate dehydration
dry mucous membraness
sunken eyes
sunken fontanels
delayed cap refill
abnormal skin turgor
tachypnea
decreased urine output
S/S of severe dehydration
tachycardia
cold extremities
decreased LOC/impaired cognition
increased RR
hypotension (LATE sign)
oliguria
Dehydration treatment
oral rehydration therapy (pedialyte)
breastfeed as normal
encourage food
rest
IV therapy (severe)
treat underlying cause (fever, vomiting, etc)
Pediatric bolus
10-20 mg/kg
infused over 30 minutes
Diabetic ketoacidosis
more common in T1DM
ketosis
metabolic acidosis
hyperglycemia >11.1 pediatrics (13.8 adults)
DKA symptoms
dehydration
weight loss
hypokalemia
polyphagia
polyuria
polydipsia
weakness
nausesa/vomiting
hypotension + tachycardia
*kussmaul breathing
*acetone breath
Pseudohyponatremia
false normal serum levels of Na+ caused by intracellular shift of H2O to ECF
What does insulin do to K+?
causes K+ to shift from ECF into ICF –> hypokalemia
What should K+ be before beginning insulin?
> 3.3 mmol
DKA treatment
IV fluids (crystalloid –> dextrose when glucose drops)
IV insulin
potassium supplements
foley –> monitor urine output
cardiac monitor
What fluid is used for bolus?
normal saline
balanced crystalloids –> RL, plasmalyte
When is insulin initiated in pediatrics with DKA?
1 hour after fluid therapy
when potassium is >/= 3.3 mmol/L
RF for cerebral edema
bicarbonate
DKA tests
plasma glucose
electrolytes (calcium, magnesium, phosphate)
anion gap
urea/creatinine
blood gas
serum osmolality
serum/urine ketones
beta hydroxyburate
Acid-base
balance of pH, bicarbonate, paCO2
Types of acidosis
respiratory acidosis (paCO2)
metabolic acidosis (HCO3-)
Diabetic tests
oral glucose tolerance test
fasting blood glucose
hemoglobin A1C
Lipolysis
glycerol –> gluconeogenesis
free fatty acids –> converted into ketones in liver
DKA Patho
insulin deficiency –> hyperglycemia -> diuresis –> fluid/electrolyte imbalance –> dehydration –> reduced intravascular volume –> impaired perfusion
inability to use glucose –> lipid/protein catabolism
protein + glycerol –> gluconeogenesis –> worsens hyperglycemia
free fatty acids –> ketones –> ketosis/acetone breath
S/S hyperglycemia
nausea/vomiting
headache
polydipsia
polyuria
polyphagia (T1DM)
paresthesia
recurrent infection/UTi
fatigue (d/t reduced intravascular volume)
blurry vision
weight loss (T1DM)
Causes of hyperglycemia
missed insulin
corticosteroids
growth
stress
Causes of hyperglycemia
missed insulin
corticosteroids
growth
stress
Types of dehydration
hypotonic
isotonic
hypertonic
Kidneys & HCO3-
kidneys reabsorb & produce HCO3-
decreased renal perfusion = less reabsorption
in acidosis kidneys exchange ammonia for bicarbonate –> less bicarbonate retained
3 processes r/t acid-base balance
acid production (cellular metabolism)
acid buffering
acid excretion
How is CO2 transported in blood?
dissolved in plasma
bicarbonate
attached to hemoglobin
Carbonic anhydrase equation
CO2 enters RBC
CO2 binds with water –> carbonic acid
carbonic acid –> hydrogen + bicarbonate
bicarbonate exchanged for Cl- in plasma
Buffer systems
bicarbonate (can only buffer metabolic acids)
transcellular hydrogen-potassium exchange
body proteins
bone
IV fluids used to manage DKA
initial fluid bolus (NS or isotonic fluids)
IV insulin
20-40 mEq/L K
after glucose levels –> dextrose fluids
What BG would you begin dextrose fluids in the setting of DKA?
14-17 mmol/L
How quickly should you drop BG in the setting of DKA?
2.8-5 mmol/L an hour
Fasting blood glucose
4-7 mmol/L
2 hour postprandial blood glucose
5-10 or 5-8 mmol/L
Random BG indicating hyperglycemia
> 11.1 mmol/L
How to calculate daily fluid requirements
100, 50, 20
<10kg: 100 mL/kg
10-20 kg: 1000 mL + (50 mL per kg over 10 kg)
>20kg: 1500 mL + (20 mL per kg over 20 kg)
How to calculate hourly fluid requirements
<10 kg: 4 mL/kg
10-20 kg: 40 + (2 mL/kg for each kg >10)
>20 kg: 60 + (1 mL/kg for each kg >20)
How to calculate hourly output
1-3 mg/kg/hr
Mild dehydration ORT recommendations
50 mL/kg over 4 hours
Moderate dehydration ORT recommendations
100 mL/kg over 4 hours
Which cells require insulin to intake glucose?
skeletal muscle
fat cells
(GLUT4 transporter located inside cells. insulin promotes insertion of GLUT4 into cell membrane allowing glucose to enter cells)
Volume for fluid bolus
10-15 mL/kg
Anion gap acidosis
caused by retention/increased production of acids
causes an INCREASE in anion gap (cations - anions)
increases b/c available serum bicarbonate (anion) is decreased in acidotic state
Hyperchloremic acidosis
caused by a LOSS of bicarbonate –> decreased buffering capacity
GI, renal, exogenous causes
What is the only insulin that can be given IV?
regular human insulin
When should K+ supplements be given?
when K+ is </= to 5.0 mmol/L
avoids hypokalemia during insulin treatment
What is NSP4
only toxin known to be produced by a virus
non-structural protein 4
What does NSP4 do
blocks transport of glucose and sodium into enterocytes
flattens villi –> decreased absorption
paracrine effect
increases release of calcium from endoplasmic reticulum –> increased GI motility/secretion
calcium stimulates vagal nerve –> vomiting
how long does acute gastroenteritis typically last
4-7 days
usually self-resolving
S/S of rotavirus
fever
watery diarrhea (non-bloody, explosive)
vomiting
Causes of metabolic acidosis
increased lactic acid
increased ketones
decreased serum bicarbonate
increased serum hydrogen
Types of dehydration
hypotonic <135
isotonic 135-145
hypertonic >145
Types of ketones
acetone
beta hydroxyburate
ACAC
Mild dehydration weight loss
3+-5%
Moderate dehydration weight loss
6-10%
Severe dehydration weight loss
> 10%
Mild dehydration treatment
oral rehydration
continue breastfeeding
avoid fluids high in sugar (worsen diarrhea)
age-appropriate foods in small amounts
rest
Moderate dehydration treatment
50-100 mL/kg oral rehydration solution every 2-4 hours
additional rehydration to compensate for ongoing losses
Severe dehydration treatment
rapid rehydration –> fluid bolus isotonic fluids
glucose, electrolyte, urinalysis tests
Methods of fluid replacement
IV
NG
subc
Function of insulin
protein & fat anabolism
glucose entry into skeletal/fat cells
inhibits glycogenolysis
promotes glycogenesis
inhibits glucagon
Nursing interventions DKA
start IV access
monitor weight (sign of hydration status)
foley catheter –> monitor output
cardiac monitor (arrhythmia s/t hypokalemia)
administer fluids per doctor’s order
frequent assessments (blood glucose, VS, PAT)
IV potassium administration
confirm lab values for potassium
assess kidney function –> need working kidneys to prevent hyperkalemia
NEVER bolus potassium
Most common causes of DKA
missed insulin
illness, infection, stress (increase insulin requirement)
Complications of T1DM
hypoglycemia (more common d/t use of insulin)
DKA
Hyperglycemia and cerebral edema
hyperglycemia –> acidosis d/t dehydration
acidosis –> vasodilation of cerebral arteries –> cerebral edema
cognitive fx do not occur until this occurs
S/S of DKA
ketonuria
hyperglycemia >13.8
acetone breath
kussmaul resps (when pH <7.3)
abdominal pain
nausea/vomiting (d/t inflammatory mediators)
S/S of DKA
ketonuria
hyperglycemia >13.8
acetone breath
kussmaul resps (when pH <7.3)
abdominal pain
nausea/vomiting (d/t inflammatory mediators)
Cushing reflex
d/t increased ICP
bradycardia
widened pulse pressure
irregular respiration