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BSNC 5000 > Module 5 - Viral AGE, DKA, Acid-base > Flashcards

Module 5 - Viral AGE, DKA, Acid-base Flashcards

1
Q

Gastroenteritis

A

inflammation of stomach/small/large intestine s/t infection

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2
Q

Common viruses causing AGE

A

rotavirus
norovirus
adenovirus

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3
Q

Rotavirus pathophysiology

A

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

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4
Q

S/S of AGE

A

fever
nausea
vomiting
abdominal cramping/pain
++ diarrhea
dehydration s/t to fluid losses
anorexia –> hypoglycemia

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5
Q

S/S of mild dehydration

A

dry mucous membranes
increased thirst
asymptomatic

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6
Q

S/S of moderate dehydration

A

dry mucous membraness
sunken eyes
sunken fontanels
delayed cap refill
abnormal skin turgor
tachypnea
decreased urine output

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7
Q

S/S of severe dehydration

A

tachycardia
cold extremities
decreased LOC/impaired cognition
increased RR
hypotension (LATE sign)
oliguria

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8
Q

Dehydration treatment

A

oral rehydration therapy (pedialyte)
breastfeed as normal
encourage food
rest
IV therapy (severe)
treat underlying cause (fever, vomiting, etc)

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9
Q

Pediatric bolus

A

10-20 mg/kg
infused over 30 minutes

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10
Q

Diabetic ketoacidosis

A

more common in T1DM
ketosis
metabolic acidosis
hyperglycemia >11.1 pediatrics (13.8 adults)

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11
Q

DKA symptoms

A

dehydration
weight loss
hypokalemia
polyphagia
polyuria
polydipsia
weakness
nausesa/vomiting
hypotension + tachycardia
*kussmaul breathing
*acetone breath

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12
Q

Pseudohyponatremia

A

false normal serum levels of Na+ caused by intracellular shift of H2O to ECF

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13
Q

What does insulin do to K+?

A

causes K+ to shift from ECF into ICF –> hypokalemia

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14
Q

What should K+ be before beginning insulin?

A

> 3.3 mmol

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15
Q

DKA treatment

A

IV fluids (crystalloid –> dextrose when glucose drops)
IV insulin
potassium supplements
foley –> monitor urine output
cardiac monitor

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16
Q

What fluid is used for bolus?

A

normal saline
balanced crystalloids –> RL, plasmalyte

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17
Q

When is insulin initiated in pediatrics with DKA?

A

1 hour after fluid therapy
when potassium is >/= 3.3 mmol/L

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18
Q

RF for cerebral edema

A

bicarbonate

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19
Q

DKA tests

A

plasma glucose
electrolytes (calcium, magnesium, phosphate)
anion gap
urea/creatinine
blood gas
serum osmolality
serum/urine ketones
beta hydroxyburate

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20
Q

Acid-base

A

balance of pH, bicarbonate, paCO2

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21
Q

Types of acidosis

A

respiratory acidosis (paCO2)
metabolic acidosis (HCO3-)

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22
Q

Diabetic tests

A

oral glucose tolerance test
fasting blood glucose
hemoglobin A1C

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23
Q

Lipolysis

A

glycerol –> gluconeogenesis
free fatty acids –> converted into ketones in liver

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24
Q

DKA Patho

A

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

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25
Q

S/S hyperglycemia

A

nausea/vomiting
headache
polydipsia
polyuria
polyphagia (T1DM)
paresthesia
recurrent infection/UTi
fatigue (d/t reduced intravascular volume)
blurry vision
weight loss (T1DM)

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26
Q

Causes of hyperglycemia

A

missed insulin
corticosteroids
growth
stress

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27
Q

Causes of hyperglycemia

A

missed insulin
corticosteroids
growth
stress

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28
Q

Types of dehydration

A

hypotonic
isotonic
hypertonic

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29
Q

Kidneys & HCO3-

A

kidneys reabsorb & produce HCO3-
decreased renal perfusion = less reabsorption
in acidosis kidneys exchange ammonia for bicarbonate –> less bicarbonate retained

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30
Q

3 processes r/t acid-base balance

A

acid production (cellular metabolism)
acid buffering
acid excretion

31
Q

How is CO2 transported in blood?

A

dissolved in plasma
bicarbonate
attached to hemoglobin

32
Q

Carbonic anhydrase equation

A

CO2 enters RBC
CO2 binds with water –> carbonic acid
carbonic acid –> hydrogen + bicarbonate
bicarbonate exchanged for Cl- in plasma

33
Q

Buffer systems

A

bicarbonate (can only buffer metabolic acids)
transcellular hydrogen-potassium exchange
body proteins
bone

34
Q

IV fluids used to manage DKA

A

initial fluid bolus (NS or isotonic fluids)
IV insulin
20-40 mEq/L K
after glucose levels –> dextrose fluids

35
Q

What BG would you begin dextrose fluids in the setting of DKA?

A

14-17 mmol/L

36
Q

How quickly should you drop BG in the setting of DKA?

A

2.8-5 mmol/L an hour

37
Q

Fasting blood glucose

A

4-7 mmol/L

38
Q

2 hour postprandial blood glucose

A

5-10 or 5-8 mmol/L

39
Q

Random BG indicating hyperglycemia

A

> 11.1 mmol/L

40
Q

How to calculate daily fluid requirements

A

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)

41
Q

How to calculate hourly fluid requirements

A

<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)

42
Q

How to calculate hourly output

A

1-3 mg/kg/hr

43
Q

Mild dehydration ORT recommendations

A

50 mL/kg over 4 hours

44
Q

Moderate dehydration ORT recommendations

A

100 mL/kg over 4 hours

45
Q

Which cells require insulin to intake glucose?

A

skeletal muscle
fat cells
(GLUT4 transporter located inside cells. insulin promotes insertion of GLUT4 into cell membrane allowing glucose to enter cells)

46
Q

Volume for fluid bolus

A

10-15 mL/kg

47
Q

Anion gap acidosis

A

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

48
Q

Hyperchloremic acidosis

A

caused by a LOSS of bicarbonate –> decreased buffering capacity
GI, renal, exogenous causes

49
Q

What is the only insulin that can be given IV?

A

regular human insulin

50
Q

When should K+ supplements be given?

A

when K+ is </= to 5.0 mmol/L
avoids hypokalemia during insulin treatment

51
Q

What is NSP4

A

only toxin known to be produced by a virus
non-structural protein 4

52
Q

What does NSP4 do

A

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

53
Q

how long does acute gastroenteritis typically last

A

4-7 days
usually self-resolving

54
Q

S/S of rotavirus

A

fever
watery diarrhea (non-bloody, explosive)
vomiting

55
Q

Causes of metabolic acidosis

A

increased lactic acid
increased ketones
decreased serum bicarbonate
increased serum hydrogen

56
Q

Types of dehydration

A

hypotonic <135
isotonic 135-145
hypertonic >145

57
Q

Types of ketones

A

acetone
beta hydroxyburate
ACAC

58
Q

Mild dehydration weight loss

A

3+-5%

59
Q

Moderate dehydration weight loss

A

6-10%

60
Q

Severe dehydration weight loss

A

> 10%

61
Q

Mild dehydration treatment

A

oral rehydration
continue breastfeeding
avoid fluids high in sugar (worsen diarrhea)
age-appropriate foods in small amounts
rest

62
Q

Moderate dehydration treatment

A

50-100 mL/kg oral rehydration solution every 2-4 hours
additional rehydration to compensate for ongoing losses

63
Q

Severe dehydration treatment

A

rapid rehydration –> fluid bolus isotonic fluids
glucose, electrolyte, urinalysis tests

64
Q

Methods of fluid replacement

A

IV
NG
subc

65
Q

Function of insulin

A

protein & fat anabolism
glucose entry into skeletal/fat cells
inhibits glycogenolysis
promotes glycogenesis
inhibits glucagon

66
Q

Nursing interventions DKA

A

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)

67
Q

IV potassium administration

A

confirm lab values for potassium
assess kidney function –> need working kidneys to prevent hyperkalemia
NEVER bolus potassium

68
Q

Most common causes of DKA

A

missed insulin
illness, infection, stress (increase insulin requirement)

69
Q

Complications of T1DM

A

hypoglycemia (more common d/t use of insulin)
DKA

70
Q

Hyperglycemia and cerebral edema

A

hyperglycemia –> acidosis d/t dehydration
acidosis –> vasodilation of cerebral arteries –> cerebral edema
cognitive fx do not occur until this occurs

71
Q

S/S of DKA

A

ketonuria
hyperglycemia >13.8
acetone breath
kussmaul resps (when pH <7.3)
abdominal pain
nausea/vomiting (d/t inflammatory mediators)

72
Q

S/S of DKA

A

ketonuria
hyperglycemia >13.8
acetone breath
kussmaul resps (when pH <7.3)
abdominal pain
nausea/vomiting (d/t inflammatory mediators)

73
Q

Cushing reflex

A

d/t increased ICP
bradycardia
widened pulse pressure
irregular respiration

BSNC 5000 (11 decks)

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