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Critical Care I > test 3 > Flashcards

test 3 Flashcards

1
Q

What are the methods for determining maintenance fluid needs

A

Holliday Segar Method

4-2-1 (still holliday segar)

BSA

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2
Q

what weight requirement for determining maintenance fluid needs using the BSA method

A

> =10kg

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3
Q

formula for maintenance fluid needs BSA

normal vs critical

A

1600ml/m2/day

if critically ill
1200mL/m2/day

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4
Q

why would critical ill children need 1200mL/m2/day instead of 1600

A

increased ADH (SIADH) secretion due to stress response

AKI risk - don’t want to fluid overload them if kidneys are not functioning at full capacity

Ventilators, headers and humidification cut the need by 20-50%

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5
Q

why would we not fluid restrict to 1200mL/m2/day in critically ill?`

A

insensible fluid losses
-Febrile or Tachypnea or GI (diarrhea, ileostomy, NG with suction)

so maybe febrile patients
persistently febrile or spiking high
increase fluid needs by 12% for every degree above 37C

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6
Q

Basic insensible fluid loses estimation

A

400ml/m2/day

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7
Q

Dehydration classifications is categorized how based on what?

A

mild, moderate or severe

based on serum sodium levels

Hypernatremic, Hyponatremic and isotonic dehydration

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8
Q

Name that dehydration

A dehydrated pt who has lost salt over a period of time. lost water and salt.

maybe seen in diarrhea. especially if replacing with water without electrolytes

A

Hyponatremic dehydration

hypernatremia would be diarrhea but here you are replacing water without electrolytes

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9
Q

name that dehydration

rate of water loss is greater than the solute. (salt did not follow)

A

Hypernatremic dehydration

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10
Q

most common type of dehydration

A

isotonic

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11
Q

type of dehydration where water and salt loss is equal (acute process)

A

isotonic dehydration

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12
Q

what type of osmolality is

1/2 NS

A

Hypotonic

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13
Q

what type of osmolality is

1/4 NS

A

Hypotonic

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14
Q

what type of osmolality is

3% NS

A

Hypertonic

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15
Q

what type of osmolality is

Albumin 5%

A

Colloid

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16
Q

what type of osmolality is NS

A

Isotonic

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17
Q

what type of osmolality is LR

A

Isotonic

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18
Q

what does LR contain that NS does not

A

K

HCO3

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19
Q

normal Na

A

135-145

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20
Q

Sodium is key to what mentioned functions

A

skeletal muscle function

nerve and myocardial action potentials

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21
Q

Hypervolemia
Hypovolemia
Normovolemic

Congestive Heart failure puts you at risk for what?

A

Hypervolemia

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22
Q

Hypervolemia
Hypovolemia
Normovolemic

renal failure puts you at risk for what?

A

Hypervolemia

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23
Q

Hypervolemia
Hypovolemia
Normovolemic

Nephrotic syndrome puts you at risk for what?

A

Hypervolemia

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24
Q

Hypervolemia
Hypovolemia
Normovolemic

Water Intoxication puts you at risk for what?

A

Hypervolemia

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25
Q

Hypervolemia
Hypovolemia
Normovolemic

Diarrhea puts you at risk for what?

A

Hypovolemia

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26
Q

Hypervolemia
Hypovolemia
Normovolemic

Renal Losses puts you at risk for what?

A

Hypovolemia

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27
Q

Hypervolemia
Hypovolemia
Normovolemic

diuretics puts you at risk for what?

A

Hypovolemia

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28
Q

Hypervolemia
Hypovolemia
Normovolemic

cerebral salt wasting may put you in what fluid status?

A

Normovolemic

low sodium levels

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29
Q

Hypervolemia
Hypovolemia
Normovolemic

Meningitis may put you in what fluid status?

A

Normovolemic

low sodium levels

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30
Q

Hypervolemia
Hypovolemia
Normovolemic

Burns puts you at risk for what?

A

Hypovolemic

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31
Q

Acute Hyponatremia symptoms

A

Nausea
lethargy
seizures
coma

can lead to neurological consequences

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32
Q

In acute hyponatremia the symptoms are _______

A

more severe

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33
Q

how to diagnose hyponatremia

A

check serum Na and osmols

urine studies if unsure of cause

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34
Q

How to treat Hyponatremia

A

Replace deficit slowly
-Goal rise of Na 2-4 mEq/L every 4 hours (10-20 in 24 hours)

If they are seizing
- Replace to 125 quickly with HTS (3%) - bolus using formula for amount

formula
- 0.6x(weight in kg) x (target Na-measured Na)

after bolus to achieve 125 you calculate out what you need to get to 135 and this should be given over 24 hours.

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35
Q

formula for Na treatment

A

0.6x(weight in kg) x (target Na - measured current Na) = ____mEq of Na needed

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36
Q

3% hypertonic has how much Na per L

A

513mEq Na per L

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37
Q

Causes mentioned of Hypernatremia

A

Breastfeeding failure (baby not getting enough)

Severe Diarrhea

Diabetes Insipidus

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38
Q

presentation of hypernatremia

A

weakness

lethargy

decreased DTRs (deep tendon reflexes)

irritability

muscle cramps

renal failure

AMS

Seizures

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39
Q

how to diagnose hypernatremia

A

serum Na levels

osmols

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40
Q

treatment for hypernatremia

A

Avoid decreasing more than 12-15 mEq/L in 24 hours

At risk for cerebral edema if drops too fast

If hypovolemic - calculate free water deficit
0.6xkg x (current Na/desired Na) - (0.6 x wt kg) = gives you how much water they need in 24 hours - if they can drink it, they can PO

you can use D5 water for IV

Check electrolytes q 2-4 hours to make sure you aren’t dropping too fast

These patients will be on regular maintenance plus D5W or 1/2NS or 1/4NS to help bring it down slower

Balancing game with constant monitoring

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41
Q

Potassium is needed for ____ gradients and important for

A

transmembrane voltage gradients

important for muscle and nerve cells

important with acid base balance

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42
Q

primary route of excretion for potassium is

A

kidneys

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43
Q

normal potassium

A

3.5-5.2

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44
Q

EKG changes with hyperkalemia

A

increasing in severity from top to bottom

Peaked T waves

Wide PR interval
Wide QRS duration
Peaked T waves
(precursor to V.Fib)

Loss of P waves
Sinusoidal wave

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45
Q

acidosis causes K to

A

rise

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46
Q

alkalosis causes k to

A

drop

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47
Q

DKA patients come in acidotic….when do you add k

A

your first bags usually don’t have K but then you add it in later

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48
Q

causes of Hyperkalemia

A

Acute or chronic renal failure

Tissue injuries ( crush injuries)

hemolysis

Acidosis

Medications (Spironolactone, Bactrim, ACE inhibitors)

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49
Q

what medications cause hyperkalemia

A

spironolactone

Bactrim

ACE inhibitors

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50
Q

Treatment for Hyperkalemia

A

Calcium Chloride - to stabilize that cardiac membrane

Sodium Bicarb - shifts the potassium to cell

D25/50% with insulin - Insulin causes potassium to shift intracellularly

Albuterol - helps shift k to intracellular

Kayexalate - removes potassium for exchanging for sodium in the GI tract and excretes through stool

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51
Q

Hypokalemia symptoms

A

can by asymptomatic

Diastolic dysfunction

ECG changes

Cramping

Fatigue

ileus

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52
Q

ECG changes seen in Hypokalemia

A

flat or absent T waves

long QT

Prolonged QRS

Presence of U-waves

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53
Q

diagnosis for hypokalemia

A

BMP with magnesium - magnesium and potassium work together

Urine osmolality

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54
Q

Treatment for hypokalemia

A

identify cause

replace K
-KCL 0.5-1meq/kg/dose

you can also give this other ways

remember minimum is over an hour……has to be given very slow

think central line or peripheral…….ect

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55
Q

where is magnesium mostly found

A

less than 1% of Mg is extracellular, much is stored in our bones

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56
Q

what is Mg used for

A

ATP generation, DNA transcription, Membrane stabilization, regulation of K excretion

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57
Q

what electrolyte works together with K

A

Magnesium

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58
Q

normal Mg levels

A

1.7-2.2 mg/dL

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59
Q

causes of hypomagnesemia

A

GI losses: diarrhea, vomiting, refeeding syndrome, pancreatitis

IBD, Celiac disease, CF

Renal: hypercalcemia, diuretic use, RTA

Endocrine: DM, DKA, Hyperaldosteronism

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60
Q

Presentation of hypomagnesemia

A

Anorexia, nausea, vomiting

Seizures, ataxia, hyperreflexia

EKG changes: Torsades de pointes, long QT

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61
Q

Diagnostic eval for hypomagnesemia

A

Mg level

iCal

EKG

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62
Q

Management of hypomagnesemia

A

Repletion with Magnesium sulfate or chloride

Consider K repletion (mag and K are buddies and go together)

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63
Q

Hypermagnesemia causes

A

excessive intake
-mg containing laxatives, antacids

Chronic renal failure

tumor lysis

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64
Q

presentation for hypermagnesemia

A

hypotonia

decreased reflexes

hypotension

flushing

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65
Q

diagnosing hypermagnesemia

A

Mg level

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66
Q

Management for hypermagnesemia

A

Stop any mag intake

fluid for volume expansion

inotropes for BP management

Ventilatory assistance for muscle weakness

For rapid removal, dialysis can be used or exchange transfusion

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67
Q

chloride has a direct relationship with

A

sodium

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68
Q

chloride has an inverse relationship with

A

bicarb

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69
Q

what can lead to hypochloremia

A

CF
Bulimia
Diuretics

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70
Q

high chloride and ph

A

acidosis

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71
Q

presentation of hypochloremia

A

rarely occurs by itself

arrhythmias
decreased resp effort
seizures
tachycardia

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72
Q

Treatment for hypochloremia

A

find cause

replace with potassium, sodium or ammonium chloride or arginine chloride

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73
Q

hyperchloremia causes

A

diarrhea
chloride administration
metabolic acidosis

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74
Q

presentation of hyperchloremia

A

often no symptoms but have symptoms r/t acidosis such as:

kussmaul respirations

lethargy

headache

confusion

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75
Q

treatment for hyperchloremia

A

find underlying cause

treat acidosis: can use sodium bicarb

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76
Q

when can you see hypophosphatemia

A

refeeding syndrome

DKA

severe resp alkalosis

Vit D deficiency

Burns

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77
Q

symptoms of hypophosphatemia

A

impaired energy utilization

diaphragmatic/resp muscle weakness

tissue hypoxia

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78
Q

treatment for hypophosphatemia

A

IV phos

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79
Q

Hyperphosphatemia causes

A

renal failure

phosphate containing enemas

tumor lysis syndrome

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80
Q

Treatment for hyperphosphatemia

A

phosphate binders
mannitol
diuresis

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81
Q

Calcium is present in how many different forms?

A

3 forms

  • Bound to albumin (plasma protein)
  • Diffusible (CaCitrate or CaPhoshate)
  • Unbound ion
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82
Q

what type of calcium is most important for body functions

A

ionized Ca

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83
Q

normal Ca

A

8.8-10.8

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84
Q

at risk for hypocalcemia

A

Post PRBC infusion - because of the preservatives….citrate —calcium binds with citrate
so your CRRT patients and ECMO as well
-CRRT uses citrate to keep them from clotting but can drop their calcium

Hypoparathyroidism
Sepsis
tumor lysis
DiGeorge syndrome

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85
Q

symptoms of hypocalcemia

A 
neuromuscular irritability
confusion
muscle cramps
numbness
tingling

cardiac: prolonged QT, AV blocks, sinus tachy

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86
Q

diagnosing hypocalcemia

A

Ca level (total and iCal)
CMP
PTH
EKG

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87
Q

Treatment for hypocalcemia

A

Calcium chloride (10-20mg/kg/dose)

Calcium gluconate (100mg/kg/dose)

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88
Q

risk for hypercalcemia

A

Williams syndrome
excessive intake
immobility
malignancy - cancer attacks the bones - the breakdown causes a calcium spike

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89
Q

presentation of hypercalcemia

A 
nausea
anorexia
constipation
lethargy
headaches
seizures
arrhythmias
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90
Q

Diagnostic for Hypercalcemia

A 
Total calcium
iCal
PTH
pH
EKG
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91
Q

Treatment for Hypercalcemia

A

Hydration
loop diuretics for diuresis
Calcitonin for rapid correction

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92
Q

what electrolyte imbalance is Williams syndrome at risk for?

A

Hypercalcemia

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93
Q

what electrolyte imbalance is DiGeorge syndrome at risk for?

A

Hypocalcemia

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94
Q

what electrolyte imbalances can cause seizures

A

Hypercalcemia

Hypochloremia

Hypomagnesemia

Hyponatremia

Hypernatremia

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95
Q

What electrolyte imbalances are you at risk for with DKA

A

Hypophosphatemia

Hyperchloremia

Hypomagnesemia

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96
Q

What electrolyte imbalances can cause EKG changes

A

Hypocalcemia

Hypomagnesemia

Hypokalemia

Hyperkalemia

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97
Q

what electrolyte imbalances can cause arrhythmias

A

Hypochloremia

Hypercalcemia

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98
Q

what electrolyte imbalances are associated with tumor lysis syndrome or cancer

A

Tumor lysis syndrome

  • hypocalcemia
  • hyperphosphatemia
  • hypermagnesemia

Cancer when it attacks the bone

  • bone breaks down and releases Ca+
  • Hypercalcemia
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99
Q

what electrolyte imbalances are you at risk for in renal impairment/failure

A

hyperphosphatemia

hypermagnesemia

hyperkalemia

hypernatremia

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100
Q

What electrolyte imbalances associated with acidosis

A

hyperchloremia

hyperphosphatemia

hyperkalemia

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101
Q

what electrolyte imbalance is associated with loop diuretics

A

hypercalcemia

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102
Q

what electrolyte imbalance associated with diuretics

A

hypochloremia

hypomagnesemia

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103
Q

what electrolyte imbalance associated with sepsis

A

hypocalcemia

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104
Q

What electrolyte imbalances associated with constipation

A

Hypercalcemia

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105
Q

what electrolyte imbalance associated with anorexia and nausea

A

hypercalcemia

hypomagnesemia

Nausea only
-Hyponatremia

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106
Q

what electrolyte imbalance associated with acute diarrhea

A

hypernatremia

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107
Q

what electrolyte imbalance are you at risk for with PRBCs

A

hypocalcemia

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108
Q

what electrolyte imbalance associated with Ataxia

A

hypomagnesemia

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109
Q

what electrolyte imbalance associated with confusion, AMS

A

hypocalcemia

hypernatremia

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110
Q

what electrolyte imbalance associated with muscle cramps

A

hypokalemia

hypernatremia

hypocalcemia

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111
Q

what electrolyte imbalance associated with hyporeflexia

A

hypermagnesemia

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112
Q

what electrolyte imbalance associated with hyperreflexia

A

hypomagnesemia

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113
Q

what electrolyte imbalance associated with resp weakness or decreased resp effort

A

hypophosphatemia

Hypochloremia

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114
Q

the lower the pH the ____ the H ion concentration

A

Higher

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115
Q

the higher the pH the ___ the H ion concentration

A

Lower

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116
Q

normal pH range

A

7.35-7.45

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117
Q

normal PCO2 (partial pressure)

A

35-45

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118
Q

normal Bicarb

A

22-26

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119
Q

carbonic anhydrase helps with what formula important in acid base balance

A

CO2 + H20 H2Co3

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120
Q

If your hyperventilating or your vent settings are too high, you could become

A

alkalotic

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121
Q

If your hypo-ventilating you could become

A

acidotic

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122
Q

pH < 7.35

CO2 >45

A

Respiratory acidosis

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123
Q

Asthma can cause what type of acid base imbalance

A

Resp acidosis

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124
Q

How can kidneys compensate if your building up CO2 becoming acidotic

A

makes more bicarb which will pair with Hydrogen ions and excreted in urine.

This takes days

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125
Q

pH > 7.45

CO2 <35

A

Respiratory alkalosis

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126
Q

what type of acid base balance

Pt who is hyperventilating

On a ventilator and settings are too high

salicylate intoxication

Hyperthyroidism

A

Resp alkalosis

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127
Q

How can kidneys compensate if your in resp alkalosis

A

getting rid of bicarb

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128
Q

pH < 7.35

HCO3 < 22

A

Metabolic acidosis

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129
Q

Diarrhea
and hyperchloremia
can cause what type of acid base imbalance

A

Metabolic acidosis

Diarrhea you are loosing bicarb through your GI tract

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130
Q

normal anion gap

A

4-12

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131
Q

pH <7.35
HCO3 <22
anion gap >12

A

Anion Gap Metabolic Acidosis

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132
Q

Calculate anion GAP

A

Na
K
Chloride
HCO3

Take your positives
Na+ and subtract potassium, chloride and Bicarb to get your gap.

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133
Q

Kussmaul breathing happens because you are trying to get rid of

A

CO2

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134
Q

Vomiting or Ng Suctioning can lead to what acid base imbalance

A

Metabolic Alkalosis

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135
Q

pH >7.35

HCO3 >26

A

Metabolic Alkalosis

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136
Q

when you loose your chloride your body starts to make more

A

bicarb

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137
Q

diuretics can lead to what type of acid base imbalance

A

Metabolic alkalosis bc your dumping Na, K, Ca, Cl and your bicarb starts to come up bc of this

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138
Q

How does your lungs compensate in Metabolic acidosis

A

because you have a higher bicarb your lungs compensate by increasing CO2 that you have

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139
Q

If I told you a pt had chronic renal failure, what would you think about in regard to acid base balance

A

kidneys may not be able to keep up with excreting Hydrogen ions

metabolic acidosis

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140
Q

If I told you a pt had vomiting the last few days, what would you think about in regard to acid base balance

A

Metabolic alkalosis

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141
Q

If I told you a pt had drug ingestions, what would you think about in regard to acid base balance

A

Respiratory alkalosis - depressed resp

Metabolic alkalosis

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142
Q

If I told you a pt taking Lasix, what would you think about in regard to acid base balance

A

Metabolic alkalosis (you can see a bump in bicarb)

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143
Q

If I told you a pt had cyanosis, what would you think about in regard to acid base balance

A

Respiratory acidosis

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144
Q

If I told you a pt had Kussmaul breathing, what would you think about in regard to acid base balance

A

Metabolic acidosis - your trying to hyperventilate to breathe off CO2

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145
Q

If I told you a pt had AMS from seizures, what would you think about in regard to acid base balance

A

Respiratory acidosis - if you aren’t breathing well, cant blow off CO2

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146
Q

pH 7.15
bicarb 6
PCO2 18

His serum levels reveal
Na 135
chloride 114
potassium 4.5
bicarb 11

what does the pH tell you?
what kind of acid base disorder is this?

what is the anion gap?

A

Metabolic Acidosis

PCO2 is low bc of compensation

135-114 = 21 - 11= 10 (anion gap)

Non-anion gap hyperchloremic metabolic acidosis

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147
Q

poorly controlled asthma

pH 7.54
pO2 of 60
PCO2 29
Na 138
Chloride 103
bicarb 25
A

Resp alkalosis

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148
Q

3 month old
chronic lung disease
home meds include lasix

pH 7.37
pCO2 70
Na 136
Cl 88 
Bicarb 37
A

compensated resp acidosis

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149
Q

what do ketones produce

A

B-Hydroxybutyrate &raquo_space;»acetoacetate (6:1)

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150
Q

How is B-Hydroxybutyrate measured

A

blood

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151
Q

How is acetoacetate detected

A

Urine ketone strips

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152
Q

whats your renal threshold for glucose excretion? - point at which osmotic diuresis occurs

A

180 mg/dL

Osmotic diuresis ->dehydration ->electrolyte wasting ->further stimulates stress hormones

severe dehydration, poor tissue perfusion leads to lactic acidosis

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153
Q

what electrolytes are DKA pts depleted of

A

K+
May be high initially and should fall as the acidosis corrects pulling K back into the cells

Na+ - sodium level that you see is actually lower than what you see - calculate 1.6mEq to sodium levels for every 100 rise above 100 glucose level

if Na appears normal on arrival - reflects extreme free water loss

Phosphorous

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154
Q

Cl is normally ____ in DKA

A

high

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155
Q

DKA pt who during treatment, as b-hydroxy levels are decreasing but bicarb isnt correcting, what should you consider

A

Chloride is rising with fluids

May need to change fluids

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156
Q

What lab can be a predictor for cerebral edema in DKA pt

A

BUN - elevated - have to be more careful of DKA

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157
Q

when is cerebral edema more likely in DKA

A

first 3-12 hours after start of treatment

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158
Q

< __ yrs old has increased risk of cerebral edema

A

5 yrs

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159
Q

Serum test for DKA

A 
K, Na, K, HCO3, Cl, glucose
Bun/creatinine
B-hydroxybutyrate
Venous blood gas
Ca, Mg, Phos

if fever - blood and urine cultures

  • lactate if shock or sepsis
  • CBC
  • Hematacrit

ECG

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160
Q

labs to collect for new onset diabetes

A

Diabetes associated antibodies (glutamic acid decarboxylase antibodies, insulin auto-antibodies, islet cell antibodies, zinc transporter 8 antibodies)

HA1C
insulin
C-peptide

Celiac panel

Thyroglobulin antibodies

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161
Q

Anion Gap =

A

Na-(Cl+HCO3)

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162
Q

Normal anion gap

A

around 12

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163
Q

what Anion gap do you normally see in DKA

A

20-30

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164
Q

If you have a DKA with an anion gap >35, this suggests concomitant ___ ____

A

lactic acidosis

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165
Q

mild, moderate or severe DKA?

pH <7.30 or serum bicarb <15

A

mild

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166
Q

mild, moderate or severe DKA?

venous pH <7.2 or serum bicarb <10

A

moderate

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167
Q

mild, moderate or severe DKA?
venous pH <7.1
serum bicarb <5

A

Severe

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168
Q

These factors make the pt ICU status for DKA (at some facilities)

A

Severe DKA <7.1

Age < 5yrs

AMS

Received >40mL/kg of fluid

Sepsis/SIRS

Received sodium bicarb treatment

High BUN at presentation

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169
Q

intubation is encouraged or discouraged in DKA

A

discouraged if possible. At high risk for cardiac event due to level of acidosis

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170
Q

fluid resuscitation in DKA pt who is not in shock and has no evidence of cerebral edema

A

NS or LR bolus of 10-20ml/kg over 30-60 min

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171
Q

fluid resuscitation in DKA pt who is in shock

A

rapid fluid resuscitation with 20mL/kg and reassessment after each bolus

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172
Q

DKA fluid management calculation

A

replace remaining fluid deficit:
-use deficit estimate of 5-7% body weight for moderate DKA

-use deficit estimate 7-10% body weight for severe DKA

fluid deficit plus maintenance fluids volume over 24-48 hours

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173
Q

DKA fluid management - what fluid type should you consider using if there is a concern for hyperchloremic acidosis

A

LR instead of NS

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174
Q

when is insulin started in DKA management

A

after fluid replacement

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175
Q

Insulin in DKA management

A

insulin infusion at 0.05-0.1 units/kg/hr while receiving IV fluids

0.05 units/kg/hr is for children <5yrs of age

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176
Q

Why do you not want to bolus insulin in DKA

A

increased risk of cerebral edema

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177
Q

When do you add dextrose to fluids in DKA treatment

A

when plasma glucose falls to 250-300 mg/dL or if its correcting too quickly

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178
Q

In DKA treatment you do not want your glucose to come down more than ___ mg/dL/hr

A

100

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179
Q

Insulin management in mild DKA (7.2-7.3) or when insulin infusion is not feasible

A

may administer subcutaneous rapid-acting insulin every 1-2 hours or regular insulin every 4 hours

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180
Q

In DKA management when is Potassium chloride or Potassium phosphate added to fluids

A

K<5.5

Pt has voided

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181
Q

Severe hypophosphatemia in DKA should be treated. Don’t forget to monitor for

A

hypocalcemia

when your replacing phosphate can lead to hypocalcemia

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182
Q

Bicarb in DKA treatment

A

Do not give - no benefit in DKA and associated with worse outcomes and cerebral edema

Reserved for cases of life threatening hyperkalemia or severe acidosis with cardiac compromise

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183
Q

As your glucose comes down what should your sodium be doing

what happens if this does not occur

A

Serum Na should increase

Failure of Na+ to increase prompts intense neurologic monitoring due to risk associated with cerebral edema

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184
Q

2 bag system for DKA what are in the 2 bags

A

Bag A: NS or LR
Bag B: 10% dextrose added to NS or LR

Add KCL and Kphos according to serum K level (<5.5)

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185
Q

For DKA pt how do you calculate the IVF rate

A

2.5L/m2 - bolus given and then divide by 24 hours

example BSA = 1.6, received 400ml bolus

Total IVF rate = (2,500 ml * 1.6) - 400=3,600mL/24 hours = 150ml/hr

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186
Q

what resolves first in DKA

Hyperglycemia or metabolic acidosis

A

hyperglycemia

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187
Q

once hyperglycemia resolves, maintain glucose levels between

A

100-200mg/dL

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188
Q

In DKA management, where the glucose is falling too fast or the acidosis is not correcting what do you do?

A

Change to D12.5% or increase fluid rate

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189
Q

what labs are you monitoring every 2-4 hours in DKA

What else are you monitoring closely

A

hourly capillary blood glucose checks

labs

  • electrolytes
  • blood gas
  • B-hydroxybutyrate
  • BUN/Cr
  • Serum glucose
  • Ca, Mg, Phos every 4-6 hours

hourly neurologic exams

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190
Q

when do you transition them off the 2 bag system in DKA treatment

A

HCO3 >15 mEq/L
B-hydroxybutyrate <1.0-1.5
Abd pain and vomiting resolved, patient can tolerate oral intake

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191
Q

when do you transition to subcutaneous insulin in mgmt of DKA

A
  • Before a meal
  • carbohydrate consistent diet
  • administer basal insulin along with a short acting insulin
  • to prevent rebound hyperglycemia and ketoacidosis, administer subcutaneous insulin 30 min before discontinuing insulin infusion
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192
Q

in Pediatric DKA the incidence of cerebral edema is ____ and the mortality rate is ___

A

rare

high

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193
Q

risk factors for cerebral edema in DKA

A

severe acidosis on presentation

High initial serum BUN

Low initial pCO2

Failure of corrected serum Na+ to rise during treatment

Age <5 years

new onset diabetes

Received NaHCO3 treatment

Rapid administration of hypotonic fluid

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194
Q

signs/symptoms of cerebral edema in DKA

A

onset headache after treatment

progressively worsening headache

Altered sensorium

changes in neurologic status

inappropriate slowing of HR

increase in BP

decrease oxygen sats

Cushing’s triad (late signs) - rising BP, bradycardia and resp depression

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195
Q

cerebral injury clinical diagnosis (DKA)

A

Can be one diagnostic criteria

  • abnormal motor or verbal response to pain
  • decorticate or decerebrate posture
  • cranial nerve palsy
  • abnormal neurogenic resp pattern (grunting, tachypnea, cheyne-stokes, apneusis)

-or-
2 major criteria
-AMS, confusion, fluctuating level of consciousness
-Sustained HR deceleration (>20 beats/min) not attributable to improved intravascular volume
-Age inappropriate incontinence

or 1 major and 2 minor (>5 yrs old)
1 major and 1 minor (<5 yrs old)

minor 
vomiting
headache
lethargy or not easily arousable
Diastolic BP >90 mmHg
Age <5 yrs

-only count signs that occurred after treatment

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196
Q

treatment of cerebral edema (DKA)

A

initiate treatment as soon as cerebral edema is suspected. Do not delay for CT imaging

-Adjust fluid rate to maintain normal bp or avoiding excessive fluid administration

  • Give mannitol or hypertonic (3%) saline
  • mannitol 0.5-1g/kg IV over 10-15 min
  • Hypertonic saline (3%) 2.5-5mL/kg over 10-15 min
  • Head of bed elevated to 30 degrees keep the head in midline position
  • intubation may be necessary - hyperventilation below pCO2 appropriate to pt degree of acidosis associated with poorer outcomes
  • after treatment, consider CT
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197
Q

Mannitol dosing and time to give Mannitol for DKA related cerebral edema

A

mannitol 0.5-1g/kg IV over 10-15 min

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198
Q

Hypertonic Saline dosing and time to give for DKA related cerebral edema

A

2.5-5mL/kg over 10-15 min

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199
Q

The top zone on the adrenal cortex, Zona Glomerulosa makes ___ that turns into ___

A

Angiotensin II

Aldosterone

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200
Q

The second from top zone on the adrenal cortex, Zona fasciculata makes ___ that turns into ___

A

ACTH

Cortisol

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201
Q

The third zone on the adrenal cortex, Zona Reticularis makes ___ that turns into ___

A

ACTH

Androgens

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202
Q

The adrenal medulla makes ___

A

Catecholamines

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203
Q

The hypothalamic-pituitary adrenal axis

the main mechanism is

A

regulating cortisol production

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204
Q

ACTH is made in the

A

pituitary gland

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205
Q

congenital adrenal hyperplasia is affecting the ____and not the pituitary

A

gland

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206
Q

A group of autosomal recessive disorders characterized by impaired cortisol synthesis ->hypersecretion of CRH and ACTH that leads to hyperplasia of adrenal glands

A

Congenital Adrenal Hyperplasia

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207
Q

what enzyme deficiency is associated with Classical Congenital Adrenal hyperplasia

A

21-Hydroxylase Deficiency (for 90% of the cases)

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208
Q

Classical Congenital adrenal hyperplasia is more prevalent in what race

A

1: 15000 - Caucasians
1: 42,000 African Americans

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209
Q

what forms of congenital adrenal hyperplasia

A

Salt-wasting - 67%

Simple viralizing-33%

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210
Q

Classical Congenital adrenal hyperplasia is diagnosed by

A

elevated 17-hydroxyprogesterone level

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211
Q

21 Hydroxylase Deficiency in CAH

A

Hypotension
salt wasting

Cortisol deficiency

your progesterone and 17-OH progesterone go up which leads to hyper-androgenism

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212
Q

salt wasting =

A

mineralocorticoid deficiency

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213
Q

what organs are involved in blood pressure regulation

A

liver
lungs
kidneys
adrenal cortex

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214
Q

When you don’t make aldosterone….what happens

A

Hyponatremia
hyperkalemia
acidosis
hypotension

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215
Q

medication for CAH to replace cortisol

dosing to start

A

hydrocortisone 20mg/m2/day divided TID

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216
Q

medication for CAH to replace mineralocorticoid (aldosterone)

A

Fludrocortisone 0.1mg BID and

salt solution since they salt waste

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217
Q

what does the newborn screen test for in regards to CAH

A

focuses on 21-hydroxylase deficiency by testing for 17-hydroxyprogesterone

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218
Q

if you get an abnormal newborn screen back for CAH, what needs to be ordered

A 
clinical eval
lytes
confirmatory 17OHP
High dose ACTH stim test
Preterm-> different normative values
Referral
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219
Q

treatment for acute/new diagnosis for CAH

A

Hydrocortisone 100mg/m2 Iv/IM
(HC at high doses has mineralocorticoid activity so you dont have to give fludrocortisone)

+/- IVF with dextrose - hypoglycemia is common with adrenal insufficiency due to low cortisol

Fludrocortisone (mineralocorticoid) - after hydrocortisone is at maintenance dosing

ECG
frequent neuro checks
NS bolus 20ml/kg
D5 or D10LR or NS approx 1800ml/m2/day
Hydrocortisone 25 mg/m2 per dose every IV 6 hours after the initial dosing or PO q8

lytes q 2-4 hours till stable

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220
Q

signs/symptoms of adrenal crisis

A

hyponatremia
hyperkalemia
hypotension
hypoglycemia

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221
Q

daily treatment for adrenal insuf s/t CAH

what does this do

A

Hydrocortisone 10-20mg/m2/day (infants are 20)

  • suppresses ACTH and adrenal androgens
  • maintains normal growth and weight

-tablets, not suspension (does not stay in suspension and will not be even dosing

stress doses when sick is usually 3 xs usual dose

if salt waster
Fludrocortisone 0.1mg

Salt 17-34 mEq/day in infancy

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222
Q

at start of illness for a CAH pt

A 
stress dose steroids
IV med (solucortef) if not tolerating PO
early/aggressive rehydration
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223
Q

long term complications in CAH

A

growth can be accelerated then later stunted if undertreated

virilization continues to occur in girls who are undertreated

BP

Excessive glucocorticoids -> Cushings

  • HTN
  • obesity
  • short stature
  • metabolic syndrome
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224
Q

elevated renin in CAH

A

need more mineralocorticoid

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225
Q

we dont want to normalize 17-OHP in CAH because we can cause

A

Cushing’s by overtreating

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226
Q

inadequate treatment of CAH can lead to

A

virilization

early puberty

Reduced adult final height

Advancement of bone age -> leads to early epiphyseal closure

Infertility ->
males: testicular adrenal rests (can cause testicular function)
Females: PCOS/anovulation

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227
Q

autosomal recessive in CAH means that every ___ in ____ will have CAH

A

1 in 4

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228
Q

a life-threatening condition that causes salt wasting and adrenal insufficiency in most cases

A

Classical Congenital Adrenal Hyperplasia

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229
Q

A girl with clitoromegaly

what should you suspect

A

Classical Congenital Adrenal Hyperplasia

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230
Q

A boy with microphallus or bilat undescended testes

What should you suspect

A

Classical Congenital Adrenal Hyperplasia

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231
Q

non-classical forms may present with premature adrenarche or as polycystic ovary syndrome

A

Classical Congenital Adrenal Hyperplasia

does not require stress dose steroids

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232
Q

2 things to draw in the EC when you suspect CAH

A

17 Hydroxyprogesterone

Cortisol levels

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233
Q

which type of CAH needs the Fludrocortisone

A

Salt wasters

the non classical or the virilizers do not

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234
Q

which type 1 DM is auto immune mediated

A

Type 1A

Type 2B is not

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235
Q

Name 5 rare forms of Diabetes

A

MODY (maturity onset diabetes of young)

Neonatal Diabetes (<6mos age)

Gestational Diabetes (2nd or 3rd trimester)

Steroid induced diabetes

  • usually post organ transplant
  • Cystic Fibrosis related Diabetes (CFRD)
  • 2/2 disease of exocrine pancreas

Mitrochondrial forms of diabetes

  • MELAS
  • look for neuro, other abnormal exam findings)
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236
Q

risks based screening for Diabetes (Type 2 or pre-diabetes

A

obesity/overweight: BMI >= 85th percentile PLUS
maternal history of DM or gestational DM

Metabolic syndrome: Acanthosis nigricans (sign of insulin resistance), HTN, Dyslipidemia, PCOS, SGA or LGA

Family history of T2 DM

Race/ethnicity (native American, Hispanic, AA, Latino, Asian American, pacific islander)

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237
Q

normal A1C

A

<5.7

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238
Q

Prediabetes A1C

A

5.7-6.4

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239
Q

Diabetic A1C

A

> 6.4

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240
Q

Normal fasting blood glucose

A

<100

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241
Q

prediabetic fasting blood glucose

A

100-125

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242
Q

Diabetic fasting blood glucose

A

> 125

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243
Q

Oral glucose tolerance test normal glucose

A

<144

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244
Q

oral glucose tolerance test prediabetic

A

144-199

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245
Q

oral glucose tolerance test diabetic

A

> 199

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246
Q

ADA diagnostic criteria for diabetes

A

FBG >=126

or

2 hour pG>=200 during OGTT

or

HA1C >=6.5

or
pt with classic symptoms of hyperglycemia, hyperglycemic crisis, a random plasma glucose >200

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247
Q

classic symptoms of diabetes

A 
polyuria (include nocturia)
Polydipsia
Polyphagia
Weight loss
fatigue/lack of energy
DKA

other concurrent illness?

  • frequent infections (vaginal yeast infections, abscess, UTI)
  • Flu like symptoms
  • strep throat
  • gastroenteritis
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248
Q

pathophysiology of T2DM

A

Genetic (molecular defect identified- insulin secretion)

Environmental factors

  • Diet
  • Sedentary lifestyle (BMI >=85%)

Dysregulation - insulin secretion and sensitivity

Heterogenous disorder

Insulin resistance (lack of same biological effect) - Obesity, Puberty

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249
Q

treatment guideline for new onset DM in overweight youth with HA1C <8.5% without acidosis or ketosis

A

Metformin PO BID
titrate up to 2,000mg per day as tolerated (start with 500mg once daily)

draw pancreatic antibodies

negative -> continue metformin
if unable to manage with metformin, start insulin

positive -> insulin as indicated for type 1 DM

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250
Q

treatment guideline for new onset DM in overweight youth with HA1C >=8.5% no acidosis, with or without ketosis

A

start basal insulin at 0.5/units/kg/day - titrate up every 2-3 days as indicated by glucometer reading

Metformin
-Titrate up to 2,000mg/day as tolerated
(start with 500mg once daily)

draw pancreatic antibodies

negative -> continue metformin (wean insulin)
if unable to manage with metformin, start insulin

positive -> insulin as indicated for type 1 DM

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251
Q

treatment guideline for Acidosis under DKA and/or HHNK

A

manage DKA/HHNK

IV insulin until acidosis resolves. then subq insulin until pancreatic antibodies are known

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252
Q

lifestyle modifications for someone in pre-diabetes. Research shows metformin does not prevent diabetes full blown progression at this time

A

Healthy diet

  • portion control
  • complex carbohydrates
  • caloric reduction: (500kcal/day => 1lb/wk weight loss)

Daily exercise
-moderate to vigorous activity for at least 60min/day

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253
Q

How does metformin work

A

A biguanide that

  • insulin sensitizer
  • inhibits gluconeogenesis
  • helps with weight loss
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254
Q

Metformin is used as monotherapy in Type 2DM when A1C is less than

A

8.5%

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255
Q

Black box warning for Rosiglitazone

A

Congestive heart failure and bladder cancer in diabetics

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256
Q

when you start someone on metformin, what is your initial dose and how often do you titrate up based on glucose readings

A

500mg once a day with the goal of 2000mg daily or 1000mg BID

  • increasing by 500mg weekly
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257
Q

what baseline labs do you need prior to starting metformin

A

LFTs
Renal function

If AST/ALT 2.5 times the norm, consult liver team to see what they say…..if 3-4 x we dont start

The concern is fatty liver

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258
Q

pt education for metformin

A

Avoid alcohol - Black box warning - lactic acidosis

can cause pernicious anemia

glucose targets 90-130 fasting and post prandial glucose concentration <180
(check BID BG) specifically fasting

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259
Q

side effects metformin

A

nausea
vomiting
diarrhea

can try extended release

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260
Q

Contraindications for metformin

A 
Hepatitis
impaired renal function
cirrhosis
alcoholism
cardiopulmonary insufficiency
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261
Q

If Type 2DM failing therapy with Metformin and insulin, you can add a 3rd agent as adjunct therapy ….which agent are you thinking

A

Victoza (Liraglutide)

Refer to endocrinology

this is a once a day shot

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262
Q

How does Victoza (Liraglutide) work

A

Glucagon-like-peptide (GLP-1) receptor agonist

Incretin hormone

  • Increases glucose dependent insulin secretion
  • Increases B cell growth/replication
  • slows gastric emptying and PO intake
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263
Q

what is C-peptide lab

A

marker of the B cell function

If I am looking to see if the body is naturally making any insulin we look at this lab

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264
Q

HHS and ketosis

A

HHS does not present with ketosis

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265
Q

what are the antibodies test for type 1 DM

A

Islet cell antibodies (Alpha, Beta, Delta)

GAD 65 (targets enzyme glutamic acid decarboxylase)

Insulin AutoAB

Zinc Transporter

if any are positive - definitive diagnosis for type 1 DM

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266
Q

B - Hydroxybutyrate are essentially

A

blood ketones

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267
Q

what are some labs that you should be drawing on DKA -new onset

A 
POC glucose
C-peptide
HgA1C
Beta-hydroxybutrate
chem10
VBG
celiac panel
GAD autoantibody
ICA 512AutoAB
Insulin AutoAB
IgA
Thyroglobulin AB
Thyroid panel
tissue Transglut IGA
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268
Q

leading cause of death in T1DM

A

DKA

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269
Q

ISPAD guidelines for diagnosis of DKA

A 
uncontrolled hyperglycemia (>200)
metabolic acidosis (pH <7.3)
Ketonemia
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270
Q

risk factors for DKA

A

sepsis and infections

Inadequate insulin intake including pump malfunction

Pancreatitis (7-20% r/t hypertriglyceridemia)
Age <2 yrs 
delayed diagnosis
recurrent DKA
underlying mental health issues
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271
Q

s/s DKA

A

n/v/abd pain (rule out pancreatitis)

Tachypnea/kaussmal resp

tachycardia

fruity odor

lethargy/obtunded (concern for cerebral edema)

3 Ps

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272
Q

how can you explain insulin to pt

A

Your body needs insulin to open up all of the cells so that glucose can enter the cells and make energy (generate ATP).

When the body cant get the glucose, the body looks at other sources like fat cells, muscle cells. from that you get fatty acids and glycerol and your body will convert to ketones. and thats where you get B hydroxybutyrate.

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273
Q

type 1 DM age of onset

A

6 mos - adulthood, peaks at age 12

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274
Q

Type 2 DM age of onset

A

> =10 yrs

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275
Q

Acanthosis Nigricans is common in what DM

A

type 2

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276
Q

which type DM has diabetic ketoacidosis at onset

A

> 50% for type 1

<50% type 2

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277
Q

C-peptide high or normal seen in what type DM

A

Type 2 DM

In type 1 its low or undetectable

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278
Q

Pancreatic antibodies are likely to be positive in what type of DM

A

DM type 1

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279
Q

what does positive pancreatic antibodies mean

A

it just means there has been B cell loss

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280
Q

type 1a DM patho

A

autoimmune B cell destruction leading to absolute insulin deficiency

does not happen overnight

genetic predisposition…..with a precipitating event

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281
Q

When you have one autoimmune, your at risk for more. What other autoimmune diseases are they at risk for with type 1 DM?

A

Hashimoto’s thyroiditis (most common)

Celiac disease

Adrenal insufficiency

other

  • Multiple sclerosis
  • Lupus
  • Gastritis
  • Autoimmune arthritis
  • Vitiligo
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282
Q

what labs are obtained at diagnosis for Type 1 DM and every year (after 5 years into Diabetes)

A

Thyroid Antibodies plus TFTs

Celiac Disease Antibodies

Screening for Addison’s disease and others based on symptoms

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283
Q

insulin is a ____ hormone produced by ___ ____

A

peptide hormone

beta cells

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284
Q

how does insulin work

A

regulated and secreted in oscillations (typically every 3-6 min) as a response to increased blood glucose

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285
Q

Newest ultra long acting insulin
what is it
how long does it last

A 
Insulin Degludec (Tresiba)
up to 42 hours
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286
Q

Rapid acting insulins

A

Aspart (Fiasp) - ultra rapid acting
Lispro (Humulog)
Apidra

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287
Q

Short acting insulin

A

Regular

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288
Q

Intermediate acting insulin

A

NPH

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289
Q

long acting insulin

A

glargine (Lantus, Toujeo)

detemir (Levemir)

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290
Q

Ultra rapid acting insulin

A

Fiasp

Lyumjev

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291
Q

what does basal insulin cover

A

glucose released by liver

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292
Q

what does bolus insulin cover

A

carbohydrates and correct high blood glucose levels

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293
Q

dosage of insulin in type 1 DM depends on what factors

A

Age of presentation (DKA?)

Honeymoon period/partial remission (10-15% pancreas is functioning for a short period - longest milli has seen is 2 years)

Family preference

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294
Q

Insulin starting dose guide formula

A

TDD = 0.x unit/kg/day (x= age in years)

if in DKA
1unit/kg/day (max)

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295
Q

Basal dosing for insulin should be ___ -___% of TDD

A

50-60%

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296
Q

Bolus dosing for insulin should be ___-____ of TDD

A

40-50%

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297
Q

Target BG for Type 1 DM normally

A

80-120mg/dl

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298
Q

Target BG for Type 1 DM if toddler, developmental delays or CF

A

150 mg/dl

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299
Q

How often should a type 1 DM be injecting insulin

A

3-4 times/day

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300
Q

How is insulin given when using a pump

A

continuous basal rate
Food bolus
correction bolus

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301
Q

Insulin side effects

A

hypoglycemia
- rule out alcohol intake

Lantus/Basaglar can burn: may use Tresiba

weight gain

Lipoatrophy or Lipohypertrophy: Rotate sites

302
Q

when a pt is on insulin having frequent hypoglycemia, what needs to be ruled out

A

alcohol intake

303
Q

If a DM pt is using Lantus/Basaglar and its burning. What can you switch to?

A

Tresiba

304
Q

For insulin dependent pt. How do you prevent Lipoatrophy or Lipohypertrophy?

A

Rotate sites

305
Q

In diabetic pt low glucose is considered low

A

70mg/dl

Adrenergic: Palpitations, tremors anxiety

Cholinergic: Sweating, hunger, paresthesias

306
Q

In diabetic pt low glucose is considered severely low

A

<55

Headache, irritability, difficulty concentrating, confusion, seizures, coma

307
Q

what can you give a diabetic pt for severe hypoglycemia

A

Glucagon (peptide hormone, alpha cells)

308
Q

how many times per day should a diabetic check blood sugars

A

at least 4xs

309
Q

MODY

A

maturity onset diabetes of Youth

monogenic disorder

misdiagnosed as type 1 or type 2

High genetic predisposition (50% chance if parent has it)

14 genes identified for mutation causing MODY

Pathogenesis - insulinopenia - subtle onset - insulin often not required

occurs before age 25 yrs

islet autoimmunity is absent

treatment depends on type of MODY

310
Q

Signs of MODY

A

Mild fasting hyperglycemia = about 140

insulin requirement <= 0.5 units/kg/day
(some endogenous insulin beyond 3-5 yrs after onset of diabetes)

Negative autoantibody testing

Measurable C-peptide

Lack of significant obesity

Strong family history

lack of insulin resistance

311
Q

treatment for MODY

A

Sulfonylureas
-Glyburide

Refer to endocrinology for initiation of therapy

312
Q

Acute complications for DM

A

hypoglycemia
DKA (Diabetic Ketoacidosis)
HHS (hyperglycemic hyperosmolar state)

313
Q

Chronic complications for DM

A

Microvascular

  • Retinopathy
  • Nephropathy

Neuropathy
Macrovascular: Cardiovascular

Delayed puberty
Growth disturbance (short stature)
psychosocial/Psychiatric

314
Q

what screening should be done for a type 2 DM at diagnosis, then yearly

A

Retinopathy: dilated eye exam

Nephropathy: spot urine albumin to creatinine ratio

Neuropathy: foot exam

HTN should be evaluated at diagnosis and every visit

Dyslipidemia should be evaluated at diagnosis. If abnormal - reevaluate yearly. If normal, every 3-5 years

315
Q

what screenings should be done in patients 10 yrs old and older in Type 1DM who has been a diabetic for 5 years. These should be done yearly after the initial

A

Retinopathy: dilated eye exam

Nephropathy: spot urine albumin to creatinine ratio

Neuropathy: foot exam

Dyslipidemia should be evaluated at diagnosis. If abnormal - reevaluate yearly. If normal, every 3-5 years

316
Q

what screenings should be done in Type 1DM shortly after diagnosis; if normal - repeat every 1-2 yrs

A

autoimmune thyroid disease: TSH

317
Q

what screenings should be done in Type 1DM shortly after diagnosis or with symptoms

A

Celiac
IgA
TTG
IgA

318
Q

if your HA1C is 7.0 your average blood glucose over the past 90 days

A

170

319
Q

If your HA1C is 5.0, your average blood glucose over the past 90 days

A

100

320
Q

If your HA1C is 8.0, your average blood glucose over the past 90 days

A

204

321
Q

why do we recommend keeping the HA1C 7%

A

reduces the risk of long term complications significantly

Retinopathy - 76%
Nephropathy - 54%
Neuropathic - 60%

322
Q

what is the depression screening called

A

PHQ-9 Depression screening

323
Q

number of solute particles in 1 kg of solvent

A

osmolality

this is the term used in medicine

324
Q

number of solute particles in 1 L of solvent

A

Osmolarity

325
Q

formula for serum osmolality

A

(2x {Na}) + {glucose} + (Bun)

326
Q

effective osmolality or the measure of the osmotic pressure gradient that reflects the concentration of solutes that don’t cross cell membrane easily and affect distribution of water

A

Serum tonicity

327
Q

transfer of soluble components (not protein) from blood into glomerulus

A

filtration

328
Q

water and solutes move from renal tubule back into circulation

A

reabsorption

329
Q

transfer of solutes and waste from plasma into the renal tubule for excretion (urine)

A

secretion

330
Q

content of urine, end result of above processes

A

Excretion

331
Q

content of urine, end result of filtration, reabsorption, secretion

A

Excretion

332
Q

what does Antidiuretic hormone (ADH) aka Vasopressin do

A

recruits renal water channels in collecting duct -> water reabsorption in renal tubules -> concentrates urine (decreases urine volume)

“Adds
Da
H2O”

333
Q

drinking water increases or decreases your plasma osmolality

A

decreases

334
Q

at what plasma osmolality does thirst begin to autoregulate osmolality

A

280 mosmol/kg

335
Q

at what plasma osmolality does plasma ADA start to risk to autoregulate osmolality

A

285 mosmol/kg

336
Q

when there are problems with ADH and water homeostasis regulation what can it affect

A

thirst

urine output

Intravascular volume status

Serum osmolality

Serum Sodium (Na) level

Urine osmolality

Urine Na level

337
Q

decreased production of ADH

A

central diabetes insipidus

338
Q

decreased renal response to ADH

A

nephrogenic Diabetes insipidus

339
Q

decreased ability to reabsorb water in the renal tubules ->cannot concentrate urine ->excess loss of water in urine

(inappropriately dilute urine and serum hyperosmolality)

A

Diabetes Insipidus

340
Q

what causes central DI - Hypothalamus doesn’t produce ADH

A 
Cancer (craniopharyngioma, germinoma)
trauma
meningitis
hypoxic brain injury
infiltrative disorders (histiocytosis, leukemia)
surgery, radiation
holoprosencephaly, congenital
hypopituitarism
Anorexia nervosa
idiopathic
341
Q

what causes nephrogenic DI - collecting ducts don’t respond to ADH

A

kidney disease (polycystic kidney disease, sickle cell)

Medications - lithium, foscarnet, amphoteracin)

pregnancy

Bartter syndrome

Bardet Biedl syndrome

Hypercalcemia

Hypokalemia

Hereditary (Aquaporin-2 gene mutation)

342
Q

what medications can cause nephrogenic DI

A

lithium, foscarnet, amphotericin

343
Q

what syndromes can cause nephrogenic DI

A

Bartter syndrome

Bardet Biedl syndrome

344
Q

what gene mutation is associated with nephrogenic DI

A

Aquaporin-2 gene mutation

345
Q

DI symptoms

A

symptoms of dehydration and hypernatremia

  • Tachycardia, hypotension
  • irritability, restlessness
  • weakness
  • seizures
  • AMS, Coma
  • FTT or obesity
  • Fever (infants)
  • Polyuria
  • Nocturia
  • Absence of primary polydipsia
  • Absence of excess solute excretion or osmotic diuresis (hyperglycemia, high protein diet)
  • Patients not taking diuretics
346
Q

In DI what is their volume status

A

Hypovolemic

347
Q

In DI what should their urine output be

A

increased

348
Q

In DI what should their serum sodium be

A

High >150 mEq/L

349
Q

In DI what should their serum osmolality be

A

High >300 mOsm/L

350
Q

In DI what should your urine specific gravity be

A

Low (<1.010)

351
Q

In DI what should your urine sodium be

A

Low (<20 mEq/L)

352
Q

In DI what should your urine osmolality be

A

low (<100-300 mosm/L)

353
Q

when does water deprivation test start

A

after breakfast and after 1st void of the day and you don’t get any fluids

354
Q

when you give DDADP (vasopressin) and your urine osmols do not rise this is

A

nephrogenic DI

355
Q

when you give DDADP (vasopressin) and your urine osmols do rise this is

A

central DI

356
Q

DI: Acute management - hypernatremia

A

Severe dehydration - NS bolus 20mL/kg

Free water replacement over 24-48 hours

  • Goal is to correct Na 0.5mEq/L per hr (12mEq/L/day)
  • Risk cerebral edema - plasma osm drops to quickly

Monitor Na level frequently

remember that NS is hypotonic in this situation….may need 0.45% NaCl

or use NS for bolus then go with D5W

357
Q

Free water deficit formula (DI)

A

Free water deficit (liters) = measured Na - Goal Na all divided by goal Na then multiply by 0.6L/kg x weight (kg)

358
Q

what is key to regulate plasma osmolality in a pt with DI

A

someone that has an intact thirst mechanism

359
Q

monitoring in DI

A

intake/output
Na levels
adjustments to daily fluid requirement based in I/O, Na levels, change in insensible losses, growth

360
Q

medication used for acute management for DI

A

Vasopressin

361
Q

what med is most commonly prescribed for DI management

A

Desmopressin (DDAVP)

  • longer half life
  • no pressor effect
  • every 12-24 hr dosing for IV/nasal; q 8-12 hr dosing for oral

monitor for breakthrough mild polyuria-occurs when dose is due (good sign that the dose is right)

362
Q

Nephrogenic DI management

A

if drug induced - stop if able

Low salt, low protein diet

NSAIDS - indomethacin is more effective than ibuprofen

Diuretics - hydrochlorothiazide, amiloride

Partial nephrogenic DI - higher doses of DDAVP may work

363
Q

inability to suppress ADH

impaired water excretion

inappropriately concentrated urine + serum hypo-osmolality

A

SIADH - syndrome of inappropriate ADH

364
Q

list pulmonary causes of SIADH

A

mechanical ventilation

pneumonia

bronchiolitis

asthma

cystic fibrosis

365
Q

list neurologic causes of SIADH

A

tumor

surgery

trauma

hemorrhage

meningitis

Encephalitis

severe nausea

366
Q

list oncology causes of SIADH

A

Medulloblastoma

lymphoma

367
Q

list medications that causes of SIADH

A

Oxcarbazepine

Valproate

chemotherapies

narcotics

nsaids

368
Q

list other causes of SIADH

A

Anesthesia

idiopathic

post-op

369
Q

s/s of SIADH

A

symptoms of hyponatremia

  • n/v
  • anorexia
  • headache
  • cramps or tremors
  • irritability
  • confusion
  • malaise
  • seizure
  • stupor or coma

normal cardiac, renal, liver, adrenal, thyroid function

patient not taking diuretics

Absence of renal salt wasting

no evidence of hypovolemia

BUN usually low

uric acid low

370
Q

volume status in SIADH

A

Euvolemic to hypervolemic

371
Q

urine output in SIADH

A

Decreased (<1mL/kg/hr)

372
Q

serum sodium in SIADH

A

low (<135 mEqu/L)

373
Q

serum osmolaltiy in SIADH

A

low (<280 mOsm/L)

374
Q

Urine specific gravity in SIADH

A

High (>1.020)

375
Q

Urine Sodium in SIADH

A

High (>20-40 mEq/L)

376
Q

treatment for SIADH

A

severe symptoms - treat immediately with 3% saline

gradual correction of hyponatremia - 1st line therapy is fluid restriction

377
Q

Acute hyponatremia

duration
severity?
goal Na correction?

A

develops within 48 hours
severe symptoms more likely
at risk for complications
more tolerant of sodium correction

goal Na Correction is 6-8mEq/L per 24 hours

378
Q

Chronic hyponatremia

duration
severity?
goal Na correction?

A

Duration >48 hours
cerebral volume adaption
less likely to be symptomatic
at risk for osmotic demyelination if corrected too quickly

requires more gradual correction
goal Na correction 4-6 mEq/L per 24 hours

379
Q

treatment for severe symptomatic hyponatremia (seizure, obtunded, coma)

(SIADH)

A

3% saline 3-5mL/kg (max 100mL) raises by 2.5-4 mEq/L

380
Q

SIADH management

A

fluid restriction is first line

  • restrict to 1/2 to 3/4 daily maintenance fluid requirement
  • Monitor sodium levels
  • Goal rate of Na correcting 4-8mEq/L per 24 hours depending on acuity
381
Q

Alternative therapy for chronic SIADH

A
  • low diuretic (+/- sodium supplementation)
  • Urea supplementation - increases water excretion
  • Vasopressin receptor antagonist (Vaptans, rarely used in pediatrics)
382
Q

hyponatremia + hypovolemia due to inappropriate sodium wasting in urine

A

Cerebral salt wasting (CSW)

383
Q

What is cerebral salt wasting seen in

A

CNS insult: subarachnoid hemorrhage, post-surgery, trauma, meningitis, encephalitis, tumors, status epilepticus

384
Q

Volume status in Cerebral salt wasting

A

Hypovolemic

385
Q

urine output in Cerebral salt wasting

A

increased

386
Q

Serum sodium in Cerebral salt wasting

A

Low (<135 mEq/L)

387
Q

Serum osmolality in Cerebral salt wasting

A

low

388
Q

urine specific gravity in Cerebral salt wasting

A

High (>1.050)

389
Q

urine sodium in Cerebral salt wasting

A

High (>40 mEq/L)

390
Q

Urine osmolaltiy in Cerebral salt wasting

A

High (>100-300 mOsm/L)

391
Q

Managing Cerebral salt wasting

A

Treat underlying cause

Volume repletion and treat hyponatremia

  • isotonic saline - provide fluid and restore sodium stores
  • Moderate-severe hyponatremia
    • Provide additional sodium as 3% saline or salt tabs
    • limit free water (not volume)

Monitor sodium levels
-avoid quick correction of hyponatremia - risk osmotic demyelination syndrome

-correct Na no more than 8-10 mEq/L per day

Fludrocortisone may be useful

392
Q

what lab represents the unbound, biologically active T4

A

Free T4

393
Q

If free T4 is high …most likely

A

Hyperthyroidism

394
Q

If free T4 is low …most likely

A

Hypothyroidism

395
Q

If free TSH is high …most likely

A

Hypothyroidism

396
Q

If free TSH is low …most likely

A

Hyperthyroidism

397
Q

3 types of hypothyroidsm

A

congenital
acquired
Transient

398
Q

what are the types of congenital hypothyroidism

A

dysgenesis - did not form correctly

dyshormonogenesis - it formed, but doesnt function properly

399
Q

If not caught and treated early, what can happen

A

developmental delay

400
Q

T3, T4 and TSH and placenta

A

do not cross the placenta - when your testing the baby at day of life 1 - those are the babies numbers

401
Q

Thyroid meds that mom takes can cause

A

Transient hypothyroidism - can last 3-4 weeks (this can be over or underproduction)

402
Q

what are the causes of transient hypothyroidism

A

maternal antithyroid drugs

Maternal TSH receptor blocking antibodies

403
Q

what are the causes of acquired hypothyroidism

A

hashimoto thyroiditis

Iodine deficiency

404
Q

causes of secondary hypothyroidism

A

Hypothalamus or pituitary
-Free T4 and TSH low or normal

Malformation
-Holoprosencephaly - midline defects (cleft lip/palate)

405
Q

what does hypothyroidism look like in baby

A 
low hr
low energy so dont feel well
Acrocyanosis
abd distension
umbilical hernia
mottled skin
thick lips
large fontanel
weakness
hypotonia
constipation
prolonged jaundice
cold intolerance
406
Q

Congenital Hypothyroidism and goiter

A

RARE 1:30k live births - most often r/t dsyhormonogenesis or transient

407
Q

Newborn screen and congenital hypothyroidism

A

We do screen for this in all 50 states

408
Q

Acquired Hypothyroid/hashimoto Thyroiditis

Setup and symptoms

A

Subtle

decline in growth velocity without weight loss

25-33% have family history

Common in Turner & Trisomy 21

iodine deficiency (table salt (not sea salt), milk products, eggs, fish) - Cretinism (when cause is iodine deficiency)

409
Q

Acquired Hypothyroid/hashimoto Thyroiditis

Evaluation

A

Goiter

Antithyroid peroxidase & antithyroglobulin antibodies
Elevated TSH, low FREE T4
Elevated TSH and normal T4 may be prelude to failure

410
Q

Treatment Acquired Hypothyroid/hashimoto Thyroiditis

A

Congenital or Acquired

  • Levothyroxine
  • Infants 15mcg/kg and children 3mg/kg
411
Q

Hyperthyroidism is most commonly cause by ____ in children

A

Graves Disease

412
Q

Graves Disease Setup and Symptoms

A

Adolescent girls

emotional lability, personality changes, school performance

Tremor, anxiety, inability to concentrate

Weight loss

413
Q

Graves Disease Evaluation

A

Free T4, T3 high

TSH low

414
Q

Hyperthyroid symptoms

A

increase sensitivity to heat

sudden weight loss

frequent bowel movements

sweating

Thyroid storm

Rapid pounding heartbeat

nervousness

irritability

tremor

difficulty sleeping

change in menstrual patterns

415
Q

Treatment Graves disease

A

Methimazole x 1-2 yrs (watch for agranulocytosis(aplastic anemia) - can switch to PTU - 2nd option (risk for liver failure) (the idea is to get you to a euthyroid state)

Surgery (needs to be a skilled surgeon) (goal is to get you to a euthyroid state)

Iodine (in a hyperthyroid state, iodine is suppressive) - temp till surgery

Radioiodine - this one you will need thyroid hormone replacement after

Beta blocker =- symptom control

416
Q

Thyroid storm setup and symptoms

A

Medical emergency

rare complication of hyperthyroidism

Tachycardia
disorientation
elevated BP
Hyperthermia

417
Q

Evaluation of Thyroid storm

A

Free T4 and T3 - high

TSH low

418
Q

Treatment for thyroid storm

A 
cooling blanket
beta blocker
iodine
hydrocortisone support if they have adrenal insufficiency associated with the thyroid storm
heart failure therapy - if needed
419
Q

Neonatal Hyperthyroid/neonatal graves disease setup and symptoms

A

Hyperthyroid mom - transplacental passage of maternal thyroid stimulating immunoglobulins (TSI)

may be masked for few days - due to maternal antithyroid treatment

Hallmark: Irritability, tachycardia, heart failure, polycythemia, craniosynostosis, advanced bone age, poor feeding, FTT

420
Q

Evaluation for Neonatal Hyperthyroid/neonatal graves disease

A

Free T4 high

TSH low

421
Q

treatment for

Neonatal Hyperthyroid/neonatal graves disease

A

none if symptoms are minimal
methimazole
B Blocker
spontaneous resolution 2-3 mos based on half life of TSIs

422
Q 
obesity
muscle wasting
muscle weakness
decreased glucose tolerance
hyperglycemia
buffalo hump
A

Cushing Syndrome symptoms

423
Q

what 3 types of hormones do the adrenal glands produce

A

Glucocorticoid (cortisol, corticosterone)

mineralocorticoid (Aldosterone, dehydroepiandrosterone)

sex hormones (androgens, progestins and estrogens)

424
Q

acute adrenal insufficiency

A

adrenal crisis

425
Q

chronic adrenal insufficiency

A

Addison disease

426
Q

the most common causes of acute adrenal insufficiency are

A

Waterhouse-Friderichsen syndrome - sudden withdrawal of long term corticosteroid therapy

427
Q

in primary adrenal insufficiency what hormones are not produced in sufficient amounts?

which one in particular

A

Glucocorticoid
mineralocorticoid

cortisol

428
Q

what is the most commonly identified cause of primary adrenal insufficiency in children

A

Congenital adrenal hyperplasia (CAH)

429
Q

Congenital adrenal hyperplasia (CAH) is an _____ _____ disorder

A

autosomal recessive disorder

430
Q

Congenital adrenal hyperplasia (CAH) is due to a defect in what enzyme

A

largely due to 21-hydroxylase deficiency required in the synthesis of cortisol to cholesterol

431
Q

what gender has a higher incidence of Congenital adrenal hyperplasia (CAH) at birth

A

females

432
Q

when do males usually present with Congenital adrenal hyperplasia (CAH)

A

with a life-threatening salt-wasting crisis in the first month of life

433
Q 
between 1-4 weeks of life
-Vomiting
-dehydration
-cardiac arrhythmias
-hyponatremia
-hyperkalemia
-salt-losing crisis
All results in circulatory collapse
A

Congenital adrenal hyperplasia (CAH)

434
Q 
fatigue
loss of weight
hyperpigmentation of the creases of the skin
nausea
vomiting
A

Adrenal insufficiency

435
Q

vomiting
abd pain
hypovolemic shock

A

adrenal crisis

436
Q

Morning 17-OHP levels may be _____ in a partial enzyme deficiency

A

elevated

437
Q

Congenital adrenal hyperplasia (CAH)

testosterone in females

A

elevated

438
Q

Congenital adrenal hyperplasia (CAH)

Androstenedione is seen in

A

males and females

439
Q

Congenital adrenal hyperplasia (CAH)

karyotyping is important for

A

ambiguous genitalia

440
Q

CAH dosing of hydrocortisone

A

10-20 mg/m2/day daily

441
Q

Adrenal insufficiency dosing for hydrocortisone

A

6-9mg/m2/day daily

442
Q

Stress dosing of hydrocortisone

A

25-50mg/m2/day IV/IM

443
Q

severe illness or surgical procedures, stress dosing of hydrocortisone

A

50-123 mg/m2/day IV

444
Q

dosing for mineralocorticoid maintenance therapy in adrenal insufficiency

A

0.1-0.2mg oral fludrocortisone acetate daily

445
Q

sodium supplementation for infants in adrenal insufficiency

A

17-34 mEq of sodium supplementation daily

446
Q

when does cerebral salt wasting occur

A

following an acute CNS injury

447
Q

Results in volume depletion and hyponatremia typically occurring within the first few days of an inciting intracranial injury, surgery or disease process

A

Cerebral salt wasting

448
Q

symptoms of cerebral salt wasting

A 
headache
n/v
depressed/AMS
lethargy
dehydration
agitation
seizures
hypotension
coma

the rate of renal sodium loss, degree of hyponatremia and overall fluid status impact the severity of the presenting symptoms

449
Q 
serum sodium <135
serum osmolarity <280
urine sodium >80
urine osmolarity >200
Urine specific gravity >1.010
A

cerebral salt wasting

450
Q

urine output in cerebral salt wasting is - ml/kg/hr

A

2-3ml/kg/hr

451
Q

what other studies should be done in cerebral salt wasting

A

CT/MRI - looking for structural abnormalities, tumors, AV malformation, hemorrhage

Lumbar puncture
-infection

452
Q

In cerebral salt wasting serum sodium level should rise no more than __-__ mEq/day

A

10-12 - to reduce risk of central pontine demyelination of white matter in brain

unless having severe neuro symptoms

453
Q

genetics of DI

A

typically x linked recessive

454
Q

What syndrome is linked to DI

A

Wolfram syndrome

455
Q

congenital DI typically X linked recessive involving what mutations

A

VR2 or AQP2

456
Q

What conditions lead to the inability of the kidneys to respond to ADH in DI

A 
Chronic renal failure
Renal tubulointerstitial diseases
Potassium depletion
sickle cell disease 
medication induced from drugs
alcohol
lithium
diuretics
amphotericin B
Demeclocycline
457
Q

what dietary abnormalities can lead to DI

A

Primary polydipsia
decreased sodium chloride intake
severe protein restriction or depletion

458
Q

is DI reversible?

A

Nephrogenic DI that results from a metabolic condition may be reversed if the medication is stopped or the metabolic condition is corrected

459
Q 
Polyuria
Dilute urine
Polydipsia
inappropriately low urine sodium and osmolality
urine specific gravity <1.005
Hypernatremia
Serum Hypo-osmolality
Dehydration
A

DI

460
Q

the primary causes of polyuria and polydipsia are

A

Diabetes Mellitus
Central DI

other causes:
UTI
relief of renal obstruction
psychogenic polydipsia (excessive water intake)

461
Q 
Serum sodium >150
Osmolality >295
Urine sodium <30
Urine osmolality <200
specific gravity <1.005
A

DI

462
Q

water deprivation test results:

concentrated urine output following ADH administration

A

Central DI

463
Q

water deprivation test results:

excessive, dilute urine despite hypernatremia and hyperosmolality

A

nephrogenic DI

464
Q

fluids are restricted until as much as 5 % of body weight has been lost to evaluate urinary response when the serum osmolality exceeds 295

A

water deprivation test

465
Q

management of DI

A

restore hemodynamics

replace water deficit and correct electrolyte disturbances

decrease Urine output to within normal range (Vasopressin, desmopressin)

Treat underlying

Volume replacement:
-Maintenance IV fluids, plus mL per ML urine output replacement (usually allow 1-2 ml/kg/hr urine output and replace the remainder)

monitor serum sodium closely

central DI needs ADH replacement to control polyuria

466
Q

critical care setting treat for DI

A

Vasopressin continuous IV
-short half life (10-20 min)

initiated at dose of 0.5milli-units/kg/hr and titrated until urine output is decreased
-urine output goal <4mL/kg/hr

467
Q

other than critical care setting treat for DI

A

Desmopressin
Oral and intranasal

chronic therapy: dose range is 5-30ug/day with peak effect 1-5 hrs

468
Q

what type of DI is resistant to vasopressin

A

Nephrogenic DI

469
Q

diagnosis of DKA

A 
blood glucose >200
presence of serum ketones
urine ketones
blood pH <7.3
serum bicarbonate <15
470
Q

hyperglycemia leads to

A 
osmotic diuresis
electrolyte loss
Dehydration
Decreased glomerular filtration
Hyperosmolarity
471
Q

physical exam findings in DKA

A 
Tachycardia
decreased pulses
poor perfusion
dry mucous membranes
enophthalmos
poor skin turgor
hypotension
deep or labored breathing
472
Q

what systems need to be monitored in DKA

A

Cardiac monitoring
-watch for T wave alterations seen in hyperkalemia or hypokalemia

Neuro monitoring
-cerebral edema

473
Q

corrected sodium formula

A

={Na+} + {1.6 x (plasma concentration mg/dL-100}/100

474
Q

In DKA treatment …as hyperglycemia improves, serum sodium should ___. If it ____ or does not _____, there is concern for what?

A

improve

if sodium does level increases or does not begin to fall, there is concern for the development of cerebral edema

475
Q

Potassium in DKA treatment

A

serum K can start low, normal or high…you lose k as an effect of water moving out of the cells due to increase in serum osmolarity ….

add K to fluid when K level <6 and pt has voided

correction of hyperglycemia and giving insulin will shift potassium back into the cells

476
Q

Phosphorous in DKA

A

cells are depleted as a result of acidosis, osmotic diuresis and insulin administration

477
Q

risk of giving bicarbonate to DKA

A

CNS acidosis
Hypokalemia
cerebral edema

478
Q

timing of blood glucose monitoring DKA

A

prior to meals and 2 hours after meal ends

479
Q

a potentially fatal complication of diabetes, usually type 2 due to insulin deficiency and an increase in counterregulatory hormones

A

Hyperglycemic Hyperosmolar state (HHS)

480
Q

enough endogenous insulin to suppress ketosis, although insufficient amount of insulin to prevent hyperglycemia

A

Hyperglycemic Hyperosmolar state (HHS)

481
Q

Accumulation of ketoacids that cause cap metabolic acidosis

A

DKA

482
Q 
severe dehydration
polyuria
polydipsia
weight loss
AMS
hyperglycemia
increased serum osmolality
no ketosis or mild
Plasma glucose >600
pH >7.3
serum bicarb >15
small ketonuria
serum osmolality >320
A

Hyperglycemic Hyperosmolar state (HHS)

483
Q

Mgmt Hyperglycemic Hyperosmolar state (HHS)

A

ABCs
restore circulatory volume and correct fluid deficit

correct hyperglycemia, hyperosmolality, and electrolyte imbalances
-fluid mgmt and insulin

frequent lab eval
-hourly serum glucose in acute phase, electrolytes and other lab studies

treat underlying (infection is most common precipitating factor)

Monitor signs of cerebral edema
-correcting fluids over a longer period (48 hrs) may reduce r/o cerebral edema

484
Q

An increase in serum levels of T3 and T4 will result in what in regards to TSH

A

Lower levels of TSH

485
Q

An decrease in serum levels of T3 and T4 will do what to TSH

A

higher levels of TSH

486
Q

abnormal fetal thyroid development or a disturbance in production of thyroid hormone

A

Congenital hypothyroidism

487
Q

autoimmune or iatrogenic hypothyroidism

A

acquired hypothyroidism

488
Q

immune system response results in damage and altered function of thyroid

A

Autoimmune hypothyroidism

489
Q

Chronic lymphocytic thyroiditis (Hashimoto) affects what gender more often

A

females

490
Q

Common comorbidities of Chronic lymphocytic thyroiditis (Hashimoto) include

A

Type 1 DM
Juvenile RA
Trisomy 21

491
Q

can be caused by head or neck radiation therapy, surgery or induced by drugs that increase thyroxine metabolism

A

iatrogenic hypothyroidism

492
Q

occurs in infants of mothers with Graves disease, causing a transplacental transfer of the thyroid stimulating immunoglobulin (TSI) from mother to infant

A

Congenital or neonatal hyperthyroidism

493
Q

Autoimmune and iatrogenic causes of hyperthyroid

A

Acquired hyperthyroidism

494
Q

most common cause of acquired hyperthyroidism resulting in an overproduction of the thyroid hormone

A

Graves disease

495
Q

Autoimmune disorder resulting in hyperthyroid state often associated with other disorders such as type 1 DM or celiac disease - usually followed by hypothyroid after initial surge of thyroid hormone

A

Hashimoto thyroiditis

496
Q

congenital hypothyroidism symptoms typically develop within first - weeks of life

A

2-6 weeks

497
Q

in congenital hypothyroidism what is critical due to the risk of irreversible neurocognitive deficits if untreated

A

Early diagnosis

498
Q 
lethargy
hoarse cry 
bradycardia
large size for gestational age
large fontanels
constipation
hypothermia
jaundice
dry skin
elevated Free T4
elevated TSH
A

Congenital hypothyroidism

499
Q 
linear growth deceleration
weight gain
fatigue
dry skin
brittle hair
muscle cramps
cold intolerance
delayed tooth eruption

lab studies - elevated TSH
low T4 and low free T4 levels

A

Acquired hypothyroidism

500
Q

thyroid peroxidase antibodies

thyroglobulin antibody titers

A

Hashimoto Thyroiditis

501
Q

congenital hyperthyroidism findings usually develop when

A

initial days after birth

502
Q 
small fontanels
fever
irritability
tachycardia
vomiting
diarrhea
poor weight gain despite increased feeding

birth history might be positive for IUGR or premature birth

elevated free T3 and T4
decreased TSH

Antithyroid peroxisomal antibodies may be present

A

congenital hyperthyroidism

503
Q 
diffuse enlargement of the thyroid
anxiety
sweating
weight loss
tachycardia
eyelid lag or retraction, periorbital edema, exophthalmus

elevated T3 and T4
Decreased TSH

+/- antithyroid peroxisomal antibodies present

A

Acquired Hyperthyroidism

504
Q

what imaging used to look at thyroid for initial eval of acquired hyperthyroidism

A

US - soft tissue of thyroid

Scintigraphy - evaluates the function of thyroid gland

radiographic testing not commonly used in screening

505
Q

evaluates the function of the thyroid gland

A

Scintigraphy

506
Q

treatment of congenital hypothyroidism

A

L Thyroxine Administration
life long monitoring
normalization of T4

507
Q

Treatment of congenital hyperthyroidism

A

Methimazole or Propylthiouracil (blocks thyroid hormone stimulation

Iodine - blocks the release of thyroid hormone already synthesized

508
Q

treatment of acquired hypothyroidsim

A

L-Thyroxine - thyroid replacement

509
Q

treatment Acquired hyperthyroidism

A

Propylthiouracil or methimazole

radioactive iodine

surgery (some cases)

510
Q

primary function of the parathyroid gland and parathyroid hormone (PTH) is to

A

regulate the amount of calcium present in blood and bones

511
Q

in Hyperparathyroidism, excessive secretion of PTH, leads to

A

hypocalcemia

hypocalciuria

hypophosphatemia

hyperphosphaturia

512
Q

secretion of PTH is triggered by a reduction in the serum ____ level

A

calcium

513
Q

When released, PTH targets musculoskeletal, renal and gI systems to regulate

A

serum calcium levels

514
Q

PTH triggers ______ bone resorption - resulting in

A

increased

serum calcium and serum phosphate

515
Q

in the kidney, PTH stimulates the reuptake of

A

calcium and magnesium and increases phosphorous excretion

516
Q

In the intestine, PTH activates the enzyme responsible for

A

Vit D Absorption -> which controls the absorption of intestinal calcium

517
Q

most common congenital cause of hypoparathyroidism

A

DiGeorge syndrome (22q11 deletion)

518
Q

autoimmune hypoparathyroidism is usually associated with ____ disease or other endocrine diseases such as adrenal insufficiency with polyglandular autoimmune syndrome type 1

A

Addison

519
Q

ingestion of anticonvulsants causing hypocalcemia can lead to

A

Acquired hypoparathyroidism

520
Q

primary hyperparathyroidism is associated with

A

multiple endocrine neoplasia syndromes or adenomas

521
Q

secondary hyperparathyroidism is largely due to

A

hypocalcemic states associated with chronic renal failure, vit D deficiency, rickets

522
Q

PTH level decreased
serum and urinary calcium decreased
Hyperphosphatemia

EKG - shortened or prolonged QTc interval

A

hypoparathyroidism

523
Q 
Hypercalcemia
abd pain
vomiting
constipation
bone pain and paresthesias
renal stones
HTN

elevated PTH
Hypercalcemia
Hypophosphatemia
Alkaline phosphatase normal or elevated

A

Primary hyperparathyroidism

524
Q 
Hypercalcemia
abd pain
vomiting
constipation
bone pain and paresthesias
renal stones
HTN

serum calcium low or normal

EKG with prolonged QTc interval

nephrolithiasis
parathyroid adenoma

A

secondary hyperparathyroidism

525
Q

management of hypoparathyroidism

A

calcium and vit d supplementation

ECG monitoring

long term monitoring of dietary calcium intake

labs every 3-6 months to check:
serum calcium
serum phosphorous
serum magnesium
alkaline phosphate levels
25-(OH)D3
1.25-(OH)2D3

urine calcium to creatinine level monitoring

526
Q

Management of hyperparathyroidism

A

aggressive hydration and diuretics

restriction of calcium and vit D intake

Hydrocortisone

calcitonin

surgical removal of parathyroid glands

527
Q

Neuroendocrine tumor arising from the adrenal medulla (chromaffin cells)

can be benign or malignant
often bilat

A

Pheochromocytomas

528
Q

associated with von Hippel-Lindau disease, multiple endocrine neoplasia type 2, familial paraganglioma syndrome or neurofibromatosis type 1

A

Pheochromocytomas

529
Q

Sustained HTN (due to tumor associated catecholamine release)

triad (headache, diaphoresis, palpitations)

tachycardia

abnormal skin sensation

anxiety

Hyperglycemia

A

Pheochromocytomas

530
Q

diagnosis of Pheochromocytomas

A

metanephrine or catecholamine levels; plasma or urine

  • 24 hr urine collection
  • urinary vanillylmandelic acid
  • eval for causes
  • CT scan: head, neck, chest, abdomen - used to localize tumor
  • Scintigraphy or positron emission tomography may also be used to localize tumor
531
Q

mgmt of Pheochromocytomas

A

HTN control
-A or B blockers may be used presurgically

-surgical resection

metastatic Pheochromocytomas requires antineoplastic therapy

532
Q

a common cause of hyponatremia

A

SIADH

533
Q

excessive release of ADH from pituitary gland

A

SIADH

534
Q

Hyponatremia
decreased serum osmolarity and increased urine osmolarity

decreased urine output with increased urine concentration

cerebral edema may ensue in severe cases of hyponatremia

A

SIADH

535
Q

serum sodium <135

serum osmolarity <280

urine osmolarity >200

BUN < 10

Urine sp gravity >1.020

urine sodium >25

A

SIADH

536
Q

managing SIADH

A

identify and treat underlying

fluid restriction to <75% daily maintenance fluid requirement

Avoid hypotonic IV fluids

correct hyponatremia slowly by 0.5 - 1mEq/hr

for severe hyponatremia, correct to 125 with 3% Hypertonic saline

Na+ deficit = (body wt in kg) x (0.6% in extracellular fluid: ECF) x (Desired serum sodium level {125}) - Actual serum sodium level = mEq

537
Q

labs for initial eval for child newly diagnosed with diabetes

A

CBC with diff
BMP
HA1C - >=6.5 supports diagnosis for type 2 DM

insulin level
Insulin antibodies
-islet cell antibodies
-GAD-65

C peptide

12 lead EKG
Celiac disease
thyroiditis

538
Q

measures adrenal gland response to administration of ACTH

A

ACTH stimulation testing

539
Q

how to perform ACTH stim test

A

obtain baseline cortisol level

30-60 min following injection, a second cortisol level is obtained

results: Cortisol levels
- <16ug/d: suggests failing or insufficient response

-18-20ug/dL is minimal response

> 30 ug/dL is a normal response

540
Q

As much as ___ % of lean body mass in infants is water

A

70%

541
Q

Children, in general, have approx ___% of lean body mass as water and an overall higher concentration of extracellular fluid than adults

A

60%

542
Q

daily maintenance fluids for healthy children include fluid for

A

physiologic needs

daily output

insensible losses

543
Q

dehydration is a concern for morbidity and mortality in children

A

< 5yrs of age

544
Q

___ is generated in the process of metabolism

A

H2O

heat regulation requires H2O
solute excretion requires H2O

545
Q

Metabolic rate (kcals/day) approximates _______

A

fluid requirements (mL/day)

546
Q

Holliday segar method for calculating maintenance fluid requirements for 24 hr period in children

A

2-10kg: 100ml/kg

11-20kg: 1,000mL + 50ml/kg for each kg between 11 and 20kg

21-70kg: 1,500mL + 20ml/kg for each kg between 21 and 70 kg

calculate the total volume for 24 hrs and then divide by 24

547
Q

4-2-1 method

A

first 10 kg: 4 mL of fluid per kg (ie) 4 kg pt = 4kg x 4 mL = 16ml/Hr)

for second 10kg- 2mL/kg

each kg over 20kg, 1 mL/hr given

548
Q

BSA maintenance fluids calculation

A

Square root of kgxcm/3600

maintenance fluids calculation using BSA = 1,500-2000 mL/m2/day

549
Q

the proper balance between water and electrolytes

A

hydration

550
Q

conditions that alter maintenance fluid requirements

A

fever

tachypnea

hyperpnea

postop state

increased physical activity

diarrheal illness

altered kidney function (anuria, polyuria)

very low birth weigh infants: decreased skin integrity - surface area to weight ratio_

burns

trauma

excessive sweating

Endocrine disorders (SIADH, DI, Hyperthyroidism)

551
Q

___ and ____ are involved in the dehydration and rehydration process

A

fluid and electrolytes

552
Q

in dehydration what can usually explain changing lab values in many cases

A

shifts from intracellular to extracellular

553
Q

_____ is released in response to the renin-angiotensin-aldosterone release in cases of extracellular volume depletion

A

Aldosterone

554
Q

______ is released in response to volume depletion, which results in decreased urine output and increased absorption of water by kidneys

A

Antidiuretic hormone (ADH)

555
Q

hydration status more common in young children and has classic components on physical exam

  • mental status
  • HR
  • presence of tears
  • skin condition
  • cap refill
  • blood pressure
  • UOP

Hydration can be classified based on serum sodium levels

A

dehydration

556
Q

Serum Sodium 130-150

A

isotonic dehydration

557
Q

serum sodium <130

A

Hypotonic/hyponatremic dehydration

558
Q

serum sodium >150

A

Hypertonic/hypernatremic dehydration

559
Q

time frame to restore intracellular and extracellular water and electrolyte deficits in hyponatremic and isonatremic dehydration

A

24 hours

560
Q

time frame to restore intracellular and extracellular water and electrolyte deficits in hypernatremic dehydration

A

48 hours

561
Q

infants can develop _____ from incorrect mixing of formula with too much water

A

hyponatremia

562
Q

formula to calculate volume of fluid to replace

A

current weight x 1,000 x %dehydration = volume of fluid to replace

563
Q

the most precise method of determining fluid deficit is

A

weight loss, however not typical to have recent pre-illness weight results

564
Q

Fluid deficit calculation

A

fluid deficit = pre-illness weight - illness weight

% dehydration = (pre-illness weight-illness weight) all divided by illness weight and x 100%

once fluid deficit is calculated, subtract boluses and then calculate hourly

565
Q

oral rehydration fluids should have goal of replacing deficit volume over

A

4-6 hours, then to replace ongoing losses

566
Q

IV fluid replacement in isotonic and hyponatremic dehydration

A

replace half of the deficit plus 1/3 of the maintenance over 8 hours

then the remaining half of the deficit and 2/3 of the maintenance over the next 16 hours

or replace the whole deficit over 8 hours then the whole day’s maintenance over 16 hours

567
Q

IV fluid replacement in hypernatremic dehydration

A

combine the total volume deficit plus the maintenance volume for 48 hours; administer this total volume divided over 48 hours.

Prevents osmotic fluid shifts resulting in cerebral edema and seizures. Ensure serum sodium level is not corrected by ?10meq/l/d

568
Q

calculation of insensible loss

A

300mL x BSA = approx insensible loss for 24 hours. Divide by 24 to get the hrly rate of insensible loss

569
Q

daily electrolyte replacement

A

Sodium: 2-3 mEq/100mL fluid

Potassium: 2mEq/100mL fluid

chloride: 5-6 mEq/100mL fluid

570
Q

calculation for sodium deficit

A

Na deficit = (135-measured Na) x 100/L

571
Q

It is difficult to assess ____ electrolyte deficit as its mainly intracellular and shifts based on catabolism, cell-injury and acid base balance

A

Potassium

estimated that 1meq/L = 10-30% total body potassium loss

572
Q 
component of multisystem body functions
-neuronal activity
muscular contraction
myocardial contraction
hemocoagulation
bone formation
A

Calcium

573
Q

Calcium is present in 3 forms in plasma

A

bound to albumin (plasma protein)
diffusible (calcium citrate or phosphate)
unbound ion

574
Q

____ calcium is the form most important for body functions

A

ionized

575
Q

calcium concentrations is regulated by what systems

A

renal
skeletal
GI

576
Q

serum calcium <9

ionized Calcium <1.1

A

hypocalcemia

577
Q

serum calcium >10

A

hypercalcemia

578
Q

ethylene glycol ingestion can lead to

A

hypocalcemia

579
Q

PRBC transfusion can lead to

A

hypocalcemia _ binding of ionized calcium to citrate after transfusion

580
Q

malabsorption and hypoparathyroidism can lead to

A

hypocalcemia

581
Q

renal failure can lead to

A

hypocalcemia

582
Q 
rhabdomyolysis
sepsis
tumor lysis syndrome
pancreatitis
can lead to,,,
A

hypocalcemia

583
Q

what medication can lead to hypocalcemia

A

furosemide

584
Q

What syndrome is connected to hypercalcemia

A

Williams syndreome

585
Q

what electrolyte disorder is associated with malignancy, sarcoidosis

A

Hypercalcemia

586
Q

what medication can lead to hypercalcemia

A

excessive Vitamins A and D

Thiazide diuretics

587
Q

what electrolyte abnormalities associated with hyperphosphatemia and hypomagnesemia

A

hypocalcemia

588
Q

risk of hypocalcemia in neonates

A

increased due to decreased calcium intake
increased fetal calcium levels leading to transient parathyroid suppression
PTH resistance

589
Q

Can include neuromuscular irritability, Chvostek sign, confusion, irritability, laryngospasm, muscle cramps, numbness and tingling, parasthesias and weakness, seizures, tetany, and Trousseau sign.

ECG changes include sinus tachycardia, long QT interval, and AV blocks. • Evidence of myocardial irritability with severe hypocalcemia can include hypotension and bradycardia.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 716). Wolters Kluwer Health. Kindle Edition.

A

Hypocalcemia

590
Q

can be asymptomatic

severe ->nausea, anorexia, constipation, neurologic signs such as anxiety, depression, headache, lethargy, hypotonia, seizures, and coma. Cardiac arrhythmias include shortened QT interval, sinus bradycardia, first-degree heart block, and ventricular tachycardia.

can lead to polyuria, renal calculi and renal tubular dysfunction

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 716-717). Wolters Kluwer Health. Kindle Edition.

A

hypercalcemia

591
Q

hypocalcemia workup

A

total serum calcium

ionized calcium

CMP

PTH

pH

25-hydroxy vit D

1, 25-dihydroxy vitamin D

urine calcium, phosphate, creatinine

xray of ankle and wrist for bone density

Chest x ray -looking for thymus

ECG

592
Q

Hypercalcemia workup

A

total serum calcium

ionized calcium

CMP

PTH

pH

25-hydroxy vit D

1, 25-dihydroxy vitamin D

urine electrolytes

PTH related protein level if suspected malignancy

ECG

Abd radiographs - KUB or renal US to look for calculi

593
Q

treatment for hypocalcemia

A

10-20mg/kg/dose calcium chloride (only give through central venous catheter)

Calcium gluconate (100mg/kg/dose) given through either peripheral or CVC

594
Q

treatment for chronic hypocalcemia

A

enteral supplements such as calcium carbonate, citrate, calcium gluconate, glubionate, lactate, along with vit d supplements and 1, 25 dihydroxy vitamin D fo rpt unable to convert vit d

595
Q

Hypercalcemia treamtent

A

hydrate with NS (2-3 xs maintenance rate)
-Hypercalcemia may cause increased UOP results in dehydration

-Loop diuretics - helps excrete calcium
(no thiazides - preserves calcium)

Glucocorticoids - reduce effects and level vit D

only calcitonin for rapid correction of calcium or if hypercalcemia is refractory to hydration and diuresis

Bisphosphonates for rapid treatment of severe hyperphsophatemia

if severe or refractory- hemodialysis may be needed

596
Q

Hypomagnesemia may lead to

A

hypocalcemia

597
Q

If hypocalcemia is refractory, replace

A

magnesium

598
Q

Correct severe hyperphosphatemia prior to correction of related ______ to avoid soft tissue calcification

A

hypocalcemia

599
Q

the major role of ______ is to maintain electrical neutrality by balancing cations (usually sodium) in the blood

A

chloride

600
Q

regulates acid base balance in body due to inverse relationship with bicarbonate

A

Chloride

601
Q

serum chloride normal

A

97-108

602
Q

serum chloride <97

A

hypochloremia

603
Q

serum chloride >108

A

hyperchloremia

604
Q

metabolic alkalosis contributes to ____chloremia

A

hypochloremia

605
Q

electrolyte imbalance associated with Bartter syndrome

A

Hypochloremia

606
Q 
electrolyte imbalance associated with Cystic fibrosis
bulimia nervosa
diuretic usage
Removal of gastric secretions by ng tube
permissive hypercapnia
A

hypochloremia

607
Q 
electrolyte imbalance associated with 
diarrhea
excessive chloride administration
metabolic acidosis
Renal tubular acidosis
urinary diversion into colon or ileum
A

hyperchloremia

608
Q

passively follows renal sodium reabsorption and passively follows sodium absorption in GI tract

A

Chloride

609
Q

When associated with metabolic alkalosis, may exhibit arrhythmias, decreased respiratory effort, seizures in severe states. •

When associated with volume depletion or dehydration, may exhibit thirst, lethargy, tachycardia, tachypnea, and delayed capillary refill.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 719-720). Wolters Kluwer Health. Kindle Edition.

A

Hypochloremia.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 719). Wolters Kluwer Health. Kindle Edition.

610
Q

Often does not result in any symptoms. • May exhibit Kussmaul respirations (especially in diabetes ketoacidosis); possible neurologic symptoms include lethargy, headache, and confusion. • Altered cardiac function and response to inotropes. • Associated with hypernatremia and hyperkalemia.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 720). Wolters Kluwer Health. Kindle Edition.

A

Hyperchloremia.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 720). Wolters Kluwer Health. Kindle Edition.

611
Q

diagnostics for hypochloremia

A

• Serum electrolyte evaluation and serum pH. •

Urine chloride and sodium.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 720). Wolters Kluwer Health. Kindle Edition.

612
Q

treatment of hypochloremia

A

First address known causes, including fluid resuscitation, and add potassium-sparing diuretics or acetazolamide to reduce reabsorption of bicarbonate. •Chloride repletion: can be replaced with sodium, potassium, and ammonium chloride compositions. Arginine chloride or hydrochloric acid can be used for severe hypochloremia-related seizures, arrhythmias, or respiratory depression.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 720). Wolters Kluwer Health. Kindle Edition.

613
Q

treatment for hyperchloremia

A

Address underlying cause and treat associated acidosis. • Consider sodium bicarbonate IV if severe metabolic acidosis.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 720). Wolters Kluwer Health. Kindle Edition.

614
Q

chloride has a direct relationship with

A

sodium

615
Q

chloride has a inverse relationship with

A

bicarbonate

616
Q

about 50% of magnesium stores are contained

A

in bone

617
Q

magnesium is primarily excreted and regulated in the

A

kidney

618
Q

normal mag levels

A

1.7-2.2

619
Q

GI causes of hypomagnesemia

A

GI losses with diarrhea, vomiting, steatorrhea, refeeding syndrome, pancreatitis.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 721). Wolters Kluwer Health. Kindle Edition.

620
Q

diseases and syndromes associated with hypomagnesemia

A

Celiac disease, cystic fibrosis, inflammatory bowel disease, and short gut syndrome.

Bartter and Gitelman syndromes, autosomal dominant hypoparathyroidism, and mitochondrial hypomagnesemia.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 721). Wolters Kluwer Health. Kindle Edition.

621
Q

renal causes of hypomagnesemia

A

hypercalcemia, chemotherapy, chronic adrenergic stimulants, diuretic use, hypercalciuria, nephrocalcinosis, and RTA.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 721). Wolters Kluwer Health. Kindle Edition.

622
Q

Medication causes of hypomagnesemia

A

amphotericin, cisplatin, loop and osmotic diuretics.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 721-722). Wolters Kluwer Health. Kindle Edition.

623
Q

endocrine causes of hypomagnesemia

A

diabetes mellitus, diabetic ketoacidosis (DKA), excessive bone uptake after parathyroidectomy, hyperaldosteronism, and PTH disorders.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 722). Wolters Kluwer Health. Kindle Edition.

624
Q

causes of hypermagnesemia

A

Excessive intake, including magnesium-containing laxatives or antacids, total parenteral nutrition, maternal magnesium therapy in neonates. • Altered renal function, renal failure, tumor lysis syndrome, milk alkali syndrome, and lithium ingestion.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 722). Wolters Kluwer Health. Kindle Edition.

625
Q

neonates may experience transient hypomagnesemia or develop idiopathic hypomagnesemia associated with

A

maternal magnesium depletion

626
Q

GI symptoms of hypomagnesemia

A

anorexia
nausea
vomiting

627
Q

Neuro symptoms of hypomagnesemia

A

depression, malaise, nonspecific psychiatric symptoms, hyperreflexia, seizures, paresthesias, ataxia, tetany, decreased deep tendon reflexes, weakness, paralysis, muscle weakness, delirium, carpopedal spasm, and clonus.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 722). Wolters Kluwer Health. Kindle Edition.

628
Q

Cardiac symptoms of hypomagnesemia

A

ECG changes - atrial or ventricular ectopy, torsades de pointes and long QT interval

629
Q

endocrine symptoms of hypomagnesemia

A

Hyperglycemia can occur if hypomagnesemia is related to insulin resistance.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 722). Wolters Kluwer Health. Kindle Edition.

630
Q

Neuro s/s of hypermagnesemia

A

impairment of the neuromuscular junction; hypotonia, decreased deep tendon reflexes, weakness, paralysis, CNS depression, lethargy, and confusion.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 723). Wolters Kluwer Health. Kindle Edition.

631
Q

cardiac s/s hypermagnesemia

A

altered vascular tone, hypotension, flushing, possible ECG changes (prolonged PR, QRS, or QT intervals), heart block.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 723). Wolters Kluwer Health. Kindle Edition.

632
Q

GI s/s hypermagnesemia

A

abdominal cramping, nausea, and vomiting.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 723). Wolters Kluwer Health. Kindle Edition.

633
Q

resp symptoms hypermag

A

resp failure

634
Q

hypo mag workup

A

serum laboratory studies; basic metabolic panel with magnesium and ionized calcium; ECG and arrhythmia monitoring.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 723). Wolters Kluwer Health. Kindle Edition.

635
Q

hyper mag workup

A

serum laboratory studies; basic metabolic panel with magnesium and ionized calcium; ECG and arrhythmia monitoring.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 723). Wolters Kluwer Health. Kindle Edition.

636
Q

management of hypomagnesemia

A

• Severe, acute management. • Magnesium sulfate or magnesium chloride. •

Consider potassium repletion, particularly if refractory. •

Mild, subacute management. • Magnesium gluconate, oxide, or sulfate.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 723). Wolters Kluwer Health. Kindle Edition.

637
Q

management of hypermagnesemia

A

Cessation of magnesium intake. • Monitoring of renal function and support of cardiovascular and respiratory function. • Parenteral calcium supplements (calcium chloride or calcium gluconate) for heart block. •Removal of magnesium with volume expansion, forced diuresis, loop diuretics, dialysis if life-threatening or exchange transfusion if life-threatening and unable to perform dialysis.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 723). Wolters Kluwer Health. Kindle Edition.

638
Q

hypomagnesemia may result in refractory

A

hypokalemia

639
Q

A rapid increase in serum mag r/t rapid bolus may cause

A

increased mag excretion -> give it slow

640
Q

if torsades de pointes on ECG, give

A

magnesium

641
Q

phosphorous absorbed through

A

jejunum

642
Q

phosphorous excreted through

A

kidneys

643
Q

normal phosphorous

A

2.5-4.1

644
Q

what vit def can cause hypophosphatemia

A

Vit D def and Vitamin D-resistant rickets

645
Q

causes of hypophosphatemia

A

Malnutrition or starvation situations such as protein energy malnutrition or malabsorption, respiratory or metabolic alkalosis. • DKA treatment without adequate repletion. • Corticosteroid use. • Renal tubular defects or diuretic use. • Vitamin D deficiency and vitamin D-resistant rickets. • Reduced intake/supplementation in very low-birth-weight infants. • Chronic use of aluminum-containing antacids. • Tumor-induced osteomalacia resulting in renal phosphorus wasting. • Extensive burns. • Hyperparathyroidism.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 724-725). Wolters Kluwer Health. Kindle Edition.

646
Q

causes of hyperphosphatemia

A

Excessive administration or intake. • Tumor lysis syndrome. • Hypoparathyroidism. • Rhabdomyolysis. • Renal failure when decreased glomerular filtration rate <25% or smaller glomerular filtration rate reductions in neonates. Pathophysiology

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 725). Wolters Kluwer Health. Kindle Edition.

647
Q

A sudden increase in serum phosphorus may result in precipitation of

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 725). Wolters Kluwer Health. Kindle Edition.

A

calcium, thus resulting in symptoms of hypocalcemia such as tetany.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 725). Wolters Kluwer Health. Kindle Edition.

648
Q

s/s hypophosphatemia

A

Neurologic signs of confusion, irritability, coma, muscle weakness, paresthesias, seizures, and apnea in very low-birth-weight infants. • Hemolytic anemia. • Hypoxia. • Impaired granulocyte activity. • Thrombocytopenia. • Rhabdomyolysis. • Myocardial depression. • Rickets.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 725-726). Wolters Kluwer Health. Kindle Edition.

649
Q

s/s hyperphosphatemia

A

Altered mental status, seizures. • Tetany, weakness, paresthesias. • Fatigue. • Cramping. • Laryngospasm. • Neuromuscular irritability. • Cardiac arrhythmias. • Chronic hyperphosphatemia may result in calcium deposits in soft tissue.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 726). Wolters Kluwer Health. Kindle Edition.

650
Q

diagnostic hypophosphatemia

A

Serum: basic metabolic panel, phosphorous, magnesium and ionized calcium, vitamin D levels, and PTH. • Urine: calcium, phosphorous, creatinine, pH.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 726). Wolters Kluwer Health. Kindle Edition.

651
Q

diagnostic hyperphosphatemia

A

• Serum: basic metabolic panel, ionized calcium, phosphorous and magnesium, PTH, vitamin D, complete blood count, and arterial blood gas. • Urine: calcium, phosphorous, creatinine.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 726). Wolters Kluwer Health. Kindle Edition.

652
Q

treatment for hypophosphatemia

A

Acute. • Parenteral repletion is indicated with potassium or sodium phosphate. • Subacute or gradual onset of symptoms. • Replace with potassium or sodium phosphate enteral supplements.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 726). Wolters Kluwer Health. Kindle Edition.

653
Q

treatment for hyperphosphatemia

A

restrict dietary intake of phosphorus (protein restriction). • Phosphate binders which include sevelamer hydrochloride, lanthanum carbonate, calcium carbonate, or aluminum hydroxide. • If cell lysis with normal renal function, forced diuresis with NS and osmotic diuretic such as mannitol. • Consider dialysis if severe and underlying poor renal function; dialysis may be of limited effectiveness.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 726-727). Wolters Kluwer Health. Kindle Edition.

654
Q

risk of calcium-phosphorous precipitation particularly with

A

tumor lysis syndrome or renal failure

655
Q

______ is important in potassium regulation by the kidney

A

aldosterone

656
Q

Serum potassium normal

A

3.7-5.2

657
Q

medications that can cause hypokalemia

A

amphotericin B, decongestants, diuretics, dopamine, dobutamine, and bronchodilators.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 728). Wolters Kluwer Health. Kindle Edition.

658
Q

causes of hypokalemia

A

Medications: amphotericin B, decongestants, diuretics, dopamine, dobutamine, and bronchodilators. • Anorexia nervosa. • Bartter and Cushing syndromes. • Fanconi, Liddle, and Gitelman syndromes. • Hematologic: leukemia. • GI: diarrhea, use of laxatives and enemas, and vomiting. • Endocrine causes: DKA, hyperaldosteronism, increased insulin levels, and excess mineralocorticoid. • Renal: increased renin levels, renovascular disease, metabolic alkalosis, and type I RTA. • Magnesium depletion and malnutrition.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 728). Wolters Kluwer Health. Kindle Edition.

659
Q

causes of hyperkalemia

A

Acidosis, acute increase in serum osmolarity. • Addison disease, aldosterone insensitivity, hypoaldosteronism, pseudohypoaldosteronism, and associated aldosterone resistance. • Medications: angiotensin II receptor blockers, ACE inhibitors, theophylline, and nonsteroidal anti-inflammatory drugs. • Congenital adrenal hyperplasia. • Trauma: crush injury. • Excess supplementation. • Rhabdomyolysis. • Tumor lysis syndrome. • Renal impairment or RTA. • Spitzer–Weinstein syndrome. •Technical problems in obtaining a blood sample can result in hyperkalemia if the blood is hemolyzed, if there is existing thrombocytosis, or leukocytosis at the time of serum sample, or if the child has received blood that has been stored for a long time.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 728-729). Wolters Kluwer Health. Kindle Edition.

660
Q

s/s hypokalemia

A

Often, no symptoms. • Diastolic dysfunction, hypertension, or ventricular arrhythmias in patients with heart disease, heart failure, or left ventricular hypertrophy. •ECG changes can include delayed depolarization, flat or absent T waves, long QT, prolonged QRS, ST changes, and the presence of U waves. • Cramping. • Decreased perfusion. • Fatigue. • Ileus. • Impaired insulin release. • Impaired muscle contraction, paralysis. • Polyuria.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 729). Wolters Kluwer Health. Kindle Edition.

661
Q

s/s hyperkalemia

A

ECG changes: most commonly peaked T waves, low-voltage P waves, prolonged PR and QRS interval, ST changes, AV block, ventricular tachycardia and fibrillation, loss of PR interval, merging of QRS, and T waves to produce a sine wave pattern, asystole. • Neurologic: muscle weakness, paresthesias, and tetany with severe hyperkalemia (≥9 mEq/L).

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 729-730). Wolters Kluwer Health. Kindle Edition.

662
Q

diagnostics hypokalemia

A

• Serum: basic metabolic panel with magnesium, creatine kinase, renin, pH, and cortisol levels. • Urine studies: urinalysis, electrolytes, osmolality, and urine 17-ketosteroids. • ECG.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 730). Wolters Kluwer Health. Kindle Edition.

663
Q

diagnostics hyperkalemia

A

Serum: basic metabolic panel with magnesium, creatine kinase, renin, pH, and cortisol levels. • Urine studies: urinalysis, electrolytes, osmolality, and urine 17-ketosteroids. • ECG.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 730). Wolters Kluwer Health. Kindle Edition.

664
Q

treatment of hypokalemia

A

• Identification of cause. • Potassium repletion. • Acute, risk for arrhythmia. • Calculate electrolyte deficiency to minimize risk of hyperkalemia with treatment. • Potassium chloride 0.5 to 1 mEq/kg/dose IV; maximum 20 mEq/dose; central administration is preferred and cardiac monitoring required. • Subacute, chronic repletion. • Potassium chloride, phosphate, or bicarbonate enteral supplement, based on etiology.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 730). Wolters Kluwer Health. Kindle Edition.

665
Q

treatment for hyperkalemia

A

• Evaluate for accuracy of the laboratory sample (may be falsely elevated with hemolysis, thrombocytosis, or leukocytosis). • Remove all exogenous potassium sources. • Hyperkalemia with ECG changes. • Administer calcium chloride or calcium gluconate IV for membrane stabilization. • Administer IV insulin and glucose (e.g., D25 or D50), IV sodium bicarbonate, inhaled β-agonists (e.g., albuterol); all temporarily shifts potassium intracellularly. • Diuretics, if normal renal function (results in potassium removal). • Cation exchange resin, such as sodium polystyrene sulfonate (exchanges potassium for sodium in the GI tract, resulting in potassium removal).

dialysis

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 730-731). Wolters Kluwer Health. Kindle Edition.

666
Q

Potassium should be interpreted in relation to the serum pH. Why

A

bc it shifts intracellularly with alkalosis and extracellularly with acidosis

667
Q

Severe ___kalemia is a medical emergency

A

hyperkalemia >7

668
Q

normal Na

A

135-145

669
Q

hypervolemic hyponatremia is caused by

A

• Congestive heart failure. • Renal failure. • Nephrotic syndrome. • Water intoxication. • Cirrhosis.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 732). Wolters Kluwer Health. Kindle Edition.

670
Q

hypovolemic hyponatremia is caused by

A

Renal losses through osmotic diuresis or RTA. • Extrarenal losses through diarrhea, vomiting, burns, or pancreatitis.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 732). Wolters Kluwer Health. Kindle Edition.

671
Q

normovolemic hyponatremia is caused by

A

SIADH, adrenal insufficiency. • CNS diseases: cerebral salt wasting, meningitis, intracranial tumors. • Pulmonary disease: cystic fibrosis. • Diuretic use.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 732). Wolters Kluwer Health. Kindle Edition.

672
Q

• Rapid decrease in serum sodium level is associated with more severe symptoms. • Irritability, poor feeding, nausea, lethargy, seizures, coma, seizures. • Can lead to cerebral edema.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 734). Wolters Kluwer Health. Kindle Edition.

A

Acute hyponatremia

673
Q

Weakness, lethargy, decreased deep tendon reflexes, fever, high-pitched cry, irritability, muscle cramps, rhabdomyolysis, renal failure, respiratory failure, altered mental status, seizures.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 734). Wolters Kluwer Health. Kindle Edition.

A

acute hypernatremia

674
Q

workup for hypo/hypernatremia

A

Serum: sodium and osmolality. • Urine: sodium, specific gravity, and osmolality.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 734). Wolters Kluwer Health. Kindle Edition.

675
Q

treatment for hyponatremia

A

Identify and treat cause of hyponatremia. • Restore normal intravascular volume. • Replete sodium deficit. • Serum sodium correction must be done in a slow, controlled manner to avoid central pontine myelinolysis. • Goal rate of sodium rise is 2 to 4 mEq/L every 4 hours or 10 to 20 mEq/L in 24 hours. • If seizures are present, goal is to raise serum sodium acutely to 125 mEq/L for seizure cessation. • Hypertonic saline solution; NS bolus 20 mL/kg may be administered if hypertonic saline is not available. • Hypertonic saline is calculated based on this formula: mEq sodium to raise sodium to desired level. • 0.6 × (Weight in kg) × (target sodium − measured sodium).

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 734-735). Wolters Kluwer Health. Kindle Edition.

676
Q

Treatment for hypernatremia

A

•Avoid decreasing serum sodium more than 15 mEq/L in 24 hours to minimize risk for cerebral edema or no faster than 0.5 to 1.0 mEq/L/hour. • Therapy is guided by a combination of sodium level and serum osmolarity, and intravascular volume status. • Hypernatremic, hypovolemic dehydration. • Calculation of free-water deficit, solute fluid deficit, solute sodium deficit, solute potassium deficit, maintenance fluid requirements, and ongoing losses determines composition of IV fluids and rate of administration. • Hypernatremic, hypervolemic dehydration. • May require natriuretic agent for increased weight.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 735). Wolters Kluwer Health. Kindle Edition.

677
Q

reported sodium concentrations may be low in association with

A

hyperlipidemia
hyperproteinemia
hyperglycemia

678
Q

who is at a increased risk for hypernatremia and associated hypovolemic dehydration

A 
infants
small children
developmental delay hx
AMS
critical illness rendering them unable to respond to thirst mechanism
679
Q

a serum level of

A

<125

680
Q

hyperkalemia - what on ECG

A

peaked T waves

681
Q

ventricular arrhythmias, prominent u waves, ST segment depression

A

hypokalemia

682
Q

electrolyte imbalances that can cause seizures

A

Hyponatremia Hypernatremia Hypophosphatemia Hypochloremia Hypocalcemia Hypercalcemia

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 736). Wolters Kluwer Health. Kindle Edition.

683
Q

Ventricular ectopy, torsades de pointes

A

hypomagnesemia

684
Q

Hypotension

AV block

A

hypermagnesemia

685
Q

Long QT interval

AV block

A

hypocalcemia

686
Q

electrolyte abnormality associated with eating disorders

A

chloride responsive metabolic alkalosis and significant hypophosphatemia

687
Q

eating disorders carry risk for cardiac arrhythmias due to electrolyte abnomalities

A

abnormalities: depletion of total body potassium, hypomagnesemia, serum hypophosphatemia, and altered acid–base balance.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 737). Wolters Kluwer Health. Kindle Edition.

688
Q

evaluating degree of malnutrition in eating disorders

A

serum complete metabolic panel, carotene levels, zinc, copper, prealbumin, amylase and lipase, cholesterol, and liver function tests.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 738). Wolters Kluwer Health. Kindle Edition.

689
Q

analysis for fluid and electrolyte evaluation

A

BMP or CMP

690
Q

indicate dehydration but not predictive alone

A

BUN

691
Q

serum bicarb levels of ____, along with clinical findings of moderate to severe dehydration

A

<17

692
Q

serum bicarb levels of ____, associated with high risk of failing oral rehydration therapy

A

<13

693
Q

normal chloride levels

A

98-108

694
Q

normal k

A

3.5-4.5

695
Q

what does CMP include

A

electrolytes - sodium, potassium, chloride, carbon dioxide, BUN, creatinine, magnesium, phosphorous, LFTs (AST or SGOT and SLT or SGPT), bilirubin level, serum total protein and alkaline phosphatase

696
Q

pH of < ____ with normal PCO2 and normal or low bicarbonate may indicate dehydration

A

7.35

697
Q

Urinalysis: dark color, high specific gravity and presence of ketones can indicate

A

dehydration

698
Q

urine electrolytes: if Na+ is low, kidneys may

A

be conserving sodium due to dehydration

699
Q

fractional excretion of sodium assists in differentiating

A

between dehydration and poor kidney function

700
Q

What would a CBC show in dehydreation

A

elevated RBC, WBC or both

701
Q

most metabolic disorders are inherited as

A

autosomal recessive traits

702
Q

a group of disorders that result in abnormalities in the synthesis or catabolism of proteins, carbohydrates, or fats.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 753). Wolters Kluwer Health. Kindle Edition.

A

Genetic metabolic disorders

703
Q

Acute finding vs chronic findings of inborn errors of metabolism

Seizures/lethargy/coma

A

Hypotonia

704
Q

Acute finding vs chronic findings of inborn errors of metabolism

Poor feeding/vomiting

A

FTT

705
Q

Acute finding vs chronic findings of inborn errors of metabolism

Hypoglycemia

A

Recurrent unexplained illnesses

706
Q

Acute finding vs chronic findings of inborn errors of metabolism

Signs of sepsis

A

Developmental delay/loss of milestones

707
Q

Acute finding vs chronic findings of inborn errors of metabolism

Hyperammonemia

A

Cardiomegaly

708
Q

Acute finding vs chronic findings of inborn errors of metabolism

ketosis

A

macro/microcephaly

709
Q

Acute finding vs chronic findings of inborn errors of metabolism

Metabolic/lactic acidosis

A

Eyes/hair/skin abnormalities

710
Q

Acute finding vs chronic findings of inborn errors of metabolism

abnormal urine odor

A

“course” appearance”

711
Q

Urine odors associated with IEM

Maple Syrup

A

Maple syrup urine disease

712
Q

Urine odors associated with IEM

Musty

A

Phenylketonuria

713
Q

Urine odors associated with IEM

sweaty feet

A

Isovaleric/Glutaric acidemia

714
Q

Urine odors associated with IEM

Boiled cabbage

A

Tyrosinemia

715
Q

Urine odors associated with IEM

Fishy

A

Trimethylaminuria

716
Q

Metabolic labs

what do you grab first when you have a suspicion

if anything is positive then what do you snag

A 
CBC
Blood gas
Serum glucose (looking for hypoglycemia)
Serum electrolyte panel (look at anion gap)
Liver function tests 
Ammonia (look for hyperammonemia)
Urinalysis
Urine pH
urine color and specific gravity
odor
urine ketones

then
Plasma amino acids
Acylcarnitine profile
lactate

urine amino acids
urine organic acids
urine reducing substances

717
Q

what tests can be done for glucocorticoid excess

A

24 hr urinary free cortisol

midnight salivary or plasma cortisol

overnight low dose dexamethasone suppression test

718
Q

tests for adrenal insufficiency

A

8AM plasma cortisol and ACTH concentration

Low dose ACTH stim test

High dose stim test

Metyrapone test

Serum renin level

Aldosterone level

719
Q

Test for congenital Adrenal hyperplasia

A

High dose ACTH stim test
17-hydroxyprogestrone

Cyp21 analysis

720
Q

tests for calcium homeostasis

A

Total calcium

ionized calcium

parathyroid hormone

PTH-related protein

Urine Calcium: Creatinine ratio

721
Q

Test for Vit D status

A

25-OH

1-25 (OH) 2D

722
Q

Markers of bone turnover

A

Osteocalcin

bone specific alkaline phosphatase

N-telopeptides

723
Q

tests for water homeostasis

A

serum and urine osmolality

urine sp. gravity

water deprivation test

vasopressin challenge

serum vasopressin levels

724
Q

tests for autoimmune thyroid disease

A

TSH

Thyroid receptor antibody (TRAb)

Antithyroglobulin (ATG)

Thyroid peroxidase antibodies (TPO)

725
Q

from 2 years of age until puberty approx __ -___cm linear growth/year is considered normal

A

4-5

726
Q

mid-parental height calculation: Target height

A

male: {paternal height +maternal height}/2 +5cm

females same just minus 5 cm

727
Q

if I want to look at ambiguous genitalia what radiographic study?

A

US

728
Q

if I want to look at thyroid nodules what radiographic study?

A

US

729
Q

if I want to look at pituitary tumors what radiographic study?

A

CT or MRI

730
Q

if I want to look at osteoporosis or osteomalacia what radiographic study?

A

Plain film or DEXA scan

731
Q

tanner staging male

early adolescence (10.5-14 yrs)
no pubic hair
preadolescent penis
prepubescent testes

A

Tanner 1

732
Q

tanner staging male

early adolescence (10.5-14 yrs)
scanty pubic hair
penis - slightly increased in size
enlarging testes

A

Tanner 2

733
Q

tanner staging male

middle adolescence (12.5-15 yrs)
pubic hair - darker with curls
longer penis
larger testes

A

Tanner 3

734
Q

tanner staging male

middle adolescence (12.5-15 yrs)
pubic hair - course and curly
larger penis
scrotum darkens

A

Tanner 4

735
Q

tanner staging male

late adolescence (14-16 yrs)
pubic hair - adult
adult penis
scrotum adult

A

Tanner 5

736
Q

tanner staging female

early adolescence (10-13 yrs)
preadolescent pubic hair 
preadolescent breasts
A

Tanner 1

737
Q

tanner staging female

early adolescence (10-13 yrs)
sparse, straight pubic hair
small mound breasts

A

Tanner 2

738
Q

tanner staging female

middle adolescence (12-14 yrs)
dark curls pubic hair
breasts - larger with no overt contour separation

A

tanner 3

739
Q

tanner staging female

middle adolescence (12-14 yrs)
course and curly pubic hair
breasts - secondary mound of areola

A

tanner 4

740
Q

tanner staging female

late adolescence (14-17 yrs)
pubic hair adult triangle shape appearance
breasts - Nipple projects, areola becomes a part of the breast

A

tanner 5

741
Q

what type of AI is a result of a destroyed or inactive adrenal gland or hormone production failure

A

Primary AI

742
Q

in infancy, what is the most common cause of primary AI

A

CAH

743
Q

what type of AI is associated with a deficiency of ACTH

A

Secondary AI

744
Q

hypothalamic decrease in CRH secretion or production is what type of AI

A

Secondary AI

hypopituitarism secondary to primary pituitary disease, congenital pituitary lesions and developmental anomalies (ancephaly, holoprosencephaly, and craniopharyngiomas are the causes of ACTH deficiency).

745
Q

what are the most common reason for ACTH deficiency in childhood

A

Craniopharyngiomas

Secondary AI

746
Q

hypothalamic decrease in CRH secretion or production falls under what type of AI

most often from suppression of the HPA axis from prolonged use of glucocorticoids

A

Tertiary AI

747
Q

drugs that associated with tertiary AI

A

Glucocorticoids
spironolactone
etomidate
ketoconazole

748
Q

HPA axis may not return to normal for up to how long after long term steroid treatment

A

more than 1 month

749
Q

what type of AI is experienced to some degree by every critically ill pt

A

relative AI

750
Q

If a child is responsive to fluids in shock, what is their AI status

A

absent

751
Q

explain neonatal adrenal insufficiency

A

infant HPA axis is immature

further limit infants ability to increase cortisol production in response to stress

752
Q

cortisol level that suggests AI

A

<16 ug/dl or <440 nmol/L

Critical Care I (27 decks)

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