Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

> =10kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

formula for maintenance fluid needs BSA

normal vs critical

A

1600ml/m2/day

if critically ill
1200mL/m2/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Basic insensible fluid loses estimation

A

400ml/m2/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

name that dehydration

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

A

Hypernatremic dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

most common type of dehydration

A

isotonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

isotonic dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what type of osmolality is

1/2 NS

A

Hypotonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what type of osmolality is

1/4 NS

A

Hypotonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what type of osmolality is

3% NS

A

Hypertonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what type of osmolality is

Albumin 5%

A

Colloid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what type of osmolality is NS

A

Isotonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what type of osmolality is LR

A

Isotonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what does LR contain that NS does not

A

K

HCO3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

normal Na

A

135-145

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Sodium is key to what mentioned functions

A

skeletal muscle function

nerve and myocardial action potentials

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Hypervolemia
Hypovolemia
Normovolemic

Congestive Heart failure puts you at risk for what?

A

Hypervolemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Hypervolemia
Hypovolemia
Normovolemic

renal failure puts you at risk for what?

A

Hypervolemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Hypervolemia
Hypovolemia
Normovolemic

Nephrotic syndrome puts you at risk for what?

A

Hypervolemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Hypervolemia
Hypovolemia
Normovolemic

Water Intoxication puts you at risk for what?

A

Hypervolemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Hypervolemia Hypovolemia Normovolemic Diarrhea puts you at risk for what?
Hypovolemia
26
Hypervolemia Hypovolemia Normovolemic Renal Losses puts you at risk for what?
Hypovolemia
27
Hypervolemia Hypovolemia Normovolemic diuretics puts you at risk for what?
Hypovolemia
28
Hypervolemia Hypovolemia Normovolemic cerebral salt wasting may put you in what fluid status?
Normovolemic low sodium levels
29
Hypervolemia Hypovolemia Normovolemic Meningitis may put you in what fluid status?
Normovolemic low sodium levels
30
Hypervolemia Hypovolemia Normovolemic Burns puts you at risk for what?
Hypovolemic
31
Acute Hyponatremia symptoms
Nausea lethargy seizures coma can lead to neurological consequences
32
In acute hyponatremia the symptoms are _______
more severe
33
how to diagnose hyponatremia
check serum Na and osmols urine studies if unsure of cause
34
How to treat Hyponatremia
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.
35
formula for Na treatment
0.6x(weight in kg) x (target Na - measured current Na) = ____mEq of Na needed
36
3% hypertonic has how much Na per L
513mEq Na per L
37
Causes mentioned of Hypernatremia
Breastfeeding failure (baby not getting enough) Severe Diarrhea Diabetes Insipidus
38
presentation of hypernatremia
weakness lethargy decreased DTRs (deep tendon reflexes) irritability muscle cramps renal failure AMS Seizures
39
how to diagnose hypernatremia
serum Na levels | osmols
40
treatment for hypernatremia
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
41
Potassium is needed for ____ gradients and important for
transmembrane voltage gradients important for muscle and nerve cells important with acid base balance
42
primary route of excretion for potassium is
kidneys
43
normal potassium
3.5-5.2
44
EKG changes with hyperkalemia
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
45
acidosis causes K to
rise
46
alkalosis causes k to
drop
47
DKA patients come in acidotic....when do you add k
your first bags usually don't have K but then you add it in later
48
causes of Hyperkalemia
Acute or chronic renal failure Tissue injuries ( crush injuries) hemolysis Acidosis Medications (Spironolactone, Bactrim, ACE inhibitors)
49
what medications cause hyperkalemia
spironolactone Bactrim ACE inhibitors
50
Treatment for Hyperkalemia
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
51
Hypokalemia symptoms
can by asymptomatic Diastolic dysfunction ECG changes Cramping Fatigue ileus
52
ECG changes seen in Hypokalemia
flat or absent T waves long QT Prolonged QRS Presence of U-waves
53
diagnosis for hypokalemia
BMP with magnesium - magnesium and potassium work together Urine osmolality
54
Treatment for hypokalemia
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
55
where is magnesium mostly found
less than 1% of Mg is extracellular, much is stored in our bones
56
what is Mg used for
ATP generation, DNA transcription, Membrane stabilization, regulation of K excretion
57
what electrolyte works together with K
Magnesium
58
normal Mg levels
1.7-2.2 mg/dL
59
causes of hypomagnesemia
GI losses: diarrhea, vomiting, refeeding syndrome, pancreatitis IBD, Celiac disease, CF Renal: hypercalcemia, diuretic use, RTA Endocrine: DM, DKA, Hyperaldosteronism
60
Presentation of hypomagnesemia
Anorexia, nausea, vomiting Seizures, ataxia, hyperreflexia EKG changes: Torsades de pointes, long QT
61
Diagnostic eval for hypomagnesemia
Mg level iCal EKG
62
Management of hypomagnesemia
Repletion with Magnesium sulfate or chloride Consider K repletion (mag and K are buddies and go together)
63
Hypermagnesemia causes
excessive intake -mg containing laxatives, antacids Chronic renal failure tumor lysis
64
presentation for hypermagnesemia
hypotonia decreased reflexes hypotension flushing
65
diagnosing hypermagnesemia
Mg level
66
Management for hypermagnesemia
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
67
chloride has a direct relationship with
sodium
68
chloride has an inverse relationship with
bicarb
69
what can lead to hypochloremia
CF Bulimia Diuretics
70
high chloride and ph
acidosis
71
presentation of hypochloremia
rarely occurs by itself arrhythmias decreased resp effort seizures tachycardia
72
Treatment for hypochloremia
find cause replace with potassium, sodium or ammonium chloride or arginine chloride
73
hyperchloremia causes
diarrhea chloride administration metabolic acidosis
74
presentation of hyperchloremia
often no symptoms but have symptoms r/t acidosis such as: kussmaul respirations lethargy headache confusion
75
treatment for hyperchloremia
find underlying cause treat acidosis: can use sodium bicarb
76
when can you see hypophosphatemia
refeeding syndrome DKA severe resp alkalosis Vit D deficiency Burns
77
symptoms of hypophosphatemia
impaired energy utilization diaphragmatic/resp muscle weakness tissue hypoxia
78
treatment for hypophosphatemia
IV phos
79
Hyperphosphatemia causes
renal failure phosphate containing enemas tumor lysis syndrome
80
Treatment for hyperphosphatemia
phosphate binders mannitol diuresis
81
Calcium is present in how many different forms?
3 forms - Bound to albumin (plasma protein) - Diffusible (CaCitrate or CaPhoshate) - Unbound ion
82
what type of calcium is most important for body functions
ionized Ca
83
normal Ca
8.8-10.8
84
at risk for hypocalcemia
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
85
symptoms of hypocalcemia
``` neuromuscular irritability confusion muscle cramps numbness tingling ``` cardiac: prolonged QT, AV blocks, sinus tachy
86
diagnosing hypocalcemia
Ca level (total and iCal) CMP PTH EKG
87
Treatment for hypocalcemia
Calcium chloride (10-20mg/kg/dose) Calcium gluconate (100mg/kg/dose)
88
risk for hypercalcemia
Williams syndrome excessive intake immobility malignancy - cancer attacks the bones - the breakdown causes a calcium spike
89
presentation of hypercalcemia
``` nausea anorexia constipation lethargy headaches seizures arrhythmias ```
90
Diagnostic for Hypercalcemia
``` Total calcium iCal PTH pH EKG ```
91
Treatment for Hypercalcemia
Hydration loop diuretics for diuresis Calcitonin for rapid correction
92
what electrolyte imbalance is Williams syndrome at risk for?
Hypercalcemia
93
what electrolyte imbalance is DiGeorge syndrome at risk for?
Hypocalcemia
94
what electrolyte imbalances can cause seizures
Hypercalcemia Hypochloremia Hypomagnesemia Hyponatremia Hypernatremia
95
What electrolyte imbalances are you at risk for with DKA
Hypophosphatemia Hyperchloremia Hypomagnesemia
96
What electrolyte imbalances can cause EKG changes
Hypocalcemia Hypomagnesemia Hypokalemia Hyperkalemia
97
what electrolyte imbalances can cause arrhythmias
Hypochloremia Hypercalcemia
98
what electrolyte imbalances are associated with tumor lysis syndrome or cancer
Tumor lysis syndrome - hypocalcemia - hyperphosphatemia - hypermagnesemia Cancer when it attacks the bone - bone breaks down and releases Ca+ - Hypercalcemia
99
what electrolyte imbalances are you at risk for in renal impairment/failure
hyperphosphatemia hypermagnesemia hyperkalemia hypernatremia
100
What electrolyte imbalances associated with acidosis
hyperchloremia hyperphosphatemia hyperkalemia
101
what electrolyte imbalance is associated with loop diuretics
hypercalcemia
102
what electrolyte imbalance associated with diuretics
hypochloremia hypomagnesemia
103
what electrolyte imbalance associated with sepsis
hypocalcemia
104
What electrolyte imbalances associated with constipation
Hypercalcemia
105
what electrolyte imbalance associated with anorexia and nausea
hypercalcemia hypomagnesemia Nausea only -Hyponatremia
106
what electrolyte imbalance associated with acute diarrhea
hypernatremia
107
what electrolyte imbalance are you at risk for with PRBCs
hypocalcemia
108
what electrolyte imbalance associated with Ataxia
hypomagnesemia
109
what electrolyte imbalance associated with confusion, AMS
hypocalcemia hypernatremia
110
what electrolyte imbalance associated with muscle cramps
hypokalemia hypernatremia hypocalcemia
111
what electrolyte imbalance associated with hyporeflexia
hypermagnesemia
112
what electrolyte imbalance associated with hyperreflexia
hypomagnesemia
113
what electrolyte imbalance associated with resp weakness or decreased resp effort
hypophosphatemia Hypochloremia
114
the lower the pH the ____ the H ion concentration
Higher
115
the higher the pH the ___ the H ion concentration
Lower
116
normal pH range
7.35-7.45
117
normal PCO2 (partial pressure)
35-45
118
normal Bicarb
22-26
119
carbonic anhydrase helps with what formula important in acid base balance
CO2 + H20 H2Co3
120
If your hyperventilating or your vent settings are too high, you could become
alkalotic
121
If your hypo-ventilating you could become
acidotic
122
pH < 7.35 | CO2 >45
Respiratory acidosis
123
Asthma can cause what type of acid base imbalance
Resp acidosis
124
How can kidneys compensate if your building up CO2 becoming acidotic
makes more bicarb which will pair with Hydrogen ions and excreted in urine. This takes days
125
pH > 7.45 | CO2 <35
Respiratory alkalosis
126
what type of acid base balance Pt who is hyperventilating On a ventilator and settings are too high salicylate intoxication Hyperthyroidism
Resp alkalosis
127
How can kidneys compensate if your in resp alkalosis
getting rid of bicarb
128
pH < 7.35 | HCO3 < 22
Metabolic acidosis
129
Diarrhea and hyperchloremia can cause what type of acid base imbalance
Metabolic acidosis Diarrhea you are loosing bicarb through your GI tract
130
normal anion gap
4-12
131
pH <7.35 HCO3 <22 anion gap >12
Anion Gap Metabolic Acidosis
132
Calculate anion GAP
Na K Chloride HCO3 Take your positives Na+ and subtract potassium, chloride and Bicarb to get your gap.
133
Kussmaul breathing happens because you are trying to get rid of
CO2
134
Vomiting or Ng Suctioning can lead to what acid base imbalance
Metabolic Alkalosis
135
pH >7.35 | HCO3 >26
Metabolic Alkalosis
136
when you loose your chloride your body starts to make more
bicarb
137
diuretics can lead to what type of acid base imbalance
Metabolic alkalosis bc your dumping Na, K, Ca, Cl and your bicarb starts to come up bc of this
138
How does your lungs compensate in Metabolic acidosis
because you have a higher bicarb your lungs compensate by increasing CO2 that you have
139
If I told you a pt had chronic renal failure, what would you think about in regard to acid base balance
kidneys may not be able to keep up with excreting Hydrogen ions metabolic acidosis
140
If I told you a pt had vomiting the last few days, what would you think about in regard to acid base balance
Metabolic alkalosis
141
If I told you a pt had drug ingestions, what would you think about in regard to acid base balance
Respiratory alkalosis - depressed resp Metabolic alkalosis
142
If I told you a pt taking Lasix, what would you think about in regard to acid base balance
Metabolic alkalosis (you can see a bump in bicarb)
143
If I told you a pt had cyanosis, what would you think about in regard to acid base balance
Respiratory acidosis
144
If I told you a pt had Kussmaul breathing, what would you think about in regard to acid base balance
Metabolic acidosis - your trying to hyperventilate to breathe off CO2
145
If I told you a pt had AMS from seizures, what would you think about in regard to acid base balance
Respiratory acidosis - if you aren't breathing well, cant blow off CO2
146
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?
Metabolic Acidosis PCO2 is low bc of compensation 135-114 = 21 - 11= 10 (anion gap) Non-anion gap hyperchloremic metabolic acidosis
147
poorly controlled asthma ``` pH 7.54 pO2 of 60 PCO2 29 Na 138 Chloride 103 bicarb 25 ```
Resp alkalosis
148
3 month old chronic lung disease home meds include lasix ``` pH 7.37 pCO2 70 Na 136 Cl 88 Bicarb 37 ```
compensated resp acidosis
149
what do ketones produce
B-Hydroxybutyrate >>>>acetoacetate (6:1)
150
How is B-Hydroxybutyrate measured
blood
151
How is acetoacetate detected
Urine ketone strips
152
whats your renal threshold for glucose excretion? - point at which osmotic diuresis occurs
180 mg/dL Osmotic diuresis ->dehydration ->electrolyte wasting ->further stimulates stress hormones severe dehydration, poor tissue perfusion leads to lactic acidosis
153
what electrolytes are DKA pts depleted of
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
154
Cl is normally ____ in DKA
high
155
DKA pt who during treatment, as b-hydroxy levels are decreasing but bicarb isnt correcting, what should you consider
Chloride is rising with fluids May need to change fluids
156
What lab can be a predictor for cerebral edema in DKA pt
BUN - elevated - have to be more careful of DKA
157
when is cerebral edema more likely in DKA
first 3-12 hours after start of treatment
158
< __ yrs old has increased risk of cerebral edema
5 yrs
159
Serum test for DKA
``` 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
160
labs to collect for new onset diabetes
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
161
Anion Gap =
Na-(Cl+HCO3)
162
Normal anion gap
around 12
163
what Anion gap do you normally see in DKA
20-30
164
If you have a DKA with an anion gap >35, this suggests concomitant ___ ____
lactic acidosis
165
mild, moderate or severe DKA? pH <7.30 or serum bicarb <15
mild
166
mild, moderate or severe DKA? | venous pH <7.2 or serum bicarb <10
moderate
167
mild, moderate or severe DKA? venous pH <7.1 serum bicarb <5
Severe
168
These factors make the pt ICU status for DKA (at some facilities)
Severe DKA <7.1 Age < 5yrs AMS Received >40mL/kg of fluid Sepsis/SIRS Received sodium bicarb treatment High BUN at presentation
169
intubation is encouraged or discouraged in DKA
discouraged if possible. At high risk for cardiac event due to level of acidosis
170
fluid resuscitation in DKA pt who is not in shock and has no evidence of cerebral edema
NS or LR bolus of 10-20ml/kg over 30-60 min
171
fluid resuscitation in DKA pt who is in shock
rapid fluid resuscitation with 20mL/kg and reassessment after each bolus
172
DKA fluid management calculation
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
173
DKA fluid management - what fluid type should you consider using if there is a concern for hyperchloremic acidosis
LR instead of NS
174
when is insulin started in DKA management
after fluid replacement
175
Insulin in DKA management
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
176
Why do you not want to bolus insulin in DKA
increased risk of cerebral edema
177
When do you add dextrose to fluids in DKA treatment
when plasma glucose falls to 250-300 mg/dL or if its correcting too quickly
178
In DKA treatment you do not want your glucose to come down more than ___ mg/dL/hr
100
179
Insulin management in mild DKA (7.2-7.3) or when insulin infusion is not feasible
may administer subcutaneous rapid-acting insulin every 1-2 hours or regular insulin every 4 hours
180
In DKA management when is Potassium chloride or Potassium phosphate added to fluids
K<5.5 | Pt has voided
181
Severe hypophosphatemia in DKA should be treated. Don't forget to monitor for
hypocalcemia | when your replacing phosphate can lead to hypocalcemia
182
Bicarb in DKA treatment
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
183
As your glucose comes down what should your sodium be doing what happens if this does not occur
Serum Na should increase Failure of Na+ to increase prompts intense neurologic monitoring due to risk associated with cerebral edema
184
2 bag system for DKA what are in the 2 bags
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)
185
For DKA pt how do you calculate the IVF rate
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
186
what resolves first in DKA | Hyperglycemia or metabolic acidosis
hyperglycemia
187
once hyperglycemia resolves, maintain glucose levels between
100-200mg/dL
188
In DKA management, where the glucose is falling too fast or the acidosis is not correcting what do you do?
Change to D12.5% or increase fluid rate
189
what labs are you monitoring every 2-4 hours in DKA What else are you monitoring closely
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
190
when do you transition them off the 2 bag system in DKA treatment
HCO3 >15 mEq/L B-hydroxybutyrate <1.0-1.5 Abd pain and vomiting resolved, patient can tolerate oral intake
191
when do you transition to subcutaneous insulin in mgmt of DKA
- 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
192
in Pediatric DKA the incidence of cerebral edema is ____ and the mortality rate is ___
rare | high
193
risk factors for cerebral edema in DKA
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
194
signs/symptoms of cerebral edema in DKA
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
195
cerebral injury clinical diagnosis (DKA)
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
196
treatment of cerebral edema (DKA)
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
197
Mannitol dosing and time to give Mannitol for DKA related cerebral edema
mannitol 0.5-1g/kg IV over 10-15 min
198
Hypertonic Saline dosing and time to give for DKA related cerebral edema
2.5-5mL/kg over 10-15 min
199
The top zone on the adrenal cortex, Zona Glomerulosa makes ___ that turns into ___
Angiotensin II Aldosterone
200
The second from top zone on the adrenal cortex, Zona fasciculata makes ___ that turns into ___
ACTH Cortisol
201
The third zone on the adrenal cortex, Zona Reticularis makes ___ that turns into ___
ACTH Androgens
202
The adrenal medulla makes ___
Catecholamines
203
The hypothalamic-pituitary adrenal axis | the main mechanism is
regulating cortisol production
204
ACTH is made in the
pituitary gland
205
congenital adrenal hyperplasia is affecting the ____and not the pituitary
gland
206
A group of autosomal recessive disorders characterized by impaired cortisol synthesis ->hypersecretion of CRH and ACTH that leads to hyperplasia of adrenal glands
Congenital Adrenal Hyperplasia
207
what enzyme deficiency is associated with Classical Congenital Adrenal hyperplasia
21-Hydroxylase Deficiency (for 90% of the cases)
208
Classical Congenital adrenal hyperplasia is more prevalent in what race
1: 15000 - Caucasians 1: 42,000 African Americans
209
what forms of congenital adrenal hyperplasia
Salt-wasting - 67% | Simple viralizing-33%
210
Classical Congenital adrenal hyperplasia is diagnosed by
elevated 17-hydroxyprogesterone level
211
21 Hydroxylase Deficiency in CAH
Hypotension salt wasting Cortisol deficiency your progesterone and 17-OH progesterone go up which leads to hyper-androgenism
212
salt wasting =
mineralocorticoid deficiency
213
what organs are involved in blood pressure regulation
liver lungs kidneys adrenal cortex
214
When you don't make aldosterone....what happens
Hyponatremia hyperkalemia acidosis hypotension
215
medication for CAH to replace cortisol | dosing to start
hydrocortisone 20mg/m2/day divided TID
216
medication for CAH to replace mineralocorticoid (aldosterone)
Fludrocortisone 0.1mg BID and salt solution since they salt waste
217
what does the newborn screen test for in regards to CAH
focuses on 21-hydroxylase deficiency by testing for 17-hydroxyprogesterone
218
if you get an abnormal newborn screen back for CAH, what needs to be ordered
``` clinical eval lytes confirmatory 17OHP High dose ACTH stim test Preterm-> different normative values Referral ```
219
treatment for acute/new diagnosis for CAH
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
220
signs/symptoms of adrenal crisis
hyponatremia hyperkalemia hypotension hypoglycemia
221
daily treatment for adrenal insuf s/t CAH | what does this do
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
222
at start of illness for a CAH pt
``` stress dose steroids IV med (solucortef) if not tolerating PO early/aggressive rehydration ```
223
long term complications in CAH
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
224
elevated renin in CAH
need more mineralocorticoid
225
we dont want to normalize 17-OHP in CAH because we can cause
Cushing's by overtreating
226
inadequate treatment of CAH can lead to
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
227
autosomal recessive in CAH means that every ___ in ____ will have CAH
1 in 4
228
a life-threatening condition that causes salt wasting and adrenal insufficiency in most cases
Classical Congenital Adrenal Hyperplasia
229
A girl with clitoromegaly | what should you suspect
Classical Congenital Adrenal Hyperplasia
230
A boy with microphallus or bilat undescended testes | What should you suspect
Classical Congenital Adrenal Hyperplasia
231
non-classical forms may present with premature adrenarche or as polycystic ovary syndrome
Classical Congenital Adrenal Hyperplasia does not require stress dose steroids
232
2 things to draw in the EC when you suspect CAH
17 Hydroxyprogesterone | Cortisol levels
233
which type of CAH needs the Fludrocortisone
Salt wasters the non classical or the virilizers do not
234
which type 1 DM is auto immune mediated
Type 1A Type 2B is not
235
Name 5 rare forms of Diabetes
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)
236
risks based screening for Diabetes (Type 2 or pre-diabetes
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)
237
normal A1C
<5.7
238
Prediabetes A1C
5.7-6.4
239
Diabetic A1C
>6.4
240
Normal fasting blood glucose
<100
241
prediabetic fasting blood glucose
100-125
242
Diabetic fasting blood glucose
>125
243
Oral glucose tolerance test normal glucose
<144
244
oral glucose tolerance test prediabetic
144-199
245
oral glucose tolerance test diabetic
>199
246
ADA diagnostic criteria for diabetes
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
247
classic symptoms of diabetes
``` 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
248
pathophysiology of T2DM
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
249
treatment guideline for new onset DM in overweight youth with HA1C <8.5% without acidosis or ketosis
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
250
treatment guideline for new onset DM in overweight youth with HA1C >=8.5% no acidosis, with or without ketosis
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
251
treatment guideline for Acidosis under DKA and/or HHNK
manage DKA/HHNK IV insulin until acidosis resolves. then subq insulin until pancreatic antibodies are known
252
lifestyle modifications for someone in pre-diabetes. Research shows metformin does not prevent diabetes full blown progression at this time
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
253
How does metformin work
A biguanide that - insulin sensitizer - inhibits gluconeogenesis - helps with weight loss
254
Metformin is used as monotherapy in Type 2DM when A1C is less than
8.5%
255
Black box warning for Rosiglitazone
Congestive heart failure and bladder cancer in diabetics
256
when you start someone on metformin, what is your initial dose and how often do you titrate up based on glucose readings
500mg once a day with the goal of 2000mg daily or 1000mg BID - increasing by 500mg weekly
257
what baseline labs do you need prior to starting metformin
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
258
pt education for metformin
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
259
side effects metformin
nausea vomiting diarrhea can try extended release
260
Contraindications for metformin
``` Hepatitis impaired renal function cirrhosis alcoholism cardiopulmonary insufficiency ```
261
If Type 2DM failing therapy with Metformin and insulin, you can add a 3rd agent as adjunct therapy ....which agent are you thinking
Victoza (Liraglutide) Refer to endocrinology this is a once a day shot
262
How does Victoza (Liraglutide) work
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
263
what is C-peptide lab
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
264
HHS and ketosis
HHS does not present with ketosis
265
what are the antibodies test for type 1 DM
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
266
B - Hydroxybutyrate are essentially
blood ketones
267
what are some labs that you should be drawing on DKA -new onset
``` 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 ```
268
leading cause of death in T1DM
DKA
269
ISPAD guidelines for diagnosis of DKA
``` uncontrolled hyperglycemia (>200) metabolic acidosis (pH <7.3) Ketonemia ```
270
risk factors for DKA
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 ```
271
s/s DKA
n/v/abd pain (rule out pancreatitis) Tachypnea/kaussmal resp tachycardia fruity odor lethargy/obtunded (concern for cerebral edema) 3 Ps
272
how can you explain insulin to pt
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.
273
type 1 DM age of onset
6 mos - adulthood, peaks at age 12
274
Type 2 DM age of onset
>=10 yrs
275
Acanthosis Nigricans is common in what DM
type 2
276
which type DM has diabetic ketoacidosis at onset
>50% for type 1 | <50% type 2
277
C-peptide high or normal seen in what type DM
Type 2 DM In type 1 its low or undetectable
278
Pancreatic antibodies are likely to be positive in what type of DM
DM type 1
279
what does positive pancreatic antibodies mean
it just means there has been B cell loss
280
type 1a DM patho
autoimmune B cell destruction leading to absolute insulin deficiency does not happen overnight genetic predisposition.....with a precipitating event
281
When you have one autoimmune, your at risk for more. What other autoimmune diseases are they at risk for with type 1 DM?
Hashimoto's thyroiditis (most common) Celiac disease Adrenal insufficiency other - Multiple sclerosis - Lupus - Gastritis - Autoimmune arthritis - Vitiligo
282
what labs are obtained at diagnosis for Type 1 DM and every year (after 5 years into Diabetes)
Thyroid Antibodies plus TFTs Celiac Disease Antibodies Screening for Addison's disease and others based on symptoms
283
insulin is a ____ hormone produced by ___ ____
peptide hormone | beta cells
284
how does insulin work
regulated and secreted in oscillations (typically every 3-6 min) as a response to increased blood glucose
285
Newest ultra long acting insulin what is it how long does it last
``` Insulin Degludec (Tresiba) up to 42 hours ```
286
Rapid acting insulins
Aspart (Fiasp) - ultra rapid acting Lispro (Humulog) Apidra
287
Short acting insulin
Regular
288
Intermediate acting insulin
NPH
289
long acting insulin
glargine (Lantus, Toujeo) | detemir (Levemir)
290
Ultra rapid acting insulin
Fiasp | Lyumjev
291
what does basal insulin cover
glucose released by liver
292
what does bolus insulin cover
carbohydrates and correct high blood glucose levels
293
dosage of insulin in type 1 DM depends on what factors
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
294
Insulin starting dose guide formula
TDD = 0.x unit/kg/day (x= age in years) if in DKA 1unit/kg/day (max)
295
Basal dosing for insulin should be ___ -___% of TDD
50-60%
296
Bolus dosing for insulin should be ___-____ of TDD
40-50%
297
Target BG for Type 1 DM normally
80-120mg/dl
298
Target BG for Type 1 DM if toddler, developmental delays or CF
150 mg/dl
299
How often should a type 1 DM be injecting insulin
3-4 times/day
300
How is insulin given when using a pump
continuous basal rate Food bolus correction bolus
301
Insulin side effects
hypoglycemia - rule out alcohol intake Lantus/Basaglar can burn: may use Tresiba weight gain Lipoatrophy or Lipohypertrophy: Rotate sites
302
when a pt is on insulin having frequent hypoglycemia, what needs to be ruled out
alcohol intake
303
If a DM pt is using Lantus/Basaglar and its burning. What can you switch to?
Tresiba
304
For insulin dependent pt. How do you prevent Lipoatrophy or Lipohypertrophy?
Rotate sites
305
In diabetic pt low glucose is considered low
70mg/dl Adrenergic: Palpitations, tremors anxiety Cholinergic: Sweating, hunger, paresthesias
306
In diabetic pt low glucose is considered severely low
<55 Headache, irritability, difficulty concentrating, confusion, seizures, coma
307
what can you give a diabetic pt for severe hypoglycemia
Glucagon (peptide hormone, alpha cells)
308
how many times per day should a diabetic check blood sugars
at least 4xs
309
MODY
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
Signs of MODY
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
treatment for MODY
Sulfonylureas -Glyburide Refer to endocrinology for initiation of therapy
312
Acute complications for DM
hypoglycemia DKA (Diabetic Ketoacidosis) HHS (hyperglycemic hyperosmolar state)
313
Chronic complications for DM
Microvascular - Retinopathy - Nephropathy Neuropathy Macrovascular: Cardiovascular Delayed puberty Growth disturbance (short stature) psychosocial/Psychiatric
314
what screening should be done for a type 2 DM at diagnosis, then yearly
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
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
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
what screenings should be done in Type 1DM shortly after diagnosis; if normal - repeat every 1-2 yrs
autoimmune thyroid disease: TSH
317
what screenings should be done in Type 1DM shortly after diagnosis or with symptoms
Celiac IgA TTG IgA
318
if your HA1C is 7.0 your average blood glucose over the past 90 days
170
319
If your HA1C is 5.0, your average blood glucose over the past 90 days
100
320
If your HA1C is 8.0, your average blood glucose over the past 90 days
204
321
why do we recommend keeping the HA1C 7%
reduces the risk of long term complications significantly Retinopathy - 76% Nephropathy - 54% Neuropathic - 60%
322
what is the depression screening called
PHQ-9 Depression screening
323
number of solute particles in 1 kg of solvent
osmolality this is the term used in medicine
324
number of solute particles in 1 L of solvent
Osmolarity
325
formula for serum osmolality
(2x {Na}) + {glucose} + (Bun)
326
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
Serum tonicity
327
transfer of soluble components (not protein) from blood into glomerulus
filtration
328
water and solutes move from renal tubule back into circulation
reabsorption
329
transfer of solutes and waste from plasma into the renal tubule for excretion (urine)
secretion
330
content of urine, end result of above processes
Excretion
331
content of urine, end result of filtration, reabsorption, secretion
Excretion
332
what does Antidiuretic hormone (ADH) aka Vasopressin do
recruits renal water channels in collecting duct -> water reabsorption in renal tubules -> concentrates urine (decreases urine volume) "Adds Da H2O"
333
drinking water increases or decreases your plasma osmolality
decreases
334
at what plasma osmolality does thirst begin to autoregulate osmolality
280 mosmol/kg
335
at what plasma osmolality does plasma ADA start to risk to autoregulate osmolality
285 mosmol/kg
336
when there are problems with ADH and water homeostasis regulation what can it affect
thirst urine output Intravascular volume status Serum osmolality Serum Sodium (Na) level Urine osmolality Urine Na level
337
decreased production of ADH
central diabetes insipidus
338
decreased renal response to ADH
nephrogenic Diabetes insipidus
339
decreased ability to reabsorb water in the renal tubules ->cannot concentrate urine ->excess loss of water in urine (inappropriately dilute urine and serum hyperosmolality)
Diabetes Insipidus
340
what causes central DI - Hypothalamus doesn't produce ADH
``` Cancer (craniopharyngioma, germinoma) trauma meningitis hypoxic brain injury infiltrative disorders (histiocytosis, leukemia) surgery, radiation holoprosencephaly, congenital hypopituitarism Anorexia nervosa idiopathic ```
341
what causes nephrogenic DI - collecting ducts don't respond to ADH
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
what medications can cause nephrogenic DI
lithium, foscarnet, amphotericin
343
what syndromes can cause nephrogenic DI
Bartter syndrome Bardet Biedl syndrome
344
what gene mutation is associated with nephrogenic DI
Aquaporin-2 gene mutation
345
DI symptoms
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
In DI what is their volume status
Hypovolemic
347
In DI what should their urine output be
increased
348
In DI what should their serum sodium be
High >150 mEq/L
349
In DI what should their serum osmolality be
High >300 mOsm/L
350
In DI what should your urine specific gravity be
Low (<1.010)
351
In DI what should your urine sodium be
Low (<20 mEq/L)
352
In DI what should your urine osmolality be
low (<100-300 mosm/L)
353
when does water deprivation test start
after breakfast and after 1st void of the day and you don't get any fluids
354
when you give DDADP (vasopressin) and your urine osmols do not rise this is
nephrogenic DI
355
when you give DDADP (vasopressin) and your urine osmols do rise this is
central DI
356
DI: Acute management - hypernatremia
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
Free water deficit formula (DI)
Free water deficit (liters) = measured Na - Goal Na all divided by goal Na then multiply by 0.6L/kg x weight (kg)
358
what is key to regulate plasma osmolality in a pt with DI
someone that has an intact thirst mechanism
359
monitoring in DI
intake/output Na levels adjustments to daily fluid requirement based in I/O, Na levels, change in insensible losses, growth
360
medication used for acute management for DI
Vasopressin
361
what med is most commonly prescribed for DI management
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
Nephrogenic DI management
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
inability to suppress ADH impaired water excretion inappropriately concentrated urine + serum hypo-osmolality
SIADH - syndrome of inappropriate ADH
364
list pulmonary causes of SIADH
mechanical ventilation pneumonia bronchiolitis asthma cystic fibrosis
365
list neurologic causes of SIADH
tumor surgery trauma hemorrhage meningitis Encephalitis severe nausea
366
list oncology causes of SIADH
Medulloblastoma lymphoma
367
list medications that causes of SIADH
Oxcarbazepine Valproate chemotherapies narcotics nsaids
368
list other causes of SIADH
Anesthesia idiopathic post-op
369
s/s of SIADH
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
volume status in SIADH
Euvolemic to hypervolemic
371
urine output in SIADH
Decreased (<1mL/kg/hr)
372
serum sodium in SIADH
low (<135 mEqu/L)
373
serum osmolaltiy in SIADH
low (<280 mOsm/L)
374
Urine specific gravity in SIADH
High (>1.020)
375
Urine Sodium in SIADH
High (>20-40 mEq/L)
376
treatment for SIADH
severe symptoms - treat immediately with 3% saline gradual correction of hyponatremia - 1st line therapy is fluid restriction
377
Acute hyponatremia duration severity? goal Na correction?
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
Chronic hyponatremia duration severity? goal Na correction?
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
treatment for severe symptomatic hyponatremia (seizure, obtunded, coma) (SIADH)
3% saline 3-5mL/kg (max 100mL) raises by 2.5-4 mEq/L
380
SIADH management
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
Alternative therapy for chronic SIADH
- low diuretic (+/- sodium supplementation) - Urea supplementation - increases water excretion - Vasopressin receptor antagonist (Vaptans, rarely used in pediatrics)
382
hyponatremia + hypovolemia due to inappropriate sodium wasting in urine
Cerebral salt wasting (CSW)
383
What is cerebral salt wasting seen in
CNS insult: subarachnoid hemorrhage, post-surgery, trauma, meningitis, encephalitis, tumors, status epilepticus
384
Volume status in Cerebral salt wasting
Hypovolemic
385
urine output in Cerebral salt wasting
increased
386
Serum sodium in Cerebral salt wasting
Low (<135 mEq/L)
387
Serum osmolality in Cerebral salt wasting
low
388
urine specific gravity in Cerebral salt wasting
High (>1.050)
389
urine sodium in Cerebral salt wasting
High (>40 mEq/L)
390
Urine osmolaltiy in Cerebral salt wasting
High (>100-300 mOsm/L)
391
Managing Cerebral salt wasting
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
what lab represents the unbound, biologically active T4
Free T4
393
If free T4 is high ...most likely
Hyperthyroidism
394
If free T4 is low ...most likely
Hypothyroidism
395
If free TSH is high ...most likely
Hypothyroidism
396
If free TSH is low ...most likely
Hyperthyroidism
397
3 types of hypothyroidsm
congenital acquired Transient
398
what are the types of congenital hypothyroidism
dysgenesis - did not form correctly dyshormonogenesis - it formed, but doesnt function properly
399
If not caught and treated early, what can happen
developmental delay
400
T3, T4 and TSH and placenta
do not cross the placenta - when your testing the baby at day of life 1 - those are the babies numbers
401
Thyroid meds that mom takes can cause
Transient hypothyroidism - can last 3-4 weeks (this can be over or underproduction)
402
what are the causes of transient hypothyroidism
maternal antithyroid drugs Maternal TSH receptor blocking antibodies
403
what are the causes of acquired hypothyroidism
hashimoto thyroiditis Iodine deficiency
404
causes of secondary hypothyroidism
Hypothalamus or pituitary -Free T4 and TSH low or normal Malformation -Holoprosencephaly - midline defects (cleft lip/palate)
405
what does hypothyroidism look like in baby
``` 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
Congenital Hypothyroidism and goiter
RARE 1:30k live births - most often r/t dsyhormonogenesis or transient
407
Newborn screen and congenital hypothyroidism
We do screen for this in all 50 states
408
Acquired Hypothyroid/hashimoto Thyroiditis | Setup and symptoms
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
Acquired Hypothyroid/hashimoto Thyroiditis | Evaluation
Goiter Antithyroid peroxidase & antithyroglobulin antibodies Elevated TSH, low FREE T4 Elevated TSH and normal T4 may be prelude to failure
410
Treatment Acquired Hypothyroid/hashimoto Thyroiditis
Congenital or Acquired - Levothyroxine - Infants 15mcg/kg and children 3mg/kg
411
Hyperthyroidism is most commonly cause by ____ in children
Graves Disease
412
Graves Disease Setup and Symptoms
Adolescent girls emotional lability, personality changes, school performance Tremor, anxiety, inability to concentrate Weight loss
413
Graves Disease Evaluation
Free T4, T3 high TSH low
414
Hyperthyroid symptoms
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
Treatment Graves disease
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
Thyroid storm setup and symptoms
Medical emergency rare complication of hyperthyroidism Tachycardia disorientation elevated BP Hyperthermia
417
Evaluation of Thyroid storm
Free T4 and T3 - high | TSH low
418
Treatment for thyroid storm
``` cooling blanket beta blocker iodine hydrocortisone support if they have adrenal insufficiency associated with the thyroid storm heart failure therapy - if needed ```
419
Neonatal Hyperthyroid/neonatal graves disease setup and symptoms
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
Evaluation for Neonatal Hyperthyroid/neonatal graves disease
Free T4 high | TSH low
421
treatment for | Neonatal Hyperthyroid/neonatal graves disease
none if symptoms are minimal methimazole B Blocker spontaneous resolution 2-3 mos based on half life of TSIs
422
``` obesity muscle wasting muscle weakness decreased glucose tolerance hyperglycemia buffalo hump ```
Cushing Syndrome symptoms
423
what 3 types of hormones do the adrenal glands produce
Glucocorticoid (cortisol, corticosterone) mineralocorticoid (Aldosterone, dehydroepiandrosterone) sex hormones (androgens, progestins and estrogens)
424
acute adrenal insufficiency
adrenal crisis
425
chronic adrenal insufficiency
Addison disease
426
the most common causes of acute adrenal insufficiency are
Waterhouse-Friderichsen syndrome - sudden withdrawal of long term corticosteroid therapy
427
in primary adrenal insufficiency what hormones are not produced in sufficient amounts? which one in particular
Glucocorticoid mineralocorticoid cortisol
428
what is the most commonly identified cause of primary adrenal insufficiency in children
Congenital adrenal hyperplasia (CAH)
429
Congenital adrenal hyperplasia (CAH) is an _____ _____ disorder
autosomal recessive disorder
430
Congenital adrenal hyperplasia (CAH) is due to a defect in what enzyme
largely due to 21-hydroxylase deficiency required in the synthesis of cortisol to cholesterol
431
what gender has a higher incidence of Congenital adrenal hyperplasia (CAH) at birth
females
432
when do males usually present with Congenital adrenal hyperplasia (CAH)
with a life-threatening salt-wasting crisis in the first month of life
433
``` between 1-4 weeks of life -Vomiting -dehydration -cardiac arrhythmias -hyponatremia -hyperkalemia -salt-losing crisis All results in circulatory collapse ```
Congenital adrenal hyperplasia (CAH)
434
``` fatigue loss of weight hyperpigmentation of the creases of the skin nausea vomiting ```
Adrenal insufficiency
435
vomiting abd pain hypovolemic shock
adrenal crisis
436
Morning 17-OHP levels may be _____ in a partial enzyme deficiency
elevated
437
Congenital adrenal hyperplasia (CAH) | testosterone in females
elevated
438
Congenital adrenal hyperplasia (CAH) | Androstenedione is seen in
males and females
439
Congenital adrenal hyperplasia (CAH) | karyotyping is important for
ambiguous genitalia
440
CAH dosing of hydrocortisone
10-20 mg/m2/day daily
441
Adrenal insufficiency dosing for hydrocortisone
6-9mg/m2/day daily
442
Stress dosing of hydrocortisone
25-50mg/m2/day IV/IM
443
severe illness or surgical procedures, stress dosing of hydrocortisone
50-123 mg/m2/day IV
444
dosing for mineralocorticoid maintenance therapy in adrenal insufficiency
0.1-0.2mg oral fludrocortisone acetate daily
445
sodium supplementation for infants in adrenal insufficiency
17-34 mEq of sodium supplementation daily
446
when does cerebral salt wasting occur
following an acute CNS injury
447
Results in volume depletion and hyponatremia typically occurring within the first few days of an inciting intracranial injury, surgery or disease process
Cerebral salt wasting
448
symptoms of cerebral salt wasting
``` 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
``` serum sodium <135 serum osmolarity <280 urine sodium >80 urine osmolarity >200 Urine specific gravity >1.010 ```
cerebral salt wasting
450
urine output in cerebral salt wasting is _-_ ml/kg/hr
2-3ml/kg/hr
451
what other studies should be done in cerebral salt wasting
CT/MRI - looking for structural abnormalities, tumors, AV malformation, hemorrhage Lumbar puncture -infection
452
In cerebral salt wasting serum sodium level should rise no more than __-__ mEq/day
10-12 - to reduce risk of central pontine demyelination of white matter in brain unless having severe neuro symptoms
453
genetics of DI
typically x linked recessive
454
What syndrome is linked to DI
Wolfram syndrome
455
congenital DI typically X linked recessive involving what mutations
VR2 or AQP2
456
What conditions lead to the inability of the kidneys to respond to ADH in DI
``` Chronic renal failure Renal tubulointerstitial diseases Potassium depletion sickle cell disease medication induced from drugs alcohol lithium diuretics amphotericin B Demeclocycline ```
457
what dietary abnormalities can lead to DI
Primary polydipsia decreased sodium chloride intake severe protein restriction or depletion
458
is DI reversible?
Nephrogenic DI that results from a metabolic condition may be reversed if the medication is stopped or the metabolic condition is corrected
459
``` Polyuria Dilute urine Polydipsia inappropriately low urine sodium and osmolality urine specific gravity <1.005 Hypernatremia Serum Hypo-osmolality Dehydration ```
DI
460
the primary causes of polyuria and polydipsia are
Diabetes Mellitus Central DI other causes: UTI relief of renal obstruction psychogenic polydipsia (excessive water intake)
461
``` Serum sodium >150 Osmolality >295 Urine sodium <30 Urine osmolality <200 specific gravity <1.005 ```
DI
462
water deprivation test results: | concentrated urine output following ADH administration
Central DI
463
water deprivation test results: | excessive, dilute urine despite hypernatremia and hyperosmolality
nephrogenic DI
464
fluids are restricted until as much as 5 % of body weight has been lost to evaluate urinary response when the serum osmolality exceeds 295
water deprivation test
465
management of DI
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
critical care setting treat for DI
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
other than critical care setting treat for DI
Desmopressin Oral and intranasal chronic therapy: dose range is 5-30ug/day with peak effect 1-5 hrs
468
what type of DI is resistant to vasopressin
Nephrogenic DI
469
diagnosis of DKA
``` blood glucose >200 presence of serum ketones urine ketones blood pH <7.3 serum bicarbonate <15 ```
470
hyperglycemia leads to
``` osmotic diuresis electrolyte loss Dehydration Decreased glomerular filtration Hyperosmolarity ```
471
physical exam findings in DKA
``` Tachycardia decreased pulses poor perfusion dry mucous membranes enophthalmos poor skin turgor hypotension deep or labored breathing ```
472
what systems need to be monitored in DKA
Cardiac monitoring -watch for T wave alterations seen in hyperkalemia or hypokalemia Neuro monitoring -cerebral edema
473
corrected sodium formula
={Na+} + {1.6 x (plasma concentration mg/dL-100}/100
474
In DKA treatment ...as hyperglycemia improves, serum sodium should ___. If it ____ or does not _____, there is concern for what?
improve if sodium does level increases or does not begin to fall, there is concern for the development of cerebral edema
475
Potassium in DKA treatment
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
Phosphorous in DKA
cells are depleted as a result of acidosis, osmotic diuresis and insulin administration
477
risk of giving bicarbonate to DKA
CNS acidosis Hypokalemia cerebral edema
478
timing of blood glucose monitoring DKA
prior to meals and 2 hours after meal ends
479
a potentially fatal complication of diabetes, usually type 2 due to insulin deficiency and an increase in counterregulatory hormones
Hyperglycemic Hyperosmolar state (HHS)
480
enough endogenous insulin to suppress ketosis, although insufficient amount of insulin to prevent hyperglycemia
Hyperglycemic Hyperosmolar state (HHS)
481
Accumulation of ketoacids that cause cap metabolic acidosis
DKA
482
``` 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 ```
Hyperglycemic Hyperosmolar state (HHS)
483
Mgmt Hyperglycemic Hyperosmolar state (HHS)
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
An increase in serum levels of T3 and T4 will result in what in regards to TSH
Lower levels of TSH
485
An decrease in serum levels of T3 and T4 will do what to TSH
higher levels of TSH
486
abnormal fetal thyroid development or a disturbance in production of thyroid hormone
Congenital hypothyroidism
487
autoimmune or iatrogenic hypothyroidism
acquired hypothyroidism
488
immune system response results in damage and altered function of thyroid
Autoimmune hypothyroidism
489
Chronic lymphocytic thyroiditis (Hashimoto) affects what gender more often
females
490
Common comorbidities of Chronic lymphocytic thyroiditis (Hashimoto) include
Type 1 DM Juvenile RA Trisomy 21
491
can be caused by head or neck radiation therapy, surgery or induced by drugs that increase thyroxine metabolism
iatrogenic hypothyroidism
492
occurs in infants of mothers with Graves disease, causing a transplacental transfer of the thyroid stimulating immunoglobulin (TSI) from mother to infant
Congenital or neonatal hyperthyroidism
493
Autoimmune and iatrogenic causes of hyperthyroid
Acquired hyperthyroidism
494
most common cause of acquired hyperthyroidism resulting in an overproduction of the thyroid hormone
Graves disease
495
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
Hashimoto thyroiditis
496
congenital hypothyroidism symptoms typically develop within first _-_ weeks of life
2-6 weeks
497
in congenital hypothyroidism what is critical due to the risk of irreversible neurocognitive deficits if untreated
Early diagnosis
498
``` lethargy hoarse cry bradycardia large size for gestational age large fontanels constipation hypothermia jaundice dry skin elevated Free T4 elevated TSH ```
Congenital hypothyroidism
499
``` 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
Acquired hypothyroidism
500
thyroid peroxidase antibodies | thyroglobulin antibody titers
Hashimoto Thyroiditis
501
congenital hyperthyroidism findings usually develop when
initial days after birth
502
``` 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
congenital hyperthyroidism
503
``` 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
Acquired Hyperthyroidism
504
what imaging used to look at thyroid for initial eval of acquired hyperthyroidism
US - soft tissue of thyroid Scintigraphy - evaluates the function of thyroid gland radiographic testing not commonly used in screening
505
evaluates the function of the thyroid gland
Scintigraphy
506
treatment of congenital hypothyroidism
L Thyroxine Administration life long monitoring normalization of T4
507
Treatment of congenital hyperthyroidism
Methimazole or Propylthiouracil (blocks thyroid hormone stimulation Iodine - blocks the release of thyroid hormone already synthesized
508
treatment of acquired hypothyroidsim
L-Thyroxine - thyroid replacement
509
treatment Acquired hyperthyroidism
Propylthiouracil or methimazole radioactive iodine surgery (some cases)
510
primary function of the parathyroid gland and parathyroid hormone (PTH) is to
regulate the amount of calcium present in blood and bones
511
in Hyperparathyroidism, excessive secretion of PTH, leads to
hypocalcemia hypocalciuria hypophosphatemia hyperphosphaturia
512
secretion of PTH is triggered by a reduction in the serum ____ level
calcium
513
When released, PTH targets musculoskeletal, renal and gI systems to regulate
serum calcium levels
514
PTH triggers ______ bone resorption - resulting in
increased | serum calcium and serum phosphate
515
in the kidney, PTH stimulates the reuptake of
calcium and magnesium and increases phosphorous excretion
516
In the intestine, PTH activates the enzyme responsible for
Vit D Absorption -> which controls the absorption of intestinal calcium
517
most common congenital cause of hypoparathyroidism
DiGeorge syndrome (22q11 deletion)
518
autoimmune hypoparathyroidism is usually associated with ____ disease or other endocrine diseases such as adrenal insufficiency with polyglandular autoimmune syndrome type 1
Addison
519
ingestion of anticonvulsants causing hypocalcemia can lead to
Acquired hypoparathyroidism
520
primary hyperparathyroidism is associated with
multiple endocrine neoplasia syndromes or adenomas
521
secondary hyperparathyroidism is largely due to
hypocalcemic states associated with chronic renal failure, vit D deficiency, rickets
522
PTH level decreased serum and urinary calcium decreased Hyperphosphatemia EKG - shortened or prolonged QTc interval
hypoparathyroidism
523
``` Hypercalcemia abd pain vomiting constipation bone pain and paresthesias renal stones HTN ``` elevated PTH Hypercalcemia Hypophosphatemia Alkaline phosphatase normal or elevated
Primary hyperparathyroidism
524
``` 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
secondary hyperparathyroidism
525
management of hypoparathyroidism
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
Management of hyperparathyroidism
aggressive hydration and diuretics restriction of calcium and vit D intake Hydrocortisone calcitonin surgical removal of parathyroid glands
527
Neuroendocrine tumor arising from the adrenal medulla (chromaffin cells) can be benign or malignant often bilat
Pheochromocytomas
528
associated with von Hippel-Lindau disease, multiple endocrine neoplasia type 2, familial paraganglioma syndrome or neurofibromatosis type 1
Pheochromocytomas
529
Sustained HTN (due to tumor associated catecholamine release) triad (headache, diaphoresis, palpitations) tachycardia abnormal skin sensation anxiety Hyperglycemia
Pheochromocytomas
530
diagnosis of Pheochromocytomas
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
mgmt of Pheochromocytomas
HTN control -A or B blockers may be used presurgically -surgical resection metastatic Pheochromocytomas requires antineoplastic therapy
532
a common cause of hyponatremia
SIADH
533
excessive release of ADH from pituitary gland
SIADH
534
Hyponatremia decreased serum osmolarity and increased urine osmolarity decreased urine output with increased urine concentration cerebral edema may ensue in severe cases of hyponatremia
SIADH
535
serum sodium <135 serum osmolarity <280 urine osmolarity >200 BUN < 10 Urine sp gravity >1.020 urine sodium >25
SIADH
536
managing SIADH
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
labs for initial eval for child newly diagnosed with diabetes
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
measures adrenal gland response to administration of ACTH
ACTH stimulation testing
539
how to perform ACTH stim test
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
As much as ___ % of lean body mass in infants is water
70%
541
Children, in general, have approx ___% of lean body mass as water and an overall higher concentration of extracellular fluid than adults
60%
542
daily maintenance fluids for healthy children include fluid for
physiologic needs daily output insensible losses
543
dehydration is a concern for morbidity and mortality in children
< 5yrs of age
544
___ is generated in the process of metabolism
H2O heat regulation requires H2O solute excretion requires H2O
545
Metabolic rate (kcals/day) approximates _______
fluid requirements (mL/day)
546
Holliday segar method for calculating maintenance fluid requirements for 24 hr period in children
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
4-2-1 method
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
BSA maintenance fluids calculation
Square root of kgxcm/3600 maintenance fluids calculation using BSA = 1,500-2000 mL/m2/day
549
the proper balance between water and electrolytes
hydration
550
conditions that alter maintenance fluid requirements
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
___ and ____ are involved in the dehydration and rehydration process
fluid and electrolytes
552
in dehydration what can usually explain changing lab values in many cases
shifts from intracellular to extracellular
553
_____ is released in response to the renin-angiotensin-aldosterone release in cases of extracellular volume depletion
Aldosterone
554
______ is released in response to volume depletion, which results in decreased urine output and increased absorption of water by kidneys
Antidiuretic hormone (ADH)
555
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
dehydration
556
Serum Sodium 130-150
isotonic dehydration
557
serum sodium <130
Hypotonic/hyponatremic dehydration
558
serum sodium >150
Hypertonic/hypernatremic dehydration
559
time frame to restore intracellular and extracellular water and electrolyte deficits in hyponatremic and isonatremic dehydration
24 hours
560
time frame to restore intracellular and extracellular water and electrolyte deficits in hypernatremic dehydration
48 hours
561
infants can develop _____ from incorrect mixing of formula with too much water
hyponatremia
562
formula to calculate volume of fluid to replace
current weight x 1,000 x %dehydration = volume of fluid to replace
563
the most precise method of determining fluid deficit is
weight loss, however not typical to have recent pre-illness weight results
564
Fluid deficit calculation
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
oral rehydration fluids should have goal of replacing deficit volume over
4-6 hours, then to replace ongoing losses
566
IV fluid replacement in isotonic and hyponatremic dehydration
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
IV fluid replacement in hypernatremic dehydration
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
calculation of insensible loss
300mL x BSA = approx insensible loss for 24 hours. Divide by 24 to get the hrly rate of insensible loss
569
daily electrolyte replacement
Sodium: 2-3 mEq/100mL fluid Potassium: 2mEq/100mL fluid chloride: 5-6 mEq/100mL fluid
570
calculation for sodium deficit
Na deficit = (135-measured Na) x 100/L
571
It is difficult to assess ____ electrolyte deficit as its mainly intracellular and shifts based on catabolism, cell-injury and acid base balance
Potassium estimated that 1meq/L = 10-30% total body potassium loss
572
``` component of multisystem body functions -neuronal activity muscular contraction myocardial contraction hemocoagulation bone formation ```
Calcium
573
Calcium is present in 3 forms in plasma
bound to albumin (plasma protein) diffusible (calcium citrate or phosphate) unbound ion
574
____ calcium is the form most important for body functions
ionized
575
calcium concentrations is regulated by what systems
renal skeletal GI
576
serum calcium <9 | ionized Calcium <1.1
hypocalcemia
577
serum calcium >10
hypercalcemia
578
ethylene glycol ingestion can lead to
hypocalcemia
579
PRBC transfusion can lead to
hypocalcemia _ binding of ionized calcium to citrate after transfusion
580
malabsorption and hypoparathyroidism can lead to
hypocalcemia
581
renal failure can lead to
hypocalcemia
582
``` rhabdomyolysis sepsis tumor lysis syndrome pancreatitis can lead to,,, ```
hypocalcemia
583
what medication can lead to hypocalcemia
furosemide
584
What syndrome is connected to hypercalcemia
Williams syndreome
585
what electrolyte disorder is associated with malignancy, sarcoidosis
Hypercalcemia
586
what medication can lead to hypercalcemia
excessive Vitamins A and D | Thiazide diuretics
587
what electrolyte abnormalities associated with hyperphosphatemia and hypomagnesemia
hypocalcemia
588
risk of hypocalcemia in neonates
increased due to decreased calcium intake increased fetal calcium levels leading to transient parathyroid suppression PTH resistance
589
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.
Hypocalcemia
590
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.
hypercalcemia
591
hypocalcemia workup
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
Hypercalcemia workup
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
treatment for hypocalcemia
10-20mg/kg/dose calcium chloride (only give through central venous catheter) Calcium gluconate (100mg/kg/dose) given through either peripheral or CVC
594
treatment for chronic hypocalcemia
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
Hypercalcemia treamtent
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
Hypomagnesemia may lead to
hypocalcemia
597
If hypocalcemia is refractory, replace
magnesium
598
Correct severe hyperphosphatemia prior to correction of related ______ to avoid soft tissue calcification
hypocalcemia
599
the major role of ______ is to maintain electrical neutrality by balancing cations (usually sodium) in the blood
chloride
600
regulates acid base balance in body due to inverse relationship with bicarbonate
Chloride
601
serum chloride normal
97-108
602
serum chloride <97
hypochloremia
603
serum chloride >108
hyperchloremia
604
metabolic alkalosis contributes to ____chloremia
hypochloremia
605
electrolyte imbalance associated with Bartter syndrome
Hypochloremia
606
``` electrolyte imbalance associated with Cystic fibrosis bulimia nervosa diuretic usage Removal of gastric secretions by ng tube permissive hypercapnia ```
hypochloremia
607
``` electrolyte imbalance associated with diarrhea excessive chloride administration metabolic acidosis Renal tubular acidosis urinary diversion into colon or ileum ```
hyperchloremia
608
passively follows renal sodium reabsorption and passively follows sodium absorption in GI tract
Chloride
609
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.
Hypochloremia. Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 719). Wolters Kluwer Health. Kindle Edition.
610
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.
Hyperchloremia. Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 720). Wolters Kluwer Health. Kindle Edition.
611
diagnostics for hypochloremia
• 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
treatment of hypochloremia
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
treatment for hyperchloremia
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
chloride has a direct relationship with
sodium
615
chloride has a inverse relationship with
bicarbonate
616
about 50% of magnesium stores are contained
in bone
617
magnesium is primarily excreted and regulated in the
kidney
618
normal mag levels
1.7-2.2
619
GI causes of hypomagnesemia
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
diseases and syndromes associated with hypomagnesemia
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
renal causes of hypomagnesemia
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
Medication causes of hypomagnesemia
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
endocrine causes of hypomagnesemia
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
causes of hypermagnesemia
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
neonates may experience transient hypomagnesemia or develop idiopathic hypomagnesemia associated with
maternal magnesium depletion
626
GI symptoms of hypomagnesemia
anorexia nausea vomiting
627
Neuro symptoms of hypomagnesemia
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
Cardiac symptoms of hypomagnesemia
ECG changes - atrial or ventricular ectopy, torsades de pointes and long QT interval
629
endocrine symptoms of hypomagnesemia
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
Neuro s/s of hypermagnesemia
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
cardiac s/s hypermagnesemia
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
GI s/s hypermagnesemia
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
resp symptoms hypermag
resp failure
634
hypo mag workup
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
hyper mag workup
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
management of hypomagnesemia
• 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
management of hypermagnesemia
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
hypomagnesemia may result in refractory
hypokalemia
639
A rapid increase in serum mag r/t rapid bolus may cause
increased mag excretion -> give it slow
640
if torsades de pointes on ECG, give
magnesium
641
phosphorous absorbed through
jejunum
642
phosphorous excreted through
kidneys
643
normal phosphorous
2.5-4.1
644
what vit def can cause hypophosphatemia
Vit D def and Vitamin D-resistant rickets
645
causes of hypophosphatemia
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
causes of hyperphosphatemia
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
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.
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
s/s hypophosphatemia
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
s/s hyperphosphatemia
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
diagnostic hypophosphatemia
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
diagnostic hyperphosphatemia
• 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
treatment for hypophosphatemia
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
treatment for hyperphosphatemia
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
risk of calcium-phosphorous precipitation particularly with
tumor lysis syndrome or renal failure
655
______ is important in potassium regulation by the kidney
aldosterone
656
Serum potassium normal
3.7-5.2
657
medications that can cause hypokalemia
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
causes of hypokalemia
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
causes of hyperkalemia
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
s/s hypokalemia
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
s/s hyperkalemia
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
diagnostics hypokalemia
• 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
diagnostics hyperkalemia
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
treatment of hypokalemia
• 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
treatment for hyperkalemia
• 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
Potassium should be interpreted in relation to the serum pH. Why
bc it shifts intracellularly with alkalosis and extracellularly with acidosis
667
Severe ___kalemia is a medical emergency
hyperkalemia >7
668
normal Na
135-145
669
hypervolemic hyponatremia is caused by
• 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
hypovolemic hyponatremia is caused by
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
normovolemic hyponatremia is caused by
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
• 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.
Acute hyponatremia
673
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.
acute hypernatremia
674
workup for hypo/hypernatremia
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
treatment for hyponatremia
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
Treatment for hypernatremia
•   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
reported sodium concentrations may be low in association with
hyperlipidemia hyperproteinemia hyperglycemia
678
who is at a increased risk for hypernatremia and associated hypovolemic dehydration
``` infants small children developmental delay hx AMS critical illness rendering them unable to respond to thirst mechanism ```
679
a serum level of
<125
680
hyperkalemia - what on ECG
peaked T waves
681
ventricular arrhythmias, prominent u waves, ST segment depression
hypokalemia
682
electrolyte imbalances that can cause seizures
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
Ventricular ectopy, torsades de pointes
hypomagnesemia
684
Hypotension | AV block
hypermagnesemia
685
Long QT interval | AV block
hypocalcemia
686
electrolyte abnormality associated with eating disorders
chloride responsive metabolic alkalosis and significant hypophosphatemia
687
eating disorders carry risk for cardiac arrhythmias due to electrolyte abnomalities
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
evaluating degree of malnutrition in eating disorders
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
analysis for fluid and electrolyte evaluation
BMP or CMP
690
indicate dehydration but not predictive alone
BUN
691
serum bicarb levels of ____, along with clinical findings of moderate to severe dehydration
<17
692
serum bicarb levels of ____, associated with high risk of failing oral rehydration therapy
<13
693
normal chloride levels
98-108
694
normal k
3.5-4.5
695
what does CMP include
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
pH of < ____ with normal PCO2 and normal or low bicarbonate may indicate dehydration
7.35
697
Urinalysis: dark color, high specific gravity and presence of ketones can indicate
dehydration
698
urine electrolytes: if Na+ is low, kidneys may
be conserving sodium due to dehydration
699
fractional excretion of sodium assists in differentiating
between dehydration and poor kidney function
700
What would a CBC show in dehydreation
elevated RBC, WBC or both
701
most metabolic disorders are inherited as
autosomal recessive traits
702
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.
Genetic metabolic disorders
703
Acute finding vs chronic findings of inborn errors of metabolism Seizures/lethargy/coma
Hypotonia
704
Acute finding vs chronic findings of inborn errors of metabolism Poor feeding/vomiting
FTT
705
Acute finding vs chronic findings of inborn errors of metabolism Hypoglycemia
Recurrent unexplained illnesses
706
Acute finding vs chronic findings of inborn errors of metabolism Signs of sepsis
Developmental delay/loss of milestones
707
Acute finding vs chronic findings of inborn errors of metabolism Hyperammonemia
Cardiomegaly
708
Acute finding vs chronic findings of inborn errors of metabolism ketosis
macro/microcephaly
709
Acute finding vs chronic findings of inborn errors of metabolism Metabolic/lactic acidosis
Eyes/hair/skin abnormalities
710
Acute finding vs chronic findings of inborn errors of metabolism abnormal urine odor
"course" appearance"
711
Urine odors associated with IEM Maple Syrup
Maple syrup urine disease
712
Urine odors associated with IEM Musty
Phenylketonuria
713
Urine odors associated with IEM sweaty feet
Isovaleric/Glutaric acidemia
714
Urine odors associated with IEM Boiled cabbage
Tyrosinemia
715
Urine odors associated with IEM Fishy
Trimethylaminuria
716
Metabolic labs what do you grab first when you have a suspicion if anything is positive then what do you snag
``` 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
what tests can be done for glucocorticoid excess
24 hr urinary free cortisol midnight salivary or plasma cortisol overnight low dose dexamethasone suppression test
718
tests for adrenal insufficiency
8AM plasma cortisol and ACTH concentration Low dose ACTH stim test High dose stim test Metyrapone test Serum renin level Aldosterone level
719
Test for congenital Adrenal hyperplasia
High dose ACTH stim test 17-hydroxyprogestrone Cyp21 analysis
720
tests for calcium homeostasis
Total calcium ionized calcium parathyroid hormone PTH-related protein Urine Calcium: Creatinine ratio
721
Test for Vit D status
25-OH 1-25 (OH) 2D
722
Markers of bone turnover
Osteocalcin bone specific alkaline phosphatase N-telopeptides
723
tests for water homeostasis
serum and urine osmolality urine sp. gravity water deprivation test vasopressin challenge serum vasopressin levels
724
tests for autoimmune thyroid disease
TSH Thyroid receptor antibody (TRAb) Antithyroglobulin (ATG) Thyroid peroxidase antibodies (TPO)
725
from 2 years of age until puberty approx __ -___cm linear growth/year is considered normal
4-5
726
mid-parental height calculation: Target height
male: {paternal height +maternal height}/2 +5cm females same just minus 5 cm
727
if I want to look at ambiguous genitalia what radiographic study?
US
728
if I want to look at thyroid nodules what radiographic study?
US
729
if I want to look at pituitary tumors what radiographic study?
CT or MRI
730
if I want to look at osteoporosis or osteomalacia what radiographic study?
Plain film or DEXA scan
731
tanner staging male early adolescence (10.5-14 yrs) no pubic hair preadolescent penis prepubescent testes
Tanner 1
732
tanner staging male early adolescence (10.5-14 yrs) scanty pubic hair penis - slightly increased in size enlarging testes
Tanner 2
733
tanner staging male middle adolescence (12.5-15 yrs) pubic hair - darker with curls longer penis larger testes
Tanner 3
734
tanner staging male middle adolescence (12.5-15 yrs) pubic hair - course and curly larger penis scrotum darkens
Tanner 4
735
tanner staging male late adolescence (14-16 yrs) pubic hair - adult adult penis scrotum adult
Tanner 5
736
tanner staging female ``` early adolescence (10-13 yrs) preadolescent pubic hair preadolescent breasts ```
Tanner 1
737
tanner staging female early adolescence (10-13 yrs) sparse, straight pubic hair small mound breasts
Tanner 2
738
tanner staging female middle adolescence (12-14 yrs) dark curls pubic hair breasts - larger with no overt contour separation
tanner 3
739
tanner staging female middle adolescence (12-14 yrs) course and curly pubic hair breasts - secondary mound of areola
tanner 4
740
tanner staging female late adolescence (14-17 yrs) pubic hair adult triangle shape appearance breasts - Nipple projects, areola becomes a part of the breast
tanner 5
741
what type of AI is a result of a destroyed or inactive adrenal gland or hormone production failure
Primary AI
742
in infancy, what is the most common cause of primary AI
CAH
743
what type of AI is associated with a deficiency of ACTH
Secondary AI
744
hypothalamic decrease in CRH secretion or production is what type of AI
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
what are the most common reason for ACTH deficiency in childhood
Craniopharyngiomas | Secondary AI
746
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
Tertiary AI
747
drugs that associated with tertiary AI
Glucocorticoids spironolactone etomidate ketoconazole
748
HPA axis may not return to normal for up to how long after long term steroid treatment
more than 1 month
749
what type of AI is experienced to some degree by every critically ill pt
relative AI
750
If a child is responsive to fluids in shock, what is their AI status
absent
751
explain neonatal adrenal insufficiency
infant HPA axis is immature further limit infants ability to increase cortisol production in response to stress
752
cortisol level that suggests AI
<16 ug/dl or <440 nmol/L

Critical Care I (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions