Mine Flashcards

(500 cards)

1
Q

Monosaccharides

A

Glucose, galactose, fructose

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2
Q

Primary fuel source for brain after 48 hr fast

A

Ketone bodies

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3
Q

What aids diarrhea in centrally fed patients

A

Soluble fiber
Soluble = sponge
Aids in diarrhea

Common Foods High in Soluble Fiber:
Oats: Oatmeal and oat bran .
Barley:
Legumes: Beans (like kidney beans, black beans, and chickpeas) and lentils
Apples
Carrots

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4
Q

Nitrogen output equation

A

UUN + 4 g = nitrogen output

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5
Q

What vitamins do not require sodium as a transporter

A

B12 and folate
B12 = needs IF
Folate = folate transporter

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6
Q

Vitamin C absorption

A

Ileum , some in jejunum

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7
Q

Riboflavin absorption

A

Proximal small intestine ie duodenum/jejunum

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8
Q

Pantothenic acid absorption (vitamin B5)

A

Jejunum via
Passive diffusion or sodium dependent active transport

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9
Q

Niacin deficiency

A

Pallegra aka the 3 D’s= dermatitis diarrhea dementia
Foods= meat fish poultry enriched and fortified grains
Patients in antitiburculosis meds or ioniazids or mercaptopurine

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10
Q

Metabolic alkalosis pH

A

> 7.45
Renal losses, diuretics, loss of intravascular volume, decr chloride
Chronic diuretic therapy

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11
Q

When is high protein / low calorie nutrition not appropriate

A

Obesity with uremia

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12
Q

Treat mild hypercalcemia with

A

Hydration

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13
Q

Treat severe hypercalcemia with

A

Aggressive IV saline hydration and IV lasix/loop diuretics

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14
Q

Basic structure of triglyceride

A

Glycerol backbone with 3 fatty acid molecules attached via ester linkage

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15
Q

Hemoglobin does what

A

Transports oxygen from lungs to other parts of body

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16
Q

Vitamins that require bile salts

A

Fat soluble
a D e k

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17
Q

Wilson’s disease

A

Copper toxicity
genetic deficiency of copper metabolism -> Cu accumulates in liver and other organs

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18
Q

Fat in distal ileum

A

Slows transport
Ileal break slows transit in response to enteric hormones like GLP1,GLP2, PYY

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19
Q

ATP production occurs in

A

Cells that contain mitochondria

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20
Q

Intracellular fluid

A

Inside cells , 60% of total bw
K phos mag

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21
Q

Extracellular fluid

A

Na cl and bicarb main electrolytes

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22
Q

In extended periods of fasting the body uses what as the main source of energy

A

Fatty acid oxidation

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23
Q

Critical Illness and the acute phase responses of serum iron and ferritin

A

in critical illness, serum iron will decrease, serum ferritin will increase increases

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24
Q

Organs necessary for gluconeogenesis

A

Liver small intestine and kidney

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25
Ursodial facilitates absorption of
Fat Can dissolve some gall stones and treat primary cholangitis
26
Where is essential amino acids oxidized
Liver
27
Patient with ileostomy at risk for what def
B12
28
Vitamin A absorption
Primarily in upper small intestine
29
k absorption
Primarily jejunum
30
Thiamine (b1) absorption
Primarily in proximal small intestine primarily in jejunum
31
Patient with back pain and abd pain, hx of pancreatitis and recent binge drinking.Reports bloating and oily stools. Should be evaluated for
Pancreatic exocrine insufficiency PERT may help
32
Inadequate chromium intake on PN may have
Hyperglycemia Chromium potentiates action of insulin
33
Insoluble fiber
think "Broom" Increases stool weight and bulk and increase regularity of bowel movements Foods High in Insoluble Fiber: Whole Wheat Products Wheat Bran: Vegetables: Many common vegetables contribute insoluble fiber, such as:Green beans, Cauliflower, Broccoli, Carrots Fruits with Edible Skins: Apples, pears, and berries consumed with their skins on
34
Mct
Water soluble Do not require bile salts or pancreatic enzymes for absorption Transported directly to liver Excess can cause GI upset
35
Fat digestion begins in
Majority in duodenum
36
50 year old male who weighs 80kg. Calculate his TBW and intravascular space.
TBW= 80 kg x 60% = 48 Liters ECF= 1/3 x 48 =16 Intravascular space is 1/4 of the ECF. SO 16 x 1/4 =4 liters
37
SBS with best outcome
With all segments of small bowel and colon in continuity - jejunoileocolonic anastomosis
38
SBS most difficult
End jejunostomy - likely needs PN
39
Phytobezoar tx
Enzymes such as cellulase or endoscopic intervention Do not use meat tenderizer that contains papain
40
EFAD sx and tx
Dry scaly rash Impaired wound healing Increased infections & immune dysfunction Treatment: give 100 grams weekly of SO-ILE; 20% ILE formulation, 250 mL 2x weekly, or 500 mL x1 weekly
41
AMDR set for (-acceptable macronutrient distribution range)
protein carbs and fat including omega 3 and omega 6
42
Choline for
Lipid transport and metabolism Investigated as tx for hepatic steatosis. PN does not contain
43
Pt with NG suction x 48 hrs at risk for
Low potassium Normal gastric fluid is 10’mEq/L of K Also hyponatremia and hypochloremia And can cause metabolic alkalosis
44
Metabolic alkalosis causes DAMPEN
D : diuretics A: adenoma / colonic adenoma m: misc: bulimia excessive upper GI losses p: post hypercapnia (build up of co2 in copd) E: emesis n: NG output
45
Swinamer equation
Uses body surface area
46
Absence of Glutamine
Can cause mucosal atrophy It is the principle metabolic fuel for intestinal cells
47
Supplemental arginine
Considered therapeutic for wound healing and immune function Controversial for critically ill septic patient
48
Hyperkalemic emergency - first line tx
Calcium gluconate Used for symptomatic pts with ECG changes
49
Deficiency of brush border oligosaccharides causes
Diarrhea bloating and flatulence after sugar intake
50
When determining nitrogen balance, urea accounts for what % of total urine nitrogen losses
80% Nitrogen intake = 24 hour protein intake (g/day) / 6.25 Nutrition output = 24 UUN (grams) + 20% UUN + 2 grams
51
Accuracy of nitrogen balance can be effected by
Wounds fistulas ostomy stool and urine output
52
Glycogen stores can sustain normal activities in a healthy adult for
1 day
53
Pt with poor renal function and on sulfamethoxazole/trimethoprim for a UTI likely to have
Hyperkalemia - trimethoprim can induce hyperkalemia by impairing renal K excretion
54
All of these hydrolyze fat in the small intestine
Pancreatic lipase, cholesterol ester hydrolase and phospholipase
55
Vitamin D toxicity results in
Soft tissue calcification
56
Vitamin D deficiency results in
Osteomalacia Bone pain Tetany Low Ca
57
Majority of peptide absorption
Takes place in small intestine
58
Dietary folate absorbed via
Enterohepatic circulation
59
What limits folate absorption
Zinc deficiency, chronic ETOH use, changes in jejunal pH, impaired bile secretion
60
What is glycogen
Is storage form of carbs in the body Stored primarily in liver and skeletal muscle
61
Glutamine is a
Conditionally essential AA and primary source of fuel for enterocytes
62
Glucose and galactose transport requires
Sodium glucose transporter 1
63
Tests for selenium status
Plasma selenium level Erythrocyte selenium concentration Plasma glutathione peroxidase
64
Most serous complication of hyperphos
Metastatic calcification of non skeletal tissues When ca/phos product exceeds 55 mg2/dL Also causes secondary hyper parathyroidism and renal osteodystrophy
65
Patient in ICU with severe diarrhea will likely have what acid base disorder
Metabolic acidosis Diarrhea induces GI losses of bicarb and can cause metabolic acidosis (with normal anion gap)
66
Albumin half life
14-20 days albumin is a negative acute phase response - decreases in times of stress/inflammation
67
Retinal binding protein half life
12 hrs
68
69
Ascites tx
Fluid restrict Sodium restrict 1.5g/kg/d protein Max concentration PN
70
Clinical symptoms of SIADH
Increased urinary sodium - sodium wasting , causing labs notable for hyponatremia Inappropriate release of ANTIDIURETIC HORMONE. Result is increased total body water and dilutional hypontremia
71
Tx for SIADH
Fluid restriction and increased sodium intake
72
Urine osmolality tells what
How well kidneys are concentrating urine Increased = dehydration, kidney disease, DI, SIADH decreased= excessive fluid intake, CHF, adrenal insufficiency , diluted urine
73
Urine osmolality in SIADH
Will be increased as well as urinary sodium Due to excessive water reabsorpton
74
Meds for SIADH
Loop diuretics or vasopressin2 receptor agonists
75
Iron def sx
Pallor Fatigue Microcytic anemia
76
Tyrosine becomes essential in
PKU - deficiency of phenylalanine hydroxylase enzyme
77
Aggressive zinc supplementation can lead to
Can lead to copper deficiency
78
Copper toxicity is common with
Liver disease - excreted via bile *same with manganese
79
Zinc def can cause a secondary def of
Vitamin A
80
A creatine clearance <50 ml/min can compromise
Reliability of urinary urea nitrogen therefore cannot calculate nitrogen balance
81
Cheilosis is associated with
Riboflavin def Also includes hyperemia of oral mucosa, angular stomatitis, glossitis or magenta tongue
82
Folic acid def sx
Macrocytic or megaloblastic anemia
83
Which predictive equation most accurate for healthy obese and nonobese adults
MSJ
85
Normal length of small intestine in healthy adult
300-600 cm
86
If small bowel is <120 cm to an end jejunostomy or ileostomy pt will
Likely require PN and hydration
87
Thiamin def can result in ___
Lactic acidosis Needed for metabolism of CHO AND conversion of pyruvate to acetylcoA Without thiamine, Cho metabolism at risk for lactic acid fermentation
88
RQ
0.7 is fat 0.82 is protein 0.85 is mixed 1 is carbs
89
Valproic acid can lead to
Carnitine def
90
___ reduces homocysteine concentrations
Folic acid Hyperhomocysteinemia can increase risk of coronary atherosclerosis folic acid B6 and B12 can reduce plasma levels
91
What part of bowel has least impact of nutrient absorption after a resection
Jejunum / proximal bowel; duodenum and proximal jejunum Bc ileal compensation and adaptation
92
Hepatic enceph can be improved with supplementation of
Zinc Can be used in patients not improving on lactulose and rifaximin therapy
93
Conditionally essential AA
Arginine Cysteine Glutamine Glycine Proline Tyrosine
94
PN patient with high ileostomy output - what would they need
Increased volume and increased sodium Na concentration of ileal output can be as high as 120’meq/l
95
Albumin correlates with
30 day mortality
96
Ileal and Jejunal electrolyte content is most similar to
Lactated ringers - 130 meq/l na, 109 meq/l chloride, 4 meql/ potassium, 28 meq/l lactate, 2.7 meq/l calcium
97
Whay vitamin is impacted with chronic PPI use
B12
98
What’s the bodies adaptation of starvation
Increased lipid oxidation
99
Chronic steroid use and vitamin A deficiency. How long would you supplement vitamin A
7 days
100
What happens in both acute illness malnutrition and social environmental malnutrition
Lipolysis
101
Characteristics of starvation
Hypoglycemia and ketosis
102
Characteristics of stress related malnutrition
Hyperglycemia and hyper metabolism
103
Copper def associated with ___ anemia
Microcytic hypochromic copper and iron = microcytic anemia
104
Deficiencies of folate or b12 result in ___ anemia
Macrocytic anemia
105
Iron def results in ___ anemia
Microcytic hypochromic
106
Iron mostly absorbed in
Jejunum
107
Fluid requirements for age 18-55
35 ml/kg
108
Fluid requirements for age 55-75
30’ml/kg
109
Fluid requirements for age 75 or older
25 ml/kg
110
Dietary fat primarily absorbed in ___ of GI tract
Duodenum and proximal jejunum
111
Immune modulating formula most appropriate for ___ patient
TBI ASPEN cautions against use in ICU
112
Presence of ___ in SBS improves outcomes
Ileocecal valve and colon May allow life without PN even with less than 60 cm of small bowel remaining
113
what kind of oral rehydration solution best for end jejuonostomy Meq/L of sodium?
iso-osmolar, diluted juice with sodium. ideal range is 90-120 mEq/L sodium concentration. i.e isotonic IVF. recipe- 1/2 tsp salt + 32 oz water + 2 tbsp sugar
114
closed enteral system
24-48 hr hang time, decreased risk of microbial contamination
115
EAD site infection sx
foul smelling drainage, peristomal infection most common
116
pt should be able to meet ___ % of needs orally to wean TF
66%-75% or 2/3-3/4 needs
117
TF pt has N/V, if delayed gastric empyting is expected, what should you do
d/c or reduce narcotic meds, use low fat/low fiber formula and or isotonic formula (1-1.2kcal/mL), room temperature formula, reduce rate of TF infusion
118
Long term TF pt has new onset diarrhea, what should be first intervention
Cdiff should be ruled out in any pt receiving abx prior to ordering antidiarheal medication, these meds are not indicated with pt who have Cdiff
119
Blue dye
no longer recommended to assess aspiration
120
what should be first trialed to restore EAD patency
water - if water does not workk, an enzymatic declogging kit or mechanical device for clearing tubes may be used
121
what type of insulin should be used for a non-insulin dependent diabetic who is starting on enteral nutrition. BG is between 160-200 mg/dl.
regular insulin *Short acting* may minimize incidence of hypoglycemia when initiating EN, as titration and tolerance of EN is unpredictable at first
122
what type of insulin should a non-insulin dependent diabetic be on , when enteral nutrition is STABLE
basal/bolus insulin
123
when starting EN in the not critically ill hospital patient, what is best
full strength formula, 40-50 mL/hr advanced to goal rate within 1-2 days. bolus feeds can then be advanced by volumes of 60-120 mL every 8 to 12 hours until goal volume reached
124
Pt on an isotonic formula continuously at goal rate for 2 days. Ordered 30 mL FWF. Pt now c/o bloating and is distended. he has not had a BM in 36 hrs. GRVs are WNL. what intervention would be best initial strategy?
initiate a bowel regimen other strategies- obtain image to r/o abdominal etiology, reduce narcotics or anticholinergic meds, fiber*but may incr gas*, providing additional free water
125
___ feeding may improve nutrient delivery in the ICU patient
volume based feeding protocol FEED ME and PEP UP protocols have been used w/ positive outcomes small bowel feeding is superior to gastric feeding in terms of nutrient delivery, however, can still be interrupted during the day and likely not as effective as volume based feeding
126
Terminally ill patient - what is true regarding feeding at end of life
the most common symptom when nutrition/hydration withheld is dry mouth- ellivated with good mouth care, ice chips, hard candy EN and hydration do not always ensure comfort - feeding even small amounts can prevent ketonemia and prolong sense of hunger, IVF in these pts can also increase discomfort and respiratory distress
127
Cyclic vs Nocturnal feeds
cyclic- 8-20 hours nocturnal- supplement intake and promote unobstructed day activity; would benefit stroke pt in rehab
128
optimal sodium concentration of oral rehydration solution for a pt with SBS
90-120 mEq/L
129
EN initiation should be delayed for ___
hemodynamically unstable pt risk of refeeding should not delay initiation of EN
130
Pt with GRV of ___ should hold EN
>500 mL
131
NG/NJ tube indicated for pt who requires EN for ___
4-6 weeks
132
What type of pt would be at risk for small bore tube misplacement
pt who is s/p stroke on inpatient medical unit, pt with head and neck trauma admitted to ICU, sedated pt s/p tracheostomy *ideal- pt who is alert and cooperate, as passage of feeding tube may be facilitated by concurrent pt swallowing to decr risk of entering respiratory system
133
___ tube requires IMMEDIATE replacement If disloged
Jejunostomy - closes quickly direct jejunostomy tube requires surgical, endoscopic, or fluouroscopic replacement NG/ND can be replaced by RN or medical provider bed side gastrostomy tube is priority, however if standard tube not immediately available, comparable sized Foley or red rubber catheter can be used to keep stomach open
134
What is most likely cause of diarrhea in enterally fed pt
sorbitol content of liquid meds as little as 10-20 g of sorbitol can lead to diarrhea
135
how to administer meds via EAD
administer each med separately, followed by 15-30 mL water flush enteric coating, controlled release, and sustained release meds should not be crushed and given via EAD
136
risk factor for aspiration in critically ill patients
decreased LOC, >70 years of age, GERD, delayed gastric emptying, supine position, vomiting, bolus feeds, mechnical ventilation, poor oral care
137
treatment for hypergranulation around PEG/PEJ site
cauterization with silver nitrate trimmed with scissors then treated w silver nitrate topical steroids may also be given
138
pt with ___ should be prioritized for feeding pump in time of shortage
jejunostomy feeding
139
EAD patency intervention
flush EAD with 30 mL water every 4 hours with continuous feeding also before and after intermittent feedings, and after each GRV measurement
140
Infectious complications in the EN patient can come from
patients own throat, lungs, and stomach can occur both exogenously through feeding tube equipment and endogenously via retrograde contamination from pt own infected secretions there is a correlation between prolonged enteral hang time and bacterial contamination no need for routine cultures in uncomplicated enterally fed pt
141
new occurrence of pain at or near the EAD site , weight gain, pressure, but no redness at site - should prompt what intervention
referral to physician or surgeon who placed tube - c/f buried bumper syndrome, infection, pressure necrosis
142
example of intermittent TF schedule
240 mL delivered over 45 min, five times per day 240-720 mL over 20-60 minutes -4-6 x day
143
example of bolus TF schedule
240-480 mL delivered over 4-15 min via gravity or syringe, at least 3 hours between feeds
144
oozing stools likely from
fecal impaction
145
change EN feeding set every ___ for open system
every 24 hrs and disposable feeding sets should not be reused
146
how much formula should be added to the open system administration feeding set at a time
formula supply for 8-12 hrs
147
ready to feed formula hang time
12 hrs
148
what should be labeled on EN order
pt info, EN formula name, delivery route and access device, admin method including rate/volume
149
trendelenberg position
used when HOB elevation of 30-45 degrees is contraindicated supine (laying on back) and HOB tilted down below feet
150
what patients should be included in refeeding protocol
ALL PATIENTS as nutrition screen does not always identify malnutrition
151
___ type of feeding would be best for critically ill pt with poorly controlled BG
continuous
152
oral nutrition supplements mostly made up of
CHO - taste better most enteral products for PO intake are 40-60 percent kcal from carbs,, 15-25% protein, and 15-35% from fat also usually have a blend of soluble and insoluble fiber
153
what formula most likely to occlude EAD
high fiber formula *increase in accumulation of formula sediment in the inner lumen of the EAD is seen more often with high fiber orrr high protein formulas
154
factors that increase risk for clogging of feeding tubes
fiber containing formulas, small diameter tubes, silicone tubes rather than polyurethane, checking GRVS, improper med administration
155
___ provides real time 3D view of EAD tip location during placement
electromagnetic placement highly accurate
156
constipation in the enterally fed pt may be associated with
lack of adequate hydration, inadequate or excessive fiber intakm prolonged bed rest/minimal physical activity, use of narcotics
157
pts should receive a minimum of __ of fluid per kcal when on high fiber feedings
1 mL/kcal
158
what interventions are effective in reducing risk of aspiration
oral care twice daily, HOB 30-45 degrees, post pyloric tube placement
159
when weaning TPN, a ___ prior to d/c is recommended
1-2 hour taper or 50% rate reduction to prevent rebound hypoglycemia
160
pinch off syndrome
when catheter is compressed between first rib and clavicle leads to intermittent occlusion of infusion and increased risk of catheter fracture change in arm position can relieve occlusion - Hallmark sign if catheter tears, tx is removal and replacement
161
___ is most effective for clearing catheter occlusion d/t precipitation of calcium phosphate
0.1N hydrochloric acid *note this can be associated w/ fever, phlebitis, sepsis
162
___ used for clearing occlusions d/t meds high in pH (tobramycin, phenytoin)
sodium bicarb 1 mEq/L solution
163
___ most effective for clearing catheter occlusion d/t lipid residue
70% ethanol
164
excessive CHO in PN Can result in
hepatic steatosis, as excess CHO deposits in liver as fat also can increase CO2 production
165
metabolic bone disease
chronic complication of PN -from potential aluminum contamination, inadequate Ca provision, Mg and Copper def, also both vitamin D toxicity and def can lead to bone loss
166
Best practices to reduce CVAD related infections during insertion
during insertion process- hand hygeine, cleaning site with 0.5-2% chlorhexedine/70% alcohol preparation, use max barrier precautions
167
Pt reports difficulty aspirating blood from CVAD but can still infuse PN - what is this most likely caused by
fibrin sheath - usually allows meds and PN to infuse but aspirating blood difficult
168
Pt has fever, chills, positive peripheral and central blood cultures, no redness or purulence at cath exit site. likely has
catheter related blood stream infection *often present with no redness or purulence
169
tunnel infection presents with
tenderness, erthyema, induration from catheter site along subcutaneous tract of a tunneled catheter
170
exit site infections present with
erythema or induration within 2 cm of cath exit site, abscense of concomitant blood stream infection and without purulence
171
catheter related phlebitis presents with
inflammation of vessel wall as well as erythema and pain near cath insertion site or along the affected vein
172
`elevated conjugated (direct) bilirubin indicates
cholestasis *elevated Alk Phos, GGT, conjugated bili usually indicate cholestasis or biliary obstruction elevated direct bili; >2 mg/dL
173
70 kg patient receiving 3000 kcal/day from PN has mild-mod elevations of serum aminotransferases and mild elevated bilirubin and alk phos. likely exhbiting what type of PN associated liver disease?
hepatic steatosis - overfeeding with 43 kcal/kg
174
hepatic dysfunction facts
neomycin (antiobiotic) can cause partial villious atrophy and steatorhea lab markers are poor indicators in cirrhosis anthropometrics are also poor d/t ascites muscle and fat wasting is common
175
hepatic steatosis in adults presents with
usually with moderate elevations of aminotransferases, usually c/b overfeeding
176
cholestasis in children
characterized by impaired biliary secretion elevated conjugated (direct) bilirubin is common lab manifestation in this population
177
gallbladder sludge
complication of PN d/t lack of enteral stimulation
178
clinical presentation of refeeding includes
dyspnea, seizures, cardiac arrthymias -electrolyte abormalites- low Phos, Mg, K, sodium retention uusually in early phase d/t excessive sodium and fluid intake--leads to pulmonary edema, cardiac decompensation
179
PN dependent pt with ileostomy output of 3L/day presents with a BUN/serum Creatinine ratio of 30:1 and mild hyponatremia. what would be an appropriate PN intervention?
Increase sodium and increase fluid BUN/Cr ration of >/=20:1 indicates volume depletion
180
42 y/o patient s/p bowel resection is on PN for a post op ileus. NG output is 2.5-3 L/day. Arterial blood gas ABG reveals a pH of 7.49 and PCO2 of 45 mm Hg, serum bicarb of 34 mEq/L. What is an appropriate PN intervention
increase chloride:acetate ratio Bicarb 34 is high (22-26) pH of 7.49 indicates alkalosis (7.35-7.45) PCO2 is normal (34-45)
181
Manganese toxicity effects the __
brain Parkinson like sx pt with impaired biliary secretion / liver diseases are at risk for toxicity bc manganese is excreted via bile can be visualized via brain MRI or monitor whole blood manganese levels since 60-80% of it is contained in red blood cells
182
Management of catheter exit site infection
topical antibiotic ointment if no purulence or clinical signs of sepsis present
183
pt on PN and AKI.. ABG reveals pH 7.31, PCO2 36, serum bicarb 20 mEq/L. What would you do?
increase acetate (bicarb) or decrease chloride metabolic acidosis likely r/t AKI pH indicates acidosis (7.35-7.45) PCO2 is normal (35-45) Bicarb is low (22-26) -- so decreased chloride:acetate ratio
184
refractory hypokalemia should be assessed for what other electrolyte disorder
hypomagnesemia
185
what is most likely responsible for elevated serum bicarbonate in a PN patient 1. excess chloride salts 2. diarrhea 3. excess acetate salts 4. acute renal failure
3- excess acetate salts; metabolic alkalosis other causes of metabolic alkalosis- NG suctioning, volume depletion, diuretic use *excess chloride, diarrhea, acute renal failure are common causes of metabolic ACIDOSIS
186
pressure sensitive 3 way valve catheter
groshong
187
best approach to reduce cholelithiasis
early initiation of EN to improve bile flow
188
best approach to reduce PNALD - PN associated liver disease
cyclic PN
189
risk factors for development of rebound hypoglycemia after abrupt cessation of PN
malnutrition, hepatic dysfunction, renal insufficiency
190
190
potential causes of hyperglycemia in a pt receiving TPN
pancreatitis, obesity, sepsis
191
renal failure pt's experience ___ with insulin
longer half life=higher incidence of severe hypoglycemia
192
Pt receiving TPN via CVC. they now present with SOB, cough, cyanosis of face, neck, shoulder, arms. WHat type of device complication are they experiencing?
superior vena cava syndrome
193
Thrombosis sx with PN
chest pain, ear ache, jaw pain, swelling of arm, shoulder, neck or face on ipsilateral catheter side, or leaking at the exit or insertion site
194
Tunnel infection is characterized by
pain, swelling, erythema, induration along the subcutaneous tract of a tunneled catheter
195
Pinch off syndrom
complication of subclavian tunneled central catheters, with intermittent or permanent occlusion related to postural changes
196
superior vena cava syndrome
SOB, dyspnea, cough, cyanosis of face, neck, shoulder, arms, distended check or neck veins
197
Pt is receiving 45 kcal/kg via TPN. Consequences of over feeding a critically ill patient on TPN are =
respiratory acidosis (incr CO2 production), elevated TG (fatty liver), elevated BG suggested feeding range= 12-25 kcal/kg
198
45 kg patient, 60 years old, on PN for high output fistula. he is receiving 67 g AA, 400 grams Dex, 25 g Lipid (SO-ILE), in 1500 mL volume. What is he at risk for developing?
Hyperglycemia from dextrose = pt receiving more than recommended dose, GIR of 6.2 mg/kg/min Other components are WNL (0.56 g/kg ILE, 1.5 g/kg protein, 33 mL/kg fluid) Ideal GIR range is 4-5 mg/kg/min
199
pt on PN via PICC presents with arm, shoulder, and neck swelling. also has dilated collateral veins over the arms, neck, and chest. what is he likely experiencing
catheter related central venous thrombosis central venous catheters can cause endothelial trauma and inflammation which lead to venous thrombosis
200
fibrin sheath / fibrin sleeve
thrombotic catheter occlusion, and develops when fibrin adheres to external surfaces of the catheter
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40 year old M on long term TPN (15 years). He is on a 12 hour cyclic formulation and provides 5 g/kg/d Dex, 2 g/kg protein daily, and 1 g/kg fat daily. He has developed metabolic bone disease. W is an appropriate intervention to reduce hypercalciuria?
reduce AA content of PN solution *most important contributer to MBD is a negative calcium balance.
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factors that cause hypercalciuria
excessive Ca and inadequate Phos supplementation, excessive protein in PN solution, cyclic PN infusions, chronic metabolic acidosis Hyper parathyroidism; Pth pulls Ca out of bone and into blood and kidneys try to excrete via urine Too much vit D Loop diuretic like lasix
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factors that cause hypocalcemia
decreased Ca intake and or increased Ca urinary excretion
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Risk factors for developing PN associated liver complications
prolonged use of SO-ILE - proinflammatory and contain toxic phytosterols, which may impair bile flow reduce risk by= cycling PN, supplementing with enteral feeds, adding Ursodiol to stimulate bile flow, use alternative ILE that contain olive oil/fish oil with higher omega3:omega6 ratio- can reduce LFTs
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Pt w diabetes on TPN have increased risk of
catheter related infections
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DM and PN pt recs for BG checks and dextrose
glucose checks every 2-6 hrs, max GIR of 5 mg/kg/min, start dextrose at 100-150 g/day to reduce hyperglycemia and refeeding
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benefits of cyclic TPN
allows body to oxidize fat and results in lower insulin levels, improves liver enzymes
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Carnitine
essential carrier molecule in fatty acid metabolism, added as Levocarnitine in TPN, can help with elevated TG
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Pt with refeeding is starting on TPN, what should be supplemented?
Thiamine - involved in energy metabolism usually depleted in times of malnutrition, weight loss, chronic alcoholism. supplementation of 100-200 mg before feeding or before introduction of dextrose containing IVs. Continue supp for 5-7 days or longer depending on pt nutrition status.
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pt presents with suspected catheter occlusion, what are appropriate initial actions?
systematic approach to determine cause and prevent unnesessary cath removals/replacements. for ex= determine if occlusion is relieved via postural changes, remove dressing and check for kinks in tubing, review recent flushing techniques, check patency and blood aspiration, assess for signs of edema, redness, pain, dilated vessels
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sentinel event
pt safety event of an unexpected occurence involving death or serious physical injury or the risk thereof need for immediate investigation or response ex= pneumothorax after placement of CVC
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Risks associated with elevated TG in TPN pt
hypertriglyceridema; >400 mg/dL pancreatitis, fat overload syndrome, hypercoagulation, decr immune function, hepatic injury, pulmonary compromise, infection risk
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the most common route of infection for a tunneled CVAD is
contamination of catheter hub most common cause of infections for CVADs or implantable devices, with intraluminal colonization
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Ways to diagnose MBD
dual energy x ray absorptiometry, urinary phos concentrations, quantitative ultrasounds NOT serum calcium concentrations
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Fibrin sheath is an example of a ___
thrombotic catheter occlusion
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Examples of non-thrombotic catheter occlusions
mechanical obstructions, drug or mineral precipitates, lipid deposits
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Most appropriate pharmacological intervention to clear intraluminal clot in the CVAD device?
Alteplase 2 mg/2mL - cathflow only FDA approved thrombolytic agent for CVAD occlusions
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Osmolarity of amino acids
1 gram = 10 mOsm add all PN components together and divide by total volume
219
Osmolarity of dextrose
1 gram = 5 mOsm add all together and divide by total volume
220
Calculate osmolarity of this PN admixture= 75 grams AA, 210 grams Dextrose, at 125 mL/hr
Volume=3000 mL 75 grams AA x 10 = 750 mOsm 210 grams Dex x 5= 1050 mOsm = 1800 mOsm total 1800 mOsm / 3000 mL = 600 mOsm/L
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preferred site for placement of central venous access device in an adult patient
subclavian vein >>> less risk of infections compared to jugular or femoral placement external jugular NOT preferred, internal jugular and femoral placement have high risk of infection
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antibiotic ointment / prophylaxis for cathether associated sepsis prevention
NOT recommended - encourages resistant flora
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Pt on long term TPN develops involuntary movements, tremors, facial muscle spasms. what could be a cause?
manganese toxicity early phase = weakness, anorexia, headache, apathy late phase = Parkinson like sx toxicity may occur in pt on long term therapy supplemented by multiple trace elements. cholestasis and biliary obstruction also increase risk of toxicity; as more than 90% of manganese is excreted via bile into feces
224
63 kg, 75 y/o M with PNA is receiving TPN with 2800 kcal, 100 grams AA daily. his ABG reveals pH 7.32, PCO2 49, serum bicarb 25. WHat is an appropriate PN intervention? a. increase calories b. increase chloride:acetate ratio c. decreased chloride:acetate ratio d. decreased calorie content
Pt experiencing respiratory acidosis as evidenced by decreased pH, and elevated PCO2. He is also receiving 45 kcal/kg. Most appropriate nutrition intervention is to decrease calories. Overfeeding can lead to hypercapnia, excessive CO2 production
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What is most likely to contribute to metabolic bone disease in PN dependent patients? a. aluminum contamination b. calcium supplementation c. moderate AA dose d. correction of acidosis with acetate in PN
aluminum contamination *highest in PN calcium and Phos salts, trace minerals, and vitamins in PN solutions Renal insufficient patients at highest risk for toxicity due to impaired renal aluminum excretion causes osteomalacia by impairing calcium bone fixation, inhibiting conversion of 25H Vitamin D to active form, reduced PTH secretion
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Home EN covered by Medicare part B if
pt has permanent condition or disorder (defined as >90 days) that impairs food from reaching small bowel, or disease of small bowel impairs digestion or absorption of adequate nutrition I.e - dysphagia dx not covered= malnutrition, anorexia, dementia
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indication for home TPN
disease of small intestine or exocrine glands that significantly impair nutrient absorption, or motility disorders of GI tract which results in severe nutrient absorption i.e=need for bowel rest x 3 months
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Zinc deficiency symptoms
loss of taste and altered smell, night blindness (as zinc def can lead to vit A def), gonadal hypofunction, dermatitis if severe, alopecia, growth retardation
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what does MD note need to include to get HPN covered
must document failure of enteral feeding trial (doesnt need to say how long) or explain why enteral feeding tube is not an option
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most effective way to improve discharge teaching
teach back method
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what is required in the home for a PN patient at discharge
access to telephone, electricity, sanitary water, refrigeration
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the amount of aluminum in the PN bag is usually ___ times larger than packages state
10 times more
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enteral feeding pump will be covered by Medicare if
pt being fed via jejunal tube
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Medicare covers tube feeding expenses when the prescribed regimen provides
sole source of nutrition 25-30 kcal/kg
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which is not appropriate for home a. hickman catheter b. PICC c. midline d. implanted port
midline - peripheral
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which trace element def is likely to occur in long term PN patient a. iron b. copper c. chromium d. manganese
iron - not included in TNA d/t compatibility iron dextran can be added to 2-in-1, after given test to evaluate tolerance/allergy. serum iron and ferritin levels should be routinely monitored (every 1-3 weeks) to prevent iron overload
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home infusion providers should have policies that address
education, training, evaluation of pt/caregiver competency
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Best way to determine chromium status
no known reliable indicator role in glucose, protein, lipid metabolism, potentiates action of insulin. pregnancy and t2DM can lead to excess chromium excretion; if def is suspected, can treat hyperglycemic pt with chromium and observe for resolution of sx, lab detection very difficult
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increased risk of aluminum toxicity in pt's with
renal failure or iron deficiency anemia majority of aluminum in bloodstream is bound to protein, primarily transferrin, and cannot be excreted=excessive exposure to aluminum accumulation sx neither specific or sensitive
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written education materials
6th grade reading level, broad principles in plain language clear graphics and typography design
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home EN pt suddenly develops N/V, most likely cause is?
gastric outlet obstruction also- too rapid of a bolus administration, feeding tube migration, excessive feeding volume, gastroparesis
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DME companies are responsible for providing
formula delivery, equipment and supplies delivery, infusion nursing care
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Pt receiving high protein and high fiber enteral formula, at 65 mL/hr via PEG. FLushes are not scheduled, only as needed. Also checks GRV every 6 hrs and receives liquid medications twice daily. Tube is now occluded. This is likely d/t
inadequate flushing
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best practices to maintain EAD patency
use largest tube bore that is feasible, flush tubes before and after intermittent feeds or at standard intervals for continuous feeds, before and after meds, limit GRV checks
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recertify PN by medicare after ___ months
6 months
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DXA recommendation for long term PN pt
all pts on PN for >1 year should be recommended for a dual-energy x ray (DXA) scan absorptiometry
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initially, how often should labs be obtained for the home PN pt
weekly at first for 4 weeks or until labs are stable once stable, can be increased to monthly
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managed care and private insurance companies usually follow ___ guidelines for HPN coverage
Medicare criteria
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check micronutrients on the home PN pt every ___ months
every 6 months a micronutrient assessment should be obtained
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insurance companies usually cover
tubing, syringes, equipment not always formula
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home prepared or blenderized EN should be discarded after
24 hrs
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clinical manifestations of copper def can be similar to
B12 def symptoms anemia, leukopenia,foot numbness, gait difficulty
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max hang time for open system in the home setting
12 hours at home 8 hours in hospital
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closed system hang time
24-48 hrs
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most common complication after PEG placement
peristomal infection
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nutrition education is reimbursed for medicare for pt's with
DM and renal disease
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normal ABG values pH=
7.35-7.45 measures H+ concentration - acid base status of blood
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normal ABG values PCO2 (mmg Hg) =
35-45 this is the respiratory component of acid base regulation regulated by the lungs, acidic component
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normal ABG values PO2 (mm Hg)
80-100
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normal ABG values HCO3 (mEq/L)
22-26
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base deficit =
less base than necessary aka acidosis present
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base excess =
more base (HCo3) than necessary = alkalosis present
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respiratory alkalosis
primary problem is low PCO2, high pH (>7.45) -move in opposite directions- patient is blowing off too much PCO2 respiratory rate quickens, hyperventilation causes: pain, anxiety, fever, stimulated respiration (I.e. ventilator)
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respiratory acidosis
primary problem is high PCO2, and a low pH (<7.35) aka acidic -move in opposite directions- compensatory response is increase in HC0O3, respiratory rate has slowed down (hypoventilation) so there is retention of CO2 and causes a buildup of acid causes: COPD, stroke, cardiac arrest, airway obstruction, depressed RR, overfeeding
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metabolic disorders -acid/base
result from disturbances in plasma HCO3 (bicarbonate//base component) regulated by kidneys
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metabolic acidosis
primary problem is low HCO3 (bicarb) and low pH = so the body is in an ACIDIC state -move in same way- causes: severe diarrhea, laxatives, renal failure, DKA, CKD hyperkalemia is common HCO3 also decreases as GFR rises, so this is common in CKD too compensatory response: lungs will hyperventilate, increase RR, to blow off CO2
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A patient presents with metabolic acidosis. which ABG pattern will you see??
pH is low HCO3 is low
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acid/base balance - secondary change
compensatory response that acts to minimize pH changes produced by the primary disorder also called COMPENSATION -for example, when lungs are causing acidosis, the kidneys will step in and retain HCO3
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compensation for respiratory alkalosis
there is alkalosis = elevated pH, and decreased PCO2 the kidneys will then increase HCO3 (base) excretion
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compensation for respiratory acidosis
there is acidosis= decr pH, elevated PCO2 the kidneys will retain HCO3 (base) and lose H+ anions
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compensation for metabolic alkalosis
there is alkalosis = >pH, >HCO3 and high bicarb the lungs will retain CO2 (acid)
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compensation for metabolic acidosis
there is acidosis =
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for a patient with metabolic acidosis, what is the appropriate method for compensation seen on ABG?
metabolic acidosis = decreased pH, decreased HCO3 present = more acid present the lungs will lose acid (CO2) and breathe it off aka hyperventilation leading to a decrease in PCO2 lab
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simple acid base disorder means
presence of one primary acid-base disorder PCO2 and HCO3 move in same direction
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mixed acid base disorder means
simultaneous occurence of two or more primary disorders; 2 simple acid-base disorders at the same time pCO2 and HCO3 move in opposite direction= mixed acid base disorder example - high output fistula presenting with respiratory failure example - DKA presenting with PNA
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what is the renal compensation for respiratory acidosis
decreased pH due to increased PCO2 (acid) so the kidneys will decrease bicarbonate (HCO3) excretion to increase HCO3 levels
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acute respiratory acidosis etiologies
acute airway disorders that cause HYPOVENTILATION = build up of CO2 - airway obstruction, asthma/COPD exacerbation acute CNS depression (drug overdose, head trauma, stroke, infections) acute neuromuscular disorders (guillian barre, spinal cord injury) meds (opioids, sedatives, neuromuscular blockers) acute respiratory disorders (PNA, pulmonary edema, embolus, hemothorax, pneumothorax)
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chronic respiratory acidosis etiologies
asthma, COPD, emphysema, OSA, myasthenia gravis, spinal cord injury, MS, hypothyroidism
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respiratory acidosis treatment
indentify/treat underlying cause ventilator support, respiratory treatments, antimicrobial therapy as needed, antidotes for overdoses, d/c offending meds, avoid alkali therapy - bc this does not treat the underlying cause
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in respiratory alkalosis, the kidneys will compensate how?
alkalosis d/t lungs = >pH, breathing off too much PCO2 this means there is hyperventilation - breathing all of the acid off, making the blood basic the kidneys will then excrete bicarbonate (HCo3) and increase levels of H+
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respiratory alkalosis etiologies
HYPERVENTILATION CNS disorders - anxiety/panic attack, infections, head traumas, cancer hypoxia, elevated altitude pneumonia, pulmonary edema, embolism, hyperventilation, interstitial fibrosis mechanical ventilation - improper settings medications - xanthine derivatives, nicotine, catecholemines, salicylates pregnancy - progesterone leads to incr ventilation cirrhosis sepsis renal insuffiency - impaired compensation
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respiratory alkalosis treatments
identify/treat underlying cause d/c offending meds if present ventilator support respiratory suppresants- decr ventilation reassurance for anxiety antimicrobial therapy as approproate; PNA
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metabolic acidosis is defined 2 ways -
normal or elevated anion gap Anion Gap Basics • It’s a simple blood calculation to figure out where the acid is coming from. • Anion gap = (Sodium) – (Chloride + Bicarbonate) • Normal anion gap ≈ 8–12 (depending on lab).
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metabolic acidosis
lungs will hyperventilate
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Anion Gap equation
AG = Na - (Cl + HCO3) =
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Anion gap and albumin
hypo-albuminemia can falsely decrease the anion gap so you have to correct AG *Corrected AG = AG + 2.5 x (4.5 - measured albumin)
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Anion Gap results
normal = 3-11 increased AG = incresed unmeasured anions (PO4, SO4, albumin, ketones) Non-AG = bicarb losses from the ECF are replaced by chloride (every 1 mEq/L increase in Cl should result in 1 mEq/L decrease in HCO3) decreased AG = decreased unmeasured anions (when albumin is low)
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Etiology of normal anion gap metabolic acidosis USEDCAR
U=urinary diversion; loss of bicarb S=small bowel (pancreatic/biliary) fistula; loss of bicarb E= excessive chloride (IVF/PN) D= diarrhea; loss of bicarb C= CKD/carbonic anyhydrase inhibitors (diamox or acetazolimide) decr renal bicarb absorption A= aldosterone or adrenal insufficiency R=renal tubular acidosis; decr renal bicarb absorption
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etiology of elevated anion gap metabolic acidosis GOLDMARK
increase levels of acid in the body G= glycols - ethylene and propylene O= oxoproline (acetaminophen;chronic use) L= lactic acidosis (most common; d/t hypoperfusion/sepsis) D=D-lactate acidosis (small bowel bacteria overgrowth), undigested CHO in colon M= methanol toxicity A= aspirin toxicity R=renal failure K=ketoacidosis; DKA and starvation
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treatment of metabolic acidosis
identity/treat underlying cause antidiarrhea/antisecretory meds to d/c GI losses of bicarb d/c chloride (acid) based fluids adjust PN to have higher acetate (bicarb/base) :chloride ratio fluid resus - insulin for DKA or antimicrobials for sepsis bicarb replacement(oral or IV) antimicrobials for bacterial overgrowth
291
2 classifications of metabolic alkalosis
saline resistant (urine chloride >10 mEq/L) and saline responsive (urine chloride <10 mEq/L)
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metabolic alkalosis is what
primary problem is high HCO3 (bicarb) and increased pH (>7.45) -causes; excessive loss off H+ (acid) from kidney or stomach, ingestion or administration of bicarb rich fluids, loss of fluid containing chloride (Acid) *persistent vomiting, NGT output, diuretics DAMPEN lungs compensate by= increase PCO2= lungs will do this by decreasing respiratory rate/hypoventilation, retain CO2 to increase acid levels Metabolic alkalosis --> lungs hypoventilate
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Saline responsive metabolic alkalosis causes DAMPEN
Metabolic alkalosis. Caused by losing too much acid or having too much base in blood D=diuretics; loops and thiazides A=adenoma (secrete chloride and K) M=miscellaneous aka bulimia (Excessive upper GI losses) P=post hypercapnia (build up of CO2 as in COPD) and incr PCO2 E=emesis N=NG suction/losses
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Saline resistant metabolic alkalosis causes ABELCH
Saline resistant = saline won’t fix A= alkali ingestion B= beta hydroxylase deficiency E= exogenous steroids L= licorice ingestion C=Cushing's syndrome H=hyperaldosteronism; enhanced H+ secretion/losses the higher the urine chloride, the greater the shift of H+ into cells or increase in H+ secretion
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metabolic alkalosis treatment
indentify/treat underlying cause volume replacement d/c acetate (bicarb) based fluids; change to chloride based salts adjust PN to have higher chloride:acetate ratio antiemetics, acid suppressive therapy for emesis or high NG output K replacement when K is low acetazolamide; can cause metabolic acidosis, so can help with this , instead of lasix give diamox spironolactone hydrochloric acid=severe/rare cases
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Which can lead to metabolic alkalosis? 1. pulmonary embolism 2. septic shock 3. high NG output 4. morphine overdose
NG output pulmonary embolism= respiratory problem septic shock= high lactic acid/lactate buildup d/t tissue hypofunction, so likely metabolic acidosis w/ AG morphine overdose= leads to decr resp rate, so likely acute resp acidosis
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Acid base considerations for TPN
use acetate salts instead of chloride salts when low HCO3 present (acidosis) acetate is converted to bicarbonate in the liver ; HCO3 additives are incompatible in PN solutions Excess CHO can lead to increased PCO2 production, difficult weaning from the vent Excess Cl salts can cause non-AG metabolic acidosis Albumin is largest source of unmeasured anions in the blood; can falsely effect AG
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pt comes in w/ c/o vomiting x 3 days. NG tube was placed. she is NPO on IVF (LR at 125 mL/hr). Her chloride is 92 (low) her K is 3.1 (low), her PCO2 is elevated at 47, pH is 7.53 (also elevated), and HCO3 is 36 (elevated). what is the primary acid base disorder? and what is the source?
metabolic alkalosis - pH >7.45, HCO3 (bicarb) is also elevated. what is the source= GI losses of chloride rich fluids - vomiting, NG tube what would the compensation response be? = lungs will retain CO2, decr resp rate (hypovent) how to treat = fluid resus, replete K, give isotonic fluids
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IVF for gastric fluid loss
0.45%NaCl (1/2 normal saline) + 10-20 mEq/L KCL Stomach fluid: ~60 mEq Na, 130 mEq Cl, 15 mEq K, 0 mEq HCO3
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Colon fluid
60 mEq Na, 40 mEq Cl, 30 mEq K, 0 mEq HCO3
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Duodenum fluid
140 mEq Na, 80 mEq Cl, 5 mEq K, 0 mEq HCo3
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Pancreas fluid
140 mEq Na, 75 mEq Cl, 5 mEq K, 115 mEq HCO3
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Bile is made up of how much Na, Cl, K, Bicarb?
145 mEq Na, 100 mEq Cl, 5 mEq K, 35 mEq HCO3
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Ileum fluid
140 mEq Na, 104 mEq Cl, 5 mEq K, 30 mEq HCO3
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62 y/o male s/p emergent bowel resection 9 days ago. now with high output enterocutaneous fistula. ECF output = 1000-1200 mL/d x 3 days. Getting normal saline at 125 mL/hr and Is NPO. His labs are notable for hyponatremia, hypokalemia, hyperchloridemia, low CO2, low pH, low PCO2, low HCO3. what is his primary acid base disorder? what is the cause?
high output = anything >500 ml/d primary disorder=metabolic acidosis; low pH and low bicarb (HCO3) cause = ECF output with high bicarbonate losses; now he is acidic expected compensation; lungs will increase RR, breathe off CO2 treat= change NS to a balanced crystaloid like LR or PLasmalyte
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Small bowel fluid loss replacement: IVF
balanced crystalloid; LR, Plasmalyte bicarb or acetate-based custom fluid *pancreas, bile, ileum= all contain bicarb and ~140-145 mEq/L Na, 75-100 mEq/L Cl, 5 mEq/l K, ~30-115 mEq/L bicarb *highest bicarb in pancreatic fluid
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65 y/o F underwent ileal conduit. she is NPO d/t large volume emesis post-op. now with aspiration PNA on antibiotics. she is NPO for ileus and IVF is NS at 100 mL/hr. Labs= elevated chloride, low CO2, low Ph, low HCO3. what does she likely have? cause of primary disorder? what is expected compensation? how do you treat?
pH and HCO3 are low = metabolic acidosis cause= loss of bicarb from ileal conduit, receiving NS IVF expected compensation= lungs will incr RR, to breathe off CO2 (acid) how would you treat= change IVF to balanced crystalloid, bicarb containing IVF
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ileal conduit
invasive bladder cancer surgery complication- metabolic acidosis; normal/non anion gap hyperchloremic, U in the USEDCAR mnemonic experiences= excess losses of bicarb and sodium, increased absorption of ammonium,hydrogen, and chloride *know common to have loss of bicarb and Na
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3 types IBD
Crohn's, UC, and colitis indeterminant
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features of Crohn's disease
transmural unpredicatable small bowel involvement - rectal sparing fistulas, granulomas, lesions, 25-30% have no bleeding
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features of ulcerative colitis
mucosal disease, starts from rectum up, colonic involvement only, bleeding very common, pain when defecating
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features of colitis indeterminant
features of both crohns and UC 10% of cases
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IBD drugs and nutrient reactions -Sulfasalazine and methotrexate
folate metabolism
314
IBD drugs and nutrient reactions TNF-a-Antibody
protein metabolism
315
IBD drugs and nutrient reactions Steroids
alters mineral and protein metabolism
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IBD common effected vitamins/minerals
Vitamin D, B12, vitamin C and vitamin A Zinc, Selenium Calcium, Magnesium, Iron
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IBD nutrition overview
IBD = significant nutritional risk - bowel rest with PN not superior to EN unless high output fistula or high grade SBO present - Elemental formulas not better than polymeric - CD fistula treated with PN may close but high rate of recurrence -peri operative PN is appropriate if malnourished
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Intestinal failure definitiion
IV supplementation is required to maintain health and or growth vs intestinal insuffiency; doesn't require IV supplementation but still+reduction of gut absorptive function
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Short bowel syndrome def
patients with <200 cm of functional small bowel 2 subgroups - colon in/not in continuity - possible reconnection - total colectomy
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how to know pt's remaining bowel in SBS
operative report at time of surgery, or radiologically via opsiometer
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SBS with greatest nutritional risk
1. duodenostomy or jejunoileal anastomosis with <35 cm residual bowel 2. Jejunocolic or ileocolic anastomosis with <60 cm remaining bowel 3. end jejunostomy with <115 cm remaining bowel
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Sites of Absorption - Small intestine
Carbs, Fats, Proteins Calcium, Magnesium, Trace Elements, Vitamins
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Sites of Absorption - Small & large intestine
water, electrolytes
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normal fluid reabsorbed via intestines
small bowel - ~7 L (max 12 L) colon - ~1.4 L (max 5 L)
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Jejunal Resection considerations
pt will still have good absorption unless >75% resected good ileal adaptation preserves absorption of B12 and bile salts normal intestinal transit peptide YY is present least common type of SBS
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Ileal Resection considerations
adequate absorption if >/=60 cm of jejunum to colon remaining malabsorption of B12 and bile salts Poor jejunal adaptation rapid transit- reduced peptide YY small bowel bacterial overgrowth
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Extensive Bowel Resection considerations
>/=100 cm of small bowel to avoid TPN large fluid losses, malabsorption, poor jejunal adaptation, acid hypersecretion, rapid gastric emptying, rapid intestinal transit, most challenging
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SBS and why there is malabsorptionh
acid hypersecretion - decr activation of pancreatic enzymes rapid intestinal transit - no time to mix food in intestine decreased peptide YY loss of surface area bacterial overgrowth bile acid wasting
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Meds to slow transit
loperamide, codeine, diphenoxylate-atripine
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How long does it take for bowel adaptation in SBS
~ 2 years
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common chronic pancreatitis nutritional issues
catabolic state, up to 150% REE, 35 kcal/kg, 1-1.5 g/kg protein +MCT, pancreatic enzymes mild-likely just need IVF and adv PO as toleranced mod/severe- start EN via NG, or NJ if NG poorly tolerated; likely benefit from semielemental formula for acute pancreatitis decr B12 and increase malabsorption of fat soluble vitamins, lower levels of antioxidants, insulin dependent diabetes APACHE and Ranson are 2 criteria to determine severity of pancreatitis
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types of pancreatic insuficiency
chronic pancreatitis CF Schwachman syndrome (short stature, nutropenia, anemia, PI, thrombocytopenia)
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pancreatic disease key nutrition concepts
acute -wacth for hypocalcemia (25%) alcoholic - thiamine, folate, mg, zinc, Selenium, b12 chronic - B12 and ADEK, evaluate fat metabolism, TG, steatorrhea PI - focus on growth and weight gain for children- assess nutrient needs, may have increased energy needs
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function of the liver
metabolic organ regulates protein and energy metabolsim vitamin storage and activation detoxifies and excretes waste products
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tx for ETOH hepatitis
abstain from alcohol corticosteroids nutrition - MCT EN as affective as steroids, PN may be beneficial on liver function, no published studies for EN vs PN
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malnutrition and liver disease
severity of malnutrition correlates with severity of liver disease frequently underdiagnosed
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liver disease nutrition requirements
25-35 kcal/kg (ICU), normal needs if stable 1-1.2 g/Kg protein, up to 2 g/kg if malnourished/renal function is up Zinc can help in hepatic encephalopathy; cofactor for ammonia break down metabolic dysfunction-associated steatotic liver disease- new term for non alcoholic fatty liver disease
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overnight fast in ESLD patients
need late night snack to reduce - increased fat oxidation, catabolism of protein cirrhosis is a catabolic state cirhotic patients utilize fat as fuel more; increased ketone production
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caloric needs in liver disease
REE measured with indirect calorimetry general estimates: 25-30 kcal/kg ascites increases REE by 10% use actual, ideal, or dry weight 1-1.2 g/kg protein, or 1.5 g/kg if malnourished high complex carbs frequent small meals and bedtime snacks MVI with Ca, Znc, Mg
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pediatric nutrition screening tools
STAMP, STRONGkids, PYMS
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normal neonate gestation
37-42 weeks
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prematurity classifications
low birth weight - <2500 g very low birth weight - <1500 g -> almost always on PN, no electrolytes at first, peripheral calcium can cause skin damage, start GIR 5-6, goal 8-12, target BG 120-150, treat hyperglycemia by decreasing GIR, not starting insulin, watch TG if >1000 g birth weight, max lipid 3g/kg extremely low - <1000 g micronate - < 750 g
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small for gestational age
birth weight <10%ile on intrauterine growth curve or birth weight / length below -2 SDS for gestational age - causes: pregnancy induced HTN, maternal malnutrition, maternal substance abuse, chromosomal abnormalities *infant can be low body weight but full term
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large for gestational age
birth weight >90%ile on intrauterine growth chart -causes: maternal diabetes (most common), genetic predisposition, miscalculation of due date
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excessive protein intake can contribute to
metabolic acidosis and azotemia azotemia- build up of nitrogen containing waste; BUN>100
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infants less than ~6 months do not need ___ d/t inadequate nutrient intake and risk of electrolyte disturbances
free water
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cystic fibrosis MNT
increased nutrient needs PERT - max of 2500 units of lipase/kg/meal or 10,000 units lipase/kg/day high calorie diet - 110-200% of DRIs supplement fat soluble vitamins-ADEK in water miscible form supplement salt for infants - 1/8 tsp day from 0-6 months, or 1/4 tsp day >6 months
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human milk
liquid gold macronutrient content - 20 kcal/oz, 0.9-1.4 g/protein per 100 mL, 3.5-3.9 g fat/100 mL varies
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neonatal bone growth most rapid in the ___ trimester
third trimester *this is why neonate/premie formulas include incr Ca, Phos, Zinc for bone growth
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Antireflux formulas
10% more viscous than standard, wont work with antacid meds indicated for babies with severe GER
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4 month old male with elevated conjugated bili of 3.2 mg/dL. he has a h/o biliary atresia. what type of formula would you recommend? 1. standard 2. calorie dense 3. soy based 4. formula high in MCT
4. formula high in MCT
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basic indications for use of a standard infant formula
all infants *except galactosemia*
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indications for use of soy based formula
galactosemia
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vitamin D supplementation for babies
exclusively breast fed - 400 units/day breast fed and formula - assess and supplement accordingly formula fed - no supplementation if daily volume of formula consumed meets needs
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vitamin K and new borns
prophylactic supplementation in all new borns
356
risk factors for vitamin D deficiency in babies
breast fed w/o supplementation dark skin birth prior to 32 weeks gestation recent immigration from developing country, where they live (is it sunny/cold/cloudy?) at risk conditions -malabsorption, epilepsy/cerebral palsy *phenobarbitol*
357
when would you want to supplement neonate pt with B12
c/f breast fed infant if mother is vegan possible concern for IF infants/children
358
neonate and iron needs
fortify in breast fed infants by 4-6 months, as their endogenous supply is depleted commercial formulas contain iron may need supplementation in times of malabsorption
359
neonate and flouride needs
no need to supplement from birth to 6 months after 6 months may need supplementation based on water supply -well water will need flouride ex: 0.25 mg/d for 6 month-3 years of age if water contains < 0.3 ppm
360
no ___ before age 1 year
cows milk *low in iron, low in vitamin C & E, low in essential fatty acids, high renal solute load
361
insufficient oral intake definition - pediatric EN indication
inability to consume <60-80% of nutrient needs for >5 days in children over 1 year of age or >3 days in children less than 1 year
362
feeding modality for infant <32 weeks or small gestation premises, or basalscull fracture present
orogastric tube
363
manipulated formula and human milk hang time
4 hours
364
PN indications for pediatrics
if it is evident that full PO feeds or EN goals are not going to be met, start PN: infants: within 1-3 days children/adolescents: 4-5 days critical illness: not recommended within 24 hr of PICU admission, start of PN depends on intake of EN and overall nutritional status
365
Lipid infusion rates
pediatric: 0.15 g/kg/hour adults: 0.11 g/kg/hour
366
fish oil ILE indications for peds
use for cholestasis (d bili > 2 mg/dL) dosage is 1 g/kg/day Omegaven
367
prevention of EFA deficiency in peds
soy based - 0.5 g/kg/day for infants/children multi oil based -30% of calories
368
PN lipid hang time - pediatrics
fat emulsion should run over 12 hrs if possible. if not possible, infusion should be completed in 24 hrs with 2 separate doses of no more than 12 hrs hang time each
369
2-in-1 vs 3-in-1 for babies
2-in-1 neonates/infants receive IV fat emulsion separate from dex and AA
370
PN composition for pediatrics
dex: 40-60% kcal fat: 20-40% kcal >60% from fat will cause ketosis protein: based on g/kg, type of AA solution differs from birth to 1 year and after 1 year
371
Amino Acid solutions for <1 year old
taurine is added pH is lower higher levels of tyrosine, histadine lower - phenylalanine, methionine, glycine
372
___ trace element will be increased if +enterocutaneous fistula or diarrhea present
zinc
373
___ trace element should be decreased/removed in instances of cholestasis
manganese And copper-also excreted via bile
374
you have a child on TPN with cholestasis, how can you manipulate the TPN to be more liver friendly
reduce/change lipids- soy to SMOF or SMOF to omegaven cycle TPN GIR within range adjust trace elements
375
Pediatric MVI dosing
<1 kg: 1.5 mL/day <3 kg: 3.25 mL/day 3 kg-11 years: 5 mL/day >11 years: 10 mL/day of adult formulation
376
long term pediatric PN pt will need ___ added to TPN for fat metabolism
carnitine - as Levocarnitine transports LCT along membrane low levels of carnitine associated with elevated TG, elevated alk phos
377
cysteine and pediatric PN
Conditionally essential. cysteine added to preterm/infant PN to reduce the pH and increase calcium/Phos solubility
378
aluminum and PN
PN components with lowest aluminum amount should be used to reduce exposure in pediatrics FDA recommends <5 mcg/kg/day
379
can check urine __ if pediatric patient has poor weight gain/growth on PN
urine sodium
380
neonate classification
neonate is first 28 days of life preterm: <37 weeks GA term: >/= 37 weeks GA
381
neonates: SGA, LGA, AGA
small for gestational age - <10%ile large of gestational age- >90%ile appropriate for gestational age -10th-90th%ile
382
indications for PN in neonates
1. VLBW who cannot be adequately fed enterally 2. premature neonates with severe respiratory distress syndrome 3. neonatal congenital defects (volvulus, meconium ileus, atresia, gastrochesis, hirshprungs, enteric fistula, diaphragmatic hernia)
383
when to start PN in neonates
VLBW - ideally within first few hours of life, use starter/vanilla/base PN LBW premature- within 24-48 hrs and continue until adequate EN established
384
NICU starter PN
provides immediate protein for extremely premature infant often contains dex (5-10%) and AA (3-4%), can also contain heparin, calcium, MVI
385
maintenance fluid requirements for PRE TERM neonate
75-120 mL/kg/day
386
maintenance fluid requirements for TERM neonate
60-120 mL/kg/day
387
maintenance fluid requirements for neonate 3-10 kg (>1 month)
100 mL/kg
388
fluid requirements vary depending on age of neonate and specific circumstances like
decreased fluid requirements for first 48 hrs of life to allow natural diuresis (70-90mL/kg) increased fluid for: increased insensible losses, provision of optimal nutrition (140-160 mL/kg/d for full enteral nutrition)
389
volume of PN for neonates
PN is part of maintenance fluids PN total volume = (total 24 hr fluid goal - fluids from drips - ILE - EN feeds)
390
amino acids and neonates
special formulations metabolized to ammonia-> converted to urea->eliminated in urine high AA can incr ammonia in bloodstream d/t immature urea cycle activity, can result in incr BUN and organic acids formation
391
nenates and dextrose
BG guidelines not the same in neonates tolerance of GIR is indicated by glucose screening values of 60-150 mg/dL with negative to trace amounts of glucose in urine GIR 10-14 mg/kg/min, max 14-18
392
ILE and neonates
EFAD can happen very quickly - minimal fat stores smallest neonates become deficient in 3-7 days provided as either 10%, 20%, or 30% emulsions
393
normal IV fluids for neonates
first 24 hrs neonates receive no electrolytes - D10W after first 24 hrs, can add sodium - D10 0.2%NS
394
importance of Ca and Phos for neonate
extremely important to prevent MBD preterm infants lost out on accrual during 3rd trimester
395
Ideal Ratio of Ca:Phos that promotes greatest retention / for neonates
1.7 : 1 mg:mg or 1.3 mol : 1 mol
396
MVI requirements in neonates PN
<2.5 kg = 2 mL/kg/day >/= 2.5 kg = 5 mL/day
397
L-cysteine function- neonates
precursor of glutathione antioxidant allows for reduction of methionine added at 40 mg per gram of AA lowers pH- improve Ca:Phos solubility not required if providing at least 3g/kg/day
398
cartinine and neonates
quaternary amine recquired for transport of LCT across mitochondrial membrane for oxidation premature infants are at risk for def d/t limited reserves supplementation required in premature infants <32-34 weeks gestational age
399
heparin and neonates
cofactor of lipoprotein lipase: enhances lipid clearance only in NICU PN, recommended dose: 0.25-1 unit/mL of PN remains patency of catheter, reduces vein irritation
400
breastfeeding contraindicated for ___
mother with HIV/AIDS if mother not on anti-retroviral (ART), needs to have undetectable levels if a mothers med could cause harm to infant if passes through human milk
401
breastfeeding recs
recommended feeding method for virtually all infants gold standard AAP recs exclusively breast feed for first 6 months of life supplement after 6 months with formula and additional foods
402
___ can be used if mother does not have human milk for baby
donor milk
403
neonates foritifies
not all created equally recommend fortification for BW < 1500 g human milk based - prolacta cows milk based hydrolyzed and Elemental formulas
404
neonate: if fortifying with prolacta, baby will need additional
0.5 mL PVS, Fe and folic acid (depends on weight), 200 IU vitamin D
405
neonates: if fortifying with HMF fortifier, baby will need additional
Iron (depends on weight) and vitamin D
406
neonates: if fortifying with formula powder fortifier, baby will need additional
poly vi sol - depends on weight
407
Saline-Responsive Metabolic Alkalosis
You can fix it by giving saline - These patients are usually low on fluids and low on chloride. - Giving them saline helps correct the alkalosis. Cause: •Vomiting (losing stomach acid and chloride) •Diuretics (pee out too much salt and water) •Dehydration Think: “They’re DRY and SALTY — just give them saline!”
408
Saline Resistant Metabolic Alkalosis
Meaning: Giving saltwater won’t fix it. • These patients aren’t low on fluids, or their problem is hormonal, not just salt loss. • You have to fix the underlying disease, not just rehydrate them. Causes: •Hyperaldosteronism (body makes too much aldosterone, which keeps pushing out acid and potassium) •Cushing’s syndrome •Severe low potassium Think: “They’re HORMONALLY MESSED UP — saline alone won’t help.”
409
Non-Anion Gap Metabolic Acidosis (NAGMA) what it is, causes
Anion gap is normal. •Problem isn’t new acids — it’s losing bicarbonate or gaining chloride. •Chloride usually rises to “replace” the lost bicarbonate (hence sometimes called hyperchloremic acidosis). Causes you’ll see: •Diarrhea (lose bicarb through your gut) •Renal tubular acidosis (kidneys fail to reabsorb bicarb) •Certain IV fluids (like normal saline overload) Simple memory tip: Losing base, not gaining bad acid
410
Elevated Anion Gap Metabolic Acidosis (AGMA) what it is, general info
Anion gap is HIGH (>12–16+). •There are extra acids in the blood that shouldn’t be there. •These acids eat up bicarbonate while they flood the blood. Causes you’ll see: (Use the famous mnemonic: MUDPILES) • Methanol (antifreeze poisoning) • Uremia (kidney failure) • Diabetic ketoacidosis (DKA) • Propylene glycol (another toxic alcohol) • Isoniazid or Iron overdose • Lactic acidosis (shock, sepsis) • Ethylene glycol (antifreeze again) • Salicylates (aspirin overdose) Simple memory tip: “Too much poison acid.”
411
PN dextrose contains 3.4 kcal/kg, glycerol or glycerin in IV solutions contains ___ kcal/kg
4.3 kcal/kg - used in IVF shortages
412
standardized comercially available PN (SCAPN) or a multichamber bag (MCB) - two brands out there.
Clinamix -1 and 2 liter dual chamber -dextrose with or without Ca -amino acids with or without lytes Kabiven -3 chamber, 4 sizes avail -need to be activated by pharmacy , limited amounts of protein and lytes, need to add MVI and trace minerals
413
ILE filter size
1.2 micron filter
414
ILE contains ___ and ____ - lyte/vitamin
phosphate (from phospholipid) around 1.5 mmol/100 mL and vitamin K from soy and or olive oil
415
10% and 20% ILE are appropriate for
central and peripheral PN 30% only for central -TNA only
416
__ ILE not appropriate for fish allergy
SMOF or Omegaven
417
caution 3 ILE with ___ and ___ allergies
soy and egg alllergies can test prior to admin for allergy
418
Omegaven - indicated for pediatric pt's with
PNAC - PN associated cholestasis d bili >2 dosed 1 g/kg day max 1.2 micron filter
419
filter for a Y-sited 2-in-1 infusion with lipids
1.2 micron filter
420
Extravasation - PN complication. What is it?
leakage of intravenous (IV) fluids, medications, or PN administered through the same line, out of the vein and into the surrounding tissues. Causes: catheter dislodgement or perforation of the vein wall, fragile veins, improper insertion technique, increased venous pressure.
421
Extravasation - what are the complications, sx?
can lead to a range of local complications, including: pain, swelling, redness, and blistering. Tissue damage, ranging from irritation to necrosis, depending on the osmolarity and vesicant properties of the fluid or medication. delayed medication or nutrient delivery. *Identifying patients at higher risk for extravasation (e.g., those with fragile veins, altered mental status who may dislodge lines)
422
Thrombus - PN complication. what is it?
a blood clot that forms inside a blood vessel, obstructing the flow of blood. it can occur within the vein where the catheter is placed or within the catheter itself. Causing a partial or complete occlusion of the IV catheter, resulting in difficulty infusing or aspirating. Local symptoms such as pain, swelling, and redness along the vein. More serious complications like deep vein thrombosis (DVT) or catheter-related bloodstream infections (CRBSI).
423
Thrombus - causes? and what kind of pt's have higher risk of PN thrombus?
causes -damage to the inner lining of the vein during insertion, slow or turbulent blood flow around the catheter, presence of the foreign body (catheter) itself, which can activate the coagulation cascade. pt's with a hypercoagulable states, those with a history of DVT, hypercoagulable conditions, or certain medical conditions
424
what macronutrient dosing limits will provide the most stable 3-in-1 admixtures?
TNAs maintain final concentrations of amino acid ≥4%, monohydrated dextrose ≥10%, and injectable lipid emulsion ≥2% are more likely to remain stable for up to 30 hr at room temperature orrrr for 9 days refrigerated followed by 24 hr at room temperature
425
Should heparin be included in the PN admixture to reduce the risk of central vein thrombosis?
no, it can increase risk of central vein thrombosis.
426
Filter for TPN per ASPEN 2020 guidelines
ASPEN recommends using a 1.2 micron in-line filter for administration of total nutrient admixtures (TNAs), dextrose-amino acid admixtures and lipid injectable emulsion (ILE). For TNAs, place the filter as close to the catheter hub as possible. For dextrose-amino acid admixtures, place below the Y-site where the dextrose-amino acid admixture and the ILE co-infuse
427
3 etiology-based nutrition diagnoses in adults in clinical practice settings are as follows
1. Starvation-related malnutrition: Chronic starvation without inflammation (eg, anorexia nervosa). 2. Chronic disease-related malnutrition: Inflammation is chronic and of mild to moderate degree (eg, organ failure, pancreatic cancer, rheumatoid arthritis, sarcopenic obesity) 3. Acute disease or injury-related malnutrition: Inflammation is acute and of severe degree (eg, major infection burns,trauma, closed head injury).2
428
Nutritionally-At-Risk Adult
** Involuntary weight loss of 10% of usual body weight within 6 months or 5% within 1 month ** Involuntary loss of 10 lb within 6 months ** Body mass index (BMI) less than 18.5 kg/m2 ** Increased metabolic requirements ** Inadequate nutrition intake, including not receiving food or nutrition products for more than 7 days
429
Nutritionally-At-Risk Child
** Weight for length, weight for height, or sex less than 10th percentile (–1.28 z score) ** BMI for age or sex less than 5th percentile (–1.64 z score) ** Increased metabolic requirements ** Impaired ability to ingest or tolerate oral feeding Documented inadequate provision of or tolerance to nutrients ** Inadequate weight gain or a significant decrease in usual growth percentile
430
Nutritionally-At-Risk Neonate
High Risk ** Preterm less than 28 weeks at birth ** Extremely low birth weight less than 1000 g ** Infant establishing feeds after episode of NEC or GI perforation ** severe congenital gastrointestinal malformations (eg, gastroschisis) Moderate Risk ** Preterm 28th–31st weeks, otherwise well ** Intrauterine growth restriction (weight less than 9th percentile) ** Very low birth weight 1000–1500 g ** Illness or congenital anomaly that may compromise feeding
431
Selecting Appropriate Vascular Access for PN Administration
Global Recommendations 5A: Individualize the selection of vascular access device (VAD) for PN administration based on an evaluation of the risks and benefits of the device, clinical factors, and psychosocial considerations. 5B: Choose the smallest device with the fewest number of lumens necessary for the patient’s needs. 5C: Dedicate 1 lumen of the VAD for PN administration when possible. 5D: Position the tip of the central venous access device (CVAD) in the lower third of the superior vena cava near the junction with the right atrium. 5E: Confirm optimal position of the CVAD tip prior to initiating PN
432
Peripheral PN Adult - ASPEN recs
Use peripheral PN only for short-term purposes, no more than 10–14 days, as supplemental PN or as a bridge therapy during transition periods, where oral intake or EN is suboptimal or clinical circumstances do not justify placing a CVAD. 6B: Estimate the osmolarity of peripheral PN formulations. 6C: Maintain an upper limit of 900 mOsm/L for the peripheral PN formulations.
433
Perioperative PN Adult
8A: Consider preoperative PN in severely malnourished patients unable to tolerate sufficient oral intake or EN. 8B: Reserve postoperative PN for severely malnourished patients unable to tolerate EN for more than 7 days, unless initiated preoperatively. Neonate and Pediatric 8C: Consider preoperative and postoperative PN in malnourished neonates and children who are unable to tolerate oral intake or EN.
434
increase zinc for patients with
High GI losses, decubitus ulcers, wounds, burns consider additional 10-15 mmol/day
435
Copper and Manganese are both eliminated via ___
via bile hold or remove for cholestasis
436
consider increased selenium for patients with
burns, malabsorptive states, critical illness consider additional 20-40 mcg/day
437
Chromium excreted via
kidneys consider holding or decreasing in renal failure
438
Selenium deficiency can lead to
cardiomyopathy
439
chromium deficiency can lead to
glucose intolerance
440
manganese deficiency can lead to
not well documented
441
copper deficiency can lead to
anemia (microcytic), dipigmentation of hair, neurologic abnormalities
442
ideal macronutrient content for adult PN
Dextrose: ~50% kcal, or 60-85% of non protein calories (most PN's will have 150-350 g/day) Protein: g/kg as appropriate, can initiate at goal caution with azotemia (BUN >100 mg/dL) Fat: 15-30% kcal, do not exceed 2.5 g/kg/day]]
443
Hypoglycemia requiring dextrose containing fluids is most likely to occur in which type of liver disease
Acute liver failure Also known as fulminant hepatic failure. During this, glycogen stores are rapidly depleted and insulin’s metabolism is impaired. Oral intake also usually reduced
444
Pregnant women with hyperemesis is starting feeds. What formula do you pick? NG feeds of isotonic formula or a polymeric formula?
Polymeric
445
Supplementation of ___ is usually restricted during early stages of stem cell transplant
Iron Blood products are typically recruited before stem cell trans plant and can lead to iron overload
446
Which kind of enterocutaneous fistula would have the greatest degree of nutritional loss
A proximal high output The higher the fistula occurs in the GI tract , the greater the output and higher risk of metabolic derangements. As seen in proximal high out put fistulas. High output = >500 mL/d.
447
___ containing enteral nutrition may be possible in pt with low output esophageal, gastric, duodenal, or proximal jejunal fistulas
Fiber containing EN Opposite for distal ileal or colonic low output fistulas— those require low fiber or fiber free EN, and site should be as high up as possible to increase surface area of absorption
448
Loop diuretics can lead to
Azotemia Med leads to increased urine output and lyte abnormalitie. Specifically low K and Mg due to increased K and Mg excretion. Loop diuretics can lead to azotemia due to volume depletion
449
Whatbis true about EFAD and patients with CF?
EFAD profiles have been shown to improve in patients with CF AFTER lung transplant Usually, EFAD signs are uncommon in patients with CF. usually causes poor growth and poor pulmonary function. Sometimes omega 3 can be used in management of CF, however mixed results from trials.
450
Iron and calcium are absorbed in the___
Duodenum
451
Folic acid is absorbed in the ___
Proximal jejunum
452
In pulmonary insuffiency, excessive calorie intake can increase blood PCO2 resulting in
Respiratory acidosis
453
A 4-year-old presents with 3 days of frequent vomiting. Labs show elevated serum bicarbonate and hypochloremia. What is the most likely acid-base disorder? A. Respiratory acidosis B. Metabolic alkalosis C. Metabolic acidosis D. Respiratory alkalosis
B metabolic alkalosis
454
Vomiting leads to which primary electrolyte loss? A. Sodium B. Bicarbonate C. Chloride D. Potassium
Chloride
455
Which acid-base disorder is most commonly associated with profuse diarrhea? A. Metabolic alkalosis B. Respiratory alkalosis C. Metabolic acidosis D. Respiratory acidosis
Answer: C. Metabolic acidosis
456
Diarrhea leads to a loss of which substance that causes acidosis? A. Hydrochloric acid B. Bicarbonate C. Carbon dioxide D. Ammonia
Answer: B. Bicarbonate
457
Q: Why does vomiting cause metabolic alkalosis?
Loss of gastric acid (H⁺) increases blood bicarbonate levels And causes metabolic alkalosis
458
Q: What acid-base disorder is caused by diarrhea? Q: Why does diarrhea cause metabolic acidosis?
Loss of bicarbonate (HCO₃⁻) from intestinal secretions Causes Metabolic acidosis (non-anion gap)
459
a patient with unexplained skin rashes and alopecia on nutrition-focused physical exam, could be started on what supplementation?
Zinc supplementation at risk populations = older adults, postoperative GI surgery , liver disease, renal disease, malabsorptive conditions Plasma and urinary zinc have been confirmed as the most reliable biomarkers of zinc status in healthy populations. However, plasma zinc should be interpreted with caution in patients with low albumin, inflammation or hemodilution. Pt with wounds who are deficient or shown to be losing zinc in wound exudates (negative pressure therapy) may benefit from supplementation. Supplementation for all patients with wounds is not recommended due to the risks of copper deficiency and adverse effects on wound healing with zinc toxicity. Clinical manifestations of zinc deficiency are evident at plasma levels < 33 mcg/dL If signs of zinc deficiency such as alopecia and skin rash are noted on nutrition focused physical exam it is most likely a deficiency is prese Treatment for zinc deficiency in adults is typically 220 mg zinc sulfate (50 mg elemental zinc) twice daily for a total of 100 mg elemental zinc per day. Oral replacement will generally alleviate all clinical manifestations within 1-2 weeks.
460
A pt with CHF and on chronic diuretic therapy - what vitamin deficiency are they at risk for having?
Thiamin = this deficiency is more common in heart failure patients than the general population Mechanisms include decreased intake, poor absorption (due to cardiac cachexia and splanchnic congestion), increased urinary excretion with diuretics , altered thiamin metabolism. High dose loop diuretics ( urosemide) are thought to be the most important factor contributing to thiamin deficiency. Furosemide causes thiamin deficiency due to increased urinary thiamin excretion Clinical trials in patients with CHF have shown that thiamine supplementation increases systolic, diastolic and central venous pressures with a decline in heart rate and increase in LVEF.
461
A 51-year-old female is 10 years post gastric bypass surgery for obesity, presents with numbness and tingling in her distal lower extremities that has worsened. She had been on an oral multivitamin supplement. She was significantly anemic and neutropenic. Her vitamin B12 level was normal as were her serum iron, ferritin, and transferrin levels. What nutritional deficiency is the most likely cause of all of these symptoms?
COPPER Nutritional deficiencies of iron, vitamin B12, folate, copper, thiamin and zinc have all been described after gastric bypass surgery. B12 was normal, but when deficient can also cause anemia, neurological and psychiatric symptoms including numbness, paresthesia and memory disturbance. Thiamin deficiency can lead to neuropathy such as beriberi or Wernicke ’s encephalopathy but not anemia. Zinc deficiency can lead to pica, dysgeusia, hair loss and skin lesions, not anemia. Copper deficiency though rare, can present with anemia (microcytic, normocytic, or macrocytic) and also neutropenia. In addition, it can manifest as myelopathy and peripheral neuropathy.
462
In the first 1 - 3 months after a hematopoietic stem cell transplant the nutritional needs of a patient are
30-35 kcal/kg IBW daily with >= 1.5 g protein per kg body weight Energy needs will vary with the individual, but energy requirements are usually estimated at 1.3 - 1.5 x basal energy expenditure (BEE), or approximately 30 to 35 kcal per kilogram IBW. Protein intake should be aimed at 1.5 - 2.0 g per kilogram IBW during the first 1 to 3 months after transplantation.
463
Nutrition support for solid-organ transplant patients receiving cyclosporine or tacrolimus may need to be modified due to the presence of -
hyperkalemia Cyclosporine or tacrolimus, commonly used after solid organ transplantation for immune suppression, can frequently cause nutrient disorders such as hyperkalemia, hypomagnesemia, hyperglycemia, and hypercholesterolemia, and has a direct effect on the renin-angiotensin-aldosterone system contributing to altered potassium homeostasis. Tacrolimus and cyclosporine also affect the renal tubular excretion of potassium
464
What are the protein requirements for a stable patient receiving peritoneal dialysis (PD)?
1-1.2 g/kg
465
In critically ill patients with chronic obstructive pulmonary disease (COPD), accumulation of energy deficit throughout a hospital stay can result in which of the following?
delayed weaning from the vent prolonged underfeeding of patients with chronic respiratory disease may lead to deficits in lean body mass that may increase mortality. Patients with COPD frequently have an increased REE secondary to their disease, although the exact etiology of this hypermetabolism is not fully understood. Accumulation of an energy deficit throughout a hospitalization has been associated with a greater risk of increased length of stay, complications, infections, days on antibiotics, and time on mechanical ventilation.
466
Which of the following antisecretory medications would be most appropriate for addition to a parenteral nutrition (PN) solution of a patient who has recently undergone an extensive small bowel resection resulting in short bowel syndrome?
= famotidine NOT octreotide since it is recent surgery Histamine 2-receptor antagonists/famotidine and octreotide can be added to PN solutions; however, octreotide may impair small intestinal adaptation if used in the early phase following significant resection of the bowel. Omeprazole or a Proton pump inhibitor are effective antisecretory agents but cannot be added to parenteral nutrition. Clonidine can only be taken by oral route or patch.
467
A critically ill patient with hyperglycemia receiving continuous enteral nutrition with a history of insulin dependent diabetes should ideally be placed on -
continuous IV insulin In the critical care setting, continuous intravenous insulin infusion has been shown to be the best method for achieving glycemic targets and allows for off cycles during the 24-hour period when enteral feeding is discontinued.
468
critically ill patient with a BMI of 35 kg/m2, what are the calorie recommendations for parenteral and enteral nutrition?
11 - 14 Kcal/kg actual body weight BMI is >30 kg/m2, the goal of the parenteral and enteral regimen should not exceed 65% to 70% of target energy requirements as measured by indirect calorimetry. If indirect calorimetry is unavailable then 11 - 14 Kcal/kg of actual body weight is recommended for individuals with a BMI 30 - 50 kg/m2. For individuals with a BMI > 50 kg/m2 the recommendation is 22 - 25 kcal/kg of ideal body weight.
469
Which of the following is the most appropriate distal catheter tip placement of a peripherally inserted central catheter (PICC)?
PICC is defined as a catheter inserted via peripheral vein whose distal tip lies in the lower third of the superior vena cava or the cavoatrial junction. The cephalic or basilic veins are often used as the insertion site for PICCs. Central or peripheral access is not defined by the initial point of entry into the vascular system but rather by the position of the distal catheter tip. Central lines are defined as catheters with the distal tip in either the superior or inferior vena cava. Therefore, by definition, a PICC is used as central venous access.
470
key difference between extravasation and infiltration of an IV catheter
difference is the type of fluid or medication that leaks out of the vein into the surrounding tissue Infiltration: when a non-vesicant solution or medication leaks into the surrounding tissue. non-vesicant does not typically cause significant tissue damage or irritation. Common examples of non-vesicant fluids = normal saline, dextrose solutions, and some non-irritating antibiotics. Extravasation: when a vesicant solution or medication leaks into the surrounding tissue. this vesicant can cause significant tissue damage, blistering, or even necrosis (tissue death). Examples = certain chemotherapy drugs, vasopressors (like norepinephrine), and some electrolyte solutions (like calcium chloride).
471
IV catheter thrombosis =
blood cot alteplase=Thrombolytic agent
472
adult reference ranges for electrolytes
Sodium: 135-145 Potassium: 3.5-5 Chloride: 98-108 CO2: 23-30 Calcium: 9-10.5, or 8.5-10.5 Phosphorus: 2.5-4.5 Magnesium: 1.7-2.4
473
stomach fluid is high in
highest in chloride (130 mEq), and H+ ions -aka ACID- decent amount of sodium (60 mEq), and highest in potassium (15 mEq), NO BICARB!
474
intestinal fluid (duodenum, pancreas, bile, ileum) are high in
sodium; ~140-145 mEq/L chloride; 75-104 mEq/L K; 5 mEq/L and ileum, bile, pancreas contain bicarb. highest fluid in bicarb is pancreas; 115 mEq/L
475
a concern for infant formula being reconstituted in water high in flouride
can lead to too much flouride, fluorosis, or impair bone growth
476
NEC concerns
human maternal milk/donor milk can decreas risk of NEC or sepsis minimal enteral feeding is not recommended anymore probiotics are not widely used for treatment of NEC
477
human milk fortifiers/formula fortificaion
increases kcals, but also increase osmolarity. want to keep it <400 mOsm/L to prevent renal solute load, malabsorption, poor tolerance AAP recs max osmolarity if 450 mOsm/L for infant formulas
478
sepsis
intense inflammatory state, highly catabolic body oxidizes lipid as fuel glucose production increased / glucose uptake decreased hyperglycemia and insulin resistance is common energy expenditure increases at first, tapers after ~21 days feed high protein
479
AKI vs CKD
AKI = 20-30 kcal/kg can require increased protein anuric: 1-1.2L fluid/d Oliguric: fluid as tolerated CKD= 30-35 kcal/kg protein 1 g/kg appropriate PD= 30-35 kcalk/kg - subtract dextrose absorbed via dialystate 25-35 kcal/kg for outpatient PD, 1-1.2 g/kg stable PD outpatient
480
do not correct acid base balance in PN for ____
respiratory acid/base disorders, fix the respiratory issue
481
Isotonic Hyponatremia (Pseudohyponatremia) vs Hypertonic
Pathophysiology: Normal serum osmolality with low measured sodium due to laboratory artifact. • Causes: • Hyperlipidemia • Hyperproteinemia (e.g., multiple myeloma) • Clinical Features: Typically asymptomatic; discrepancy between serum sodium and osmolality. • Management: No specific treatment; address underlying cause. Hypertonic Hyponatremia • Pathophysiology: Increased serum osmolality due to the presence of osmotically active substances drawing water into the ECF, diluting sodium concentration. • Causes: • Hyperglycemia • Mannitol administration • Clinical Features: Symptoms related to underlying cause; signs of hyponatremia may be present. • Management: Treat underlying cause (e.g., insulin for hyperglycemia); correct sodium levels cautiously.
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Hepatic steatosis vs cholestasis
Steatosis = fat buildup * elevated liver enzymes Cholestasis = bile flow obstruction * elevated alk phos, elevated bilirubin Feature Hepatic Steatosis (Fatty Liver) Cholestasis (Bile Flow Blockage) Cause Fat buildup in liver cells Impaired bile flow (inside or outside liver) Common Triggers Alcohol, obesity, TPN, meds Gallstones, liver disease, TPN, sepsis Main Lab Finding Elevated AST & ALT High Alk Phos & Direct Bilirubin Symptoms Often none; fatigue, RUQ pain Jaundice, dark urine, pale stool, itching Reversible? Often yes (with lifestyle change) Depends on cause (some reversible) Risk if Untreated Fibrosis → cirrhosis Liver damage, fat-soluble vit def, infection
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Pre albumin half life
2-3 days
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Transferrin half life
8-10 days
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Hypovolemic hyponatremia
occurs when both sodium and water are lost, but more sodium is lost than water, leading to a low serum sodium concentration. Depletion of ECF volume Cause; Renal losses, diuretics, GI fistula output, excessive sweating, burns, wounds/drains, SAH and cerebral salt wasting Urine sodium concentratio < 20 meq/l Urine osm > serum osm Clinical Features: Signs of volume depletion such as hypotension, tachycardia, dry mucous membranes, and decreased skin turgor. Management: Volume repletion with isotonic saline to restore ECF volume and suppress antidiuretic hormone (ADH) secretion. Give isotonic fluids to expand ECF
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Euvolemic hyponatremia
Total body water increases while total body sodium remains normal, leading to dilutional hyponatremia without signs of volume overload. Usually due to excess anti diuretic hormone Also due to medications, central nervous system disorders, pulmonary diseases, or malignancies. • Endocrine disorders: Hypothyroidism, adrenal insufficiency. • Primary polydipsia: Excessive water intake. • Low solute intake: “Tea and toast” diet, beer potomania. SIADH (Syndrome of Inappropriate Antidiuretic Hormone): Patients can be euvolemic despite having low sodium, because the excess water is evenly distributed. SIADH- usually from brain/CNS injury or malignancy, head trauma, lung Ca, pneumonia, can also be psychogenic High urine sodium and high urine osmolarity Urine osm > serum osm Clinical Features: Typically asymptomatic or mild symptoms; no signs of volume depletion or overload. • Management: Address underlying cause, fluid restriction, salt tabs, and in some cases, administration of vasopressin receptor antagonist or loop diuretic Often present with normal Blood pressure, heart rate, and tissue perfusion /// No signs of fluid retention (like edema) or fluid loss (like dry mucous membranes)
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Hypervolemic hypothermia
Fluid OVERLOAD • Pathophysiology: Both sodium and water content increase, but water retention >>>> sodium retention, leading to edema and dilutional hyponatremia. Fluid retention, 3rd spacing Causes: end organ damage, heart failure / ESRD / ESLD / ascites, nephrotic syndrome Tx: fluid AND sodium restriction Think ascites- we limit fluid and Na for treatment Clinical Features: Signs of fluid overload such as peripheral edema, ascites, and pulmonary congestion. • Management: Fluid and sodium restriction, diuretics, and treatment of the underlying condition
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Electrolyte renewal guidelines
If low, increase by 50% of prior day provision If trending down but still WNL, increase by 25% of prior day provision
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PN Macronutrients and their volumes The patient weighs 70 kg with needs assessed at 25 kcal/kg (1750 kcal) and 1.5 g/kg protein (105g). The TPN recommendation includes 105g amino acids, 280g dextrose, and 40g lipids. Given the availability of a standard 10% amino acid stock solution and assuming 150 ml volume needed for electrolytes, what volume is needed to prepare this TPN regimen?
A standard 10% amino acid stock solution provides 1 g AA per 10 ml. Dextrose and lipid each require 0.5 ml per kcal. Each g dextrose provides 3.4 kcal and each g lipid provides 10 kcal. 105 grams x 10 mL/g = 1050 mL 280 grams Dex = 952 kcal x 0.5 kcal/mL =476 mL 40 g lipids x 10 kcal/g = 400 kcal x 0.5 kcal/mL = 200 mL 200+476+1050= 1726 mL
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What is the maximum infusion rate of IV phosphorus administration provided to prevent thrombophlebitis and soft tissue calcification?
7 mmol/hr
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Magnesium repletion of ___mEq is needed to increase serum Mg by 0.1 mg/dL.
8 meq Each 8 meq of magnesium repletion should increase serum magnesium by 0.1 mg/dL
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Potassium repletion of ____ _mEq is required to increase serum K+ by —
Each 10 mEq of potassium repletion should increase serum K+ by 0.1 mmol/L
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Which of the following is appropriate medication treatments can bring down potassium levels in acute symptomatic hyperkalemia? a. Albuterol b. Calcium gluconate c. Kayexalate d. Lokelma
Answer: a. Albuterol Albuterol and insulin can both shift potassium into cells within 60 minutes. Dextrose is administered with insulin to prevent hypoglycemia. Calcium gluconate is given concurrently for cardioprotection. Both Kayexalate and Lokelma take > 60 minutes to take effect and are not first line treatment for acute hyperkalemia.
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A patient presents with an Na level of 132 mg/dL following a few days of diarrhea. What kind of hyponatremia is he likely experiencing?
Answer: b. Hypovolemic hypotonic hyponatremia Because the patient was experiencing diarrhea, the patient is hypovolemic with sodium losses exceeding fluid losses. Euvolemic hypotonic hyponatremia is more commonly seen in SIADH, head trauma or malignancy. Normal sodium I/O but retaining water/ normal fluid volume in the body hypervolemic hypotonic hyponatremia is more common in end-organ failure. Hypertonic hyponatremia is seen in hyperglycemia, HHNK (hyperglycemic hyperosmolar non-ketotic syndrome) also called psuedohyponatremia
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Which IV fluid solution is most appropriate in acute trauma or surgery? a. ½ Normal Saline (1/2 NS) b. Normal Saline (NSS) c. 5% Dextrose in Water (D5W) d. Lactated Ringers (LR)
Answer: d. Lactated Ringers (LR) Normal Saline and Lactated Ringers are both isotonic. NSS is most appropriate for resuscitation. LR is most similar to blood plasma and appropriate for acute trauma and surgery. D5W is indicated for increased free water needs following resuscitation. ½ NS is used in DKA and hypernatremia but contraindicated in acute trauma, burns and liver failure.
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18. Which IV fluid solution is isotonic and effective for resuscitation? a. ½ Normal Saline (1/2 NS) b. Normal Saline (NSS) c. 5% Dextrose in Water (D5W) d. Lactated Ringers (LR)
B normal saline
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Which electrolyte is critical in energy utilization, with deficiency resulting in neurologic dysfunction? a. Magnesium b. Phosphorus c. Potassium d. Sodium
Answer: b. Phosphorus Phosphorus is a component of ATP and critical in energy utilization. Hypophosphatemia is a hallmark of refeeding syndrome due to AP demand. Neurologic dysfunction can result from phosphorus deficiency.
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Which amino acid cannot be provided in PN, thus requiring enteral administration? a. Arginine b. Carnitine c. Choline d. Glutamine
Answer: c. Choline Choline is not included in PN and must be repleted enterally. Choline is not an amino acid- it is a water soluble vitamin
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15. Which amino acid is important in immune function and wound healing? a. Arginine b. Carnitine c. Choline d. Glutamine
Arginine Arginine is important in immune function and wound healing. Carnitine is required for transformation of long-chain fatty acids. Choline is essential to membrane structure. Glutamine is necessary for colonic health.