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p2 year > cirrhosis, vitamins/minerals, nutrition > Flashcards

cirrhosis, vitamins/minerals, nutrition Flashcards

1
Q

what is cirrhosis

A

cell injury in liver, death of hepatocytes

hepatocytes: functional unit of liver

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2
Q

causes of cirrhosis

A
  • # 1 cause: alcohol use (severe amounts of drinking)
  • hepatitis C
  • fatty liver disease (obesity)

continual hepatocyte damage –> no time for hepatocytes to recover –> death > regeneration –> organ failure

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3
Q

cirrhosis s/s

A
  • ascitic belly
  • altered mental status
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4
Q

cirrhosis labs to look at – 4 main ones

A
  • jaundice / high bilirubin
  • low platelets
  • low albumin
  • high PT/INR (low clotting factors, dec clotting)

bc liver makes: platelets, albumin, clotting factors

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5
Q

other labs to look at for cirrhosis

A

LTFs: ALT, AST –> released by liver when cell damage occuring
- acute damage: LFT inc –> bc there are hepatocytes that can release LFTs and regenerate
- chronic damage: LFT dec –> bc no more hepatocytes around to release LFTs

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6
Q

cirrhosis complications in order of progression

A
  • ascites
  • portal HTN
  • variceal bleeding
  • spontaneous bacterial peritonitis (SBP)
  • hepatic encephalopathy
  • hepatorenal syndrome
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7
Q

ascites Dx

A

step 1: abdominal ultrasound** –> look for fluid
step 2: parcentesis
step 3: compare albumin in serum to albumin in ascitis fluid with SAAG –> portal HTN

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8
Q

paracentesis

A

put a needle in the ascitic belly and remove the fluid accumulated

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9
Q

SAAG

A

serum ascites albumin gradient
SAAG = serum albumin - ascitic albumin
if SAAG >/= 1.1 –> portal HTN

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10
Q

sodium restriction MoA

A

sodium will cause further fluid retention – do not want more fluid retention when already a bunch of fluid in peritoneal

DO NOT FLUID RESTRICT – already dehydrated bc alcoholic

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11
Q

aldosterone antagonist MoA

A

aldosterone drive:
not enough blood through liver –> not enough blood volume to heart –> low cardiac output –> trigger a inc HR, kidney water retention, direct blood away from peripheral to central –> BUT when fluid gets to GI, will go into extravascular space bc portal HTN–> STILL low cardiac output –> will continue to rev up this drive

aldosterone antagonist: inhibit this process

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12
Q

what is a more potent diuretic in cirrhosis? loops or aldosterone antagonists

A

aldosterone antagonists!!
therefore always do spironolactone over furosemide if need to pick one!

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13
Q

midodrine MoA

A

alpha activity –> inc BP

**allows toleration of other two diuretics

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14
Q

large volume paracentesis MoA

A

remove all the fluid from the extravascular space

** if > 5L: the intravascular fluid will rush back into the extravascular space when the fluid is removed, therefore dropping BP –> therefore need IV albumin

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15
Q

IV albumin MoA

A

hypertonic, therefore will keep fluid in the intervascular space instead of it rushing back into the extravascular space after LVP –> prevents the drop in BP that would occur

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16
Q

aldosterone antagonist AE

A

inc K

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17
Q

loop diuretic AE

A

dec K

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18
Q

what diuretic ratio do you need to optimize diuresis and keep K normal

A

40mg furosemide : 100mg spironolactone

**THESE ARE DAILY AMOUNTS – CAREFUL OF BID!

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19
Q

benefit of IV albumin with LVP

A

may dec mortality !

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20
Q

cons of IV albumin with LVP

A
  • expensive
  • short circulating half life (hours)
  • short term solution to help with the transition
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21
Q

TIPS procedure MoA

A

put in a shunt from the portal vein to the hepatic vein –> bypass the liver –> this bypasses the highly pressurized area that will prevent fluid from getting through/prevents backups

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22
Q

TIPS AE and therefore CIs

A

AE: hepatic encephalopathy
**bc ammonia in blood no longer going through liver –> ammonia not detoxified by liver –> ammonia goes to CNS –> mental changes

CI: pts with refractory hepatic encephalopathy
pts with history of hepatic encephalopathy

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23
Q

what to avoid in acities

A

thiazide diuretics (HCTZ)
- will dec Na (Na is already low)

ACEi/ARB
- will lower bowman capsule pressure –> WILL CAUSE AKI

fluid restricition
- patients are already drhydrated

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24
Q

if do TIPS, what do you need to do

A

START HEPATIC ENCEPHALOPATHY PROPHYLAXIS
- bc such a high risk of it

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25
Q

portal HTN definition

A

high BP in portal vein

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26
Q

portal HTN Dx

A

SAAG greater than or equal to 1.1

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27
Q

varices definition

A

abnormally distended floppy vessels, form in the GI tract to GI organs

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28
Q

varices patho

A

FORM DUE TO PORTAL HTN
* more blood flow in GI tract –> form varices (other vessels to GI organs)

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29
Q

varices Dx

A

***EDG –> upper endoscopy

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30
Q

portal HTN/varices treatment goal

A

prevent varix enlargement and bleeding

**WILL NOT PREVENT VARIX FORMATION BC THE PORTAL HTN IS STILL CAUSING BLOOK BACKUP!

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31
Q

portal HTN/varix treatment indication

A

ONLY when have varix present!!!

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32
Q

non-selective BB options

A

nadolol, propranolol –> will NOT dec BP
carvedilol –> WILL dec BP bc of alpha activity

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33
Q

non-selective BB MoA

A

treat the portal HTN by 2 methods:
1) beta-1 blockage activity
- dec HR –> dec cardiac output –> less CO to get backed up into the varices and cause enlargement/rupture

2) beta-2 bloackage activity
- inhibit the splanchnic vessle vasodilation –> therefore prevent more blood into varices to prevent enlargement/rupture

**need to have both effects, hence why not use selective BBs

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34
Q

what do we titrate non-selective BB to?

A

HR around 60bpm

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35
Q

non-selective BB holding parameters

A

SBP < 90
DBP < 60
HR < 50-60

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36
Q

what is acute variceal bleeding a risk for?

A

SBP! –> bc bleeding around GI tract, bacteria in blood could move into peritoneum

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37
Q

s/s acute variceal bleeding

A
  • low BP
  • high HR
  • low Hgb
  • low Hct
  • pt is out of it
  • black stool
  • hemetameous
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38
Q

how to determine when acute variceal bleeding has stabilized

A

no more changes in
- HR (has lowered)
- BP (has increased)
- Hgb (has increased) –> not dropping/changing by more than 2
- Hct (has increased)

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39
Q

why do we wait until bleed stabilized to initiate non-selective BB

A

will dec BP
during a bleed…
1) already dec BP losing blood
2) could be an infection –> potential sepsis –> lowering BP even more could push infection into shock

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40
Q

acute variceal bleeding treatment

A

1) supportive care –> IV isotonic (NS, LR), O2
2) packed RBC
3) octreotide
4) EVL with EDG
5) SBP prophylaxis
6) non-selective BB

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41
Q

when PRBC indicated?

A

Hgb less than 7 or 8

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42
Q

octreotide MoA

A

vasoconstricts splanchnic vessels

IV bolus –> IV continuous infusion

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43
Q

endoscopic variceal ligation (EVL) with EDG MoA

A

do the EDG, while looking find the bleeding varix
–> “banding”: choke off the bleeding varix until the vessel dies

**varix can regrow, therefore do in hospital, then again in like 2 weeks, etc…

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44
Q

SBP prophylaxis

A

ceftriaxone or 3rd gen ceph (cefotaxime, …)
x7 days –> do all 7 days, start IV, if discharged before done with course switch to po to finish the 7 days

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45
Q

non-selective BB

A

only if varix (would be present in this case), and bleed has stabilized

if bleed not stable –> means still bleeding, repeat EVL and EDG !

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46
Q

spontaneous bacterial peritonitis (SBP)

A

bacterial infection in ascitic fluid

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47
Q

common causes of SBP

A

enteric gram (-)
- e coli
- k pneumoniae

gram (-)
- strep pneumoniae

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48
Q

SBP Dx

A

1) infection s/s
- fever
- malaise
- abdominal pain
- elevated WBC
- weakness

2) paracentesis for cultures
i) absolute PMN = (WBC in ascitic fluid) x (% PMN)
if abs PMN >/= 250
ii) cultures
delayed, so use for narrowing or d/c

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49
Q

active SBP treatment and duration

A

1) antibiotics
- 1st: 3rd gen ceph ; 2nd: cipro
- x5 days

2) IV albumin
- day 1: 1.5 g/kg
- day 3: 1 g/kg
- indication: SCr > 1, BUN > 30, bili > 4

3) repeat paracentesis in 48 hours
-PMN dec by 25%
yes –> no change
no –> carbapenems (meropenem) x5 days (new day count)

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50
Q

prophylaxis SBP indications

A

acute variceal bleeding –> 7 days
previous Hx SBP –> infinite
ascitic protein < 1.5 AND one of: —> infinite
- SCr >/= 1.2
- BUN >/= 25
- Na </= 130
- CP > 9 + bili >/= 3

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51
Q

acute variceal SBP prophylaxis

A

1st: 3rd gen ceph iv
2nd: cipro if allergic

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52
Q

indefinitie SBP prophylaxis

A

bactrim
cipro

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53
Q

hepatic encephalopathy patho

A

decline in hepatic function + portosystemic shunting (either TIPS or portal HTN)

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54
Q

s/s of HE

A

1) inc ammonia levels
- check level to ensure ammonia cause
- DO NOT RECHECK FOR EFFICACY –> use AMS as efficacy!
- higher level does NOT mean worse AMS – different for each pt

2) AMS
slowed responses all the way to coma

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55
Q

HE treatment

A

1) remove precipitating factors
- benzos, antiseizure, bipolar

2) give branched amino acid protein from veggies and dairy
- ammonia in these proteins are less likely to cross BBB

3) target ammonia in GI
1st: lactulose
2nd: rifaximin

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56
Q

lactulose MoA

A

2
1) non-absorbable sugar
- gut flora will ferment lactulose in LI –> produce organic acid –> dec colon pH –> inc movement of ammonia from blood into bowel –> in bowel, converts NH3 to NH4+ –> ammonia now trapped in GI –> eliminated

2) cathartic
- causes bowel contraction –> have bowel movement

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57
Q

lactulose dosage forms

A

PO: 25mL po q1-2 hr until 2+ watery stools had
can change to po if not working or pt is out of it
enema: 300mL retention enema, retain for 1 hr, give q6-12hr

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58
Q

when will lactulose start working

A

WHEN THE PT HAS BOWEL MOVEMENTS –> does not work until then!!!!!!!

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59
Q

rifaximin MoA

A

antibiotic that is poorly absorbed and stays in GI tract –> decreases the bacteria that normally produce ammonia in GI as part of normal flora

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60
Q

rifaximin indication

A

when still AMS when at 2-3 soft stools per day on lactulose

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61
Q

is rifaximin monotherapy

A

NO –> still need lactulose with it!!

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62
Q

prevention for HE

A

after acute episode (on discharge) to prevent further episodes

1) lactulose
doses vary, **titrate to 2-3 soft stools per day

2) rifaximin
can add on too if needed

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63
Q

hepatorenal syndrome

A

liver failure (cirrhosis) + renal failure

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64
Q

hepatorenal patho

A

portal HTN –> splanchnic vasodilation –> dec effective circulating volume and dec intravascular pressure –> dec kidney perfusion and will cause AKI if intravascular low enough

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65
Q

heptorenal Dx

A

cirrhosis
+
ascities
+
SCr inc by 0.3 mg/dL or more in 48 hours
SCr inc by more than 50% from baseline in 7 days
+
no improvement in SCr (dec) with 2 days of holding diuretics and giving IV albumin 1 g/kg/day

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66
Q

IV norepinephrine MoA

A

vasopressor –> constrict periphery and get heart pumping to save life via adrenergic response

67
Q

when do we evaluate hepatorenal treatment response

A

4 days
then
2 weeks max of therapy

68
Q

what PKPD changes occur in cirrhosis?

A

1) dec liver bloodflow
2) loss of hepatocyte function
3) decreased albumin production
4) dec kidney function (in presence of high SCr)
5) increase in CNS active therapeutic reponse

69
Q

1) dec liver bloodflow impacts

A

dec liver bloodflow –> dec first pass
THEREFORE
will have significant inc systemic circulation of high first pass drugs
- cavedilol, propanolol, morphine
THEREFORE dec dose
- carvedilol, propanolol: titrate dose to effect
- morphine: titrate to effect, change to hydromorphone

70
Q

2) dec hepatocyte function

A

dec hepatocyte function
THEREFORE
decreased metabolic capacity of liver bc fewer cells to metabolize drugs –> inc therapeutic effect
- impacts phase I (CYP) more
THEREFORE
change drugs to phase II elimination drugs
ex benzos: diazepam –> lorazepam

71
Q

3) dec albumin production

A

liver makes albumin –> hence dec albumin
THEREFORE
will have less protein binding –> inc unbound (the active form) –> inc therapeutic effect
- impact high protein bound drugs
- ex: phenytoin
THEREFORE
monitor and dec dose to compensate

72
Q

4) dec renal function (with a high SCr)

A

portal HTN –> dec intravascular volume –> dec kidney perfusion –> inc SCr and hepatorenal syndrome

73
Q

5) inc CNS therapeutic effect

A

cirrhosis –> inc permeability of BBB
THEREFORE
more of a drug can move into the brain –> inc therapeutic effect of CNS active drugs
- opioids, benzos
THEREFORE
monitor and dec dose to compensate
**if patient has AMS (very out of it) –> HOLD the dose until AMS resolves, then can redose

74
Q

vitamins

A

organic compounds

function: metabolism (create/use energy), cell function regulation

75
Q

minerals

A

chemical elements

76
Q

vitamins and minerals

A

required as nutrients in small amounts but are not produced by body –> have to get via diet

77
Q

vit and min supplementation

A

only to fill gaps, not replace
- daily value: recommended amount or not to exceed per day
- %DV: how much in one serving vs daily diet

78
Q

malnutrition

A

undernutrition or overnutrition (obesity) DUE TO nutrient imbalance

79
Q

supplementation indication

A

1) malnutrition
- alcoholism, elderly, low income

2) increased physiologic need
- pregnancy, lactation, infants, trauma, infection, genetic disorder

3) decreased absorption
- GI disorder, GI surgery (small bowel resection, gastric bypass), chronic pancreatitis, CF, severe diarrhea

80
Q

which vitamin is folic acid?

A

B9 – water soluble

neural tube formation, dec in pregnancy, therefore need supplementation

81
Q

vitamin A

A

vision

82
Q

vitamin D

A

Ca/Phos homeostasis
bone development

83
Q

vitamin E

A

antioxidant

84
Q

vitamin K

A

clotting factor formation

85
Q

general vit B

A

promoted carb, protein, lipid metabolism

86
Q

B1

A

thiamine
- produce ATP

87
Q

B6

A

pyridoxine
- amino acid metabolism

88
Q

B9

A

folic acid
- neural tube development

89
Q

B12

A

cobalamin
- DNA/RNA synthesis

90
Q

C

A

antioxidant
iron absorption

91
Q

which are the major minerals

A

Ca
Cl
Phos
Mg
K
Na
sulfur

need >100mg/day

92
Q

which are the minor minerals

A

IRON
zinc
selenium
nickel
copper
fluroide
iodine
chromium

93
Q

which are the minor minerals

A

IRON
zinc
selenium
nickel
copper
fluoride
iodine
chromium

need <100mg/day

94
Q

populations at risk for mineral deficieny

A
  • elderly
  • chronic illness
  • vegetarian/vegan
  • pregnant
95
Q

when low Ca level, need to check

A

if low albumin
**need to calculate corrected Ca if low albumin

96
Q

when low K level, need to check

A

for low Mg
**Mg regulates K
**need to correct Mg before correct K

Mg inhibits ROMK channels that efflux K

97
Q

special populations at risk for deficiencies

A

1) eating disorders
- nutritional rehab slowly
2) alcohol use disorder
- fat soluble vit
- thiamine
- folic acid
3) pregnancy
- folic acid
- iron
4) pediatric
- vitamin D
- iron
5) elderly
- B12
5.5) macular degeneration
- AREDS-2 (vit A,C,E)

98
Q

1) eating disorders

A

anorexia, bulimia
- restricition of energy intake –> low body weight

therapy goals: nutritional rehab, restore weight slowly to prevent refeeding syndrome

99
Q

refeeding syndrome

A

aggressive nutritional rehab leading to fluid and electrolyte shifts
- hypoxia, myocardial dysfunction, respiratory failure

100
Q

2) alcohol use disorder

A

chronic alcohol –> dec oral intake, dec absorption –> malnutrition

101
Q

AUD treat

A

1) fat soluble vitamins ADEK
2) thiamine B1 –> prevent wernicke’s encephalopathy
3) folic acid (b9)—> prevent macrocytic anemia

4) minerals: Ca, Phos, Mg
5) fluids and electrolytes

102
Q

3) pregnancy

A

have an increased physiological requirement

therefore give prenatal vitamin
- folic acid: NTD prevention
- iron: placenta/fetal development, anemia prevent
- Ca
- vit D
- idoine

103
Q

what do you give with a prenatal vitamin

A

stool softener –> bc iron AE is constipation!

104
Q

4) pediatric

A

if breastfeeding, supplement with:
- vitamin D –> right away until milk
- iron –> 4 months until iron-containing foods

if formula, no supplementation

no whole cow milk until 12 months!

105
Q

5) elderly

A

dec calorie requirement, inc nutrient requirement

**B12
- absorbed by stomach acid, less stomach acid produced in elderly!
- DO NOT START WITHOUT BLOOD TEST

106
Q

5.5) macular degeneration

A

central vision loss due to damage of macula

want to treat with vitamin A, C, E
–> use AREDS-2 (best)

107
Q

AREDS

A

vitamin C
vitamin E
zinc
copper
beta-carotene (vit A precursor)

108
Q

AREDS-2

A

**Better

vitamin C
vitamin E
zinc
copper
lutein
zeaxanthin
*omega-3 tried – but not significant reduction so removed from formula!

109
Q

DNI with methotrexate

A

dec folic acid
MUST supplement folic acid, do not take on same day

110
Q

DNI with PPIs

A

dec calcium and others –> osteoporosis
if need Ca supplement –> calcium citrate!

111
Q

what is enteral nutrition

A

using the gut to eat (GI tract)

112
Q

who is at risk for malnutrition

A

1) cancer
2) AIDS
3) infant (esp premature)
4) elderly
5) NG tubes
6) neurologic impairment (stroke)
7) developmental impairment (cerebrapaulsey)
8) hospitalized (inc need when sick + dec intake)
9) GI conditions
- IBD Chron’s –> bc si impacted
- bariatric surgery –> bc bypass SI
- pancreatitis –> bc no pancreatic enzymes to break down food in si

113
Q

when to consider starting nutritional support

A

inpatient
- normal: 7 days
- ICU: sooner than 7 days to dec mortality

outpatient
- normal: never
- have malnutrition or risk for malnutrition: start

114
Q

why do we always use the gut if possible

A
  • biggest immune system organ
  • will maintain gut integrity
  • will keep bile flowing which is bacteriostatic, prevents bile stones
115
Q

enteral nutrition tube placement

A

1) nasal placement (N-tubes)
i) NG - gastric
ii) ND – duodenal
iii) NJ – jejunal

**for short term use!

116
Q

NG tube characteristics

A
  • easy to place
  • inc aspiration risk -> pneumonia
  • larger diameter
  • allows for stomach decompression (removal of contents)
117
Q

ND and NJ tube characteristics

A
  • harder to place
  • dec aspiration risk
  • smaller diameter –> easier to clog
118
Q

1) feed limitations

A

gastric tubes: can do bolus feed
duodenal and jejunal tubes: can only do continuous feeds

119
Q

2) crush limitations

A

gastric and duodenal tubes: can do crush and flush
jejunal tubes: can only give as liquid

**ALWAYS check if can crush – not SR, ER, enteric coated!

120
Q

crush and flush

A

crush med, 10-15mL flush before and after med

*MUST GIVE MEDS SEPARATELY

121
Q

giving as liquid

A

crush with spoon, mix with 10mL sterile water

**MUST GIVE MEDS SEPARATELY

122
Q

3) liquid limitations

A

if mOsm > 600 –> dilute in sterile water (prevent diarrhea)
if viscous –> dilute (prevent occlusion)

123
Q

enteral feed drug DDIs

A

have to hold feed 1-2 hours before and after:
PO..
- phenytoin
- warfarin
- quinolones
- levothyroxine

*if on continuous feed, can give these as IV to avoid having to stop the feed/the DDI

124
Q

steps to determine enteral formulation

A

step 1: total calorie requirement
step 2: special considerations
step 3: administration strategy
step 4: fluid consideration
step 5: monitoring

125
Q

step 1: total calorie requirement

A

20-30 mg/kg/day

126
Q

step 2: special considerations

A

1) renal, HF: need high cal/mL –> more concentrated so less fluid
2) renal: need less K and Phos
3) DM: need more calories from lipid, less from glucose
4) burns, trauma: need more protein
5) pancreatitis: need low lipid

127
Q

step 3: administration strategy

A

bolus feed: need gastric tube
step 1: convert total kcal to mL
step 2: total mL / 200 mL = number of feeds per day

continuous feed: hospital
step 1: convert total kcal to mL
step 2: total mL / 24 hours = GOAL rate
step 3: start at 20mL/hr, every 4 hours try to inc if tolerant

128
Q

step 4: fluid requirements

A

step 1: 1 mL/kcal/day or 30-40 mL/kg/day
step 2: daily need - formula mL = free water needed
step 3: free water needed / 4 or 6 = mL of free water to give q 6 or 4 hours

129
Q

step 5: monitor

A
  • diarrhea
  • bloating, abdominal pain –> dec rate, use continuous, dec bolus mL, post-pyloric feed
  • electrolytes
  • abdominal wall tube
  • nasal tube
  • head elevated 30-45 degrees
  • prevent clog
130
Q

parenteral nutrition/TPN

A

providing nutrients through IV
- to prevent malnutrition
- is expensive, have side effects –> therefore know indications, monitor, individualize, transition to enteral asap

131
Q

tpn goals

A

1) provide physiologic energy needs when you can’t through enteral
2) provide macronutrients and micronutrients through IV

132
Q

adult tpn indications

A

all of them are when EN not feasible/not likely to reach goal/not provide 50% or more of daily value:

  • stable, wellnourished: 7 days
  • risk of malnutrition: 3-5 days
  • mod-sev malnutrition: asap
133
Q

risk of malnutrition

A
  • involuntary weight loss (10% in 6 mon)
  • BMI < 18.5
  • inc metabolic requirements
  • altered diets
134
Q

adult tpn CI

A

metabolic instability
- sepsis
- hemodynamic instability
- fluid shifts

DELAY until condition improves

135
Q

pediatric tpn indication

A
  • infant (1month - 1 year) –> 1-3 days
  • child (1yr - adolescent) –> 4-5 days
  • self limiting illness, likely to resolve –> 7 days

shorter days bc: less energy storage, more energy needs

136
Q

neonate tpn indication

A

neonate: 0-28 days

  • very low birthweight (<1.5kg) : asap
  • critically ill, preterm: as soon as EN not sufficient

NEVER WITHOUT FAT FOR MORE THAN 3 DAYS –> essential fatty acid deficiency can develop and impact brain development

137
Q

refeeding syndrome electrolytes impacted

A

potassium
magnesium
phosphate

all low

138
Q

TPN complications

A
  • metabolic: glucose, refeeding, triglycerides, liver
  • mechanical: pneumothorax, thrombus, occlude catheter, phlebitis
  • infection
139
Q

three tpn administration options

A

peripheral: PIV
central: PICC, tunneled catheter

140
Q

peripheral tpn CI

A

900 mOsm/L –> hard stop bc of phlebitis risk!

141
Q

TPN product options

A

3-in-1: protein + carb + lipid
*more risk incompatibilty/lipid cracking

2-in-1: protein + carb
**peds

142
Q

TPN approaches

A

standard: commerical TPN bags
**CI in PEDS!

individualized: prepare unique for each pt
*use in peds

cycled TPN: have some time off on continuous to avoid IFALD

143
Q

therefore, if peds, you are likely using

A

individualized approach with a 2-in-1 bag + lipid bag

144
Q

components of tpn

A

1) fluid goals
2) total energy requirements
3) macronutrients
4) micronutrients
5) special population consideration

145
Q

1) fluid goals

A

neonates: 60-80 mL/kg/day –> 120-150 mL/kg/day

pediatric: 4-2-1 method
first 0-10kg: 4mL/kg/hr
next 10-20kg: 2mL/kg/hr
any >20kg: 1mL/kg/hr

146
Q

2) total energy requirements

A

neonate: 80-120 kcal/kg/day
child: 60-90 kcal/kg/day
adolescent: 40-55 kcal/kg/day

147
Q

amino acid/protein energy values

A

4 kcal/g
100 mOsm/%

148
Q

nitrogen balance

A

want (+) –> if (-), inc protein in TPN

Nbalance = Nin - (Nout + 4)

Nin = g protein / 6.25
Nout = UUN result
4 = insensible loss

149
Q

dextrose/carb energy values

A

3.4 kcal/g
50 mOsm/%

MAX IN PERIPHERAL IS 12.5% –> above, need central!

150
Q

lipid energy values

A

Intralipid 20% –> 2 kcal/mL (NOT GRAM)

151
Q

lipid CIs

A

infusion rate max hard stop:
peds: 0.15 g/kg/hr
adult: 0.11 g/kg/hr

allergies
intralipid: egg, soybean
SMOF-lipid: egg, soybean, fish
omegaven: egg, fish

max hang time for lipid bag: 12 hours
need 1.2 micron filter (NOT SMALLER – will filter out lipid!)

152
Q

lipid monitoring

A

lipid/triglyceride balance
IFALD, hypertriglyceridemia, EFAD –> balance

153
Q

4) micronutrients

A

electrolytes
vitamins
trace elements

154
Q

electrolytes note

A

all come as salts –> can’t inc one without inc another
*Na, K, Phos

155
Q

electrolyte caution

A

calcium-phosphate ppt
- concentration dependent

156
Q

how to minimize risk CaPhos ppt (aka how to inc solubility of Ca and Phos)

A
  • dec temp
  • dec pH
  • dec time in bag
  • dec concentration of Ca and Phos
  • use calcium gluconate
  • add phos –> then rest –> then ca
157
Q

multivitamin

A

include at standard dose –> need it for development

MONITOR PTS ON WARFARIN CLOSELY –> contains vitamin K

158
Q

trace elements

A

commercially available

159
Q

5) special population consideration

A
  • liver: more branch-chain amino acids
  • DM: dec carb, inc fat
  • COPD/pulmonary: dec carb, inc fat
  • trauma, burn: inc protein needs
160
Q

anion balance

A

if metabolic acidosis: inc acetate, dec chloride
if metabolic alkalosis: inc chloride, dec acetate

161
Q

3-in-1 compatibility

A

creaming: can reverse, safe to use
cracking: cannot reverse, not safe to use

162
Q

3-in-1 minimum stability values

A

4% amino acid
10% dextrose
2% lipid

163
Q

filter requirements

A

if lipids (3-in-1, or lipid bag) – 1.2 micron
if no lipids (2-in-1) – 0.22 micron

164
Q

TPN safety limit checks

A

1) dextrose peripheral max: 12.5%
2) lipid max infusion rate: 0.15 g/kg/hr peds, 0.11 g/kg/hr adult
3) glucose max infusion rate: 4 mg/kg/min adult
4) peripheral osmolality limit: 900 mOsm
5) 3-in-1 stability minimims: 4% protein, 10% dextrose, 2% lipid

p2 year (9 decks)

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