cirrhosis, vitamins/minerals, nutrition Flashcards
what is cirrhosis
cell injury in liver, death of hepatocytes
hepatocytes: functional unit of liver
causes of cirrhosis
- # 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
cirrhosis s/s
- ascitic belly
- altered mental status
cirrhosis labs to look at – 4 main ones
- jaundice / high bilirubin
- low platelets
- low albumin
- high PT/INR (low clotting factors, dec clotting)
bc liver makes: platelets, albumin, clotting factors
other labs to look at for cirrhosis
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
cirrhosis complications in order of progression
- ascites
- portal HTN
- variceal bleeding
- spontaneous bacterial peritonitis (SBP)
- hepatic encephalopathy
- hepatorenal syndrome
ascites Dx
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
paracentesis
put a needle in the ascitic belly and remove the fluid accumulated
SAAG
serum ascites albumin gradient
SAAG = serum albumin - ascitic albumin
if SAAG >/= 1.1 –> portal HTN
sodium restriction MoA
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
aldosterone antagonist MoA
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
what is a more potent diuretic in cirrhosis? loops or aldosterone antagonists
aldosterone antagonists!!
therefore always do spironolactone over furosemide if need to pick one!
midodrine MoA
alpha activity –> inc BP
**allows toleration of other two diuretics
large volume paracentesis MoA
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
IV albumin MoA
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
aldosterone antagonist AE
inc K
loop diuretic AE
dec K
what diuretic ratio do you need to optimize diuresis and keep K normal
40mg furosemide : 100mg spironolactone
**THESE ARE DAILY AMOUNTS – CAREFUL OF BID!
benefit of IV albumin with LVP
may dec mortality !
cons of IV albumin with LVP
- expensive
- short circulating half life (hours)
- short term solution to help with the transition
TIPS procedure MoA
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
TIPS AE and therefore CIs
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
what to avoid in acities
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
if do TIPS, what do you need to do
START HEPATIC ENCEPHALOPATHY PROPHYLAXIS
- bc such a high risk of it
portal HTN definition
high BP in portal vein
portal HTN Dx
SAAG greater than or equal to 1.1
varices definition
abnormally distended floppy vessels, form in the GI tract to GI organs
varices patho
FORM DUE TO PORTAL HTN
* more blood flow in GI tract –> form varices (other vessels to GI organs)
varices Dx
***EDG –> upper endoscopy
portal HTN/varices treatment goal
prevent varix enlargement and bleeding
**WILL NOT PREVENT VARIX FORMATION BC THE PORTAL HTN IS STILL CAUSING BLOOK BACKUP!
portal HTN/varix treatment indication
ONLY when have varix present!!!
non-selective BB options
nadolol, propranolol –> will NOT dec BP
carvedilol –> WILL dec BP bc of alpha activity
non-selective BB MoA
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
what do we titrate non-selective BB to?
HR around 60bpm
non-selective BB holding parameters
SBP < 90
DBP < 60
HR < 50-60
what is acute variceal bleeding a risk for?
SBP! –> bc bleeding around GI tract, bacteria in blood could move into peritoneum
s/s acute variceal bleeding
- low BP
- high HR
- low Hgb
- low Hct
- pt is out of it
- black stool
- hemetameous
how to determine when acute variceal bleeding has stabilized
no more changes in
- HR (has lowered)
- BP (has increased)
- Hgb (has increased) –> not dropping/changing by more than 2
- Hct (has increased)
why do we wait until bleed stabilized to initiate non-selective BB
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
acute variceal bleeding treatment
1) supportive care –> IV isotonic (NS, LR), O2
2) packed RBC
3) octreotide
4) EVL with EDG
5) SBP prophylaxis
6) non-selective BB
when PRBC indicated?
Hgb less than 7 or 8
octreotide MoA
vasoconstricts splanchnic vessels
IV bolus –> IV continuous infusion
endoscopic variceal ligation (EVL) with EDG MoA
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…
SBP prophylaxis
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
non-selective BB
only if varix (would be present in this case), and bleed has stabilized
if bleed not stable –> means still bleeding, repeat EVL and EDG !
spontaneous bacterial peritonitis (SBP)
bacterial infection in ascitic fluid
common causes of SBP
enteric gram (-)
- e coli
- k pneumoniae
gram (-)
- strep pneumoniae
SBP Dx
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
active SBP treatment and duration
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)
prophylaxis SBP indications
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
acute variceal SBP prophylaxis
1st: 3rd gen ceph iv
2nd: cipro if allergic
indefinitie SBP prophylaxis
bactrim
cipro
hepatic encephalopathy patho
decline in hepatic function + portosystemic shunting (either TIPS or portal HTN)
s/s of HE
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
HE treatment
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
lactulose MoA
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
lactulose dosage forms
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
when will lactulose start working
WHEN THE PT HAS BOWEL MOVEMENTS –> does not work until then!!!!!!!
rifaximin MoA
antibiotic that is poorly absorbed and stays in GI tract –> decreases the bacteria that normally produce ammonia in GI as part of normal flora
rifaximin indication
when still AMS when at 2-3 soft stools per day on lactulose
is rifaximin monotherapy
NO –> still need lactulose with it!!
prevention for HE
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
hepatorenal syndrome
liver failure (cirrhosis) + renal failure
hepatorenal patho
portal HTN –> splanchnic vasodilation –> dec effective circulating volume and dec intravascular pressure –> dec kidney perfusion and will cause AKI if intravascular low enough
heptorenal Dx
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
IV norepinephrine MoA
vasopressor –> constrict periphery and get heart pumping to save life via adrenergic response
when do we evaluate hepatorenal treatment response
4 days
then
2 weeks max of therapy
what PKPD changes occur in cirrhosis?
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
1) dec liver bloodflow impacts
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
2) dec hepatocyte function
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
3) dec albumin production
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
4) dec renal function (with a high SCr)
portal HTN –> dec intravascular volume –> dec kidney perfusion –> inc SCr and hepatorenal syndrome
5) inc CNS therapeutic effect
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
vitamins
organic compounds
function: metabolism (create/use energy), cell function regulation
minerals
chemical elements
vitamins and minerals
required as nutrients in small amounts but are not produced by body –> have to get via diet
vit and min supplementation
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
malnutrition
undernutrition or overnutrition (obesity) DUE TO nutrient imbalance
supplementation indication
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
which vitamin is folic acid?
B9 – water soluble
neural tube formation, dec in pregnancy, therefore need supplementation
vitamin A
vision
vitamin D
Ca/Phos homeostasis
bone development
vitamin E
antioxidant
vitamin K
clotting factor formation
general vit B
promoted carb, protein, lipid metabolism
B1
thiamine
- produce ATP
B6
pyridoxine
- amino acid metabolism
B9
folic acid
- neural tube development
B12
cobalamin
- DNA/RNA synthesis
C
antioxidant
iron absorption
which are the major minerals
Ca
Cl
Phos
Mg
K
Na
sulfur
need >100mg/day
which are the minor minerals
IRON
zinc
selenium
nickel
copper
fluroide
iodine
chromium
which are the minor minerals
IRON
zinc
selenium
nickel
copper
fluoride
iodine
chromium
need <100mg/day
populations at risk for mineral deficieny
- elderly
- chronic illness
- vegetarian/vegan
- pregnant
when low Ca level, need to check
if low albumin
**need to calculate corrected Ca if low albumin
when low K level, need to check
for low Mg
**Mg regulates K
**need to correct Mg before correct K
Mg inhibits ROMK channels that efflux K
special populations at risk for deficiencies
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)
1) eating disorders
anorexia, bulimia
- restricition of energy intake –> low body weight
therapy goals: nutritional rehab, restore weight slowly to prevent refeeding syndrome
refeeding syndrome
aggressive nutritional rehab leading to fluid and electrolyte shifts
- hypoxia, myocardial dysfunction, respiratory failure
2) alcohol use disorder
chronic alcohol –> dec oral intake, dec absorption –> malnutrition
AUD treat
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
3) pregnancy
have an increased physiological requirement
therefore give prenatal vitamin
- folic acid: NTD prevention
- iron: placenta/fetal development, anemia prevent
- Ca
- vit D
- idoine
what do you give with a prenatal vitamin
stool softener –> bc iron AE is constipation!
4) pediatric
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!
5) elderly
dec calorie requirement, inc nutrient requirement
**B12
- absorbed by stomach acid, less stomach acid produced in elderly!
- DO NOT START WITHOUT BLOOD TEST
5.5) macular degeneration
central vision loss due to damage of macula
want to treat with vitamin A, C, E
–> use AREDS-2 (best)
AREDS
vitamin C
vitamin E
zinc
copper
beta-carotene (vit A precursor)
AREDS-2
**Better
vitamin C
vitamin E
zinc
copper
lutein
zeaxanthin
*omega-3 tried – but not significant reduction so removed from formula!
DNI with methotrexate
dec folic acid
MUST supplement folic acid, do not take on same day
DNI with PPIs
dec calcium and others –> osteoporosis
if need Ca supplement –> calcium citrate!
what is enteral nutrition
using the gut to eat (GI tract)
who is at risk for malnutrition
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
when to consider starting nutritional support
inpatient
- normal: 7 days
- ICU: sooner than 7 days to dec mortality
outpatient
- normal: never
- have malnutrition or risk for malnutrition: start
why do we always use the gut if possible
- biggest immune system organ
- will maintain gut integrity
- will keep bile flowing which is bacteriostatic, prevents bile stones
enteral nutrition tube placement
1) nasal placement (N-tubes)
i) NG - gastric
ii) ND – duodenal
iii) NJ – jejunal
**for short term use!
NG tube characteristics
- easy to place
- inc aspiration risk -> pneumonia
- larger diameter
- allows for stomach decompression (removal of contents)
ND and NJ tube characteristics
- harder to place
- dec aspiration risk
- smaller diameter –> easier to clog
1) feed limitations
gastric tubes: can do bolus feed
duodenal and jejunal tubes: can only do continuous feeds
2) crush limitations
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!
crush and flush
crush med, 10-15mL flush before and after med
*MUST GIVE MEDS SEPARATELY
giving as liquid
crush with spoon, mix with 10mL sterile water
**MUST GIVE MEDS SEPARATELY
3) liquid limitations
if mOsm > 600 –> dilute in sterile water (prevent diarrhea)
if viscous –> dilute (prevent occlusion)
enteral feed drug DDIs
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
steps to determine enteral formulation
step 1: total calorie requirement
step 2: special considerations
step 3: administration strategy
step 4: fluid consideration
step 5: monitoring
step 1: total calorie requirement
20-30 mg/kg/day
step 2: special considerations
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
step 3: administration strategy
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
step 4: fluid requirements
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
step 5: monitor
- 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
parenteral nutrition/TPN
providing nutrients through IV
- to prevent malnutrition
- is expensive, have side effects –> therefore know indications, monitor, individualize, transition to enteral asap
tpn goals
1) provide physiologic energy needs when you can’t through enteral
2) provide macronutrients and micronutrients through IV
adult tpn indications
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
risk of malnutrition
- involuntary weight loss (10% in 6 mon)
- BMI < 18.5
- inc metabolic requirements
- altered diets
adult tpn CI
metabolic instability
- sepsis
- hemodynamic instability
- fluid shifts
DELAY until condition improves
pediatric tpn indication
- 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
neonate tpn indication
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
refeeding syndrome electrolytes impacted
potassium
magnesium
phosphate
all low
TPN complications
- metabolic: glucose, refeeding, triglycerides, liver
- mechanical: pneumothorax, thrombus, occlude catheter, phlebitis
- infection
three tpn administration options
peripheral: PIV
central: PICC, tunneled catheter
peripheral tpn CI
900 mOsm/L –> hard stop bc of phlebitis risk!
TPN product options
3-in-1: protein + carb + lipid
*more risk incompatibilty/lipid cracking
2-in-1: protein + carb
**peds
TPN approaches
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
therefore, if peds, you are likely using
individualized approach with a 2-in-1 bag + lipid bag
components of tpn
1) fluid goals
2) total energy requirements
3) macronutrients
4) micronutrients
5) special population consideration
1) fluid goals
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
2) total energy requirements
neonate: 80-120 kcal/kg/day
child: 60-90 kcal/kg/day
adolescent: 40-55 kcal/kg/day
amino acid/protein energy values
4 kcal/g
100 mOsm/%
nitrogen balance
want (+) –> if (-), inc protein in TPN
Nbalance = Nin - (Nout + 4)
Nin = g protein / 6.25
Nout = UUN result
4 = insensible loss
dextrose/carb energy values
3.4 kcal/g
50 mOsm/%
MAX IN PERIPHERAL IS 12.5% –> above, need central!
lipid energy values
Intralipid 20% –> 2 kcal/mL (NOT GRAM)
lipid CIs
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!)
lipid monitoring
lipid/triglyceride balance
IFALD, hypertriglyceridemia, EFAD –> balance
4) micronutrients
electrolytes
vitamins
trace elements
electrolytes note
all come as salts –> can’t inc one without inc another
*Na, K, Phos
electrolyte caution
calcium-phosphate ppt
- concentration dependent
how to minimize risk CaPhos ppt (aka how to inc solubility of Ca and Phos)
- dec temp
- dec pH
- dec time in bag
- dec concentration of Ca and Phos
- use calcium gluconate
- add phos –> then rest –> then ca
multivitamin
include at standard dose –> need it for development
MONITOR PTS ON WARFARIN CLOSELY –> contains vitamin K
trace elements
commercially available
5) special population consideration
- liver: more branch-chain amino acids
- DM: dec carb, inc fat
- COPD/pulmonary: dec carb, inc fat
- trauma, burn: inc protein needs
anion balance
if metabolic acidosis: inc acetate, dec chloride
if metabolic alkalosis: inc chloride, dec acetate
3-in-1 compatibility
creaming: can reverse, safe to use
cracking: cannot reverse, not safe to use
3-in-1 minimum stability values
4% amino acid
10% dextrose
2% lipid
filter requirements
if lipids (3-in-1, or lipid bag) – 1.2 micron
if no lipids (2-in-1) – 0.22 micron
TPN safety limit checks
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
