Exam 3 Flashcards

1
Q

basic nutritional support steps

A

1.determine nutritional risk
assess nutritional status
3.calculate protein and kcal requirements

  1. evaluate available routes
  2. identify special nutritional requirements
  3. select appropriate formula
  4. evaluate for drug nutrient interactions
  5. devise monitoring plan
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2
Q

nutritional screening tools

A
  1. simple malnutrition screening tool
    if score is >2 or more, pt is at risk for malnutrition
  2. ICU malnutrition screening tool
  3. NUTRIC ICU screening tool: high risk: >/5 without IL-6, > 6 with IL-6
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3
Q

Assessment of Nutritional Status

A

system based approach to determining if pt needs nutritional support

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4
Q

components of nutritional supports assessment

A
  1. a focused medical, surgical, and dietary history
  2. physical exam: general appearance, skin, musculoskeletal, neurologic, etc.
    a. ways to interpret physical examination: using subjective assessment tool-> classifies pts based on physical exam data
  3. Anthropometrics(measuring size of human body)
    a. BMI, IBW, body composition w. bioelectric impedance, functional assessment (hand grip strength
  4. Visceral proteins: hepatic ally synthesized and presumed to reflect decreased organ functional protein mass: Albumin, Transferrin, Prealbumin
  5. immune function
    malnutrition results in decreased lymphocytes: TLC: <1.2 x 10^9 cells/L

6.Nutritional deficiencies:

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5
Q

Calculating nutritional requirements

A. Estimating energy requirements

  1. healthy.
  2. Ill stress, Bmi<30
  3. Ill,stress, BMI 30-50
  4. Ill, stress BMI>50:
  5. Burns
    a. BMI <30
    b. BMI>/= 30
A

Kcal/kg/day

Healthy: 20-25

Ill, stress, BMI<30: 25-30

Ill, Stress, BMI 30-50: 11-14 (ABW)

Ill, stress BMI>50: 22-25 IBW

Burns based on BSA or
25-35 BMI< 30
21 BMI >/=30

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6
Q

Calculating nutritional requirements

A. Estimating protein requirements

  1. in critics illness
  2. in burns

if pt is obese
BMI 30-40
BMI >40

A

stress level determines amount (g/kg/day)

  1. 2-2g/kg/day in critical illness
  2. 5-3.5g/kg/day in burns

obesity based on BMI
30-40= 2g/kg/day IBW
>40= 2.5g/kg IBW

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7
Q

Calculating nutritional requirements

A. Estimating fat rquirements

A

10-35% of total calories in adults

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8
Q

Calculating nutritional requirements

A. Establihsing fluid requirements

A

usual fluid requirements: 30-40mL/kg/day or

1mL/kcal/day

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9
Q

impact of baseline nutritional status on the timing of nutrition support iniitiation

A

for NUTRIC nutritional risk tool

if LOW RISK

  • normal baseline:
  • NUTRIC <5
  • may withhold nutrition up to 7 days

if HIGH RISK

  • compromised baseline
  • NUTRIC>/= 5
  • initiation of nutrition should be done asap. >80% OF ESTIMATED OR CALCULATED GOAL AND ENERGY AND PROTEIN WITHIN 48-72 HOURS
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10
Q

TPN indications

A

overall: inability to use the enteral route

  1. GI tract dysfunction:
    * short bowel
    * severe vomiting
  2. adjunctive treatment for cancer
    * malnourished and not EN candidates
  3. pancreatitis
    * if EN exacerbates symptoms or disease
  4. critically ill
    * EN route not available r tolerance is a problem
    * withold fo Ruperts to 7 days
  5. Preoperative
  6. Hyperemesis
  7. Eating disorders
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11
Q

cons/complications of parenteral nutrition

A
  1. economic: costly
  2. mechanical:
    * pneumothorax: from line placement
    * thrombosis
    * thrombophlebitis
  3. Infectious:
    * line sepsis/fungemia
    * increased bacterial translocation
  4. Metabolic:
    * electrolyte imbalances
    * hyper-hypoglycemia
    * hypertriglyceridemia
    * FLuid overload
    * osteoporosis/osteomalacia
  5. GI tract:heptobiliary
  6. refeeding syndrome
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12
Q

refeeding syndrome

A

rapid severe depletion of K, Mg, and phosphate in starved patient.

the more nutritionally depleted the slower nutritional support should be initiated

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13
Q

Parenteral nutrition component

macronutrients

a. about kcal/g
b. notes

Last macronutrient also:
a.allergies to consider
b. time frame of when cant u give it in critical care unit
c. infusion adverse events
D. Oher warnings
A

A.Protein:

  • 4kcal/g
  • 6.25 g protein =1g nitrogen
  • contains both essential and non essential amino acids

B. carbohydrates (dextrose)
3.4 kcal/g
pH range: 3.5-6.5

C: Lipids

  • 9 Kcal/g
  • given via oil suspensions in aq. medium in parenteral nutrition
  • don’t give if pt has egg allergy due to egg phospholipid emulsifying agent
  • cant use if soybean oil allergy
  • source of vitamin K
  • contains omega-6 PUFA promote production of pro inflammatory cytokines. avoid in 1stweek of pt being in critical care unit and provide max of 100g/week
  • adverse events:
    a. infusion reactions ->dyspnea, chest tightness, palpitation, chills, rash, headache nausea
    b. hypertryglyceridemia(TF>400 MG/DL)
    c. hepatotoxicity
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14
Q

steps to initiating tpn

A
  1. ESTABLISH VASCULAR ACCESS
  2. calculate macro requirements
    * provide 25-50% on first day
    * CHO 150-200 g initially
  3. evaluate electrolyte needs
  4. evaluate trace element and vitamin needs
  5. evaluate fluid requirements
  6. determine ened for insulin

7, review compatibility

8.ASPEN guidance

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15
Q

designing tpn formula

macros: what kind of formulas can be used?

A
  • can use standard formula or *individualized formula

* determine nutrionial requirements, lipid, protein, and dextrose, and then volume

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16
Q

designing tpn formula: electrolytes

what to consider

A

consider extraordinary losses (renal/GI) as well a renal and hepatic failure reducing requirements

also consider acid base balance

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17
Q

designing TPN formula

Micronutrients(vitamins) considerations

A

water soluble vitamins most important, but dry should be met

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18
Q

designing TPN formula

trace elements

when do trace element deficiencies usually occur

A

trace elements deficiencies usually occur in unsupplemented long term tpn

REQUIREMENTS VARY ON BASIS of pts. clinical condition

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19
Q

factors effecting calcium phosphate compatibility

A
  1. amino acid conc: increases pH
  2. amino acid product composition: affect solubility
  3. calcium and po4 conc. :decreases solubility
  4. calcium salt: only calcium gluconate that should be added to tpn. NEVER chloride
  5. dextrose conc: lowers pH( increases solubility)
  6. pH of formulation: low pH increase more soluble calcium form
  7. temp: inverse solubility: higher the temp, less the solubility
  8. order of mixing: ADD PHOSPHATE BEFORE CALCIUM
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20
Q

monitoring for nutritional plan in hospital pts.

A

fluid/weights: daily

glucose: 1-6 hrs
electrolytes: daily-TIW

LFTS: 1-2 x week

Visceral proteins: 1-2x/week

CBC, PT/PTT 1-2x/week

protein turnover: weekly

lipids: triglycerides weekly

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21
Q

why is it important to use enteral route

A

“if the gut works, use it”

maintains intestinal integrity and immune function

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22
Q

enteral feeding access devices

naso/orogastric tube

indication:
placement: 
advantages:
disadvantages:
crushed meds?:
A

enteral feeding access devices

naso/orogastric tube

indication: short term, intact gag, normal Gastric emptying
placement: bedside
advantages: ease of placement, inexpensive, all feeding methods
disadvantages: tube displacement, aspiration

crushed meds?: YES

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23
Q

enteral feeding access devices

nasoduodenal, nasojejunal tube

indication:
placement:
advantages:
disadvantages:
crushed meds?:
A

enteral feeding access devices

indication: short term, aspiration, impaired gastric emptying
placement: bedside
advantages: potential reduced aspiration risk, earlier feeding
disadvantages: skills for placement, smaller tube. NO MOLUS FEEDING

crushed meds?: yes.10 fr or larger

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24
Q

enteral feeding access devices

Gastrostomy G-tube

indication:
placement:
advantages:
disadvantages:
crushed meds?:
A

enteral feeding access devices

indication: long term, normal gastric emptying
placement: surgery
advantages: all feeding methods, comfort, larger tube
disadvantages: procedure risk, aspiration, site complications

crushed meds?: Yes

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25
Q

enteral feeding access devices

jejunostomy J-tube

indication:
placement:
advantages:
disadvantages:
crushed meds?:
A

enteral feeding access devices

indication: long term, impaired GE, aspiration
placement: surgical
advantages: earlier feeding, comfort, reduced aspiration
disadvantages: procedure risk, smaller tube, site complications, NO BOLUS FEEDS

crushed meds?:NO

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26
Q

enteral formula selection

A

standard formulas are recommended for most patients

how we choose a formula typically is based on how much protein a pt. needs

if pt has other issues (volume intolerance, impaired digestion, renal disease, stress/trauma etc.,) may warrant specialty formula

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27
Q

enteral nutrition gi INTOLERANCE

why is it problem

ways to monitor

prevention/management

A

may contribute to aspiration, requires holding feeds and impacts delivery of nutrition

ways to be monitored for intolerance:

  1. gastric volume residuals (GVR) volume rmeinig in stomach over a given interval
    * not a god indicator
  2. symptoms of intolerance
    * better than grr

prevention/maanagement:
*heep head of bead at 30-40 degrees

  • minimize opioids
  • correct fluid and electrolyte abdnormaliities
  • continuous rather than bolus feeding
  • post pyloric feeding
  • prokinetic agents: metaclopromide, erythromycin
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28
Q

complications of enteral nutrition

A

1.DIARRHEA

  1. intestinal ischemia
    * risks: neonates, critically ill, immunosuppressed, juejenal feeding, hyperosmolar feeds
    * prvention: delay feeding until fully volume resuscitated
    * iniitiate with is0-asmolor fiber free formula
    * monitor for SS, esp. if previous tolerating feeds
  2. Metabolic: glucose, fluid electrolytes, macros andmicronutrient perturbations (alterations)
  3. mechanical:
    * feeding tube occlusion: flushing maintains potency
    * malposition:
    * nasopulminar intubation
  4. infectious
    a. aspirarion
    b. sinusitis
    c. exit site infections of gastric tube
    d. intra-abdominal
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29
Q

Nutritional monitoring plan for hospitalized patients

Enteral feeding

A

Fluid/weights: daily

Glucose: q1-6hr

electrolytes: daily-TIW

visceral proteins: 1-2x/week

CBC, PT/PTT: 1-2x/week

Protein turnover: weekly

GI intolerance: daily up to every 4 hours

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30
Q

steps to med administration via enteral access device

A
  1. med ordered by provider
  2. oder reviewed by nurse or pharmaist
  3. medication prepared by nurse or pharmacist
  4. medication administered by nurse
31
Q

things to consider when admin. meds via enteral access device

A

access site:
*may affect absorption of drug

med dosage form:
*liquid vs tablet. NOT CR and enteric coated tabs
physical incompatibilities

prevention and management of tube occlusions

proper administration techniques

32
Q

med administration techniques via feeding tube

A

oral preffered.

crush immediate release tablets

administer multiple meds seperately, with water flushes done between each medication, flushingg w. at least 15-30 ml of water before and after medication

do not crush enteric coated tablets

33
Q

drug nutrient interaction mechanisms w. examples:

A

Precipitating factor- Object

drug-nutrient: carbamezapine decreases biotin status

drug-nutrient status: quetiapine causes weight gain

drug metabolic status: capecitabine causes hypertriglyceridemia

nutrition status-drug: obesity lowers ertapenem levels

nutrient-drug: vitamin D reduces atorvastatin levels

food component-drug: protein reduces levodopa absorption

food-drug: grapefruit increases simvastatin concentrations

34
Q

meds not impacted by enteral access device feed

A
  1. atovaquone
  2. azalea antifungals (fluconazole, posazonazole and voriconazole)
  3. linezolid
  4. metronidazole
  5. h2 receptor blockers
  6. levetiracetam
  7. pantoprazole
  8. tacrolimus
35
Q

meds impacted by enteral access device feed

phenytoin

A
  1. phenytoin
    * reduced absorption requiring substantially higher doses
    * managed by escalating dose, holding feeds 2 hours before/after admin(not reliable), dilution of suspension, use of IV formulation enterally
36
Q

meds impacted by enteral access device feed

carbamezapine

A

improved bioavailability w. slow gastric emptying

*1:1 dilution w. water and rigorous tube flushing

37
Q

meds impacted by enteral access device feed

fluroquinolones

A

reduced bioavailability

bind multi-valent cations

give 2 hours before or 4 hours after antacids (calcium, magnesium)

38
Q

meds impacted by enteral access device feed

amiodarone

digoxin

A

amiodarone: absorption is improved with food. make sure it is administered in stomach
digoxin: soluble fiber reduces digoxin absorption . reduced bioavailability

39
Q

meds impacted by enteral access device feed

levothyroxine

A

levothyroxine : absorption best in fasting state

continuous enteral foods reduce efficacy

40
Q

meds impacted by enteral access device feed

proton pump inhibitors

A

admin. with alkaline solution or as one of the powder formulations

41
Q

meds impacted by enteral access device feed

warfarin

A

must increase dose for warfarin due to protein content of the feeds

monitor pt/inr closely-especially when feeds are DC’d

42
Q

meds impacted by enteral access device feed

itraconazole

Sevelamer

sucralfate

A
  1. poor viability
  2. can clog tube
  3. binds phosphate
43
Q

meds impacted by enteral access device feed

DOACs

A

*rivaroxaban
*apixaban
*dabigatran: DO NOT CRUSH
edoxaban

44
Q

who has increased requirements for vitamin deficiency

A

malabsorption, medications, alcohol, hemodialysis and hyperthyroidism

45
Q

purpose of vitamins

B vitamins:

A

1.thiamine, riboflavin, niacin, biotin, pantothenic acid

energy releasing

  1. vit. b6, b12, folate:
    * hematopoeisis
46
Q

purpose of vitamins

A

fat soluble

vit. A,D,E,K
greater potential for toxicity

47
Q

Elements of Dietary reference intakes

A

RDA= recommended dietary allowance

AI: adequate intake

EAR= estimated average requirement: average daily intake estimated t meet the requirements of 50% of healthy individuals

uL=tolerable upper intake level (max amount)

48
Q

Thiamine deficiencies

A

requirements are increased with high carb consumption:

deficiency in alcoholics

49
Q

riboflavin . vitamin b2 deficiency

A

increased requirements during periods of metabolic stress. isolated deficiencies are rare

50
Q

Niacin deficiency

A

called Pellagra

characterized by the 3 d’s

dermatitis
diarrhea
dementia

treat agressively with high doses

51
Q

pyridoxine b6

ddi

A

levadopa and high doses >5 mg/day

phenobarbital, phenytoin

52
Q

vitamin b12 deficiency

A

older>50 yrs have decreased absorption

macro-lyritic anemia

can cause irreversible nerve damage

53
Q

folic acid. vitamin b9deficiencies

A

pregnant patients require supplementation to prevent neural tube defects

54
Q

vitamin c deficiency

A

scurvy

defect in collagen synthesis
difficulty in healing wounds

55
Q

cirrhosis complications

A

ascites

portal hypertension

vatical bleeding

spontaneous bacterial peritonitis

hepatic encephallopathy

Hepatorenal syndrome

56
Q

Child-Pugh grading

why is it used:
scoring:

A

used for dosage adjustments

  1. bilirubin:
    Score 1: 1-2
    Score 2: 2-3
    score 3: >3

2.albumin:
Score 1: >3.5
Score 2: 2.8-3.5
score 3: <2.8

  1. Acsites:
    Score 1: none
    Score 2: mild
    score 3: moderate

4.PT (prothrombin time
Score 1: 1-4
Score 2:4-6
score 3:>6

Grade A:<7 points
Grade B: 7-9 points
Grade C: 10-15 points

57
Q

Mayo end-stage Liver disease score

what is it used for

A

staging cirrhosis. also used for transplant considerations

meld score=3.78[in serum bilirubin (mg/dL)]+11.2[ln INR] + 9.57[ln serum creatinine (mg/dL)]+6.43

58
Q

Ascites

Patho

physical examination

abdominal paracentesis

A

Patho: as a result of portal hypertension. increase sinusoidal pressure->causes back up of blood flow to sphlanic vessels around gi track. body produces NO

PE: full, tense, bulging abdomen

abdominal paracentesis

  • removes fluid: therapeutic and
  • SAAG>/=1.1 g/dL indicates portal hen from cirrhosis
  • can be used to see abc in peritoneum, dx of SBP
  • note: paracentesis should not be avoided even if pt has low platelets or increased pt/INR
59
Q

ascites treatment

non pharm

pharm
*what if conventional pharm not working

A

non pharm:
* Na+ restriction

*NOT FLUID RESTRICT: because circulating intravascular volume is low due to moving into extravaasculr space

pharm:
1)aldosterone antagonists: RAAS (counter RAAS system activation due to body sensing decreased circulating volume
a)sprinolactone 50-100 mg up to 400 mg
causes k+, sooooo.. paired with
b)loop diuretics:
 to prevent hyperkalemia 40 mg
RATIO: 100mg/40mg
* do not give thiazide diuretics: because they worsen already hyponatremia in cirrhosis 

what if a pt is not tolerating diuretic therapy, bp is low

  • HOLDING THRESHOLD IS systolic bp<90
  • add midodrine (vasoconstrictor in periphery and raises bp inorder to tolerate diuresis)

*large volume paracentesis (4-8L) ever 2 weeks
-> can cause decreased bp even more
-> increased SCr(due to organ hypoperfusion)
to combat that, if removing greater than 5L, give 8g IV 25% albumin(hypertonic) for q L of fluid removed
**$$, short tpx t1/2, but could reduce mortality

TIPS procedure:
Transjugular intrahepatic portosystemic shunt
*refractory ascites pts intolerant of large volume paracentesis
*also used for refractory vatical bleeding
*shunt bypasses liver providing immediate relief for the high pressure portal vein
*increases ammonia-> cases increased hepatic encephalopathy

60
Q

Portal hypertension -(variceal bleeding prevention)

define:

dx:

complications

goal of portal htn treatment

A

define: difference in pressures btw portal vein and inferior vena cava
dx: SAAG >/=1.1

compliacations:
* variceal bleeding
- > causes 1/3 of cirrhotic death
* ascites (as mentioned b4)

goals:
prevent vatical enlargementt and bleeding
(NOT to prevent variceal development)
treatment only used in confirmed varies through EGD

61
Q

Portal HTN treatment

goals

pharm:
*also holding parameters for pharm

A

goals:
prevent vatical enlargementt and bleeding
(NOT to prevent variceal development)
treatment only used in confirmed varies through EGD

pharm:
*non selective beta blockers
*propanolol, nadolol, carvedilol
*b1 blockade: reduce HR, reduce CO-> reduces portal pressure
b2 blockade: causes sphlannic vasodilation, so blockade will vasoconstrict
*propanolol: 20-40 bid
*nadolol: 20-40 mg daily
*carvedilol: 3.125 mg bid
titrate up needs to resting HR ~60- bpm

holding parameters:
decreaes/hold dose 
*systolic BP<90 or DBP<60
*HR<60
*hepatorenal syndrome (HRS)
*refractory ascites 
*SBP
62
Q

Acute variceal bleeding

define:

what is biggest risk for acute variceal bleeding

A

define: gastric and esophageal varies form as a result of shunting of blood away.
varices: abnormally dilated vessels. as total pressure increases increases risk for rupture and bleeding

big risk of variceal bleeding: SBP

63
Q

acute variceal bleeding treatment

A

supportive care measures

  • IV fluids
  • PRBC
  • hgb ~8 g/dL

octeotride IV: somatostatin analog.
moa: inhibits glucagon->causes vasoconstriction of sphlancnic circulation

EVL: endoscopic variceal ligation (rubber banding) :squeezes off varies-> with EGD

best results when octreotide IV and evl occur together

SBP prophylaxis: 7 DAY CEFTRIAXONE iv

*if octreotide IV+evl doesn’t work and bleeding persists, consider TIPS

once bleed stabilizes:
*non selective BB

64
Q

Spontaneous bacterial peritonitis

what is it
causative organisms
Dx

A

bacterial infection of the ascitic fluid

caused by enteric gram _(E. Coli)

Dx:

  • fever, malaise, increased WBC, pain/tenderness in abdomen
  • paracentesis: absolute polymorphonucleated leukocyte count>/=250 mm^3
  • take WBC x PMN= absolute PMN cel count
  • +bacterial culture (the culture might come back neg., but pt are still treated
65
Q

SBP treatment

prophylaxis (as mentioned b4)

active infection

A

prophylaxis:
* IV cetriaxone, (or ciprafloxacin) for 7 days

  • indefinitE sap ppt:
    a. previous hx of sbp
    b. ascitic protein <1.5 + other criteria
  • Ciprofolax 750 mg weekly (in guidelines), but more practical -> 250-500 mg daily
  • bactrim Double strength (DS) 5 days a week (guideline) more practical 1 tab daily
active:
for absolute PMN>/=250
*3rd gen ceph
*cephotaxime
*ceftriaxone (more widely available)
*cipro if true PCN allergy

if specific org. is identified, can streamline therapy within 48-72 hrs of starting IV abx

Duration: 5 days

*IV albumin 25%: 1.5g/kg on day 1 + 1g/kg on day 3
indicated for pts with Scr>1, BUN>30, OR bilirubin >4.
*reduces mortality

66
Q

Hepatic encephalopathy

A

define: accumulations of toxins from declining hepatic function and portal-systemic blood flow shunting

toxins:
ammonia results in altered mental status
*NOTE: ammonia levels don’t determine severity. elevated ammonia indicated yes they have hepatic encephalopathy. don’t need to keep checking ammonia levels when treating

67
Q

treatment for hepatic encephalopathy

A
  1. remove precipitating factors
    * meds: opioids, benzos,
  2. dietary protein: switch pt to dairy or vegetable protein sources because less likely to cause BBB
  3. ammonia in GI tract
    * Lactulose- nonabsoprbale disaccharides
    * but bacteria ferments this, decreases colonic ph with acid production, causes bowel movement where NH34 GETS trapped in bowel.
    * eliminated fecally

acute hepatoencephalopathy

  • PO lactulose 25 mL q1-2h until have atlas 2 loose/watery stools
  • enema : 300 mL retention enema, retin for 1 hour q 6-12 hours

Prevention HE:

  • after active treatment:
  • give lactulose 15-60mLq 6-12 hours (2-3 soft BM/day)

other therapies: Rifaximin (Xifaxen)
*abx: reduce bacteria that produce ammonia
acute dose: 40 mg po q8h
maintenance: 550 mg po BID
*ADD ON, NOT SUBSTITUTION. almost all trial pts used this in combo

68
Q

Hepatorenal syndrome

A

sphelncnic vasodilation secondary to portal HTN, causing reduced intravascular volume, causing reduced renal perfusion

  • very high mortality rate
  • sort of last stage of cirrhosis

dx:

  • cirhosis with ascites
  • Scr: >/= 0.3 mg/dL in 48hrs or >/=50% increase in baseline in last 7 days
  • no improvement in scrabble after 2 days of diuretic d/c + iv albumin 1g/kg/day
69
Q

hepatorenal syndrome treatment

A
  • ultimately liver transplant
  • iv NORPEPINEHRINE+ iv albumin 1g/kg/day

response to therapy: Scr decrease to < 1.5mg/dl or return within 0.3 mg/dL of baseline over a max of 2 weeks.

if after 4 days of therapy he scr remains the same, d/c therapy

70
Q

pkpd changes in cirrhosis

decrease in blood flow

A

*impact dugs that have high first pass effect
ex: propanolol
morphine
coreg (carvedilol)

increased in bioavailability

decrease doses to compensate

71
Q

pkpd changes in cirrhosis

loss of hepatocyte function

A

decreased metabolic activity

effects phase I (cyp) metabolism more often than phase II

solution: use agents that undergo phase II metabolic. more than phase I when possible

ex: benzos
diazepam: has more cyp
lorazepam: more phase II

72
Q

pkpd changes in cirrhosis

decreased albumin production

A

heavily protein bound drugs have more unbound drug-
> more tpx effect

ex: phenytoin: decrease dose if needed to compensate

73
Q

pkpd changes in cirrhosis

other changes

A

decreased renal function in the setting of increased Scr

increased tpx response: increase BB permeability of opioids benzos (decrease dose to compensate)