MNT liver Flashcards

1
Q

How much blood is circulated in the liver per min

A

1500 ml

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2
Q

how does blood exit the liver

A

via the hepatic veins into the interior vena cava

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3
Q

what makes poop brown

A

bile

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4
Q

where is bile made

A

liver

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5
Q

where is bile stored and concentrated

A

gallbladder

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6
Q

steatoreaha

A

fatty greasy diharea

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7
Q

how much liver function is needed to sustain life

A

10-20% cannot survive totally wihtout it

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8
Q

functions of the liver

A

activation/storage of vits and minerals
converts vit D to active form
formation/excreation of bile
metabolism of steriods
conversion of amonia to urea (affects MNT)
synthesis of clotting factors(bleeding affects MNT)

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9
Q

thorugh all liver diseases what can happen

A

10-20% liver function

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10
Q

Viral Hepitis

A

won’t impact us unless it gets to ESLD

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11
Q

Steatosis

A

fat in the liver or fatty liver

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12
Q

How much wt loss can improve steatosis

A

3-5% wt loss

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13
Q

how much wt loss is needed to reverse NASH

A

10%

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14
Q

meds for NAFLD

A

Vit e if no TD2
coffee unsweetend =protective

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15
Q

ALD

A

most common liver disease
40% of deaths from cirrhosis atributed to ETOH

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16
Q

ALD charaterized by

A

fatty liver hepatitis or cirrhosis

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17
Q

Alchoholic cirrhosis may lead to

A

GI bleed hepatic encephalopathy, portal HT ascites

18
Q

Necrosis

A

death of cells

19
Q

Alcoholic liver micronutrient deficiency

A

thiamin is most common

20
Q

Bottom line for Hepatitis

A

liver disease is a spectrum of severity
MNT is for complications

21
Q

Cirrhosis

A

irreversible fibrotic changes ( scarring) of the liver with inflamtion blood wont flow thorugh as well

22
Q

Portal HTN

A

increased pressure in portal vein

23
Q

varices

A

englarged blood vessels in esophagus
we care if feeding tube has to be placed and nick can cause bleed due to lack of cltting factors being made

24
Q

increased prothrimbin time

A

increased clotting time

25
Q

MNT for Portal HTN and Esoph Varices

A

if acute GI bleed no EN
PN if NPO 5-7 days
No PEG either dt the acites

26
Q

Ascites

A

accumulation of fluid in the abdominal cavity

27
Q

Medical treatment for ascites

A

paracentesis
diuretics

28
Q

MNT for ascites

A

NA restriction 2 g ( not lower to avoid decrease oral intake)
adequate protein

29
Q

MOnitor for ascites

A

wt to know energy needs
electrolytes (NA and pottasium)
abdominal girth know where the wt is

30
Q

Paracentesis

A

remove 5 liters of fluid , does pull off electrolytes and protein
need to get the dry wt after the fluid is removed for energy calulations

31
Q

Hyponatremia

A

low sodium
dt decreased water excretion
sodium losses with paracentesis

32
Q

Hyponatremia MNT

A

fluid restriction 1-1.5 l day
low sodium 2 g /d

33
Q

Hepatic Encephalopathy

A

impaired mentiaiton or thinking neuromuscualr diturbances and altered conciousness

34
Q

Hepatic encephalopathy possible mechanism

A

high ammonia impaired urea synthesis

35
Q

Sources of ammonia

A

GI tract protein metabolism blood from GI bleed

36
Q

HE MEds

A

lactulose and antibiotics both cause diharea to get rid of the ammonia in the body

37
Q

MNT encephalopathy

A

avoid unnecessary protein restriction
fiber increases aids in excretion of N compunds
intake of .25 g/kg of oral BCAA

38
Q

DIseased liver isn’t able to

A

maintain blood glucose levels or keep bs from tanking in periods of fasting

39
Q

MNT for ESLD

A

recomend carb consistent intake
consitent meal intake (3-6) day including bedtime snack conating carb and protein
nocturnal EN for malnurished pts

40
Q

milk thistle

A

may help liver butn ot in liver disease

41
Q

VIt def in ESLD

A

vit A D E K

42
Q

Liver transplant

A

established treatment for ESLD
malnutrion is common at time of transplant