Week 1 Liver Flashcards

(101 cards)

1
Q

What is cirrhosis?

A

extensive scarring of the liver

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2
Q

Most common causes for cirrhosis in the US

A

hepatitis C, alcoholism, and biliary obstruction

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3
Q

Basic functions of the liver

A

digestion, nutrition metabolism, protein synthesis, detoxify blood, produce bile, converts glucose to glycogen, converts ammonia, regulates platelets, produces heme

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4
Q

What happens when there is a lack of albumin (a protein created by the liver)?

A

Because of the large molecule keeping pressure in the vascular system, patients will start third spacing huge volumes of fluid in their gut and lower extremities

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5
Q

What is the tx for tylenol overdose?

A

Mucomyst

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6
Q

What medications cause the most liver problems?`

A

Tylenol, “glitazone” diabetic drugs and anti-TB drugs

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7
Q

What happens when someone doesn’t make bile?

A

They can’t emulsify fat and develop steatorrhea and fat leave through the stool. Also can not get fat soluble vitamins (AEDK)

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8
Q

Function of vitamin K in liver patients

A

responsible for much of the blood clotting cascade

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9
Q

Why give FFP over FP to a liver PT?

A

FFP has more clotting factors (7&9) that the PT lacks

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10
Q

Will the PT with ESLD by hypo or hyper glycemic?

A

Hypoglycemic because the liver can not convert glucose to glycogen for storage

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11
Q

Ammonia and ESLD

A

the liver is unable to convert ammonia which is a bi-product of protein and excrete it so it builds up in the body

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12
Q

Anemia and ESLD

A

the liver processes heme so you will be anemic in ESLD

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13
Q

What medication is used to remove ammonia?

A

Lactulose

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14
Q

Which antibiotic is commonly used in liver disease?

A

Rifaximin according to Rita

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15
Q

Function of antibiotic use in liver disease

A

Helps prevent episodes of HE and keeps PTs out of the hospital

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16
Q

Kupffer cells

A

found in the liver and involved in the immune system and infection response. They decrease as your liver function decreases and you are less able to fight infections

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17
Q

AST/ALT levels in liver disease

A

Both will be elevated, ALT is more specific to liver cells

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18
Q

Bilirubin levels in liver disease

A

they will be very high because the body can’t excrete it. It will cause urine to be light to dark brown

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19
Q

Level of ammonia in liver disease

A

elevated

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20
Q

Level of albumin in liver disease

A

decreased

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21
Q

Level of Ca2+ in liver disease

A

decreased

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22
Q

Qty of platelets in liver disease

A

drastically decreased

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23
Q

Number of WBCs in liver disease

A

decreased

the immune system is inhibited

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24
Q

PT/INR levels in liver disease

A

prolonged

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25
Function of EGD test
looking for esophageal varicies. If there are, you have portal HTN (over 5mmHg of pressure)
26
MARs procedure
Dialysis of the liver to purify their blood
27
Why give aldactone in liver disease?
It decreases aldosterone which regulates H2O and Na in the body
28
What type of diet should liver patients be on?
High calorie, high carb, low/moderate fat, high protein, LOW salt 6 meals/ day
29
What is hepatitis?
Inflammation of the hepatocytes in the liver
30
How is Hep A transmitted
fecal-oral route, contaminated H2O, food, more common in underdeveloped areas
31
Hep A vaccine?
Yes
32
Hep B vaccine?
Yes but people who are overweight should have their titers checked because the vaccine may not remain as effective
33
Hep B infection series of events
May not know infection has occurred, most recover and develop immunity, a small # become carriers and need lifelong tx
34
Tx for chronic Hep B infection
lifelong Ribavirin and pegylated interferon only if you become a chronic carrier, otherwise, you won't need these meds
35
Hep C Sx
Most people a asymptomatic which delays tx and can lead to ESLD
36
Hep C transmission
Parenteral
37
Hep C vaccine?
No
38
Hep D incidence
rare, must have coexisting Hep B to be infected
39
Hep D vaccine?
No but getting the Hep B vaccine will likely keep you from getting Hep D
40
Hep E transmission
fecal-oral route | Mostly seen in Asia and Africa
41
fulminant hepatitis
A severe, acute and often fatal form of hepatitis | Liver cells fail to regenerate and necrosis takes over
42
When is hepatitis considered chronic?
when liver inflammation lasts longer than 6 months
43
Cause of chronic hepatitis
Hep B, C or B superimposed with hep D
44
Complications of chronic hepatitis
cirrhosis and liver cancer | infections, especially the combination of HBV with HCV, HDV, or HIV infections.
45
Measures to prevent HAV infection include
handwashing especially after handling shellfish Receiving immunoglobulin within 14 days of virus exposure Being vaccinated
46
Clinical manifestations of hepatitis to look for on assessment
* Abdominal pain * Changes in skin or sclera (icterus) * Arthralgia (joint pain) or myalgia (muscle pain) * Diarrhea/constipation * Changes in color of urine or stool * Fever * Lethargy * Nausea/vomiting * Pruritus (itching)
47
Confirmatory test for HAV, HBV and HCV
acute elevations of liver enzymes indicating liver damage
48
. Serum total bilirubin levels in hepatitis
elevated and are consistent with the clinical appearance of jaundice Elevated levels are also seen in urine
49
When is the presence of hepatitis A established
when hepatitis A virus (HAV) antibodies (anti-HAV) are found in the blood
50
When is the presence of the hepatitis B virus (HBV) established
in the presence of hepatitis B antigen-antibody systems in the blood and a detectable viral count
51
How long is the Hep B PT contagious?
as long as HBsAg (hepatitis B surface antigen) is present in the blood, presence after 6 months indicates a carrier state or chronic hepatitis. People who have been vaccinated against HBV have a positive HBsAb because they have immunity
52
Liver biopsy
biopsy may be used to confirm the diagnosis of hepatitis and to establish the stage and grade of liver damage
53
Interventions during the acute stage of viral hepatitis
aimed at resting the inflamed liver to promote hepatic cell regeneration
54
Hepatitis nutrition
high in carbohydrates and calories with moderate amounts of fat and protein, small frequent meals, supplement vitamins
55
STEATOSIS
Fatty liver
56
Cause of fatty liver
accumulation of fats in and around the hepatic cells, may be caused by alcohol abuse or other factors
57
Causes of Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH)
* Diabetes mellitus * Obesity * Elevated lipid profile
58
Common findings in fatty liver disease
asymptomatic | elevated ALT and AST or normal ALT and elevated AST
59
Tx for fatty liver
Weight loss, glucose control, and aggressive treatment using lipid-lowering agents
60
Biproducts of protein breakdown
Ammonia and bacteria
61
Levels of AST/ALT, bilirubin and alkaline phosphatase through liver disease
They will all go up until the end stage and then they will go down
62
Critically low platelet value
40,000
63
Sx of portal HTN
anorexia excess fluid/3rd spacing HF
64
Teaching plan for liver disease PTs
``` No alcohol Watch OTC (tylenol/NSADIS) Take rest periods Low salt diet Need bleeding precautions Daily WT ```
65
When to get liver dialysis (MARs procedure)
increased weakness, tremulous, change in mental status
66
What to teach about meds for liver
Teach why they use each med Lactulose, they dont like the diarrhea Diuretics, Lasix, aldactone, not HCTZ (too weak)
67
Why do we give aldactone?
decreases aldosterone levels
68
Phases of hepatitis
Pre-icteric Icteric Convalescent
69
Pre-Icteric phase of hepatitis
No jaundice but you won't feel well | Sx: anorexia, N/V, fatigue, rash, possible RUQ pain
70
Icteric phase of hepatitis sx
Jaundice (first seen in the sclera), itching, dark urine due to bilirubin excretion, clay colored stool, fatigue, wt loss
71
Convalescent phase of hepatitis
PTs will feel better but they need more rest, appetite returns, no jaundice
72
NAFLD is correlated with what disease?
Diabetes and being obese
73
Stages of liver damage
steatosis steatohepatitis Cirrhosis
74
Steatosis in NAFLD
deposits of fat cause liver enlargement
75
steatohepatitis in NAFLD
scar tissue begins to form
76
S/Sx of NAFLD
``` Asymptomatic RUQ discomfort (possibly) Fatigue Belly fat (very common Diabetes HTN Hyperlipidemia Hepatomegaly (especially when they are in the inflammatory phase) Splenomegaly Acanthosis nigricans ```
77
Tx for NAFLD
No FDA approved treatment TZD possibly statins TLC = therapeutic lifestyle changes (lose 10% of body wt)
78
Complications of cirrhosis
``` Portal hypertension Ascites Bleeding esophageal varices Coagulation defects Jaundice Portal systemic encephalopathy (Hepatic Encephalopathy) Hepatorenal syndrome Spontaneous bacterial peritonitis ```
79
Tx for portal HTN
TIPS procedure (trans-jugular intrahepatic portal shunt.)
80
Portal HTN
caused by obstruction of blood through the portal vein Can result in ascites, esophageal varices, anorexia Over years, it can result in HF
81
Issues with albumin and ascites
Free fluid in peritoneum pulls albumin with it. Need to give albumin post paracentesis If liver unable to make albumin then have oncotic pressure issues in the blood vessels
82
Sx and Tx of bleeding esophargeal varicies
Sx: hematemesis, melana Tx: Endoscopy to stop bleeding, Banding, Sclerosing
83
Portal Systemic Encephalopathy (Hepatic Encephalopathy) cause
Unknown cause, possibly due to toxins, not due to ammonia
84
Portal Systemic Encephalopathy (Hepatic Encephalopathy)
causes changes in LOC and personality | There are 4 stages of severity
85
Sx seen in early stage of Portal Systemic Encephalopathy (Hepatic Encephalopathy)
asterixis (flapping) of the hands when hands are put up
86
Hepatorenal Syndrome
As liver fails the kidneys fail | Prognosis is poor
87
Hepatorenal Syndrome sx
Sudden decrease in urine output ↑ BUN/Cr, urine osmolarity ↓ urine sodium GFR declines
88
Spontaneous Bacterial Peritonitis
Seen in ESLD | Translocation of bacteria from intestines into peritoneal fluid
89
Spontaneous Bacterial Peritonitis sx
ascites, rigid abdomen, belly button may be popping out, caput medusa, Gynecomastia, palmar erythema, abnormal bruising, and spider angiomas.
90
Spontaneous Bacterial Peritonitistx
Low Na, fluid restriction, vitamin/nutrition supplements, diuretics, Rifaximin, paracentesis
91
Spontaneous Bacterial Peritonitis labs
Increased: AST/ALT, Alkaline phosphatase, Bilirubin, Coags Decreased: Albumin, Platelets, RBCs
92
TIPS procedure
creates a tunnel in the liver, connects the portal vein to a hepatic vein, stent is placed to keep open
93
Nursing interventions post TIPS procedure
Bedrest, assess for fluid leaking or abd distention, monitor urine, check VS
94
4 problems seen in ESLD patients
Decreased bile production Anemia Coagulation issues Decrease in albumin and other proteins
95
S/Sx seen when bile production is decreased
Steatorrhea Jaundice Decrease in fat-soluble vitamins (that’s a biggie) High cholesterol (because the bile doesn’t carry it out)
96
Why are ESLD Pts anemic?
liver bifurcates the heme from the globin and store it and produce it
97
Nursing interventions for decreased bile production
Modify diet: decreased fat, increase protein, supplement vitamins Skin care: no hot soapy water, anti-itch cream
98
Interventions for anemia
if Hct is < 25%, administer blood, try to reduce liver toxins
99
Interventions for coagulation problems
FFP, Vitamin K, Bleeding precautions, administer platelets
100
Interventions for decreased albumin
small frequent high protein meals, give albumin, low salt, diuretics, beta blockers
101
Ways to promote appetite in liver disease
Paracentesis relieve pressure) Dark chocolate will relieve portal HTN Maintain clean environment Administer anti-emetics cautiously (can be toxic to liver)