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Nur 326 > Exam 2 - Liver Problems > Flashcards

Exam 2 - Liver Problems Flashcards

1
Q

Major Functions of the Liver

A

Metabolism and storage
Blood volume reservoir
Blood filter (cutfirst cells)
Blood clotting factors (prothrombin and fibrinogen)
Drug metabolism and detoxification

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2
Q

What does the liver metabolize and store

A

Fat, CHO, PRO, vitamins and minerals

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3
Q

Lobes of the Liver

A

Functional units of the liver. made of hepatocytes arranged around a central vein. One of only cells that can regrow and regenerate. Can regrow from healthy liver tissue

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4
Q

Cutfirst cells

A

Line inner liver capillaries (sinusoids). Responsible for removing bacteria from blood

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5
Q

Portal circulation

A

The portal circulatory system brings blood to the liver from the stomach, intestines, spleen, and pancreas

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6
Q

blood enters the liver through

A

the portal vein

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7
Q

the absorbed products of digestion

A

come directly to the liver and are sent to the lobules

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8
Q

portal circulation is

A

the first pass effect

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9
Q

Liver function tests

A

AST, ALT, alk phos

dont worry about them until over 150

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10
Q

Jaundice

A

caused by increased level of bilirubin in the bloodstream

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11
Q

Jaundice usually causes problems

A

Is noticeable with total bilirubin is greater than 2-2.5.

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12
Q

Jaundice look at

A

look at conjugated versus unconjugated to determine possible cause

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13
Q

what is jaundice

A

yellowish discoloration of skin and deep tissues

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14
Q

three classifications of jaundice

A

hemolytic, hepatocellular, obstructive

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15
Q

Hemolytic jaundice

A

from increased breakdown of RBCs

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16
Q

Hepatocellular jaundice

A

from liver unable to take up bilirubin from blood or unable to conjugate it

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17
Q

Obstructive jaundice

A

from decreased or obstructed flow of bile (gallstones)

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18
Q

Bilirubin

A

by product of heme breakdown - mainly hemoglobin

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19
Q

Direct

A

conjugated

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20
Q

Indirect

A

unconjugated

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21
Q

Elevations of indirect bilirubin

A

bilirubin overproduction or impaired liver functioning (hemolytic)

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22
Q

Elevations of direct bilirubin

A

liver working but cant get bilirubin out (obstruction, gallstones)

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23
Q

Jaundice clinical manifestations

A

darker urine
elevated liver enzymes
stools are normal or clay colored (depends on direct or indirect)
pruritis

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24
Q

Viral hepatitis

A

systemic virus that mainly affects liver - causes inflammation

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25
Q

Various strains

A

HAV, HBV, HCV – rarer viruses caused by Epsten-Barr, cytomegalovirus

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26
Q

Hepatitis can occur from other causes

A

Alcohol abuse, drugs, chemical, bacteria

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27
Q

Viral Hepatitis Pathogenesis

A

Viral infection >
Immune response: inflammatory mediators >
Lysis of infected cells >
Edema and swelling of tissue >
Tissue hypoxia >
Hepatocyte death! – Liver failure

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28
Q

Clinical manifestations of viral hepatitis

A

Similar between all types

Many are asymptomatic - but can range from none to mild to liver failure

causes abnormal elevated LFTs - but NOT consistent with cellular damage within the liver - trend and know patient

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29
Q

Prodromal phase

A

2 weeks after exposure

fatigue, anorexia, malaise, nausea, vomiting, HA hyperalgesia, cough, low grade fever

HIGHLY transmissible

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30
Q

What is hyperalgesia

A

increased sensitivity to pain

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31
Q

Icteric phase

A

begins with jaundice, dark urine, clay-colored stools

liver enlarged and may be painful to palpation

fatigue abdominal pain persists or increases in severity

32
Q

Recovery

A

resolution of jaundice
6-8 weeks after exposure, symptoms diminish
Liver remains enlarged/tender

33
Q

Complications of viral hepatitis

A

most most patients recover completely with no complications
overall morbidity less than 1% - higher with elderly and comorbidities

34
Q

complications of viral hepatitis

A

chronic hepatitis - prolonged damage
liver cirrhosis
liver cancer
fulminant viral hepatitis - acute liver failure

35
Q

Hepatitis A

A

Food born - transmission fecal-oral, parental, sexual

acute onset with fever
usually mild severity
does NOT lead to chronic hepattis
usually affects children and adult
Hand hygiene, HEP A vaccine

36
Q

Hepatitis B

A

Parental, sexual

insidious onset
severe disease, may be prolonged course or develop into chronic (10%)
any age group affected
HBV vaccine and safe sex and hygiene

37
Q

Hepatitis C

A

parental, sexual, mother to baby
insidious onset
mild to severe symptoms
can develop into chronic hepatitis (80%)
any age affected
screening blood, hygiene, no vaccine
leads to hepatocellular carcinoma or liver transplant

38
Q

Hep A series vaccines

A

2 doses 6 months apart
recommended for children at 12 months or special “high risk” populations

39
Q

Hep B vaccination

A

3 doses at least 4 months apart
recommended for all infants beginning as newborns

40
Q

Hep C vaccination

A

No vaccine

41
Q

Pharm for HBV

A

Two classes of drugs
Interferons
Nucleoside analogs

42
Q

Treatment of HBV

A

for Chronic
Only for high risk patients

43
Q

who are high risk patients

A

increased AST levels
hepatic inflammation
advanced fibrosis

44
Q

disadvantages of treatment

A

prolonged therapy
costs and adverse effects
high relapse**

45
Q

Considerations for Pharm for HCV

A

Treatment is only recommended for patients with chronic disease, however this thought process is changing with the evolution of newer, very effective drugs.

Now easily treatable and eliminated in most patients.

46
Q

Pharm for HCV

A

Treated with direct-acting antiviral therapy and interferon-based regiments. (may also require a nucleoside analogue medication).

47
Q

Drugs not on Matrix

A

Pegylated interferon-alpha
Ribavirin
Entacavir
Tenofovir alafenamide
Sofosbuvir
Daclatasvir

Expensive and lots of side effects!

48
Q

Tylenol?

A

Recommended <2g a day

49
Q

Serious end stage

A

Don’t take Tylenol or NSAIDS

50
Q

Cirrhosis

A

Irreversible, inflammatory, fibrotic liver disease

structural changes from injury and fibrosis

51
Q

Chaotic fibrosis leads

A

to obstructive biliary channels and blood flow – jaundice and portal hypertension

52
Q

Regeneration disrupted by

A

hypoxia, necrosis, atrophy, and liver failure

53
Q

Cirrhosis common causes

A

Hepatitis B and C
Excessive alcohol intake
Idiopathic
Non-alcoholic fatty liver disease (NASH, NAFLD)

54
Q

Alcoholic cirrhosis is

A

most common type but only accounts for 25%

55
Q

Alcoholic liver disease has

A

various stages/spectrum

56
Q

Alcoholic fatty liver

A

mildest, asymptomatic, reversible

57
Q

Alcoholic steatohepatitis

A

precursor to cirrhosis

inflammation, degeneration of hepatocytes

stimulating irrevirsible

anorexia, edema, jaundice

58
Q

Alcoholic cirrhosis

A

fibrosis and scarring alter liver structure

59
Q

Cirrhosis pathogenesis - 7 steps

A

Liver cells destroyed
cells try to regenerate
disorganized process
abnormal growth
poor blood flow and scar tissue
hypoxia
liver failure

60
Q

Early manifestations cirrhosis

A

slow/insidious
Gi disturbances - N/v, anorexia, flatulence, change in bowel habits
fever, weight loss
palpable liver

61
Q

Late manifestations cirrhosis -9

A

jaundice
ascites
endocrine problems
peripheral edema (lose albumin)
skin lesions
esophageal and anorectal varices
decreased albumin and PT
hematologic problems (bleeding/anemia)
encephalopathy (can’t clear toxins)

62
Q

Portal hypertension

A

resistant portal blood flow leads to varices and ascites (blood can’t flow freely)

63
Q

cause of portal hypertension

A

systemic hypotension, vascular underfilling, stimulation of vasoactive (RAAS system), plasma volume expansion, increased cardiac output – causes varices

64
Q

symptoms of portal hypertension

A

asymptomatic until complications

variceal hemorrhage, ascites, peritonitis, hepatorenal syndrome, cardiomyopathy

65
Q

hepatic encephalopathy

A

30-45% of cirrhosis patients

66
Q

primary driver of diagnosis

A

LOC

67
Q

Hepatic encephalopathy graded

A

Based on severity. Grade 1 is changes in behavior, mild confusion, slurred speech, disordered speech.

Grade 4 is coma, unresponsive to pain

68
Q

Hepatic encephalopathy is

A

correlated with liver labs- mainly ammonia that is primary chemical driver of LOC changes

but diagnosis is not BASED on ammonia

69
Q

Acute liver failure also called

A

fulminant liver failure

70
Q

acute liver failure is

A

NOT caused by cirrhosis or other type of liver disease

71
Q

Most common cause of acute liver failure

A

acetaminophen overdose - treated with acetylcysteine

72
Q

patho of acute liver failure

A

edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrates and disrupts the liver tissue

73
Q

acute liver failure can happen

A

6-8 weeks after a viral hepatitis or metabolic liver disease – 5-8 weeks after an acetaminophen overdose

74
Q

signs of acute liver failure

A

similar to cirrhosis symptoms

75
Q

acute liver failure treatment

A

not much, liver transplant

Nur 326 (6 decks)

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