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liver issues Flashcards

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1
Q

what are the 4 major functions of the liver

A

Metabolism &/or storage of:
Fat, CHO, PRO, vitamins and minerals

Blood volume reservoir
Distends/compresses to alter circulating blood volume

Blood filter
Helps purify blood

Blood clotting factors
Including prothrombin & fibrinogen

Drug metabolism and detoxification

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2
Q

what is jaundice

A

caused by increased level of bilirubin in the bloodstream

usually when total bilirubin is greater than 2-2.5 mg/dl

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3
Q

3 classes of jaundice

A

Hemolytic  increased breakdown of RBCs

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

Obstructive  decreased or obstructed flow of bile

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4
Q

what is bilirubin

A

By product of heme breakdown  mainly hemoglobin

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5
Q

Elevations of INDIRECT bilirubin =

A

bilirubin overproduction OR impaired liver functioning

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6
Q

Elevations of DIRECT bilirubin =

A

liver working, but can’t get the bilirubin out

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7
Q

clinical manifestations of jaundice

A

Urine  darker

Liver enzymes = elevated

Stools = Normal or clay colored

Pruritis

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8
Q

what can cause hepatitis other than the infection

A

alcohol abuse

drugs

chemicals

bacteria

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9
Q

Viral hepatitis patho

A

Viral infection

Immune response: inflammatory mediators

Lysis of infected cells

Edema and swelling of tissue

Tissue hypoxia

Hepatocyte
death!

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10
Q

T/F Many cases of ALL types of hepatitis are asymptomatic

A

TRUE

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11
Q

prodromal hepatitits

A

2 weeks after exposure

Fatigue, anorexia, malaise, nausea, vomiting, HA hyperalgesia, cough, low-grade fever

HIGHLY transmissible

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12
Q

Iceteric hepatitis

A

Begins with jaundice

Jaundice, dark urine, clay-colored stools

Liver enlarged and may be painful to palpation

Fatigue abdominal pain persists or increases in severity

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13
Q

Recovery hepatitis

A

Resolution of jaundice

6-8 weeks after exposure, symptoms diminish

Liver remains enlarged/tender

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14
Q

Complications of viral hepatitis

A

Chronic hepatitis

Liver cirrhosis (next section)

Liver cancer

Fulminant viral hepatitis – acute liver failure

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15
Q

transmission of Hep A

A

fectal-oral, parental, sexual

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16
Q

Hep A characteristics

A 
Acute onset with fever
Usually mild severity 
Does NOT lead to chronic hepatitis 
Usually affects children and adult 
Hand hygiene, Hep A vaccine
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17
Q

hep b transmission

A

parental, sexual

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18
Q

hep b characteristics

A

Insidious onset
Severe disease, may be prolonged course or develop into chronic
Any age group affected
HBV vaccine and safe sex and hygiene

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19
Q

hep c transmission and characteristics

Study These Flashcards
A

Transmission  parental, sexual
Insidious onset
Mild to severe symptoms
Can develop into chronic hepatitis (80%)
Any age is affected
Screening blood, hygiene; NO vaccine
Leads to hepatocellular carcinoma, liver transplant
New treatment is developing and becoming more widely available

20
Q

Hep A Series

Study These Flashcards
A

2 doses 6 months apart

Recommendations
All children beginning at age 12 months

Special “high risk” populations

21
Q

Hep B Series

Study These Flashcards
A

3 doses at least 4 months apart

Recommendation: All infants beginning as newborns

22
Q

Hep C =

23
Q

Two classes of drugs are used for chronic HBV:

Study These Flashcards
A

Interferons

Nucleoside analogs

24
Q

What is high risk from treatment with HBV

Study These Flashcards
A

↑ AST levels
Hepatic inflammation
Advanced fibrosis

25
disadvantages of HBV treatment
Prolonged therapy Costs and adverse effects High relapse
26
how is HCV treated
direct-acting antiviral therapy and interferon-based regiments Some require treatment along with a nucleoside analogue medication as well
27
what is cirrhosis
Irreversible, inflammatory, fibrotic liver disease Structural changes from injury (alcohol/viruses) and fibrosis Chaotic fibrosis leads to obstructive biliary channels and blood flow  jaundice and portal hypertension Regeneration is disrupted by hypoxia, necrosis, atrophy, and liver failure
28
Common causes of cirrhosis
Hepatitis B&C Excessive alcohol intake Idiopathic Non-alcoholic fatty liver disease [NASH, NAFLD]
29
stages of alcoholic liver disease
most common type Alcoholic fatty liver Mildest, asymptomatic Alcoholic steatohepatitis Precursor to cirrhosis Inflammation, degeneration of hepatocytes Alcoholic cirrhosis Fibrosis and scarring alter liver structure
30
cirrhosis patho
``` Liver cells destroyed Cells try to regenerate Disorganized process Abnormal growth Poor blood flow and scar tissue Hypoxia Liver failure ```
31
early manifests of cirrhosis
``` GI disturbances N/V Anorexia Flatulence Change in bowel habits Fever, weight loss Palpable liver ```
32
late manifests of cirrhosis
``` Jaundice Peripheral edema Decreased albumin & PT Ascites Skin lesions Hematologic problems (anemia, bleeding) Endocrine problems Esophageal & anorectal varices Encephalopathy ```
33
what is portal hypertension
Resistant portal blood flow leads to varices & ascites
34
cause of portal hypertension
systemic hypotension, vascular underfilling, stimulation of vasoactive (RAAS system) systems, plasma volume expansion, increased cardiac output -> ascites
35
T/F Can’t do anything for the portal hypertension except liver transplant
True
36
what is the primary driver of diagnosis in hepatic encephalopathy
LOC
37
Grades of hepatic encephalopathy
Grade I: Changes in behavior, mild confusion, slurred speech, disordered sleep Grade II: Lethargy, moderate confusion Grade III: Marked confusion (stupor), incoherent speech, sleeping but arousable Grade IV: Coma, unresponsive to pain
38
what is the primary chemical driver in LOC changes
ammonia
39
most common cause of acute liver failure
Acetaminophen overdose
40
patho of acute liver failure
Patho: edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrates and disrupts the liver tissue Can occur 6-8 weeks after a viral hepatitis or metabolic liver disease 5 days to 8 weeks after an acetaminophen overdose Signs are similar to cirrhosis symptoms Treatment: not much, liver transplant
41
Class of lactulose
hyperosmotic laxative
42
indication of lactulose
reduction of ammonia absorption in hepatic encephalopathy
43
MOA of lactulose
reduces blood ammonia levels by converting ammonia to ammonium
44
route of lactulose
po, enema.rectal
45
contraindication of lactulose
hypokalemic
46
rifaximin MOA
inhibits bacterial RNA synthesis by binding to bacterial DNA (initially used as an antibiotic for GI infections)
47
S/E of rifaximin
peripheral edema, nausea, ascites, dizziness, fatigue, pruritis, skin rash, abdominal pain, anemia Has been associated with an increased risk of C diff

Pharm 1 (28 decks)

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