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Pharm 1 > liver issues > Flashcards

liver issues Flashcards

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

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

A

2 doses 6 months apart

Recommendations
All children beginning at age 12 months

Special “high risk” populations

21
Q

Hep B Series

A

3 doses at least 4 months apart

Recommendation: All infants beginning as newborns

22
Q

Hep C =

A

No vaccine

23
Q

Two classes of drugs are used for chronic HBV:

A

Interferons

Nucleoside analogs

24
Q

What is high risk from treatment with HBV

A

↑ AST levels
Hepatic inflammation
Advanced fibrosis

25
Q

disadvantages of HBV treatment

A

Prolonged therapy
Costs and adverse effects
High relapse

26
Q

how is HCV treated

A

direct-acting antiviral therapy and interferon-based regiments

Some require treatment along with a nucleoside analogue medication as well

27
Q

what is cirrhosis

A

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
Q

Common causes of cirrhosis

A

Hepatitis B&C

Excessive alcohol intake

Idiopathic

Non-alcoholic fatty liver disease [NASH, NAFLD]

29
Q

stages of alcoholic liver disease

A

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
Q

cirrhosis patho

A 
Liver cells destroyed
Cells try to regenerate
Disorganized process
Abnormal growth
Poor blood flow and scar tissue
Hypoxia
Liver failure
31
Q

early manifests of cirrhosis

A 
GI disturbances
	N/V
	Anorexia
	Flatulence
	Change in bowel habits
Fever, weight loss
Palpable liver
32
Q

late manifests of cirrhosis

A 
Jaundice
Peripheral edema
Decreased albumin & PT 
Ascites
Skin lesions
Hematologic problems (anemia, bleeding)
Endocrine problems
Esophageal & anorectal varices
Encephalopathy
33
Q

what is portal hypertension

A

Resistant portal blood flow leads to varices & ascites

34
Q

cause of portal hypertension

A

systemic hypotension,

vascular underfilling,

stimulation of vasoactive (RAAS system) systems,

plasma volume expansion,

increased cardiac output -> ascites

35
Q

T/F Can’t do anything for the portal hypertension except liver transplant

A

True

36
Q

what is the primary driver of diagnosis in hepatic encephalopathy

A

LOC

37
Q

Grades of hepatic encephalopathy

A

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
Q

what is the primary chemical driver in LOC changes

A

ammonia

39
Q

most common cause of acute liver failure

A

Acetaminophen overdose

40
Q

patho of acute liver failure

A

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
Q

Class of lactulose

A

hyperosmotic laxative

42
Q

indication of lactulose

A

reduction of ammonia absorption in hepatic encephalopathy

43
Q

MOA of lactulose

A

reduces blood ammonia levels by converting ammonia to ammonium

44
Q

route of lactulose

A

po, enema.rectal

45
Q

contraindication of lactulose

A

hypokalemic

46
Q

rifaximin MOA

A

inhibits bacterial RNA synthesis by binding to bacterial DNA (initially used as an antibiotic for GI infections)

47
Q

S/E of rifaximin

A

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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