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Advanced Patho Exam 2 > Exam 2: Hepatitis > Flashcards

Exam 2: Hepatitis Flashcards

1
Q

Define Hepatitis

A
  • Non- specific inflammation of the hepatocytes, liver cells
  • etiology can be single or multifactorial
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2
Q

the pathophysiology of hepatitis

A
  • inflammation triggers fibrogenesis
    -hepatic stellate cells are activated, which cause fibrosis
  • fibrosis can lead to cirrhosis
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3
Q

what does inflammation in the liver cells activate?

A

it activates stellate cells and these cells make fibrosis

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4
Q

can cirrhotic be reversed?

A

no, once cirrhotic, it cannot be reversed. there is no cure.

-early stages of cirrhosis, may be reversed with anti-fibrotic agents

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4
Q

what can cause hepatitis? (5)

A

-heavy alcohol use
-toxins
-some medications
-certain medical conditions
-virus

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5
Q

the common hepatitis viruses in the US

A

-hepatitis A virus
-hepatitis B virus
-hepatitis C virus

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5
Q

what is the portal triads composed of?

A

composed of three major tubes
- hepatic artery
-portal vein
-bile duct

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5
Q

function of the hepatic artery

A

carry oxygenated blood to the hepatocytes

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6
Q

function of the portal vein

A

carry blood with nutrients from the small intestines

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7
Q

function of the bile duct

A

carries bile products away from the hepatocytes, to the larger ducts and gallbladder

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8
Q

Serologic Markers (5)

A
  • IgM
    o means “Miserable NOW= acute”
     if you are worried for an acute infection, you order this!
  • IgG
    o Means “good to go, Gone= chronic”
     Exposed at some point in your life
  • Either by vaccine or actual infection
  • Antibody (Ab) Total
    o Just checks immunity
     When it comes back + = exposed, or vaccinated.
     You have immunity towards the virus!
  • ALT
    o More specific for Liver damage
     Important lab to follow and monitor!
  • Antigen (Ag)
    o Looking for something infecting, acute!
     Surface (sAg)
  • Outside of the virus
     Envelope (eAg)
  • Around the virus
     Core (cAg)
  • Inside the virus
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9
Q

what is Nonalcoholic Steatohepatitis (NASH)

A
  • Significant form of chronic liver disease in adults and children
  • Presence of hepatic steatosis and inflammation with hepatocyte injury (ballooning) with or without fibrosis
    o Fat in liver, with inflammation surrounding it. Liver cells blow up like a balloon, then can progress to fibrosis
    o Only diagnosed by biopsy
  • Seen as early as 8 years of age, most common liver abnormality in children from 2 to 19 yrs
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10
Q

the pathogenesis of NASH

A

o NASH is hepatocellular injury, inflammation, and fibrosis
 The most severe forms of NASH progress to cirrhosis, end stage liver disease, and increased risk for hepatocellular carcinoma
o Insulin resistance
o Change in lipogenesis
o Mitochondrial dysfunction
o Cytokine and adipokine association –liver damage and alterations in repair in the fatty liver
o 2 “hit” model or theory
 steatosis can be reversible process
 “Hit” 1 is excessive hepatocyte triglyceride accumulation resulting from insulin resistance
 “Hit” 2 involves an inflammatory injury to the liver possibly by oxidative stress, associated with lipid peroxidation and cytokines

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11
Q

What is Hepatitis A? And what injuries can you get from it?

A

o Only an ACUTE illness!!!
o A highly contagious, short-term liver infection, caused by the virus Hep A.
o You can get two type of injuries; hepatocellular injury or Cholestasis

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12
Q

what is hepatocellular injury?

A
  • “Basically, injury to the actual liver cells”
  • Diffuse liver necrosis
  • Prominent Centrilobular damage
  • Increased portal cellularity
  • Regional lymph node enlargement
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13
Q

what is cholestasis?

A
  • “causing injury to bile ducts, therefore bile leaks out, gets absorbed in the blood, causing jaundice”
  • Jaundice, this is a more severe case of Hep. A
  • Hyperbilirubinemia
     Impaired Synthetic Function
  • Prolonged PT
  • Decreased albumin
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14
Q

pathophysiology of hepatitis A

A

 Viral replication on the liver cells
 After entry into cell (virus), RNA is uncoated and ribosomes bind to form polysomes
* -> viral proteins are then synthesized
* -> genome is copied by polymerase
* -> assembled virus particles are shed into biliary tree and excreted into the feces

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15
Q

incubation period for hepatitis A

A

28 days
-symptoms last about 4-6 weeks

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16
Q

transmission of hepatitis A

A

o Fecal-oral
 Hep A virus bile excretion with shedding in stool occurring 2 weeks prior to and 1 week after onset of symptoms/illness

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17
Q

pertinent patient hx (hep A)

A

recent travel outside of US

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18
Q

presentation of Hepatitis A (8)

A

o Flu-like symptoms
o Anorexia
o Headache
o Abdominal pain
o Myalgia
o Dark urine
o Clay colored stools
o Jaundice (common)

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19
Q

Abnormal Liver Enzymes/Serologic Markers: hepatitis A

A

o AST/ ALT usually elevated >500 in acute infection
o Serological testing
 HAV Ab IgG- chronic marker- + test = immune/cleared
 HAV Ab IgM- acute marker- + test = acute
 HAV Ab Total- does not differentiate between the two tests
* It is helpful to determine immunity, not active acute infection
* May have acquired immunity

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20
Q

complications of hepatitis A

A

-extremely rare
-transplantation

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21
Q

preventative measures for hepatitis A

A

o HAV vaccine!!
 Available for adults and children
 Given to “risky” population
* Military, travelers, moving to endemic areas, illicit drug users, gays

• Serum immunoglobulin is given to
those exposed (HAV Immunoglobulin)

− Pre-exposure prophylaxis
• < 2 week trip
• < 2 y/o
− Post-exposure prophylaxis
• Up to 2 weeks post exposure
• Household, sexual contact, daycare, food
handlers etc.

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22
Q

what is hepatitis B

A

o Liver infection caused by Hep. B virus
o Member of the hepadnavirus family
o Acute and chronic infection
 Some people are sick for a few weeks, others the disease progresses to a serious lifelong illness, chronic HBV.
 30% acute, 15% chronic
* 95% clear the infection and develop a lifelong immunity
o **rmbr it is not curable, you can stop the activity, but since it is replicated in the nucleus you cannot get rid of the virus’ DNA

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23
Q

pathophysiology of hepatitis B

A

 Once the body is exposed to HBV, a cell-mediated immune response is triggered
 Cytotoxic T cells and natural killer cells are sent to the virus and release inflammatory cytokines
 Liver cells are attacked and are infiltrated by HBV
* Ground glass appearance
 Virus is constantly being shed into the blood
 Replication TAKES PLACE IN NUCLEUS OF THE CELL. “DEEP IN THE CELL” THEREFORE THERE IS NO CURE!

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24
Q

incubation period for hepatitis B

A

30-60 days
-can survive 7 days outside of the body and still cause infection

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25
Q

transmission of hepatitis B

A

o Mother to child
 20% transmission rate, if HBs Ag positive
 90% transmission rate, if HBe Ag positive
o Blood to blood
 Mucosal contact with infected blood or body fluid
* Hemodialysis patients are always at risk
 Can be transmitted sexually, if mucosal gets torn
* Sometimes semen or saliva has blood
* Having sex on your menstrual cycle
* Perinatal infection is common

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26
Q

pertinent patient hx (risk factors) for hepatitis B

A

o Are they getting HD
o Have they had transfusion, outside of US
o Sexual encounters
o Someone at home who has it
o Are they IV drug users
o What kind of work do they do

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27
Q

what are three initial testing for HBV

A

-HBsAg (surface antigen): it is the marker of active disease–first detectable viral antigen
-HBcAb Total (core total): the core protein is part of the nucleus, it will remain positive for life, if they have been exposed or had it
-HBsAb (surface antibody): marker of immunity–it will be (+) if you have had vaccine

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28
Q

complications of HBV

A

o HBV can progress to CIRRHOSIS if not treated
o HUGE Risk for hepatocellular carcinoma (HCC), even without cirrhosis
 Some people die of liver cancer without knowing they had hep B
o Common form of fulminant hepatic failure
 Massive necrosis of the liver parenchyma and decrease in liver size
o Watch and wait
 may need transplantation

29
Q

preventive measures for HBV

A

vaccine!
- some populations need a second dose/booster

30
Q

what is hepatitis C

A

o Liver disease, caused by Hep C virus
o Curable disease
o Primarily a chronic infection (85%)
 Acute disease not often detected
o SLOW, with varying progression rates
 Predictors for progression; >40 years old, alcoholic, male, steatosis, HIV+, HBV+
 Can lead to cirrhosis, but again, it takes a long time to get to that stage!
o Species is classified into 7 genotypes and several subtypes

31
Q

pathophysiology of hepatitis c

A

 Replicated in the cytoplasm, NOT nucleus
* That is why it is curable, powerful drugs stop replication all together
* Treatment averages 12 weeks

32
Q

incubation period for hepatitis c

A

o 14 to 160 days (2 to 22 weeks)
 Can remain outside the body
* 16 days at 77F 2 days at 98.6F, 4 weeks at </=39.2 F

33
Q

transmission of hepatitis c

A

parental transmission, blood to blood

34
Q

what should people with cirrhotic liver be screen for?

A

for liver cancer for the rest of their life

35
Q

pertinent patient hx for HCV

A

o HISTORY IS IMPORTANT TO ESTBALISH A TIME FRAME!
o May have no known or won’t admit their risk factors
 Are they HIV +?
 Do they have a past or current injection drug use or intranasal drug use
 Hemophilia with receipt of clotting factor concentrates before 1987, long term hemodialysis, persistently abnormal ALT
 Received organ transplant/transfusion before July 1992 or received blood from a donor who later tested HCV positive
 They cocaine users
 Where they Incarcerated
 Recognized exposure
* health care workers exposed after needle sticks, sharps or mucosa,
* exposures to HCV positive blood, children born to HCV positive mothers
* Received tattoo with unsterile instruments

36
Q

patient screening for HCV (2)

A

 Birth Cohort Screening-
* Person born between 1945 and 1965
* ONE time screening/blood test, may identify infected patients at earlier stages of disease
 Risk Factor-Based Screening-
* ^^^all of the risk factors from above^
o Let’s say someone comes for birth cohort screening, and hep C is negative, but then comes back 8 months later and wants to be screened again because they tried IV heroin, you now do the RISK FACTOR BASED SCREENING. Not the birth cohort one.

37
Q

presentation for hcv

A

o 75% asymptomatic
o Jaundice (uncommon)
o Fatigue, RUQ pain**
 Usually has chronic fatigue
o May present initially with variceal bleed
o May present with elevated LFT’s and/or HCV Ab Positive test
 Found common after insurance physicals/blood donations

38
Q

diagnosis and serological testing for HCV (6)

A

*Hepatitis C virus antibody
 Can’t tell you if you have active viral infection
 Can only tell you exposure, can take 6 months to become positive
* If you think someone was truly exposed and it initially came back negative, you have to repeat the test, since it takes up to 6 months to become positive.
*Hepatitis C virus RNA Polymerase Chain Reaction (PCR) QUANTitative result
 Viral load!!!
 Positive 1-2 weeks after infection
 Threshold is low most <15 or <29
* If the antibody test is positive, next thing you draw is the HCV PCR QUANT!!
*HCV Ab with reflex PCR
 If you have someone at risk, you do a REFLEX to know antibody and PCR (viral load)
* This is the one you will order!!!
*HCV PCR qualitative
 Positive or negative result
 Not utilized, since the QUANT is more sensitive
*HCV genotype
 This is done when someone is positive for further characterize the virus
 when looking at treatment options
*Hepatitis C virus RIBA
 Determines exposure to the virus vs a false positive Ab
* Not used anymore  usually do a DNA virus test instead

39
Q

complications of hepatitis c virus

A

o May develop Hepatocellular Carcinoma (HCC), once cirrhotic though
o Cirrhosis
 How to tell if someone is cirrhotic?? You draw;
* Albumin, INR level, platelet count

40
Q

preventative measures for HCV

A

o There is no vaccine
o Latex condoms of multiple partners
o Avoid sharing toothbrushes, razors, combs
o Cover open wounds

41
Q

treatments for HCV

A

o Curable with 12 week PO treatment
 YOU ARE CURED BUT *RMBR- YOU HAVE NO IMMUNITY TO IT
* If you get re exposed, you can get it again
 After 4 weeks people have cleared the virus, but there is no evidence that says that is really how much time you need.
* Therefore, if someone stops taking meds prematurely, perform a PCR blood test at 12 weeks to confirm they are “cured”
o Before you start treatment for HCV, you NEED TO CHECK FOR HEP B
 “black box warning” PO meds for Hep C can “reactivate” Hep B
* Those people who are positive for both, need to also start treatment for hep B, to prevent the acute phase.

42
Q

what is hepatitis d?

A

o Also known as “DELTA”, a liver infection caused by the hepatitis D virus
o Can only occur in people who are also infected with hepatitis B
 “parasitic virus” cannot infect on its own, needs HBV
o Similar to HBV
o Inflammatory infiltrates causing interface hepatitis (necrosis cells)
 Periportal fibrosis or bridging necrosis may be present with the process of bridging necrosis places the patient at increased risk of cirrhosis

43
Q

what are the two types of hepatitis delta?

A

 Co-infection
* Simultaneous infection with hepatitis B and D at the same time (both acute)
o You can become cirrhotic much quicker!
 Superinfection
* Acute hepatitis Delta infection of someone with chronic Hep B
o You have had Hep B for a while (chronic), then all of sudden get really sick quick, while being complaint with your HBV medications
* Leads to chronic HDV infection in up to 80% of patients
* If associated with fulminant acute hepatitis and severe chronic active hepatitis that can often progress to cirrhosis
o fulminant hepatic failure- Massive necrosis of the liver parenchyma and decrease in liver size
* severe acute hepatitis with a short incubation period

44
Q

incubation period for hepatitis d

A

o 3 to 7 weeks
 Requires an associated HBV infection

45
Q

transmission for hepatitis d

A

o Parenteral
 IV drug use, is a common way

46
Q

pertinent patient hx for hepatitis D

A

o High prevalence Mediterranean basin, middle east, central Asia, west Africa and amazon basic of S. America and some south pacific islands

47
Q

presentation for hepatitis D

A

o Jaundice (common)
o Pre-icteric (prodromal- nonspecific symptoms occur) begins with fatigue, lethargy, anorexia, nausea
 Lasts 3-7 days
 AST/ALT abnormal
 Jaundice typical
 Clay colored stools and dark urine
 Total bili abnormal
o Once symptoms resolve disease usually in convalescence (gradual recovery)
o Superinfection
 Hepatic encelopathy can develop

48
Q

diagnosis for hepatitis D

A

-consider evaluation in all patients who are HBsAg positive or recent HBV infection
-antibody (IgM IgG), PCR testing
**anyone who has HBV rather its historically or currently but its controlled and they get worse, look at them for HDV!

**faster progression to cirrhosis when coinfected vs hbv infection alone

49
Q

DESCRIBE THE GENERAL SIGNS AND SYMPTOMS OF ACUTE VIRAL HEPATITIS

A
  • 70% of infections in children <6 are not accompanied by symptoms
  • Immunological response to virus
    o Fever, fatigue, loss of appetite, N/V, ab pain, dark urine, diarrhea, clay-colored stools, joint pain, jaundice
  • Flu like symptoms
50
Q

DISCUSS THE IMPLICATIONS OF CHRONIC VIRAL HEPATITIS

A
  • Inflammation triggers fibrinogenesis
  • During inflammation stellate cells become active and make fibrosis, cirrhosis is advanced fibrosis
  • Once cirrhotic, cannot be reversed
51
Q

How is HBV transmitted?

A

o HBV is transmitted through activities that involve percutaneous (i.e., puncture through the skin) or mucosal contact with infectious blood or body fluids (i.e., semen, saliva), including blood and semen
 Sex with an infected partner
 Injection drug use that involves sharing needles, syringes, or drug-preparation equipment
 Birth to an infected mother
 Contact with blood or open sores of an infected person
 Needle sticks or sharp instrument exposures
 Sharing items such as razors or toothbrushes with an infected person
 HBV is not spread through food or water, sharing eating utensils, breastfeeding, hugging, kissing, hand holding, coughing, or sneezing

52
Q

How long does HBV survive outside the body?

A

HBV can survive outside the body at least 7 days and still be capable of causing infection

53
Q

What should be used to remove HBV from environmental surfaces?

A

o Any blood spills — including dried blood, which can still be infectious — should be cleaned using 1:10 dilution of one part household bleach to 10 parts of water for disinfecting the area.
o Gloves should be worn when cleaning up any blood spills

54
Q

Who is at risk for HBV infection?

A

 Infants born to infected mothers
 Sex partners of infected persons
 Men who have sex with men
 Injection drug users
 Household contacts or sexual partners of known persons with chronic HBV infection
 Health care and public safety workers at risk for occupational exposure to blood or blood-contaminated body fluids
 Hemodialysis patients

55
Q

IDENTIFY THE FACTORS THAT PROMOTE THE PROGRESSION AND SEVERITY OF HEPATITIS C.

A
  • 75% are asymptomatic with vague symptoms until more chronic stages
  • Only half people infected know they are infected
  • People aren’t compliant with treatment
  • Medications are expensive
56
Q

DISCUSS REASONS FOR AND IMPLICATIONS OF, THE CHRONICITY OF HEP C. (What does it impact)

A
  • Impacts more than just the liver-
    o neuropathy, insulin resistance, cutaneous manifestations, glomerulonephritis, lymphoproliferative disorders, vasculitis
  • 70-80% of people have no signs and symptoms of an acute infection.
57
Q

the definition of Nonalcoholic fatty liver disease (NAFLD)

A

defined as the presence of fat in the liver (hepatic steatosis) either in imagining or on liver histology after the exclusion of secondary causes of fat accumulation in the liver
o Triglycerides are the primarily form of fat
o (e.g., significant alcoholic consumption, certain medications, and other medical conditions, or hereditary disorders)

58
Q

what does the most severe form of NASH progress to? (3)

A

-cirrhosis
-end stage liver disease
-increased risk for hepatocellular carcinoma

59
Q

risk factors associated with NAFLD: Conditions with established association (4)

A

o Obesity
o DM2
o Dyslipidemia (high levels of triglycerides and cholesterol)
o metabolic syndrome

**with NAFLD, its not trying to get to ideal body weight. a lot of these patients, a 10% reduction of their body weight will lead to improvement in their liver test

60
Q

metabolic syndrome criteria

A

(elevated BP, HDL/LDL/triglycerides out of wack)
 Presence of 3 or more of the following features;
* Waist circumference >102 cm in men >88 cm in women
o APPLE vs pear
* Triglyceride level 150 mg/dL or >
* High-density lipoprotein (HDL) cholesterol level < 40 mg/dL in men and < 50 mg/dL in women
* SBP 130 mmHg or greater or DBP 85 mmHg or greater
* Fasting plasma glucose level 110 mg/dL or greater

61
Q

risk factors associated with NAFLD: Conditions with emerging association

A

o Polycystic Ovary Syndrome (PCOS)
o Hypothyroidism
o Obstructive Sleep Apnea (OSA)
o Hypopituitarism
o Hypogonadism
o Pancreato-duodenal resection
* Seen in children as young as 2 years of age

62
Q

what does adipose tissue lead to?

A
  • it is metabolically active and leads to insulin resistance
    also leads to:
    -thrombophilia
    -HTN
    -hyperuricemia
    -dyslipidemia
    -hyperglycemia
    -macrovascular disease
    -central obesity
63
Q

what does an increased influx of free fatty acids to the liver and mitochondria lead to?

A

oxidative stress and liver damage
o Despite increased mitochondrial oxidation, the liver is unable to adapt to the chronic substrate oversupply

64
Q

functions of adipose tissue:

A
  • plays a central role in energy metabolism through its ability to store energy in the fed state and to release it in the fasting state
    -influence systemic energy homeostasis through the endocrine system
65
Q

Visceral adipose tissue generates multiple signals that alter lipid and glucose metabolism can lead to what?

A

-lead to hepatic fat accumulation
-creates a pro inflammatory environment that triggers cellular injury in the liver and other tissues

The inability to suppress injurious processes, such as oxidative stress, dysregulation of the unfolded protein response (leading to endoplasmic reticulum stress), lipotoxicity, and apoptotic pathways, contribute to liver damage, progressive fibrosis that can lead to cirrhosis, and the development of hepatocellular cancer in some patients

66
Q

list other causes of NAFLD

A
  • Modern diets, insufficient activity/play, Obstructive sleep Apnea, altered gut microbiome
  • Macro vesicular Steatosis
    o Excessive alcohol consumption
    o Hep C Genotype 3
    o Wilson’s Disease
    o Lipodystrophy
    o Parenteral nutrition
    o Abetalipoproteinemia
    o Medications (amiodarone, methotrexate, tamoxifen, corticosteroids)
  • Micro vesicular Steatosis
    o Reye’s syndrome
    o Medications (valproate, anti-retroviral medications)
    o Acute fatty liver of pregnancy
    o HELLP syndrome
    o Inborn errors of metabolism
67
Q

IDENTIFY THE MOST COMMON CLINICAL MANIFESTATIONS OF NAFLD IN PEDIATRIC AND ADULT PATIENTS

A
  • Non-specific or asymptomatic
    o Some report RUQ pain
    o Apple obesity (central)
    o Hepatomegaly
    o Dorsocervical hump
  • Once cirrhosis develops-
    o Palmar erythema, spider angiomata, gynecomastia, upper abdominal veins
     More severe- ascites, icterus, nail changes, splenomegaly, asterixis (shaking of the hands)
68
Q

diagnosis of NAFLD

A

-US
-CT
-MRI
-Fibro scan

69
Q

Diagnosis of NASH

A

liver biopsy

70
Q

Diagnosis for Advanced fibrosis

A

o FIB4 index, APRI, ALT/AST, NAFLD fibrosis score
 Fibrosis score is a blood test where is the fibrosis and the level of it
o FibroScan
o MR elastography
o Liver biopsy

71
Q

Physical finding of chronic hepatitis b (5)

A
  • hepatosplenomegaly
  • spider telangiectasias (vascular abnormality not exclusive to liver disease but often correlates)
  • jaundice
  • ascites
  • peripheral edema
72
Q

Decompensated cirrhosis in HCV (4)

A
  • hepatic encephalopathy
  • esophageal varices
  • ascites
  • cancer

Advanced Patho Exam 2 (4 decks)

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