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PT1 B3 > Lecture 71/73 - Pathology of Liver Disease > Flashcards

Lecture 71/73 - Pathology of Liver Disease Flashcards

1
Q

what are the different zones of a liver microscopic anatomy? why is this important?

acetaminophen toxicity damages which zone first?

A

Zone 1 – closest to heaptic arteries – sees the most oxygen

Zone 2 - Intermediate oxygenation

Zone 3 closest to the central Central vein – least amount of oxygen, but this is typically more than sufficient
But becomes oxygen deficient with any ischemic/toxic event

Acetaminophen Tox – Zone 3 toxicity first
but overall, drug toxicities and zone order of damage cannot be predicted

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2
Q

for what reason are liver biopsies taken?

how are they taken?

A

why: to establish severity of liver disease or evaluate progression. Never (rarely) taken to establish the diagnosis itself

how ? Percutaenous, Transjugular, Laproscopic/operative

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3
Q

Cholestatic pattern of liver injury on histology

  • what is the mechanism
  • what does it look like
  • lab findings
A

Bile in hepatocytes/canaliculi

Elevated BR and Alk Phosph

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4
Q

Apoptotic pattern of liver injury on histology

  • what does it look like ?
  • lab findings
A

small pink cells with white space around them

↑ AST/ALT

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5
Q

Necrotic pattern of liver injury on histology

labs

A

Loss of hepatocytes (appears blue)
- may have inflammation

↑↑↑ AST/ALT
May ↓ AST/ALT late – -which is very concerning finding; it means all the heaptocytes have been depleted and enzymes exhausted

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6
Q

Steatosis pattern of liver injury on histology

labs

is this reversible?

A

Steatosis – Fat accumulation within the hepatocytes
§ Appears white fat droplets;

		Normal to Mild ↑ AST/ALT

this is reversible

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7
Q

Steatohepatitis pattern of liver injury on histology

– what is a pathognomonic finding here? what do they look like?

labs

is this reversible ?

A

The more aggressive cousin in Steatosis – fat accumulation with evidence of injury and inflammation

    § Cells balloon up -- leading to Mallory bodies 
§ Mallory bodies -- appear with pink inclusions that are meant to be removed but damaged cells cannot get rid of them

Other signs of inflammation and apoptosis

↑ AST/ALT

fatty changes are reversible, but not the scarring that may occur

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8
Q

Hepatitis pattern of liver injury on histology

labs

A

Inflammation (mostly lymphocyte)

↑ AST/ALT

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9
Q

what are the 2 types of fatty liver disease ?
how common are they?

can these be distinguised on histology

A

Alcoholic Fatty Liver disease – 5 to 10 %

Non-alcoholic fatty liver disease – 20 - 30 % of US adults

No – cannot be distinguished on histology

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10
Q

NAFLD / AFLD – at what stages can changes be reversed? how can they be reversed?

describe the progression of disease if not reversed …

A

Steatosis – very common and reversible.
Steatohepaptitis – fibrosis is not not reversible; fatty changes are.

have patients decreased fat and alcohol consumption; lose weight

Fibrosis(Cirrhosis) –> HCC

Progression of NAFLD:
NAFLD –> NASH –> Cirrhosis –> HCC

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11
Q

what is the difference between grading and staging of chronic hepatitis

A

Grading – the severity of the current inflammation, this may resolve

Staging – the severity of the fibrosis – this does not regress. Assessing how much damage has already been done

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12
Q

Grading of hepatitis – what are 4 grades?

A

□ Grade 1 - confined to the interface plate

□ Grade 2 - some leak across the plate into the parenchyma

□ Grade 3

□ Grade 4 - severe inflammation; treat regardless of etiology; can lead to necrosis (lymphocytes killing hepatocytes)

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13
Q

Staging of Hepatitis – what are the 4 stages?

what causes the “nodular/bumpy” appearance

A

□ Stage 1 - no Bridging
□ Stage 2 – some bridging

□ Stage 3 - bridging fibrosis between portal tracts, but no change in architecture and do not get portal HTN. No compression of the vessels. The fibrosis begins to define curved nodules of the liver

□ Stage 4- extensive bridging fibrosis, nodules and bumpy contour as the liver attempts to regenerate. Full bridging.

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14
Q

what are the etiologies of chronic hepatitis:

A

Viral Hepatitis – HBV and HCV

Auto-immune –

Drug/Meds/Alcohol

Inherited/Metabolic Diseases – Wilson’s disease, Hereditary hemochromatosis, A1AT Deficiency

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15
Q

what are the two primary viral origins or chronic hepatitis? what percentage of each acute infection leads to chronic hepatitis?

what causes most of the damage to hepatocytes in chronic hepatitis?

A

HCV – 85% chronic hepatitis (20% of whome develop cirrhosis).

HBV – 4% develop persistent infection; 30% of whom develop chronic hepatitis

The immune repsonse itself is what causes most of the damage in chronic hepatitis. The attempts at repair lead to scarring / cirrhosis

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16
Q

Auto Immune Chronic Hepaptitis –

What are some histological findings:

what labs can be run to help with the dx?

what is a common treatment?

A

Histo: Lots of plasma cells; +/- multinucleated giant hepatocytes

Labs: IgGs, ANA Titers
Females > Males

Common treatment: steroids

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17
Q

what are three inherited disease that can lead to chronic hepatitis?

A

Alpha 1 Anti-Trypsin Deficiency – the misfolded protein accumulates in the liver;

Hereditary Hemocrhomatosis

Wilson’s Disease –

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18
Q

Hereditary Hemochromatosis –
what is it ? (what gene)

Dx?

Treatment?

A

AR mutation in C282Y – There is no negative feedback for iron uptake (enterocyte iron binding complex). In this, the enterocytes and other organs keep taking up iron

Dx - Stains blue; can make definitive dx with genetic testing

Treatment: Phlebotomy/bloodletting

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19
Q

Wilson’s Disease:
What is it? (gene)

Phagonomonic physical exam finding

Definitive Dx:

Treatment;

A

Autosomal recessive mutation in ATP7B (nomrlaly excretes copper into bile); therefore leads to abnormal copper retention and accumulation

Leads to cirrhosis; decreased cerruloplasmin

Pathog – Kayser Fleischer Rings in the corner

Definitive dx – liver bx

Treatment - Chelation

20
Q 
Alpha 1 Anti Trypsin Deficiency -- 
what is it? 
lung findngs? 
liver findings? 
Treatment for liver vs lung ??
A

ALpha 1 anti-trypsin (with either PiZ or PiS mutations) – the protein is misfolded leading to abn accumulation in hepatocytes

Lung findings – panacinar emphysema

Liver findings — Globules (accumulation of misfolded protein); best seen on Immnostain

Treatment:
lungs – infuse the protein
liver – cannot do much except advise patients to avoid alcohol in order to prevent further damage

21
Q

what is the role of bile?

describe how it is formed?

A

Bile – helps eliminate waste (bilirubin); fat emulsifier

Bilirubin is formed from heme.
Heme –> Biliverdin –> Bilirubin (not water soluble; travels in blood to the liver bound to albumin)
Conjugated UDP gluconuryl transferase (UDPT1A1) to Glucuronic Acid (water soluble); which is then excrted in bile

22
Q

what is indirect (unconjugated) vs direct (conjugated) Hyperbilirubininemia

give examples of both

A

Indirect (unconjugated) – § A defect in the bilirubin metabolism pathway BEFORE the glucuronidation; or there is simply too much bilirubin production

examples: Hemolytic, physiologic, Crigler Najjar (1 and 2), Gilbert’s disease

Conjugated (direct) – Defect in bilirubin metabolism/excretion (AFTER) the gluconuridation step. BIle transport is impared in the haptocytes

examples: Dubin Johnson Syndrome

23
Q

what are the hereditary unconjugated hyperbilirubinemias ? which is the most severe
which are the most benign

A

□ Crigler Najjar 1 – AR — Not compatible with life

□ Crigler Najjar II -- AD -- Usually mild and worsened by stress

□ Gilbert (french pronunciation) – 5 to 10%; benign; common and does not correlate to a disease state
® Small Group: mild scleral icterus during periods of stress, starvation, exercise

24
Q

what are the conjugated hyperbilirubinemias

A

□ Dubin Johnson — AR – benign; turns liver black; but never biopsied bc its asymptomatic
□ Rotor — AR — benign and even more mild than Dubin Johnson

25
Q

what is kernicterus?

A

end organ, including the gray matter in the brain seen in unconjugated bilirubinemias

worse in ped patients

26
Q

what are the three cholestatic diseases of the biliary tract?

what lab findings would you expect? (what pattern of LFTs)

Physical exam findings/History?

A

Primary Biliarly Cirrhosis

SEcondary Biliary Cirrhosis

Primary Sclerosing Cholangitis –

Increased conjugated BR, Increased ALP
LFTs c/w Choestatic pattern of LFTs
History: Pruritis, dark urine, light colored stool
Exam: Jaundice, heaptosplenomegaly

27
Q

Primary Biliarly Cirrhosis –

cause/what is it?
Characteristic histology?
characteristic patient?
Common lab finding ?

A

Cause: Idiopathic; Lymphocytic, granulomatous destruction of intrahepatic bile ducts; as bile escapes out into parenchyma, there is an immune reaction to it, forming granulomas

Histo: Granulomas; destruction of the ducts

Patient: Middle aged women

Labs: + AMA (anti-mitochondrial antibody)

28
Q

Secondary Biliary Cirrhosis –
pathology?

Gross pathology?
Histology?

A

Path – extrahepatic Biliary Obstruction (tumors, stones, pancreatitis, parasites); leading to increased pressure in intrahepatic ducts –> injury/fibrosis and cholestasis

Gross Path – green liver
Histo – Islands of liver parenchyma surrounded by fibrosis; lots of bile ductules

29
Q

Primary Sclerosing Cholangitis

  • Pathology?
  • Histology?
  • Commonly a/w? typical patient
  • whats seen on ERCP?
    Treatment?
A

pathology: unknown cause of inflammation, constriction and fibrosis

Histology – “Onion skinning” bile duct fibrosis; much less inflmmation than Primary Biliary Cirrhosis

Typical patient: young men with IBD (UC or CD)

ERCP: “Skip pattern” or “beading”

Treatment: Transplant

30
Q

Name three causes of Acute hepatitis

A

infectious

toxic

Metabolic

31
Q

Infectious causes of acute hepatitis – hepatotropic vs non hepatocropic

A

hepatotropic – hepatitis A, B, C, D, E, Yellow Fever

Non hep – EBV, CMV

Liver flukes

32
Q

Toxic causes: what is the difference between intrinsic hepatotoxicity and idiosyncratic hepatotoxicity

Metabolic causes of hepatitis

A

intrinsic – cuase injury in everyone (acetaminophen)

Indiosyncratic – causes injury in only vary rare cases (eg 1/100 people get liver toxicity from a specific drug).

Metabolic: A1AT def, Wilsons, hemocrhomatosis etc

33
Q

What are the three classes of vascular injury to the liver?

A

Pre hepatic –

Intra hepatic

Post hepatic

34
Q

Pathology and manifestations of pre - hapatic injury –

transaminase levels normal or elevated?

A
  • Mechanisms: Hepatic artery compromised, portal vein obstruction, thrombosis
    * Manifestations – esophageal varices, splenomegaly, intestinal congestion
    * The Liver (Usually) does not infarct as it has dual vascular supply

normal transaminases

35
Q

Etiologies and manifestations of intra - hapatic injury –

transaminase levels normal or elevated?

A

Cirrhosis – by the far the most common (intrahepatic vessels are compressed by the nodularity of the scarring liver)

Sinusoidal Diseases – DIC, Eclapsia, Tumor, Sickle Cell, Toxins

Can give rise to portal HTN and cirrhosis, even if cirrhosis is not already present

dManifestations – ascites, varices, + hepatomegaly +

some evidence of liver damage (elevated AST, ALT)

36
Q

Etiologies and manifestations of post - hapatic injury –

transaminase levels normal or elevated?

A

hepatic venous outflow obstruction

Budd Chiari (hepatic vein thrombosis) — hepatomegaly, pain ascites
□ Causes: malignancies, coagulative disorders (PCV, HCC)
□ The liver can’t get rid of the blood and it swells up; necrosis

Other causes: Veno-occlusive disease (VOD) / Sinusoidal obstruction syndrome (SOS) — less common

Manifestations: Congestive liver disease (ascites, hepatomegaly, varices; no JVD)

37
Q

name three benign liver tumors?

A

Hemangioma

Focal nodular hyperplasia

Adenoma

38
Q

name the malignancies of the liver/biliary tree

what is the most common?

A

Dysplasia
HCC
Cholangiocarcinoma
HEpatoblastoma

Metastatic disease – most common

39
Q

Hepatic Hemangioma –
clinical approach?
should you biopsy?

A

very common — clinically negligible

Bx is contraindicated; risk of bleeding

40
Q

Focal Nodular Hyperplasia

  • clinical approach?
  • gross pathology/radiographic appearance
A

clinically negligible
but can become symptomatic if large enough

radiographic / path – central scar; “focal cirrhosis”

41
Q

Adenoma

  • clinical approach?
  • commonaly associated with what type of therapy?
  • treatment?
A

Typically Benign but is a true neoplasm and has the potential to develop into a malignancy

Tumors are hormone response
commonly associated with young women taking OCPs or an athletes taking anabolic steroids

Treat: discontinue steroids; resection

42
Q

Hepatic Dysplasia

what is it?
risk factors?

A

indicates that the liver is at risk for developing into HCC

□ Cirrhosis, recurrent injury (inflammation and repair);
□ Viral integration (HBV)
□ Inherited

Sporadic/idiopathic

43
Q

Hepatocellular Carcinoma

etiologies:
what protein can be used to screen?
pathology/growth patterns?
treatment?

A

HBV (+/-) cirrhosis; and all other causes of cirrhosis (HCV, alcoholic and non alcoholic FLD, Auto immune, hematochromatosis, A1AT def, Wilson disease)

what protein can be used to screen? – AFP
pathology/growth patterns? – may be single or multiple
treatment? – resection, transplant, chemo-embolization, radiation, etc

44
Q

Fibrolamellar HCC

  • who gets it?
  • progonosis?
  • histology?
A

□ Occurs in young patients w/o risk factors
□ Often large at Diagnosis
□ But Good Prognosis

Histology: Fibrous bands passing through tumor; large hepatocytes

45
Q

Cholangiocarcinoma
- what is it? / where does it arise?

risk factors?
histo?

prognosis?

A

Tumor arising from the bile duct;

Risk factors: disease of bile duct (PSC, Liver flukes), cirrhosis

Histo: Looks like adenocarcinoma (glandular), likes to travel along nerves, vessels

		○ Poorer prognosis
46
Q

Hepatoblastoma
- who gets it?
morphology?
treatment?

A

Most common liver malignancy in young children

○ Morphology:
□ Epithelial component, resembling developing liver
Mesenchymal component

○ Treatment: Surgery Or Transplantation; possibly preceded by neoadjuvant therapy

47
Q

Metastatic disease to the Liver
presentation? pathology

most common primary diseases that like to go to the liver?

A

Metastatic- by far the most common malignancy in the Liver

* Most common is carcinoma
	* Colon, stomach, pancreas, breast, lung

Usual: multiple round masses, often near capsule

PT1 B3 (16 decks)

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