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Pathology > liver , gallbladder & exocrine pancrease > Flashcards

liver , gallbladder & exocrine pancrease Flashcards

1
Q

cause Jaundice

A

retention of bile
1) Predominantly Unconjugated Hyper-bilirubinaemia
* Excess Production of Bilirubin
* Reduced Hepatic Uptake
* Impaired Bilirubin Conjugation

2) Predominantly Conjugated Hyper-bilirubinaemia:
* Decreased Hepatocellular Excretion (decreased clearance)
* Impaired Intra- or Extra-hepatic bile flow

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2
Q

patho of Jaundice

A

Disruption of the equilibrium between Bilirubin
production and clearance; Bilirubin is the end
product of haeme degradation

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3
Q

CM of Jaundice

A

Patients with a yellow discolouration of skin and sclerae (icterus)

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4
Q

cause of Neonatal Jaundice

A

Due to immaturity of the liver in conjugating and
excreting Bilirubin –> Development of transient
and mild unconjugated hyper-bilirubinaemia

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5
Q

state the diffrence between UnConjugated/Conjugated Bilirubin of Jaundice

A

–> Unconjugated Bilirubin:
* Insoluble in water at physiologic pH
* Exists in tight complexes with serum albumin
* Cannot be excreted in the urine
* Small amount of unconjugated Bilirubin, present as an albumin-free anion in plasma
* Increase of this unbound fraction (e.g. in haemolytic disease of the newborn [erythroblastosis fetalis]) can lead to accumulation of unconjugated Bilirubin in the brain –> Kernicterus

–> Conjugated Bilirubin:
* Water-soluble
* Non-toxic
* Loosely bound to albumin
* Can be excreted in urine
* Bilirubin delta fraction: With prolonged conjugated hyper-bilirubinaemia, a portion of circulated pigment becomes covalently bound to albumin

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6
Q

state the 3 mechanisms that disrupt the clearance and production of Bilirubin -> which casue Unconjugated Hyper-bilirubinaemia

A
  1. Excessive extra-hepatic production of Bilirubin
  2. Reduced hepatocyte uptake
  3. Impaired conjugation
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7
Q

state the 2 mechanisms that disturb the clearance and production of Bilirubin -> which casue conjugated Hyper-bilirubinaemia

A
  1. Decreased hepatocellular excretion
  2. Impaired bile flow
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8
Q

cause of Crigler-Najjar Syndrome

A

Mutations in the UGT1A1 gene –> Deficient
bilirubin uridine diphosphate glucuronosyl transferase
(bilirubin-UGT) enzyme

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9
Q

Types of Crigler-Najjar Syndrome

A

– Type 1 (CN1): Very severe; no enzyme function; affected individuals can die in childhood due to Kernicterus
– Type 2 (CN2): Less severe; <20% of normal enzyme’s function; people with CN2 are less likely to develop Kernicterus, and most affected individuals survive into adulthood

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10
Q

CM of Crigler-Najjar Syndrome

A

– Jaundice , at birth or in infancy
– Severe unconjugated hyper-bilirubinaemia –> Kernicterus

*Kernicterus –> brain damage due to high levels of bilirubin in a baby’s blood

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11
Q

Clinical picture of babies with Kernicterus

A
  • Extremely tired (lethargic)
  • Weak muscle tone (hypotonia)
  • Episodes of increased muscle tone (hypertonia) and arching of the backs
  • Involuntary writhing movements of the body
    (choreo-athetosis)
  • Hearing problems, or intellectual disability
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12
Q

casue of Dubin-Johnson Syndrome

A

Absence of the canalicular protein, multidrug
resistance protein 2 ([MRP2]–> (responsible for the transport of bilirubin glucuronides & related organic anions into bile)

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13
Q

patho of Dubin-Johnson Syndrome

A

Defect in hepatocellular excretion of
bilirubin glucuronides across the canalicular membrane

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14
Q

CM of Dubin-Johnson Syndrome

A

Chronic or recurrent Jaundice of
fluctuating intensity

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15
Q
  • Macroscopic findings: Darkly pigmented liver
  • Microscopic findings: Coarse pigmented granules within the cytoplasm of hepatocytes

Are the features of what type of Syndrome?

A

Dubin-Johnson Syndrome

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16
Q

cause of Rotor Syndrome

A

unknown

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17
Q

patho of Rotor Syndrome

A

Multiple defects in hepatocellular
uptake and excretion of Bilirubin pigments

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18
Q

CM of Rotor Syndrome

A

Jaundice, but otherwise
normal lives

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19
Q

Micro findings of Rotor Syndrome

A

Normal liver

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20
Q

cause of Cholestasis

A

Extra-hepatic or intra-hepatic obstruction of
bile channels or Defects in hepatocyte bile secretion

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21
Q

CM of Cholestasis

A

– Jaundice
– Pruritus
– Skin Xanthomas (focal accumulations of
Cholesterol)

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22
Q

Patho/Morphology:
1. Accumulation of Bile pigment within Hepatocytes –> fine, foamy appearnace (feathery degeneration)
2. Dilated canalicular spaces
3. Apoptotic cells
4. Kupffer cells with regurgitated bile
pigments (green-brown)
5. Bile ductular proliferation
6. Bile pigment retention
7. Swollen and degenerated Hepatocytes

–> There is also oedema and neutrophilic infiltrates

Feaures of what type of syndrome ?

A

Cholestasis

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23
Q

Factors that influence the development and severity of alcoholic liver disease (Renal Failure)

A

1) Gender: W>M
2) Ethnic differences
3) Genetic factors (Genetic polymorphisms in
detoxifying enzymes and some cytokine promoters)
4) Co-morbid conditions: Iron overload and infections (HBV and HCV) –> Increase in the severity of alcoholic liver disease

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24
Q

Complications of short-term alcohol consumption on the liver

A

mild, reversible Hepatic Steatosis

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25
Q

Macroscopic features:
– Large, heavy (4-6 kg) and soft liver (Hepatomegaly)
– Yellow and greasy organ

Microscopic findings:
– Micro-vesicular lipid droplets in hepatocytes
– Chronic alcohol intake:
* Clear macro-vesicular globules –> Compression and displacement of the hepatocyte nucleus to the cell periphery
* Fibrous tissue around terminal hepatic veins with
extension to adjacent sinusoids

Are the features of what type of Alcoholic liver disease?

A

Hepatic Steatosis (Fatty Liver Disease)

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26
Q

The 3 distinctive forms of Alcoholic liver disease

A
  1. Hepatic Steatosis (Fatty Liver Disease)
  2. Alcoholic Hepatitis
  3. Cirrhosis
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27
Q

Microscopic findings :
– Hepatocyte swelling (ballooning*) and necrosis
– Cholestasis and Haemosiderin deposition in
hepatocytes and Kupffer cells
– Mallory bodies: Eosinophilic cytoplasmic clumps in hepatocytes
– Neutrophilic infiltrates around degenerating
hepatocytes. Accumulation of lymphocytes and
macrophages within parenchyma
– Activation of sinusoidal stellate cells and portal
tract fibroblasts –> Fibrosis (mostly sinusoidal and
peri-venular)

Are the features of what type of Alcoholic liver disease?

A

Alcoholic Hepatitis

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28
Q

casues of Cirrhosis

A

– Chronic viral infections
– Alcoholic or Non-Alcoholic Steato-Hepatitis
– Autoimmune diseases
– Iron overload

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29
Q

Main characteristics:
1) Fibrous septa: Delicate bands or broad scars
around multiple adjacent nodules
2) Parenchymal nodules:
* Encircled by the fibrous septa
* Size: Small (<3mm) to large (>1cm)
* Hepatocytes within nodules (i. Pre-existent, long-lived, ii. Newly formed and capable of replication)

Are the Characteristics of what type of Alcoholic liver disease?

A

Cirrhosis

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30
Q

Morphology:
– Yellow-tan, fatty and enlarged liver (>2kg)
– Brown, shrunken, non-fatty organ (<1kg) [over the span of years]
– Regenerative activity of entrapped parenchymal
hepatocytes –> Uniform micro-nodules –> diffuse Nodularity
becomes more prominent –> Scattered larger nodules
(“hobnail” appearance on the surface of the liver)
– Engulfment of parenchymal islands by wide bands of
fibrous septa –> Mixed micro- & macro-nodular pattern
– Ischaemic necrosis and fibrous obliteration of nodules –> Development of broad expanses of tough, pale scar tissue (“Laennec Cirrhosis”)

Are the features of what type of Alcoholic liver disease?

A

Cirrhosis

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31
Q

Clinical features of Cirrhosis

A

– Anorexia
– Weight loss
– Weakness
– Frank debilitation (advanced disease)
– Incipient or Overt Hepatic Failure

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32
Q

Conditions with an end-result of Fatal Cirrhosis

A
  1. Progressive Liver Failure
  2. Portal Hypertension
  3. Hepatocellular Carcinoma
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33
Q

Morphology:
– Steatosis
– Multifocal parenchymal inflammation (neutrophils)
– Mallory bodies
– Hepatocyte death (balooning degeneration and apoptosis)
– Fibrosis (sinusoidal, but also within portal tracts and around terminal hepatic venules)

of what type of Non-alcoholic fatty liver syndrome?

A

Non-Alcoholic Steato-Hepatitis (NASH)

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34
Q

Types of NAFLD (non-alcoholic fatty liver disease)

A

– Simple Hepatic Steatosis
– Steatosis accompanied by minor non-specific
inflammation
– Non-Alcoholic Steato-Hepatitis (NASH)

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35
Q

What are the 2 sequential events of the “two-hit model of NAFLD pathogenesis

A
  1. Hepatic fat accumulation
    and
  2. Hepatic oxidative stress; The oxidative stress
    acts upon the accumulated hepatic lipids,
    resulting in lipid peroxidation and the release
    of lipid peroxides, which can produce reactive
    oxygen species (ROS)
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36
Q

Morphology:
Large (macro-vesicular) and small (micro-vesicular)
droplets of fat (predominantly triglycerides), within hepatocytes

Are the features of what type of NAFLD?

A

Steatosis

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37
Q

Macro/micro feature diffrence btw NASH(non-alcoholic steato Hepatitis) and Steatosis

A
38
Q

Clinical features of NAFLD

A

1) Individuals with Simple Steatosis, generally asymptomatic
2) Some patients show general symptoms, such as fatigue and right-sided abdominal discomfort caused by Hepatomegaly
3) Patients with NASH: Cardiovascular Disease –> Death

39
Q

Imaging studies of NAFLD?

A

fatty liver

40
Q

Labratory findings of NAFLD

A

1) Elevated serum AST and ALT (90% of
patients with NASH)
– AST/ALT ratio:
* Non-Alcoholic Steato-Hepatitis (NASH): <1
* Alcoholic Steato-Hepatitis: >2.0 to 2.5

41
Q

Managment of NAFLD

A

Goal of treatment: Reversion of Steatosis and
prevention of Cirrhosis –>
–> Correction of the underlying risk factors: Obesity and Hyperlipidaemia and
–> Treatment of Insulin resistance

42
Q

Portal Hypertension –> is the result of increased resistance to portal blood flow
state the casues

A

– Pre-Hepatic
– Intra-Hepatic (Mainly: Cirrhosis; Less frequent: Massive Fatty Change, Granulomatous Diseases)
– Post-Hepatic

43
Q

How does Cirrhosis result in portal hypertension?

A

– Increased resistance to portal flow at the level
of sinusoids
– Compression of Central Veins by peri-venular
fibrosis and expanded parenchymal nodules
–Anastomoses between the arterial and portal
system in the fibrous bands –> Portal Hypertension
– Hyper-dynamic circulation, resulting from arterial
vasodilation in the splanchnic circulation, due to
increased production of NO in the vascular bed

44
Q

Four major Clinical Consequences of Portal Hypertension:

A

– Ascites
– Formation of PortoSystemic Venous Shunts
– Congestive Splenomegaly
– Hepatic Encephalopathy

45
Q

complications of the Acute setting of hepatic Encephalpathy

A

Elevation in blood Ammonia –> Impairment of neuronal function –> Generalised
Brain Oedema

46
Q

complications of the Chronic setting of hepatic Encephalpathy

A

Deranged neuro-transmitter production (especially in mono-aminergic, opioidergic, GABAergic and endo-cannabinoid systems) –> Neuronal dysfunction

47
Q

CF of Hepatic Encephalopathy

A

– Spectrum of brain dysfunction, ranging from subtle behavioural abnormalities –> Marked Confusion and Stupor–> Deep Coma and Death
– Rigidity, Hyper-reflexia, EEG changes (non-specific), Seizures (rarely)
– Asterixis (Flapping Tremor): Non-rhythmic, rapid extension-flexion movements of the head & extremities

48
Q

—————-:Collection of excess fluid in the peritoneal cavity

A

Ascites

49
Q

mechanisms responsible for the development of Ascites

A

1) Sinusoidal Hypertension and Hypo-Albuminaemia (–> Increased movement of intravascular fluid into the extravascular space of Disse)
2) Leakage of fluid from the liver into the peritoneal cavity; Cirrhosis
3) Renal retention of Na and H2O(, due to secondary Hyper-Aldosteronism)

50
Q

loc. of porto-Systemic Shunt

A

Veins around and within:
1) The Rectum (Haemorrhoids)
2) The Cardio-Oesophageal junction (OesophagoGastric varices)
3) The Retro-Peritoneum and the Falciform ligament
of the Liver (peri-umbilical and abdominal wall
collaterals) –> “Caput medusae”

51
Q

clinical features of Hepato-renal Syndrome

A

Decreased Urine output

52
Q

Laboratory findings of Hepato-Renal Syndrome

A

1) ↑Urea,Nitrogen and Creatinine in blood
2) Hyperosmolar Urine (devoid of proteins and
abnormal sediment), with ↓ sodium levels*
(unlike in Renal Tubular Necrosis)

53
Q

Treatment of Hepato-renal syndrome

A

Liver transplantation

54
Q

Porto-Pulmonary hypertension involves

A

1) Portal Hypertension (cirrhotic or non-cirrhotic cause)
2) Excessive pulmonary vasoconstriction
3) Vascular remodeling

55
Q

Clincial features of Porto-pulmonary Hypertension

A

– Dyspnoea on exertion
– Clubbing of the fingers
– Palpitations
– Chest pain

56
Q

clincial features of Heptao-pulmonary Syndrome

A

1) Platypnoea (easier breathing in a horizontal position)
2) Orthodeoxia (fall of arterial blood Oxygen with upright posture)

57
Q

Phases of Acute Symptomatic viral hepatitis w/ recovery

A
  1. Incubation period
  2. Symptomatic pre-icteric period
  3. Symptomatic icteric phase
  4. Convalescence (Recovery)
58
Q

epi of Chronic Viral Hepatitis

A

– High frequency: HCV-infection –> Chronic Hepatitis
– Small number of HBV-infection cases –> Chronic
Hepatitis

59
Q

clincial features of Chronic Viral Hepatitis

A

– Fatigue
– Malaise
– Loss of appetite
– Occasional bouts of mild Jaundice

60
Q

Clinical findings:
– Spider Angiomas
– Palmar Erythema
– Mild Hepato-Splenomegaly
– Hepatic Tenderness

Are the features of what type of Syndrome?

A

Chronic Viral Hepatitis

61
Q

Labratory findings:
– Prolongation of prothrombin time
– Hyper-globulinaemia
– Hyper-bilirubinaemia
– Mild elevations in Alkaline Phosphatase levels

are the LF of?

A

Chronic Viral Hepatitis

62
Q

Chronic Viral Hepatitis Complications in cases of HBV and HCV

A
  • Vasculitis
  • Glomerulonephritis
  • Cryoglobulinaemia
63
Q

Microscopic features:
* Diffuse swelling (“ballooning degeneration”)
* Cholestasis, with bile plugs in canaliculi and brown pigmentation of hepatocytes
* fatty change (Hepatitc C)
* Apoptosis
* peioportal necrosisConfluent necrosi
* Hypertrophy and hyperplasia of Kupffer cells,
often laden with lipofuscin pigment
* Mixed inflammatory cell infiltrate in the portal tracts

Are the feature of Acute/Chronic viral Hepatits?

A

Acute Viral Hepatits

64
Q

microscopic features:
infected hepatocytes with intra-cytoplasmic
sphaeres and tubules, giving the characteristic
appearance of “ground-glass hepatocytes”

is the feature of what type of syndrome?

A

Viral Hepatits associated w/ HBV
*HBV: Hepatitis B Virus

65
Q

Microscopic features:
infected livers with lymphoid aggregates
within portal tracts and focal lobular regions of
hepatocyte Macro-Vesicular Steatosis

Are the features of what type of Condition?

A

Viral Hepatitis associated w/ HCV
*HCV : Hepatitis C Virus

66
Q

What is the Histological Hallmark of chronic Viral hepatitis B (HBV) infection?

A

“Ground glass Hepatocyte”

67
Q

cause of liver Abscess

A

– Parasitic infections (developing countries)
– Complication of a bacterial infection elsewhere in
body (Western world)

68
Q

Macroscopic features:
– Solitary or multiple lesions
– Size: From tiny to massive lesions

Microscopic findings:
– Liquefactive necrosis
– Abundant neutrophils

Are the features of what type of condition?

A

Liver Abscess

68
Q

Clinical manifestaions of Liver Abscesses

A

– Fever
– Right upper quadrant pain
– Tender Hepatomegaly
– Jaundice (in cases of biliary obstruction)

69
Q

Tx of Liver Abscesses

A

– Antibiotic therapy and
– Percutaneous or surgical drainage

70
Q

patho+ triggers of Autoimune Hepatitis

A

– T-Cell mediated autoimmunity
– Hepatocyte injury caused by IFN-γ (produced by CD4 and CD8 T-cells) and CD8 T-cell-mediated cytotoxicity
– Defect in regulatory T-cells –> Uncontrolled activation of pathogenic self-reactive lymphocytes

Triggers:
- Viral infections, certain drugs (e.g. Atorvastatin, Simvastatin, Methyldopa, Interferons etc.), herbal products

71
Q

Laboratory findings:
– Absence of serologic evidence of viral infection
– Elevated serum IgG
– High titers of autoantibodies (80% of cases)
– Autoantibodies: Detected by Immuno-Fluorescence
(IF) or Enzyme-Linked Immunosorbent Assays (ELISA)
* Antinuclear Abs
* Anti-Smooth Muscle Abs
* Liver/Kidney microsomal Abs
* Anti-soluble Liver/Pancreas Abs

Are the findings of whattype of condition ?

A

Autoimune Hepatitis

72
Q

Microscopic findings:
– Severe hepatocyte injury –> Confluent necrosis
– Simultaneous, marked inflammation and advanced scarring
– Burned-out Cirrhosis (No histological hallmarks
present)
– Abundant plasma cells

Are the features of what type of conditio?

A

Autoimmune Hepatitis

73
Q

CM of Autoimmune Hepatitis

A

Mild to severe Chronic Hepatitis

74
Q

Clinical features of Haemochromatosis

A

– Hepatomegaly
– Skin pigmentation
– Diabetes mellitus
– Cardiac dysfunction
– Atypical arthritis

75
Q

Diagnosis of Haemochromatosis

A

– High levels of serum Iron and Ferritin
– Exclusion of secondary causes of Iron overload (for
Hereditary Haemochromatosis)

76
Q

Management of Haemochromatosis

A

Phlebotomy; Use of Iron Chelators* -> Decrease total body Iron

*(Chelators: Agents that are able to bind metal ions for drastic reduction in their reactivity)

77
Q

Secondary Iron Overload -> Acquired forms of Iron
accumulation; known sources of excess Iron?

A

– Multiple transfusions
– Ineffective Erythropoiesis (β-Thalassaemia and
Myelodysplastic Syndromes)
– Increased Iron intake

78
Q

Wilson disease is Charactersied by?

A

accumulation of toxic levels of Copper in many tissues and organs (Liver, Brain and Eye)

79
Q

casue of Wilson disease

A

Loss-of-function mutations in ATP7B gene
(Chromosome 13); ATP7B gene encodes an ATPase
metal ion transporter, localised to the Golgi region
of hepatocytes

80
Q

Clinical features of Wilson disease

A

– Acute or Chronic Liver Disease
– Neuropsychiatric manifestations (mild Behavioural
Changes, frank Psychosis, Parkinson disease-like
syndrome)

81
Q

Treatment of Wilson disease

A

Long-term therapy with Copper Chelators (D-Penicillamine) and Zinc salts

82
Q

Wilson disease is charactersised by Progressive accumulation of Copper in Hepatocytes –>Toxic injury. what are the 3-step mechanism of this process?

A
  1. Induction of free radical formation
  2. Binding to sulfhydryl groups of cellular proteins
  3. Displacement of other metals in hepatic metalloenzymes
83
Q

Wilson disease may mimic?

A

1) Fatty Liver Disease (with mild to moderate Steatosis,
Steato-Hepatitis and similar patterns of Scarring)
2) Acute Hepatitis-like injury: In its most severe form,
manifests as Fulminant Hepatic Failure
3) Chronic Hepatitis-like picture, with coexistence of
Fatty Liver Disease features; Progression of Chronic
Hepatitis –> Development of Cirrhosis

84
Q

Special stains used to identify Copper deposits in Wilson Disease

A

i. Rhodanine stain for Copper and
ii. Orcein stain for Copper-associated protein)

85
Q

fxn of α1-Antitrypsin

A

Inhibition of neutrophil elastase
released at sites of inflammation

86
Q

complications of AAT (α1-Antitrypsin) Deficiency

A

1) Hepatocellular Carcinoma
2) Pulmonary Emphysema

87
Q

Morphology:
– Hepatocytes with round to oval cytoplasmic
globules (PAS+ and PASd+ [DD: Glycogenosis of
Diabetic Hepatopathy, and Glycogen Storage
Diseases])
– Patterns of Hepatocyte injury associated with PiZZ
homozygosity:
* Marked Cholestasis with Hepatocyte necrosis
in newborn
* Childhood Cirrhosis
* Smoldering Chronic Hepatitis
* Cirrhosis (apparent late in life)

Are the features of what type of syndrome ?

A

α1-Antitrypsin Deficiency

88
Q

CM of α1-Antitrypsin Deficiency

A

– Cholestasis: 10-20% of newborns with AAT
deficiency
– Chronic Hepatitis
– Cirrhosis or
– Pulmonary disease

89
Q

Treatment of α1-Antitrypsin Deficiency

A

Orthotopic Liver transplantation

Pathology (11 decks)

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