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Pathophysiology II > Week 5 > Flashcards

Week 5 Flashcards

1
Q

Fibrosis caused by what three mechanisms?

A

Inflammation- cytokines signal collagen deposition
Wound healing (scar tissue)
Direct stimulators of fibrosis (HBV, Carbon Tetrachloride)

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2
Q

Types of cirrhosis: Laennec Cirrhosis, other name?

A

Micronodular Cirrhosis

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3
Q

Attributes of micro nodular cirrhosis?

A
  • Acute manifestation
  • < 3 mm in diameter
  • No landmarks of lobular
    architecture in the form of portal
    tracts or central vein
  • Connective tissue is thin
  • Primary Etiology:
  • Alcoholic cirrhosis is the prototype
  • Hemochromatosis
  • Wilson disease
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4
Q

Types of Cirrhosis: Chronic hepatitis, other name?

A

Macronodular Cirrhosis

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5
Q

Attributes of Chronic Cirrhosis?

A
  • Submassive confluent necrosis in
    which the liver is grossly misshapen
  • Connective tissues are
    characteristically broad and contain
    elements of portal tracts,
    mononuclear inflammatory cells and
    proliferated ductules
  • Micronodular may be converted into a
    macro pattern by continued
    regeneration and expansion of
    existing nodules
  • Etiology: HBV, HCV
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6
Q

Manifestations of Cirrhosis?

A
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7
Q

What does albumen do?

A

Moves fluid

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8
Q

Where is albumen made?

A

Liver

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9
Q

what happens when liver is impaired and can’t make albumen?

A

fluid builds up in interstitial tissues and around other vessels

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10
Q

What’s in a portal triad?

A

branch of bile duct
branch of hepatic portal vein
branch of hepatic artery

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11
Q

Hepatic lobules

A
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12
Q

Portal Hypertension caused by

A

Tissue destruction causes loss of hepatic vascular volume, increasing pressure in the portal vein

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13
Q

Portal hypertension results in:

A

Increased congestion at portocaval anastomoses results in the following manifestations:
* Esophageal varices
* Hemorrhoids
* Caput medusae
* Splenomegaly and hypersplenism with pancytopenia

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14
Q

What disease is this?
Autosomal recessive genetic
disorder
* Defect in WD gene codes
(ATP7B chromosome 13)
* Decreased incorporation of
copper into ceruloplasmin
(copper binding protein)
production
* Defect in hepatic copper
transport into bile

A

Wilson Disease

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15
Q

Pathogenesis of Wilson Disease?

A

Accumulation of free copper, toxic to many tissue

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16
Q

Wilson Disease expressions?

A
  • Hepar: Fatty change, chronic hepatitis, micronodular cirrhosis
  • Basal Ganglia: Movement disorders similar to Parkinson disease with additional psychiatric
    manifestations
  • Eyes: Kayser-Fleischer rings around the iris
17
Q

Treatment for Wilson Disease?

A

Life-Long:
* Penicillamine (Cuprimine, Depen)
* Chelating agent
* Can cause serious side effects à Skin and kidney problems, bone marrow suppression and worsening of neurological symptoms
* Used cautiously if having penicillin allergy
* Suppress vitamin B-6 (pyridoxine)

  • Trientine (Syprine)
  • Trientine works much like penicillamine but tends to cause fewer side effects
  • Neurological symptoms can also worsen
18
Q

Other treatment for Wilson Disease

A
  • Zinc acetate (Galzin)
  • Prevents body from absorbing copper from the diet
  • Typically used as maintenance therapy to prevent copper from building up
    again after treatment with penicillamine or trientine
  • Zinc acetate might be used as primary therapy if unable to take penicillamine
    or trientine
  • Zinc acetate can cause stomach upset
19
Q

Disease of increased blood and tissue iron levels that leads to injury, called what?

A

Hemochromatosis

20
Q

Primary (hereditary) hemochromatosis cause?

A
  • Autosomal recessive mutation on HFE gene (C28Y)
  • Increased small Intestine absorption of Iron
21
Q

Secondary Hemochromatosis cause?

A

Chronic transfusion in anemias, build up of too much iron

22
Q

Results of Hemochromatosis

A
  • Toxic iron deposits in multiple organs:
  • Liver > Micronodular cirrhosis and
    increased risk of HCC
  • Heart > Restrictive cardiomyopathy
  • Pancreas > Acquired diabetes mellitus
  • Skin > Bronze pigmentation (bronze
    diabetes)
  • Gonads > Hypogonadism
23
Q

Spectrum of gallbladder diseases

A
24
Q
  • Stone formation in Gall Bladder
  • Colicky pain (waves, with peristalsis)
  • Worse with fatty foods
  • Diagnose > RUQ Ultrasound
  • Tx > Elective cholecystectomy
A

cholelithiasis

25
Q

cholelithiasis treatment?

A

Cholecystectomy

26
Q
  • Obstruction of gall stone in the cystic duct
  • Murphy’s sign +
  • Constant ( vs colicky pain )
  • Fever, leukocytosis
  • Diagnose > RUQ Ultrasound, HIDA Scan
    (Hepatobilliary scintigraphy)
  • Treatment > Cholecystectomy
A

Cholecystitis

27
Q

Cholecystitis treatment?

A

Cholecystectomy

28
Q

what is Morphy’s Sign?

A

Asking the patient to take in and hold a deep breath while palpating the right subcostal area. If pain occurs on inspiration, when the inflamed gallbladder comes into contact with the examiner’s hand, Murphy’s sign is positive.

29
Q
  • Gall stone obstructs in the common bile duct
  • Proximal inflammation
  • Obstructive jaundice
  • Dilated hepatic bile ducts
  • Treatment > ERCP
A

Choledocholithiasis

30
Q
  • Also known as Ascending Cholangitis
  • Choledocolithiasis + Infection
  • Charcot’s triad
  • Fever, Abdominal Pain, Jaundice
  • Reynold’s pentad
  • Fever, Abdominal Pain, Jaundice, Confuse,
    Hypotension
  • Diagnose > RUQ Ultrasound
  • Treatment > Emergency ERCP
A

Cholangitis

Pathophysiology II (5 decks)

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