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253-Green Patho > The Liver > Flashcards

The Liver Flashcards

1
Q

What is Cirrhorsis?

A

End stage of Liver disease in which the hepatocyte are progressively replaced with fibrous scartissue.

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2
Q

Are liver cells good at regeneration?

How is this affected in Cirrhosis

A

Yes, Liver cell reporduce well and the liver has a large fx reserve.

However, cirrhosis progressively replaces hepatocyte ares with scartcissue

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3
Q

What does a liver with cirrhosis look like

A

Fibrous, nodular

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4
Q

Etiologies of Cirrhosis

A
  • Alcohol abuse (60-70% of cases) (This is a kind of toxic hepatitis)
  • Hepatitis (10% ish)
  • Drugs (e.g. methotrexate)
  • Biliary disease (liver, bile ducts, gallbladder) (10% ish)

• Metb disorders (eg hemochromatosis)
o Inc Iron levels and deposition in liver

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5
Q

What is cryptogenic?

A

Same as idiopathic. Occasionally cirrhosis cause can be cryptogenic

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6
Q

Patho- Steps leading to portal HTN

A

• Hepatocytes destroyed -> cells regenerate -> fibrous scar tissue forms -> Vessel constriction -> portal HTN

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7
Q

What other issue will be present with vessel constriction in the liver?

A

Impeded perfusion to liver

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8
Q

Portal HTN will lead to what other major complications?

A

Fluid shift or ascites- (r/t inc pressure in peritoneal capillaries

Duct constriction -> bile flow impeded -> bile stasis

Reduction in Metabolic waste clearance- Normal or essential components in high levels can become toxic

Liver Failure

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9
Q

Common MNFTS of Cirrhosis.

Some vague, some specific

A

VAGUE
Anorexia, weakness, wt loss

SPECIFIC -
Hepatomegaly and jaundice (some forms do not present w/ jaundice)

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10
Q

How is the spleen potentially affected by Cirrhosis?

Why?

A

Splenomegaly

Portal HTN leads to increased hydrostatic pressure in splenic veins

Also r/t Anemia, leukopenia, thrombocytopenia (r/t bone marrow deficiencies from reduced components being provided by liver)

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11
Q

What is Varices?

A

Another potential MNFTS/Complication of Portal HTN

Refers to dilation of associated veins. (It is not localized like an aneurism )

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12
Q

What Gi issues is associated with Portal HTN

A

GI bleeds

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13
Q

What is the Tx for Cirrhosis?

A

• Maximize regeneration (reduce workload)
o Diet modification
• small meals,
• high carb (high calorie)
• no fat (liver has to produce bile for breakdown)
o No alcohol
o Treat Compiications

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14
Q

Distinguish between Portal vein, Hepatic arteries and hepatic veins and hepatic duct?

(% of total fluid volume, source and output)

A

PORTAL- ~ 70% of total blood to liver. from GI tract to liver

HEPATIC A- ~30% of total blood to liver. From heart to Liver

HEPATIC V- Draining blood from liver emptying to inferior vena cava

Hepatic Duct- Bile- L+R lead to common hepatic -> common bile Duct-> sphincter of Oddi -> Duodenum

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15
Q

What is normal pressure for the portal vein system and how does this change in Portal HTN

A

Portal HTN is defined as: >12mmHg:

Normal= 5-10mmHg

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16
Q

How do you describe the site of blockage causing Portal HTN?

Where are most?

A

Description could be pre, intra or post hepatic for blockages.

Most is Intra hepatic
Ex. Cirrhosis

17
Q

What is portosystemic shunting?

Common areas?

A

Obstruction of venous blood flow through liver, leading the development of collateral channels between portal and venous system. Meaning some blood bypasses liver.

Hemerrhoidal and esophageal commonWhat

18
Q

Describe the complications of portosystemic shunting

A

Esophogeal Varices

Caput medusea

Hemorrhoids

Hepatic encephalopathy

19
Q

What are Esophogeal Varices?

A

Thin waled varicosities (twisted/collateral veins) that develop along esophageal mucosa and are subject to rupture. (i.e GI Hemorrhage)

Often MNFTS as Frank Blood

20
Q

What is Frank Blood?

A

Frank blood is bleeding via rectum. Often associated with hemorrhage in the GI tract. (Beyond occult blood)

21
Q

Why are toxin likely to develop in blood with portal HTN?

A

HTN leads to collateral connections (or channels) Passing of blood for Portal System to hemoroidal or other venous system, liver gets bypassed -> no metabolization or filtration in liver -> toxic compounds enter rest of venous system

22
Q

What is Ascites

A

Excess fluid accumulation in peritoneal cavity

23
Q

What might lead to Ascites?

A 
• ET and Patho
o	Cirrhosis and portal HTN
o	Right sided heart failure
o	Severe changes in HP or OP
o	Water/Na retention
24
Q

Two key MNFTS of Ascites

A

Dyspnea (Inc abdm cavity pressure oushing against lung expansion, reduces tidal volume)

Abd distension (fluid build up in abdominal cavity)

25
Q

Tx of Ascites

A

o Small volume: use diuretics, Provide fluids and electrolytes

o Large volume: Paracentesis + volume expender (eg albumin)

26
Q

What fx capacity of liver must be lost to lead to failure?

Implications?

A

• l/o >80% fx capacity before failure

> 50% mortality (r/t late diagnosis)

27
Q

Common Et

Examples of Acute vs Chronic Liver failure?

A

o Fulminant hepatitis (ACUTE)
o Toxic liver damage – Alcohol (ACUTE)
o Cirrhosis (chronic)

28
Q

VERY basic path and MNFTS of Liver failure

4 broad categories of complication involved in the failure?

A

Hepatic insuff and multi organ failure

Hepatic encephalopathy
Hepatorenal
Hematology
Metabolism

29
Q

4 major issues r/t hematology in Liver failure

A

o Impaired protein synthesis (Specific to hematology -clotting factors and fibrinogen)
• The liver also breaks down clots and this is impaired

o Depressed marrow function (r/t limited protein (aka resources) for the marrow to produce cells)
• Thrombocytopenia, leukopenia

o Inadequate clearance of activated clotting factors (Liver has major role in clot breakdown)
• DIC (Disseminated intravascular coagulation)
This refers many small clots develop across blood stream, this cause obstruction but also depletes resources for stopping actual bleeds

o GI bleeds (r/t to above)

30
Q

Key Issues related to Metabolism complications in Liver failure

A

• inadequate bilirubin clearance
o jaundice

• Hypoalbuminemia (key colloid in Colloid osmotic pressure, less pull pressure in vessels- risk of hypervolemia)
o edema and ascites

• Defective urea cycle 
   o Hyperammonemia (ammonia is byproduct of protein metb)

• Reduced estrogen catabolism
o Hyperestrogenism

31
Q

Describe hepatorenal syndrome

A

• idiopathic renal failure (though reasons are discussed)

• severe reduction in renal perfusion
o link show liver improves so does kidney

• oliguria (limited urine leading to anuria…basically no urine) And azotemia (build up of nitrogenous waste products in blood)

32
Q

Why is there a reduction in renal perfusion in liver failure

A

o Reduced perfusion r/t
• portal hypertension (stealing volume)
• fluid shifts
• Albuminopenia

33
Q

What is Hepatic encephalopathy?

A

Hepatic encephalopathy is:
• Neuro mnfts of liver failure
• Toxic compounds that can affect the brain are not detoxified
(Ex. ammonia, urea, nitrogenous compounds)

34
Q

2 reasons toxins aren’t processed properly in liver failure

A

o Liver impaired (hepatocytes impaired casuing reduced processing toxins)

o Porto systemic shunts (venous return skips the liver outright)

35
Q

2 different ways changes in concentrations of toxic compounds could negatively affect the brain

A

Changing concentration
(Eg. ammonia -> glutamate -> alter neurotransmission and osmolarity. Effecting action potentials with increasing concentration)

Changing Osmolarity
(Blood in brain vessels pulls out fluid and brain dehydration occurs)

36
Q

Early MNFTS of hepatic encephalopathy

A

Asterixis (hand trembling) and hyperflexia (over active reflex)

37
Q

Tx for liver failure

A
  • Reverse cause
  • Deal with Mnfts and complications

• Purgative
o (potent laxative clears gut of proteins- source of ammonia) azotemia (nitro compounpounds)

• Non absorbable Abx
o act at level of gut, continue through all of the gut and impact flora in colon

• liver transplant in many cases (sometimes only option and difficult one)

253-Green Patho (21 decks)

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