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Big Ol' Patho. > Cirrhosis + Portal HTN + Liver Failure > Flashcards

Cirrhosis + Portal HTN + Liver Failure Flashcards

1
Q

Cirrh =

What is Cirrhosis?
What kind of changes occur?

A

Yellow

  • Very serious, considered to be end stage of liver disease (will go into liver failure from here)
  • Major cause of death
  • Fibrosis–> Nodular liver (bumps)
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2
Q

What is fibrosis?

A

Fibrosis of the liver is excessive accumulation of scar tissue that results from ongoing inflammation and liver cell death that occurs in most types of chronic liver diseases. Nodules, abnormal spherical areas of cells, form as dying liver cells are replaced by regenerating cells.

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3
Q

Et of cirrhosis?

A
  • Alcohol abuse (60-70%)
  • Hepatitis
  • Drugs
  • Biliary disease
  • Metb disorders
  • Cryptogenic ( idiopathic)
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4
Q

WHat is an example of a metabolic disorder that can result in cirrhosis?

What are the primary problems that occur in cirrhosis?

A

hemochromatosis = iron overload in body leading to deposition of this iron into tissues including liver

dec liver fx and portal htn

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5
Q

Pathophysiology of Cirr?

A
  • Repetitive assault on hepatocytes –> eventually not able to regenerate; instead will form scar tissue (collagen fibers) to replace these hepatocytes; collagen fibers surround the area of the dead hepatocyte, appear as nodules
  • As scar tissue forms, compressed ducts and blood vessels → perfusion impacted
  • Vessel constriction → impeded perfusion → portal HTN (pressure inside of vessel increases (inc hydrostatic P) , causing more push pressure → fluid shift → ascites (fluids moves into empty body cavity)
  • Duct constriction → bile flow impeded → bile stasis (can result in gallstones)
  • Dec in metb waste clearance
  • Liver failure
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6
Q

Fx’s of the liver?

A
  • Production of bile salts
  • Elimination of bilirubin
  • Metabolism of steroid hormones (sex hormones, glucocorticoids, aldosterone)
  • Metabolism of drugs
  • Carbohydrate metabolism
  • Fat metabolism
  • Protein metabolism
  • Storage of vitamins and minerals
  • Filtration of blood and removal of bacteria and pacticular matter from Kupffer cells
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7
Q

What fx does the liver play in carb metabolism?

A

Stores glycogen and synthesizes glucsoe from amino acids, lactic acid, and glycerol

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8
Q

What fx does the liver play in fat metabolism?

A
  • Formation of lipoproteins
  • Conversation of carbs and proteins to fat
  • Synthesis, recycling, and elimination of cholesterol
  • Formation of ketones from fatty acid
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9
Q

Liver fx in protein metb?

A
  • Deamination of proteins
  • Formation of urea from ammonia
  • Synthesis of plasma proteins
  • Synthesis of clotting factors
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10
Q

Manifestations and complications of cirrhosis?

A

Manifestations:
• Vary
• Common: anorexia, weakness, wt loss
• Hepatomegaly, jaundice

Complications:

  • Portal HTN
  • Ascites
  • Varices
  • GI bleeds
  • Splenomegaly
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11
Q

What are varices and were are they seen to form cirrhosis?

A

varix=singular
= dilation of an associated vein
(associated vein = not a vein within the hepatic portal system itself, but rather extending pressure to other neighbouring veins such as esophopharageal?)

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12
Q

Why does splenomegaly results with cirrhosis?

A

d/t engorgement of surround vessels (portal htn)

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13
Q

Tx of cirrhosis?

A

• Maximize regeneration
–> Diet (to dec workload)
–> No alcohol
• Address complications - Need to ensure varix doesn’t rupture, etc (complications will set in as liver failure progresses)

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14
Q

What does the word portal mean?

A

Pertains to the porta hepatis.
The porta hepatis is a deep fissure in the inferior surface of the liver through which all the neurovascular structures (except hepatic veins) and hepatic ducts enter or leave the liver 1. It contains: right and left hepatic ducts. right and left branches of hepatic artery. portal vein.

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15
Q

2 sources of blood supply to the liver?

A

1) From hepatic portal vein

2) Arterial supply through the hepatic artery –> supplies nutrients to liver tissue itself

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16
Q

Where does blood in the hepatic portal vein come from?

What does this blood contain?

A

Hepatic vein carries blood from: intestines, major abdominal organs including pancreas and spleen

This blood carries nutrient and toxic materials absorbed in the intestine, blood cells and their breakdown products from the spleen, and insulin and glucagon from the pancreas

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17
Q

Where does blood exit the liver?

Where does this lead?

A

hepatic veins

Drain into the inferior vena cava

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18
Q

What occurs in portal htn?

A
  • Inc pressure in hepatic-portal system
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19
Q

What is the parameter for determining when portal htn occurs?

A

when exceeds >12 mmHg, is portal HTN

N=5-10

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20
Q

Et of portal HTN

3 kinds?

A

3 kinds of et based on site of obstruction:

1) Pre-hepatic – blockage in vessel before liver
2) Intra-hepatic – with cirrhosis
3) Post-hepatic – after liver

  • Mostly d/t cirrhosis
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21
Q

Complications of portal HTN?

A
  • Most serious complication = ruptured varix (in assoc vein, such as esophageal varix)

Others:

  • Ascites
  • Portosystemic shunts
  • Splenomegaly
22
Q

How does ascites result form portal HTN?

A

Increased pressure in peritoneal capillaries –> fluid moves into interstitial spaces, then into body cavity

23
Q

Portosystemic shunts

A

when build up of pressure within hepatic-portal system, collateral connection form with vessels outside of HPS, distributes some of that blood into the adjoining veins, (ex: splenic vein shunts some blood into esophageal vein…)
• This relieves some pressure but ends up passing same problem to other vessel
• This also bypasses liver, so toxic compounds now going to reach brain and tissues

24
Q

Why does splenomegaly result form portal HTN?

A

veins such as splenic vein are engorged, causing inc push pressure, fluid shift into interstitial space of the spleen

25
Q

What does splenomegaly result in?

A
  • Anemia, leukopenia, thrombocytopenia (and resulting bleeding)
    (See Fig 38-14 p. 930)
26
Q

How does portosytemic shunting of blood result in hepatic encephalopathy?

What is HE?
(See Fig 38-14 p. 930)

A

Causes shunting of ammonia and toxins from the intestine in to general circulation

Hepatic encephalopathy (HE), also known as portosystemic encephalopathy, is the occurrence of confusion, altered level of consciousness, and coma as a result of liver failure

27
Q

What are 3 things result from development of collateral channels in portal htn?
(See Fig 38-14 p. 930)

A
  • Caput medusae (spider-web like appearance, displacement of blood to superficial veins around umbilicus)
  • Hemorrhoids
  • Esophageal varices
28
Q

What is ascites?

A
  • FOrm of third spacing
  • Fluid accum in peritoneal cavity
    • Is NOT just the presence of fluid in this cavity…there is always some fluid.
29
Q

Etiology and Patho of ascites?

A
  • Cirrhosis + portal HTN
  • Right sided HF
  • Severe changes in HP &/or OP (within vessels of GI tract)
  • Water/Na+ retention (by kidneys)
    or protein loss (impaired syntehsis of albumin in liver)
30
Q

Manifestations of ascites?

A
  • Are many but are going to choose 2 here
  • Dyspnea
  • Abdominal distension (note, this is not bowel distension but rather d/t fluid displacement into cavity) → if small volume, will not be as detectable
31
Q

Why do you see dyspnea from ascites?

A

p from fluid in abm cavity; for thoracic cavity vol to increase, need to be able to displace diaphragm…is now p countering this push, so can’t adequate inflate lungs

32
Q

Tx of ascites?

A

• Small vol: Diuretic (small if

33
Q

Why is a diuretic used for small volume ascites?

A

moving fluid from vasculature → decreasing blood volume → dec in CHP and relative inc in hydrostatic pressure in the cavity→ less push pressure from vessels in hp system → overall net flow of fluid into vasculature (our of body cavity)

34
Q

Why is paracentesis with vol expander used in large vol ascites?

A

→ albumin will prevent rush of fluid from vasculature by serving as plasma vol expander
o Paracentesis alone would not work because would remove counter pressure against vasculature, fluid will rush into the cavity once the 5L has been removed…severe risk of hypovolemia

35
Q

Is liver failure acute or chronic?

A

Can be either

36
Q

What constitutes liver failure?

Mortality rate?

A
  • L/o >80% fx capacity (this is when liver will stop working all together…have smaller scale liver failure before this)
  • > 50% mortality
37
Q

Why is liver so important?

A

• Liver supports function of many other organs (brain, heart)

38
Q

Et of liver failure?

A
  • Fulminant hepatitis
  • Toxic liver damage (d/t environmental component, etc)
  • Cirrhosis (ex of cause of chronic liver failure)
39
Q

What does it mean if something is fulminant?

A

fulminant refers to any condition that arises abruptly and is very severe

40
Q

Describe the mnfsts/patho that result from liver failure r/t hematology:

A
  • Impaired hemostasis & anemia d/t
  • -> Impaired protein synthesis (clotting factors and fibrinogen)
  • -> Marrow function depressed because doesn’t have resources it needs → thrombocytopenia, leucopenia
  • -> Inadeq clearance of activated clotting factors → DIC (disseminated intravascular coagulation = clotting in the vessels), disseminated meaning throughout vasculature
  • -> GI bleeds -
41
Q

Describe the mnfsts/patho that result from liver failure r/t metabolism:

A

a. Inadequate bilirubin clearance → jaundice
b. Hypoalbuminemia → Edema and ascites (fluid shift)
c. Defective urea cycle – build up of ammonia can be toxic, liver functions to make this into urea (reverse of cycle seen before, can go both ways) → hyperammonemia
d. Dec estrogen catabolism → hyperestrogenism (loss of libido, inc cancers, gynecomastia in men, etc)

42
Q

4 major categories of manifestations resulting from liver failure?

A

1) Hematology
2) Metb
3) Hepatorenal syndrome
4) Hepatic encephalopathy

43
Q

Describe Hepatorenal syndrome as manifesation of liver failure
Why does kidney damage result?
How does this manifest?

A

a. Idiopathic renal failure – can’t accept this! What do we know….
- -> Severe dec in renal perf with liver failure → becomes ischemic, infarction
- -> Also know that if we reverse the liver failure, kidney fx will return to normal = definite
- -> Why is kidney not getting enough blood? Answer lies in portal htn → if blood is shunted into portal system, other areas deprived of blood
- -> Oliguria and azotemia

44
Q

Oliguria?

Azotemia?

A

dec urine output

build up of nitrogenous waste products in the circulation (ammonia, urea, etc)

45
Q

Hepatic encephalopathy

  • What is it?
  • Example of how this occurs?
A

a. Neuro manfestations of liver failure
b. Toxic compounds not detoxified → reach brain through circulation (b/c liver impaired, portosystmeic shunts)
c. Eg: ammonia → converted to glutamate, which accumulates (neurotrans) → alters neurotransmission & osmolarity

46
Q

Manifestations of hepatic encephalopathy

A
  • Early manifestations: asterixis (trembling of hands) & hyperreflexia (hyperactive reflexes)
  • Confusion?
  • Coma?
  • Death?
47
Q

Tx of liver failure?

A
  • May be able to reverse cause (but not likely)
  • Treat manifestations and complications
  • Use purgative in some instances
  • Non-absorbable abx
  • Liver transplant in many cases (only long term solution)
48
Q

When is it more likely that you’ll be able to reverse the cause of liver failure?

A

more likely if acute, such as exposure to toxic compound, which you can then remove

49
Q

Why is purgative used in liver failure?

A

is very strong laxative to rid bowels of protein in contents
- used because primary source of ammonia is proteins ==> This ammonia causes encephalopathy

50
Q

Why are non-absorbable abx used with liver failure?

A

not absorbed into circ, will remain in gut to limit normal flora (as these flora are responsible for producing ammonia through their metabolism

Big Ol' Patho. (17 decks)

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