Liver 5 (test 1) Flashcards

1
Q

What is the definition of cirrhosis?

A

Adiffuse process characterized by: -

fibrosis and conversion of normal lobular architecture into structurally abnormal nodules (regeneration) - ↓ liver size (from scarring)

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2
Q

What is the result of chronic hepatitis resulting from a number of chronic, progressive disorders?

A

End stage liver failure

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3
Q

What is portal hypertension, and what are some of the causes?

A

Portal hypertension ↑ resistance to hepatic blood flow, due to - –Fibrosis (compression of sinusoids and central veins by scar tissue) –Abnormal lobular architecture –Development of arteriovenous anastomoses within the scars –etc.

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4
Q

What are come consequence of portal hypertension?

A

a] Ascites -may also be due, in part, to: •decreased plasma oncotic pressure •liver’s secondary effects on renal function (fluid retention)

b] ACQUIRED portosystemic shunts → Hepatic Encephalopathy

c) Splenomegaly (diffuse, symmetrical) = SPLENIC CONGESTION: secondary to decreased blood flow through the liver & portal hypertension

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5
Q

What is Hepatic Encephalopathy?

A

(HE) is a disorder of mental activity, neuromuscular function and consciousness that occurs as a result of either chronic or acute liver failure. This complex neuropsychiatric syndrome is primarily caused by metabolic abnormalities.

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6
Q

What is the pathogenesis of an acuired portosystemic shunt?

A

Fibrosis impedes hepatic blood flow and produces portal hypertension •Due to this increase in portal blood pressure, blood seeks the path of least resistance and –may shunt around the liver or –move directly through the liver via shared capillary beds Typically, many small shunts, not a single large vessel

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7
Q

What is the primary cause of cirrhosis?

A

Chronic persistent stumuli - chronic toxins / drugs (aflatoxin, alcohol, barbiturates) - chronic canine hepatitis -persistent viral infections (Human hepatitis virus) -Autoimmune and drug therapy are most common causes in dogs

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8
Q

What are some causes of passive congestion, and the pathogenesis to hepatic problems?

A

Passive congestion CAUSE: Right sided heart failure e.g. cardiomyopathy, heartworms, … ↓ cardiac output, ↓ venous pressure producing CONGESTION of – central veins & centrilobular sinusoids

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9
Q

What is caval syndrome?

A

This is a Dz caused by Dirofiliara Immitis (heartworm), where it deposits in the vena cava causing hypertension and inflammation of the liver.

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10
Q

How would you describe centrilobular fibrosis, and is the main cause?

A

↑ fibrous connective tisue around central veins CHF specifically RHF

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11
Q

Although centrilobular necrosis is generally caused by RHF, what are some other causes for this, and why?

A

overt hepatocyte necrosis

hemorrhage anemia shock

pathogenesis is centrilobular hypoxia

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12
Q

What are the two types of portosystemic shunts?

A

Congenital and acquired

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13
Q

What are the two options for a congenital portosystemic shunt?

A

Congenital = A congenital anomalous connection between the portal vein and a systemic vein

Portal blood is:

a] diverted around liver (Extrahepatic shunt) Small breed dogs

OR

b] shunted through liver (Intrahepatic shunt) Large breed dogs

Result is - BYPASS OF LIVER Toxins absorbed from the GI have direct access to the systemic circulation (e.g. ammonia) Usually a SINGLE relatively large caliber vessel

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14
Q

What is the signalment for a dog with portosystemic shunt?

A
  • stunting
  • high blood ammonia •hepatic encephalopathy
  • +/- PU/PD
  • Microhepatica = small liver = hepatic atrophy - due to a lack of hepatotropic factors •+/- ammonium biurate crystals in urine (this is a key one)
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15
Q

What abnormalities would you see in a PSS on blood profiles?

A

Abnormalities include:

  • Elevated serum bile acids (especially postprandial) •Hyperammonemia
  • +/- ammonium biurate crystals formation in alkaline urine Usually also:
  • Hypoalbuminemia
  • Decreased BUN
  • +/- hypoglycemia
  • +/- hypocholesterolemia
  • +/- hypoglobulinemia Liver enzymes are often normal or only mildly increased! Hematology: Microcytosis (small RBCs)
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16
Q

What are the types of an acquired portosystemic shunt and some examples, and the net cause?

A

–Prehepatic: Restricted blood flow through the portal vein

•Portal vein thrombosis, tumor, local abscess

–Intrahepatic: Restricted blood flow through the sinusods •Hepatic fibrosis

–Posthepatic: restricted blood flow through the hepatic vein/caudal vena cava

•Rt.-sided heart failure, vena cava syndrome, Increased blood pressure in portal vascular system

17
Q

What lab results can help to distinguish congenital from acquired shunts?

A

need pic

18
Q

what are 2 vascular anomalies that “may” produce portal hypertension?

A

•1) Portal vein hypoplasia (microvascular dysplasia) –Abnormally small portal vein in intrahepatic or extrahepatic sites leads to inadequate portal perfusion of the liver –Produces the same histologic image as porto-systemic shunt •2) Arterioportal shunts (anastomoses) –Abnormal connections between hepatic veins and hepatic arteries. Congenital. –Reverse flow in the portal vein can occur in severe cases most cause portal hypertension

19
Q

why would you not see ascites with a congenital PSS?

A

you have a single large vein that bypasses the liver, and thus no portal hypertension = no ascites

20
Q

what is Telangiectasis

A

a condition characterized by dilation of the capillaries, which causes them to appear as small red or purple clusters, often spidery in appearance, on the skin or the surface of an organ –Common in feedlot cattle. Also in older cats –No clinical significance

21
Q

what is tension lipidosis

A

–Localized area of diminished liver perfusion in areas adjacent to site of ligament attachments

22
Q

what is Glucocorticoid-induced hepatocellular degeneration (steroid hepatopathy)

A

this is VERY COMMON •Glucose is normally stored within hepatocytes as glycogen •Excessive hepatic accumulation of glycogen occurs with metabolic perturbations involving glucose regulation (e.g. diabetes mellitus, glycogen storage diseases) •Most common causes: •Endogenous glucocorticoids (Cushing’s disease) •Exogenous administration of glucocorticoids (prednisone, Dexamethasone..) •Gross: Pale and enlarged liver •Micro: Swelling of hepatocytes - engorgement with glycogen.