Elimination & Detox 2: Circulatory Hepatopathology Flashcards by Nellie O'Leary

majority of the PORTAL CIRCULATION comes from….

VENOUS DRAINAGE from CENTRAL VEIN in hepatocyte… (4)

MAJORITY of the blood flow to the liver comes from the ____ ____

majority of the PORTAL CIRCULATION comes from VENOUS DRAINAGE of SPLEEN/INTESTINES from SPLANCHNIC VEIN

VENOUS DRAINAGE from CENTRAL VEIN in hepatocyte…
1. CENTRAL VEIN
2. HEPATIC VEIN
3. CAUDAL VENA CAVA
4. RIGHT SIDE OF HEART

MAJORITY of the blood flow to the liver comes from the PORTAL VEIN

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HEPATOCELLULAR/CYTOSOLIC LIVER ENZYMES…

when do they appear? (2)

what 3 are they? list what SPECIES/WHERE they’re found in

include subs about 2 other CBC parameters that can be important

appear when there’s..
1. HEPATOCELLULAR INJURY
2. HEPATOCELLULAR STRESS

what 3 are they?
1. ALT = LIVER-SPECIFIC, DOG/CAT

AST = LIVER & MUSCLE, DOG/CAT

–> CK elevated = muscle or liver
–> ALT elevated = lliver
–> ALT & CK = BOTH

SDH = LARGE ANIMALS

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INDUCIBLE LIVER ENZYMES

when do they appear?

what are the 2?

appear via INCREASED PRODUCTION with CELL STRESS

what are the 2?
1. GGT
2. ALP

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if the liver is STRANGULATED and LOSES OXYGEN, which enzymes should we expect to be elevated?

INDUCIBLE

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COMMON or UNCOMMON? (1 is rare)

CONGESTION?

PORTAL THROMBI?

PSS/VASCULAR ANOMALIES?

PELIOSIS HEPATIS?

INFARCTION?

GALL BLADDER INFARCTS?

CONGESTION = COMMON

PORTAL THROMBI = UNCOMMON

PSS/VASCULAR ANOMALIES = COMMON

PELIOSIS HEPATIS = COMMON

INFARCTION = RARE

GALL BLADDER INFARCTS = UNCOMMON

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LOBAR TORSION causes ____, which is UNCOMMON/COMMON

TORSION, COMMON

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PSS is MORE common in ____ vs. ____

SA, LA

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PELIOSIS HEPATIS is common in WHAT 2 SPECIES?

CATS
CATTLE

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why are INFARCTS RARER in the liver? (2)

DUAL BLOOD SUPPLY from SYSTEMIC (hepatic arteriole) & PORTAL VEIN
SLOW VENOUS POOLING GOING THROUGHOUT ENTIRE LIVER

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2 findings in this liver?

OVERALL?

NICE SHARP LOBAR MARGINS
HOMOGENOUS BROWN COLOR

OVERALL NORMAL!

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what’s the MOST IMPORTANT finding we can report to a PATHOLOGIST about LIVER?

SIZE = IS IT ACROMEGALY OR MICROHEPATICA?

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HEPATIC CONGESTION

due to WHAT 2 things?

what do we see if it’s ACUTE? (2)

what do we see if it’s CHRONIC? (1)

due to…
1. RIGHT-SIDED HEART FAILURE
2. or OBSTRUCTION OF CAUDAL VENA CAVA

ACUTE?
1. DILATION OF CENTRAL VEINS
2. CENTRILOBULAR SINUSOIDS FILL WITH BLOOD

CHRONIC?
1. ATROPHY OF CENTRILBOULAR HEPATOCYTES –> FIBROSIS

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what happens to the LIVER if we have RIGHT-SIDED HEART DISEASE causing CAVAL PRESSURE? (5, including this as the first step)

RIGHT-SIDED HEART DISEASE causing INCREASED CAVAL PRESSURE
HEPATIC VEIN PRESSURE INCREASES
SINUSOIDS & VESSELS in liver get CONGESTED/SWOLLEN with BLOOD
blood is eventually DRAINED OF OXYGEN & NUTRIENTS
HEPATOCYTES DIE

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what DISEASE process is this?

what does it cause? (2)

DISEASE = VEGETATIVE BACTERIAL ENDOCARDITIS on HEART VALVES

causes…
1. RIGHT-SIDED HEART FAILURE
2. FLUID ACCUMULATION & INCREASED CAVAL PRESSURE

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describe the PATHOLOGIC PROCESS occurring here

PASSIVE CONGESTION with RED-BLACK VENOUS BLOOD

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what is the arrow pointing to?

what PATHOLOGY does this indicate/why?

arrow = FIBRIN TAGS

usually indicates PASSIVE CONGESTION from FIBRINOGEN PUSHING OUT OF LIVER (if not PERITONITIS)

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3 words to describe this PATHOLOGY? (& more common name)

3 findings?

CHRONIC PASSIVE CONGESTION (nutmeg liver)

3 findings?
1. DEATH OF HEPATOCYTES
2. CENTRILOBULAR FIBROSIS from CHRONIC INFLAMMATION
3. HEPATOCELLULAR VACUOLATION (reversible cell injury, turns yellow)

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name PATHOLOGY on histopath liver (3 words)

what are the red foci?

CHRONIC PASSIVE CONGESTION

RED = DEAD HEPATOCYTES with POOLED BLOOD IN SINUSOIDS

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ID PATHOLOGY

LOBAR TORSION

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what 3 pathologic processes in LOBAR TORSION?

common other Ddx?

tends to occur in WHICH LOBE & potentially why?

etiology?

3 things?
1. POOLING OF BLOOD

NECROSIS OF HEPATOCYTES from lack of fresh blood flow
ENLARGED/SWOLLEN SINGLE LIVER LOBE from injury

common Ddx = HEPATIC NEOPLASM/TUMOR

tends to occur in LEFT LATERAL LIVER LOBE, maybe due to LEFT COLLATERAL LATERAL LIGAMENT

IDIOPATHIC

what happens to a patient if we CUT OFF BLOOD SUPPLY TO PORTAL VEIN?

THE PATIENT WILL DIE! SPLEEN, INTESTINE & ABDOMINAL ORGANS DRAIN THROUGH PORTAL VEIN, so BLOOD CANNOT BE OXYGENATED BACK TO THE HEART

ID PATHOLOGY (blue outline)

chronicity?

PORTAL VEIN THROMBOSIS

more CHRONIC (fibrin)

ID PATHOLOGY

chronicity?

PORTAL VEIN THROMBOSIS

more ACUTE (less fibrin)

patients with a PORTAL VEIN THROMBOSIS often…

DIE SUDDENLY, usually with UNDERLYING LIKELIHOOD FOR DEVELOPING PORTAL VEIN THROMBOSIS

PORTOSYSTEMIC SHUNTS... = definition what 3 CBC findings are INCREASED? 2 kinds?

= VASCULAR CONNECTION between PORTAL and SYSTEMIC CIRCULATION so that the LIVER DOES NOT HAVE ABILITY TO FILTER PORTAL BLOOD COMING IN 3 CBCs INCREASED.. 1. BILE ACIDS 2. AMMONIA 3. BUN 2 kinds? 1. CONGENITAL 2. ACQUIRED

INTRAHEPATIC CONGENITAL PORTOSYSTEMIC SHUNTS are more common in = (1) EXTRAHEPATIC CONGENITAL PORTOSYSTEMIC SHUNTS are more common in = (3) PSS often leads to WHAT pathologic change? why?

INTRAHEPATIC = LARGE BREED DOGS EXTRAHEPATIC = 1. CATS 2. SMALL BREED DOGS 3. FERRETS PSS often leads to MICROHEPATICA/HYPOPLASIA because the liver is dependent on GROWTH FACTORS from the INTESTINE & PANCREAS

what kind of PSS is RARELY reported in LARGE animals?

EXTRAHEPATIC

TRUE/FALSE in PSS, there is NO BLOOD being sent into PORTAL VEIN

FALSE

why do INTRAHEPATIC PORTOSYSTEMIC SHUNTS occur?

= occurs because we have PATENT DUCTUS VENOSUS, where a vessel is ABNORMALLY PATENT & connecting the PORTAL VEIN to CAUDAL VENA CAVA

EXTRAHEPATIC PORTOSYSTEMIC SHUNTS are ___ COMMON than INTRAHEPATIC

2 ways in which an EXTRAHEPATIC PSS can manifest/connections?

1. PORTAL VEIN --> GASTRIC VEIN --> VENA CAVA --> SYSTEMIC (PORTOCAVAL) 2. PORTAL VEIN --> AZYGOUS VEIN --> SYSTEMIC (PORTOAZYGOUS)

what does the AZYGOUS vein drain? where is it located?

drains the SPINAL COLUMN, located at DORSAL ASPECT OF LIVER

what are the GROWTH FACTORS that the LIVER DEPENDS ON? & name where one of them comes from what 2 organs produce them?

GROWTH FACTORS... 1. EPITHELIAL GROWTH FACTOR 2. HEPATIC GROWTH FACTOR 3. INSULIN-LIKE GF 4. AMINO ACIDS 5. GLUCAGON & INSULIN (pancreas) 2 organs? 1. INTESTINES 2. PANCREAS

3 histologic findings for CONGENITAL PORTOSYSTEMIC SHUNT?

1. SMALL LOBULES 2. HEPATIC ARTERIOLAR HYPERPLASIA (compensatory for lack of blood flow) 3. BILE DUCT HYPERPLASIA (many growth factors in this area can cause this)

FOUR GENERAL CLINICAL SIGNS OF PSS? NEURO signs? (3) GI signs? (4) URINARY signs? (4)

GENERAL signs? 1. RUNTED 2. UNTHRIFTY 3. HYPOREXIA 4. MALAISE NEURO signs? 1. HEAD-PRESSING 2. DEPRESSION 3. ATAXIA GI signs? 1. V+ 2. D+ 3. ANOREXIA 4. PTYALISM (cats) URINARY signs? 1. DYSURIA (pain while urinating) 2. STRANGURIA (straining to urinate) 3. POLLAKURIA (frequent small urinations) 4. HEMATURIA (blood in urine)

HEPATOENCEPHALOPATHY.. often secondary to WHAT disease? why? what do we usually see POST-PRANDIAL?

often secondary to PSS, because AMMONIA FROM GI is NOT BEING CONVERTED TO NON-TOXIC UREA IN LIVER & ENTERS BRAIN can see BLINDNESS POST-PRANDIAL

describe LESION in these KIDNEYS what DISEASE can cause these? what DANGEROUS PATHOLOGY can this cause?

UROLITHIASIS (URATE STONES) in RENAL PELVIS PSS, AMMONIA is NOT PROCESSED so EXCRETING MORE URATES can cause OBSTRUCTION

CIRRHOSIS... = definition 3 pathognomonic findings on histo? what does this cause GROSSLY? usually causes SMALL/LARGE liver

= END-STAGE LIVER DZ 1. BRIDGING FIBROSIS 2. NODULAR REGENERATION 3. BILIARY HYPERPLASIA increases in PORTAL VENOUS PRESSURE because BLOOD CANNOT TRAVEL THROUGH, so PORTAL HYPERTENSION usually causes SMALL liver

how can we tell GROSSLY in between CONGENITAL & ACQUIRED shunt? (2)

1. if ACQUIRED from CIRRHOSIS, then can see MULTIPLE, SMALL TORTUOUS ACQUIRED PORTOSYSTEMIC SHUNTS from INCREASED PORTAL HYPERTENSION 2. ASCITES

why can we see ASCITES in liver dz? (2) overall, indicates a ____ PSS

1. due to PORTAL HYPERTENSION 2. HYPOALBUMINEMIA secondary to CIRRHOSIS (unable to make albumin from liver) indicates a ACQUIRED PSS

in ACQUIRED PSS, usually see SMALL VESSELS between WHAT 2 veins? why?

RENAL & PORTAL VEIN because THEY'RE IN CLOSE PROXIMITY

PRIMARY PORTAL VEIN HYPOPLASIA... = overall effect & how it works? clinical signs... can affect ___ lobe or the ___ liver

= REDUCES PORTAL BLOOD FLOW via CONGENITAL lack of PORTAL VENULES present clinical signs VARY from ASYMPTOMATIC to SEVERE with PORTAL HYPERTENSION can affect ONE lobe or the ENTIRE liver

2 ALTERNATIVE NAMES for PRIMARY PORTAL VEIN HYPOPLASIA?

1. MICROVASCULAR DYSPLASIA 2. NON-CIRRHOTIC PORTAL HYPERTENSION

PELIOSIS HEPATIS.. ___ finding in WHAT 2 species? what do we se GROSSLY? on BLOODWORK...

INCIDENTAL finding in... 1. CATTLE 2. CATS GROSSLY = see DILATED VESSELS throughout LIVER PARENCHYMA on BLOODWORK, NO FUNCTIONAL ABNORMALITIES (that's why it's INCIDENTAL)

ID DZ (2 names)

PELIOSIS HEPATIS TELANGIECTASIA

HEPATIC NECROSIS/INFARCTS in LIVER are how common? what PATHOGEN is it commonly associated with?

HEPATIC NECROSIS/INFARCTS = RARE PATHOGEN = CLOSTRIDIUM HEMOLYTICUM; causes HEPATIC NECROSIS

ID LESION & PATHOGEN

HEPATIC NECROSIS (infarct) PATHOGEN = CLOSTRIDIUM HEMOLYTICUM

ID LESION

BILIARY MUCOCELE

ID ORGAN & PATHOLOGY

GALL BLADDER INFARCT