Elimination & Detox 2: Circulatory Hepatopathology Flashcards
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
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
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
if the liver is STRANGULATED and LOSES OXYGEN, which enzymes should we expect to be elevated?
INDUCIBLE
- GGT
- ALP
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
LOBAR TORSION causes ____, which is UNCOMMON/COMMON
TORSION, COMMON
PSS is MORE common in ____ vs. ____
SA, LA
PELIOSIS HEPATIS is common in WHAT 2 SPECIES?
- CATS
- CATTLE
why are INFARCTS RARER in the liver? (2)
- DUAL BLOOD SUPPLY from SYSTEMIC (hepatic arteriole) & PORTAL VEIN
- SLOW VENOUS POOLING GOING THROUGHOUT ENTIRE LIVER
2 findings in this liver?
OVERALL?
- NICE SHARP LOBAR MARGINS
- HOMOGENOUS BROWN COLOR
OVERALL NORMAL!
what’s the MOST IMPORTANT finding we can report to a PATHOLOGIST about LIVER?
SIZE = IS IT ACROMEGALY OR MICROHEPATICA?
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
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
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
describe the PATHOLOGIC PROCESS occurring here
PASSIVE CONGESTION with RED-BLACK VENOUS BLOOD
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)
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)
name PATHOLOGY on histopath liver (3 words)
what are the red foci?
CHRONIC PASSIVE CONGESTION
RED = DEAD HEPATOCYTES with POOLED BLOOD IN SINUSOIDS
ID PATHOLOGY
LOBAR TORSION
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
MORE
2 ways in which an EXTRAHEPATIC PSS can manifest/connections?
- PORTAL VEIN –> GASTRIC VEIN –> VENA CAVA –> SYSTEMIC (PORTOCAVAL)
- 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?
- SMALL LOBULES
- HEPATIC ARTERIOLAR HYPERPLASIA (compensatory for lack of blood flow)
- 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
- BRIDGING FIBROSIS
- NODULAR REGENERATION
- 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)
- if ACQUIRED from CIRRHOSIS, then can see MULTIPLE, SMALL TORTUOUS ACQUIRED PORTOSYSTEMIC SHUNTS from INCREASED PORTAL HYPERTENSION
- ASCITES
why can we see ASCITES in liver dz? (2)
overall, indicates a ____ PSS
- due to PORTAL HYPERTENSION
- 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?
- MICROVASCULAR DYSPLASIA
- 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
