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VTS ECC 2024 > Hepatobiliary/Pancreas > Flashcards

Hepatobiliary/Pancreas Flashcards

1
Q

Liver is responsible to produce

A

–Bile acids/salts = help absorb lipids and bilirubin

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2
Q

Bilirubin is considered

A

Waste from RBC’s after being destroyed by splenic macrophages

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3
Q

Liver Functions:

#3

A
  1. Metabolism
  2. Detoxification
  3. Synthesis of plasma proteins/cholesterol/coag factors
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4
Q

Fat Soluable Vitamins

A

K.E.D.A
– GI, Liver and Pancreas work intangent to absorb fat soluable vitamins and fat
–If any portion malfunctions → malabsorption occurs → eliminated thru stool

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5
Q

Liver Anatomy

A

–2 surfaces: diaphragmatic surface + Visceral surface
–Falciform ligament → attaches liver to diaphragm
–6 lobes LLat/Lmedial/Quadrate/Rmedial/RLat caudate lobes

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6
Q

Where is gallbladder located?

A

Between quadrate and R medial liver Lobes

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7
Q

Hepatic circulation

A

–Portal vein = 75-80% of blood supply
– Hepatic Artery 20-25% of supply
–Processes blood from GIT via Hepatic Portal vein
–Hepatic Artery (celiac artery branch) supplies blood to liver
–Ciruclation travels from peripheral lobules → interior → sinusoids → larger fenestrations of sinusoids in endothelial cells
–Blood from sinusoids leave each lobule via central vein and ultimately thru hepatic vein

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8
Q

Hepatocytes

A

–located inside sinusoids and come into contact w/ blood
–large pores allow large molecules (protiens etc) made by hepatocytes to enter blood circulation

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9
Q

Kupffer Cells

A

Macrophages in the liver that engulf foreign substances

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10
Q

Canaliculi

A

Bile Ductules located between each hepatocyte
–empty into large bile ductules → ultimately empty into bile duct @ triad → CBD empties directly into duodenum

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11
Q

Functions of Bile

#2

A

–necessary for lipid digestion intestines
–transport hemoglobin for excretion

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12
Q

Sphnicter of Oddi

A

Controls bile duct entrance into duoedenum

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13
Q

CCK’s role in gallbladder function

A

CCK released from duodenum mucosa → stimulates contraction of gallbladder or relaxation after fatty meals

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14
Q

Bilirubin Excretion Pathway

#6

A

–RBCs broken down via extravascular hemolysis
–removed via mononuclear phagocytic system in Liver/spleen/bone marrow/lungs/ lymph nodes
–Macrophages consumed RBCs causing them to rupture -> release hemoglobin via hemolysis
–Hb broken down into heme + globin
–Heme converted to Biliverdin (green pigment)
–Biliverdin converted to Free or Unconjugated bilirubin

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15
Q

Unconjugated vs conjugated Bilirubin

A

–Unconjugated: enters bloodstream → combines with albumin → goes to liver for absorption
–Conjugated : → released into bile and ultimately enters SI
–Fecal bacteria reduce bilirubin → urobilirubin to give feces/urine color

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16
Q

Carbohydrate breakdown process via Liver

A

Monosaccharides = glucose/fructose/galactose → glucose metabolized to produce ATP via Glycolysis
–Fructose/Galactose converted too glucose by liver for energy

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17
Q

Glycogen

A

Stored glucose in liver/skeletal muscles
–excess stored in fat

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18
Q

Glycogenolysis

A

Process to break down glycogen into glucose monomers for glucose use in post absorptive state (between meals)

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19
Q

Gluconeogenesis

A

Synthesis of Glucose from NONcarb sources → to provide glucose when levels decline
–utilizes pyruvate (from AA breakdown of proteins), lactate, glycerol

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20
Q

Triglycerides

A

Lipids used for energy when glucose not readily available
–Glycerol created and converted into glucose via Glyconeogenesis

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21
Q

Fatty Acid Metabolism

A

FA end up as Ketones with excessive FA metabolization
–overwhelms oxidative capability of Liver to convert FA to energy
–Too many ketones build up if not used

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22
Q

Protein Production via Liver

A

Liver responsible for nearly all plasma protein synthesis
–Alb and clotting proteins
–Converts AA into ketoacids → used by liver for energy production or glucose/FA
–Degraded AA = ammonia = converted by hepatocytes to Urea→ excreted by kidneys

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23
Q

Glucose/Na+ Diffusion gradient

A

–Glucose reliant on gradient created by Na+ for intracellular movement
–Glucose w/i enterocyte = unfavorable gradient and prevents glucose entering enterocyte
–Na+/K+ pump in enterocyte x3 Na+ OUT and x2 K+ ions IN → lowers Na+ gradient inside cell
– creates gradient that favors Na+ movement from GIT into enterocyte
–Na+ moves into cell = glucose moves by Co-transport w/ Na+

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24
Q

Pancreatic Endocrine functions

#2

A

Islets = secrete different hormones
– Beta cells = insulin
–Alpha cells = glucagon (increase BG via glucogenesis)
– delta cells = somatostatin inhibits the secretion of insulin and glucagon, as well as GH, and diminishes the activity of the GIT

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25
Q

Pancreatic Exocrine functions

#3

A

Acini groups = release secretions into lumen → duodenum
–Lipase = breaks down lipids into FFA and monoglycerides
– Proteases = breaks down proteins into AA
– Amylase = breaks down starches into maltose

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26
Q

What stimulates Pancreatic cell receptors?

#3

A

Acetylcholine
CCK
Secretin

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27
Q

Relation between Intestinal digestion and Pancreatic enzymes

A

Intestinal phase of digestion has neural and endocrine stimulus to increase pancrease secretions

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28
Q

EPI

A

Exocrine pancreatic Insufficiency
–Results from diminshed/reduced production of exocrine proteolytic enzymes
–Pancreatic atrophy/chronic pancreatitis

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29
Q

Role of CCK with pancreatic proenzymes

A

CCK stimulates duodenal mucosal cells to serete enteropeptidase in duodenal lumen -> enteropeptidase activates trypsinogen to trypsin -> activates other proenzymes release by pancreas

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30
Q

Cholecytitis types

What can cause it? #4

A
  1. Neutrophilic
  2. Lymphoplasmacytic, follicular

caused by infection/duct obstruction/trauma/systemic dz

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31
Q

Clin Path of Cholecystitis

A

Consistent with hepatobiliary dz
– elevated ALT/AST/AlkPhos/GGT
–Tbili/cholesterol
Inflammatory leukogram -> leukocytosis/Neutrophilia

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32
Q

Infection Agents with Cholecystitis

A

E.coli
Clostridium
–Can cause Emphysematous cholecystitis

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33
Q

Which breed is prone to bacterial Cholecystitis

A

Dachshunds

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34
Q

Choleliths composition

A

Calcium carbonate
bilirubin pigments

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35
Q

Gallbladder mucocele causes:

A

combination of mucin production/↓ GB motility
–dyslipidemias
–glycocorticoid excess
–hyperadrenocorticism

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36
Q

Hepatitis

A

inflammation cell infiltrates w/i hepatic parenchyma

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37
Q

Acute vs. Chronic hepatitis

A

Acute = combination of inflammation/hepatocellular apoptosis/necrosis
Chronic = presence of fibrosis with regenerative nodules + inflammatory infiltrate, apoptosis

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38
Q

Feline Cholangitis complex types

A
  1. Neutrophilic
  2. Lymphocytic
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39
Q

Neutrophilic Cholangitis in cats

what can this be associated with?

A

–Infiltration of neutrophils in intrahepatic bile ducts
– may be associated with IBD and pancreatitis in cats

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40
Q

Lymphocytic Cholangitis in cats

A

–Chronic form of dz with mixed inflammatory infiltrates
–small lymphoctyes/plasma cells
–bile duct hyperplasia

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41
Q

Role of Copper with Hepatitis

adverse efx of excess copper o

Causes/major mechanism for copper storage

A

–Excess hepatic chopper contributes to chronic hepatitis in dogs
–Related to excess dietary copper
–Biliary excretion major mechanism for maintaining copper homeostasis = any cause of cholestatsis = ↑ copper levels
–Excess copper damages hepatocytes by causing oxidative stress/cellular degeneration

Bedlington Terrier inherited defect with copper hepatic excretions

42
Q

Infectious K9 Hepatits

A

–Adenovirus type 1
–rare due to vaccine - but young unvaccinated dogs at risk
–corneal edema/anterior uveitis seen

43
Q

FIP

what causes it?

A

–caused by feline enteric coronavirus
–can affect any organ in the body
– lesions associated with neutrophil macrophages infiltration
–pyogranulomatous lesions noted on liver capsule

44
Q

Leptospirosis common serovars

A

L. icterohaemorrhagiae
L. canicola
L. pomona
L. hardjo
L. grippotyphosia

45
Q

Leptospirosis

CS seen

A

–acute renal failure +/- hepatic involvement
–pulmonary hemmorhage, uveitis, acute fever
–septicemia: bacterial seeding of liver 2nd to bacteremia via translocation

46
Q

Lepto Treatment

A

Penicillin for leptospiremic stage
Doxycycline for carrier stage

47
Q

Hepatic Failure

A

Acute = hepatocellular necrosis + fat accumulation, hepatocellular dropout
Chronic = hepatocellular necrosis but with fibrosis/inflammation/hyperplasia

48
Q

Difference between Acute Liver failure and Acute Liver Injury

A

ALI = hepatocellular damage + necrosis but maintains function
ALF = has compromised function

49
Q

Hepatic Encephalopathy

Compounds involved
Counsequences of HE

A

–Neurosynchiatric syndrome
–Typically occurs w/ more than 70% hepatic function lost
–Circulating compounds: ammonia/ aromatic AA/ endogenous benzos/ GABA/ Glutamine
– Impede neuronal/astrocyte function = cell swelling
–inhibits cell membrane pumps/ion channels
–elevation in intracellular Ca++
–Electrical activity depression
–Interference w/ oxidative metabolism

50
Q

3 Classifications of HE

A

Acute
Bypass
Chronic

51
Q

Toxic Affects of HE: Ammonia

#4

A

– Increases brain tryptophan/glutamine
– ↓ ATP availability
– ↑ excitability/glycolysis (causes sz)
–causes brain edema

Produced by GI flora; normally converted to Urea/Glutamine in Liver

52
Q

Toxic affects of HE: Bile Acids

A

–affects/alters cell membrane permeability
– BBB more permeable to HE toxins;
impaired cellular metabolism

53
Q

Toxic affects of HE: ↓ a-ketoglutaramate

A

Division from krebs cycle for ammonia detoxification; ↓ ATP availability

54
Q

Toxic Affects of HE: Endogenous Benzodiazepine

A

Neural inhibition; hyperpolarize neuronal membrane

55
Q

Toxic Affects of HE: False neurotransmitters

A

impairs norepi action ↓ ammonia detoxidication in brain urea cycle

56
Q

Toxic Affects of HE: GABA

A

Neural inhibition; ↑BBB permeability

57
Q

Toxic Affects of HE: Glutamine

A

Alters BBB AA transport

58
Q

Toxic Affects of HE: Manganese

A

Elevated levels seen with Hepatic failure/encephalopathy

59
Q

Toxic Affects of HE: Phenol

A

Synergistic w/ other toxins/ lowers cellular enzymes/ neurotoxic/hepatoxic

60
Q

Toxic Affects of HE: Tryptophan

A

Directyly neurotoxic/ increases serotinin levels

61
Q

Toxic Affects on Chronicity with HE

A

GABA and endogenous benzos surpass excitatory stimulus = coma/CNS depression

62
Q

Toxic Affects of Acute Liver Failure

A

Can lead to cerebral edema
– elevated ICP
– +/- brain herniation

63
Q

Metabolic derangements with HE

A

hypoglycemia
dehydration
hypoK+
Azotemia
Alkalemia

64
Q

Coagulation disorders with HE

#8

A

–decrease in facor synthesis
–increase in factor utilization
–decrease in factor turnover
–increase in fibrinolysis/thromboplastin release
–Dsyfibrinogenemia
–decrease plt #s/Function
–Vit K deficiency
–Increase production of anticoagulants

65
Q

Hypoglycemia see with HE

A

Liver crucial for body glucose regulation
–involved with glycogenesis, glycocenolysis, glycogen storage
–Euglycemia can still be maintained with 75% loss of liver parenchyma
–Once glycogen depleted → fat/muscle/body proteins used for ADP → creates negative nitrogen balance/decreased muscle mass

66
Q

Sepsis with Liver Failure

A

–Liver Exposed to many types of pathogens via portal blood flow/GI venous drainage
– Inhibition of metabolic activity of granulocytic cells/cell adhesion/chemotaxis
–Reduced # of Kupgger cells = allows pathogens to translocate from portal circulation to systemic circulation

67
Q

Pulmonary Edema with HE

A

–2nd to altered permeability of pulmonary capillaries
– result from hypoAlb, low colloid oncotic pressure and vasodilation

68
Q

O2 Extraction with HE

A

Lower in HE pts from tissue hypoxia
–lactic acidosis
–further exacerbated by hypoxemia = worsens cerebral dsyfunction = accelerated cerebral hypotension and edema

69
Q

Portal Hypertension with HE

A

2nd to Cirrohsis w/ chronic liver failure
–sinusoidal collapse blocks intrahepatic flow = increased protal pressure
–portal vein thrombosis

70
Q

CBC findings with HE

#5

A

–Target cells, acanthocytes, anisocytosis
–non-regen anemia = chronic dz, GI bleeding, PSS
–Regen anemia = blood loss from ulceration
–Leukocytosis OR Leukopenia = infx causes or bacterial translocation
–Consumptive thrombocytopenia = infx or immune causes

71
Q

Elevated ALT/AST

A

Leak from cells with cell membrane dysfunction

72
Q

ALT value

A

More liver specific with short half life 24-60hrs

73
Q

AST Value

A

Present in many Liver muscle RBCs

74
Q

ALP value

A

Many catalysts → bone, liver, steriod induced (dog only)
–Activity increases with cholestatic dz

75
Q

GGT value

A

Found in many tissues but biochemically measured ones located on membranes of hepatocyte canalicular cells and biliary epithelial cells
–useful for cholestatic dz diagnosis (more specific than ALP)

76
Q

When is Icterus visible?

A

Tbili 2.3-3.3 mg/dl

77
Q

What % of total proteins snythesized by liver

A

25%
–Albumin ONLY produced in liver

78
Q

What % of cholesterol is synthetized by liver?

A

50%
–hypocholecterolemia seen with liver dz

79
Q

UA sediment findings with Liver Failure

A

–Ammonium biurate crystals w/ protal systemic vascular anomalies
–Biliurbinemia seen with cats (dogs normally have small amount, cats DO NOT)

80
Q

Respiratory affects from HE

#2

A

– Centrally induced hyperventilation/respiratory alkalosis → Renal excretion of K+ excretion = worsening hypoK+ = exacerbated HE
– Hypocapnia = shifts CO2 intracellularly to extracellularly = ↑ intracellular pH/accelerating use of phosphate to phosphorylase glucose = hypoPhos = RBC hemolysis

81
Q

Diet managment for Hepatic Failure

A

Low aromatic amino acids (animal proteins)
–Milk/soy/vegetable proteins contain low AAA and high in branches chain AA
– Valine, Leucine, Isoleucine

82
Q

Nutriceutical therapy for Hepatic Failure

#3

A

SAME = hepatoprotective, antioxidant, antiinflammatory
VIT E = antioxidant minimizes lipid peroxidation of hepatocyte
Milk Thistle = antioxidant and free radical scavenger, slows hepatic collagen formation

83
Q

Liver Vascular Anatomy involved with Portal Hypertension

A

Portal vein = carries blood from GIT/gallbladder/pancreas/spleen TO liver

84
Q

Portal venous Pressure

A

Ohm’s Law P = Q x R
PVP = portal blood flow x intraheptic resistance

85
Q

Cause of Portal Hypertension

A

PH caused by ↑ resistance in portal
-pre, -intra - post hepatic circulation = ↑ portal blood flow
– ↑ resistance caused by hepatocyte damage = changes in hepatic architecture
→ fibrosis, microthrombi, regenerative nodules

86
Q

Sinussoidal Endothelial Cells

A

–Normally produce vasoactive substances to regulate sinosoidal resistance - vasodilatory and vasoconstrictive substances
–Endothelial Dsyfunction = impaired sinussoidal relaxation 2nd to overproduction of vasoconstrictors

87
Q

Hepatic Stellate cells

A

Store lipids and Vit A around sinusoids
–injury = HSCs to secrete inflammatory cytokine factors

88
Q

Sheer stress

A

Sheer stress in splanic vessels with vasodilator release = splanic arterial dilation → compensatory hyperdynamic circulatory state (↑ Cardiac index and ↓ systemic arterial resistance)

89
Q

RAAS effects with Portal Hypertension

A

– ↓ effect of circulating blood volume = RAAS/ADH activation
–Na+/H2O retention = ascites
– promotion of translocation of bacteria into portal system

90
Q

Classifications of Portal Hypertension

A

Prehepatic
Intrahepatic
Posthepatic

91
Q

Pre-hepatic Portal Hypertension

A

↑ resistance in extrahepatic portal vein
–result of intraluminal obstruction or extra compression
–Hepatic arteriovenous fistulas = PH due to arterial blood overloading portal venous system
– Congenital PSS

92
Q

Intra-hepatic Portal Hypertension

#3

A

↑ resistance in hepatic microcirulation
–presinusoidal → resistance in terminal intrahepatic protal vein tributaries
– sinusoidal → result of fibrotic hepatopathies
– post sinusoidal →veno-occlusive dz from endothelial damage and hepatoytes (toxins/chemo agents)

93
Q

Post-hepatic Portal Hypertension

A

Obstruction of larger hepatic veins
–post-hepatic vena cava or R atrium
– ↑ resistance in RA due to <3 failure/pericardial dz or pulmonary hypertension

Budd-Chiari syndrome

94
Q

Budd-Chiari Syndrome

A

Obstruction of hepatic outflow in caudal vena cava or large extrahepatic veins
– tumor, thrombosis, congenital fibrous webs causing compression (intra-luminal or extra-luminal)
– vena cava stenosis

95
Q

Diagnosis of Portal Hypertension

A

PVP via direct or indirect measurement
Direct = catheterization of protal vein, manometer or pressure transducer inserted
Indirect = angiographic balloon catheterization

96
Q

CBC findings with Portal Hypertension

A

Microcytosis w/ acquired portosystemic collaterals
–mild thrombocytopenia
–anemia

97
Q

Biochem findings with Portal Hypertension

A

Moderate - marked enzyme activity 2nd to necroinflammatory liver dz
–post-hepatic PH = mild - moderate elevated serum 2nd to hepatic necrosis or ischemia from congestion
–ammonia / total bile acids elevated with functional hepatic failure
–hyperbilirubinemia
– Intra-hepatic PH = ↓ Alb/Urea/Cholesterol

98
Q

Coag Findings with Portal Hypertension

A

Upregulation of pro and anti - coagulant factors
–platelets activated by damaged endothelium
→ intra or extra hepatic clot formation

99
Q

Peritoneal Fluid findings with Portal Hypertension

A

Protein content of ascites
– Pre-hepatic/pre sinusoidal = < 2.5 g/dl
Post-hepatic / sinusoidal = > 2.5g/dl

100
Q

Ascites 2nd to Portal Hypertension

A

Imbalances of Starlings Law; ↑ hydrostatic PVP drives fluid into interstitial space
–vasodilation in splanchnic activates RAAS/SNS = volume expansion ↑ hydrostatic pressure in portal vasculature

101
Q

HypoAlb 2nd to Portal Hypertension

A

Synthetic Dysfunction ↓ vascular colloid osmotic pressure = worsens ascites

102
Q
A

VTS ECC 2024 (17 decks)

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