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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
Pancreatic Exocrine functions | #3
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
26
What stimulates Pancreatic cell receptors? | #3
Acetylcholine CCK Secretin
27
Relation between Intestinal digestion and Pancreatic enzymes
Intestinal phase of digestion has neural and endocrine stimulus to increase pancrease secretions
28
EPI
Exocrine pancreatic Insufficiency --Results from diminshed/reduced production of exocrine proteolytic enzymes --Pancreatic atrophy/chronic pancreatitis
29
Role of CCK with pancreatic proenzymes
CCK stimulates duodenal mucosal cells to serete enteropeptidase in duodenal lumen -> enteropeptidase activates trypsinogen to trypsin -> activates other proenzymes release by pancreas
30
Cholecytitis types | What can cause it? #4
1. Neutrophilic 2. Lymphoplasmacytic, follicular ## Footnote caused by infection/duct obstruction/trauma/systemic dz
31
Clin Path of Cholecystitis
Consistent with hepatobiliary dz -- elevated ALT/AST/AlkPhos/GGT --Tbili/cholesterol Inflammatory leukogram -> leukocytosis/Neutrophilia
32
Infection Agents with Cholecystitis
E.coli Clostridium --Can cause Emphysematous cholecystitis
33
Which breed is prone to bacterial Cholecystitis
Dachshunds
34
Choleliths composition
Calcium carbonate bilirubin pigments
35
Gallbladder mucocele causes:
combination of mucin production/↓ GB motility --dyslipidemias --glycocorticoid excess --hyperadrenocorticism
36
Hepatitis
inflammation cell infiltrates w/i hepatic parenchyma
37
Acute vs. Chronic hepatitis
Acute = combination of inflammation/hepatocellular apoptosis/necrosis Chronic = presence of fibrosis with regenerative nodules + inflammatory infiltrate, apoptosis
38
Feline Cholangitis complex types
1. Neutrophilic 2. Lymphocytic
39
Neutrophilic Cholangitis in cats ## Footnote what can this be associated with?
--Infiltration of neutrophils in intrahepatic bile ducts -- may be associated with IBD and pancreatitis in cats
40
Lymphocytic Cholangitis in cats
--Chronic form of dz with mixed inflammatory infiltrates --small lymphoctyes/plasma cells --bile duct hyperplasia
41
Role of Copper with Hepatitis adverse efx of excess copper o | Causes/major mechanism for copper storage
--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** ## Footnote Bedlington Terrier inherited defect with copper hepatic excretions
42
Infectious K9 Hepatits
--Adenovirus type 1 --rare due to vaccine - but young unvaccinated dogs at risk --corneal edema/anterior uveitis seen
43
FIP ## Footnote what causes it?
--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
Leptospirosis common serovars
L. icterohaemorrhagiae L. canicola L. pomona L. hardjo L. grippotyphosia
45
Leptospirosis | CS seen
--acute renal failure +/- hepatic involvement --pulmonary hemmorhage, uveitis, acute fever --septicemia: bacterial seeding of liver 2nd to bacteremia via translocation
46
Lepto Treatment
Penicillin for leptospiremic stage Doxycycline for carrier stage
47
Hepatic Failure
Acute = hepatocellular necrosis + fat accumulation, hepatocellular dropout Chronic = hepatocellular necrosis but with fibrosis/inflammation/hyperplasia
48
Difference between Acute Liver failure and Acute Liver Injury
ALI = hepatocellular damage + necrosis but maintains function ALF = has compromised function
49
Hepatic Encephalopathy | Compounds involved Counsequences of HE
--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
3 Classifications of HE
Acute Bypass Chronic
51
Toxic Affects of HE: Ammonia | #4
-- Increases brain tryptophan/glutamine -- ↓ ATP availability -- ↑ excitability/glycolysis (causes sz) --causes brain edema ## Footnote Produced by GI flora; normally converted to Urea/Glutamine in Liver
52
Toxic affects of HE: Bile Acids
--affects/alters cell membrane permeability -- BBB more permeable to HE toxins; impaired cellular metabolism
53
Toxic affects of HE: ↓ a-ketoglutaramate
Division from krebs cycle for ammonia detoxification; ↓ ATP availability
54
Toxic Affects of HE: Endogenous Benzodiazepine
Neural inhibition; hyperpolarize neuronal membrane
55
Toxic Affects of HE: False neurotransmitters
impairs norepi action ↓ ammonia detoxidication in brain urea cycle
56
Toxic Affects of HE: GABA
Neural inhibition; ↑BBB permeability
57
Toxic Affects of HE: Glutamine
Alters BBB AA transport
58
Toxic Affects of HE: Manganese
Elevated levels seen with Hepatic failure/encephalopathy
59
Toxic Affects of HE: Phenol
Synergistic w/ other toxins/ lowers cellular enzymes/ neurotoxic/hepatoxic
60
Toxic Affects of HE: Tryptophan
Directyly neurotoxic/ increases serotinin levels
61
Toxic Affects on Chronicity with HE
GABA and endogenous benzos surpass excitatory stimulus = coma/CNS depression
62
Toxic Affects of Acute Liver Failure
Can lead to cerebral edema -- elevated ICP -- +/- brain herniation
63
Metabolic derangements with HE
hypoglycemia dehydration hypoK+ Azotemia Alkalemia
64
Coagulation disorders with HE | #8
--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
Hypoglycemia see with HE
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
Sepsis with Liver Failure
--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
Pulmonary Edema with HE
--2nd to **altered permeability of pulmonary capillaries** -- result from **hypoAlb, low colloid oncotic pressure and vasodilation**
68
O2 Extraction with HE
Lower in HE pts from tissue hypoxia --lactic acidosis --further exacerbated by hypoxemia = worsens cerebral dsyfunction = accelerated cerebral hypotension and edema
69
Portal Hypertension with HE
2nd to Cirrohsis w/ **chronic liver failure** --sinusoidal collapse blocks intrahepatic flow = increased protal pressure --portal vein thrombosis
70
CBC findings with HE | #5
--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
Elevated ALT/AST
Leak from cells with cell membrane dysfunction
72
ALT value
More liver specific with short half life 24-60hrs
73
AST Value
Present in many Liver muscle RBCs
74
ALP value
Many catalysts → bone, liver, steriod induced (dog only) --Activity increases with cholestatic dz
75
GGT value
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
When is Icterus visible?
Tbili 2.3-3.3 mg/dl
77
What % of total proteins snythesized by liver
25% --Albumin ONLY produced in liver
78
What % of cholesterol is synthetized by liver?
50% --hypocholecterolemia seen with liver dz
79
UA sediment findings with Liver Failure
--Ammonium biurate crystals w/ protal systemic vascular anomalies --Biliurbinemia seen with cats (dogs normally have small amount, cats DO NOT)
80
Respiratory affects from HE | #2
-- 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
Diet managment for Hepatic Failure
Low aromatic amino acids (animal proteins) --Milk/soy/vegetable proteins contain low AAA and high in branches chain AA -- **Valine, Leucine, Isoleucine**
82
Nutriceutical therapy for Hepatic Failure | #3
SAME = hepatoprotective, antioxidant, antiinflammatory VIT E = antioxidant minimizes lipid peroxidation of hepatocyte Milk Thistle = antioxidant and free radical scavenger, slows hepatic collagen formation
83
Liver Vascular Anatomy involved with Portal Hypertension
Portal vein = carries blood from GIT/gallbladder/pancreas/spleen TO liver
84
Portal venous Pressure
Ohm's Law P = Q x R PVP = portal blood flow x intraheptic resistance
85
Cause of Portal Hypertension
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
Sinussoidal Endothelial Cells
--Normally produce vasoactive substances to regulate sinosoidal resistance - vasodilatory and vasoconstrictive substances --Endothelial Dsyfunction = impaired sinussoidal relaxation 2nd to overproduction of vasoconstrictors
87
Hepatic Stellate cells
Store lipids and Vit A around sinusoids --injury = HSCs to secrete inflammatory cytokine factors
88
Sheer stress
Sheer stress in splanic vessels with vasodilator release = splanic arterial dilation → compensatory hyperdynamic circulatory state (↑ Cardiac index and ↓ systemic arterial resistance)
89
RAAS effects with Portal Hypertension
-- ↓ effect of circulating blood volume = RAAS/ADH activation --Na+/H2O retention = ascites -- promotion of translocation of bacteria into portal system
90
Classifications of Portal Hypertension
Prehepatic Intrahepatic Posthepatic
91
Pre-hepatic Portal Hypertension
↑ 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
Intra-hepatic Portal Hypertension | #3
↑ 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
Post-hepatic Portal Hypertension
Obstruction of larger hepatic veins --post-hepatic vena cava or R atrium -- ↑ resistance in RA due to <3 failure/pericardial dz or pulmonary hypertension ## Footnote Budd-Chiari syndrome
94
Budd-Chiari Syndrome
**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
Diagnosis of Portal Hypertension
PVP via direct or indirect measurement Direct = catheterization of protal vein, manometer or pressure transducer inserted Indirect = angiographic balloon catheterization
96
CBC findings with Portal Hypertension
Microcytosis w/ acquired portosystemic collaterals --mild thrombocytopenia --anemia
97
Biochem findings with Portal Hypertension
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
Coag Findings with Portal Hypertension
Upregulation of pro and anti - coagulant factors --platelets activated by damaged endothelium → intra or extra hepatic clot formation
99
Peritoneal Fluid findings with Portal Hypertension
Protein content of ascites -- Pre-hepatic/pre sinusoidal = < 2.5 g/dl Post-hepatic / sinusoidal = > 2.5g/dl
100
Ascites 2nd to Portal Hypertension
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
HypoAlb 2nd to Portal Hypertension
Synthetic Dysfunction ↓ vascular colloid osmotic pressure = worsens ascites
102

VTS ECC 2024 (17 decks)

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