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41 Cards in this Set
- Front
- Back
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Trace the path of bile from the cannaliculi of the hepatocytes to the duodenal sphincter of Oddi...
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Cannaliculi --> interlobular duct --> segmental ducts --> L or R hepatic duct --> common hepatic duct --> cystic duct ---> *GALLBLADDER* (storage) --> Common Bile duct ---> Duodenum!
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Bile is isotonic. What are the 2 secretory sources of bile (what does each source secrete and what is the function of these secretions?):
1. 1 thing 2 functions 2. several things - function covered later |
1. Ductal epithelial cells: Alkaline solution (25% of bile volume)
- appropriate pH for micelle formation & digestive enzyme function - feedback control of intestinal pH via secretin 2. Hepatocytes: primary juice - inorganic ions, lipids, bile acids, lecithin, cholesterol-micelles) - detoxified metabolites |
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What happens if there is too much cholesterol in the bile?
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If there is too much cholesterol can't form Micelles. Vesicles will form instead and these are unstable and will form cholesterol crystals
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Once conjugated, bilirubin must stay where? After arriving in the gut, bilirubin is de-conjugated by bacteria, then what 2 options does it have?
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Once conjugated bilirubin must stay in vessels (blood or duct). After de-conjugation in the gut bilirubin can get carried back to the liver (recycled) or it can be reduced to urobilinogen which is either peed out or fermented by bacteria into stercobilinogen and lost in the feces.
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What type of jaundice (pre, hepatic or post) is associated with the build-up of unconjugated bilirubin? What symptoms will you see in obstructive jaundice?
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Pre-hepatic jaundice is associated with the build-up of unconjugated bilirubin. In obstructive jaundice there will be urobilinogen in the urine, and a loss of stercobilinogens = pale stool b/c bile can’t get into gut!
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In the absorptive and post-absorptive states, what does the liver do with
a. Carbohydrates b. Fats |
In the absorptive state the live will do glycogenesis and lipogenesis (glucose/aa --> TG). In the post-absorptive state the liver will do glycogenolysis & gluconeogenesis (aa/lactate/pyruvate/glycerol --> glucose); and ketogenesis (FA --> ketones)
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In terms of proteins what are 3 anabolic functions of the liver? What are 2 catabolic functions?
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The liver is responsible for making albumin, hepatic enzymes and clotting factors (except factor 8 and VMF). It is responsible for the catabolism of ketoacids (energy during absorptive state) and for deamination aa → ketones + NH3 (converted to urea for excretion via kidneys).
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Why is plasma [albumin] not a good indicator of liver function?
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Albumin is not a good marker of liver function b/c it has a T½ of 21days, therefore levels won’t go down acutely.
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What are the hormone(s) of the absorptive and post-absorptive states?
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Insulin is the only hormone of the absorptive state. The post-absorptive state is governed by adrenaline, glucagon, cortisol, and GH.
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What are the 2 types of bile acids, where does each come from and what is the significance of each (ie what illness can they cause?)
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Primary BA are made by the liver and are converted to secondary BA by colonic bacteria. If you have no gallbladder then can’t control the amount of BA released this is bad b/c secondary BA irritate the epithelium and cause secretory diarrhea.
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What happens to bile acids in each of the following locations?
- liver - S. bowel - Distal ileum - Portal vein |
In the liver BA are synthesized and conjugated. In the SB, BA emulsify fat. BA are actively absorbed from the distal ileum and returned to the liver via the portal vein.
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Is bilirubin water soluble when it’s conjugated or not? In what form is bilirubin bound to albumin?
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Unconjugated bilirubin is tightly bound to albumin and lipid soluble. Conjugate bilirubin is water soluble.
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What are the 2 blood tests for hepatocellular integrity? Which is more specific?
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ALT and AST are found in hepatocytes (released when injured). ALT is in skeletal msk, AST in skeletal, cardiac msk and intestines. Thus AST is less specific but more sensitive (use to screen!)
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What are the 3 blood tests for biliary duct integrity?
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Alkaline Phos (ALP) – also in bone, intestine & placenta; GGT – not found in bone thfr use with above; 5’NT – only in liver. None of these are directly correlated with function – they are ONLY indicative of structure!
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What are the 3 blood tests for liver FUNCTION? Which is best for acute injury? Why?
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– Albumin: half life of 21 days therefore no good in acute damage
- Clotting Factors: will affect INR v. quickly b/c F7 has half life of ~ 7hrs. - Bilirubin: * conjugated: excretion across the canaliculi is the rate limiting step (only seen in advance disease) * unconjugated: increases d/t hemolysis, hematoma re-sorption, inherited inefficiency |
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One path to ascities is to block hepatic outflow and↑ sinusoidal pressure. What is another pathway?
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The body senses portal HTN and releases NO in response. This triggers arterial v.dilation = ↓ vascular resistance and ↓ effective arterial volume. The body then sees the ↓ volume and activates the RAAS system causing Na/H20 retention that leads to ascities.
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Every pt with cirrhosis must be screened for what?
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Every pt with cirrhosis MUST be screened for hepatocellular carcinoma.
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What are the 2 functional divisions of the exocrine pancreas? What does each produce?
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The exocrine pancreas is divided into the:
- Acinar cells: grape-like clusters that secrete pancreatic enzymes - Ductal cells: secretions solution rich in HCO3 (to neutralize chime, optimize enzyme activity and allow micelle formation) |
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The 3 phases of pancreatic secretion are cephalic, gastric and intestinal. What is happening in the cephalic phase?
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Cephalic phase = see food → send signal via vagal → signal stimulates a neuron to release Ach → enzyme secretion
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The 3 phases of pancreatic secretion are: cephalic, gastric and intestinal. What is happening during the intestinal phase?
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Intestinal phase:
-CCK = fat + digested proteins stimulate the I cells to release CCK → vagal afferent → vagal efferent → Ach → acinar cells secrete enzymes! -Secretin = stomach acid stims the S cells to release secretin → ductal cells to secrete HCO3 (actual effects of secretin are small – it x’s over to + CCK) |
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There are receptors for both secretin AND Ach in acinar and ductal cells. What is the different p-way activated by secretin and Ach and how do these p-ways interact?
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In acinar cells the secretin pway is weak and potentiates the ACh pway (vice-versa).
Secretin: G-proteins → ↑ cAMP → +PKA → HCO3 release ACh: IP3 → Ca+ release DAG → (along with above Ca+ release) → +PKC → Enzyme exocytosis! |
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What is the effect of alcohol on the pancreas?
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Alcohol will block apical exocytosis of enzymes from the pancreas leading to pancreatitis!
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What are 3 factors which will prevent acinar auto-digestion?
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20. 1. Enzymes are sorted into separate lysosomes and granules with reasonably high fidelity
2. Enzymes are made in their inactive form (can have a gene mutation = ↑autoactivation = ↑ intracellular activation = hereditary pancreatitis) 3. Antiproteases in granules, cytoplasm and some in blood |
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What is the effect of the CF mutation on the pancreas? Why is this a problem?
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Secretin → ↑ cAMP → activates CFTR → ↑ Cl- secretion → ↑ Na/H2O secretion (follows Cl-). But Cl sneaks back in the cell by exchanging for HCO3. Now cell has lost a –ve charge, wants to be neutral so will kick out a Na+. Water is dragged along. In CF there is less Cl- out and thfr less H20 out = plug = Ca+ stones = inflammation/fibrosis = necrosis/atrophy = exocrine insufficiency.
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When a pancreas is stimulated, what will happen to the concentration of Cl and HCO3 in the pancreatic secretions?
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In a stimulated pancreas the secretory [Cl] will go down and the [HCO3] will go up b/c the 2 are being exchanged.
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What 3 things will activate trypsinogen → trypsin?
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Autoactivation, enterokinase and cathpsin B (stored in lysosomes; if a lysosomes mixes with a granule you will get prematurely activated trypsin = pancreatitis!)
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Between which GI layers would you find Meissner's and Aubach's plexuses? Which is sensory and which is motor?
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Aubach's (motor) - lies between the longitudinal and circular musclar layers
Meissner's (sensory) lies between the circular muscle and the submucosa |
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What is an interstitial cell of Cajal?
(Where is if found / what does it do?) |
a pacemaker that triggers gut contraction.
Found in GI tract - they organize contractions into phasic ones that are the basis of peristalsis |
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What is the difference between a NM end plate and a Smooth muscle - nerve junction?
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A NM end plate has tight interdigitation between the nerve and the muscle. In a smooth muscle junction the nerve synapses with the ICC and THEN with the smooth muscle cell.
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The gut's nueral innervation consists of:
Extrinsic <--------> Intrinsic (2subtypes) (1subtype) What is the effect of each of the subtypes of nerves listed above? |
Extrinsic:
Symp = (F or F) ↓peristalsis and ↑sphincter tone Parasymp = ↑ peristalsis and ↓sphincter tone Intrinsic: Enteric nerves ---> ICC --> SMC NO - inhibitory (relaxation) ACh - excitatory (contraction) |
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What is a slow wave and where does it happen?
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Slow waves occur in the ICC's of the GI system. These cells have unstable resting membrane potentials that cycle thru depol & repol phases however not every depol = AP. Need temporal summation of waves to trigger a contraction.
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How is contraction of the GI myocytes triggered?
Why/how do contractile waves propagate in the GI tract? |
If you get enough "spike potentials" (Ca+ influx or intracellular release) then you will get contraction of the GI myocytes. Because the cells are connected with gap junctions, they function as a syncitium and will display synchronised and rhythmic contractions.
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Slow waves are omnipresent, producing weak contractions. From where do they originate? What does their frequency depend on?
What causes spike potentials? The force of contraction is proportional to what? |
Slow waves originate from Intersitial Cells of Cajal
- myenteric plexus of stomach & SI - submucosal plexus of colon Their frequence depends on their location in the bowel. Spike potentials are cause by Ca+ influx through L-type (voltage) Ca-channels. Force is proportional to frequency and amplitude of these spikes |
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What are some diseases associated with esophageal dysmotility?
1. Pharynx (2) 2. Esophageal Body (4 SADS) 3. LE sphincter (4 AGDS) |
1. CNS - dementia, stroke, parkinson's
2. Spasm, achalasia, DM, sclerodema (contractility problem) 3. Achalasia, DM, GERD, Sclerodema |
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What are the phases of esophageal peristalsis?
Primary Secondary tertiary |
Swallowing is VOLUNTARY
1 = swallowing-UES relaxation 2 = esophageal distention triggers autonomic response --> phasic contractions 3 = LES relaxes soon after swallowing and remains relaxed until peristalsis arrives |
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What happens (motor functions) in each of the follwoing gastric regions?
1. Fundus 2. Body & Antrum 3. Pylorus |
1. Fundus - vagal mediated relaxation and accomodation
2. Body & Antrum - trituration, mixing and grinding 3. Pylorus - antropyloric coordination to produce emptying |
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Peristalsis is autonomic/involuntary and can be manifest solely by the enteric nervous system. How does this work? Ie. what will local distention trigger?
What is the role of the longitudinal muscles in peristalsis? |
Local distention will trigger ascending excitation (ACh) = circular muscle contracts behind food
AND descending inhibition (NO) = muscles relaxed in front of food. Longitudinal muscles will contract in order to shorten the passage ahead of food. |
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What is a migrating motor complex?
What are the 3 phases? Why is phase 3 called the "housekeeping phase?" (3 reasons - not in notes) |
Waves of activity that sweep along the length of the intestinges, in a regular cycle during fasting.
1 = quiescent 2 = periods of peristalsis 3 = rapid, evenly spaced peristalsis (pylorus will stay open) Phase 3 serves "housekeeping purposes: - facilitate transportation of indigestible substances - transports bacteria from SI --> LI - inhibts the migration of colonic bacteria into the terminal ileum |
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What is the direction of slow wave propagation in the right, transverse and left colon?
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Right/ascending - waves move downwards
Transverse - waves move distally Left/descending - waves move downwards |
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What is the function of the right (ascending) colon?
What happens if a person has a right hemicolectomy? |
Absorption of water and electrolytes (has the highest amount of active transport).
R hemicolectomy = watery diarrhea |
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Motor dysfunction in the colon is broadly categorized into what 2 categories?
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Transit (colon) or outlet (rectum) problems.
1. Transit: medication, diet, neuropathy (DM), scleroderma, obstruction, Hirschsprung's, Chagas' disease) 2. Outlet: Hirschprung's, pelvic floor trauma, prolapse, enterocele, large rectocele, anal stenosis, rectal ulcer syndrome. |
