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GI Final 3
Spears and Carvalho Cirrhosis
| Question | Answer |
|---|---|
| Cirrhosis is? | chronic fibrosis of the liver that impairs Hepatocyte function |
| Cirrhosis is typically caused by ______ or ______ | alcoholism; Hepatitis |
| Treatment for cirrhosis is to help manage? | variceal bleeding, Ascites, Hepatorenal syndrome, or Hepatoencephalopathy (HE) *last line (liver transplant) |
| Liver disease types include? | Hepatitis C virus (HCV); Alcohol-related liver disease (ALRD); Non-alcoholic fatty liver disease (NAFLD)/Nonalcoholic steatohepatitis (NASH) |
| Cirrhosis Pathophysiology--> is the hepatic parenhymal fibrosis that results from chronic inflammation or ______ _____ | hepatotoxic insult |
| What are the 4 complications of Cirrhois? | Ascites, Portal Hypertension/Variceal bleeding, Hepatorenal Syndrome, Hepatic encephalopathy |
| General things that occur with cirrhosis you can see is? | decreased cardiac output, increase in inflammatory responses and also increase in renal constriction and lead to injury on the kidney |
| Splanchnic Circulation System--> associate this as the? | blood flow that regulates our internal organs and how that blood flow will come from the stomach, spleen, pancreas, small intestine, and colon and flow through the portal vein where it hits the liver for filtration |
| In a cirrhotic liver, we will have scar tissue and the ultimate thing is increased _______ | resistance from the portal vein that's met because of that cirrhotic tissue |
| We will have increased resistance from blood flow contributing to that rise in portal vein _______/rupture & bleeding of Esophagus Varices | pressure *portal vein HTN will cause variceal bleeding |
| Major medications for cirrhosis is trying to control that portal vein hypertension we will use what agents? | Beta blockers as well as Somatostatin Analog |
| Beta blockers for the tx of increased portal vein/pressure/ rupture & bleeding of esophagus varicies include? | Propanolol (Inderal); Nadolol (Corgard) |
| Somatostatin Analog for the tx of increased portal vein/pressure/ rupture & bleeding of esophagus varicies include? | Octreotide (Sandostatin) |
| MOA of Beta Blockers (Propanolol and Nadolol are? Uses are? | Non-selective B-AR antagonists; decreased Cardiac Output (B1); decreased Splanchnic blood flow (B2); as well as for CV function and HTN |
| MOA for Somatostatin Analog Octreotide (Sandostatin) is? | Cyclic oligopeptide analog of Somatostatin |
| Uses for Somatostatin Analog Octreotide (Sandostatin) is? | increase Splanchnic vasoconstriction; decrease Vasodilatory GI peptides; decrease blood flow and portal pressure; as well as anti-diarrheal |
| We want to use Octreotide and our BB to try to reduce the ____ ____ going into the internal organs which can then have a downstream effect of helping to reduce the pressure going through the portal vein because of the increased resistance in the liver | blood flow |
| Somatostatin Analog (Octreotide Sandostatin) 1/2 life is? | 1-2h |
| Why are non-selective B-blockers used and not selective B-blockers? | bc you want to cut everything that could increase pressure in the liver (cut down on both CO and the flow through the arteries and veins that feed into the liver |
| Why does propranolol undergo extensive first-pass metabolism and nadolol does not? | difference in logP; Nadolol has 2 -OH groups (its already hydroxylated); so that's why Propranolol is highly metabolized whereas Nadolol is already metabolized |
| What structural features makes Propranolol and nadolol log P values different | the presence of that Diol makes it more soluble in water |
| When would Nadolol be preferred over Propranolol? | advantage of one being more water soluble (don't want it to cross that BBB; so if you want something that doesn't cross the BBB then use Nadolol |
| How does Octreotide work? looks like Somatostatin and acts the same way. Difference is that somatostatin is ______ ______ in the body (short 1/2 life). They make the change with "D" which is a? | rapidly destroyed; non-natural amino acid *Body works with L amino acids making these D amino acids having a Longer 1/2 life (1-2H and the key are the D amino acids are not recognized) |
| Ascites is? | fluid build-up in the abdomen |
| We have 3 medications for the tx of Ascites which are? | Spiranolactone (Aldcatone); Furosemide (Lasix); Midodrine (Amatine which is a Alpha-1 agonist) |
| MOA and use of Spironolactone (Aldactone) is? | MR antagonist; AR antagonist; PR agonist; Use: K+ sparing diuretic; tx of aldosteronism and hyperandrogenism |
| Why does Spironolactone (Aldactone) cause Gynecomastia? | due to that change in its receptor in activity and having stimulation of those progesterone receptors |
| MOA and use of Furosemide (Lasix) is? | NKCC2 (Na-K-Cl)-cotransporter inhibitor *loop diuretic |
| MOA and use of the alpha-1 agonist Midodrine (Amatine) is? | Active metabolite desglymidodrine agonist at a1-AR *increases renal plasma flow, Urinary Na+ excretion and can be used for Refractory ascites as well as for orthostatic hypotension |
| AE of Midodrine (Amantine) are | CV: Supine hypertension; CNS: Paresthesia "pins and needles"; Renal: polyuria; Dermatologic: itch |
| Spiranolactone has a rapid ____ ______ metabolism which will transform it into its more active metabolite ______ | first-pass; Canrenone *its a prodrug |
| Med-Chem Midodrine-->ADME? | it has poor permeability into the BBB |
| Why do we combine these 2 diuretics (Spiranolactone and Furosemide) | you want one that keeps K+ and the other that kicks away the Na+ -don't want the person to go into hyperkalemia so counterbalance that loss of K+ |
| Hepatorenal Syndrome (HRS) is? treatment options are? | Kidney injury from advanced liver disease; -Midodrine (Amantine); Octreotide (Sandostatin); and Albumin (Blood product derivative) |
| MOA of Albumin? | Increases plasma volume, Its a Colloid *it will take advantage of concentration gradients and help move water from outside of the blood vessels into the blood vessels |
| Uses of Albumin? Interactions? | increases oncotic pressure (moves fluids from intestinal to intravascular space (into the blood capillaries) -Interactions can be treating Hypoalbuminemia but to fix the issue with the increased vasodilation that can come from hepatorenal syndrome and the consequential constriction that can come to renal vessels |
| 1. Hepatorenal syndrome (HRS) pathophysiology its caused due to the increase in _________ liver, an increase in portal vein _______, an increase in _____ | cirrhotic; hypertension; ascites |
| 2. HRS: one of the responses is an increase in _______ factors | vasodilatory *will see an increase in prostaglandin release, increases in nitric oxide and one of the body's reaction to that is to increase the release of the RAAS--> causing renal vasal constriction |
| 3. So you have vasodilation of the _______ vessels which come from the other internal organs in the presence of ___________ of the renal tissue which overtime leads to severe renal damage | splanchnic; vasoconstriction *use of medications to create a balance in that effect of reducing splanchnic vasodilation and also preventing vasoconstriction of the renal vessels |
| Major reason we need to supplement albumin is because the liver is SHOT but too much supplementation leads to? | Albuminemia (excreted in the urine means that the kidney is not working |
| What is Hepatic Encephalopathy? | brain dysfunction from advanced liver disease *we get an increase in toxic factors that are circulating due to the poor function of the liver and those toxic factors can make it into the brain and potentially cause brain damage |
| What medications do we use for Hepatic Encephalopathy? | Lactulose (Chronulac) and Rifaximin (Xifaxan) |
| MOA of Lactulose? (remember its also a osmotic laxative) | Decrease plasma NH4+(ammonia) levels to lower extent of portal encephalopathy; |
| Uses of Lactulose (Chronulac)? | Hepatic Encephalopathy prevention or tx; Constipation |
| MOA of Rifaximin (Xifaxan)? | inhibits bacterial DNA-dependent RNA polymerase and RNA synthesis *decreases protein-metabolizing bacteria in GI (less formation of NH4+) |
| Use of Rixaximin (Xifaxan) | HE prevention and treatment (off-label for tx); and for IBS-D *wide spectrum abx agent |
| Med-Chem: Lactulose metabolism requires ____ _____ for drug activation | colonic flora (converting lactulose into lactic acid--> forming ammonium lactate which is now ionic and not going back |
| Med-Chem: Note about Rifaximin (Xifaxan): Derivative of ansamycins); and has BBW? | chelation properties with metals and need to avoid antacids; -similar with FQ (napthalinic ring (2 benzene rings glued with O2--> ideal format (electronic and sterically to chelate or bind metals Mg2+, Ca2+ causing interference when in circulation |
| Lactulose degradation by bacteria releases _____ _____ which reacts with NH4+ and once NH4+ gets ionized by the lactic acid it cannot and gets _______ | lactic acid; expelled |
| For Venous high pressure and bleeding, we use non-selective BB for? | used to both decrease CO and portal blood flow |
| For Venous high pressure and bleeding, we use Nadolol because? | its more hydrophilic because of the diol in its structure. less metabolized due to steric factor and bc it already is a metabolite |
| For Venous high pressure and bleeding, we use Octreotide because? | decreases portal blood flow and has D-aminio acids in its structure |
| For Fluid Build up, we use Spironolactone because? | its a K+ sparing diuretic; Antagonist of testosterone (androgens) and agonist of progesterone; Antagonist of aldosterone |
| For Fluid Build up, we use Furosemide because? | its a diuretic and helps to drain excess fluid |
| For accumulation of toxins in the blood stream, we use Lactulose because? | softens stool and increases bowel movements and is fermented by bacteria releasing acids that trap and excrete ammonia in the feces |
| For accumulation of toxins in the blood stream, we use Rifaximin because? | it kills protein-metabolizing bacteria, decreasing the amount of toxic waste products |
| For Hepatorenal syndrome, we use Midodrine and Octreotide because? | helps reduce ascites and portal vein hypertension |
| For Hepatorenal syndrome, we use Albumin because? | its a large plasma colloid that increases oncotic pressure to keep water in the blood vessels |
Created by:
Xander635
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