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GI Final 3
Long Cirrhosis
| Question | Answer |
|---|---|
| What is Cirrhosis? | late phase of fibrosis of the liver in which the structural components are altered and regenerative nodules develop |
| What is decompensated Cirrhosis? | presence of at least one complication of the disease |
| Chronic liver disease and cirrhosis are a leading | cause of death both in the United States and in Texas |
| Cirrhosis is a risk factor for | hepatocellular carcinoma (HCC) |
| The top causes of cirrhosis (liver disease) that are the most important to know are? | Alcohol (6-8 drinks per day), viral infections, and MASH (MASLD) aka fatty liver disease |
| Why is Hep B not prevalent in the US? | We have a vaccine for Hepatitis B. would see it for someone that comes to the US |
| Other causes of Liver disease are? | Genetic disorders, autoimmune disease, Cryptogenic, and medications (acetaminophen, amoxicillin, isoniazid (TB), and METHOTREXATE) |
| In a healthy (non-cirrhotic liver), the portal blood flow is under ____ ______ | low pressure (holes in b/w the cells) exchange where toxins are removed from the body. *think of it being a sponge |
| In cirrhosis, we have ______ or scarring | fibrosis *fibrosis is like a hard shell on the outside which prevents slooth blood flow through the perforations |
| 1. Pathophysiology--> what happens is, if there is fibrous tissue (liver cells are dying, causing fibrosis or scarring) this will _______ the pressure that results in liver blood flow changes. | increase |
| 2. So if there's this fibrosis or this shell, it blocks the water of the blood from going that way and therefore the blood has to find another way of going, this is what causes the? | complications of cirrhosis *the fibrosis that is causing pressure |
| Fibrosis tissue leads to increase in portal pressure leading to liver blood flow changes and lastly to? | cirrhosis and complications |
| what are the 4 major functions of the liver? | -Digestion (bile production and fat absorption, no vitamins); -Metabolism/Excretion (glucose (package as glycogen), bilirubin, hormones, fat); -Detoxification (chemicals, medications), -Proteins synthesis (*albumin, produces blood clotting factors, globulin, enzymes) |
| Patients that present with cirrhosis can look very different. Biggest effect we see are? | yellowing of the eye (Jaundice, show up in the whites of your eyes and extend throughout their skin); we also see Spider-angiomata (swollen blood vessels close to the skin); (see big-hard belly called ascites); itching from bile salts under the skin; muscle changes; edema but very variable |
| Yellowing (jaundice) is from the build up of? | bilirubin *liver helps to process it out, but will build up in the body) |
| Cirrhosis is chronic and _______ | progressive *continues to progress until they die |
| Clinical presentations: Laboratory manifestations that we see are? | increased (aspartate transaminASE (AST); Alanine transaminASE (ALT) these are your LFTs; others that go up are Alkaline phosphatase and Gamma glutamyl transpeptidase |
| LFT's are released from hepatocytes (liver cells) when those liver cells __. As your liver dies, these cells burst releasing the enzymes and therefore the amount in the blood goes _____. However at the very end of cirrhosis, these LFT's will go ____ | die; UP; DOWN *down since there are no more cells left to burst (so a steady increase and dramatic drop) |
| Clincial presentation of laboratory manifestations in cirrhosis: Bilirubin? Albumin? INR/Prothrombin time? Platelets? | UP; Down (because its made by the liver); UP (bc your not making clotting factors); Down |
| Gold-standard for cirrhosis diagnosis? | Liver Biopsy (can see the cause) |
| What makes up the Child-Pugh score? | Encephalopathy (confusion bc liver is not detoxifying); Ascites (big abdomen with build up of fluid) Bilirubin (higher is worse); Albumin (lower is worse); Prothrombin time (risk of bleeding) |
| Child-Turcotte-Pugh Class added score parameters? | Class A--> 5 to 6 points (least severe liver disease) Class B--> 7 to 9 points (moderately severe liver disease) Class C--> 10 to 15 points (most severe liver disease) *we use Child-pugh to decide, before the very ESLD, how severe is it? |
| Disease severity classification uses the MELD score which stands for? What makes up the MELD score? | Model for End-Stage Liver Disease; SCr, Tbili, and INR |
| MELD score was used to determine their risk of _______ in the next 90 days (3 months) *how to allocate livers | mortality *use at the very end to decide "who gets a liver" |
| LD is brought to the Er by her husband, who states taht she has seemed somewhat confused over the past week or so. After examining the pt, the physician determines that she has grade 1, mild confusion and no ascites. When her lab results return, she has an INR of 1.4, an albumin of 3.2, and a Tbili of 2.2. What is her Child-Turcotte-Pugh score? | 8 (encehalopathy mild is 2 points, ascites-none is 1 point, bilirubin of 2.2 is 2 points, albumin of 3.2 is 2 points, and INR was <1.7 which is 1 point) so 8 points is Class B (moderate) |
| Which of the following is NOT a typical s/sx of cirrhosis? -increased INR; -Jaundice; -Mental status changes; -Constipation | Constipation |
| Decompensated liver failure is defined as the presence of at least how many complications? | at least 1 |
| What are the complications of Cirrhosis? | PK/PD changes; Coagulopathy; Spontaneous Bacterial Peritonitis; Ascites; Portal HTN; Varices and Variceal Bleeding; Encephalopathy; Hepatorenal Syndrome |
| PK/PD changes--> pts with cirrhosis will have an increase in sensitivity to? | medication effects (opiates, BZDs, NSAIDS) *really the medications that are heavily processed by the liver *avoid NSAIDS, and we give lower doses of opioids |
| Which BZDs are SAFE for use in liver disease? | (LOT)Lorazepam, Oxazepam, and Temazepam |
| PK/PD changes: Medications overall have a decrease in clearance leading to _____ hepatic blood flow which _______ clearance and ______ 1/2 life | decrease; decrease; increase |
| PK/PD changes: The liver is responsible for metabolism for many medications and will see a ____ in protein synthesis for these enzymes and see an _____ in levels of FREE drug for protein-bound medications | decrease; increase |
| Two proteins that have another effect are Protein C and S (anticoagulants) however in cirrhosis, pts have a decrease in both C and S as well as? | albumin, clotting factors, and platelets; as well as less stable coagulation system. When you think cirrhosis, you think BLEEDING |
| Jane is a 54 yo female with a PMH significant for a seizure disorder, HTN, and gout admitted for fulminant liver failure due to an overdose of a hepatotoxic medication. She currently takes phenytoin, metoprolol tartrate, lisinopril, and allopurinol at home. Which of the following medications will require dose adj. due to her change in liver function? | Phenytoin |
| Portal HTN--> high pressure that leads to fibrosis (locking the doors)--> break a window make a new path (resistance to blood flow and leads to? | increased portal vein pressure |
| Varices and Variceal Bleeding: Splanchnic blood supply is the blood supply for organs in the abdominal cavity that answer the acronym LIPS. what does it stand for? | L (liver) I (intestines/Stomach P (Pancreas) S (Spleen) *these organs drain their blood to the liver. all doors are locked and you get a higher pressure building |
| Varices and Variceal bleeding: When these weak vessels form they are very ______ and prone to bursting | superficial Varices (swollen veins in esophageal lining that are prone to rupture and bleeding) |
| Variceal bleeding: Prophylaxis--> goal is to? | reduce portal pressure via reduction of portal venous inflow |
| Variceal bleeding prophylaxis: Why would i want to use a selective over a non-selective Beta blocker | you want to affect the blood vessels, not just the heart. Propranolol 10 mg BID or Nadolol 20 mg daily |
| When treating Variceal Bleeding prophylaxis, we want to AVOID use of Beta blockers in _____ ______ and ____ ____ cirrhosis. *give during Beta blocker window" | early stage (not going to do anything because the pressure is not great enough); end stage (blood supply systemically is going to drop and if we give them a Beta blocker, we won't be able to maintain their blood pressure high enough to sustain life and mortality goes UP |
| Once variceal bleeding happens--> Maintain hemodynamic stability with ____ ______ if necessary and _____ if necessary (severe bleeding, unconsciousness) and control bleeding with what drug? | Fluid resuscitation; Intubate; Octreotide |
| Variceal treatment: Control the bleeding with Octreotide, dose? After hemodynamically stable and out of surgery, the BEST time to start octreotide after ____-_____ hours when the bleeding STOPS. Then we will give for less than ___ days; AE of Octreotide? | 24-72; 5; Dose: 50-1000 mcg IV bolus and then 25-50 mcg/hr IV infusion; -bradycardia, hyperglycemia, fatigue, HA |
| Variceal bleeding Tx: Literature hints at other agent which is _____ ______. Most important thing to know is that its NOT _______ | isosorbide mononitrate; monotherapy (increased mortality when used alone) |
| How do we stop the bleeding (3 options) | Endoscopic variceal ligation (rubber band) Endoscopic variceal sclerotherapy (burn it shut) Transjugular intrahepatic portosystemic shunt (TIPS) (shunt blood and#1 SE is confusion since blood is not detoxified) |
| Hole from variceal bleeding--> start what abx and dose? | Ceftriaxone 1g IV Q24h (for the prevention of SBP (spontaneous bacterial peritonitis) |
| AS was just admitted w/ severe hematemesis. Due to a decrease in her blood pressure, she received fluid resuscitation and due to her Hgb (6.4) she received packet RBC (<7). she is still severely bleeding. the team plans to take her for endoscopic variceal ligation, but in the meantime, the team provides all of the following tx for the pt except? | initiate clindamycin to prevent translocation of gut bacteria |
| Why would you want to avoid ciprofloxacin if the pt has been receiving long-term prophylaxis with a FQ? | increased likelihood of resistance |
| Ascites is the? | accumulation of fluid in the peritoneal cavity *happens bc albumin is decreased in cirrhosis |
| Albumin maintains ______ ______ which is pressure that keeps fluid in blood vessels as opposed to leaking out. Albumin is _______ in cirrhosis | Oncotic pressure; decreased *pools in the peritoneal cavity; in thoracic (would have SOB) |
| Ascites (decreased protein synthesis---> low albumin--> which _____ the permeability of the capillaries (fluid seeps out)---> resulting in VOLUME OVERLOAD. At the same time you have Portal HTN (body will try to compensate for that increased pressure resulting in? | increases; increased Nitric oxide (systemic and splanchnic vasodilation to compensate for that portal HTN)--> drops pressure--> kidneys dont like that and release ADH (RAAS activation, SNS activation)--> leading to retention of renal Na+ and H2O (makes Ascites worse) |
| Ascites Tx: Non-pharm--> Acetaminophen dose? | 2g per day in cirrhosis and restrict Na+ |
| Ascites Tx for Abdominal Paracentesis for tense ascites--> Do a _____ _____ (remove the fluid). Over 5 L is considered ______. If this has to be conducted it tells us that Albumin is _____. If we take out more than 5 L, we are going to supplement them with ______ | Therapeutic Tap (removal of > 5L); therapeutic; LOW; Albumin (to prevent ascites from re-accumulating as fast) |
| Ascites Tx with Albumin, With the Therapeutic tap and knowing that Albumin is low, the dose for albumin to give a pt is dependent on the amount taken out per L. What is the dose? | 8g per L of ascitic fluid removed and MUST ROUND TO NEAREST 25g |
| Mr. Jones received a "therapeutic tap" this afternoon for which 6L of fluid were removed. The physician asks you how much albumin she should order. You recommend: | 50g |
| Ascites--> Pharmacological options are? | 100 mg Spironolactone and 40 mg Furosemide every morning given together. Max effect 3-5 days. monitor for K+ if low increase Spironolactone |
| If the fluid from ascites sits there it could get infected (Spontaneous Bacterial Peritonitis). #1 bug we suspect is E. coli. If you suspect--> perform diagnostic paracentesis and we take out _____ mL. | 25 (taking out the fluid to test for an infection). |
| WE do not give Albumin when conducting a diagnostic paracentesis. The diagnoistic paracentesis test tells us the PMN (neutrophils count) and if >/= ______ cells/mm^3 it warrants treatment with abx. <250 and have fever and other symptoms of infection we give abx. which abx? | 250. Ceftriaxone |
| How do we calculate a PMN cell count: (total WBC count or TNC) x (PMN%). Once calculated add ______ to PMN. and at the end if we see there are RBC, we subtract 1 PMN for every ______ RBC | BANDS (immature neutrophils) 250 |
| TNC: 9000; Neutrophils: 3%; Bands: 1%; RBC: 500. Calculate PMN cell count | 3% + 1% --> 4$--> 9000(0.04)--> 360 PMNs - 2 (500/2)--> 358 PMNs (over 250 so we treat with Ceftriaxone 2g IV q24h or 1g q12h for 5 days |
| SBP tx--> Abx therapy: We know there is an infection so we give them? When its variceal bleeding and we are PREVENTING an infection from happening with what dose? | Ceftriaxone 2g IV q24h or 1g IV q12h for 5 days Ceftriaxone 1g q24h |
| Aside from Ceftriaxone therapy, we would ONLY give albumin for SBP (if the serum creatinine is over ___ mg/dL and BUN > ____ mg/dL) OR Tbili > 4mg/dL (not all 3, either or) | 1; 30 Albumin dose 1.5g/kg upon deptection ---> then 1g/kg 2 days later |
| Which of the following pts would NOT require extended spectrum abx coverage for the tx of SBP? | Frank, a 63 yo make with cryptogenic cirrhosis admitted for fever, abd pain, and confusion |
| We prevent SBP when there is a ____ ______. Tx when we know there is an infection give? | variceal bleed (only 1g of Ceftriaxone 1g IV q24h (primary prohpylaxis) VS Ceftriaxone 2g IB q24h for 5 days; Add albumin if SCr >1 AND BUN>30) OR Tbili >4 mg/dL and dose on actual weight 1.5 g/kg upon deptection ---> 1g/kg two days later |
| IF after the 5 days of treatment with Ceftriaxone and albumin, we give ____-_____ prophylaxis for SBP for the following: hx of previous SBP OR ascistic fluid protein <1.5g/dL *AND* one of the following: SCr >1.2; BUN>25; Na+ >130; Bilirubin > 3---> what are the options? | Long-term; Ciprofloxacin PO daily. Bactrim is an option but NOT if pt going to be listed for transplant (not giving for long-term) |
| Which of the following pts require long-term SBP prophylaxis? | Arielle, with an ascitic fluid protein 1.2, SCr 1.3, BUN 27, Na 135, and Bilirubin 2.2 |
| Hepatic encephalopathy is? | brain dysfunction/confusion caused by liver insufficiency |
| In Hepatic encephalopathy (HE), Nitrogenous substances (NH3) accumulate in the? | systemic circulation due to hepatic dysfunction and shunting through portosystemic collaterals bypassing the liver; toxins produced by gut bacteria and a byproduct of protein breakdown. Accumulation in the CNS--> Encephalopathy due to accumulation |
| Pts that have encephalopathy have what's called ______. HE presentation is a continuum of symptoms which are? | asterixis; impaired cognition, confusion, behavior changes, somnolence, and coma. *cognition is impaired and flapping of hands and can't pull them back. Flapping is specific due to encephalopathy of the liver |
| HE management--> we restrict _____ diet because we don't want to feed the bacteria to make more toxins/ #1 tx is _____ which is also used to treat constipation. | Protein; Lactulose (treatment and prevention of Encephalopathy) |
| How does Lactulose work in HE? important to know that the dosing is titrated to the # of _____ (only drug in existence that is dosed this way) | increases excretion of the nitrogenous substances by making the pt have a bowel movement ; bowel movements ****Titrate to 2-3 bowel movements per day |
| Lactulose--> dose in morning (no poop)--> take again if no bowel movement, take more until it happens. This is for ______ of encephalopathy | TREATMENT AND PREVENTION (can be given orally and as an enema) |
| HE management--> if pt is unresponsive to Lactulose, you can add on? | Rifaximin (to kill the bacteria in the gut effectively stopping production of the toxins) *lactulose and Rifaximin would be used TOGETHER, rifaximin is NOT monotherapy |
| HE Management: Paired with Lactulose, what is the dose of Rifaximin (Xifaxin) for cirrhosis? | 550 mg PO BID (not monotherapy) *rifaximin is used for prevention of RECURRENT hepatic encephalopathy |
| Hepatorenal Syndrome (HRS) is? | worsening of renal function in pts with cirrhosis despite a lack of typical causes. *renal dysfunction secondary to liver disease |
| HRS--> Portal HTN--> increased Nitric oxide--> vasodilation of systemic circulation--> vasoconstriction of renal circulation--> leading to? | decreased renal perfusion |
| HRS management includes discontinuing nephrotoxins and d/c or decrease the dose of diuretics and we give 3 drugs together. Which ones? | HRS--> gets MOA: Midodrine; Octreotide; Albumin -Midodrine 5-7.5 mg PO TID (oral vasoconstrictor increasing kidney perfusion (b/c kidney is not getting enough perfusion); -Octreotide 100 mcg SQ TID(vasoconstricts the sphanchnic blood flow to push the blood flow to the kidney(HRS 3x daily; variceal bleed IV bolus then infusion); -Albumin 1g/kg (max dose 100g) on Day 1--> 25-50g/day (increases oncotic pressure (keeps the fluid in the blood vessels and sends it to the kidney |
| Dose of HRS management with the 3 drugs MOA doses are? | Midodrine: 5-7.5 mg PO TID; Octreotide 100 mcg SQ TID; Albumin 1 g/kg (max dose 100 g) on day 1--> 25-50 g/day |
| STAY alert on ALBUMIN DOSES--> 1. HRS treatment? 2. Therapeutic tap: removal of >5L albumin dose? 3. SBP TREATMENT? | 1. Albumin 1 g/kg (max dose 100 g) on day 1--> 25-50 g/day 2. Albumin 8 g/L of ascitic fluid removed *round to nearest 25 g 3. Add albumin IF <SCr > 1 mg/dL AND BUN< 30 mg/dL) OR Tbili >4mg (1.5g/kg upon detection--> 1g/kg two days later and round to nearest 25 g) |
| Which of the following lab values with decrease in cirrhosis? -AST -ALT -Tbili -Platelets -INR | Platelets |
| Which of the following clinical/lab critera do not contribute to the Child-Turcotte-Pugh class? -Albumin -Na+ -Bilirubin -Encephalopathy -INR | Na+ |
| Randal ha a score of 10 points on the Child-Pugh score, qualifying him as class C. What is his severity of liver disease? | Most severe liver disease |
| 100 kg pt with cirrhosis has had a declining RENAL function during his stay. Today he has SCr of 2.5, BUN 33, and his diagnositc tap was (+) for SBP. Team initiates ceftriaxone 2g IB q24h, but is unsure of the albumin dosing stating "just know it is different." what do you recommend? | meet criteria (SCr >1 and BUN > 30). Dose is 1.5g/kg on day 1 followed with 1g/kg 2 days later -150g w/in 6h of SBP detection, followed by 100 g 2 days later |
| which of the following is NOT a symptom pts with cirrhosis may experience at one point in the course of their disease? | Visual impairment |
| When a pt's varices stop bleeding, would you continue the prophylactic antibiotic? | NO (as bleeding stos, stop abx) |
| In addition to Na+, what 3 labs contribute to the calculation of a MELD score? | SCr, INR, Tbili |
Created by:
Xander635
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