CCP 217 Gastrointestinal Emergencies Flashcards

Question

liver function tests MUST KNOW + EXPLAIN PATHO

Answer 1

1. serum albumin 2. prothrombin time 3. INR 4. serum bilirubin level

Answer 2

1. Severe epigastric pain that radiates to the back | 2. nausea/vomiting

Answer 3

"Atlanta criteria" 1. “Classic” mid-epigastric abdominal pain 2. Serum lipase or amylase >3x normal 3. Confirmatory imaging findings (CT, MRI, or US)

Answer 4

1. gallstones cause pancreatic ductal obstruction 2. obstruction increases intra-pancreatic duct pressure → acid reflux into the pancreas → trypsin activation → autodigestion of pancreatic tissue

Answer 5

1. ethyl alcohol sensitizes pancreatic cells to cholecystokinin → increased trypsin production 2. trypsin activation → autodigestion of pancreatic tissue

Answer 6

inflammation of the bile duct system

Answer 7

presence of gallstones within the common bile duct

Answer 8

The presence of stones in the gallbladder

Answer 9

Lipase has higher sensitivity and specificity 1. Lipase at 3 times the upper limit of normal is 100% sensitive and 99% specific for acute pancreatitis 2. Amylase may be elevated in acute pancreatitis but is less sensitive (81%) and specific than lipase. Amylase may also be falsely negative

Answer 10

surgical removal of the gallbladder

Answer 11

1. Severe acute liver injury with encephalopathy and impaired clotting function (INR ≥1.5) in a patient without underlying cirrhosis or prior liver disease 2. diagnosed when there is evidence of acute hepatitis with coagulation abnormality (INR ≥1.5) and any degree of encephalopathy in a patient without pre-existing cirrhosis and an illness course <26 weeks in duration

Answer 12

1. may be beneficial in any patient with early, non-acetaminophen-related acute liver failure 2. prospective, double-blind trial of patients with acute liver failure not due to acetaminophen toxicity demonstrated improved transplant-free survival in patients with acute liver failure treated with IV N-acetylcysteine

Answer 13

1. IV fluid resuscitation 2. correction of electrolyte and metabolic abnormalities (hypoglycaemia) 3. Vasopressor support for shock (norepinephrine) 4. Corticosteroids for refractory shock (hydrocortisone) 5. Consider administration of N-acetylcysteine 6. Management of complications (eg. elevated ICP secondary to hepatic encephalopathy, GIB secondary to hepatic coagulopathy) 7. broad-spectrum ABX for signs of infection

Answer 14

1. acetaminophen overdose (40%) 2. indeterminate (17%) 3. idiosyncratic drug reactions (13%) 4. hepatitis B virus (6%) 5. ischemic hepatitis (6%) 6. hepatitis A virus (4%) 7. autoimmune hepatitis (4%) 8. Wilson disease (3%) 9. Budd–Chiari syndrome (2%) 10. pregnancy (2%) 11. malignancy (1%)

Answer 15

1. Grade I: mild asterixis 2. Grade II/III: pronounced asterixis 3. Grade IV: asterixis is often absent (may exhibit posturing)

Answer 16

1. sudden loss of muscle tone during sustained contraction of an outstretched limb 2. associated with a silent period on EMG 3. referred to as ‘negative myoclonus’ 4. irregular flexion–extension movements at the metacarpophalangeal and wrist joints, which increase during a sustained posture

Answer 17

1. Elevated AST/ALT/ALP/GGT/bilirubin 2. Anemia 3. Elevated serum creatinine and BUN 4. Elevated amylase/lipase 5. Hypoglycemia 6. Hypophosphatemia 7. Hypomagnesemia 8. Hypokalemia 9. Acidemia or alkalemia 10. Elevated ammonia 11. Elevated lactate dehydrogenase (LDH)

Answer 18

1. late stage of progressive hepatic fibrosis 2. characterized by distortion of the hepatic architecture and the formation of regenerative nodules 3. irreversible in advanced stages 4. only treatment option is liver transplantation

Answer 19

1. Alcohol (60-70%) 2. Chronic viral hepatitis (B or C, 10%) 3. Non-alcoholic liver disease (10%) 4. Biliary obstruction (5-10%) 5. Hemochromatosis (5-10%)

Answer 20

1. fibrosis of hepatic tissue → elevated Portal pressures due to decreased hepatic venous drainage 2. decreased hepatic venous drainage → splenomegaly and splanchnic vasodilation 3. splenomegaly → anemia, hypoalbuminemia, thrombocytopenia, and ascites 4. splanchnic vasodilation → increased splanchnic blood flow, further elevated portal pressures 5. feedback loop ensues → decreased blood volume and hypotension/shock/death

Answer 21

1. variceal hemorrhage 2. ascites 3. bacterial peritonitis 4. hepatic encephalopathy 5. hepatorenal syndrome 6. hepatopulmonary syndrome

Answer 22

1. Urinary tract infections 2. bacterial peritonitis 3. C. difficile colitis

Answer 23

1. caput medusae (network of painless, swollen veins around your bellybutton) 2. ascites 3. fetor hepaticus 4. gynecomastia 5. hepatomegaly 6. splenomegaly 7. jaundice/scleral icterus 8. muscular atrophy 9. palmar erythema 10. testicular atrophy 11. spider angiomas 12. nail changes (splinter haemorrhages) 13. parotid gland enlargement

Answer 24

1. biliary tree is a series of GI ducts allowing newly formed bile from the liver to be concentrated and stored in the gallbladder prior to release into the duodenum 2. Bile is secreted from hepatocytes and drains from both lobes of the liver via intralobular ducts and collecting ducts into the left and right hepatic ducts 3. left and right hepatic ducts join to form the common hepatic duct, which runs alongside the hepatic vein 4. common hepatic duct descends and is joined by the cystic duct which regulates bile flow in and out of the gallbladder for storage and release 5. the common hepatic duct and cystic duct combine to form the common bile duct 6. common bile duct descends and passes posteriorly to the duodenum and head of pancreas 7. common bile duct now joined by main pancreatic duct, forming the hepatopancreatic ampulla (ampulla of Vater) – which then empties into the duodenum via the major duodenal papilla 8. major duodenal papilla is regulated by a muscular valve, the sphincter of Oddi

Answer 25

clinical finding in ascending cholangitis (an infection of the bile duct in the liver) 1. jaundice 2. fever (usually with rigors) 3. right upper quadrant abdominal pain

Answer 26

acute cholescystitis 1. ask the patient to take in and hold a deep breath while palpating the right subcostal area 2. If pain occurs on inspiration, when the inflamed gallbladder comes into contact with the examiner’s hand, Murphy’s sign is positive

Answer 27

1. patient NPO 2. administer IV fluids 3. analgesics 4. Empiric IV antibiotics 5. GI consult

Answer 28

1. patient NPO 2. administer IV fluids 3. analgesics 4. Empiric IV antibiotics 5. Surgical consult

Answer 29

impacted stone or sludge in the cystic duct or the ampulla of Vater → distension and contraction of the gallbladder or biliary tract → an intermittent increase in pressure and pain

Answer 30

The most common type of stone in Western society (80%-90%) 1. imbalance in biliary cholesterol homeostasis → cholesterol crystallization 2. Formation is promoted by hepatic hypersecretion, gallbladder hypomotility, and genetic predisposition

Answer 31

1. Abnormal bilirubin metabolism with excess unconjugated bilirubin 2. Includes black (uninfected) and brown (infected) stones

Answer 32

1. biliary tree is normally a sterile environment due to the continuous flow of bile and the immunologic response of the biliary epithelial cells 2. when an obstruction leads to increased bile duct pressure and the breakdown of these defenses pathology occurs 3. Bacteria enter the biliary system primarily by ascending from the duodenum into the extrahepatic ducts 4. The portal venous system and the periportal lymphatic system are also potential routes of entry 5. E. coli, Klebsiella, and Enterococcus are the most common bugs in patients with acute cholangitis

Answer 33

inflammation of colonic diverticula

Answer 34

1. visceral 2. parietal 3. referred

Answer 35

1. the nerves that run through the walls of an organ get stretched 2. poorly localized, feels like a dull ache or cramp 3. comes directly from the organ involved 4. pain may be dull, hard to locate precisely, and may be either constant or intermittent

Answer 36

1. pain caused by irritation of fibres that innervate the parietal peritoneum 2. sharp, can be localized by pointing to a specific spot

Answer 37

1. occurs when the brain is unable to localize the source of discomfort due to nociceptive dorsal horn neurons receiving convergent inputs from different tissues

Answer 38

1. serous membrane that forms the lining of the abdominal cavity 2. covers most of the intra-abdominal organs 3. provides support and protection for the abdominal organs 4. acts as the main conduit for the lymph vessels, nerves, and abdominal arteries and veins 5. there are two layers of peritoneum; with potential space between those layers 6. parietal peritoneum (outer layer) is attached to the abdominal wall 7. visceral peritoneum (inner layer) is wrapped around the intraperitoneal organs 8. potential space between the two layers is the peritoneal cavity (contains serous fluid)

Answer 39

1. stomach 2. liver 3. spleen 4. appendix 5. transverse colon, sigmoid colon, upper third of the rectum 6. the first 5cm and the fourth part of the the duodenum 7. the jejunum, the ileum, the cecum 8. tail of the pancreas 7. uterus, fallopian tubes, ovaries, gonadal blood vessels (female)

Answer 40

1. main body of duodenum 2. ascending colon, descending colon 3. middle third of the rectum 4. remainder of pancreas (body/neck/head) 5. kidneys + adrenal glands 6. proximal ureters, renal vessels

Answer 41

1. lower 1/3 of rectum | 2. urinary bladder

Answer 42

a reversible syndrome of impaired brain function occurring in patients with advanced liver failure

Answer 43

1. cirrhosis → worsening hepatocyte dysfunction → increase serum NH₃ levels 2. cirrhosis → systemic inflammation, bacterial translocation, and release of vasoactive mediators → increased BBB permeability 3. serum NH₃ crosses the BBB → cerebral edema, altered brain glucose metabolism, astrocyte swelling, and neurotransmitter receptor dysfunction (GABA) 4. Hepatic encephalopathy ensues

Answer 44

1. Esophagogastric varices (alcohol abuse, cirrhosis, ascites, prior UGIB) 2. Peptic ulcer disease (NSAID use, H pylori infection) 3. Vascular anomalies (AVM history) 4. Mallory-Weiss tear (forceful vomiting) 5. Aortoenteric fistula (history of aortic procedure) 6. Malignancy

Answer 45

1. Diverticular disease 2. Colitis 3. Polyps 4. Malignancy 5. UGIB (Hematochezia can be a sign of severe UGIB) 6. Hemorrhoids

Answer 46

1. cirrhosis → increased intrahepatic flow resistance → portal HTN 2. portal HTN → the development of a pressure gradient between portal vein and IVC 3. high portal system pressure → development of venous collaterals to the systemic veins in the esophageal plexus 4. varicosities form

Answer 47

1. UGIB secondary to a mucosal tear at the gastroesophageal junction 2. typically secondary to repeated vomiting episodes

Answer 48

1. thrombosis or embolism of the superior mesenteric artery 2. mesenteric venous thrombosis 3. non-occlusive mesenteric ischemia due to a low flow state

Answer 49

1. The liver synthesizes both clotting factors and endogenous anticoagulant factors such as protein C and antithrombin 2. Both are equally underproduced in cirrhotic patients. 3. This phenomenon leads to “rebalanced hemostasis” 4. cirrhotic patients may have a close-to-normal clotting tendency, but abnormal routine coagulation studies 5. INR is not an accurate reflection of hemostasis in cirrhotic patients

Answer 50

1. IV/O2/Monitor 2. Volume resuscitation (blood products preferred) 3. Reverse coagulopathy (FFP/PCC/TXA/Vit K/Platelets) 4. promote gastric emptying (NG tube, metoclopramide) 5. secure airway 6. control bleeding (Blakemore/Minnesota/Linton tube, octreotide, vasopressin) 7. prevent further complications (prophylactic ABX, PPI therapy) 8. STAT GI consult

Answer 51

1. Mesenteric ischemia is classified as arterial vs venous and occlusive vs non-occlusive 2. Arterial mesenteric ischemia includes SMA embolism, SMA thrombosis, and non-occlusive mesenteric ischemia 3. Venous mesenteric ischemia is d/t mesenteric vein thrombosis 4. The abdominal aorta has three branches: the celiac artery, SMA, and IMA 5. The celiac artery is short and wide, has extensive collateral circulation. rarely involved in acute mesenteric ischemia. 6. The SMA branches off the aorta at a 45° angle and tapers, making a “funnel” for emboli. SMA is the most common culprit vessel in acute mesenteric ischemia 7. In acute mesenteric ischemia, ischemia starts at the mucosa and extends toward the serosa

Answer 52

1. SMA thrombosis can be considered the “acute coronary syndrome of the gut" (similar pathophysiology) 2. plaque deposition at the origin of the SMA causes flow-limiting stenosis and pain after eating (“intestinal angina”) 3. The acute event occurs similarly to MI, with plaque rupture and platelet aggregation

Answer 53

1. Abdominal pain described as “out of proportion” to exam (patient reports severe pain without peritonitis on exam) 2. Underlying cardiac disease 3. “Gut emptying” (N/V/D)

Answer 54

1. The normal abdominal aorta (infrarenal) measures 2.0 cm in diameter 2. AAA is defined as a focal dilation of the abdominal aorta to at least 50% larger than its expected normal diameter 3. An abdominal aorta measuring >3.0 cm is considered aneurysmal 4. AAA is a true aneurysm, meaning that the localized dilation involves all three layers of the arterial wall (intima, media, and adventitia)

Answer 55

1. abdominal pain 2. hypotension 3. pulsatile mass in abdomen

Answer 56

1. IV/O2/Monitor 2. Volume resuscitation (target SBP 70-90 mmHg with intact mental status, blood products preferred) 3. Reverse coagulopathy (FFP/PCC/TXA/Vit K/Platelets) 4. Analgesia 5. Arterial Line 6. STAT vascular surgery consult

Answer 57

1. loss of elastin and collagen leads to destruction of the aortic media and lamina, allowing for rupture 2. Aorta ruptures into retroperitoneal space, creates a tamponade effect at the rupture site 3. Often presents as back pain 4. Because rupture is contained, it allows the patient’s blood pressure to stabilize temporarily

Answer 58

1. loss of elastin and collagen leads to destruction of the aortic media and lamina, allowing for rupture 2. Aorta ruptures into the peritoneum, leading to rapid exsanguination/shock/death

Answer 59

1. Location (Small bowel vs Large bowel obstruction) 2. Etiology (mechanical vs functional obstruction) 3. Severity (complete vs partial)

Answer 60

1. the failure to pass intraluminal intestinal contents through the small or large bowel 2. This obstruction can be mechanical or functional

Answer 61

1. cancer (60%) 2. diverticulitis (20%) 3. stricture 4. fecal impaction 5. volvulus (5%)

Answer 62

1. post-operative state 2. medications 3. electrolyte abnormalities

Answer 63

1. Adhesions from a prior abdominal or pelvic surgery (>80% of cases) 2. hernias (common) 3. foreign bodies 4. malignancy (common) 5. post-radiation strictures or edema 6. congenital malformations 7. volvulus 8. infection

Answer 64

1. Volvulus is a twisting of bowel loops 2. Volvulus occurs when a part of the colon twists on the mesentery and results in obstruction 3. Cecal volvulus is due to a mobile segment of the cecum 4. sigmoid volvulus occurs with redundant sigmoid colon attached to narrow mesentery

Answer 65

1. Due to a lesion or object that occludes the bowel lumen | 2. This can be a result of extraluminal or intraluminal disorders (eg, adhesion, stricture, or mass)

Answer 66

1. Due to a lack of propulsive motor activity (eg, post-operative ileus, electrolyte disturbances [hypokalemia]).

Answer 67

1. The bowel consists of the small and large intestine 2. Obstruction causes the failure to pass intraluminal intestinal contents through the small or large bowel 3. Accumulation of intestinal material proximal to the site of obstruction → bowel dilation 4. Bowel dilation → increased peristalsis and loose bowel movements early in the disease course as contents distal to the obstruction are evacuated 5. Further Bowel dilation → Increased intraluminal pressure causing bowel wall edema and distension, nausea, and vomiting 6. Bowel wall edema → reduced intestinal absorption of intraluminal contents and decreases venous and arterial flow 7. Bacterial overgrowth d/t stasis → further dilation and increased gas production proximal to the site of obstruction 8. Bacteria translocate into the bloodstream d/t increased bowel wall permeability 9. Fluid loss from transudative fluid secretion into the bowel lumen and vomiting → dehydration, metabolic alkalosis, and electrolyte abnormalities

Answer 68

1. occurs when there are multiple sites of obstruction 2. considered more dangerous than bowel obstruction with a single transition point 3. Intraluminal pressure in the closed loop increases rapidly → rapid reductions in venous and arterial blood flow → Bowel infarction and necrosis

Answer 69

1. Bowel Strangulation occurs with ischemia or twisting of the bowel or mesentery 2. Bowel infarction and necrosis d/t poor blood flow → perforation, peritonitis, and sepsis.

Answer 70

free air under the diaphragm

Answer 71

1. idiopathic immune-mediated intestinal and extraintestinal disease process 2. caused by a disruption of the natural barriers and protective mechanisms of the gastrointestinal (GI) tract 3. Two primary inflammatory bowel disease conditions are Crohn’s disease and ulcerative colitis

Answer 72

1. More than 6 bowel movements/day 2. Moderate to severe rectal bleeding 3. High local and systemic inflammatory burden 4. evidence of stricture, deep ulceration, abscesses, obstruction, or perforation 5. Signs of other significant organ dysfunction

Answer 73

1. mediated by an inappropriate inflammatory response in bowel 2. Intestinal epithelial cells have ↑ cell permeability → increased invasion by bacteria + cellular destruction 3. invading bacteria → cellular stress responses from the endoplasmic reticulum d/t ↑ release of inflammatory mediators → GI inflammation 4. Intestinal epithelial cells have ↓ mucus-production → reduced protective barrier against chemical stress

Answer 74

1. RLQ pain 2. fever 3. nausea/vomiting/anorexia

Answer 75

1. appendicitis with perforation or peritonitis

Answer 76

1. Nonperforated appendicitis

Answer 77

1. McBurney's point lies 2/3 of the distance laterally on a line drawn from the umbilicus to the right anterior superior iliac 2. corresponds to the location of the base of the appendix

Answer 78

1. RLQ pain elicited by palpation of the LLQ in acute appendicitis 2. If this occurs, it is said to be a positive Rovsing sign.

Answer 79

1. traditionally been thought to result from obstruction of the appendix 2. Obstruction → increased intraluminal and intramural pressure (due to distention of the appendiceal lumen) 3. The increase in intraluminal and intramural pressure → inflammation and engorgement of the appendix 4. Lymphatic stasis and thrombosis + occlusion of the small blood vessels in the wall of the appendix → ischemia and eventual necrosis 5. Inflammation and necrosis increase the risk of perforation, which can → localized abscess or diffuse peritonitis 6. Bacterial overgrowth early in the disease process is usually aerobic, while a polymicrobial infection typically occurs later in the disease course

Answer 80

1. describes the clinical manifestations of the pathologic elevation of the intra-abdominal pressure (IAP)

Answer 81

1. When the IAP exceeds 12 mm Hg it is referred to as intra-abdominal hypertension (IAH) 2. When the IAP exceeds 20 mm Hg it is referred to as abdominal compartment syndrome (ACS)

Answer 82

ACS → IVC compression → decreased cardiac preload → decreased CO → tachycardia + elevated afterload → increased MVO2 and decreased coronary perfusion → myocardial dysfunction → cardiogenic shock → death

Answer 83

ACS → increased renal venous pressure → decreased renal perfusion pressure → decreased GFR → decreased urine secretion and decreased buffering capacity → oliguria + metabolic acidosis → renal failure → MODS → death

Answer 84

ACS → decreased abdominal perfusion pressure → gut ischemia → gut barrier failure → bacterial translocation → intra-abdominal sepsis → distributive shock → MODS → death

Answer 85

1. ACS → IAP transmitted across the diaphragm → elevated intra-thoracic pressure, compressive atelectasis, increased alveolar dead space, reduced FRC, VQ mismatch and hypoxic bronchial artery vasoconstriction → increased WOB + accessory muscle use → respiratory fatigue 2. In MV decreased lung and chest wall compliances result in elevated PIP + PPlat 3. increased intra-thoracic pressure increases PVR and leads to RV failure

Answer 86

1. ACS → IAP transmitted across the diaphragm → elevated intra-thoracic pressure → decreased cerebral venous outflow → elevated intracranial pressure (ICP) → decreased cerebral perfusion pressure → cerebral hypoxia → encephalopathy 2. Neuro ICU patients with elevated ICP should have their IAP monitored closely

Answer 87

1. the steady state pressure concealed within the abdominal cavity

Answer 88

1. sustained intra-abdominal pressure (IAP) of > 12mmHg

Answer 89

1. sustained IAP > 20mmHg with new organ failure

Answer 90

1. (APP) = MAP – IAP

Answer 91

1. a measure of the ease of abdominal expansion, which is determined by the elasticity of the abdominal wall and diaphragm. It should be expressed as the change in intra-abdominal volume per change in IAP

Answer 92

1. Improve Abdominal Wall Compliance 2. Evacuate Intra-Luminal Contents 3. Evacuate Abdominal Fluid Collections 4. Correct Positive Fluid Balance 5. Organ Support

Answer 93

1. sedation + analgesia (↑ Abdominal Wall Compliance) 2. HOB elevation at 30 degrees (↑ Abdominal Wall Compliance) 3. neuromuscular blockade (↑ Abdominal Wall Compliance) 4. nasogastric decompression (Evacuate Intra-Luminal Contents) 5. avoid excessive fluid (↓ Positive Fluid Balance) 6. diuretics (↓ Positive Fluid Balance) 7. maintain an APP > 60mmHg with vasopressors (organ support) APP = MAP - IAP 8. optimise ventilation strategies (organ support)

Answer 94

1. congestive hepatopathy caused by blockage of hepatic veins 2. Two of the hepatic veins must be blocked for clinically evident disease 3. Liver congestion and hypoxic damage of hepatocytes eventually result in predominantly centrilobular fibrosis 3. The obstruction may be thrombotic or non-thrombotic anywhere along the venous course from the hepatic venules to junction of the inferior vena cava (IVC) to the right atrium

Answer 95

1. NOT a goal of "normal" blood pressure. 2. target a MAP of 65 (although there is nothing wrong with aiming for a blood pressure of 85-90 mmHg systolic) 3. Do not over resuscitate these patients. This will increase the potential of bleeding. Giving unnecessary blood products can make things worse. 4. If the patient is a cirrhotic, they live at a lower blood pressure at baseline

Answer 96

Think of these patients like a bleeding trauma patient (specifically, a bleeding pelvis) 1. Do not over resuscitate these patients 2. If you give crystalloid, just give a small amount. 3. Variceal bleeding is similar to pelvic trauma in that they will need a lot of blood. 4. If you have a bleed that requires 1-2 units of blood, transfuse PRBC's with a transfusion target of Hgb of 70. If you need to give the patient 3-4 units of blood in an hour, you should probably initiate MTP with a 1:1:1 ratio 5. TXA. This is tough. The literature is fairly compelling supporting TXA in a trauma patient who receives blood. GI bleeds are a different situation. The studies available for TXA with GI bleed have been unimpressive. Consider giving it, but it is not a high priority.

Answer 97

1. Hemoglobin <70 g/L 2. Hemoglobin <90 g/L with ACTIVE acute coronary syndrome (ACS) 3. Normal hemoglobin with ACTIVE bleeding and hypotension ***If giving more than 4 units of blood in the stable patient Transfuse 1 unit FFP*** ***Transfuse for platelets below 50,000/μL [50 x109/L]***

Answer 98

1. Vitamin K 5-10 mg IV | 2. Cryoprecipitate 10 bags (approximately 10-15 mL each) OR 1 unit per 10 kg of body weight

Answer 99

Often a history of alcohol abuse, cirrhosis, ascites, prior UGIB

Answer 100

Nonsteroidal anti-inflammatory drug (NSAID) use, Helicobacter pylori infection

Answer 101

forceful vomiting → Longitudinal tear of the esophageal mucosa

Answer 102

history of aortic procedure, Massive bleeding

Answer 103

``` Arteriovenous malformation (AVM) by history Angiodysplasia ```

Answer 104

``` Diverticular disease (Elderly) Colitis Polyps Malignancy Brisk UGIB Hemorrhoids ```

Answer 105

1. Gastric, duodenal, esophageal, and stomal ulcers are the most common causes of UGIB (d/t ASA, NSAIDs, steroid use, H. pylori infection, and smoking) 2. Gastric erosion and esophagitis are also common causes of UGIB (alcohol use, NSAIDs/ASA use, stress from severe illness such as sepsis and trauma) 3. Esophageal and gastric varices result from portal HTN d/t liver cirrhosis 4. Mallory-Weiss bleeding occurs secondary to a mucosal tear at the gastroesophageal junction, usually secondary to repeated vomiting episodes

Answer 106

(bright red blood per rectum or maroon-colored rectal bleeding)

Answer 107

1. LGIB can be classified according to pathophysiologic causes: inflammatory, vascular, oncologic, traumatic, or iatrogenic. 2. Diverticulosis represents approximately 30% of LGIB 3. Diverticular bleeding is usually painless and results from a penetrating artery erosion. 4. AVM and angiodysplasia are the next most common causes of LGIB, followed by ischemic colitis and mesenteric ischemia 5. Other less common causes of LGIB include colonic polyps, malignancy, anticoagulation side effects, radiation side effects, and inflammatory bowel diseases.

Answer 108

1. thrombosis or embolism of the superior mesenteric artery 2. mesenteric venous thrombosis 3. and non-occlusive mesenteric ischemia due to a low flow state.

Answer 109

1. In liver disease, the pathophysiology of hemostasis is complex and difficult to assess accurately with the available routine laboratory tests 2. The liver synthesizes both clotting factors and endogenous anticoagulant factors such as protein C and antithrombin. Both are equally underproduced in cirrhotic patients. This phenomenon leads to “rebalanced hemostasis,” which causes cirrhotic patients to have a close-to-normal clotting tendency but abnormal routine coagulation studies

Answer 110

1. In most cases, the hemoglobin target is >70 g/L 2. Actively bleeding patients with thrombocytopenia (<50,000/μL) should receive a platelet transfusion 3. Non-cirrhotic coagulopathic patients with a prolonged PT and INR >2.0 should receive FFP transfusion (The management of coagulopathy due to cirrhosis is more complicated because the INR is not an accurate reflection of hemostasis in cirrhotic patients)

Answer 111

1. Proton Pump Inhibitor. The evidence supporting the benefit of PPIs in UGBI is limited. Current guidelines recommend an initial bolus of 80 mg, followed by a continuous infusion at 8 mg/h for 72 h 2. Prokinetics. Prokinetic agents such as erythromycin and metoclopramide improve gastric visualization at the time of endoscopy 3. TXA might be useful for cases in which MTP is req'd, in the treatment of patients with complex coagulopathic profiles (DOAC's), or in patients with evidence of hyperfibrinolysis (cirrhotic's w/ low fibrinogen levels). The loading dose is 1 g IV followed by continuous infusion of 3g over 24 h. 4.

Answer 112

1. Cirrhotic patients are prone to immunocompromise with a tendency toward developing infections secondary to the translocation of intestinal bacteria into the bloodstream. A meta-analysis concluded that antibiotic prophylaxis for cirrhotics with UGIB was associated with a reduction in overall mortality (NNT was 22 to prevent 1 death) Ceftriaxone 1 g IV 2. Somatostatin analogues (octreotide) inhibit the secretion of various gastric hormones and may reduce the risk of bleeding in patients with varices. 20-50 μg IV bolus followed by infusion of 25-50 μg/h. 3. Vasopressin is thought to be useful in variceal UGIB due to its vasoconstrictive property, reducing portal hypertension by way of vasoconstriction of the splanchnic circulation. Vasopressin might be useful in the management of hemodynamically unstable patients with variceal bleeding.

Answer 113

* Blakemore tube (BT) * OG tube * 2 three-way stopcocks * 4 dual Luer Lock caps * 1 Kelly clamp * Insufflating manometer * 50 cc syringe * Marking pen * Lube * 1L bag of fluid * Rolled gauze for traction * Basin of water

Answer 114

1. Resuscitate & Intubate. 2. Check for Leaks 3. Place Stopcocks 4. Label “G” on OG Tube (Place the OG tube next to the BT with the tip of the OG just above the gastric balloon. At the 50 cm mark on the BT, label the OG tube with “G” for gastric. 5. Label “E” on OG Tube (Place the OG tube next to the BT with the tip of the OG just above the esophagus balloon. At the 50 cm mark on the BT, label the OG tube with “E” for esophagus.) 6. Insert Balloon 7. Partially Inflate Gastric Balloon (50 cc of air) 8. Get Chest X-Ray (confirm balloon placement in the stomach) 9. Fully Inflate Gastric Balloon (250cc air) 10. Apply Traction (1kg traction using 1L NS bag) 11. Suction the Stomach 12. Insert the OG (until the “G” is at the 50 cm mark on the Blakemore) 13. Suction the Lower Esophagus

Answer 115

1. A-B-C 2. If unstable assume UPPER GI Bleeding 3. Intubate early for airway control 4. Replace blood with blood (permissive hypotension) 5. Reverse Bleeding disorders ○ Vit K if INR high (eg: 10 mg IV), ○ DDAVP (0.4mcg/kg IV over 10 minutes) if plt or renal disorder 6. PPI eg: Pantoprazole 80 mg IV, then 8 mg/hr 7. Octreotide eg: 50 mcg IV bolus 8. Call EPOS stat 9. Consider: ○ Antibiotics eg: Ceftriaxone 1 gram IV ○ Blakemore Tube or similar ○ Transport destination: Is surgery/IR available?

Answer 116

1. Upper GI bleed: typically originates proximal to the ligament of Treitz in the distal duodenum. 2. Lower GI bleed: bleeding starts distal to the ligament of Treitz.

Answer 117

duodenal ulcers, gastric ulcers, gastritis, esophageal varices and esophagitis

Answer 118

diverticula, arteriovenous malformations, polyps and cancer