UWorld-GI
Absent liver conjugation enzymes -Pt presents w/*Crigler-Najjar syndrome* → pathophys is *genetic lack of UGT enzyme* → presents as: 1-Increased bilirubin levels in infants *20-25 mg/dL but up to 50mg/dL* 2-Kernicterus --*severe jaundice* --*Neurological impairment* (Muscle rigidity, lethargy, seizures) Deficient bilirubin excretion into bile canaliculi -Seen in Dubin Johnson -> usually is asymptomatic & presents later in life with black colored liver
A 1-month-old caucasian presents w/a Hx of persistent jaundice experiences muscle rigidity, lethargy, & seizures. Which of the following causes of hyperbilirubinemia is most likely to produce this pt's abnormalities? (Absent liver conjugation enzymes OR Deficient bilirubin excretion into bile canaliculi)
Vit E deficiency -Deficiency predisposes cell membranes to oxidative injury → cells most susceptible are *neurons w/long axons & RBC's* → most common manifestations are: 1-*Neuromuscular disease* (skeletal myopathy, spinocerebellar ataxia, polyneuropathy) --Peripheral nerve dysfunction → *hyporeflexia, decreased proprioception* 2-*Hemolytic anemia* Niacin deficiency & Riboflavin deficiency -Would present w/: 1-Would not be affected by fat malabsorption
A 15B, presents for a follow-up apt. Since early childhood, he has suffered from recurrent respiratory infections & chronic diarrhea. The pt has been hospitalized several times for parenteral antibiotic tmt. Current prescribed meds include pancreatic enzyme therapy & a number of dietary supplements. PE shows decreased proprioception & hyporeflexia in the LE. Labs are suggestive of mild hemolytic anemia. Which of the following conditions is the most likely cause of these findings? (Niacin deficiency OR Riboflavin deficiency OR Vit. E deficiency)
Serum triglycerides -Top two factors predisposing to pancreatitis are alcohol & gallstones -pt is a young male & does not consume alcohol → *unlikely to have gallstones* -Other risk factors 1-ERCP 2-Drugs (Azathioprine, sulfasalazine, furosemide, valproic acid) 3-Infections (Mumps, coxsackie, mycoplasma) 4-Structural abnormalities of pancreatic duct (stricture, cancer, pancreas divisum) OR of ampullary region (Choledochal cyst, stenosis of sphincter of Oddi) Serum ceruloplasmin -describes *Wilson's disease* → Pt would present w/Cirrhosis, CNS involvement (basal ganglia), Kayser-Fleischer rings *does not predispose pts to pancreatitis*
A 23M, is hospitalized w/acute pancreatitis that resolves rapidly on fasting. He has suffered 2 similar episodes during the past 2 years. A gallbladder US obtained during a previous episode was normal. The pt has no sig PMHx & takes no meds. He does not drink alcohol. Which of the following tests should be considered during the workup of this pt? (Serum ceruloplasmin OR Serum triglycerides)
Thickening of the muscularis mucosae -CD is characterized by transmural inflammation all layers of small bowel wall → which can lead to *strictures (hypertrophy)*-> in question described as Thickening of the muscularis mucosae → can progress to *small bowel obstruction* Caseating granulomas in all layers of the intestine -Would be seen in *TB* *[Crohn's would present w/ non-caseating granulomas]*
A 25M, presents d/t worsening abd pain, distention, & nausea & vomiting for 3 days. He has a 4-yr Hx of recurrent abd pain associated w/diarrhea, low-grade fever, and easy fatiguability. The symptoms usually occur after stress & resolve spontaneously in a few days. However, this time, the pt's symptoms persisted & worsened. He has not other sig PMHx & takes no meds. Temp is 100.8F, BP is 110/70, Pulse is 104/min, & RR is 16/min. BMI is 19. Exam shows a tender mass in the RLQ of the abdomen. Imaging is consistent w/small-bowel obstruction. Laparotomy reveals that the abd mass is composed of inflamed small bowel, adherent & indurated mesentery, & enlarged abd lymph nodes. The affected region of the small bowel is resected. Which of the following is most likely to be seen on histologic exam of this pt's intestine? (Caseating granulomas in all layers of the intestine OR Thickening of the muscularis mucosae
Decreased lower esophageal tone -Pt presents w/*GERD* → which presents w/: 1-Symptoms most common in I the mins or hours after eating 2-Burning, squeezing pain in the retrosternal area 3-Regurg of acidic (sour-tasting) stomach contents into the mouth RF -↑ in pregnancy → d/t elevated estrogen & progesterone levels → *leading to decreased LES tone* Diffuse spasm of the esophageal muscle -would present w/*difficulty swallowing foods & liquids* & sensation of food getting *stuck* in the esophagus -Pregnancy does not increase the risk of esophageal spasm
A 28F, at 32 wks presents for a routine prenatal visit. The pt has had burning, squeezing pain in the middle of her chest that lasts for mins to hours at a time & usually occurs after meals. The pain is occasionally accompanied by small amounts of sour-tasting material in the back of her throat. The pt does not have any abd pain, emesis, or visible blood in her stool. Her pregnancy has been complicated by GDM, which has been well controlled w/nutritional therapy & exercise. She does not drink, smoke, or use drugs. Vitals are normal. Fundal Ht is 32cm & fetal heart tones are normal. Which of the following is the most likely cause of this pt's symptoms? (Decreased lower esophageal tone OR Diffuse spasm of the esophageal muscle)
VIP -Pt presents w/*VIPoma* which presents w/*WDHA/pancreatic cholera* 1-*Watery diarrhea* (often >3x's day) 2-Hypokalemia 3-*Achlorhydria* (pt shows total lack of gastric acid secretion) 4-Somatostatin would inhibit secretion of VIP -> *relieving her symptoms* Motilin -Stimulates smooth muscle contraction in the upper GI tract → only seen in periods of hunger
A 32F, presents d/t 6month Hx of persistent diarrhea. She has had 8-10 episodes a day of tea-colored, odorless, watery stools. The symptoms have persisted despite a lactose-free diet & a fasting trial. The pt has had no abd pain, fever, or vomiting. Temp 98F. Abd exam is unremarkable. Sampling of her gastric contents shows a total lack of gastric acid secretion. Somatostatin tmt promptly relieves the symptoms. An excess of which of the following hormones is most likely responsible for her symptoms? (Motilin OR VIP)
Hep B infection -Biopsy would show → Finely granular, diffusely homogenous, pale eosinophilic cytoplasm (ground-glass hepatocytes) *large hepatocytes filled w/granular, homogenous. pale pink cytoplasm* Non-alcoholic steatohepatitis -*Hepatic steatosis* is characterized by the accumulation of large & small vesicles of fat w/in hepatocytes → would be seen w/*obesity* in non-alcoholic steatohepatitis
A 32M, presents d/t several months of fatigue & wt loss. The patient has no sig PMHx. He drinks 1-2 alcoholic beverages daily & has used illicit IV drugs in the past. He is sexually active w/his GF. The pt has a maternal aunt w/hypothyroidism, but his family Hx is otherwise unremarkable. Temp is 98F, BP is 110/70, Pulse is 65/min, RR is 18/min. PE is normal. A liver biopsy shows large hepatocytes filled w/granular, homogenous, pale pink cytoplasm. Which of the following is the most likely Dx? (Hep B infection OR Non-alcoholic steatohepatitis)
Reduced intestinal Ca+ oxalate formation -Crohn's would present w/*calcium oxalate stones* -Crohns causes less bile acids to be reabsorbed -> this causes an imbalance in the cholesterol:Bile acid ratio -> supersaturation of cholesterol in bile leads to Gallstones -Additionally, the cholesterol will bind to calcium which will cause an increase in oxalate -> increased oxalate will cause stones Rapid cell turnover -Pt would present w/*uric acid stones* → seen in conditions such as 1-Myeloproliferative disease 2-Hemolytic anemia [pt has Crohn's]
A 33M, w/ a 2-year Hx of Crohn's presents w/left-sided flank pain that started in the morning. Urinalysis shows hematuria. A day later, the pt passes a urinary stone. Abd imaging reveals several additional kidney stones. Which of the following is the most likely underlying cause of this pt's kidney stones? (Rapid cell turnover OR Reduced intestinal Ca+ oxalate formation)
Intraabdominal pressure -Pt presents w/*mallory Weiss* → pathology is *longitudinal mucosal tears* at the esophagogastric-squamocolumnar junction → most commonly occur *secondary to rapid increase of intraabdominal & intraluminal gastric pressure → that occurs during retching & vomiting* Venous pressure -Would be seen in esophageal varices [endoscopy would not show longitudinal tears]
A 35M, alcoholic, presents to ER w/hematemesis. Prior to this, he has had three episodes of vomiting. BP is 110/80, Pulse is 98/min. He has no jaundice. Lungs are clear to auscultation. Abd is soft, non-tender, & non-distended. There is no hepatomegaly. Endoscopy shows longitudinal mucosal tears at the gastroesophageal junction. This pt's condition is most likely related to which of the following? (Intraabdominal pressure OR Venous pressure)
Gastric lymphoma -Pt presents *antral-predominant gastritis → seen w/*unchecked duodenal ulcers* → d/t *H.pylori infection* -Presentation 1-Vague epigastric pain 2-Occasional nausea 3-Bloating 4-Mild epigastric tenderness to deep palpation Ileal obstruction -Seen in *Crohn's disease* not in H.pylori
A 36F, presents d/t vague epigastric abd pain, occasional nausea, & bloating. She has no associated weight loss. PMHx is notable for moderate obesity & chronic allergic rhinitis. The pt takes no meds & does not smoke, drink, or use drugs. She was a vegetarian for several years but now consumes a wide variety of foods, including meat. The pt has traveled abroad extensively in the past. Vitals are normal. Exam shows a mild epigastric tenderness to deep palpation. Labs reveal mild anemia. Upper GI endoscopy shows diffuse erythema of the antral mucosa. Biopsy reveals an inflammatory cell infiltrate involving the superficial mucosal layers. The underlying cause of this pt's current condition can also lead to which of the following? (Gastric lymphoma OR Ileal obstruction)
Smooth muscle cells -Pt has taken an *opioid* →can cause contraction of *smooth muscle cells* in the sphincter of Oddi leading to spasm & *new on-set upper abd pain*
A 40F, presents to the ED after experiencing a right knee injury. She was mountain hiking w/some friends when she slipped down a steep slope & landed awkwardly on her right leg. After preliminary assessment, she is treated w/an opioid analgesic & her knee pain decreases significantly. Soon after administration, however, the pt experiences new-onset upper abd pain that makes it difficult for her to lie still. Vital signs are normal. BMI is 34. PE shows tenderness over the RUQ. An adverse drug effect involving which of the following structures is most likely responsible for this pt's current condition? (Gastric epithelium OR Smooth muscle cells)
Gemfibrozil -MOA of fibrates is inhibition of rate-limiting enzyme *7-alpha-cholesterol-hydroxylase* → results in *reduced bile acid production & ↓ cholesterol solubility* → increases microcrystal precipitation thereby *promoting gallstone formation* Ezetimibe -Blocks intestinal cholesterol absorption → ↓liver cholesterol stores & ↓ biliary cholesterol content -AE → *Elevated transaminases* especially w/concurrent statin use
A 42F, presents w/persistent hyperlipidemia despite 6 months of maintaining a healthy diet & exercising regularly. Although her PMHx is sig for biliary colic secondary to gallstones, the pt has refused elective cholecystectomy. Her father dies of an MI at age 54, & her mother has DM. Temp is 97F, BP is 122/79, Pulse is 78/min, & RR are 14/min. Exam shows no abnormalities. Labs obtained 1 week ago show elevated serum triglycerides & LDL cholesterol levels. Drug therapy is discussed w/the pt. Given this pt's pre-existing gallbladder disease, which of the following drugs should be avoided? (Ezetimibe OR Gemfibrozil)
Gastrin -Pt presents with *gastrinoma* d/t *ZES* → often presents w/multiple peptic ulcers that can be located *beyond the duodenal bulb* VIP -Pts typically present w/: 1-*Diarrhea that persists w/fasting* 2-Achlorhydria 3-Hypokalemia
A 46F, presents w/persistent diarrhea, weight loss, & abd pain. Her diarrhea started several months ago. She has no fever, melena, or hematochezia. The pt has not traveled outside of the country & has not drunk from any untreated freshwater sources. She has had no recent hospitalizations or antibiotic use. Her sis has a Hx of celiac disease. Upper endoscopy reveals post bulbar duodenal & jejunal ulcers. This pt most likely has tumor secreting which of the following molecules? (Gastrin OR VIP)
C.diff -May present w/: 1-Diarrhea 2-Abd pain 3-fever 4-Colonic perforation 5-Pseudomembranes Salmonella typhi -Would present w/*typhoid fever* → which would present w/Bloody diarrhea, abd pain, high fever, *salmon-colored macules mainly on trunk*
A 46M, w/HIV is hospitalized w/fever, cramping abd pain, & watery diarrhea. Evaluation shows high fever, hypotension, tachycardia, & lower abd distention & tenderness. Abd XR reveals free intraperitoneal air, & the pt is taken for urgent exploratory laparotomy. Operative findings include an erythematous & dilated colon. A focus of bowel wall necrosis w/perforation is resected. Histopath reveals acute inflammatory changes & epithelial necrosis (shown). There is a layer of denuded epithelium, fibrin, & inflammatory cells overlaying the mucosa (arrows). Which of the following is the most likely responsible pathogen? (C.diff OR Salmonella typhi)
Succinate DH -Pts presents w/*riboflavin deficiency* → suggested by *low urinary riboflavin excretion* -Riboflavin def is rare but can be seen in: 1-*alcoholics* 2-Severely malnourished → presents w/: 1-*Angular stomatitis* 2-*Cheilitis* 3-*Glossitis* 4-Seborrheic dermatitis 5-Eye changes (keratitis, corneal neovascularization) 6-Anemia Riboflavin is key for enzymes of ETC → *FAD/FADH2, FMN/FMNH2* Succinate thiokinase & isocitrate DH -Both in TCA but do not use *FAD/FMN* as co-factors
A 47M, homeless man comes to the ED d/t a "pins-and-needles" sensation in his legs. He also has painful lesions on his lips & corners of his mouth. He has had no loss of consciousness, nauseas, vomiting, or diplopia. The pt drinks alcohol heavily on a daily basis & has a Hx of IV heroin use. On PE, he appears unkempt & ill appearing. Temp is 98.2F, BP is 146/90, pulse is 106/min. He has glossitis & angular stomatitis. Abd exam reveals hepatomegaly. Labs show low urinary riboflavin (B2) excretion. Activity of which of the enzymes is most likely impaired in this pt? (Succcinate DH OR Succinate thiokinase OR Isocitrate DH)
Achalasia -Would Dx'd w/ manometry → presents w/: 1-*Dysphagia* 2-Regurgitation 3-*retrosternal pain* 4-Manometry findings → ↓ LES tone Esophageal stricture -Would present w/progressive *solid food* dysphagia → Pt would have a long Hx of GERD -would not be Dx'd w/manometry
A 48M, is evaluated for retrosternal discomfort & dysphagia for the past several months. He smokes a pack of ciggs daily & drinks alcohol on the weekends. BMI is 32.8. PE is unremarkable. Manometry results are shown. Which of the following is the most likely Dx? (Achalasia OR Esophageal stricture)
Abetalipproteinemia -Microscopic finding → normal intestinal mucosa, but *enterocytes contain clear or foamy cytoplasm* (more prominent in the tips of the vili) -D/t loss of function of *MTP-gene* → presents w/: 1-*Manifestation w/in first year of life* 2-*Malabsorption symptoms* 3-Deficiency in fat soluble Vitamins & essential FA's → resulting in Acanthocytes on PBS 4-Neuro abnormalities (progressive ataxia, retinitis pigmentosa) 3-Labs → --↓↓ plasma Triglycerides --↓↓ Cholesterol levels -- *absent* (chylomicrons, VLDL's, & apoB) Whipples -Micro finding →Distended M∅ in the lamina propria of SI → w/ M∅ staining *PAS positive* & diastase-resistant granules & *rod-shaped T.whippeli*
A 5-month-old B, is being evaluated for poor wt gain since birth. He is noted to have bulky & greasy stools.A jejunal biopsy shows the findings. This pt most likely suffers from which of the following conditions? (Abetalipproteinemia OR Whipples)
Increased absorption of nitrogenous substances by the gut -A GI bleed cause increased nitrogen delivery to the gut in the form of Hb → *Hb is then converted to ammonia* & absorbed into the bloodstream Accumulation of BUN -suggests renal failure [would not be seen w/ GI bleed]
A pt w/ a PMHx sig for Hep C infection presents to the ED w/ a GI bleed. 24 hours later, he presents w/ Hyperammonemia symptoms. Which of the following events is the most likely precipitant of this pt's altered mental status? (Accumulation of blood urea nitrogen OR Increased absorption of nitrogenous substances by the gut)
Red pulp expansion -Pt has a Hx of sig alcohol & IV drug abuse → has evidence of *alcoholic liver disease - ALD* 1-Acute hemorrhage is usually seen w/*normal MCV* 2-ALD usually causes --*Thrombocytopenia* d/t decreased plts production --Increased plts destruction --Splenic sequestration *Expansion of red pulp - enlarged spleen* Extramedullary hematopoiesis -Seen in myelofibrosis -Would have *dry tap*
A 54M, presents to the ED after an episode of bloody vomiting. He has no fever, chills, abd pain, diarrhea, or constipation. The pt has a Hx of alcohol abuse w/multiple previous hospital admissions d/t alcohol withdrawal & generalized tonic-clonic seizures. He also has a PMHx of IV drug abuse & is currently enrolled in a methadone maintenance program. BP is 96/62, pulse is 102/min. On exam, the pt appears comfortable, but develops dizziness when asked to sit up. There is no JVD. The abd is distended w/dullness to percussion at both flanks. The liver is enlarged & the tip of the spleen is also palpable. There is trace pedal edema. Labs shows: -Hb----------------9.7 -MCV--------------98 -Leuko's------------5K -Plts----------------78K Histopath exam of this pt's spleen is most likely to show which of the following? (Extramedullary hematopoiesis OR Red pulp expansion)
Malignancy mets via portal circulation -Most common cause of liver mets is *colorectal cancer* → which spreads directly from colon or superior rectum thru the *portal venous circulation* to the liver Malignancy mets via hepatic veins -Hepatic vein *drains liver* does not bring blood to liver Transcoelomic spread of malignancy -Although GI cancers can spread to the peritoneum & then invade liver → *it is far less common than hematogenous dissemination thru portal system*
A 65F, has had several months of progressive fatigue, diminished appetite, & unintentional weight loss. The pt has no chronic med conditions. She has not received medical care in many years & has not had recommended cancer screening. The pt suddenly dies while undergoing evaluation. Autopsy reveals abnormal findings associated with metastatic malignancy. Microscopic evaluation of the lesions shows neoplastic cells. Which of the following is most likely cause of this pt's liver lesions? (Malignancy spread via the hepatic veins OR Malignancy spread thru the portal circulation OR Transcoelomic spread of malignancy)
Splenic vien -Pt presents w/*gastric fundus varices only* Left gastric vein -Pt would present w/ *gastric & Esophageal varices* [Pt's esophagus is normal]
A 64M, presents to the ED after an episode of hematemesis. He also reports dark stools & abd pain for the past several days. The pt has PMHx sig for chronic pancreatitis. Abd exam shows epgatric tenderness to palpation. Rectal exam is notable for black, guaiac-positive feces. Upper GI endoscopy reveals a bleeding spot w/in a cluster of enlarged torturous veins in the gastric fundus. The rest of the stomach & esophagus appears normal. Increased pressure in which of the following vascular structures is the most likely cause of this pt's condition? (Left gastric vein OR Splenic vein)
Liver -Infarcts in liver are rare b/c it has *dual blood supply* (hepatic artery & portal venous supply) Organ susceptible to infarction after occlusion of a feeding artery are ranked from *greatest → least* CNS → Myocardium → Kidney → Spleen → *liver*
A pt presents w/a thrombus in a dilated left atrium. In the event of an interruption of blood flow secondary to arterial occlusion, which of the following organs would be least vulnerable to infarction? (Spleen OR Liver)
Malignancy mets via portal system -Most common cause of liver mets is *colorectal cancer* → which spreads directly from colon or superior rectum thru the *portal venous system* to the liver Malignancy mets via hepatic veins -Hepatic vein *drains liver* does not bring blood to liver Transcoelomic spread of malignancy -Although GI cancers can spread to the peritoneum & then invade liver → *it is far less common than hematogenous dissemination thru portal system*
A 65F, has had several months of progressive fatigue, diminished appetite, & unintentional weight loss. The pt has no chronic med conditions. She has not received medical care in many years & has not had recommended cancer screening. The pt suddenly dies while undergoing evaluation. Autopsy reveals abnormal findings (shown). Microscopic evaluation of the lesions shows neoplastic cells. Which of the following is most likely cause of this pt's liver lesions? (Malignancy spread via the hepatic veins OR Malignancy spread thru the portal circulation OR Transcoelomic spread of malignancy)
Absence of muscularis propria -Pt presents w/*diverticulosis* → which is a false diverticula & only has 1-Mucosa 2-Submucosa 3-*missing muscularis propria* herniate thru a focal weakness in the muscularis Normal colonic layers -Describes conditions where all three layers of mucosa are present (Meckles, Congenital colonic diverticulosis)
A 68F, is evaluated after recurrent episodes of bright red blood per rectum. She has had no abd pain, nausea, vomiting, or hematemesis. PMHx is sig for HTN & obesity. She is a smoker, has a sedentary lifestyle, & consumes processed food & red meat frequently. Abd exam shows no abnormalities. Colonoscopy reveals numerous mucosal outpouchings in the sigmoid colon, & sigmoid colectomy is performed. Histopath of this pt's colonic lesions is most likely to reveal which of the following? (Absence of muscularis propria OR Normal colonic layers)
Acute diverticulitis -Presents w/: 1-Constant abd pain → *classically LLQ abd pain* 2-Nausea, vomiting 3-*Change in bowel habits* (pt has loose stools) 4-*Lower abd tenderness* 5-*Palpable mass* (d/t inflammation or abscess formation) 6-*Leukocytosis* in labs Ischemic colitis -Common cause of lower abd pain in adult → however, presents w/: 1-Hematochezia 2-Postprandial pain -In pt's w/*ischemic RF's* (HTN, DM)
A 73F, presents d/t a 10-day Hx of abd pain & loss of appetite. The pt does not like "going to the doctor" & has not been seen by a physician in many years. Frequent loose stools & loss of appetite have been present since the pain began. FHx is sig for colon cancer in a maternal aunt. Temp is 100F, & pulse is 98/min. Abd exam is sig for tenderness on deep palpation of the left lower quadrant, along w/an appreciable mass. There is no inguinal lymphadenopathy. WBC count is 15K. Which of the following is the most likely cause of the abd pain in this pt? (Acute diverticulitis OR Ischemic colitis)
Left gastric -Found on the lesser curvature of the stomach Gastroduodenal -Supplies the pylorus & proximal duodenum → ulcer would have to be in *posterior duodenal bulb* [not on lesser curvature]
A pt presents w/an ulcer & dies from a complication. Autopsy shows a deep peptic ulcer localized proximally on the lesser-curvature of the stomach. The ulcer most likely penetrated which of the following arteries? (Gastroduodenal OR Left gastric)
Ileum -Pt likely has *gallstone ileus* which is an uncommon complication of long-standing cholelithiasis that occurs in elderly women → the gallstone travels until it gets stuck in the ileum (the smallest portion of the intestine) →pts may presents w/ signs of *small bowel obstruction, including: 1-Abd pain/distention 2-Nausea/vomiting 3-high pitched (tinkling) bowel sounds 4-Tenderness to palpation 5-*pneumobilia* air in the biliary tree
A female pt w/a Hx of gallstones has an abd XR that reveals air in the gallbladder & biliary tree. This pt had a gallstone that was most likely lodged where? Duodenum OR Ileum
Inhibiting viral genome replication & assembly -NS5A inhibitor → crucial for viral replication & assembly Blocking reverse transcriptase of viral RNA -HCV does not contain a reverse transcriptase
A pt has a PMHx sig for Hep C. After appropriate counseling is provided, combination therapy w/sofosbuvir & ledipasvir is planned. This tmt is most likely to help clear the infection thru which of the following mechanisms? (Blocking reverse transcriptase of viral RNA OR Inhibiting viral genome replication replication & assembly)
Duodenal S-cells → Secretin stimulates the exocrine pancreatic ductal cells to secrete a fluid that is ↑HCO3 & ↓Cl-
A pt has pancreatic deficiency. However, bicarbonate is still released from the duodenum. What cells are responsible for this?
Femoral artery → External iliac → common iliac → abd aorta → inferior mesenteric -Structures supplied by the IMA are the *Hindgut structures* → which include: -The distal 1/3 of the transverse colon -Descending colon -Sigmoid colon -Rectum
A pt is being prepped for catheterization planned via the femoral artery to the sigmoid colon. During the procedure, the arterial catheter is most likely to proceed in which of the following orders?
Each drug as its own AE, including: -Mg+ salts may cause diarrhea -Al+ hydroxide may cause constipation -Together these two drugs will offset each other's AE
A pt is given a combination of Mg+ & aluminum hydroxide as an antacid. What is the rational for this?
Pt has an infection w/ *C.diff* → C.diff has two toxins; *Toxin A (enterotoxin)* & *Toxin B (cytotoxin)*→ both act synergistically to causes disruption → the toxins bind to specific receptors on intestinal mucosal cells, & are internalized allowing them to exert their effects → *Both toxins inactivate Rho-regulatory proteins (involved in signal transduction & actin cytoskeleton structure maintenance)* → as a result they cause a *disruption of tight intracellular junctions (leading to cell rounding/retraction as well as increased paracellular intestinal fluid secretion)* → this leads to *recruitment of neutro's & induction of apoptosis*
A pt is started on a course of antibiotics & soon after develops watery diarrhea. CBC shows leukocytosis. The toxin most likely responsible for his current condition primarily damages which of the following components of intestinal mucosal cells?
Internal iliac -Channels *proximal the anal dentate line* → drain to the inferior mesenteric & *internal iliac nodes* Left colic -Would drain the left colic flexure & upper descending colon
A pt presents w/ a firm palpable mass in the rectal vault. Flexible rectosigmoidoscopy shows a large ulcerative mass in the middle third of the rectum extending to the rectosigmoid junction. Frozen section analysis reveals clear margins of the colon specimen w/ mets in the para-rectal LN's. Which of the following LN groups should be sampled in the pt for further assessment of mets? (Internal iliac OR Left colic)
Duodenum -Caused by H.pylori → unlikely to be malignant Stomach -Gastric ulcer → can be malignant especially if associated w/ gastric adenocarcinoma
A pt presents w/ an ulcer. The pt is told that based on the location of the ulcer it is very unlikely to be malignant. Where is the most likely location of the ulcer? Duodenum OR Stomach
-*↑* gastric pH → b/c of atrophic tissue leading to *achlorhydria* -*↑* gastrin → in response to increased gastric pH -*↓* parietal cell mass → b/c of atrophic mucosa leading to destruction of parietal cells
Describe the expected levels (increased or decreased) of -Gastrin -Gastric pH -Parietal cell mass seen in pernicious anemia?
Somatostatin -Also *Octreotide -> somatostatin analog* -Inhibit the release of endogenous hormones (glucagon, VIP, Intestinal peptide) that induce splanchnic vasodilation → *so directly reduce portal blood flow* CCK -Contracts the gallbladder & & expulsion of pancreatic exocrine secretions into the duodenum → would be counter-productive b/c would increase glucagon secretion (vasodilator)
After the pt (with Alcoholic liver disease) is stabilized w/IV fluids & blood products, the pt develops another bout of bloody emesis. Urgent upper GI endoscopy confirms esophageal varices. Which of the following peptides is most likely to immediately decrease the portal venous pressure in this PT? (CCK OR Somatostatin)
Galactokinase (GALK) -Pt likely has *galactosemia* → which presents w/: 1-Cataracts 2-Urine positive for reducing substrates 3-*no other serious manifestations* *Side note* → GALT deficiency would have serious systemic deficiencies and would present in infancy Aldolase B -hereditary fructose intolerance → will present w/ Hypoglycemia, hypophosphatemia, & failure to thrive *no cataracts*
Aldolase B OR Galactokinase
Failure of prrimitive foregut to separate from airway -This pt presents w/*TEF* → which presents w/: 1-*significant drooling* 2-*coughing, choking, cyanosis w/feeds* 3-XR→ stomach bubble 4-Pregnancy Hx of polyhydraminos Obstruction of posterior nasal passage -This is *choanal atresia* → can present w/cyanosis when feeding & upper airway obstruction *would not present w/ excessive drooling* Collapse of the supraglottic structures during respiration -This is laryngomalacia → presents w/inspiratory stridor that is worse in the supine position & improves w/ upright positioning *this is not described in the stem*
Collapse of the supraglottic structures during respiration OR Failure of the primitive foregut to separate from the airway OR Obstruction of posterior nasal passages
There is one mRNA for both enzymes -In prokaryotes: --*one mRNA transcript contains the sequence for many proteins --a single mRNA molecule can be translated into multiple proteins or polypeptides There are two operators for one repressor protein -Lac operon has a *single operator*
E.coli grows on a lactose-containing medium up-regulate the production of the enzymes β-galactosidase & galactosidase permeate. Which of the following best explains the synchronous production of both enzymes in response to lactose? (There are two operators for one repressor protein OR There is one mRNA for both enzymes)
*Increased Serum leptin levels are highly correlated w/ ↑BF content (↑BMI)* → leptin has two main functions: 1-Decreases the production of neuropeptide Y *(a potent appetite stimulant)* in the arcuate nucleus of the hypothalamus 2-Simulates the production of POMC in the arcuate nucleus → POMC is cleaved to form α-melanocytes stimulating hormone *αMSH* which *inhibits food intake*
How are BMI & leptin levels related?
Coating of viral particles -Hep D antigen (HDAg) *must be coated by the external coat HBsAg* to penetrate the hepatocyte
How does Hep B help Hep D? (Coating of viral particles OR Replication of viral RNA)
Metastatic liver disease -The CT shows *multiple hypodense masses in the liver* which wold be consistent w/ metastatic liver disease → Metastasis is the most common malignant neoplasm of the adult liver (20x's more common than HCC) -Pts may be *asymptomatic* → only when the hepatic parenchyma is destroyed or the major bile ducts are obstructed will pts present w/ symptoms Intrahepatic cholangiocarcinoma -Grossly → would present as tree like mass that grows along the biliary system
Intrahepatic cholangiocarcinoma OR Metastatic liver disease
GTP -Ras is in family of *G-proteins* cAMP - seen in substances that use ATP
Molecular testing of a mutation in the KRAS gene results in the constitutive activation of the Ras protein. Under normal circumstances, this protein is only active when bound to which of the following substances? (cAMP OR GTP)
Infiltrative growth w/in the stomach wall -The image shows *signet-ring carcinoma* → which is 1 of 2 types gastric adenocarcinoma → *signet rings shows a clear space w/ the nucleus in the periphery* -Pt has a presentation that more accurately present adenocarcinoma Rugal thickening w/acid hypersecretion -Seen w/H.pylori or ZES [no signet cells would be seen on Microscopy]
The lesion most likely demonstrates which of the following? (Infiltrative growth w/in the stomach wall OR Rugal thickening w/acid hyper-secretion)
Tumor cell deposits in the regional LN's -LN spread is the strongest predictor of metastatic potential & is associated w/increased risk for incurable, distant disease
The presence of which of the following indicates a poor prognosis in colon cancer? (Malignant cells invading the lamina propria OR Tumor cell deposits in the regional LN's)
Brown → Biliary tract infections (bacteria produce β-glucuronidase) Black -Chronic hemolysis
What are brown Vs black pigment stones associated with? (-Biliary tract infections -Hemolysis)
Either a toxic or ischemic injury to acing cells that leads to *premature activation of trypsin (from trypsinogen)* inside the pancreatic acini
What does the pathogenesis of acute pancreatitis involve? (in terms of enzyme activation)
Overall action → used an anti-diarrheal agent *(slows motility)* MOA - target *mu opioid receptors*
What is dhiphenoxylate? What is its MOA & overall action?
Inactivates ribosomal subunits -Shiga-like toxin inactivates the *60s ribosomal subunit leading to inhibition of protein synthesis* Disrupts the cellular cytoskeleton -Describes C.diff *toxin B/Cytotoxin*
What is the MOA of EHEC? (Disrupts the cellular cytoskeleton OR Inactivates ribosomal subunits)
Celiac artery -*Origin* → Foregut -*Spinal level* → T12/L1 -*Innervation* → vagus -*Structures → (pharynx to Lower esophagus to proximal duodenum)* --Liver --Gallbladder --Pancreas --Spleen (mesoderm)
What is the embryologic origin of the Celiac artery? What spinal level is it located at? What is its innervation? What structures does it supply?
IMA -*Origin* → Hindgut -*Spinal level* → L3 -*Innervation* → Vagus -*Structures (Distal 1/3 of transverse colon → upper portion of the rectum)* → including: --Descending colon --Sigmoid colon --Rectum
What is the embryologic origin of the IMA? What is its spinal level? What is its innervation? What structures does it supply?
SMA -*Origin* → Midgut -*Spinal level* → L1 -*Innervation* → Vagus -*Structures (distal duodenum → proximal 2/3 of transverse colon)* → including: --Jejunum --Ileum --Cecum --Ascending colon
What is the embryologic origin of the SMA? What is its spinal level? What is its innervation? What structures does it supply?
Digestive enzyme deficiency -Pancreatitis in alcoholic pts is d/t *exocrine insufficiency* (deficiency in amylase, protease, & lipase) Bile salt malabsorption -would be seen in Crohn's
What is the mechanism of action of pancreatitis in an alcoholic? (Bile salt malabsorption OR Digestive enzyme deficiency)
1-Glycosylase (cleaves the altered base) 2-Endonuclease (cleaves the 5' end)→ 3-lyase (cleaves the 3' end) 4-polymerase 5-ligase
What is the order of the enzymes involved in DNA damage repair?
*Ventral* -Main pancreatic duct (proximal part) -Uncinate process -Inferior Part of head *Dorsal* -Superior aspect of head -Body -Tail -accessory pancreatic duct
What structures are derived from: the ventral pancreatic primordium VS the dorsal pancreatic bud
Decreased & increased -Statin inhibits HMG CoA reductase → *decreasing* hepatic cholesterol synthesis -Cholestyramine Binds bile-acid resins, causing increased bile acid excretion → leading to *Increased synthesis* of new bile acids
Which of the following best describes the independent effects of simvastatin & cholestyramine, respectively, on hepatic cholesterol synthesis? (Decreased & increased OR Decreased & decreased)
Decreased FFA oxidation -Alcohol inhibits FFA oxidation by using up all of the NAD+ *(↑NADH production)* Increased glucose uptake into cells -not associated with alcoholic hepatic steatosis
Which of the following is the most likely cause of this pt's condition? (Decreased FFA oxidation OR Increased glucose uptake into cells)
Fever, anorexia, & dark colored urine -The liver biopsy & pt's Hx of traveling to an area endemic to Hep A suggests Hep A which presents w/: -Biopsy → --Areas of *spotty necrosis w/ballooning degeneration* (hepatocytes swelling w/wispy clear cytoplasm) --Councilman bodies *(eosinophilic apoptotic hepatocytes)* --*Mono-nuclear Inflammatory cell infiltrates*
Which of the following is the most likely initial clinical presentation of this pt? Fever, anorexia, & dark colored urine OR Prolonge pruritus & fatigue
Obesity -Pt presents w/a PMHx sig for *GERD* that has progressed to dysphagia w/ solid foods, wt loss, & a *mass in the lower esophagus (seen as the white pale area in the gross photo)* → This should raise suspicion for *esophageal adenocarcinoma* → RF for esophageal adenocarcinoma are: 1-Chronic GERD 2-Obesity 3-Smoking 4-Use of meds that lower esophageal sphincter pressure *nitrates* 5-Consumption of processed meats
Which of the following is the most likely predisposing RF for this pt's esophageal disease? (H.pylori infection OR Obesity)