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473 Cards in this Set
- Front
- Back
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Question
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Answer
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Baby vomits milk when fed and has a gastric air bubble.
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Blind esophagus with lower segment of esophagus attached to trachea.
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After a stressful life event, 30-year-old man has diarrhea and blood per rectum; intestinal biopsy shows transmural inflammation.l
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Crohn’s disease.
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treatment for a Young man presents with mental deterioration and tremors. He has brown pigmentation in a ring around the periphery of his cornea and altered LFTs.
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Penicillamine for Wilson’s disease.
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most common cause 20-year-old male presents with idiopathic hyperbilirubinemia.
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Gilbert’s disease.
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55-year-old male with chronic GERD presents with esophageal cancer. what is the most common subtype
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Adenocarcinoma.
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Female presents with alternating bouts of painful diarrhea and constipation. Colonoscopy is normal.
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Irritable bowel syndrome.
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derivations of GI blood supply
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Embryonic gut region Celiac = Foregut SMA = Midgut IMA = Hindgut
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Structures supplied by celiac artery
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Stomach to proximal duodenum; liver, gallbladder, pancreas
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Structures supplied by SMA artery
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Distal duodenum to proximal 2/3 of transverse colon
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Structures supplied by IMA artery
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Distal 1/3 of transverse colon to upper portion of rectum
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Branches of celiac trunk:
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common hepatic, splenic, left gastric. These comprise the main blood supply of the stomach.
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Short gastrics have poor anastomoses if ?
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splenic artery is blocked.`
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If the abdominal aorta is blocked, these arterial anastomoses (with origin) compensate name 4
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Internal thoracic/mammary (subclavian) . Superior epigastric (internal thoracic) .Inferior epigastric (external iliac) Superior pancreaticoduodenal (celiac trunk) . Inferior pancreaticoduodenal (SMA) Middle colic (SMA) . Left colic (IMA) Superior rectal (IMA) . Middle rectal (internal iliac)
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Portal-systemic anastomoses name 5
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1. Left gastric ¨ azygous (esophageal varices) 2. Superior ¨ inferior rectal (external hemorrhoids) 3. Paraumbilical ¨ inferior epigastric (caput medusae at navel) 4. Retroperitoneal ¨ renal 5. Retroperitoneal ¨ paravertebral
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what verices are are commonly seen with portal hypertension
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Varices of gut, butt, and caput
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Coordinates Motility along entire gut wall. Contains cell bodies of some parasympathetic terminal effector neurons. Located between inner (circular) outer (longitudinal) layers of smooth muscle in GI tract wall.
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Myenteric (Auerbach's)
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Enteric nerve plexi. Which one Coordinates Motility along entire gut wall.?
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Myenteric (Auerbach's)
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Enteric nerve plexi. Which one Contains cell bodies of some parasympathetic terminal effector neurons?
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Both Myenteric (Auerbach's) and Submucosal (Meissner's)
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Enteric nerve plexi. Which one Located between inner (circular) and outer (longitudinal) layers of smooth muscle in GI tract wall.?
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Myenteric (Auerbach's)
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Enteric nerve plexi. Which one Regulates local Secretions, blood flow, and absorption?
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Submucosal (Meissner's)
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Enteric nerve plexi. Located between mucosa and inner layer of smooth muscle in GI tract wall?
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Submucosal (Meissner's)
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layers in order that a knife wuold go through in the lateral abdomen
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skin superficial fascia external oblique internal oblique tranversus abdominis transversalias facia extraperitoneal tissue peritoneum
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Secrete alkaline mucus to neutralize acid contents entering the duodenum from the stomach. Located in duodenal submucosa?
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Brunner’s glands
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the only GI submucosal glands
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Brunner’s glands
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Brunner’s glands what doe they secrete and why?
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alkaline mucus to neutralize acid contents entering the duodenum from the stomach.
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Brunner’s glands where are they?
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Located in duodenal submucosa (the only GI submucosal glands)
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Hypertrophy of Brunner’s glands is seen in?
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peptic ulcer disease.
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Hypertrophy of ?????? is seen in peptic ulcer disease
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Brunner’s glands
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Unencapsulated lymphoid tissue found in lamina propria and submucosa of small intestine. Contain specialized M cells that take up antigen
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Peyer’s patches
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Peyer’s patches special cells
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M cells
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what do stimulated B cells that leave peyer's patches become and how does it work
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IgA secreting plasma cells in mesinteric lymphnodes. IgA receives protective secretory component and is then transported across epithelium to gut to deal with intraluminal antigen.
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What to think about Peyer patch related antibodies
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Think of IgA, the Intra-gut Antibody. And always say “secretory IgA.
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what layer are peyer's patches in
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lamina propria and submucosa of small intestine.
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what are spaces of Disse
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perisinusoidal space in the liver
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where is the Cystic duct
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btw the gall bladder and the common bile duct
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what joins to make the common bile duct
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Cystic duct and Common hepatic duct
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lower Pectinate line what forms it
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Formed where hindgut meets ectoderm.
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Formed where hindgut meets ectoderm.
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Pectinate line
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Name the ligament that connects the Liver to anterior abdominal wall?
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Falciform
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Name the ligament that connects the Liver the the duodenum?
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Hepatoduodenal
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Name the ligament that connects the Liver to lesser curvature of stomach?
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Gastrohepatic
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Name the ligament that connects the Greater curvature and transverse colon?
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Gastrocolic
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Name the ligament that connects the Greater curvature and spleen?
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Gastrosplenic
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Name the ligament that connects the Spleen to posterior abdominal wall?
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Splenorenal
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What Structures are contained in the Falciform Ligament?
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Ligamentum teres
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What Structures are contained in the Hepatoduodenal Ligament?
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Portal triad: hepatic artery, portal vein, common bile duct
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What Structures are contained in the Gastrohepatic Ligament?
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Gastric arteries
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What Structures are contained in the Gastrocolic Ligament?
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Gastroepiploic arteries
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What Structures are contained in the Gastrosplenic Ligament?
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No vessels
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What Structures are contained in the Splenorenal Ligament?
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Splenic artery and vein
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Important GI ligaments which one May be compressed between thumb and index finger placed in epiploic foramen (of Winslow) to control bleeding?
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Hepatoduodenal
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Important GI ligaments which one Separates R greater and lesser sacs May be cut during surgery to access lesser sac?
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Gastrohepatic
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Important GI ligaments which one is part of greater omentum?
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Gastrocolic
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Important GI ligaments which one Separates L greater and lesser sacs?
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Gastrosplenic
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what is the clinical importance of the foramen of winslow
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Portal triad can be compressed by thumb and index finger to conrtol bleeding
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Layers of gut wall (inside to outside):
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mucosa submucosa muscularis externa serosa/advetiia
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Frequencies of basal electric rhythm: in the stomach and small bowel.
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Stomach––3 Hz Duodenum––12 Hz Ileum––8–9 Hz
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layers and functions of the gut wall mucosa
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mucosa is the inner most layer and its layers are epithelium (absorption), lamina propria (support), muscularis mucosa (motility)
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internal hemorrhoids: where are they? Arterial supply? Venous drainage? nervous system?
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Above pectinate line. Superioar rectal artery (from IMA). rectal artery (branch of IMA). Venous drainage is to superior rectal vein (inferior mesenteric vein) (portal system) Internal hemorrhoids receive visceral innervation, and are therefore NOT painful.n
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external hemorrhoids: where are they? Arterial supply? Venous drainage? nervous system?
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Below pectinate line Arterial supply from inferior rectal artery (branch of internal pudendal artery). Venous drainageto inferior rectal vein (internal pudendal vein) (internal iliac vein)(IVC). External hemorrhoids receive somatic innervation and are therefore painful.i
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which hemorrhoids are painful
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external hemorrhoids
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cancer and hemorrhoids
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External hemorrhoids/ squamous cell carcinoma. often mistaken of one another
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Femoral triangle Contains
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femoral nerve, artery, vein,
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Femoral region organization
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Lateral to medial: Nerve-(Artery-Vein-Empty space- Lymphatics) N-(AVEL)
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Femoral sheath what and where? contents?
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Fascial tube 3–4 cm below inguinal ligament Contains femoral vein, artery, and canal (deep inguinal lymph nodes), but not femoral nervea
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A hernia is a
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protrusion of peritoneum through an opening, usually sites of weakness.
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Diaphragmatic hernia what is it
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Abdominal structures enter the thorax;
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Diaphragmatic hernia in infants
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may occur in infants as a result of defective development of pleuroperitoneal membrane.
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Diaphragmatic hernia most common type and desciption
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a hiatal hernia, stomach herniates upward through the esophageal hiatus of the diaphragm.
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Paraesophageal Hernia
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GE junction is normal. Cardia moves into the thorax.
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which hernia Follows the path of the descent of the testes. Covered by all three layers of spermatic fascia.
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Indirect inguinal hernia
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Indirect inguinal hernia. Path?
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Goes through the INternal (deep) inguinal ring, external (superficial) inguinal ring, and INto the scrotum. Enters internal inguinal ring lateral to inferior epigastric artery.
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Indirect inguinal hernia. Who?
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INfants owing to failure of processus vaginalis to close. Much more common in males
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Direct inguinal hernia Path?
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Protrudes through the inguinal (Hesselbach’s) triangle. Bulges directly through abdominal wall medial to inferior epigastric artery. Goes through the external (superficial) inguinal ring only. Covered by transversalis fascia.
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Direct inguinal hernia Who?
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Usually in older men.
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Femoral hernia path?
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Protrudes through femoral canal below and lateral Leading to pubic tubercle.
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Femoral hernia Who?
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More common in women.
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Leading cause of bowel incarcerationo
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Femoral hernia
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Hiatal hernias: Mech
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Sliding (most common): GE junction is displaced
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which hernia has GE junction is displaced
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Hiatal hernias:
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which hernia has GE junction is normal
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Paraesophageal:
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Inguinal hernia mnemonic
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MDs don’t LIe: Medial to inferior epigastric artery = Direct hernia. Lateral to inferior epigastric artery = Indirect hernia.e
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Hesselbach’s triangle: borders
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Inferior epigastric artery Lateral border of rectus abdominis Inguinal ligament
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-Inferior epigastric artery -Lateral border of rectus abdominis -Inguinal ligament
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Hesselbach’s triangle: borders
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Salivary secretion glands and Which glands are most serous vs Mucinous
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Parotid (most serous), submandibular,submaxillary, and sublingual (most mucinous) glands.
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Function and contents of Saliva
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1. á-amylase (ptyalin) begins starch digestion; inactivated by low pH on reaching stomach 2. Bicarbonate neutralizes oral bacterial acids, maintains dental health 3. Mucins (glycoproteins) lubricate fooda
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saliva and autonomics which nerves
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Salivary secretion is stimulated by both sympathetic (T1¨CT3 superior cervical ganglion) and parasympathetic (facial, glossopharyngeal nerve) activity.
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saliva tonicity changes
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Low flow rate leads to hypotonic. High flow rate leads to closer to isotonic
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GI secretory products what cell and organ does Intrinsic factor come from?
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Parietal cells Stomach
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GI secretory products what cell and organ does Gastric acid come from?
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Parietal cells Stomach
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GI secretory products what cell and organ does HCO3 – come from?
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Mucosal cells Stomach Duodenum
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GI secretory products what cell and organ does Cholecysto- kinin come from?
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I cells Duodenum Jejunum
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GI secretory products what cell and organ does Pepsin come from?
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Chief cells Stomach
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GI secretory products what cell and organ does Gastrin come from?
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G cells Antrum of stomach
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GI secretory products what cell and organ does Secretin come from?
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S cells Duodenum
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GI secretory products what cell and organ does Somatostatin come from?
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D cells Pancreatic islets GI mucosa
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GI secretory products what cell and organ does Gastric inhibitory peptide (GIP) come from?
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K cells Duodenum Jejunum
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GI secretory products what cell and organ does Vasoactive intestinal polypeptide (VIP) come from?
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Parasympathetic ganglia in sphincters, gall bladder, small intestine
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GI secretory products what cell and organ does Nitric oxide come from?
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Intrinsic factor Gastric acid
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GI secretory products What substances do Chief cells Stomach produce?
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Pepsin
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GI secretory products What substances do Mucosal cells Stomach Duodenum produce?
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HCO3–
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GI secretory products What substances do G cells Antrum of stomach produce?
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Gastrin
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GI secretory products What substances do I cells Duodenum Jejunum produce?
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Cholecysto- kinin
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GI secretory products What substances do S cells Duodenum produce?
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Secretin
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GI secretory products What substances do D cells Pancreatic islets GI mucosa produce?
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Somatostatin
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GI secretory products What substances do K cells Duodenum Jejunum produce?
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Gastric inhibitory peptide (GIP)r
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GI secretory products What substances do Parasympathetic ganglia in sphincters, gall bladder, small intestine produce?
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Vasoactive intestinal polypeptide (VIP)
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GI secretory products action of Intrinsic factor?
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Vitamin B12 binding protein (required for B12 uptake in terminal ileum)
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GI secretory products action of Gastric acid?
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lower stomach pH
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GI secretory products action of Pepsin?
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Protein digestion
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GI secretory products action of HCO3–?
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Neutralizes acid Prevents autodigestion
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GI secretory products regulation of Gastric acid?
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increased by histamine, ACh, gastrin decreased by somatostatin, GIP, prostaglandin, secretin
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GI secretory products regulation of pepsin?
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increased by vagal stimulation, local acid?
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GI secretory products regulation of HCO3–?
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increased by secretin
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Autoimmune destruction of parietal cells ¨leads to
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chronic gastritis and pernicious anemia.
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Inactive pepsinogen becomes pepsin by
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H+
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GI Hormones Action of Gastrin?
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Increases gastric H+ secretion Increases growth of gastric mucosa Increases gastric motility
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GI Hormones Action of Cholecysto- kinin?
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Increases pancreatic secretion Increases gallbladder contraction decreasesgastric emptying
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GI Hormones Action of Secretin?
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↑ pancreatic HCO3 – secretion ↓ gastric acid secretion
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GI Hormones Action of Somatostatin?
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↓ gastric acid and pepsinogen secretion ↓ pancreatic and small intestine fluid secretion ↓ gallbladder contraction ↓ insulin and glucagon release
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GI Hormones Action of Gastric inhibitory peptide (GIP)?
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Exocrine: ↓ gastric H+ secretion Endocrine: ↑ insulin release
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GI Hormones Action of Vasoactive intestinal polypeptide (VIP)?
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↑ intestinal water and electrolyte secretion ↑ relaxation of intestinal smooth muscle and sphincters
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GI Hormones Action of Nitric oxide?
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↑ smooth muscle relaxation, including lower esophageal sphincter
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GI hormones regulation of Gastrin?
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↑ by stomach distention, amino acids, peptides, vagal stimulation ↓ by stomach pH < 1.5
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GI hormones regulation of Cholecysto- kinin?
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↓ by secretin and stomach pH < 1.5 ↑ by fatty acids, amino acids
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GI hormones regulation of Secretin?
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↑ by acid, fatty acids in lumen of duodenum
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GI hormones regulation of Somatostatin?
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↑ by acid ↓ by vagal stimulation
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GI hormones regulation of Gastric inhibitory peptide (GIP)?
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↑ by fatty acids, amino acids, oral glucose
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GI hormones regulation of Vasoactive intestinal polypeptide (VIP)?
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↑ by distension and vagal stimulation ↓ by adrenergic input
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GI hormones regulation of Nitric oxide?
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?
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Gastrin wrt when is it Very Very high
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↑↑ in Zollinger- Ellison syndrome.
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what is ↑↑ in Zollinger- Ellison syndrome.
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gastrin
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Gastrin What are Very potent stimulators
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Phenylalanine and tryptophan are potent stimulators.
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Phenylalanine and tryptophan are potent stimulators of what GI hormone
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Gastrin
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In cholelithiasis, pain worsens after fatty food ingestion due to?
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↑ CCK.
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↑ HCO3 – neutralizes gastric acid in duodenum, allowing?
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pancreatic enzymes to function.
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Used to treat VIPoma and carcinoid tumors.
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Somatostatin
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what hormone? An oral glucose load is used more rapidly than the equivalent given by IV.
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Gastric inhibitory peptide (GIP)
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Gastric inhibitory peptide (GIP) wrt Oral Vs IV
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An oral glucose load is used more rapidly than the equivalent given by IV.
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VIPoma: what is it and what are the symps and Tx
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VIPoma: non-α, non-ß islet cell pancreatic tumor that secretes VIP. Copious diarrhea. Tx is Somatostatin
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Loss of ????? is implicated in ↑ lower esophageal tone of achalasia.
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NO secretion
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Loss of NO secretion is implicated in
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↑lower esophageal tone of achalasia.
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Pancreatic enzymes Which are secreted in their active form
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α-amylase––starch digestion, secreted in active form.
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Pancreatic enzymes name the carb ones
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α-amylase––starch digestion, secreted in active form.
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Pancreatic enzymes name the Fat ones
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Lipase, phospholipase A, colipase––fat digestion.
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Pancreatic enzymes name the protein ones
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Proteases (trypsin, chymotrypsin, elastase, carboxypeptidases)––protein digestion, secreted as proenzymes.
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activation cascade for pancratic protein enzymes
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Trypsinogen is converted to active enzyme trypsin by enterokinase, a duodenal brushborder enzyme. Trypsin activates other proenzymes and more trypsinogen (positive feedback loop).
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Pancreatic enzymes Which are secreted in their in active form
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Proteases (trypsin, chymotrypsin, elastase, carboxypeptidases)––protein digestion, secreted as proenzymes.
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Trypsinogen is converted to active enzyme trypsin by ?
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enterokinase,
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Carbohydrate digestion name all the enzymes
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Salivary amylase Pancreatic amylase Oligosaccharide hydrolases
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Carbohydrate digestion Salivary amylase where from and what it does?
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Starts digestion, hydrolyzes α-1,4 linkages to yield disaccharides (maltose, maltotriose, and α-limit dextrans).
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Carbohydrate digestion Salivary amylase where from and what it does?
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Highest concentration in duodenal lumen, hydrolyzes starch to oligosaccharides and disaccharides.
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Carbohydrate digestion Salivary amylase where from and what it does?
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At brush border of intestine, the rate-limiting step in carbohydrate digestion, produce monosaccharides from oligo- and disaccharides.
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hydrolyzes α-1,4 linkages to yield disaccharides (maltose, maltotriose, and α-limit dextrans).
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Salivary amylase
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Highest concentration in duodenal lumen, hydrolyzes starch to oligosaccharides and disaccharides.
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Pancreatic amylase
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At brush border of intestine, the rate-limiting step in carbohydrate digestion, produce monosaccharides from oligo- and disaccharides.
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Oligosaccharide hydrolases
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the rate-limiting step in carbohydrate digestion,
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Oligosaccharide hydrolases
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Carbohydrate absorption what is absorbed
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Only monosaccharides (glucose, galactose, fructose) are absorbed by enterocytes.
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Carbohydrate absorption mech for Glucose into enterocytes
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Glucose and galactose are taken up by SGLT1 (Na+ dependent).
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Carbohydrate absorption mech for Galactose into enterocytes
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Glucose and galactose are taken up by SGLT1 (Na+ dependent).
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Carbohydrate absorption mech for Fructose into enterocytes
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Fructose is taken up by facilitated diffusion by GLUT-5.
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Carbohydrate absorption mech for Glucose from enterocytes into blood
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All (Glucose, Galactose, Fructose) are transported to blood by GLUT-2.
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Carbohydrate absorption mech for Galactose from enterocytes into blood
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All (Glucose, Galactose, Fructose) are transported to blood by GLUT-2.
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Carbohydrate absorption mech for Fructose from enterocytes into blood
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All (Glucose, Galactose, Fructose) are transported to blood by GLUT-2.
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Apical surface of hepatocytes face ??????? Basolateral surface face?????
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bile canaliculi. sinusoids.
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Zones of the liver portal triads
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Zone I: periportal zone –affected first by viral hepatitis Zone II: intermediate zone Zone III: pericentral vein zone –most sensitive to toxic injury –contains P-450 system –affected first by ischemia –alcoholic hepatitis
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Zones of the liver portal triads Which Zone is periportal zone?
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I
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Zones of the liver portal triads Which Zone is most sensitive to toxic injury?
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III
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Zones of the liver portal triads Which Zone is affected first by viral hepatitis?
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I
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Zones of the liver portal triads Which Zone is intermediate zone?
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II
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Zones of the liver portal triads Which Zone is pericentral vein zone?
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III
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Zones of the liver portal triads Which Zone is contains P-450 system?
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III
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Zones of the liver portal triads Which Zone is affected first by ischemia?
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III
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Zones of the liver portal triads Which Zone is alcoholic hepatitis?
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III
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Zones of the liver portal triads blood flow direction ?
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1 to 3
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Zones of the liver portal triads bile flow direction ?
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3 to 1
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Direct bilirubin is combined with what and why
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conjugated with glucuronic acid; water soluble.
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Direct bilirubin aka
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conjugated
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Indirect bilirubin aka
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unconjugated
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Jaundice (yellow skin, sclerae) results from
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elevated bilirubin levels.
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Bile is made of
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Composed of bile salts (bile acids conjugated to glycine or taurine making them water soluble), phospholipids, cholesterol, bilirubin, water, and ions.
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The only significant mechanism for cholesterol excretion.
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Bile
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one major importance of bile
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The only significant mechanism for cholesterol excretion.
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A-chalasia =
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absence of relaxation.
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“Bird beak” on barium swallow.
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A-chalasia
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2° achalasia may arise from ?
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Chagas’ disease.
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Achalasia and cancer
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Associated with an ↑ risk of esophageal carcinoma.
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Achalasia mech
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Failure of relaxation of lower esophageal sphincter (LES) due to loss of myenteric (Auerbach’s) plexus.
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Achalasia and imaging
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Barium swallow shows dilated esophagus with an area of distal stenosis.
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High LES opening pressure and uncoordinated peristalsis leads to what wrt symptoms
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to progressive dysphagia.
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Glandular metaplasia–– replacement of nonkeratinized squamous epithelium with intestinal (columnar) epithelium in the distal esophagus. Due to chronic acid reflux.
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Barrett’s esophagus
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Barrett’s esophagus hisologic mech
|
Glandular metaplasia–– replacement of nonkeratinized squamous epithelium with intestinal (columnar) epithelium in the distal esophagus.
|
|
|
Barrett’s esophagus due to
|
Due to chronic acid reflux.
|
|
|
Barrett’s esophagus wrt cancer
|
BARRett’s = Becomes Adenocarcinoma, Results from Reflux.
|
|
|
Risk factors for esophageal cancer are:
|
ABCDE -Alcohol -Barrett’s esophagus -Cigarettes --Diverticuli (e.g., Zenker’s diverticulum) -Esophageal web (e.g., Plummer-Vinson)/ -Esophagitis (due to reflux, irritants, infection) -Familial
|
|
|
Esophageal cancer which types are most common
|
Worldwide, squamous cell is most common. In US, squamous and adenocarcinoma are equal in incidence.
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“olive”
|
Congenital pyloric stenosis
|
|
|
Congenital pyloric stenosis presentation
|
Palpable “olive” mass in epigastric region and nonbilious projectile vomiting at ≈ 2 weeks of age.
|
|
|
Congenital pyloric stenosis how common and Tx
|
Treatment is surgical incision. Occurs in 1/600 live births, often in 1st-born males.
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|
|
Malabsorption syndromes name 5
|
-Celiac sprue -Tropical sprue -Whipple’s disease -Disaccharidase deficiency -Pancreatic insufficiency
|
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Celiac sprue mech location and testing
|
Autoantibodies to gluten (gliadin) in wheat and other grains. Proximal small bowel only. Abnormal xylose test.
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|
|
Malabsorption syndromes what symptoms
|
Can cause diarrhea, steatorrhea, weight loss, weakness.
|
|
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Celiac sprue associated risks
|
Associated with ↑ risk of T cell lymphoma.
|
|
|
Malabsorption syndromes Associated with ↑ risk of T cell lymphoma.
|
Celiac sprue
|
|
|
Tropical sprue mech location and Tx
|
Probably infectious; responds to antibiotics. Can affect entire small bowel.
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|
|
Whipple’s disease mech and symptoms
|
Infection with Tropheryma whippelii; Arthralgias, cardiac, and neurologic symptoms are common. Most often occurs in older men.
|
|
|
PAS-positive macrophages in intestinal lamina propria, mesenteric nodes.
|
Whipple’s disease
|
|
|
Whipple’s disease Histo
|
PAS-positive macrophages in intestinal lamina propria, mesenteric nodes.
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|
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Disaccharidase deficiency most common and features
|
Most common is lactase deficiency → milk intolerance. Osmotic diarrhea.
|
|
|
Due to CF, chronic pancreatitis. Causes malabsorption of protein, fat, vitamins A, D, E, K.
|
Pancreatic insufficiency
|
|
|
Pancreatic insufficiency due to? What it causes?
|
Due to CF, chronic pancreatitis. Causes malabsorption of protein, fat, vitamins A, D, E, K.
|
|
|
Autoimmune-mediated intolerance of gliadin (wheat) leading to steatorrhea.
|
Celiac sprue
|
|
|
Celiac sprue who gets it
|
Associated with people of northern European descent.
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|
|
Celiac sprue histo and lab findings
|
Findings include blunting of villi, lymphocytes in the lamina propria, and abnormal D-xylose test.
|
|
|
Celiac sprue what portion of bowel
|
Tends to affect jejunum.
|
|
|
Celiac sprue associations
|
Associated with dermatitis herpetiformis. 10–15% lead to malignancy (most often T-cell lymphoma).
|
|
|
Associated with dermatitis herpetiformis. 10–15% lead to malignancy (most often T-cell lymphoma).
|
Celiac sprue associations
|
|
|
Gastritis which is erosive and which is non erosive
|
Acute gastritis (erosive) Chronic gastritis (nonerosive)
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Acute gastritis mech and causes
|
Disruption of mucosal barrier → inflammation. Canbe caused by stress, NSAIDs, alcohol, uricemia, burns (Curling’s ulcer), and brain injury (Cushing’s ulcer).
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|
|
Curling’s ulcer which type and cause
|
acute gastritis/erosive Burns
|
|
|
Cushings ulcer which type and cause
|
acute gastritis/erosive Brain injury
|
|
|
Chronic gastritis (nonerosive) types and locations
|
Type A (fundus/ body) Type B (antrum)
|
|
|
Chronic gastritis (nonerosive) Type A mech and findings
|
Autoimmune disorder characterized by Autoantibodies to parietal cells leading to pernicious Anemia, and Achlorhydria.
|
|
|
Chronic gastritis (nonerosive) Type B mech and findings
|
Caused by H. pylori infection. ↑ risk of MALT lymphoma.
|
|
|
Gastritis which has ↑ risk of MALT lymphoma.
|
Chronic gastritis (nonerosive) Type B
|
|
|
Chronic gastritis (nonerosive) mnemonic
|
AB pairing Pernicious Anemia affects gastric Body. H. pylori Bacterium affects Antrum.
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|
|
Peptic ulcer disease Gastric or Duodenal? Pain Greater with meals––weight loss.
|
Gastric
|
|
|
Peptic ulcer disease Gastric or Duodenal? Often occurs in older patients.
|
Gastric
|
|
|
Peptic ulcer disease Gastric or Duodenal? H. pylori infection in 70%; chronic NSAID use also
|
Gastric
|
|
|
Peptic ulcer disease Gastric or Duodenal? Due to ↓ mucosal protection against gastric acid.
|
Gastric
|
|
|
Peptic ulcer disease Gastric or Duodenal? Pain Decreases with meals––weight gain.
|
Duodenal
|
|
|
Peptic ulcer disease Gastric or Duodenal? Almost 100% have H. pylori infection.
|
Duodenal
|
|
|
Peptic ulcer disease Gastric or Duodenal? Due to ↑ gastric acid secretion or ↓ mucosal protection.
|
Duodenal
|
|
|
Peptic ulcer disease Gastric or Duodenal? Hypertrophy of Brunner’s glands.
|
Duodenal
|
|
|
Peptic ulcer disease Gastric or Duodenal?Tend to have clean, “punched-out” margins unlike the raised/irregular margins of carcinoma.
|
Duodenal
|
|
|
Peptic ulcer disease Gastric or Duodenal? Potential complications include bleeding, penetration, perforation, and obstruction
|
Duodenal
|
|
|
Peptic ulcer disease Gastric or Duodenal? not intrinsically precancerous
|
Duodenal
|
|
|
Potential complications Duodenal ulcer
|
bleeding, penetration, perforation, obstruction
|
|
|
Stomach cancer What type is it
|
Almost always adenocarcinoma.
|
|
|
Stomach cancer spread patterns
|
Early aggressive local spread and node/liver mets. Virchow’s node––involvement of supraclavicular node by mets from stomach.
|
|
|
Stomach cancer associated with
|
dietary nitrosamines, achlorhydria, chronic gastritis, type A blood.
|
|
|
Stomach cancer when diffusly infiltrative
|
Termed linitis plastica when diffusely infiltrative (thickened, rigid appearance
|
|
|
Stomach cancer hiso apperance
|
signet ring cells
|
|
|
Krukenberg’s tumor what
|
bilateral mets to ovaries. Abundant mucus, “signet-ring” cells. from Stomach cancer
|
|
|
bilateral mets to ovaries. Abundant mucus, “signet-ring” cells
|
Krukenberg’s tumor
|
|
|
involvement of supraclavicular node by mets from stomach.
|
Virchow’s node
|
|
|
Crohn’s disease Vs Ulcerative colitis WRT etiology
|
Crohn’s disease--- Post-infectious. Ulcerative colitis--- Autoimmune.
|
|
|
Crohn’s disease Vs Ulcerative colitis WRT Location
|
Crohn’s disease--- Any portion of the GI tract, usually the terminal ileum and colon. Skip lesions, rectal sparing. Ulcerative colitis--- Colitis = colon inflammation. Continuous lesions, always with rectal involvement.
|
|
|
Crohn’s disease Vs Ulcerative colitis WRT Gross morphology
|
Crohn’s disease--- Transmural inflammation. Cobblestone mucosa, creeping fat, bowel wall thickening (“string sign” on barium swallow x-ray), linear ulcers, fissures, fistulas. Ulcerative colitis--- Mucosal and submucosal inflammation only. Friable mucosal pseudopolyps with freely hanging mesentery.
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|
|
Crohn’s disease Vs Ulcerative colitis WRT Microscopic morphology
|
Crohn’s disease--- Noncaseating granulomas and lymphoid aggregates. Ulcerative colitis--- Crypt abscesses and ulcers, bleeding, no granulomas.
|
|
|
Crohn’s disease Vs Ulcerative colitis WRT Complications
|
Crohn’s disease--- Strictures, fistulas, perianal disease, malabsorption, nutritional depletion. Ulcerative colitis--- Severe stenosis, toxic megacolon, colorectal carcinoma.
|
|
|
Crohn’s disease Vs Ulcerative colitis WRT Extraintestinal manifestations
|
Crohn’s disease--- Migratory polyarthritis, erythema nodosum, ankylosing spondylitis, uveitis, immunologic disorders. Ulcerative colitis--- Pyoderma gangrenosum, 1° sclerosing cholangitis.
|
|
|
Crohn’s disease mnemonic
|
For Crohn’s, think of a fat granny and an old crone skipping down a cobblestone road away from the wreck (rectal sparing) (see Images 114, 115).
|
|
|
Crohn’s disease Or Ulcerative colitis Transmural inflammation.
|
Crohn’s disease
|
|
|
Crohn’s disease Or Ulcerative colitis
|
Crohn’s disease
|
|
|
Crohn’s disease Or Ulcerative colitis Post-infectious.
|
Crohn’s disease
|
|
|
Crohn’s disease Or Ulcerative colitis Strictures, fistulas, perianal disease, malabsorption, nutritional depletion
|
Crohn’s disease
|
|
|
Crohn’s disease Or Ulcerative colitis ankylosing spondylitis, uveitis, immunologic disorders.
|
Crohn’s disease
|
|
|
Crohn’s disease Or Ulcerative colitis Pyoderma gangrenosum, 1° sclerosing cholangitis.
|
UC
|
|
|
Crohn’s disease Or Ulcerative colitis Crypt abscesses and ulcers, bleeding, no granulomas.
|
UC
|
|
|
Crohn’s disease Or Ulcerative colitis Severe stenosis, toxic megacolon, colorectal carcinoma.
|
UC
|
|
|
Appendicitis who?
|
All age groups; most common indication for emergent abdominal surgery in children.
|
|
|
most common indication for emergent abdominal surgery in children.
|
Appendicitis
|
|
|
Appendicitis presentation?
|
Initial diffuse periumbilical pain →localized pain at McBurney’s point. Nausea, fever; may perforate →peritonitis.
|
|
|
pain at McBurney’s point
|
Appendicitis presentation
|
|
|
Appendicitis differential Dx
|
Differential: diverticulitis (elderly), ectopic pregnancy (use β-hCG to rule out).
|
|
|
Diverticulum true Vs False
|
“True” diverticulum––all 3 gut wall layers outpouch. “False” diverticulum or pseudodiverticulum––only mucosa and submucosa outpouch. Occur especially
|
|
|
Diverticulum where are most
|
Sigmoid colon
|
|
|
false Diverticulum occur most at what types of locations
|
Occur especially where vasa recta perforate muscularis externa.
|
|
|
Diverticulum true Vs False whcih is more common
|
FALSE
|
|
|
Diverticulosis what is it and who gets it
|
Many diverticula. Common (in ~50% of people > 60 years).
|
|
|
Diverticulosis associations
|
Associated with low-fiber diets.
|
|
|
Diverticulosis mech
|
Caused by ↑ intraluminal pressure and focal weakness in colonic wall.
|
|
|
Diverticulosis location
|
Most often in sigmoid colon.
|
|
|
Diverticulosis symps
|
Often asymptomatic or associated with vague discomfort and/or rectal bleeding.
|
|
|
Diverticulitis what is it and symps
|
Inflammation of diverticula classically causing LLQ pain, fever, May cause bright red rectal bleeding.
|
|
|
Diverticulitis wrt labs
|
leukocytosis
|
|
|
Diverticulitis complications
|
May →perforation, peritonitis, abscess formation, or bowel stenosis
|
|
|
Meckel’s diverticulum mnemonic
|
The five 2’s: -2 inches long. -2 feet from the ileocecal valve. -2% of population. -Commonly presents in first 2 years of life. -May have 2 types of epithelia (gastric/ pancreatic).
|
|
|
Meckel’s diverticulum derivation
|
Persistence of the vitelline duct or yolk stalk.
|
|
|
Meckel’s diverticulum contents
|
May contain ectopic acid–secreting gastric mucosa and/or pancreatic tissue.
|
|
|
Meckel’s diverticulum how common
|
2% and/or pancreatic tissue. Most common congenital anomaly of the GI tract.
|
|
|
Meckel’s diverticulum complications
|
Can cause bleeding, intussusception, volvulus, or obstruction near the terminal ileum.
|
|
|
Meckel’s diverticulum and something else to contrast it with
|
Contrast with omphalomesenteric cyst = cystic dilatation of vitelline duct.
|
|
|
Most common congenital anomaly of the GI tract.
|
Meckel’s diverticulum
|
|
|
omphalomesenteric cyst what
|
cystic dilatation of vitelline duct.
|
|
|
cystic dilatation of vitelline duct. aka
|
omphalomesenteric cyst
|
|
|
Zenker’s diverticulum what is it and presentation
|
False diverticulum. Herniation of mucosal tissue at junction of pharynx and esophagus. Presenting symptoms: halitosis, dysphagia, obstruction.
|
|
|
False diverticulum. Herniation of mucosal tissue at junction of pharynx and esophagus.
|
Zenker’s diverticulum
|
|
|
Intussusception what complications and cause
|
Intussusception––“telescoping” of 1 bowel segment into distal segment; can compromise blood supply (see Color Image 34). Often due to intraluminal mass.
|
|
|
Volvulus what complications where does it occur
|
––twisting of portion of bowel around its mesentery; can lead to obstruction and infection. May occur at sigmoid colon, where there is redundant mesentery.
|
|
|
Hirschsprung’s disease what is it
|
Congenital megacolon characterized by lack of enteric nervous plexus in segment (Auerbach’s and Meissner’s plexuses) on intestinal biopsy.
|
|
|
Hirschsprung’s disease mech
|
failure of neural crest cell migration. leads to lack of enteric nervous plexus in segment (Auerbach’s and Meissner’s plexuses)
|
|
|
Hirschsprung’s disease presentation
|
Presents as chronic constipation early in life.
|
|
|
Hirschsprung’s disease who gets it
|
Risk ↑ with Down syndrome.
|
|
|
Hirschsprung’s disease what is the transition zone
|
Dilated portion of the colon proximal to the aganglionic segment, resulting in a “transition zone.”
|
|
|
Hirschsprung’s disease mnemonic
|
Think of a giant spring that has sprung in the colon.
|
|
|
Colonic polyps most are
|
90% are benign hyperplastic hamartomas, not neoplasms.
|
|
|
Colonic polyps locations
|
Often rectosigmoid. Saw-tooth appearance.
|
|
|
Colonic polyps what affects prognosis
|
The more villous the polyp, the more likely it is to be malignant.
|
|
|
Colorectal cancer (CRC) cause
|
. Most are sporadic, due to chromosomal instability (85%) or microsatellite instability (15%).
|
|
|
Colorectal cancer (CRC) risk factors
|
Risk factors: colorectal villous adenomas, chronic IBD (especially ulcerative colitis, ↑ age), FAP, HNPCC, past medical or family history;
|
|
|
Colorectal cancer screenin guidlines
|
screen patients >50 years with stool occult blood test and colonoscopy.
|
|
|
Colorectal cancer marker
|
CEA
|
|
|
Colorectal cancer wrt imaging
|
“Apple core” lesion seen on barium swallow x-xay.
|
|
|
Familial adenomatous polyposis (FAP) genetics
|
Autosomal dominant mutation of APC gene on chromosome 5q. Two-hit hypothesis.
|
|
|
Autosomal dominant mutation of APC gene on chromosome 5q. Two-hit hypothesis.
|
Familial adenomatous polyposis (FAP) genetics
|
|
|
Familial adenomatous polyposis (FAP) Features
|
Thousands of polyps; pancolonic; always involving the rectum.
|
|
|
Gardner’s syndrome
|
FAP with osseous and soft tissue tumors, retinal hyperplasia.
|
|
|
FAP with osseous and soft tissue tumors, retinal hyperplasia.
|
Gardner’s syndrome
|
|
|
FAP with possible brain involvement (glioblastoma).
|
Turcot’s syndrome
|
|
|
Turcot’s syndrome
|
FAP with possible brain involvement (glioblastoma).
|
|
|
HNPCC aka
|
Lynch syndrome
|
|
|
Lynch syndrome aka
|
HNPCC
|
|
|
HNPCC mech and features
|
Mutations of DNA repair genes. ~80% progress to CRC. Proximal colon always involved.
|
|
|
Peutz-Jeghers what and risks
|
polyposis syndrome, associated with ↑ risk of CRC. ↑ risk of other visceral malignancies (breast, stomach, ovary).
|
|
|
Peutz-Jeghers findings
|
hamartomatous polyps of colon and small intestine; hyperpigmented mouth, lips, hands, genitalia.
|
|
|
polyposis syndrome, associated with ↑ risk of CRC. ↑ risk of other visceral malignancies (breast, stomach, ovary).
|
Peutz-Jeghers
|
|
|
Cirrho (Greek) =
|
tawny yellow.
|
|
|
Cirrhosis Micronodular features and causes
|
Micronodular––nodules < 3 mm, uniform size. Due to metabolic insult (e.g., alcohol, hemochromatosis, Wilson’s disease).
|
|
|
Cirrhosis Macronodular features and causes
|
Macronodular––nodules > 3 mm, varied size. Usually due to significant liver injury leading to hepatic necrosis (e.g., postinfectious or druginduced hepatitis). ↑ risk of hepatocellular carcinoma.
|
|
|
Cirrhosis which type has ↑ risk of hepatocellular carcinoma.
|
Macronodular
|
|
|
procedure to relieve protal hypertension
|
Portacaval shunt between splenic vein and left renal vein
|
|
|
11 effects of liver falure
|
• Coma • Scleral icterus • Fetor hepaticus (breath smells like a freshly opened corpse) • Spider nevi • Gynecomastia • Jaundice • Loss of sexual hair • Liver "flap" = asterixis (coarse hand tremor) • Bleeding tendency (decreased prothrombin and clotting factors) • Anemia • Ankle edema
|
|
|
Fetor hepaticus
|
(breath smells like a freshly opened corpse)
|
|
|
Liver "flap" aka
|
asterixis
|
|
|
asterixis aka
|
Liver "flap"
|
|
|
Effects of portal hypertension what leads to melena
|
Esophageal varices and Peptic ulcer
|
|
|
Enzyme markers of GI pathology name 6 enzymes
|
-Aminotransferases (AST and ALT) -GGT (γ-glutamyl transpeptidase) -Alkaline phosphatase -Amylase -Lipase -Ceruloplasmin (↓)
|
|
|
Enzyme markers of GI pathology Aminotransferases (AST and ALT) Major diagnostic use?
|
Viral hepatitis Alcoholic hepatitis Myocardial infarction (AST)
|
|
|
Enzyme markers of GI pathology GGT (γ-glutamyl transpeptidase) Major diagnostic use?
|
Various liver diseases
|
|
|
Enzyme markers of GI pathology Alkaline phosphatase Major diagnostic use?
|
Obstructive liver disease (hepatocellular carcinoma), bone disease
|
|
|
Enzyme markers of GI pathology Amylase Major diagnostic use?
|
Acute pancreatitis, mumps
|
|
|
Enzyme markers of GI pathology Lipase Major diagnostic use?
|
Acute pancreatitis
|
|
|
Enzyme markers of GI pathology Ceruloplasmin (↓) Major diagnostic use?
|
Wilson’s disease (see Color Image 51)
|
|
|
Which GI enzyme gives info on Viral hepatitis, Alcoholic hepatitis, Myocardial infarction
|
Aminotransferases (AST and ALT) Myocardial infarction (AST)
|
|
|
Which GI enzyme gives info on Obstructive liver disease (hepatocellular carcinoma), bone disease
|
Alkaline phosphatase
|
|
|
Which GI enzyme gives info on Acute pancreatitis
|
Amylase, lipase
|
|
|
Which GI enzyme gives info on mumps
|
Amylase
|
|
|
Which GI enzyme gives info on Wilson’s disease
|
Ceruloplasmin (↓)
|
|
|
Alcoholic hepatitis histo
|
Swollen and necrotic hepatocytes, neutrophil infiltration, Mallory bodies (intracytoplasmic eosinophilic inclusions), fatty change, and sclerosis around central vein (Zone III).
|
|
|
Mallory bodies
|
(intracytoplasmic eosinophilic inclusions) seen in alcoholic hepatitis
|
|
|
(intracytoplasmic eosinophilic inclusions) seen in alcoholic hepatitis
|
Mallory bodies
|
|
|
Alcoholic hepatitis mnemonic with liver enzymes
|
You've sGOT toASTed with alcoholic hepatitis. (sGOT)AST > ALT(SGPT) ALT > AST in viraL hepatitis.
|
|
|
SGOT (AST) to SGPT (ALT) ratio is usually
|
> 1.5.
|
|
|
Budd-Chiari syndrome what is it and complications
|
Occlusion of IVC or hepatic veins with centrilobular congestion and necrosis, leading to congestive liver disease (hepatomegaly, ascites, abdominal pain, and eventual liver failure).
|
|
|
Budd-Chiari syndrome causes
|
Associated with polycythemia vera, pregnancy, hepatocellular carcinoma.
|
|
|
Wilson’s disease mech
|
Inadequate hepatic copper excretion and failure of copper to enter circulation as ceruloplasmin. Leads to copper accumulation,
|
|
|
Wilson’s disease Tx
|
Treat with penicillamine.
|
|
|
Wilson’s disease inheritance.
|
Autosomal-recessive inheritance.
|
|
|
Wilson’s disease is characterized by:
|
ABDC Asterixis Basal ganglia degeneration (parkinsonian symptoms) Ceruloplasmin ↓, Cirrhosis, Corneal deposits (Kayser-Fleischer rings), Copper accumulation, Carcinoma (hepatocellular), Choreiform movements Dementia
|
|
|
What is the C in the ABCD of Wilson’s disease
|
Ceruloplasmin ↓, Cirrhosis, Corneal deposits (Kayser-Fleischer rings), Copper accumulation, Carcinoma (hepatocellular), Choreiform movements
|
|
|
Hemochromatosis mech
|
Hemosiderosis is the deposition of hemosiderin (iron); hemochromatosis is the disease caused by this iron deposition.
|
|
|
Hemochromatosis presentation
|
Classic triad of micronodular cirrhosis, pancreatic fibrosis, and skin pigmentation → “bronze” diabetes.
|
|
|
Classic triad of micronodular cirrhosis, pancreatic fibrosis, and skin pigmentation → “bronze” diabetes.
|
Hemochromatosis
|
|
|
Hemochromatosis results in
|
CHF and ↑ risk of hepatocellular carcinoma.
|
|
|
Hemochromatosis ways to have it
|
Disease may be 1° (autosomal recessive) or 2° to chronic transfusion therapy.
|
|
|
Hemochromatosis lab values
|
↑ ferritin, ↑ iron, ↓ TIBC →↑transferrin saturation
|
|
|
Associated with HLA A3.
|
Hemochromatosis
|
|
|
Hemochromatosis associated with what marker
|
HLA A3
|
|
|
Hemochromatosis cool thing!
|
Total body iron may reach 50 g, enough to set off metal detectors at airports.
|
|
|
Hemochromatosis Tx
|
-repeated phlebotomy, -deferoxamine.
|
|
|
Jaundice type Hepatocellular wrt -Hyperbilirubinemia ? -Urine bilirubin ? -Urine urobilinogen?
|
Conjugated/unconjugated ↑ Normal/↓
|
|
|
Jaundice type Obstructive wrt -Hyperbilirubinemia ? -Urine bilirubin ? -Urine urobilinogen?
|
Conjugated ↑ ↓
|
|
|
Jaundice type Hemolytic wrt -Hyperbilirubinemia ? -Urine bilirubin ? -Urine urobilinogen?
|
Unconjugated Absent (acholuria) ↑
|
|
|
Hereditary hyperbilirubinemias name them
|
Gilbert’s syndrome Crigler-Najjar syndrome, type I and II Dubin-Johnson syndrome Rotor's syndrome
|
|
|
Gilbert’s syndrome mech symptoms
|
Mildly ↓ UDP-glucuronyl transferase. Asymptomatic. Elevated unconjugated bilirubin without overt hemolysis. Associated with stress.
|
|
|
Crigler-Najjar syndrome, type I mech and outcomes
|
Absent UDP-glucuronyl transferase. Presents early in life; patients die within a few years.
|
|
|
Crigler-Najjar syndrome, type I findings
|
Findings: jaundice, kernicterus (bilirubin deposition in brain), ↑ unconjugated bilirubin.
|
|
|
Crigler-Najjar syndrome, Tx
|
Type 1 - Treatment: plasmapheresis and phototherapy. Type II --phenobarbital,
|
|
|
Crigler-Najjar syndrome, type II severity and Tx mech
|
Type II is less severe and responds to phenobarbital, which ↑ liver enzyme synthesis.
|
|
|
Dubin-Johnson syndrome mech and findings
|
Conjugated hyperbilirubinemia due to defective liver excretion. Grossly black liver. Benign.
|
|
|
Rotor’s syndrome
|
like Dubin-Johnson (conjugated hyperbilirubinemia) syndrome but milder and no black liver
|
|
|
Dubin-Johnson syndrome complications
|
Grossly black liver. Benign.
|
|
|
Charcot’s triad wrt GI:
|
Charcot’s triad of cholangitis: 1. Jaundice 2. Fever 3. RUQ pain
|
|
|
1. Jaundice 2. Fever 3. RUQ pain
|
Charcot’s triad of cholangitis: can indicate Primary sclerosing cholangitis
|
|
|
Primary sclerosing cholangitis what and where
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Inflammation and fibrosis of bile ducts →alternating strictures and dilation. Both intra- and extrahepatic.
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Primary sclerosing cholangitis appearance
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alternating strictures and dilation with “beading” on ERCP.
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Primary sclerosing cholangitis associations
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Associated with ulcerative colitis.
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Primary sclerosing cholangitis complications
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Can lead to 2° biliary cirrhosis.
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Primary sclerosing cholangitis findings
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Charcot’s triad of cholangitis: 1. Jaundice 2. Fever 3. RUQ pain
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Primary Biliary cirrhosis location, mechanism, symps, and findings
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Intrahepatic, autoimmune disorder; severe obstructive jaundice, steatorrhea, pruritus, hypercholesterolemia (xanthoma). ↑ alkaline phosphatase, ↑ serum mitochondrial antibodies.
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↑ alkaline phosphatase, ↑ serum mitochondrial antibodies.
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Primary Biliary cirrhosis
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secondary Biliary cirrhosis mech?
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Due to extrahepatic biliary obstruction. ↑ in pressure in intrahepatic ducts → injury/ fibrosis.
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Primary Biliary cirrhosis associatoins
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Associated with scleroderma, CREST syndrome.
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what is the common lab value in scleroderma/CREST and primary biliary sclerosis
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↑ serum mitochondrial antibodies.
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secondary Biliary cirrhosis complications and histo/lab findings
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Often complicated by ascending cholangitis (bacterial infection), bile stasis, and “bile lakes.” ↑ alkaline phosphatase, ↑ conjugated bilirubin.
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Most common 1° malignant tumor of the liver in adults.
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hepatocellular carcinoma
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↑ incidence of hepatocellular carcinoma is associated with
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-hepatitis B and C, -Wilson’s disease, -hemochromatosis, -α1-antitrypsin deficiency, -alcoholic cirrhosis, -carcinogens (e.g., aflatoxin B1).
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Hepatocellular carcinoma spread mech
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Commonly spread by hematogenous dissemination.
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Hepatocellular carcinoma presentation
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Can present with tender hepatomegaly, ascites, polycythemia, and hypoglycemia.
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Hepatocellular carcinoma marker
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Elevated α-fetoprotein.
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Reye’s syndrome findings
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fatty liver (microvesicular fatty change), hypoglycemia, coma.
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Reye’s syndrome cause
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fatty change), hypoglycemia, Associated with viral infection (especially VZV and influenza B) treated with salicylates
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what to give a kid to lower fever
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acetaminophen, not aspirin
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Rare, often fatal childhood hepatoencephalopathy. aka
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Reye’s syndrome
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Gallstones Form when
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solubilizing bile acids and lecithin are overwhelmed by ↑ cholesterol and/or bilirubin.
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Gallstones mnemonic
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Risk factors (4 F’s): 1. Female 2. Fat 3. Fertile 4. Forty
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Gallstones which are radiolucent
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Cholesterol stones (80-90% of them) and Mixed stones
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Gallstones which are radioopaque
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Pigment stones
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Gallstones Cholesterol stones associations
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9 of them -obesity, -Crohn’s disease, -cystic fibrosis, -advanced age, -clofibrate, -estrogens, -multiparity, -rapid weight loss, -Native American origin.
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gallstones Mixed stones what are they made of
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cholesterol and pigment components.
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Gallstones most common type
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Mixed stones
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Gallstones pigment stones associations
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4 of them seen in patients with: -chronic RBC hemolysis, -alcoholic cirrhosis, -advanced age, -and biliary infection.
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Gallstones can lead to
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Can cause ascending cholangitis, acute pancreatitis, bile stasis, cholecystitis.
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Gallstones Dx and Tx
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Diagnose with ultrasound. Treat with cholecystectomy.
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Acute pancreatitis causes
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I GET SMASHeD. Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypercalcemia/Hyperlipidemia, Drugs (e.g., sulfa drugs).
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Acute pancreatitis presentation
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Clinical presentation: epigastric abdominal pain radiating to back; anorexia, nausea.
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Acute pancreatitis labs
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Labs: elevated amylase, lipase (higher specificity).
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Acute pancreatitis leads to
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Can lead to DIC, ARDS, diffuse fat necrosis, hypocalcemia, pseudocyst formation, hemorrhage, and infection.
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Chronic calcifying pancreatitis associations
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Chronic calcifying pancreatitis is strongly associated with alcoholism
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Chronic obstructive pancreatitis associations
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Chronic obstructive pancreatitis is strongly associated with gallstones.
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Pancreatic adenocarcinoma prognosis
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Prognosis averages 6 months or less; very aggressive; usually already metastasized at presentation;
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Pancreatic adenocarcinoma location and findings
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tumors more common in pancreatic head (obstructive jaundice).
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Pancreatic adenocarcinoma who adn risk factors
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↑ risk in Jewish and African-American males. Associated with cigarettes, but not ETOH.
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Pancreatic adenocarcinoma Often presents with:
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1. Abdominal pain radiating to back 2. Weight loss (due to malabsorption and anorexia) 3. Migratory thrombophlebitis (Trousseau’s syndrome) 4. Obstructive painless jaundice with palpable gallbladder (Courvoisier’s sign)
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Courvoisier’s sign
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Obstructive painless jaundice with palpable gallbladder often means cancer in pancreatic head
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Trousseau’s syndrome
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Migratory thrombophlebitis often means adenoarcinoma of the pancreas or lung
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Obstructive painless jaundice with palpable gallbladder
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Courvoisier’s sign
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Migratory thrombophlebitis often means adenoarcinoma of the pancreas or lung
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Trousseau’s syndrome
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Tumor of endocrine cells. Comprise 50% of small bowel tumors.
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Carcinoid
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Carcinoid what type of tumor and how common
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Tumor of endocrine cells. Comprise 50% of small bowel tumors.
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Carcinoid most common site and visualization
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Most common site is appendix. “Dense core bodies” seen on EM.
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Carcinoid what they produce
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5-HT / Serotonin
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Carcinoid classic symps
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wheezing, right-sided heart lesions, diarrhea, flushing.
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H2 blockers Names
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-idine
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H2 blockers mech
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Reversible block of histamine H2 receptors →↓H+ secretion by parietal cells.
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H2 blockers clinical use
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Peptic ulcer, gastritis, mild esophageal reflux.
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H2 blockers toxicity wrt hormones
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Cimetidine has antiandrogenic effects (prolactin release, gynecomastia, impotence, ↓ libido in males);
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H2 blockers toxicity wrt CNS
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cimetidine can cross BBB (confusion, dizziness, headaches) and placenta.
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H2 blockers toxicity wrt renal
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Both cimetidine and ranitidine ↓ renal excretion of creatinine.
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H2 blockers toxicity which ones
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Cimetidine (many) ranitidine(only renal) others much much less
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H2 blockers toxicity WRT Liver
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Cimetidine is a potent inhibitor of P-450;
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Proton pump inhibitors names
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omeprazole lansoprazole -prazole
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Proton pump inhibitors mech
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Irreversibly inhibit H+/K+ ATPase in stomach parietal cells.
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Proton pump inhibitors clinical use
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Peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome.
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Bismuth, sucralfate mech
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Bind to ulcer base, providing physical protection, and allow HCO3 – secretion to reestablish pH gradient in the mucus layer.
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Bismuth, sucralfate clinical use
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↑ ulcer healing, traveler’s diarrhea.
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Triple/quad therapy of H. pylori ulcers
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MAke Tummy Better -Metronidazole, -Amoxicillin (or -Tetracycline). -Bismuth, can also Add PPI please MAke Tummy Better
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Misoprostol mech
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A PGE1 analog. ↑ production and secretion of gastric mucous barrier, ↓ acid production.
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Misoprostol clinical use
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-Prevention of NSAID-induced peptic ulcers; -maintenance of a patent ductus arteriosus. -Also used to induce labor.
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Misoprostol toxicity
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-Diarrhea. -Contraindicated in women of childbearing potential (abortifacient).
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-Prevention of NSAID-induced peptic ulcers; -maintenance of a patent ductus arteriosus. -Also used to induce labor.
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Misoprostol
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GI Muscarinic antagonists name
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Pirenzepine, propantheline.
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GI Muscarinic antagonists mech
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Block M1 receptors on ECL cells (↓ histamine secretion) and M3 receptors on parietal cells (↓ H+ secretion).
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GI Muscarinic antagonists clinical use
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Peptic ulcer.
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GI Muscarinic antagonists Toxicity
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Tachycardia, dry mouth, difficulty focusing eyes.
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Antacid overuse wrt other drugs
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Can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying.
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Aluminum hydroxide toxicity
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constipation and hypophosphatemia; proximal muscle weakness, osteodystrophy, seizures
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Magnesium hydroxide
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––diarrhea, hyporeflexia, hypotension, cardiac arrest.
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Calcium carbonate
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hypercalcemia, rebound acid ↑
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all antacids can cause
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hypokalemia.
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Infliximab mech
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A monoclonal antibody to TNF-α, proinflammatory cytokine. Infliximab Inflix Pain on TNF-α
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Infliximab Clinical use
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Crohn’s disease, rheumatoid arthritis.
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Infliximab Toxicity
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Respiratory infection, fever, hypotension.
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A monoclonal antibody to TNF-α, proinflammatory cytokine.
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Infliximab
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Sulfasalazine Mech
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A combination of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory). Activated by colonic bacteria.
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Sulfasalazine Clinical use
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Ulcerative colitis, Crohn’s disease.
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Sulfasalazine Toxicity
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Malaise, nausea, sulfonamide toxicity, reversible oligospermia.
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drug used in both Ulcerative colitis, Crohn’s disease.
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Sulfasalazine
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Ondansetron Mech
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5-HT3 antagonist. Powerful central-acting antiemetic.
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Ondansetron Clinical use
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Control vomiting postoperatively and in patients undergoing cancer chemotherapy. You will not vomit with ONDANSetron, so you can go ON DANCing.
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Ondansetron Tocicity
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Headache, constipation.
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Pro-kinetic agents names
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Cisapride Metoclopramide
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Cisapride mech and uses
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Acts through serotonin receptors to ↑ ACh release at the myenteric plexus. ↑ esophageal tone; ↑ gastric and duodenal contractility, improving transit time (including through the colon).
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Cisapride Toxicity
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No longer used. Serious interactions (torsades des pointes) with erythromycin, ketoconazole, nefazodone, fluconazole.
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No longer used. Serious interactions (torsades des pointes) with erythromycin, ketoconazole, nefazodone, fluconazole.
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Cisapride
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Metoclopramide mech
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D2 receptor antagonist. ↑ resting tone, contractility, LES tone, motility. Does not ↑ transit time through colon.
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Metoclopramide Clinical use
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Diabetic and post-surgery gastroparesis.
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Metoclopramide Toxicity
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↑ parkinsonian effects. Restlessness, drowsiness, fatigue, depression, nausea, constipation. Drug interaction with digoxin and diabetic agents.
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Metoclopramide contraindications
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patients with small bowel obstruction.
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drug Contraindicated in patients with small bowel obstruction.
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Metoclopramide
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