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249 Cards in this Set
- Front
- Back
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when does the primitive gut begin to develop?
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week 4
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Endoderm becomes what in the gut?
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Intestinal epithelium and glands
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Mesoderm becomes what in the gut?
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connective tissue, muscle and wall of intestine
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What is an omphalocele? what serum level is high?
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the failure of the herniated section of the bowel to re-enter the abdomen at week 10. It is covered by the peritoneal membrane and AFP is elevated.i n 70% of cases
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What is Gastroschisis? What serum level is elevated?
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Due to a vascular injury during development a section of the small or large bowel protrudes (normally right of midline) with NO peritoneal membrance covering it. AFP is elevated.
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In the first year of life a baby presents with severe bilious emesis, abd pain and distention, recal bleeding?
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Midgut Volvulus
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What are Ladd's bands?
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Normally the abd peritoneum attach to lateral walls of abd cavity fixing the cecum retroperitoneally. In malrotation the they cross over the duodenum to reach the high malrotated cecum which can cause duodenal atresia.
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After birth baby has bilious vomiting, double bubble on xray, and polyhydramnios was noted during pregnancy
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Duodenal atresia
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3-6 weeks post birth the child has projectile non-bilious vomiting, with no other sxs?
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Pyloric stenosis, caused by a congenital lengthening and thickening of the pyloris. more commonly seen in first born males.
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palpable epigastric mass in a 3-6 week old. with hypochloremic metabolic alkalosis.
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pyloric stenosis, hypochloremic metabolic alk. due to vomiting.
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Linea alba?
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Vertical fibrous band running from pubic symphysis to the xyphoid process.
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Linea semilunaris?
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lateral edge of rectus abdominis muscle and crosses the costal margin at the tip of the 9th costal cartilage.
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Inguinal Groove?
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formed by inguinal ligament, formed by the rolled-under margin of the aponeurosis of the external oblique muscle
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the spleen is a derivative of the?
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Mesoderm! not foregut
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peyers patches GALT produce what?
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secretory IgA
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What are the three sympathetic ganglia that supply the GI?
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1. Celiac Ganglia
2. Superior Mesenteric Ganglia 3 Inferior Mesenteric Ganglia |
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in the SNS in GI what type of receptor does the preganglionic nerve land on? And what Neurotransmitter does it use?
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Nicotinic, Ach
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What is a Splanchnic nerve?
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A SNS postganglionic fiber for the GI. They Secrete NE on their target receptor
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How far down the GI tract does the Vagus nerve innervate?
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esophagus, stomach, gall bladder, pancreas entire small intestines and PROXIMAL COLON.
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What nerves innervate the distal colon?
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Pelvic nerves from S2, S3 innervate the distal half of the colon, entire sigmoid and rectum
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What are the two main components of the enteric nervous system?
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Myenteric (Auerbach's) plexus, and submucosal (Meissners) plexus.
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Myenteric (Auerbach's) Plexis is where and does what?
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between inner circular and outer longitudinal SM layer regulating peristalsis
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Submucosal (Meissners) plexus is where and does what?
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In the submucosa and inner circular SM layer. regulates secretions, blood flow and absorption.
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Explain the difference between visceral and Parietal peritoneum pain presentation.
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visceral peritoneum nerve pain travels along Type C fibers producing a generalized cramping colicky pain. once the visceral pain spreads to the parietal peritoneum these fibers are extentions of peripheral spinal nerves (the same that innervate skin) so once the peritoneum is affected you get a localized pain that is sharp.
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What are the 4 layers of the GI tract?
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Mucosa
Submucosa Muscularis mucosa Serosa |
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What's in the Mucosa of GI tract?
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Epithelium, lamina propria, muscularis mucosa
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What's in the Submucosa of the GI tract?
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Fibrous connective tissue with Meissners submucosal nervous plexus.
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What is in the Muscularis externa of GI?
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Three layers of muscle Circular, then Myenteric (Auerbach's) plexus, outer longitudinal layer
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What is in the Serosa of the GI tract?
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Nothing.
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What type of serosa covers the esophagus?
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It doesn't
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what do parietal cells secrete?
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HCl
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What do chief cells of the stomach secrete?
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Pepsinogen and intrinsic factor
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Which part of the duodenum recieves the common bile duct and pancreatic duct at the ampulla of vater
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2nd part.
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Which parts of the duodenum are retroperitoneal?
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2nd and 3rd
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Which part of duodenum is most likely to get a duodenal ulcer and from what vein?
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First part, by the gastroduodenal artery
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which is bigger jejunum or ileum?
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Jejunum is 3/5, ileum is 2/5
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what is a crypt of Lieberkuhn? what' in it?
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spaces between intestinal villi containing multipotent stem cells for enterocytes, goblet cells, enteroendocrine cells, and paneth cells
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What do Paneth cells secrete?
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antimicrobial peptides (alpha defensins) and growth factors
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what is the tenia coli?
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a longitudinal band of SM in the colon
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what seperates the left and right lobes of the liver?
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falciform ligament
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which lobe of the liver is larger R or L?
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Right lobe
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Gall bladder to the ______duct to the ______duct to the duodenum?
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cystic duct, common bile
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what type of epithelium lines the gall bladder?
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simple columnar
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Does the gall bladder have crypts and goblet cells?
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NO
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Which nucleus of the hypothalamus senses hunger?
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lateral hypothalamic area, so it stimulates feeding.
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which nucleus of hypothalamus senses fullness?
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ventromedial nucleus, tells to stop eating
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An increase of watery saliva is stimulated by what nucleus of brain? what nerve's transmit this impulse? what receptor?
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superior and inferior Salivatory nucleus of brainstem sends signals down CN 7, 9 to muscarinic receptors in the glands to secrete watery saliva (parasympathetic)
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What causes an increase in viscous saliva? what nerves and what receptors are involved?
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sympathetic nervous system acting on Beta adrenergic receptors sends signals along the T1-T3 superior cervical ganglion.
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what does leptin do?
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a hormone released from adipocytes, acts on the acuate and paraventricular nuclei, it decreases appetite an increases metabolism
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What does peptide YY do?
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released from small intestines and colon and reduces appetite in response to eating.
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alpha amylase (ptyalin) role?
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primary secreted from parotid gland, it starts digestion of carbs at the alpha 1-4 linkage and is inactivated from Low pH of stomach.
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Lingual lipase role?
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begins breakdown of lipids into FA's and monoglycerides.it can cleave fatty acids at all three positions on the triglyceride unlike pancreatic lipase.
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at low flow rates what is the characteristics of the saliva in comparison to plasma?
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saliva is hypotonic to plasma with high Na and Cl and low K
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at high flow rates what is the characteristics of the saliva in comparison to plasma?
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Saliva is isotonic to plasma with low Na and Cl and high K
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explain the pharyngeal phase of swallowing.
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upward movement of soft palate to block nasal passage, constriction of palatopharyngeal folds creating a small passageway only allowing well chewed food through, closure of glottis, tightening of vocal cords, upper esophageal sphincter opens
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what nucleus controls the skeletal muscle of the esophagus?
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nucleus amgibuus
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what nucleus controlls lower involuntary SM of esophagus?
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dorsal nucleus of the vagus nerve.
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what three NT's are used in the enteric nervous system?
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ACh Dopamine Seratonin
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What are the resting pressures of the following?
1. UES 2. Esophagus 3. LES 4. Stomach |
1. 100mmHg
2. -5mmHg 3. 20mmHg 4. 5mmHg |
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intra-esophageal pressure ____ intra-thoracic pressure?
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equals
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Explain esophageal motility changes with scleroderma and why.
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Scleroderma decreases muscle tone in lower 2/3 of esophagus due to SM being replaced with collagen. LES is relaxed allowing for reflux.
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How does achalasia affect the esophagus?
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decreased motility in lower 2/3's due to a loss of the myenteric plexus.
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Two types of causes of achalasia?
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Autoimmune destruction of myenteric plexus assoc. with HLA-DQw1. And chagas disease (t. Cruzi) infection can also cause
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SNS stimulation of the stomach via what plexus causes decreased stomach contractions?
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celiac plexus
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what does lipids and proteins in the stomach stimulate? what what happens?
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stimulates the release of CCK from I cells in the duodenum and then moves to the pancreas and gallbladder to cause them to release their enzymes (bile, trypsin's)
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what inhibits the release of pepsinogen from chief cells in the stomach?
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somatostatin
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What secretes HCO in stomach and what stimulates that secretion.
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mucous cells secrete HCO in all parts of the stomach and is stimulated by secretin.
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what follows H into the stomach lumen from a parietal cell via the electrochemical gradient?
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Chloride
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What pumps are on the apical surface of the parietal cells?
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Cl channel into lumen
K channel into lumen H/K ATP pump (H into lumen) |
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What pumps are present on the basal side of the parietal cells?
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K channel out into interstitum
Cl/HCO exchanger, (Cl into cell, HCO into interstitum) Na/K ATPase |
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What downstream messenger in parietal cells does gastrin release?
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Calcium
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what downstream messenger in parietal cells does Histamine release?
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cAMP
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What downstream messenger in parietal cells does acetylcholine release?
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Calcium
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What cell produce gastrin in the antrum of the stomach?
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G-Cells
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what does gastrin do?
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stimulates:
1. Parietal cells- gastric acid 2. chief cells-pepsinogen 3. enterochromaffin cells- histamine 4. gastric growth 5. gastric motility |
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what stimulates gastrin release from G-cells?
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1. GRP (gastrin releasing peptide) from vagus
2. gastric distention 3. amino acids and peptides present in stomach and duodenum |
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In the duodenum glucose and galactose compete for what sodium dependent transporter? what keeps sodium low intracellularly driving this?
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SGLT-1 co-transporter. the Na/K atpase keeps Na low intracellularly
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how does glucose and galactose exit the enterocyte on the basolateral surface in the duodenum (and small intestine)?
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GLUT 2 transporter.
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what is Abetalipoproteinemia?
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an inability of chylomicrons to leave the enterocyte due to lack of Beta-apolipoproteins (B-48 B100) you get a vitamin E deficiency due to malabsorption of A, D, E, K. clinically you see ataxia due to spinocerebellar degeneration. you also see acanthocytes (spur cells) which will cause a hemolytic anemia.
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What is vitamin E's other name and what does it do?
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alpha-tocopherol, it is a lipophilic free radical scavenger, so it protects the neuron from free-radical damage which can lead do decrease conductance leading to ataxia (spinocerebellar degeneration)
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What transporter apically transports fructose? Basally?
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GLUT 5, then GLUT2 basolaterally (the same as glucose and sucrose)
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where is B12 absorbed?
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in ileum, it must be attached to intrinsic factor
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what cell secretes CCK and from where?
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I cells in duodenum and jejunum
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what stimulates the release of CCK?
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AA's and FA's in the small intestine and duodenum
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What does CCK stimulate
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pancreatic lipase, amylase, proteases. relaxes sphincter of oddi and contracts gall bladder. inhibits emptying of stomach
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what cells secrete secretin, and from where?
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S cells from the crypts of lieberkuhn of the duodenum.
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what stimulates the release of secretin from S-cells?
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decreased pH in stomach or presence of FA's in duodenum
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what does secretin do?
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stimulates pancreatic bicarb secretion, neutralizing gastric acid to allow pancreatic enzymes to digest. also stims production of bile by liver and inhibs gastric acid secretion.
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what cells secrete somatostatin? release stimulated and inhibited by what?
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D cells in the duodenum, Delta cells in pancreatic islets, and GI mucosa. release is stimulated by gastric acid. release inhibited by vagal stimulation
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what secretes gastric inhibitory peptide (GIP)? and where?
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K cells of duodenum and jejunum
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Gastric inhibitory peptide release stimulated by?
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AA's, FA's, oral glucose
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what does GIP stimulate, inhibit
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release of insulin and inhibits gastric Hydrogen secretion
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what cells secrete enteroglucagon? And where are these cells? what does Enteroglucagon do?
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L cells of small intestine, from terminal ileum and colon, enteroglucagon stims insulin release and inhibits gastric and pancreatic secretions
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what releases motilin?
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enterochromaffin cells of duodenum and jejunum.
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what pancreatic tumor can cause chronic diarrhea?
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VIPoma
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What produces VIP? and what stimulates the secretion?
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enteric neurons and the pancreas. secretion stimulated by intestinal and gastric distention and causes receptive relaxation.
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which SNS ganglion innervates the colon?
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mesenteric ganglion.
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What is the gastrocolic reflex?
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when the stomach is full it sends a signal to colon to increase peristalsis.
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what does the colon secrete mainly?
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potassium
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What can diarrhea cause (think colon)?
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hypokalemia
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what type of MMC's are located in the colon?
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There are not MMC's in the colon
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What do the F cells of the pancrease secrete?
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pancreatic peptide, its release is stimulated with AA's FA's, fat, glucose in intestine. it inhibits the release of pancreatic enzymes
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what activates trypsin from trypsinogen
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enterokinase in the brush border of intestinal mucosa.
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what is the sphincter of boyden?
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allows bile into the common bile duct from gall bladder.
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what conjugates indirect bilirubin in the liver?
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glucuronic acid
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what converts conjugated direct bilirubin in the intestines to urobilinogen?
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bacteria (its yellow) this is what make poop brown and pee yellow
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Where does urobilinogen go after conversion in the inestines?
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it can be converted to stercobilinogen (brown pigmented) and pooped out. or it can be reabsorbed and excreted in kidneys as urobilin (after oxidation in kidneys).
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What's with seeing bilirubin in the urine?
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the kidney is unable to filter unconjugated bilirubin (urobilinogen) so any bilirubin seen in urine indicates liver disease
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what is the most common oral malignant lesion? what are the 2 big risk factors?
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SCC, smoking and alcohol use
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what is Leukoplakia?
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squam. cell hyperplasia, can develop into dysplasia - carcinoma in situ- invasive carcinoma
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what is Hairy Leukoplakia?
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inflammatory lesion affecting immunocomp. (pre-aids defining lesion) caused by EBV
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Lichen Planus?
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self limiting unknown etiology. causes (wickhams striae) white lace like patterns on top of papules or plaques.
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persistant papules plaques pustules ulcers in mouth area?
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SCC
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white patches or plaques on oral mucosa
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leukoplakia
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Oral lesion with asymmetry irregular borders, color changes, increasing diameter?
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melanoma
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white plaques that can be scraped off?
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oral candidiasis
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vesicular lesions with erythematous bases?
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HSV-1 herpetic stomatitis
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localized, shallow, round ulcers with grey bases that heal in 7-14 days.
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apthous ulcers
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salivary gland biopsy of lip with lymphocytic infiltrates?
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sjogrens
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Anti-Ro/SSA or anti-La/SSB antibodies?
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sjogrens
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what do pt's with sjogrens have an increased risk for?
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lymphoma
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what type of abnormality is zenchers diverticulum associated with in the esophagus?
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motor, such as spasms, achalasia, UES/LES hyperactivity
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a zenckers diverticula is just above what muscle?
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cricopharyngeus muscle
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increased pressure in what vessel can cause esophageal varices?
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left gastric vein
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what is a good initial treatment for esophageal varices?
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vasopressin, it vasoconstricts mesenteric veins decreasing blood flow to the varices.
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what can cause indirect vasoconstriction to the esophageal varices?
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somatostatin or octreotide by inhibiting vasodilatory hormones
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difficulty swallowing food and liquid means what?
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a motility (neuromuscular) problem
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difficulty swallowing solid food only indicates a?
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anatomic (mechanical) problem.
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what is adult onset asthma associated with?
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GERD
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hypertrophy of mucus secreting cells resulting in rugal hypertrophy. Parietal cell atrophy leading to achlorhydria?
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menetriers disease, pt at risk for adenocarcinoma
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describe peptic ulcer disease
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pH around epithelial cells of stomach is kept at 6-7 pH and the gastric lumen is around 1-2 pH. whenever the mucous layer is breached by either Drugs or bacteria, the cells will be damaged by the low pH
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epigastric pain radiating to left shoulder with air under the diaphragm?
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perforated duodenal ulcer
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what's the treatment for H. pylori infections?
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CAP (clarithromycin, amoxicillin, PPI) 10-14 days
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what type of adenocarcinoma is linitus plastica assoc. with
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diffuse type because infiltrating cells lack the normal cohesion molecule making it a diffuse mass in stomach wall (leather bottle)
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what should be also ruled out with acanthosis nigricans and multiple outcroppings of seborrheic keratosis (lesser trelat sign)
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gastric neoplasia (adenocarcinoma, NHL, MALT lymphoma)
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Skin manifestation of celiac sprue?
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dermatitis herpetiformis
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Celiac Sprue associated with what Human Leukocyte antigen
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HLA-B8 and HLA-DW3
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mucosal inflammation, villous atrophy and crypt hyperplasia in duodenum and jejunum?
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Celiac Sprue
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What type of intestinal changes do you see in lactase deficiency?
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None!
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fever, polyarthralgias, generalized pain. distended lamina propria with PAS + macrophages with pale foamy cytoplasm in intestinal mucosa?
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Whipples disease, G+ (Tropheryma Whippelii)
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How do you treat whipples disease?
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TMP-SMX for 1 year
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Congenital Diverticula?
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full thickness outpouching
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acquired diverticula?
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mucosal herniation through the muscular layer.
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Diverticulosis?
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having diverticula
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Diverticulitis?
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infected diverticula
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anti-gliadin anti-endomesial antibodies?
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celiac sprue
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diarrhea, steatorrhea, weight loss, folate deficiency? Tx?
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Tropical sprue, tetracycline 6 months
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incomplete closure of omphalomesenteric duct?
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Meckels diverticula
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Lower GI bleed in children DDX?
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1. meckels diverticula. technetium-99 IV injection taken up by the parietal cells of ectopic gastric mucosa
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where do you typically see diverticulosis?
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at the origin of the mesenchymal feeder artery.
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pneumaturia (a cause of)?
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colonovesical fistula from diverticulosis can cause this.
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painless hematochezia (most common over 50yrs)?
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diverticulosis
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left sided appendicitis?
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diverticulitis
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barium enema and colonoscopy are contraindicated in what situation and why?
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during acute diverticulits infection because it can cause a perforation.
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structural difference between hirschprungs and achalasia?
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in HD, the narrowed section is without ganglia, and the widened section is structurally normal. Achalasia the dilated portion of the esophagus lacks ganglia and the narrowed portion has ganglia
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UC or CD, which has granulomas?
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CD
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UC or CD, which pre-disposes to colon cancer?
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UC
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most common causative agent for pseudomembranous colitis?
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C.diff post Abx therapy, (G+, spore forming, anaerobic rod)
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Whats cool about sulfasalazine and IBD's?
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sulfasalazine is not absorbed in the small intestine but is hydrolized by the colonic flora into 5-aminosalicylate acid (5-ASA) and sulfapyridine. 5-ASA acts as a local antiinflammatory agent in the colon
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which toxins of C. diff cause pseudomembranous colitis?
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A and B toxins, you can test for these to diagnose
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1st line tx for pseudomembranous colitis?
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in immunocompetant adult supportive treatment but with concominant disease metronidazole
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most common type of benign polyp?
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hyperplastic polyp
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adenomatous polyp, benign or dysplastic?
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by definition it is dysplastic therefore has malignant potential.
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Most common adenomatous polyp?
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Tubular adenoma
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adenomatous polyp subtype with highest rate of malignant conversion?
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villous adenoma, cauliflower-like appearance with finger-like villi extending down into the center of the polyp.
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which adenomatous polyp subtype has an intermediate rate of malignant conversion?
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tubulovillous polyp
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explain K-ras mutation and colorectal cancer.
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mutated ras stays in an active state constantly sending mitotic signals which prevents apoptosis
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are reducible hernia's painful?
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no
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Jaundice at birth good or bad
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Pathologic
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Jaundice 48-72hrs after birth, good or bad?
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physiological jaundice usually due to a relative deficiency of glucuronyl transferase.
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What is Dubin Johnson syndrome? what is rotor syndrome
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Dubin johnson: increased direct bilirubin, due to inability to transport it out of the hepatocyte.causes black appearance of liver.
Rotor syndrome: same as dubin johnson but less severe without black liver |
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How does phenobarbital treat dubin johnson and rotor syndromes?
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induces hypertrophy of hepatocellular ER, improving bilirubin conjugation
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Jaundice shows during stressful periods?
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Gilberts, hyperbilirubinemia due to transient reduction of glucuronyl transferase activity
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neonate with severe jaundice at birth?
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CJ 1, complete absence of glucuronyl transferase, so no conversion from indirect to direct bilirubin. leads to kernicterus
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CJ 1 tx?
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agressive phototherapy and exchange transfusion with a liver transplant or death within 18months if left untreated. Pt's do not respond to phenobarbital because there is no enzyme activity to enhance.
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what is CJ 2?
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the less severe form of CJ because there is some activity of glucuronyl transferase. pt's will respond to phenobarbital.
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TX of alcoholic hepatitis?
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thiamine, folate, Vitamin K
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why do kids with reyes syndrome get hyperammonemia
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due to destruction of mitochondria in hepatocytes, you see elevated AST, hyperammonemia due to inhibited urea cycle in mitochondria and an elevation of short chain FA's that are also not being broken down in the mitochondria
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what type of lobular necrosis is nutmeg liver associated with?
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centrilobular fibrosis/ alternating congestion
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why does increased portal hypertension cause centrilobular fibrosis?
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because in the center of each lobule is the vein and if the vein gets backed up from either R sided heart failure, cirrhosis etc. the blood with it's toxins will pool in the zone 3 around the vein
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what's the gold standard for Dx of cirrhosis?
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tissue biopsy
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elevated AST, ALT, extremely elevated ALP, antimitochondrial antibodies. biopsy shows lymphocytic infiltrate in portal regions, and loss of bile ducts in liver parenchyma?
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primary biliary sclerosis
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elevated GGT and ALP?
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biliary tract, problem with epithelium, these are two transport proteins in the wall of the epithelium and when destroyed they (GGT,ALP) are increased in the blood.
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anti IgG antibodies against mitochondria?
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Primary biliary cirrhosis
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explain hemochromatosis pathophys.
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HFE gene mutation causes the protein product which normally (in the cell membrane) binds transferrin and allows it to be endocytosed. when this mutation occurs the the transfer rate of mucosal cell iron stores to transferrin is always maximized which means high serum iron level which leads to deposition of too much iron tissues its not supposed to be in.
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where does excess normally deposit in hemochromatosis?
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pancreatic islet cells, can lead to type 1 DM
Skin: increases melanin production giving bronze appearance myocardium, liver, |
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when do you see elevated % of serum transferrin saturation, TIBC ratio > 50%. elevated iron and ferritin?
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hemochromatosis
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Hemosiderosis?
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acquired disorder of iron overload due to repeated transfusion (i.e. pt with thalassemia)
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ATP7B gene? encodes for what?
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wilsons disease on chrom 13 encodes for P-type ATPase which transports copper into bile and incorporates it into ceruloplasmin. the mutated form inhibits copper release into bile.
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why low ceruloplasmin levels with wilsons?
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copper fails to enter circulation as ceruloplasmin so low levels.
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decreased ceruloplasmin, increased serum an urine copper, liver damage seen on biopsy. How do you treat?
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penicillamine. Copper chelators
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Tumor primarily in right liver lobe large (~>10cm), pain palpable mass and signs of intratumor hemorrhage? OCC's
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Hepatocellular adenoma usually in women 3-4 decade of life on OCC's. spontaneous regression after DC of OCC's.
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solid tumor in right lobe consisting of fibrous core with stellate projections? found accidentally. asymptomatic? biopsy shows biliary epithelium and kupffer cells?
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focal nodular hyperplasia
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you see a tumor mass in right lobe and administer technetium and it is take up by the mass. Explain what it is and why?
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its a focal nodular hyperplasia because kupffer cells are present and eat the technetium. in Hepatocellular adenomas there are no kupffer cells so you do not get uptake of the technetium
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Risk factors for HCC?
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HEP B, C, aflatoxin B1, hemochromatosis, tyrosinemia, cirrhosis, alpha 1 antitrypsin deficiency, long term androgenicn steroid use. anything that can cause chronic liver disease
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elevated afp alp, right upper lobe mass in liver.
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HCC
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what is the gold standard for HCC DX?
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liver biopsy
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what is more common in the US, mets to liver or primary HCC?
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Mets from GI mainly, but can come from lungs breasts and melanoma
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Most common mets to liver mnemonic: Cancer Sometimes Penetrate Benign Liver
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Colon>stomach>pancreas>Breast>lung
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LIver hemangioma?
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benign and generally left untreated
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Cholangiocarcinoma?
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liver flukes (clonorchis sinensis), increased risk in immigrants
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angiosarcoma (liver)?
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vinyl chloride use
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Hepatoblastoma (liver)?
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main primary liver tumor in children
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what type of gall stone is radiopaque?
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pigmented (bilirubin) stones
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How do cholesterol stones form?
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when the cholesterol:bile salt ratio is high (cholesterol>bile salt) either due to hypercholesterolinemia or problem with bile salt transort from intestine or hepatic failure. the extra cholesterol will precipitate forming stones.
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post prandial colicky RUQ pain radiating to scapula
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cholicystitis
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Leukocytosis + elevated amalyse and lipase =
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acute pancreatitis
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dideoxyinosine does what?
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can cause fatal pancreatitis. its a reverse transcriptase inhibitor part of HAART regimen
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what tx do you use for acute pancreatitis pain?
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Meperidine over morphine because morphine can cause sphincter of oddi spasm increasing pain associated with acute pancreatitis
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most common cause of adult acute pancreatitis in US? and in children?
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alcohol, children its cystic fibrosis
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what is the most common gene mutation associated with pancreatic adenocarcinoma? best tumor marker?
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K-RAS, CA 19-9 (for progression not dx)
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painless obstructive jaundice, migratory phlebitis signs of ?
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pancreatic adenocarcinoma. Migratory phlebitis is when visible vein clots form and then break up then form somewhere else and break up.
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most common imaging study used to dx pancreatic adenocarcinoma?
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CT scan showing mass normally in head of pancreas
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aspartate aminotransferase (AST) what is it?
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intracellular (cytosol, mito) enzyme found in liver, skeletal muscle, heart, brain and RBC's. It converts aspartate and alpha-ketoglutarate to oxaloacetate and glutamate these amino acids will form pyruvate.
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GGT?
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present in hepatic and biliary epithelial cells membrane its an amino acid transporter, its presence in plasma equals cell membrane damage.
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amylase?
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synthesized in pancreas and salivary glands hydrolyzes complex carbs
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Lipase?
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synthesized in pancreas, hydrolysis of glycerol esters and LCFA's.
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which test is most specific to detect pancreatitis?
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Lipase
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what is PT?
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it's made in the liver. it's increased with liver disease, warfarin therapy, vit K deficiency and intravascular coagulation. used to evaluate the extrinsic pathway of coag cascade
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what drugs should you not give cimetidine (an H2 antagonist) with?
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SSRI's TCA's Phenytoin, CCB's. Cimetidine inhibits C-P450 therefore increasing these other drugs in system.
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why not use PPI and H2 antagonists?
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PPI's must be turned on my acidic environment so with an H2 antagonist they will never be turned on.
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allows HCO secretion and binds bottom of ulcer? 2 drugs?
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Sucralfate: inhibs H. pylori and inhibits acid secretions with pts with duodenal ulcers. Bismuth sulfate lacks antiacidic properties.
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Misoprostol?
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prostaglandin analog, increases production and secretion of gastric mucous barrier and decreases acid production. used in maintenance of PDA, prevents peptic ulcers during NSAID use, induces labor
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Infliximab?
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anti-TNF alpha antibody (monoclonal).
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Where is TNF alpha seen with chrons disease patients?
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in the stool and you can treat with infliximab
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Chrons disease that is refractory to corticosteroids and sulfasalazine, you tx with?
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infliximab
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sulfasalazine?
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5-ASA derivative, decreases inflammatory response in colon and inhibits prostagandins. used in ulcerative colitis
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ondansetron?
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5-HT3 receptor antagonist, anti-emetic. prophylaxis with chemotherapy, post op nausea.
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A pt. with a history of MI you have to think of what in reference to future occurrences of?
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An MI suggests severe coronary atherosclerosis. Atheromatous disease most likely involves the mesenteric arteries as well which can lead to thrombosis of blood vessels perfusing the bowel.
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where can you see kaposi sarcoma on an HIV patient?
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Anywhere in the body. in stomach it will present as a reddics purple nodule in gastric mucosa, the color is because its vascular.
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Describe how H. pylori infections are associated with gastric MALT lymphomas.
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H. pylori activate T cells that secrete cytokines, these monoclonal B-cells that can become MALT lymphomas. But if you treat the H. pylori it stops the cytokine production by T-cells stopping the B-cell lymphoma growth that will regress.
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Peptic ulcers from H. pylori infections can lead to what clinical sxs?
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hematemesis
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what types of fistula's are seen with Chrons disease due to full thickness fissure formation?
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Entero-entero fistulas are most common but also enterocutaneous fistulas are possible.
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Fibrosis of esophagus without inflammation leading to a beaking appearance?
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CREST syndrome (E, for Esophageal dismotility) normally when pt. presents there is no inflammation
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V. parahaemolyticus vs. V. cholera, which causes a more severe diarrhea?
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V. Cholera, parahaemolyticus will cause a watery diarrhea that will clear on its own in healthy adult
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what can ulcerative colitis become?
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colonic adenocarcinoma
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What is neonatal necrotizing enterocolitis?
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a complication of prematurity. i't believed to result from pre-maturity of the gut immune system and is often precipitated by oral feeding.
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what autoimmune diseases are ulcerative colitis associated with?
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migrating polyarthritis, ankylosing spondylitis, primary sclerosing cholangitis
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HNPCC is what type of problem?
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Germline transmission of a defective DNA mismatch repair gene.
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multiple small ulcers throughout gastric mucosa that are confined to the mucosa that can cause melanotic stools and bleed profusely after sever burn?
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Curlings ulcers (stress ulcers)
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GI tract malignancies associated with HIV?
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Kaposi sarcoma, non-Hodgkin lymphoma, anorectal squamous cell carcinoma
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fatigue nausea, anorexia, jaundice, joint pain and generalized skin lesions that go away?
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Hep B infection that you beat
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what does not have trophic actions on the gastrointestinal tract?
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GIP and motilin. Secretin, CCK, Gastrin all cause gastric mucosal changes along with pancreatic growth or atrophy if absent. So in the case of parenteral feeding there will be atrophy of pancreas and gastrointestinal mucosa due to lack of gastrin, CCK and secretin that are normally stimulated by food entering the GI system
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at what "T" level is the celiac artery located?
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T-12
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What non endodermal origin structure does the celiac artery supply?
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Spleen, its originated from a mass of mesenchymal cells located between the layers of the dorsal mesogastrium. it is not a foregut structure nor is it derived from endodermal epithelium
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How can Cystic Fibrosis present in a neonate?
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Meconium ileus, abdominal distension, vomiting of bilious fluid no passage of meconium. air see on x-ray can be indicative of perforation.
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an idiopathic condition characterized by markedly enlarged mucosal folds of stomach?
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Mentrier's disease (hypertrophic gastritis)
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what ligament does the splenic artery and vein run in?
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splenorenal ligament, which is a part of the dorsal mesentery between the posterior abdominal wall and spleen.
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What apoprotein activates LPL to allow FA's to be pulled from chylomicrons?
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Apo-C 2
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