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149 Cards in this Set
- Front
- Back
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Name layers of abdomen
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Skin, superficial fascia (camper's fascia for liposuction, then scarpa's fibrous fascia, external, internal, transversus, transversalis, extraperitoneal, peritoneum
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Is the rectum retroperitoneal? adrenal glands?
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yes
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what can you compress between thumb and index finger to control bleeding?
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hepatoduodenal ligmanet
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what can you cut to access lesser sac?
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gastrohepatic, which separates right greater and lesser sacs
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gastrocolic is part of what?
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greater omentum
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what separates left greater and lesser sacs?
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gastrosplenic, which has short gastrics
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what is the frequency of stomach, duodenum, ileum wave slow waves/basal electric rhythm?
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stomach = 3 waves/min
duodenum = 12 ileum = 8-9 |
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what area of small intestine has most villi
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duodenum, which also has brunner's gland
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wha thas largest number of goblet cells in small intestine, along with plicae circulares
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jejunum
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what part has plicae circulares only in proximal part
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ileum
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what do meissner's gland regulate
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secretions, blood flow, absorption
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cricopharyngeal muscle dysfunction can lead to what
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zenker's diverticulum
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at what level is teh celiac trunk? SMA? renal arteries? testicular/ovarian arteries? IMA? Bifurcation?
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celiac trunk = T12
SMA = L1 renal arteries = L1 testicular/ovarian = L2 IMA = L3 bifurcation = L4 |
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wha tis SMA syndorme?
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transverse duodenum (3rd part) entrapped between SMA and aorta at L3 , cause the angle decreases due to diminished fat or lordosis.
the angle is usually 45-60 degrees, and loss of mesenteric fat pad will make the angle smaller and crush duodenum |
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3rd part of duodenum is anterior to what vessel?
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IMA at L3
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what are 2 watershed areas in intestine?
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splenic flexure and rectosigmoid junction
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if splenic artery is blocked, what will have poor circulation?
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short gastrics, upper fundus
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what supplies body and tail o fpancreas?
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splenic
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cystic artery is a branch off what? in what ligament does it lie?
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branch off hepatic artery in hepatoduodenal ligmanet
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Internal thoracic artery anastomoses with what? what about suprior rectal
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Internal thoracic from subclavian anastomoses with superior epigastric (internal thoracic) to inferior epigastric (external iliac)
superior rectal (IMA) --> middle rectal (internal iliac) |
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where is the portal vein in relation to liver and IVC
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right side of liver, anterior to IVC
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caput medusae is produced by what anastomosis
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paraumbilical with superficial and inferior epigastric veins
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above pectinate line, what kind of cancer? what is the blood supply?
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adenocarcinoma, blood from suprior rectal off of IMA
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below pectinate line, what is the venous drainage
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to inferior rectal vein, to internal pudendal, to internal iliac. innervation via pudendal nerve branch (inferior rectal)
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which side of hepatocytes face bile canaliculi? what side faces sinusoids?
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apical surface faces bile canaliculi, basolateral surface faces sinusoids
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sinusoids - how big are pores? basement membrane?
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pores 100-200 nm
no BM |
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in what ligament does the tail of the pancreas source with?
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splenorenal ligament, which has splenic vessels and its blood supply
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femoral sheath contains what?
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femoral vein, artery and canal (deep inguinal lymph nodes) but NOT FEMORAL NERVE.
canal is bordered by sartorius, adductor longus, and inguinal ligament |
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where arethe medial umbilical ligament, inferior epigastric vessels, and median umbilical ligaments located?
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all located between transversalis fascia and parietal peritoneum
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layers of the spermatic cord?
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tunica vaginalis, then internal spermatic fascia (transversalis), cremaster muscle (internal oblique), external spermatic fascia (external oblique - has superficial ring)
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all hernias protrude through what?
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superficial ring
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what is hesselbach's triangle and associated hernia?
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rectus abdominis, inguinal ligament (poupart's ligament), and inferior epigastric vessels.
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what hernia is more common in women? what is predisposing factor? what is a complication?
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femoral. can lead to incarceration. predisposed to by previous abdominal surgeries
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what are the 3 trophic hormones?
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gastrin, CCK secretin
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what is the regulation of gastrin? what 2 amino acids are the most potent stimulators?
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increased y stomach distention, peptides, vagal stimulation by stomach (uses GRP as signaling peptide, atropine doesn't work).
most potent amino acids are phenylalanine an dtryptophan |
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what does CCK do?
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increases pancreatic secretion
gallbaldder contraction decreases gastric emptying increases intestinal blood flow increases satiety |
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Name the locations of the following cells:
I S D K |
I == duodenum, jejunum
S - duodenum D - pancreatic islets, GI mcuosa K - duodenum, jejnum (GIP) |
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what do S cells secrete? what is teh stimulus?
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secrete bicarb, bile. decrease gastric acid
stimulus - gastric acid, fatty acids in duodenum |
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name 4 actions of somatostatin
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decreases gastric acid and pepsinogen
decreases pancreatic and small intestine fluid secretion decreass gallbladder contraction (biliary stones) decreases insulin and glucagon |
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what is somatostatin also known also?
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antigrowth hormones, cause it inhibits digestions nad absorption of substances. inhibotry hormone. used to treat VIPoma and carcinoid tumors
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What is GIP's MOA?
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decreases gastric acid, increases insulin
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what hormones decrease gastric acid?
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GIP, somatostatin, secretin, maybe CCK through somatostatin
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what is VIP released from? what does it causes? how is it regulated?
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released from NEURONS in ganglia in sphincters, bladder, intestine
increases water and electrolyte secretion and relaxes intestinal smooth muscle sphincters increased by distention and vgal stimulation, decreases by adrenergic input |
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Ghrelin - produced by what cells? action? regulation. associated with what syndrome? how does gastric bypass surgery affect it?
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secreted by P/D1 cells in stomach
increases GH, ACTH, cortisol, and prolactin secretion. associated with prader willi hyperphagia lost following gastric bypass |
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Motilin produces what? when is it increased?
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MMCs from stomach to the ileum,
increased in fasting state |
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where are parietal cells located in glands? what decreases gastric acid secretion
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located in superificla gastric glands
decreased by somatostatin, GIP, prostaglandin, secretin |
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where are chief cells? what increases them?
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in deep gastric glands, increased by vagal stimulation or loal acid
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where is bicarb trapped in stomach?
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in the mucus that covers the epithelium
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how does gastrin increase acid primarily?
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through stimulatin of ECL cells, rather than parietal cells
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what is the most serous salivary gland? most mucinous?
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serous on the sides (parotides)
mucinous in the middle (sublingual) |
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what is ptyalin?
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alpha amylase, in saliva
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what are the components of saliva?
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alpha amylase (ptyalin), ciarb (to neutralize oral acids), mucins (glycoproteins), antibacterial secretory products, grwoth factors
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in saliva, what is the compoisiton of low flow rate? what about high flow rate?
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low flow = hypotonic, high flow is isotonic. low flow has more potassium and bicarb
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what nerves runs through the parotid gland and makes pleomorphic adenoma hard to resect?
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facial nerve
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what enzyme is necessarily in parietal cells?
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carbonic anhydrase, to produce alkaline tide and H secretion
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hypertorphy of brunner's glands is seen in what disease?
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peptic ulcer disease
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name the four phases of eating?
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cephalic phase (vagal mechanism increases acid, due to sight of food)
gastric (increases gastrin and thus acid through distention and chemical stimulus) intestinal (protein in duodenum) first 2 contribute to acid secretion, decreased acid in intestinal phase due to somatostatin, peptide YY |
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what is the composition of pancreatic uice?
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same Na and K as serum. more bicarb, less chloride (at higher flow rates)
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what are 4 proteases secreted by pancreas and in what form are they?
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zymogens - trypsin, chymotrypsin, elastase, carboxypeptidases
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what is the amount of kcalories/g of protein, fat, ehtanol?
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protein = 4, fat = 9, ethanol = 7
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what are the products of salivary amylase?
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maltose, maltotriose, alpha limit dextrans. pancreatic amylase makes disacchrides form oligosacchrides
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what is the trnapsorter for the MONOSACCHARIDES (which are the only absorbable form) glucose/galactose
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(SGLT1 - Na dependent).
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what is the transporter for fructose? how is it taken up?
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Glut-5
facilitated diffusion |
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where are peyer's patches located?
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LP and submucosa of ileum. has M cells that take up antigen. produce IgA for gut mucosa
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what is the composition of bile salts?
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bile acids conjugated to glycine or taurine, making them water soluble
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where are lipids digested and absorbed?
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digested in duodenum, absorbed in jejunum
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what is most bilirubin in blood - conjugated or not?
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not conjugated
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what enzyme makes biliverdin form heme (makes the green color in bruises)
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heme oxygenase
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what % of urobilinogen (the product of gut bacteria) is excreted as stercobilin? what percent% is reabsorbed? how much of that reabsorbed amount is excreted as urobilin
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80% excreted as stercobilin
20% reabsorbed (10% of which is excreted as urobilin) |
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what is warthin's tumor? what is the most common malignant salivary tumor?
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warthins tumor - benign, heterotopic salivary gland tissue trapped in a lymph node, surrounded by lymphatic tissue
mucoepidermoid carcinoma is the most common malignant tumor |
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2 most common locations of oral SCC?
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lower lip and floor of the mouth
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what plexus is lost in achalasia? how does scleroderma contrast to achalasia?
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auerbach's plexus is lost in achalasia
scleroderma has low pressure proximal to LES. achalasia ahas high LES opening pressure |
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what is the histo of GERD?
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basal zone hyperplasia, elongation of LP papillae, eosinophils, neutrohpils
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what is the finding in diffuse esophageal spasm? what does it mimic?
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DES is a "corkscrew" esophagus. mimics angina
muscles contract all at once. periodic non peristaltic contractions |
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plummer vinson triad?
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dysphagia (esophageal webs)
glossitis iron deficiency anemia |
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if dysphagia for solids, then liquids, what should you think? What about just straight dysphagia for solids and liquids wihtout progression?
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think obstruction if solids, then liquids
think dysmotility if dysphagia for both |
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what is the 5 year survivial of esophgeal cnacer?
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10% (like pancreatic cancer)
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what are th risk factors for esophageal cancer?
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alcohol/achalasia
barrett's esophagus cigarettes (most common cause) diverticuli (zenkers) esophgeal web (plummer vinson) or esophagitis familial (tylosis) |
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what test do you do to distinguish malabsorpitoi due to GI versus pancreas?
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d-xylose test (it doesn't need to be digested by pancreas, so a positive test means GI problem)
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what does tropical sprue effect (what part of GI tract)?
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can affect entire small bowel
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whipple's disease stain?
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PAS positive, with diastase resistant granules (lysosomes and bacteria). PAS is a stain for glyocprotein. Tropheryma is an actinomycete
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what are the symptoms of whipples?
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arthalgias, cardiac, and neurologic
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what is the best screen for celiacs? what cancer is associated with celiac?
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tissue transglutaminase (IgA primarily)
T-cell lymphoma (also NHL, esophageal) |
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what are 5 causes of acute gastritis (erosive)
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stress, NSAIDS, alcohol, uremia, burns (curling's ulcer sloughs off gastric mucosa), brian injury (cushing's ulcer --> due to vagal stimulation that increase ACh and thus hydrogen)
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what is type A chronic gastritis?
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in the fundus/body. autoimmune disorder. can see lymphocytic infiltration. associated with atrophic gsatritis
type B is more common (H. pylori) |
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menetrier's disease loses what? what cell is atrophied? which cell is increased? can it lead to cancer
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loses protein
parietal cell atrophy mucus cells increased precancerous |
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what type blood is stomach cancer associated with? are the edges raised or not (opposite of ulcers)?
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Type A blood
edges are raised |
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what are the 2 types of stoamch cancer?
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intestinal - solid mass, gland forming cells, looks like colon cancer
diffuse - linitis plastica, signet ring cells. not h. pylori associated. nonperistalsing |
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which ulcer is due to increased acid secretion (versus decreased mucosal protection)
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duodenal ulcers are due to increased acid (and they thus respond to antacids more).
ulcers have clean, punched out margins, not raised or irregular margins |
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pathogenesis of H.pylori duodenal ulcers?
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H. pylori destroys D cells, increasing gastrin, acid drips into duodenum, h. pylori travels down there
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what is dumping syndrome? what should you eat?
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dumping syndrome is when chyme is passed too quickly to small intestine from stomach. eat fat rich meals in small proportions
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ulcerative colitis characterisitcs?
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autoimmune probably. friable pseudopolyps. loss of haustra --> "lead pipe" imaging apperaance.
crypt abscess is big histo finding pyoderma gangrenosum (ulcers), PSC colectomy is curative |
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crohn's disease characteristics?
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cobblestone mucosa, creeping fat on serosa, stricutres (string sign), fissures, fistulas.diarhea that may or may not be bloody
migratory polyarthritis, erythema nodosum, ankylosin gpsondylitis, uveitis, apthous ulcers corticosteroids for flare ups |
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what are the criteria (2/3) for IBS?
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pain improves with defecation
change in stool frequency change in appearance |
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where are most diverticulae located?
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sigmoid colon - at places where vasa recta perforate muscularis externa
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how common is diverticulosis? whow does it present?
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50% people>60 years old
presents with painless rectal bleeding |
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what are complicaiton sof diverticulitis?
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bleeding, colovesical fistula (pneumaturia)
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what is the difference between meckel's and omphalomesenteric cyst
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omphalomesenteric cyst = cystic dilation of vitelline duct (peripheral, but not central portions, obliterate
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where does intussuception usually happen?
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ileocecal valve
will see "currant jelly" stools |
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where do most volvulus occur/
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sigmoid colon, cause it's poorly supported. also at cecum
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where should you biopsy for hirschsprungs?
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submucosa of the narrowed part
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who is most affected by necrotizing enterocolitis?
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preemies and bottlefed (decreased immunity when that young)
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what is characteristic presenting sign of ischemic colitis? where does it infarct?
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presents with postprandial pain
infarct at the watershed regions (splenic flexure, rectosigmoid junction) |
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where does angiodysplsia most often occur?
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cecum, ileum, ascending colon
confirm by angiography |
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are villous polyps pedunculated or sessile?
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sessile
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what are the nonneoplastic polyps?
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hyperplastic polyp (90% of all polyps,most found at rectosigmoid colon)
juvenile (80% in rectum) - but juvenile polyposis syndrome has increased risk of adenocarcinoma Peutz-Jeghers (single polyps ok. AD condition with hamartomas) |
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what % of CRC patients have a family hx?
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25%
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how is FAP inherited? where is it always located?
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AD mutation, 2 hit hypothesis. always in rectum
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gardner's syndrome?
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FAP+osseous and soft tissue tumors, retinal hyperplasia
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Lynch syndrome?
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AD, genes are MSH and MCH. 80% progress to CRC. proximal colon always involved
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UC is more likely to cause cancer with what characteristics?
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pancolitis and right side colitis
no polyps |
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molecular pathway of CRC (not microsatellite instability - which is 15% of cancers sporadic and lynch syndrome)
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Loss of APC (less intercellular dehesion and increased proliferation), then K-ras (creates adenoma - unregulaed signal transudction) then loss of P53/DCC (carcinoma).
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carcinoid tumors comprise what % of small bowel tumors? what is EM finding? LM finding? What are determinants of metastasis?
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50% of small bowel tumors
EM = dense core bodies LM - uniform cells in sheets metastasis determined by size and location |
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fetor hepaticus?
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breath smells like freshly opened corpse.
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macronodular cirrhosis?
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nodules> 3mm. due to significant live injury leading to hepatic necrosis (postinfectious or drug induced hepatitis)
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what do mitochondria look like in reye's. what is cerebral finding? what 2 diseases is it associated with? has does aspirin cause damage?
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mitochondria are enlarged
cerebral edema is brain finding via hyperammonemia associated with influenza B and VZV aspirin metabolites decrease beta oxidation by reversible inhibition of mitochondrial enzyme |
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when do mallory bodies become present?
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alcoholic hepatitis
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what does liver look like in alcoholic cirrhosis
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micronodular, shurnken liver iwth "hobnail" apperance. perivenular fibrosis
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what is most common hepatic tumor?
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metastasis. nodules are umbilicated
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most common benign liver tumor?
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cavernous hemangioma. blood filled space, single epithelial layer. don't biopsy (can bleed)
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what is inheritance of A1AT deficiency? what stain should you use? what is the cause of the dysfunction?
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inherited as codominant trait
PAS positive globules (discrete intracellular inclusions) misfolded gene product |
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what are the uribine bilirubin and urobilinogen levels in hepatocellular, obstructive, and hemolytic jaundice types?
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in hepatocellular (mixed hyperbilirubinemia) - increase urine bilirubin, and normal to decrease urobilinogen
obstructive - increase urine bilirubin (light brown urine), decrease urobilinogen hemolytic - absent urine bilirubin, high urobilinogen |
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what produces the radical in CCL4?
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p450 oxidation system, which causes lipid peroxidaiton
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difference of rotors and DJ syndrome?
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rotors does not cause black liver
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what is the deficiency in Gilberts?
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uptake and glucuronidation
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what symptoms does basal ganglia degeneration have in Wilson's?
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parikinsonian. also choreiform movements.
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treatment of wilsons"
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trientine, zinc, penicillamine. mutated copper transporting ATPase.
low total copper in serum, but high free concentration |
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what condition has florid duct lesions? what does the urine look like and the stool?
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PBC -
urine is dark stool is light |
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what ducts are affect by PSC? what is the ERCP finding?
what is it associated with? what condition can it lead to |
intra and extrahepatic ducts are affected
ERCP shows beading associated with hypergammaglobulinema (IgM) and can lead to secondary biliary cirrhosis |
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what condition has florid duct lesions? what does the urine look like and the stool?
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PBC -
urine is dark stool is light |
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what ducts are affect by PSC? what is the ERCP finding?
what condition can it lead to |
intra and extrahepatic ducts are affected
ERCP shows beading associated with hypergammaglobulinema (IgM) and can lead to secondary biliary cirrhosis |
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what is charcot's triad?
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jaundice, fever, RUQ pain
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brown stone?
black stone |
brown - infection
balck - hemolysis (small spiculated crumbly with calcium carbonate or bilirubinate, mostly radioopaque) |
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tests for gallstones?
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HIDA scan (no gallbladder seen)
US |
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causes of cholecystitis?
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stones, rarely ischemia or CMV infection. if acalculous, think hospitalized
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what are causes of acute pancreatitis?
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trauma
steroids mumps autoimmune hypercalcemia/hyperlipidemia, sulfa drugs ERCP (3rd most common cause) |
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complciations of acute pancreatitis?
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DIC, ARDS, pseudocyst (walls are grnaulation tissue and fibrotic, not epithelial)
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where are most tumors of pancreas located? what are 2 serum markers? what is courvoisier's sign?
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mostly in head
use CA 19-9, CEA sign = nontender palpable gallbladder |
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what M receptor is on ECL cell? on parietal cell?
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ECL = M1 (remember M1 is CNS, ENS)
parietal = M3 |
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cimetidine side effects?
which 2 H2 blockers cause decreased renal excretion of creatinine? |
cimetidine - prolactin release, gynecomastia, impotence, decreased libido, confusion (crosses BBB), and crosses placneta
cimetidine and ranitidine decrease creatinine excretion |
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PPI - reversible or irreversible?
H2 blockers? |
PPI are irreversible
H2 are reversible |
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what is sucralfate made of? why don't you use PPI with it?
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made of aluminum sucrose sulfate. polymerizes in acid. used to allow bicarb secretion to restablsih pH gradient
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misoprostol?
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PgE1
causes diarrhea as side effect 9stimulates contractions |
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WHICH ANTACID CAUSES CONSTIPATION? diarrhea? what do all antacids cause?
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Aluminum hydroxide - constipation and hypophosphatemia, muscle weakness, osteodrystphy, seizures
MgOH2 - diarrhea, hyporeflexia, hypotension, cardiac arrest calcium carbonate all cause hypokalemia |
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what is sulfasalazine a combo of?
Side effect? |
sulfapyridine (antibacterial and 5-ASA)
can cause reversible oligospermia |
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ondansetron, granisetron, dolasetron MOA?
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5-HT3 antagonist
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metoclopramide MOA and uses?
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D2 antagonist.
use in gastroparesis and antiemetic increases resting tone, contractility, LES tone, motility, but not colon transport time |
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docusate?
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anionic surfactant, a detergent. decreases surface tension at feces, acts as a stool softener
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prochloperazine use?
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blocks dopamine, antiemetic
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