Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
294 Cards in this Set
- Front
- Back
|
Endoderm forms what
|
Epithelium of gut, liver, and pancreas
|
|
|
Mesoderm forms what
|
Muscularis propria, lamina propria, vessels and hematopoetic cells
|
|
|
Ectoderm forms what
|
Cloacal membrane
|
|
|
Neural crest cells form what
|
Enteric neurons of myenteric and submucosal plexii
|
|
|
The foregut is supplied by which artery
|
Celiac artery
|
|
|
The foregut includes/forms which structures
|
oral cavity, pharynx, tongue, tonsils, salivary glands, upper respiratory system, lungs, esophagus, stomach, proximal duodenum, liver, pancreas
|
|
|
The cranial aspect of the hepatic diverticulum becomes the
|
Liver
|
|
|
The caudal aspect of the hepatic diverticulum becomes the
|
Gallbladder and ventral pancreas
|
|
|
The midgut is supplied by what artery
|
Superior mesenteric artery
|
|
|
The midgut forms what structures
|
Distal duodenum to proximal transverse colon
|
|
|
The hindgut is supplied by what artery
|
Inferior mesenteric artery
|
|
|
The hindgut forms what structures
|
Distal transverse colon to superior anal canal as well as lining of urinary bladder and most of urethra
|
|
|
Below the pectinate line in the anal canal, the blood supply comes from...
|
Internal iliac artery
|
|
|
List, in order, the layers of the GI tract
|
Mucosa
Lamina propria Muscularis mucosa Submucosa Circular muscularis propria Myenteric plexus Longitudinal muscularis propria Serosa/adventitia |
|
|
Gastric pits have what cells (of importance) in them
|
Parietal cells
Chief cells Mucus cells G-cells |
|
|
Parietal cells do what
|
secrete hydrochloric acid and intrinsic protein
|
|
|
Chief cells do what
|
Secrete pepsinogen
|
|
|
Mucus cells do what
|
secrete mucus and bicarbonate
|
|
|
G-cells do what
|
Release gastrin
|
|
|
Gastrin does what
|
Stimulates parietal cells to secrete HCl
|
|
|
Where are Brunner's glands and what do they do
|
Make bicarbonate in the duodenum
|
|
|
Where are Paneth cells and what do they do
|
Make lysozyme in the small intestine
|
|
|
What are the three types of acini that can be found in salivary glands
|
Serous, Mucous, and Seromucous
|
|
|
What are the exocrine secretions of the pancreas
|
Trypsin, chymotrpsin, elastase, lipase, amylase and bicarbonate
|
|
|
How do pancreatic acini differ in appearance from salivary acini
|
Dual staining (base is basophilic and apex eosinophilic)
No striated ducts |
|
|
What are the cells in the liver
|
Hepatocytes
Bile duct cells Kupffer cells Stellate cells |
|
|
Kupffer cells can be identified with what stain
|
India ink
|
|
|
What do slow waves of GI smooth muscle determine
|
Maximum frequency of contraction
|
|
|
Spontaneous electrical activity of GI smooth muscles originates in
|
Interstitial cells of Cajal in deep muscular plexi
|
|
|
Spike potentials do what
|
Produce phasic smooth muscle contractions and dictate strength of contraction (recall frequency depends on slow waves)
|
|
|
What mediators effect contraction strength of GI smooth muscle
|
Acetylcholine increases contraction strength
VIP/NO decrease contraction strength |
|
|
What are the excitatory neurotransmitters of the ENS
|
ACh and Substance P
|
|
|
What are the inhibitory neurotransmitters of the ENS
|
VIP and NO
|
|
|
Where is CCK released from
|
I cells of duodenum and proximal jejunum
|
|
|
CCK does what
|
Stimulates Gallbladder contraction, pancreatic enzyme secretion, and sphincter of Oddi relaxation
|
|
|
Where is secretin released from
|
S cells of duodenum and proximal jejunum
|
|
|
Secretin does what
|
Stimulates - pancreatic water and bicarb. secretion
Inhibits - acid secretion |
|
|
Gastric Inhibitory Peptide does what
|
Stimulates insulin release
|
|
|
Where is somatostatin released from
|
D cells in pancreatic islets
|
|
|
Somatostatin does what
|
Mediates gut relaxation
A potent inhibitor of gut hormone release, secretion, and motility |
|
|
Somatostatin can be used as a treatment for what
|
Carcinoid syndrome and variceal bleeding
|
|
|
Vasoactive intestinal peptide does what
|
Mediates gut relaxation (esp. sphincters)
|
|
|
Xerostomia is what
|
Insufficient saliva production (caused by drugs and autoimmune diseases)
|
|
|
What is Sjugren's syndrome
|
Autoimmune disease against salivary and lacrimal glands
Dry eyes and dry mouth |
|
|
List the chemical stimuli of gastric acid secretion
|
Histamine (major)
ACh and gastrin stimulate ECL histamine release caffeine, calcium |
|
|
List the chemical inhibitors of gastric acid secretion
|
Somatostatin and prostaglandins
|
|
|
Discuss intrinsic factor release and function
|
Released from parietal cells
Binds B12 for absorption in distal ileum |
|
|
Glucose molecules are connected by what type of bond in starch? Cellulose?
|
Starch - alpha 1,4
Cellulose - beta 1,4 |
|
|
List the disaccharidases on the small intestine brush border
|
Maltase, lactase, sucrase
|
|
|
What are a couple of major protein digesting enzymes
|
Pepsin and pancreatic trypsin
|
|
|
What are the fat soluble enzymes
|
ADEK
|
|
|
Describe iron absorption
|
Fe3+ converted to Fe2+ by ferrireductase
Absorbed into cell Either stored by ferritin or transported to plasma by mobilferrin |
|
|
Describe trypsin activation
|
Released as trypsinogen
Trypsinogen either cleaved to trypsin by enterokinase or by already activated trypsin Trypsin cleaves proteins |
|
|
Describe the release and function of pancreatic lipase and its function
|
Released in active form (can be inactivated at low pH)
Binds colipase to stay functional in low pH Breaks the 1 and 3 ester bonds of triglycerides (cholesterolesterase cleaves 2 position) |
|
|
Describe the basal phase of pancreatic stimulation
|
minimal secretion
|
|
|
Describe the cephalic phase of pancreatic stimulation
|
CNS stimulation via vagus
|
|
|
Describe the gastric phase of pancreatic stimulation
|
Triggered by gastric distension via vagus
More enzyme than bicarb |
|
|
Describe the intestinal phase of pancreatic stimulation
|
CCK and secretin cause bicarb release
|
|
|
Briefly describe the path that pain receptors will travel from the GI tract (or in general)
|
Nociceptors stimulated (fast/sharp - myelinated A, or visceral/slow/burning - unmyelinated C)
Transmission to spinal cord via dorsal horn Second order ascend via spinthalamic tract to thalamic and reticular formation Third orders to somatosensory cortex or limbic system |
|
|
Describe visceral pain stimuli
|
Innervation by few unmyelinated C fibers = dull pain with poor localization
Response to stretch or chemical stimuli |
|
|
Describe somatoparietal pain stimuli
|
Innervation by fast myelinated fibers = precise localization with intense sudden pain
Stimulation often chemical due to inflammation |
|
|
Define nausea
|
feeling urge to vomit
|
|
|
Define retching
|
somatic and gastrointestinal contractions against closed glottis
|
|
|
Define vomiting
|
retching but with an open glottis
|
|
|
Define regurgitation
|
passive return of esophageal contents into hypopharynx
|
|
|
Define rumination
|
regurgitation of gastric contents into hypopharynx
|
|
|
List some of the basic triggers of the CTZ
|
Toxins, uremia, hypoxia, and drugs
|
|
|
List some of the receptors present in the CTZ
|
Dopamine, serotonin, histamine, and muscarinic receptors
|
|
|
List the different types of antiemetics
|
Muscarinic receptor antagonists, Histamine H1 receptor antagonists, Dopamine receptor antagonists, Serotonin Receptor antagonists, Steroids, Sedatives, Neurokinin-1 receptor antagonists
|
|
|
Describe muscarinic receptor antagonists as antiemetics
|
Blocks receptors in area postrema
Good for vestibular triggers |
|
|
Describe Histamine H1 receptor antagonists as antiemetics
|
Blocks H1 receptors in area postrema and CTZ
|
|
|
Describe dopamine receptor antagonists as antiemetics
|
Blocks CTZ receptors
Best against gut triggers |
|
|
Describe serotonin receptor antagonists as antiemetics
|
Acts on area postrema, NTS, and vagal afferents in gut
|
|
|
When are neurokinin-1 receptor antagonists used
|
Prevention of chemotherapy induced emesis
|
|
|
Esophageal atresia usually presents with what
|
Polyhydramnios, respiratory distresss, gastric distension
|
|
|
What are the two proposed mechanisms for intestinal atresisa
|
Failure of recanalization
In utero mesenteric vascular disturbance |
|
|
Intestinal atresia generally presents with what
|
Polyhydramnios, obstruction, abdominal distension, bilious vomiting, failure to pass meconium
|
|
|
What are the notable characteristics of duodenal atresia
|
No distension
Association with down syndrome "Double bubble" on x-ray |
|
|
Double-bubble on x-ray is associated with what
|
Duodenal atresia
|
|
|
What are the notable characteristics of ileal atresia
|
Neonate fails to pass meconium
Distended loops of bowel with possible "dystrophic" calcification secondary to necrosis |
|
|
What are the notable characteristics of anal atresia
|
aka Imperforate anus
Most common congenital intestinal atresia |
|
|
What is the clinical presentation of extrahepatic biliary atresia
|
White/grey stool
Infants appear orange colored from increased bilirubin |
|
|
How is extrahepatic biliary atresia treated
|
Kasai portoenterostomy before 10 weeks
Transplantation after 10 weeks |
|
|
Describe the rule of twos as it relates to Meckel's Diverticulum
|
Presents around 2yo
2% of population 2in long 2 types of ectopic tissue (gastric and pancreatic) 2 feet from ileocecal valve |
|
|
Necrotizing enterocolitis usually effects which region
|
ileocolic region
|
|
|
What are the major causes of infectious esophagitis
|
HSV
CMV Candida HIV |
|
|
HSV esophagitis is characterized by what
|
Three "M"s - Multinucleated giant cells, Margination of chromatin, and molding of nucleus (ground glass)
|
|
|
Describe the esophageal cancers
|
SCC - More common worldwide, upper/mid region, AA>W
Adenocarcinoma - Most common western, lower/GEJ Hyperkeratosis of hands and feet may tip off |
|
|
What is a Zenker's diverticulum
|
Outpouching of esophagus posterior to cricopharyngeous
|
|
|
Describe a traction diverticulum
|
Diverticulum in mid-esophagus
Caused by granulomatous inflammation (histoplasma or TB) |
|
|
What is a mucosal ring at the GE junction known as
|
Schiatzki's ring
|
|
|
What is Plummer-Vinson syndrome
|
Esophageal webs with iron deficiency and glossitis
|
|
|
What are the major causes of acute gastritis
|
NSAIDs (most common)
H. pylori |
|
|
Acute gastritis is characterized by
|
Erosive gastropathy
|
|
|
Chronic gastritis caused by H. pylori has what microscopic characteristics
|
Injury in primarily in antrum
Neutrophilic infiltration of lamina propria, pit epithelium, and/or lumina of pits Subepithelial plasma cells are present in superficial lamina propria |
|
|
Describe the progression of autoimmune chronic gastritis
|
Injury primarily in body
Abs develop against parietal cells and intrinsic factor Acid production decreases Antral G cells increase gastrin release and undergo hyperplasia Glands atrophy |
|
|
Describe peptic ulcer disease
|
Most commonly in antrum and proximal duodenum
Ulcers have a punched out round/oval appearance |
|
|
What are the hypertrophic gastropathies
|
Zollinger-Ellison Syndrome
Menetrier's Disease |
|
|
A patient with a gastrinoma in the small bowel or pancreas with duodenal ulcers and chronic diarrhea also has a large increase in parietal cell number. What might they have?
|
Zollinger-Ellison Syndrome
|
|
|
Describe menetrier's disease
|
Hypoproteinemia with diffuse hyperplasia of foveolar epithelium of body and fundus
Caused by excessive TGF-alpha Also see glandular atrophy |
|
|
Multiple Endocrine Neoplasia (MEN1) is associated with what
|
Tumors of the 3 Ps - Pancreatic (most common), parathyroid, and pituitary
|
|
|
Gastrointestinal stromal tumor is associated with what
|
c-kit mutation
Originates from cells of cajal |
|
|
What are the phases of deglutition
|
Oral
pharyngeal esophageal |
|
|
The esophageal phase of deglutition requires what sensory innervation to be intact
|
CN V, IX, X
|
|
|
The esophageal phase of deglutition requires what motor innervation to be intact
|
CN V, VII, IX, X, XII
|
|
|
The upper esophageal sphincter does what and what is the main muscle
|
Separates the oropharyngeal cavity from esophagus
Cricopharyngeas |
|
|
What are the phases of the MMC
|
Fasting
Phase I: quiescence Phase II: irregular contractile activity Phase III: (aka housekeeper), regular high amplitude coordinated contractions |
|
|
Fat and hyperosmolar contents in intestines does what to gastric emptying
|
inhibits it
|
|
|
Relaxation of anal sphincters is controlled by what
|
Parasympathetics S2,3,4 releasing NO
|
|
|
Achalasia is
|
Complete failure of esophageal peristalsis and LES relaxation
|
|
|
Achalasia is caused by
|
A defect in the myenteric plexus (mostly idiopathic, can be T. cruzi)
|
|
|
Bird-beak sign on x-ray is suggestive of
|
achalsia
|
|
|
Achalsia can be treated by
|
Botulinum toxin
Dilation Heller's myotomy (surgical sphincter cutting) |
|
|
Nutcracker esophagus is characterized by
|
High amplitude peristaltic contractions often seen with acid reflux
|
|
|
How does scleroderma esophagus differ from achalasia
|
Normal upper motility and weak LES
No birdbeak sign Severe acid reflux |
|
|
Treatment for GERD
|
Bland food
Antacids Histamine H2 receptor antagonists PPIs (-azoles) Cytoprotectives |
|
|
What are the risk factors for esophageal cancer
|
ABCDEF
|
|
|
What are the highly significant symptoms of esophageal cancer
|
Progressive dysphagia and weight loss
|
|
|
Esophageal cancer typically metastasizes to what locations
|
3 Ls and to bone
|
|
|
Gastric cancers can be associated with what predispositions/factors
|
H pylori infection
Type A blood APC, E-cadherin, and TP53 mutations Precursor lesions like polyps |
|
|
Gastric adenocarcinomas might present with what
|
Virchow's node
Sister Mary Joseph nodule |
|
|
Describe the two types of gastric adenocarcinoma
|
Intestinal type - more common, heaped mass with central ulceration most often in lesser curvature of antrum
Diffuse infiltrative type - linitis plastica (leathery thickened stomach), and signet ring cells |
|
|
A patient has colorectal adenocarcinoma with iron deficiency anemia and vague pain. Which side is the adenocarcinoma most likely on
|
Right side
|
|
|
A patient has colorectal adenocarcinoma with lower left quadrant pain, blood-streaked stool, and decreased stool caliber. Which side is the adenocarcinoma most likely on
|
Left side
|
|
|
Diagnostic tests for colorectal adenocarcinomas may include what
|
Fecal occult blood testing
Colonoscopy Cacinoembryonic antigen |
|
|
Colorectal cancer typically metastasizes where
|
Three Ls
|
|
|
How might colorectal adenocarcinomas develop from adenomas
|
Adenomas lose cancer suppressing genes APC, K-ras, and/or p53
Mismatch repair problems lead to microsatellite instab. Increased CpG island methylation without instability |
|
|
What are the chemotherapeutic drugs that might be used to treat stage 3+ colorectal adenocarcinomas
|
5-FU
Leucovorin Oxaliplatin |
|
|
Describe hyperplastic colon polyps
|
In the left colon with a serrated surface architechture
No malignant potential outisde of polyposis syndromes |
|
|
Describe adenomatous colon polyps
|
Can be pedunculated or sessile
Tubular - smooth Tubulovillous - some irregularity Villous - highly irregular, high risk of adenocarcinoma |
|
|
What gene is mutated in FAP
|
APC
|
|
|
What drug(s) slows the progression of FAP
|
COX-2 inhibitors
|
|
|
Describe Gardner syndrome
|
FAP + osteomas + desmoids (retroperitoneal fibrous tumors)
|
|
|
Turcot Syndrome DESCRIBE IT NOW!!!!
|
FAP + CNS Gliomas
|
|
|
Describe MYH-Associated Polyposis (MAP)
|
Mutation of MYH (an excision repair gene)
Similar to FAP, but fewer polyps |
|
|
Describe HNPCC
|
Mismatch repair deficiency and microsatellite instability
|
|
|
What are the Hamartomatous Polyposis diseases
|
Peutz-Jegher's Syndrome
Juvenile Polyposis |
|
|
Describe Peutz-Jeger's Syndrome
|
Multiple GI hamartomas in christmas tree arrangement
Mucocutaneous hyperpigmentation from melanin deposits |
|
|
Describe Juvenile Polyposis
|
Kids <5yo
Multiple juvenile polyps in stomach and colon |
|
|
Describe anal cancers
|
Associated with HPV
Usually SCC |
|
|
What is Trousseau's syndrome
|
Migratory superficial thrombophlebitis
Associated with pancreatic cancer |
|
|
What is Courvoisier's sign
|
Palpable gall bladder due to large obstructive mass in head of pancreas
|
|
|
Pancreatic cancer typically metastasizes where
|
Three Ls
|
|
|
What is the best diagnostic test for pancreatic cancer
|
Abdominal CT
|
|
|
What are some hereditary predispositions to developing pancreatic cancer
|
Lynch II: p53, KRAS
BRCA P16 |
|
|
Describe some of the etiologies of hepatocellular carcinoma
|
Chronic hepatitis - HBV and HCV
Cirrhosis Aflatoxins from asperillus - indue p53 mutations |
|
|
What is Budd-Chiari syndrome
|
Painful hepatomegaly with ascites from hepatic vein invasion/obstruction
|
|
|
What can alpha-fetoprotein be used as a marker for
|
HCC screening and therapeutic response (can also be elevated in pregnancy, testicular cancer, and liver disease)
|
|
|
HCC chemotherapy may include what drug
|
sorafenib - a multikinase inhibitor
|
|
|
Right sided heart valvular fibrosis is associated with what GI cancer
|
Carcinoid cacer/ carcinoid syndrome
|
|
|
What are the treatments for carcinoid cancers
|
Octreotide (somatostatin analogue)
PPI Antidiarrheals Supplemental niacin |
|
|
What might a drug treatment for gastrointestinal stromal tumors include
|
Gleevac (imatinib, a tyrosine kinase inhibitor)
|
|
|
Acute inflammation in IBD might lead to what
|
Cryptitis (neutrophils infiltrating the epithelium)
|
|
|
Describe the morphology of Crohn disease
|
Skip lesions in colon and ileum
Transmural inflammation and granulomas Deep ulcerations Fissures Cobblestone appearance |
|
|
Describe the morphology of ulcerative colitis
|
Continuous involvement from rectum
Shallow ulcers limited to mucosa Sharp demarcation between healthy and involved areas |
|
|
Chronic inflammation in IBD may lead to what
|
Crypt architecture distortion
|
|
|
Extra-GI symptoms of IBD might include
|
Uveitis
Ankylosing spondylosis Sclerosing cholangitis carcinomas |
|
|
Other than IBD (CD or UC) what are some causes of chronic colitis
|
Diversion colitis
Microscopic colitis - collagenous and lymphocytic GVHD |
|
|
Acute mesenteric ischemia is most often due to what
|
Occlusion of the superior meseteric artery
|
|
|
Describe colonic ischemia
|
Watershed zones
LLQ pain and bloody diarrhea Hypoxic injury (decreased cardiac output, drugs, etc) worsened by reperfusion injury Appears as acute hemorrhagic necrosis with sharp demarcation between uninvolved area Chronic cases have fibrous scarring of lamina propria (hyalinization) and withering of crypts |
|
|
Granulomatous enterocolitis mimics what other disease process
|
Crohn's disease
|
|
|
Granulomatous enterocolitis may be cause by what organisms
|
Yersina and TB
|
|
|
What parasites cause infectious colitis
|
Giardia, cryptosporidium, entamoeba histolytica
|
|
|
What serologic tests may be used to diagnose celiac disease
|
anti-endomysial IgA, and anti-tissue transglutaminase IgA (anti-tTG)
|
|
|
Celiac disease presents with what morphology
|
Vilous atrophy, crypt hyperplasia, and intraepithelial lymphocytosis
|
|
|
McBurney's sign might suggest what
|
appendicitis
|
|
|
Obstruction of the small intestine most often is due to
|
adhesions
|
|
|
Obstruction of the large intestine most often is due to
|
90% from cancer, diverticulitis, or volvulus
|
|
|
What are some clinical presentations of intestinal obstruction
|
Colicky abdominal pain
High pitched bowel sounds Air-fluid levels on CT/x-ray systemic hypovolemia |
|
|
A slow increase in fiber content of diet might be used to treat what type of constipation
|
Only normal transit time constipation
|
|
|
What osmotic laxative might be used in pregnant women
|
Polyethylene glycol
|
|
|
What are some stimulant laxatives
|
Anthraquinones
Bisacodyl |
|
|
What is a prokinetic 5HT4 agaonist drug
|
Tergaserod
|
|
|
Differentiation of Th1 cells in IBD is suggestive of which disease process
|
Crohn
|
|
|
Differentiation of Th2 cells in IBD is suggestive of which disease process
|
Ulcerative colitis
|
|
|
What gene mutation predisposes a person to IBD
|
NOD2/CARD15
|
|
|
What are some complications associated with ulcerative colitis
|
Toxic megacolon
Adenocarcinoma |
|
|
What is the general pharmacologic approach to treating IBD
|
5-ASA and antibiotics -->
Steroids --> Immunosuppressants --> Biologics (infliximab a TNFa inhibitor) |
|
|
What is the first-line immunomodulator used for treating IBD and how does it function
|
Azathioprine (6-mercaptopurine)
Inhibits purine synthesis and therefore DNA synthesis of T cells Slow onset of function |
|
|
What are the important apoproteins involved in lipid transport and what do they do
|
CII - Activates LPL to bind and digest lipoproteins
B100 - Recognized by the LDL receptors on hepatocytes allowing uptake of LDL and VLDL |
|
|
Phase I biotransformation involves what
|
Oxidoreductases and hydrolases
Responsible for toxification of acetaminophen |
|
|
Phase II biotransformation involves what
|
Transferases
Stronger and more rapid than phase I Increases solubility of drug for enhanced secretion Non-toxic products |
|
|
What are the four major/important components of bile
|
Bile acids
Phospholipids Cholesterol Bilirubin |
|
|
What are the blood test markers for liver function tests
|
ALT
AST Alk phos Albumin Bilirubin |
|
|
What are the normal levels for AST and ALT
|
10-40 U/L
|
|
|
What are the five major causes of ALT levels in the thousands
|
Acute viral hepatitis (Hep A and B)
Autoimmune hepatitis Drugs/toxins like acetaminophen or cocaine Shock Acute biliary obstruction |
|
|
What increased enzyme levels indicate cholesatsis
|
Alk phos
Gamma-glutamyl transpeptidase (GGT) 5'-nucleotidase |
|
|
What is the normal level of bilirubin in the blood and when does jaundice become apparent
|
Normal = 1.0mg/dL
Jaundice > 3mg/dL in eyes, >10mg/dL in skin |
|
|
Which bilirubin is elevated in a liver disorder
|
Conjugated bilirubin
|
|
|
Which bilirubin is elevated in a hematologic disorder
|
Unconjugated bilirubin
|
|
|
What markers might be looked for in autoimmune hepatitis (other than ALT, AST, etc)
|
ANA
ASMA Anti-LKM |
|
|
What markers might be looked for in primary biliary cirrhosis (other than ALT, AST, etc)
|
AMA
|
|
|
What are the key players in the symptoms of IBS
|
Abnormal motor function (basal tone or MMC messed up)
Abnormal visceral perception (hyperalgesia) Psychological distress Increased serotonin secretion |
|
|
What are some treatments for constipation type IBS
|
Laxatives and fiber to stimulate contraction
|
|
|
What are some treatments for diarrhea type IBS
|
Fiber to bulk up stool
opiods antidepressants Alosetron (5HT3 agonist) may be used in women who fail other therabies |
|
|
What is done to treat bloating in IBS
|
Rifaximin (an antibiotic)
|
|
|
Microvesicular steatosis tends to occur in what
|
Acute fatty liver of pregnancy, drug toxicity and ALD
|
|
|
Macrovesicular steatosis more commonly in what
|
Obesity, diabetes, ALD, NASH, HCV
|
|
|
What are Mallory Denk bodies and where do they occur
|
Pink globs of intracytoplasmic hyaline inclusion due to misfolded intermediate filaments and proteins
Occurs in ALD, NASH, PBC, Wilson disease, others |
|
|
Feathery degeneration of hepatocytes occurs when
|
bile accumulation in cholestasis injures cytoskeletal elements giving cells a slightly yellow foamy appearance
|
|
|
Portal eosinophils may be seen in the liver after what
|
drug intoxication
|
|
|
Periportal plasma cells may be seen in the liver in what conditions
|
autoimmune hepatitis and chronic viral hepatitis
|
|
|
Lobular neutrophils may be seen in the liver in what conditions
|
any steatohepatitis or acute phase of viral hepatitis
|
|
|
What stain will show fibrosis in liver fibrosis
|
Trichrome stain
|
|
|
Portal fibrosis in the liver is associated with what
|
Viral, metabolic, biliary, or autoimmune processes
|
|
|
Intra-acinar/sinusoidal fibrosis in the liver is associated with what
|
Cardiac disease or steatohepatitis
|
|
|
What do labs for alcoholic hepatitis show
|
AST>ALT, both elevated, but not usually above 250
|
|
|
Alcoholic hepatitis has what histologic appearance
|
Hepatocyte swelling and necrosis with mallory bodies, neutrophils, and fibrosis
|
|
|
What are the gross and microscopic appearances of alcoholic cirrhosis
|
Gross - Brown, shrunken, nonfatty liver
Micro - micronodules |
|
|
What is the most common cause of chronic liver disease in the US
|
NASH
|
|
|
What are the labs of interest for NASH
|
ALT=AST until later in disease when ALT>AST
|
|
|
How is NASH treated
|
Exercise and weightloss
|
|
|
What is the typical presentation of Autoimmune hepatitis
|
younger female, often asymptomatic
Elevated ALT |
|
|
What are the labs of interest for autoimmune
|
ALT and AST in hundreds to thousands
ANA ASMA Anti-LKM (Also Plasma cells and rosettes on biopsy) |
|
|
What is primary biliary cirrhosis
|
an autoimmune disease mainly affecting intrahepatic bile ducts
See florid duct lesions of lymphocytes between biliary epithelium |
|
|
Pruritis, fatigue, abdominal discomfort, and elevated AMA might suggest
|
PBC
|
|
|
How is PBC treated
|
Ursodeoxycholic acid or liver transplant
|
|
|
What is Primary sclerosing cholangitis
|
Scarring around bile ducts associated with IBD, but no known cause
|
|
|
PSC increases the risk of
|
Chronic pancreatitis, HCC, and cholangiocarcinoma
|
|
|
What is the appearance of PSC
|
"beaded" biliary tree of alternating strictures and dilation of large bile ducts
Concentric periductal "onion skin" fibrosis |
|
|
What labs are of interest for PSC
|
Alk phos more than ALT or AST
ERCP pANCA often positive |
|
|
What causes Wilson's disease
|
Mutated ATP7B gene leads to impaired copper excertion into bile or incorporation into ceruloplasmin
|
|
|
How does Wilson's disease manifest
|
Acute liver disease with neuropsychiatric symptoms
|
|
|
What are the major features of Wilson's disease
|
accumulation of copper in liver, brain, corneas, and kidneys
"Kayser-Fleischer" rings Low ceruloplasmin High urinary copper |
|
|
Hemochromatosis occurs from a defect in
|
HFE (Hepcidin)
|
|
|
What is the clinical triad of hemochromatosis
|
Pigment cirrhosis with hepatomegaly, skin pigmentation, and diabetes mellitus
|
|
|
How does the liver appear in hemochromatosis
|
Chocolate brown liver with more iron in zone 1 than zone 3
|
|
|
Impaired blood flow through the liver generally lead to what
|
Impaired flow through the liver resulting in ascites, esophageal varices, hepatomegaly, and elevated aminotransferases
Liver has "nutmeg" appearance with an accentuated lobular pattern |
|
|
Acute cholecystitis presents with what increased lab value
|
Increased serum alk phos
|
|
|
What are the two most common cholelithiases and which is more common
|
Cholesterol stones - 90%
Pigmented stones - 10% |
|
|
Cholesterol stones in the gallbladder are associated with what
|
Age
Female gender Obesity Pregnancy |
|
|
Pigmented stones in the gallbladder are associated with what
|
Chronic hemolytic disorders
Biliary infection GI disorders |
|
|
What are the symptoms and complications of cholelithiasis
|
Colicky pain (possibly postprandial) - often asymptomatic
Inflammation, perforation, empyema, obstruction, and increased risk of carcinoma |
|
|
What is an empyema
|
Collection of pus within an already existing lumen
|
|
|
What is a choledocholithiasis
|
Stone (usually pigmented) in biliary tree
|
|
|
What are the types of acute cholecystitis and what altered lab value is common to each
|
Calculous and acalculous
Increased alk phos |
|
|
Describe calculous type acute cholecystitis
|
Stone in neck of gallbladder or cystic duct
Acidic irritation due to bile salts Fever, nausea, leukocytosis Diffuse inflammation of mucosa |
|
|
Describe acalculous type acute cholecystitis
|
Primarily due to ischemia of cystic artery
Associated with hospitalizations, burns, surgery, trauma, and postpartum |
|
|
Describe the pathologic features of chronic cholecystitis
|
Fibrosis of the wall with "Rokitansky-Aschoff" sinuses
Porcelain gallbladder Dystrophic calcification |
|
|
What organisms are most often involved with ascending cholangitis
|
E coli
Klebsiella Enterococcus |
|
|
What is the main duct of the pancreas also known as
|
Duct of Wirsung
|
|
|
What is the accessory duct of the pancreas also known as
|
Duct of santorini
|
|
|
What are the major congenital abnormalities of the pancreas
|
Agenesis
Annular Pancreas Pancreas Divisum Ectopic Pancreas |
|
|
80% of cases of acute pancreatitis involve what
|
alcoholism or biliary tract disease
|
|
|
What are some drugs that can cause acute pancreatitis
|
Azothioprine
Estrogens Furosemide |
|
|
How does acute pancreatitis present
|
Abdominal pain radiating to back
Elevated plasma amylase and lipase Shock symptoms |
|
|
What is the pathogenesis of acute pancreatitis
|
Inappropriate activation of pancreatic enzymes leads to autodigestion
Initiated by acinar cell injury (obstruction, defective cellular transport or direct injury) |
|
|
Describe the pathogenesis of chronic pancreatitis
|
Ductal obstruction by protein/cellular concretions
Toxins Oxidative stress |
|
|
Describe the pathologic features of chronic pancreatitis
|
Fibrosis around fewer smaller acini with dilated/obstructed ducts
PATHOMNEMONIC calcium precipitates (concretions) |
|
|
Describe Intraductal Papillary Mucinous Neoplasms of the pancreas
|
Mostly in men - benign or malignant
Head of pancreas Mucin producing |
|
|
Describe serous cystadenomas of the pancreas
|
Benign cyst of glycogen rich cuboidal cells
Looks like a sponge with many microcysts |
|
|
Describe Mucinous cystic neoplasms of the pancreas
|
95% women - benign or malignant
In tail of pancreas and not connected to main pancreatic duct Dense ovarian-like stroma Mucin producing |
|
|
Pathogenesis of pancreatic carcinoma might include
|
Molecular carcinogenesis - KRAS
PanIN (Pancreatic Intraepithelial Neoplasia) - precursor lesion in situ |
|
|
What are the gross and microscopic characteristics of pancreatic carcinoma
|
Gross - gritty grey-white solid firm masses
Micro - Adenocarcinoma with dense stromal fibrosis |
|
|
What is the appearance of acinar cell carcinoma
|
Huge ducts with strange tissue between them and acinar cell differentiation
|
|
|
Describe HAV hepatitis
|
Fecal-oral
Acute infection Jaundice Treat with rest |
|
|
What does anti-HAV IgM suggest
|
Recent infection with HAV
|
|
|
What does anti-HAV IgG suggest
|
Immunity to HAV
|
|
|
What is notable about neonatal infection with HBV
|
Immune tolerance
200x increased risk of HCC |
|
|
How is HBV damage mediated
|
Immune-mediated
|
|
|
Anti-HBsAg suggests what
|
Immunity to HBV
|
|
|
What are the serum ALT levels in chronic HCV
|
Normal to slightly elevated
|
|
|
What is EIA
|
A test to detect all the antibodies of HCV
|
|
|
What is RIBA
|
A test to detect antibodies of specific recombinant proteins. Aimed at testing false positive EIA in HCV cases
|
|
|
What should be remembered about HDV
|
Requires HBV coinfection
|
|
|
What is cholestasis
|
Excess of conjugated bilirubin>20% of total bilirubin
|
|
|
What is the difference between cholestasis and jaundice
|
cholestasis - increased conjugated bilirubin
jaundice - increased unconjugated bilirubin |
|
|
What are some causes of neonatal cholestasis
|
Biliary atresia
Genetic causes Infection Idiopathic |
|
|
What is the most common cause of pediatric liver transplant
|
Biliary atresia
|
|
|
What is the principal feature of alagille syndrome
|
Chronic colestasis due to paucity of intrahepatic bile ducts
|
|
|
Is the Kasai procedure useful for alagille syndrome
|
No
|
|
|
What is a feature of alagille syndrome that might be seen on x-ray
|
butterfly vertebra
|
|
|
What are some outwardly visible features of alagille syndrome
|
Prominent forehead, pointed chin, deep set eyes, broad nasal bridge
Xanthomas |
|
|
1+1=
|
2
|
|
|
What are the key points about Vibrio cholerae
|
profuse rice water secretory diarrhea
comma shaped rod |
|
|
How does Vibrio cholerae cause diarrhea
|
Enterotoxin that increases adenylate cyclase activity causing increased cAMP which increases openness of Cl- channels
|
|
|
Enteropathogenic E coli often has outbreaks in
|
Neonatal nurseries
|
|
|
What is the most common cause of traveler's diarrhea
|
Enterotoxigenic E coli
|
|
|
Enterohemorrhagic E coli causes
|
TTP-HUS that can lead to acute renal failure, etc.
Antibiotics increase risk |
|
|
How does enterohemorrhagic E coli cause damage
|
Releases shiiga toxin that blocks protein synthesis
|
|
|
What are the Toxigenic pathogens of the GI tract
|
Vibrio cholerae
ETEC EHEC EAEC EPEC Vibrio parahaemolyticus |
|
|
What are the invasive pathogens of the GI tract
|
Shigella
Salmonella Campylobacter Yersinia EIEC |
|
|
Invasive pathogens of the GI tract typically effect which area of the GI tract and what do they generally do
|
Distal ileum and colon
Elaborate enterotoxins that increases local synthesis of prostaglandins and cytokines Ulceration |
|
|
What are some key features of shigella infection
|
Non-motile, possible systemic manifestations (meningitis, HUS/TTP)
Multiple small-volume bloody mucoid bowel movements |
|
|
What are some key features of salmonella infection
|
Motile, penetrate small bowel epithelium, can cause bacteremia
Usually has gastroenteritis with copious bloody diarrhea |
|
|
What are some rare complications of campylobacter infection
|
Toxic megacolon
Pancreatitis Guillan-Barre |
|
|
What are some key features of yersinia enterocolitica
|
Symptoms can last several weeks
Associated with reactive polyarthritis or erythema nodosum Can mimic appendicitis |
|
|
What are the organisms responsible for toxin-mediated food-borne illnesses
|
Staph aureus
Clostridium perfringens Clostridium botulinum Bacillus cereus |
|
|
Describe S aureus caused food poisoning
|
Very short incubation
Vomiting and diarrhea, rarely febrile Recovery within 24-48 hrs |
|
|
Describe C perfringens caused food poisoning
|
10 hour incubation
usually from meat Cytotoxin and enterotoxin |
|
|
Describe C botulinum caused food poisoning
|
Most lethal - rare
Floppy baby Neurotoxin inhibits release of ACh causing progressive paralysis |
|
|
Describe B cereus cause food poisoing
|
Diarrhea similar to cholera
Spore can survive high temps Usually from contaminated rice |
|
|
Describe entamoeba histolytic infection
|
Cysts and trophozoites capable of invading tissue and causing liver abcesses
Dysentery - amoebic colitis |
|
|
Describe Tropheryma whipplei infection
|
PAS+
Typically white males Diarrhea, Dementia, Endocarditis, Arthralgias |
