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;
193 Cards in this Set
- Front
- Back
Most common tumor of the salivary gland
Most common malignant tumor of the salivary gland |
pleomorphic adenoma
mucoepidermoid carcinoma |
|
Patient presents with a painless, moveable mass on their salivary gland
histologically: polygonal and epithelial spindle shaped myoepithelial cells in a variable stroma dx? course? |
pleomorphic adenoma
benign with high rate of recurrence |
|
Salivary gland tumor
Patient has salivary gland tissue trapped in a LN, surrounded by germinal centers (lymphatic tissue) dx and course |
Warthin's tumor, benign
|
|
Child presents with a painless, slow growing, hard mass on salivary gland
histo: see squamous cells, mucus-secreting cells, intermediate cells dx? course? |
mucoepidermoid carcinoma
malignant |
|
Patient has progressive dysphagia to solids and liquids
-on barium swallow, you see dilated esophagus with an area of distal stenosis (bird's beak) dx? what is the cause? increases risk of what? |
achalasia
loss of myenteric (aurebach's) plexus --> failure of LES to relax --> high LES opening pressure and uncoordinated peristalsis increased risk of esophageal carcinoma |
|
Patient with Chagas' disease develops dysphagia to solids and liquids
-see stenosis on barium swallow dx? |
achalasia secondary to chagas disease
|
|
Patient has esophageal dysmotility involving low pressure proximal to the LES
one disease association |
scleroderma (CREST)
|
|
Patient presents with
-heartburn -regurgitation upon lying down -nocturnal cough and dyspnea dx? |
GERD
|
|
Patient presents with painless bleeding of submucosal veins in lower 1/3 of esophagus
histo: can see sclerosed area with esophageal mucosa normal dx? |
esophageal varices
|
|
3 conditions associated with esophagitis
|
Reflux
Infection (HSV, CMV, Candida) Chemical ingestion |
|
Patient is an alcoholic/bulemic who presents with hematemesis
on endoscopy, you see mucosal lacerations at GE junction dx? what caused it? |
Mallory-weiss
severe vomiting |
|
patient has been violently retching --> transmural esophageal rupture
dx |
BoerHaave Syndrome
Been Heaving Syndrome |
|
Esophageal strictures
associated with 2 conditions |
lye ingestion
acid reflux |
|
Patient is a post-menopausal woman, comes in with triad of
-dysphagia (esophageal webs) -glossitis -iron deficiency anemia |
plummer vinson syndrome
|
|
What happens in Barret's esophagus
associated with what three conditions |
Chronic acid reflux (GERD) --> replacement of stratified squamous epithelium with intestinal (columnar) epithelium in distal esophagus
esophagitis, esophageal cancers, esophageal ulcers |
|
Risk factors for esophageal cancer (mnemonic)
|
ABCDEF
Alcohol/achalasia Barrett's Cigarettes Diverticuli Esophageal web (plummer vinson), Esophagitis Familial |
|
Patient who smokes, drinks, has Barrett's and a family history of esophageal cancer comes in with progressive dysphagia (solids --> liquids) --> weight loss
most common type in world and where is the lesion? most common type in US and where is the lesion |
Esophageal cancer
world = sq cell - upper and middle 1/3 US = adenocarcinoma - lower 1/3 |
|
Patient has diarrhea, steatorrhea, weight loss, weakness
You suspect she cannot absorb her food 6 possible diagnoses |
Tropical sprue
Whipple's Celiac sprue Disaccharidase deficiency Abeta-lipoproteinemia Pancreatic insufficiency These Will Cause Devestating Absorption Problems |
|
How is tropical sprue different from celiac sprue (2 ways)
|
1. tropical is infectious, celiac is autoimmune
2. tropical affects whole small bowel, celiac just the proximal (jejunum) |
|
How do you treat tropical sprue
|
Antibiotics
|
|
An older man gets diarrhea, steatorrhea, weight loss, and weakness
-also has arthralgias, cardiac, neuro symptoms you recover a gram positive organism with PAS-positive macrophages in the intestinal lamina propria and mesenteric nodes dx? organism |
Whipple's disease (malabsorption)
Tropheryme whippelii |
|
Celiac sprue
cause |
autoantibodies to gluten (gliadin) in wheat and other grains
|
|
Following an injury (like viral diarrhea) to the intestinal vili, a patient drinks milk, develops osmotic diarrhea
what happened |
lactase is located in tips of villi, so if these are damaged, you experience self-limited disaccaridase deficiency
|
|
Most common disaccharidase deficiency
how do the villi look |
lactase deficiency --> milk intolerance
normal appearing villi |
|
Malabsorption syndromes
Young child presents with malabsorption and neuro smptoms -on histo, you see fat accumulation in enterocytes dx? what 's going on |
abeta lipoproteinemia
decreased synth of apo B --> cannot generate chylomicros --> cannot secrete cholesterol, VLDL into blood stream --> accumulates in enterocytes |
|
Pancreatic insufficiency
3 causes |
Cystic fibrosis
obstructing cancer chronic pancreatitis |
|
Patient gets malabsorption of fat and fat-soluble vitamins (A, D, E, K)
patient also has chronic pancreatitis dx? |
pancreatic insufficiency
|
|
Patient is of N. European descent, gets steatorrhea
-find antibodies to gliadin and tissue transglutaminiase histo: villous blunting, crypt hyperplasia, lymphocytes in lamina propria dx? associated with what conditions? |
Celiac sprue = autoimmune intolerance of gliadin, decreases mucosal absorption in jejunum
assoc with dermatitis herpetiformis, increases risk of malignancy (T-cell lymphoma from lymphocyte infiltrate) |
|
How do NSAIDS --> acute gastritis
|
NSAIDs reduce PGE2 --> decreases gastric mucosa protection
|
|
How do burns lead to acute gastritis
|
burns --> decreased plasma volume --> sloughing of gastric mucosa (Curling's ulcer)
BURNed by a CURLING iron |
|
How does brain injury lead to acute gastritis
|
Increased ICP --> vagal stimulation --> increased ACh --> increased H production (Cushing's ulcer)
"alway's CUSHION the brain" |
|
Patient with an autoimmune disorder gets
-autoantibodies to parietal cells -pernicious anemia -achlorhydria dx? |
Chronic gastritis type A (fundus/body)
|
|
Most common type of chronic gastritis?
cause? increases what? |
Type B (antrum)
H. pylori increases risk of MALT |
|
Patient gets gastric hypertrophy with protein loss, parietal cell atrophy, and increased mucous cells
also see that rugae of stomach are hypertrophied, look like brain gyri dx? course? |
menetrier's disease
precancerous |
|
stomach cancer
a. common type b. course c. common features |
a. adenocarcinoma
b. early, aggressive local spread and node/liver mets c. signet ring cells, acanthosis nigricans |
|
Dietary nitrosamines (smoked fod), achlorhydria, chronic gastritis, type A blood
associated with what condition |
stomach cancer
|
|
what is linitis plastica
|
stomach cancer that is diffusely infiltrative (thickened, rigid appearance, "leather bottle")
|
|
Patient has stomach cancer, metastasizes to left supraclavicular node
what is the node called |
Virchaow's node
|
|
Patient has stomach cancer that progresses to bilateral ovaries
there are abundant mucus and signet ring cells dx? |
Krukenberg's tumor
|
|
Patient has stomach cancer, metastasizes to subcutaneous periumbilical region
dx? |
sister mary joseph nodule
|
|
Patient comes in with abdominal pain that gets worse with meals, weight loss
-patient is older -they take NSAIDS -have a positive urease test dx? cause? |
Gastric ulcer
H. Pylori in 70% Due to decrease in protection against gastric acid |
|
Difference in pain sequelae between a gastric and a duodenal ulcer
|
gastric = pain worse with meals --> wt. loss
duodenal = pain better with meals --> wt. gain |
|
Duodenal ulcer
cause |
nearly 100% have H. pylori infection
gastric acid secretion (eg. ZE syndrome) or decrease in mucosal protection |
|
duodenal ulcer
what happens to brunner's glands |
hypertrophy
|
|
stomach cancer
a. common type b. course c. common features |
a. adenocarcinoma
b. early, aggressive local spread and node/liver mets c. signet ring cells, acanthosis nigricans |
|
Dietary nitrosamines (smoked fod), achlorhydria, chronic gastritis, type A blood
associated with what condition |
stomach cancer
|
|
what is linitis plastica
|
stomach cancer that is diffusely infiltrative (thickened, rigid appearance, "leather bottle")
|
|
Patient has stomach cancer, metastasizes to left supraclavicular node
what is the node called |
Virchaow's node
|
|
Patient has stomach cancer that progresses to bilateral ovaries
there are abundant mucus and signet ring cells dx? |
Krukenberg's tumor
|
|
Patient has stomach cancer, metastasizes to subcutaneous periumbilical region
dx? |
sister mary joseph nodule
|
|
Patient comes in with abdominal pain that gets worse with meals, weight loss
-patient is older -they take NSAIDS -have a positive urease test dx? cause? |
Gastric ulcer
H. Pylori in 70% Due to decrease in protection against gastric acid |
|
Difference in pain sequelae between a gastric and a duodenal ulcer
|
gastric = pain worse with meals --> wt. loss
duodenal = pain better with meals --> wt. gain |
|
Duodenal ulcer
cause |
nearly 100% have H. pylori infection
gastric acid secretion (eg. ZE syndrome) or decrease in mucosal protection |
|
duodenal ulcer
what happens to brunner's glands |
hypertrophy
|
|
How are the margins of a duodenal ulcer different from those of a carcinoma
|
ulcer = clean, "punched out" margins
carcinoma = raised/irregular margins |
|
4 complications of duodenal ulcer
Is it cancerous? |
bleeding, penetration to pancreas. perforation, obstruction
No |
|
IBD: Crohn's vs. UC
etiology |
C = disordered response to intestinal bacteria
UC = autoimmune |
|
IBD: Crohn's vs. UC
location? Skipping? Rectum? |
C = any portion of GI (often terminal ileum and colon), skip lesions, rectal sparing
UC = colon, continuous, involves rectum |
|
IBD: Crohn's vs. UC
a. barium swallow x-ray image |
C = string sign from bowel wall thickening
UC = lead pipe from loss of haustra |
|
IBD: Crohn's vs. UC
layers of inflammation |
C = transmural
UC = mucosal and submucosal |
|
IBD: Crohn's vs. UC
gross appearance of mucosa and surrounding |
C = cobblestone mucosa with creeping fat + linear ulcers, fissures, fistulas
UC = friable mucosal pseudopolyps with freely hanging mesentary |
|
IBD: Crohn's vs. UC
Micro: nonccaseating granulomas and lymphoid aggregates |
Crohns
|
|
IBD: Crohn's vs. UC
Micro: crypt abscesses and ulcers, bleeding, NO granulomas |
UC
|
|
IBD: Crohn's vs. UC
Complications include strictures, fistulas, perianal disease, malabsorption, nutritional depletion, colorectal cancer |
Crohn's
|
|
IBD: Crohn's vs. UC
complications include malnutrition, toxic megacolon, colorectal carcinoma |
UC
|
|
IBD: Crohn's vs. UC
Bloody diarrhea + -pyoderma gangrenosum -primary sclerosing cholangitis treat? |
UC
ASA prep (sulfasalazine), 6-MP, infliximab, colectomy |
|
IBD: Crohn's vs. UC
Diarrhea (may be bloody) + -migratory polyarthritis -erythema nodosum -ankylosing spondylitis -uveitis -immunologic disorders treat? |
Crohn's
corticosteroids, infilximab |
|
Patient has recurrent, chronic abdominal pain with alternating diarrhea and constipation
also has 2 or more of the following 1. pain improves with defecation 2. change in stool frequency 3. change in stool appearance dx? Treat? |
Irritable Bowel syndrome
treat symptoms - SSRI's, TCA's, loperamide |
|
Most common indication of emergent abdominal surgery in kids
|
appendicitis
|
|
Patient presents with diffuse periumbilical pain --> localizes to area between iliac crest and umbilicus
also has nausea, fever possible cause in kids? 2 causes in adults? |
appendicitis
kids - lymphoid hyperplasia after viral infection adults - obstruction, fecalith |
|
Patient presents with diffuse periumbilical pain --> localizes to area between iliac crest and umbilicus
What must you rule out if patient is elderly? If a woman? |
Appendicitis symptoms
elderly = diverticulitis woman = ectopic pregnancy (use B-hCG) |
|
patient has appendicitis
what is one complication you fear |
perforation --> periotonitis
|
|
Where do diverticula most often affect?
|
sigmoid colon
|
|
What is a diverticulum?
difference between true and real? |
blind pouch in gut
true = all three layers outpouch (Meckel's) false = divertculum or pseudodiverticulum - only mucosa and submucosa outpoutch (occurs especially where vasa recta perforate muscularis externa) |
|
Patient with vague discomfort and/or painless rectal bleeding eats a low fiber diet, is over 60 yo
what is he at risk for? cause? |
diverticulosis = many diverticula, most often in sigmoid colon
high intraluminal pressure --> focal weakness in colonic wall |
|
Patient has
-bright red rectal bleeding -bubbles in pee (pneumaturia) due to colovesical fistula (colon and bladder fistula) -LLQ pain, fever, leukocytosis dx? what is happening? what do you fear? treat? |
diverticulitis = inflammation of diverticula (macrophages)
fear perforation --> peritonitis, abscess formation, or bowel stenosis give antibiotics |
|
Patient presents with halitosis, dysphagia, obstruction
on barium swallow, you see herniation of mucosal tissue at junction of pharynx and esophagus dx? |
Zenker's diverticulum (false)
|
|
Most common congenital anomaly of GI tract
what is the congenital problem |
Meckel's diverticulum
persistence of the vitelline duct or yolk stalk |
|
Patient has
-bleeding -intussusception (part of bowel invaginated on another) -volvulus (obstruction do to abnormal bowel twisting) near terminal ileum pectenate scan finds ectopic acid-secreting gastric mucosa and pancreatic tissue dx? 5 "rule of 2's"? |
Meckel's diverticulum (true)
2 inches long 2 feet from ileocecal valve 2% of population 2 year-olds or younger 2 types of epithelium (gastric/pancreatic) |
|
What is an omphalomesenteric cyst
what can it be confused with |
cystic dilation of vitelline duct
Meckel's diverticulum = persistence of vitelline duct or yolk stalk |
|
Patient is a kid that gets 'telescoping' of 1 bowel segment into a distal segment
dx? cause in kids? cause in adults? treat? |
intussusception - can compromise blood supply
kids - idiopathic, adenovirus adults (rare) - intraluminal mass treat: surgery |
|
Patient gets twisting of portion of bowel around it's mesentary --> obstruction, infarction
who does this affect mostly? where does it affect mostly? |
elderly
cecum and sigmoid colon area (redundant mesentary) |
|
Baby fails to pass meconium
Presents with chronic constipation early in life On intestinal biopsy, you see no meissner's or aurebach's plexuses Baby also has Down Syndrome Dx? pathology/embryological problem |
Hirschsprung's disease (risk increases with Down's)
Failure of neural crest cell migration --> lack of enteric nerve plexus --> constricted aganglionic segment with megacolon proximally |
|
Kid with Down's syndrome has early bidious vomiting and proximal stomach distention
you see closed off small bowel dx? what happened? |
duodenal atresia
failure of recanalization of small bowel |
|
Baby born with CF cannot poop
dx? what happens? |
meconium ileus
meconium plug obstructs intestine --> no POO |
|
What is the condition
necrosis of intestinal mucosa, possible perforation, often involving colon, can involve whole GI more often seen in preemies dx? |
necrotizing enterocolitis
|
|
Elderly person has pain after eating --> weight loss
caused by low intestinal blood flow what is happening? where? |
ischemic colitis
splenic flexure and distal colon |
|
what is an adhesion
|
acute bowel obstruction, often from recent surgery --> well-demarcated necrotic zones
|
|
older patient presents with bleeding in intestine
angiography shows tortuous dilation of vessels in cecum, terminal ileum, and ascending colon dx? |
angiodysplasia
|
|
2 types of colonic polyps
what do they look like and how dangerous are they |
tubular adenomas = small, rounded, less malignant potential
villous adenomas = long, finger-like, more malignant potential |
|
What are colonic polyps
where do they often occur are the cancerous |
masses protruding into gut lumen, giving a sawtooth appearance
often rectosigmoid 90% non-neoplastic |
|
type of polyps that are precancerous
factors affecting malignancy |
adenomatous
increasing size, villous histology, increased epithelial dysplasia --> colorectal cancer |
|
What is the most common non-neoplastic polyp in the colon and where are they found
|
hyperplastic
>50% at rectosigmoid |
|
mostly sporadic polyps in children < 5
where? what if they are single? what if multiple? |
juvenile
rectum if single, no malignant potential If multiple, indicates juvenile polyposis syndrome -> increases risk of adenocarcinoma |
|
Autosomal dominant syndrome featuring nonmalignant hamartomas in GI +
-hyperpigmented mouth, lips, hands, genitalia dx? increases risk of what |
Peutz-Jeghers
increases risk of CRC and visceral malignancies |
|
3rd most common cancer, 3rd most deadly in USA, mostly affects men >50, 25% have a family history
|
colorectal cancer
|
|
Patient has thousands of polyps all over colon, always involves rectum
what is the genetic defect? |
Familial adenomatous polyposis
autosomal dominant - APC gene (5q) Requires two hits --> CRC |
|
Familial adenomatous polyposis + osseous and soft tissue tumors, retinal hyperplasia
|
Gardner's syndrome
|
|
Familial adenomatous polyposis + malignant CNS tumor
|
Turcot's syndrome
TURcot's = TURban |
|
HNPCC
a. genetics b. how many progress to CRC c. what is always involved |
a. autosomal dominant mutation in DNA mismatch repair genes
b. 80% c. proximal colon |
|
IBD
Strep bovis bacteremia tobacco use large villous adenoma Juvenile polyposis syndrome Peutz-Jeghers syndrome risk factors for what |
Colorectal cancer
|
|
Where is the colorectal cancer
obstruction, colicky pain, hematochezia |
distal colon
|
|
Where is the colorectal cancer
dull pain iron deficiency anemia fatigue |
proximal colon
|
|
Patient is an older male with iron deficiency anemia
-stool occult blood test positive -see CEA tumor marker -apple core lesion on barium xray dx? |
colorectal cancer
|
|
2 molecular pathways to colorectal cancer
|
1. microsattelite instability (15%): DNA mismatch repair gene mutations --> sporadic, HNPCC syndrome
-mutations accumulate, but no morphology 2. APC/b-catenin (85%) |
|
What is the order of genetic mutations that lead from a normal colon to carcinoma
|
1. loss of APC --> decreased intercellular adhesion, increased proliferation
2. K-RAS mutation - unregulated intracellular signal transduction --> adenoma 3. p53 --> tumorigenesis --> carcinoma |
|
Carcinoid tumor
tumor of what kind of cells? 3 most common sites? where is it most malignant? |
neuroendocrine cells (secrete 5-HT)
appendix, ileum, rectum small intestine |
|
Carcinoid tumor
what do you see on EM |
dense core bodies
|
|
What determines if a carcinoid tumor causes carcinoid syndrome
|
If tumor is confined to GI, no syndrome (liver metabolizes 5-HT)
if metastasizes (usually to liver) --> syndrome |
|
patient has
-wheezing -right sided heart murmur -diarrhea -flushing -high 5-HT in blood dx? |
carcinoid tumor, metastasized outside GI
|
|
-Esophageal varices (hematemesis)
-peptic ulcer --> melena -splenomegaly -caput medusae, ascites -gastropathy -hemorrhoids what is the condition |
portal HTN
|
|
-coma
-sleral icterus -breath smells like freshly opened corpse -spider nevi -gynecomastia -jaundice -testicular atrophy -asterixis -decreased prothrombin and clotting factors (bleeding up) -anemia -ankle edema effects of what |
liver cell failure
|
|
what is cirrhosis
how does the liver respond |
fibrosis of liver
nodular regeneration |
|
Metabolic insults --> Alcohol, hemochromatosis, Wilson's disease
what type of hepatocellular regeneration |
micronodular (<3mm), uniform size
|
|
injury causing necrosis (post-infectus, drug induced)
what type of hepatocellular regeneration increases risk of what |
macronodular (>3mm), variable size
increases risk of hepatocellular carcinoma |
|
what is bridging fibrosis
|
hepatocellular regeneration
regenerative lesions connected by fibrous bands |
|
How can you relieve portal HTN
|
shunt between portal and systemic circulation
|
|
What is the probable diagnosis in GI
ALT > AST |
viral hepatitis
|
|
What is the probable diagnosis in GI
AST > ALT |
alcoholic hepatitis
|
|
What is the probable diagnosis in GI
AST up |
Myocardial infarction
|
|
What is the probable diagnosis in GI
GGT (gamma glutamyl transpeptidase) |
Liver diseases, heavy alcohol consumption
|
|
What is the probable diagnosis in GI
alkaline phosphatase up (3) |
Obstructive liver disease (hepatocellular carcinoma)
Bone disease Bile duct disease |
|
What is the probable diagnosis in GI
high amylase (2) |
acute pancreatitis, mumps
|
|
What is the probable diagnosis in GI
lipase |
acute pancreatitis
|
|
What is the probable diagnosis in GI
ceruloplasmin down |
wilson's disease
|
|
A child has a VZV or influenza B infection
after treatment, gets mitochondiral abnormalities, fatty liver (microvesicular), hypoglycemia, coma what was he treated with? what is the MOA of disease |
Reye's syndrome -child given aspirin
aspirin metabolites inhibit beta oxidation by reversible inhibition of mitochondrial enzyme |
|
Patient with moderate alcohol intake has abundant fat-filled vacuoles w/o inflammation in liver
hepatomegaly dx? treat? |
hepatic steatosis
reversible --> stop alcohol! |
|
Patient with long term alcohol use has
-AST>ALT (1.5:1) -swollen and necrotic hepatocytes with PMN infiltrate -See intracytoplasmic eosinophilic inclusions that look like twisted ropes dx? |
Alcoholic hepatitis
(see mallory bodies) you're toASTed with alcoholic hepatitis (remember AST > ALT) |
|
Patient with long-term alcohol use has
-jaundice -hypoalbuminemia -histo: see sclerosis around central vein (zone III) -gross: shrunken liver with large nodules dx? |
alcoholic cirrhosis
final and irreversible |
|
Most common primary malignant tumor of liver in adults
|
hepatocellular carcinoma
|
|
hepatitis B and C
Wilson's hemochromatosis a1-antitrypsin deficiency alcoholic cirrhosis aflatoxin (peanuts) increase risk of what |
hepatocellular carcinoma
|
|
patient has
-jaundice -tender hepatomegaly -ascites -polycythemia -hypoglycemia -a-fetoprotein increases dx? may lead to what? how is it spread |
hepatocellular carcinoma
budd-chiari (occlusion of hepatic veins) hematogenous |
|
nutmeg liver
pathologically, what is happening? what can it lead to? 2 causes? |
backup of blood into liver, can lead to centrilobular congestion and necrosis --> cirrhosis
RH failure, budd-chiari |
|
Patient has congestive liver disease
-hepatomegaly -ascites -abdominal pain -can cause liver failure -varices, visible abdominal and back veins -no JVD dx? what is happening? |
Budd - Chiari
occlusion of IVC or hepatic veins --> cetnrilobular congestion and necrosis |
|
Hypercoaguable state
polycythemia vera pregnancy hepatocellular carcinoma associated with what condition that causes congestive liver disease? |
budd-chiari = occlusion of IVC or hepatic veins
|
|
Patient gets panacinar emphysema due to decrease in elastic tissue in lungs
also see PAS-positive globules in liver dx? path? genetics? |
a1-antitrypsin deficiency
misfolded gene product accumulates in hepatocellular ER, lungs lose elastic tissue codominant |
|
What is physiologic neonatal jaundice
How do you treat |
immature UDP-glucoronyl transferase --> unconjugated bilirubinemia --> jaundice, kernicterus
phototherapy (converts UCB to water-soluble form) |
|
2 types of bilirubin
which is water soluble? How is it excreted? |
conjugated and unconjugated
conjugated (direct) is soluble --> excreted in urine, goes to bile to make urobilinogen |
|
What are 2 process by which urobilinogen is made
|
direct bilirubin put into bile, converted by gut bacteria to urobilinogen
heme metabolism |
|
Patient has jaundice...what type
-high conjugated and unconjugated bilirubin -high urine bilirubin -normal to low urobilinogen |
hepatocellular
|
|
Patient has jaundice...what type
-high conjugated bilirubin -high urine bilirubin -low urine urobilinogen |
obstructive (interrupted drainage of bile in biliary system)
|
|
Patient has jaundice...what type
-high unconjugated bilirubin -acholuria (no bilirubin in urine) -high urine urobilinogen |
hemolytic
|
|
Hereditary hyperbilirubinemias
Patient has unconjugated hyperbilirubinemia with no clinical consequences -no hemolysis -increased bilirubin with fasting and stress dx? path? |
Gilbert's
Mildly decreased UDP-glucoronyl transferase or decreased bilirubin uptake |
|
Hereditary hyperbilirubinemias
Early in life, patient presents with -jaundice -kernicterus (bilirubin in brain) -high unconjugated bilirubin dx? path? |
Crigler-Najjar syndrome type I
absent UDP-glucoronyl transferase --> patients DIE within a few years |
|
Crigler-Najjar syndrome
how is type II different than type I |
disease = absence of UDP glucoronyl transferase
type II is less severe responds to phenobarbitol, which increases liver enzyme synthesis |
|
Hereditary hyperbilirubinemias
patient has conjugated bilirubinema grossly black liver dx? course? |
Dubin-Johnson = impaired excretion of conjugated bilirubin
benign |
|
How does Dubin-Johnson compare to Rotor's syndrome
|
Both are caused by defect in excretion of conjugated bilirubin
Rotor's is less severe, does not cause black liver |
|
Patient has
-Asterexis -Basal ganglia degeneration (parkinsonism) -Ceruloplasmin low, Cirrhosis, Corneal deposits (brown ring around iris) -Dementia, Dyskinesia, Dysarthria -hemolytic anemia dx? path? genetics? treat? |
wilson's (symptoms = ABCD)
(Kayser fleisher rings) inadequate hepatic copper excretion (doesn't enter circulation as ceruloplasmin) --> copper accumulation in liver, brain, cornea, kidneys, joints autosomal recessive penicllamine |
|
Patient sets off metal detector at airport. He goes to security, where they see he has
-Cirrhosis -Diabetes -Bronze skin color dx? path |
hemochromatosis (symptoms = Hemachromatosis Can Delay Boarding)
Deposition of hemosiderin (iron) in liver, other tissues 50g to set off metal detectors |
|
On histology with prussian blue stain, you see
-hemosiderin in liver cells dx? increases risk of what 2 conditions? |
Hemochromatosis
CHF, hepatocellular carcinoma |
|
Hemochromatosis
what should the levels be of a. ferritin b. iron c. TIBC d. transferrin saturation |
a. high
b. high c. low d. high |
|
2 causes of hemochromatosis
|
primary (autosomal recessive) (assoc. with HLA A3)
secondary to chronic transfusion |
|
Hemochromatosis
2 treatments |
1. phlebotomy
2. deferoxamine (chelates Fe) |
|
Patient presents with
-pruritis, jaundice, dark urine, light stool, hepatosplenomegaly labs: high conjugated bilirubin, high cholesterol, high alk phos dx? 3 types |
biliary tract disease
secondary biliary cirrhosis (obstruction), primary (autoimmune), primary sclerosing cholangitis |
|
Pathophys of secondary biliary cirrhosis
How can it be complicated |
gallstone, biliary stricture, chronic pancreatitis, pancreatic head cancer --> obstruct biliary duct --> increases pressure in intraheptatic ducts --> injury fibrosis and bile stasis
complicated by ascending cholangitis |
|
patient presents with biliary tract disease + serum mitochondrial antibodies (including IgM)
-patient also has CREST, RA, Celiac (another autoimmune disease) dx? path |
primary biliary cirrhosis
autoimmune --> lymphocytic infiltrate + granulomas |
|
Patient has biliary tract disease symptoms +
-hyper IgM -also has Ulcerative colitis ERCP = you see beading of intra and extrahepatic bile ducts dx? path? |
primary sclerosing cholangitis
unknown cause --> onion skin fibrosis of bile duct --> alternating strictures and dilation --> beading of intra and extrahepatic bile ducts |
|
3 causes of gallstones
|
increased cholesterol/bilirubin, decrease in bile salts, and gallbladder stasis
|
|
2 types of gallstones
how do they look on radiography? |
1. cholesterol stones (mostly radiolucent) = 80% of stones
2. pigment stones (radioopaque) |
|
Obesity
Crohn's CF advanced age clofibrate estrogens multiparity rapid wt. loss Native American origin associated with what |
cholesterol gallstones
|
|
chronic hemolysis
alcoholic cirrhosis advanced age biliary infection associated with what |
pigment stone
|
|
patient has jaundice, fever, RUQ pain
-Murphy's positive dx? 4 risk factors |
cholangitis
Female Fat Fertile Forty |
|
cholecystitis
ascending cholangitis acute pancreatitis bile stasis biliary colic (bile duct contraction) caused by what? |
cholelithiasis
|
|
Gallstones
what happens if a fistula grows between gall bladder and small intestine |
air in biliary tree
|
|
if you see air in biliary tree on imaging, where is the gallstone
|
obstructing ileocecal valve (gallstone ileus)
|
|
How do you diagnose gallstones?
How do you treat? |
ultrasound
cholecystectomy |
|
Cholecystitis
common causes what do you see if bile duct becomes involved |
gallstones, rarely ischemia or infection (CMV)
see increased alk phos |
|
Gallstones
Ethanol Trauma Steroids Mumps Autoimmune disease Scorpion sting Hypercalcemia/Hyperlipidemia ERCP Drugs (sulfas) all of these cause what? |
Acute pancreatitis = autodigestion of pancreas by pancreatic enzymes
GET SMASHED |
|
Patient has epigastric abdominal pain that radiates to back, anorexia, nausea
labs: elevated amylase, lipase dx? |
acute pancreatitis
|
|
DIC
Acute Respiratory Distress Syndrome diffuse fat necrosis hypocalcemia pseudocyst formation hemorrhage infection multiorgan failure possible results of what condition? |
acute pancreatitis
(Ca collects in pancreatic calcium soap deposits --> hypocalcemia) |
|
patient has steatorrhea, fat-soluble vitamin deficiency, diabetes mellitus
dx? |
chronic pancreatitis --> pancreatic insufficiency
|
|
Choronic calcifying pancreatitis
strongly associated with what 2 factors? what does it cause? |
alcoholism, smoking
pancreatic cancer |
|
Patient presents with
1. abdominal pain radiating to back 2. wt loss (malabsorption and anorexia) 3. migratory thrombophlebitis = red, tender palpation of extremities 4. obstructive jaundice with palpable gallbladder Labs: CEA and CA-19-9 Dx? prognosis? Associated factors? |
pancreatic adenocarcinoma (usually in pancreatic head)
very aggressive, 6 months survival associated with cigarettes and chronic pancreatitis (not alcohol) |
|
Cimetidine, ranitidine, famotidine, nizatidine
class? MOA? |
H2 blockers (DINE for 2)
reversible block of H2 receptors on parietal cell --> decreases H secretion |
|
Treatment for peptic ulcer, gastritis, mild esophageal reflux
|
H2 blockers: cimetidine, ranitidine, famotidine, nizatidine
|
|
1. inhibits P450
2. antiandrogenic (PRL release, gynecomastia, imotence, low libido in males) 3. cross BBB (confusion, dizzy headache) 4. cross placenta 5. decreases renal excretion of creatine side effects of what GI drug |
Cimetidine (H2 blocker)
|
|
Negative effect common to cimetidine and ranitidine
|
decreases renal excretion of creatinine
|
|
Omeprazole, lansoprazole
class? MOA |
PPI
irreversible inhibit H/K ATPase in stomach parietal cells |
|
Treatment for Peptic ulcer, gastritis, esophageal reflux, ZE syndrome
|
PPI - omeprazole, lansoprazole
|
|
Drug used to increase ulcer healing, traveler's diarrhea
MOA |
Bismuth, scuralfate
Binds to ulcer base --> physical protection, allows HCO3 secretion to reestablish pH gradient in mucous layer |
|
5 drugs to treat peptic ulcer from h.pylori
|
PPI
Metronidazole Amoxicillin Tetracycline Bismuth Please MAke my Tummy Better |
|
Drug used to prevent NSAID-induced peptic ulcers, maintain patent ductus arteriosus, used to induce labor
MOA Tox |
Misoprostol
PGE1 analog --> increases production and secretion of gastric mucous barrier, decreases acid production Diarrhea, abortifacent (don't give to women of childbearing age) |
|
Pirezepine, Propantheline
MOA Tox |
Antimuscarinics = block M1 receptors on ECL cells (low histamine secretion) and M3 receptors on parietal cells (low H secretion)
Tachycardia, dry mouth, difficulty focusing eyes |
|
Drug for acute variceal bleeds, acromegaly, VIPoma, carcinoid tumors
MOA tox |
Octreotide
Somatostatin analog nausea, cramps, steatorrhea |
|
antacids
how can they affect absorption, bioavailability or urinary excretion of other drugs |
alters gastric and urinary pH, delay gastric emptying
|
|
Antacid use - what's the drug?
overuse --> -constipation -hypophosphatemia -proximal muscle weakness -osteodystrophy -seizures |
aluminium hydroxide
aluMINIMUM amount of feces |
|
Antacid use - what's the drug?
overuse --> diarrhea, hyporeflexia, hypotension, cardiac arrest |
Magnesium hydroxide
Mg = Must Go to the bathroom |
|
Antacid use - what's the drug?
overuse --> hypercalcemia, rebound acid increase |
Calcium carbonate
|
|
Common side effect to all antacids
|
hypokalemia
|
|
Drug to treat Crohn's disease, RA
MOA tox |
Infilximab
monoclonal Ab to TNF (proinflammatory cytokine) Respiratory infection (reactivation of TB), fever, hypotension |
|
Drug used for UC, Crohn's
MOA Tox |
Sulfasalazine
combination of sulfapyridine (antibact) and 5-aminosalicylic acid (anti-inflamm) --> activated by colonic bact malaise, nausea, sulfonamide tox, reversible oligospermia |
|
Drug to control vomiting post-op and in patients undergoing cancer chemo
MOA Tox |
5-HT3 antagonist --> central acting emetic
Headache, constipation |
|
Drug to treat diabetic and post-surgery gastroparesis
MOA tox |
metoclopramide
D2 receptor, 5-HT3 antagonist --> increases resting tone, contractility, LES tone, motility (Not colon transport time) -Parkinson effects -Restlessness, drowsiness, fatigue, depression, nausea, diarrhea -Drug int. with digoxin, diabetic agents -don't use if small bowel obstruction |