GI Flashcards
T-cell lymphoma (unique)
Celiac Disease
Dermatitis herpeteformis is from _____ _____ in dermal papillae
IgA deposits (celiacs)
Intusseception: child or adult? Infectious cause?
Child with Rotavirus
Double bubble sign
Duodenal atresia –> polyhydramnios, bilious vomiting
Where does volvulus occur (twisting of bowel along mesentary)?
Sigmoid colon/cecum
Celiac vs tropical sprue location
Celiac: Duodenum
Tropical sprue: infectious diarrhea that responds to antibiotics and prominent in Jejunum and Ileum (thus folate/b12 def can ensue)
where are foamy macrophages (organism in mq lysosome) typically found?
Intestinal Lamina Propria –>compresses lacteals = fat malabsorption/steatorrhea (chylomicrons need to go into lacteals)
Absent VLDL and LDL
Abetalipoproteinemia (AR def of b-48 and b-100)
b-100 needed for vldl and ldl
defective chylomicron formation (req b-48)
Abetalipoproteinemia (AR def of b-48 and b-100)
asthmatic wheezing (bronchospasm), diarrhea, flushing,
Carcinoid (neuroendocrine)
Rebound tenderness and guarding
Appendicitis
Crohn’s and UC: IBD or IBS?
IBD: Inflammatory bowel DISEASE
Hirschprung = defective relaxation and peristalsis of _____ and _______
rectum and sigmoid colon
Down syndrome GI links
Duodenal Atresia
Hirschsprungs (failure to pass meconium if severe)
Failure of ganglion (neural crest) cells to descend into: (hirschsprung)
Myenteric (Auerbach) plexus: Muscularis propria. MOTILITY
Submucosal (Meissner) plexus: Secretions/absorption
can sample EITHER of these in the narrowed area.
Rectal suction biopsy in Hirschsprungs
Shows lack of ganglion cells (neural crest-derived)
–>dont descend into submucoa and muscularis
UC: Mucosa, Submucosa, Muscularis, Serosa?
Mucosal and Submucosal ulcerations
Failure of ganglion cells (neural crest) in GI
Achalasia: damaged ganglion cells in myenteric plexus (muscularis propria)….usually from Chagas or idiopathic
Hirschsprung: failure of ganglion cells to descend into myenteric and submucosal plexus
IBD: RLQ vs LLQ pain
Crohns = RLQ pain + nonbloody diarrhea. Creeping fat UC = LLQ + bloody diarrhea
Alternating diarrhea and constipation
Irritable Bowel Syndrome
Histo/inflammation of Crohn and IBD
Crohn: Noncaseating Granuloma + Lymphoid aggregates (Th1 mediated)
UC: Crypt abscesses/ulcers with neutrophils(Th2 mediated) and bleeding
String sign vs lead pipe (loss of haustra)
String sign: crohns (strictures)
smoking protects against
UC
Diverticula : location and description
Sigmoid Colon
False: Mucosa/Submucosa outpouch (where vasa recta perforate muscularis externa)
colosvesicular fistula (pneumaturia)
Divertuculitis (give antibiotics) –> L sided appendicitis
Watershed areas that are susceptible for ischemic colitis after an episode of hypotension or occlusion
Splenic flexure (SMA and IMA watershed) Rectosigmoid (sigmoid artery and superior rectal a)
pt had abdominal pain and bloody diarrhea after surgery, will show petechial hemorrhages and pale muscosa
atherosclerosis of SMA
Ischemic colitis: Postprandial pain and weight loss;
pain and bloody diarrhea = infarction
raised protrusions of colonic mucosa
Colonic POLYPS
Hyperplastic vs Adenomatous polyp
Hyperplastic: Hyperplasia of glands. More common. usually rectosigmoid (left colon). benign and NO MALIGNANT POTENTIAL
Adenomatous: Neoplastic prolif of glands. Benign but premalignant.
Sessile growth with villous histology = greatest risk adenoma –>carcinoma progression
Role of APC, KRAS, p53 (AK-53)
APC: Increase risk of polyp formation
KRAS: leads to FORMATION of polyp
p53: this and increased COX expression = PROGRESSION to carcinoma
(aspirin impedes adenoma –>carcinoma progression)
Inherited APC mutation
Colon and rectum are removed prophylactically
Peutz Jeghers
Hamartomatous polyp (benign) + Mucocutaneous hyperpigmentation. Auto dominant.
Increased risk colorectal, breast, gynecologic cancer.
Cancer risks in HNPCC
Colorectal, ovarian, endometrial carcinoma
Goal of colonscopy
Remove adenomatous polyp (before carcinoma develops) and to detect any cancer early
An older adult with iron deficiency anemia
Colorectal cancer (occult bleed) until proven otherwise
Drooling/choking/vomiting with first feed
Esophageal atresia + distal Tracheoesophageal fistula (can see air in stomach on CXR)
acid/base disturbance from Pyloric Stenosis
Nonbiliious projectile vomiting –> Hypokalemic Hypochloremic Metabolic Alkalosis
(potassium, chloride, and acid levels are low –>from vomiting of gastric acid)
Midgut (GI)
i.e. not foregut or hindgut
duodenum to proximal 2/3 of transverse colon
Gastroschisis vs Omphalocele
both = failure of Lateral fold closure
G: Abdominal contents protrude through abdomen (no cover) –>congential malformation aka incomplete closure of the anterior abdominal wall
Omphalocele is sealed: Hernitation of bowel/abdominal contents into umbilical cord (don’t retract) –> sealed/covered by peritoneum
Small intestine atresia (D, J, I)
Duodenal: Downs –> Failure to recanalize
Jejunal/ileal, colonic: Vascular occlusion (apple peel atresia)
Week 6 and week 10 in midgut development
6: Midgut herniates through umbilical ring
10: returns to abdominal cavity and rotates around SMA
–>pathology of this = malrotation of midgut, omphalocele, atresia, voluvulus
failure to pass nasogastric tube into stomach
Tracheoesophageal anomalies
Pancreas is derived from the ______ gut
foregut
Ventral vs dorsal pancreatic buds
Ventral: Main Pancreatic duct, uncinate
Dorsal: Body, tail, isthmus, accessory duct
Head of the pancreas: both ventral and dorsal
______pancreatic bud abnormally encircles ______=ring of pancreatic tissue = duodenal narrowing –> _______ _______
Ventral bud, encircles Duodenum (2nd part)
–> Annular Pancreas
Ventral and dorsal pancreatic buds fail to ____ at 8 weeks–> _____ ______
failure of FUSION (not sep)
–>Pancreatic divisum (because they are DIVIDED)
Spleen is derived from ________ but supplied by ______ (______ artery)
Mesoderm (mesentary of stomach)
supplied by Foregut (Celiac Artery)
Retroperitoneal Structures
Suprarenal glands (Adrenals, NOT SPLEEN SON) AORTA/IVC Duodenum Pancreas Ureter COLON Kidney Esophagus Rectum
Pringle manuever: _______ ligament compressed btwn thumb and finger
Hepatuduodenal ligament, which contains
Portal Triad= Hepatic Artery, Portal Vein, Common Bile Duct.
im HAP-V after PT instructor Pringle manuevers my HugeDick
(if bleeding doesnt stop, probs IVC or hepatic vein)
Erosion Vs Ulcer
Ulcers extend UNDERNEATH an Erosion
Erosion: Mucosa only (doesnt go all the way through)
Ulcer: can extend into submucosal/muscularis
where is Basal Electric Rhythm fastest
Duodenum>ileum>stomach
Lymphoid aggregates in the Lamina Propria/Submucosa
Peyers Patches –> Ileum
Largest number of goblet cells in the small intestine
Ileum
If you remove gallbladder (i.e. gallstones), can you still get lipid absorption?
Jejunum = primary site of lipid digestion, and get passive absorption across brush border so you’re still ok without GB
GI Blood supply
Foregut - Celiac - Vagus.
Midgut - SMA - Vagus
Hindgut - IMA - PELVIC
Lower esophagus to proximal duodenum + liver, gallbladder, pancreas, spleen
Foregut supplied (celiac)
remember, spleen is mesoderm supplied by foregut
splenic flexure = watershed btwn:
SMA and IMA
Relieving portal hypertension
Shunt between portal vein and hepatic vein (Transjugular intrahepatic portosystemic shunts aka TIPS)
Hemorrhoids: Superior vs inferior rectal vein
Internal hem: Above pectinate line = Superior rectal vein –>inferior mesenteric –> Portal
External Hem: Below pectinate = Inferior Rectal vein –>Internal pudendal –> Internal iliac –> IVC
Anal fissure is also below pectinate line
Somatic innervation of external hemorrhoids
Pudendal nerve (inferior rectal branch) = painful
Lymph drainage and arterial supply of Hemmorhoids
Internal: Internal iliac LN. Superior rectal a (IMA)
External: Superficial inguinal LN. Internal pudendal a (inferior rectal branch)
Painless jaundice
Tumor in head of pancreas = obstruction of common bile duct alone
3 non-phsyiologic reasons for increased Gastrin
UP ** in Zollinger-Ellison
Up * in Chronic Atrophic Gastritis (H Pylori)
Up* In chronic PPI use (Shocker jignesh bhai!!!)
Regulation of Somatostatin
Increased by Acid
Decreased by Vagal stim (PNS)
Ocreotide: analog of Somatostatin or Secretin?
sOmatOstatin.
Inhibits GH, Sinulin, etc so use for Aromgealy, Insulinoma, Carcinoid
CCK
Secreted by Duodenum and Jejunum!
Increases Pancreatic secretion, gallbladder contraction, and sphincter of Oddi relaxation
decreases gastric emptying
Increased by fatty acids and amino acids
Acts on neural muscarinic pathways to stimulate pancreatic secretion
CCK jignesh bhai!
Secretin: Increase bicarb or bile?
Both.
What effect does Erythromycin have on the GI system?
Its a MOTILIN receptor AGONIST –> used to stimulate peristalsis.
Macrolide toxicity = Motility issues Arrythmia (from prolonged QT) Cholestatic hepatitis Rash eOsinophilia
Watery Diarrhea, Hypokalemia, Achlorhydria (no potassium and no acid)
VIPoma (VIP comes from PNS ganglia)
Chief cells secrete:
Pepsin(ogen)
Fructose is a _____sachharide and taken up by _____ into enterocytes by facilitated diffusion
only MONOsaccharides taken up by enterocytes; taken up by GLUT5.
all monosachh go into blood via GLUT2
Glucose and Galactose (monosacch) taken up into enterocytes via ________, alongside with _____ (cotransport)
SGLT1, along with Na+
all monosacch go into blood via GLUT2
Malabsorption due to pancreas or some shit that is not GI mucosal damage, normal :
D-xylose (monosaccharide) absorption test
Rate limiting step of bile synthesis catalyzed by _________. This is blocked by ________
7alpha-hydroxylase. Blocked by fibrates
Bodys only way to eliminate cholesterol
Bile
Random fact: bile has antimicrobial acivity
______ (protein) picks up Unconjugated bilirubin from the _______ where it has been released from heme and takes it to the liver to be conjugated using ____
Albumin; Macrophage; UDP-glucuronosyl-transferase
________ converts conjugated bilirubin into ________, which gives urine and feces its color
Gut bacteria; Urobilinogen
Urobilin in urine, Stercobilin in stool
Benign cystic tumor with germinal centers
Warthin tumor
In Achalasia, you lose _________ plexus and have increased risk of ________
ok so loss of motility, would it be secretions aka submucosal (meissners)? NO
its My-enteric (Auerbach), increased risk Squamous cell
Progressive dysphagia to solids and then liquids
vs
Dysphagia to solids only
Progressive to both : Achalasia, Esophageal cancer (squamous or adeno)
Solids only: Obstruction
Whats the difference btwn Boerhaave syndrome and Mallory weiss?
Both are esophageal pathologies due to violent retching, both distal
Boerhaave: TRANSMURAL, see Pneumomediastinum
MW: MUCOSAL at GE j(x), leads to hematemisis, usually alcoholics and bulimics
Plummer Vinson (Dysphagia, Iron def anemia, esophageal webs). Associated with ______ and increased risk of _______
glossitis; squamous cell carcinoma
Esophageal smooth muscle atrophy (acid reflux/dysphagia)
Sclerodermal esophageal dysmotility. Part of CREST(autoimmune, anti-centromere AB)
Calcinosis Raynaud Esophageal dysmotility Scleroderma Telangiectasia
whats the cellular metaplastic change in Barrets?
Nonkeratinized stratified squamous –>intestinal epithelium (Noncliliated Columnar with goblet cells)
Hot liquids, alcohol, obesity/fat in terms of esophageal cancer risk
Hot liquids and alcohol: Squamous
Obesity/fat: Adeno (WTF JIGNESH)
H pylori chronic gastritis (Type B for bacterial) = increased risk of _____ _____
MALT LYmphoma
Stomach cancer (early satiety/wt loss):
Intestinal vs Diffuse type
Intestinal: H pylori, nistrosamines, acholhydria, smoking, chronic gastritis. LESS CURVATURE
Diffuse: Signet ring cells, stomach wall grossly thickened and leathery (linitis plastica) (no H Pylori)
ULCERS
Hemorrage: A/P? Location?
Perforation: A/P? Locatin?
Hemorrhage: Posterior.
Gastric ulcer on lesser curvature = bleed from Left Gastric artery
Posterior wall duodenum: Gastruduodenal artery
Perforation: Anterior (duodenal)…can see free air under diaphragm and should pain from phrenic
fistulas, linear ulcers, gallstones, colorectal carcinoma are complications of
Crohns
note: colorectal carcinoma is complication of both.
Gallstones because reck terminal ileum so dont reabsorb bile acids = supersaturation of bile with cholesterol
Corticosteroids, zathioprine, antibiotics (metro, cipro), infliximab, adalimub
Tx profile for Crohns
5-ASA (Mesalamine), 6-mercaptopurine, infliximab
Tx profile for UC
Blind pouch protruding from alimentary tract that communicates with lumen of gut
Diverticulum (most often sigmoid colon)
Most are false: only mucosa and submucosa (where vasa recta perforate muscularis)
Diverticulosis
Many false diverticula, usually sigmoid colon. Ass. with low fiber diet. common cause of hematochezia
Colovesical fistula –>pneumaturia
so my first thought is fistula –>Crohns.
Its Diverticulitis classically. Give antibioitics. L sided appendicitis
herniation of mucosal tissue btwn cricopharyngeal (CRIKEY BAHENCHOD) and thyropharyngeal tissue
Zenker diverticulum (false) -->foul breath (halitosis), dysphagia, obstruction
may contain ectopic acid-secreting gastric mucosa or pancreatic tissue
Meckel diverticulum –> most common CONGENITAL anomaly of the GI tract
RLQ pain, prone to intussesception, volvulus, or terminal ileum obstruction
Meckel (Rule of 2s)
Dx ______ using Pertechnetate study for upate by ectopic ______ ______ (GI tract)
Meckels
Gastric Mucosa
(note: pertechnetate can be taken up by Na-I thyroid transporter –> so can be taken up by thyroid tissue)
failure to obliterate the omphalomesenteric (aka VITTELINE) duct
Meckels (can have ectopic gastric and/or pancreatic)
Volvulus: Midgut vs sigmoid
Midgut: kids
Sigmoid: Elderly (adults drive volvo’s while listening to Sigmoid and Garfunkel)
RET mutation in GI tract
Hirschprung –> CONGENITAL MEGACOLON due to lack of ganglion cells in COLON–> failure of neural crest cell migration
fibrous band btwn ______ and _______ = meckel
fibrous bands from cecum/colon to retroperitoneum causing duodenal compression = _______
ileum and umbilicus
Ladd (fibrous) bands –> sign of Malrotation (of midgut during fetal development). Leads to volvulus and duodenal obstruction.
Twisting of bowel around its _______ = Volvulus
Mesentary
Failure to pass meconium
- Hirschsprung (Downs):
Positive squirt sign/increased rectal tone. Rectosigmoid obstruction. Normal consistency meconium. Death by enterocolitis - Meconium Ileus (CF):
Normal rectal tone, ileum obstruction, green/dehydrated/insippiated meconium–> mortality because strongly ass. with Cystic Fibrosis so Pneumonia, Cor Pulmonale, Bronchiectasis
Vitelline duct: connects ______ to _______
- Failure to close =
- Partial closure/failure to obliterate fully
yolk sac to midgut lumen (so GI and Repro ties).
1. Vitelline fistula: Meconium from umbilicus
- Meckels (true diverticulum, attached to ileum.
can have ectopic gastric/pancreatic tissue. melena, hematochezia, abdominal pain)
Curvilinear areas of lucency that parallel the bowel
–>seen in PREMATURE, FORMULA-FED infats
Meaning AIR NIGGA.
Necrotizing Enterocolitis.
air gets into abdomen because necrosis of colonic mucosa = perforation
Chronic Autoimmune gastritis: B or T cell mediated?
CAREFUL.
Damage: CD4+ T cells (Type 4 Hypersensitivity)
Diagnosis: Antibodies against parietal cells/Intrinsic factor
–>Associated with other Autoimmune conditions i.e. Type 1 Diabetes, also when they say Hypothyroidism you can assume Hashimoto/Graves for hyperthryoid til proven otherwise = AUTOIMMUNE)
Chronic Gastritis (both autoimmune and H pylori) increase the risk for which type of gastric adenocarcinoma (Intestinal or diffuse)?
Intestinal!
–>you get chronic inflammation = Intestinal Metaplasia
Peptic Ulcer Disease = epigastric pain that _____ with mal
90% is duodenal ulcer due to H Pylori(rarely Z-E)
–> IMPROVES with meals
10% is gastric ulcers (H pylori, NSAIDS, bile reflux)
–>WORSENS with meals
Peptic Ulcer disease anatomy/bleeding
90% Duodenal ulcers
- ->Mainly anterior duodenum
- ->If Posterior duodenum, bleeding from gastroduodenal or acute pancreatitis
10% Gastric ulcer
–>Lesser curvature stomach: Left Gastric rupture bleeds
Chronic Pancreatitis in Adult and Child
Adult : Alcohol or Acute pancreatitis (or idiopathic)
Child: Cystic Fibrosis
FAP vs Lynch
FAP: Mutated Tumor APC–>Thousands of polpys, 100% progress to CRC, always involves RECTUM
Lynch (HNPCC): Mutation DNA mismatch repair genes (+ microsatellite instability), No polyp, 80% CRC, PROXIMAL COLON always involved. Ass. with endometrial and ovarian cancer
CRC location
Rectosigmoid>ascending>descending
Ascending: Iron def anemia/wt loss
Desceding: Colicky pain, hematochezia (bright blood), partial obstruction
Iron deficiency anemia in males or postmenopausal women
Think CRC
CRC pathogenesis
- Lynch: Mutation of dna repair; R sided, younger than 50
2. Sporadic: A-K-53, Adenoma to Carcinoma so begins with adenomatous polyp, L sided, older than 50
Reduced beta oxidation by reversible inhibition of mitochondrial enzymes + fatty liver (microvesicular fatty change)
Reye syndrome
Asian child less than 4, vasculitis, red eyes, adenopathy, strawberry tongue, fever, hand/foot changes (erythema/edema)
Kawasaki –> aspirin ok
Hepatic Steatosis vs Alcoholic cirrhosis
Steatosis = reversible with alcohol cessation Cirrhosis = irreversible; sclerosis around central vein (zone 3)
Intracytoplasmic eosinophilic inclusions of damaged keratin filaments
Mallory bodies –>alcoholic hepatitis (necrotic hepatocytes with neutrophil infiltration)
Tx for Hepatic encephalopathy
hyperammonemia i.e GI bleed..get depleted alpha-ketoglutarate…decreased NH3 metab = neuropsych dysfunction
- Lactulose (increase NH4+ aka ammonium)
- Rifamixin (antibiotic that decreases NH3 production by flora)
Jaundice, Tender hepatomegaly, ascites, polycythemia, anorexia
HCC (increased AFP)
Liver tumor related to oral contraceptoive or anabolic steroid use
Hepatic adenoma (risk of rupture)
Most common liver cancer
Metastatic liver cancer 20x»_space;> HCC because double blood supply, large size, kuppfer cells
Absence of JVD, nutmeg liver, congestive liver disease (hepatomegaly, varices, pain)
Budd Chiari: thrombosis/compression of hepatic veins with centrilobular congestion
–>Ass w/hypercoagulable states, plycythemia vera, postpartum, HCC
Genetics of alpha1 antitrypsin deficiency
Codominant trait (just like blood types)
Why do newborns have jaundice (physiologic)?
Immature UDP-glucoronosyltransferase –>unconjugated hyperbilirubinemia –>jaundice and kernicterus (bilirubin in basal ganglia)
causes of Kernicterus (bilirubin in basal ganglia)
Sulfonamide toxicity (avoid in pregnancy)
Physiologic (immature UDP-G-T)
Criggler-Najjar
Tx for physiologic jaundice
Phototherapy: Converts UCB biliribun to water soluble (conjugated)
Cirrhosis and PAS+ globules in liver
Alpha 1 antitrypsin def
–>misfolded protein aggregates in Endoplasmic Retic
Wilsons sx: 5 CCCCCopper is Hella B.A.DDD
Ceruloplasmin low Cirrhosis Corneal deposits (K-F ring) Carcinoma (HCC) Copper accumulation Hemolytic Anemia Basal Ganglia (Putamen) degen = Parkinsonian sx Asterixis Dementia Dysarthria Dyskinesia
Impaired ability to speak, tremor, increased serum transaminases, cousin with progresive neuro disease at young age. Whats the dx test and treatment?
Wilsons disease via Slit Lamp Exam
Penicillamine Chelation
Trientine
Oral Zinc
Testicular Atrophy, Cirrhosis (micronodular), Diabetes, Skin Pigmentation, HCC risk
Hemochromatosis
Fe labs in Hemochromatosis
Increase Iron, Increase Ferritin so Decrease TIBC
The mutation causes hepatocyte to decrease uptake of Fe-Transferrin so senses low Fe so enhances uptake:
Decreased Hepcidin = increase Ferroportin = Increased Fe secretion into Circ= INCREASED TRANSFERRIN SAT
Iron loss through menstruation slows progression in women
Tx of hemochromatosis
Phlebotomy
Chelation with Deferasirox, Fereoxamine, Deferipone
you can DEF use Phlebotomy for Hemochromatosis
Pruritis, jaundice, Dark Urine, Pale Stool, hepatosplenomegaly
Biliary Tract Diseases (PBC, PSC, secondary biliary cirrhosis)
Autoimmune destruction of Intralobular bile ducts in a Middle Aged Woman
Primary biliary cirrhosis
–>Anti-mitochondrial antibody
–>Anti-MAWtochondrial antibody
PBC is a channel for: MAW=Middle Aged Women
Lymphocytic infiltrate and granulomas in intralobular bile duct + dark urine and pale stool (Middle Aged Woman)
Primary biliary cirrhosis
Who watches PBC and what commercials are associated?
Middle aged women and Grand-ulo-ma Commericals for -CREST -Celiac Ceilings -Rheumatoid Arthritis -Sjogren Syndrome
Extrahepatic biliary obstruction that causes increased Pressure intrahepatic ducts = injury/fibrosis and bile stasis
Secondary Biliary Cirrhosis
Patients with gallstones, pancreatic carcinoma, or any known obstructive lesion are at risk for which Biliary Tract Disease?
Secondary Biliary Cirrhosis
–>can be complicated by ascending cholangitis
Concentric onion skin bile duct fibrosis
Primary Sclerosing Cholangitis
Young men with Crohns or UC (IBD) at risk for which biliary tract disease?
Primary Sclerosing Cholangitis
Hypergammaglobulinemia
p-ANCA
ass. with Ulcerative Colitis
Alt. strictures and dilation = beading of intra and extra hepatic bile ducts
Primary Sclerosing Cholangitis
Patients with Biliary Tract Disease, i.e. Primary Biliary Cirrhosis, can have prolonged biliary obstruction leading to deficiency of:
Fat soluble vitamins (bile important for this)
Why pale stool, dark urine, and pruritis in biliary tract disease (obstructive jaundice)?
“Whatever is in the bile is going to leak into the blood”
Pale stool: can’t put bile into the bowel
Pruritis: Bile acids leak into blood and deposit in skin
Dark Urine: CB is up, and remember its water soluble
CB and UCB in Viral Hepatitis?
Both are UP because Viral Hep = inflammation that disrupts hepatocytes and small bile ductules
CB: damaging small BILE ductules
UCB: damaging hepatocytes
NOTE*: Dark urine because leakage of CB which is water soluble. However, Urine urobilinogen is normal/decreased (derivative of CB into the duodenum)
Labs in Biliary tract diseases
Cholestatic pattern of LFTS =
Increased CB, Increased cholesterol, Increased ALP
Stones seen in pt with Obesity, Crohns, Clofibrate, estrogen, rapid weight loss, Native American
Cholesterol stone (radiolucent) aka cholelithiasis
Fever, RUQ pain, Jaundice
Cholangitis classic triad
Stones in in pt with Chronic hemolysis, alcoholic cirrhosis, biliary infections, TPN
Pigment stones
- ->Black = radioopaque, hemolysis
- ->Brown = radiolucent, infection
“You can lose a brown person in the crowd but you always see a black nigga”
Gallstone –> Fistula btwn gallbladder and small intestine –> air (biliary tree) and stone goes into intestinal tract –> stone obstructs ileocecal valve
Gallstone ileus
Inpiratory arrest on RUQ palpation due to pain
Murphy sign: Cholecystitis
if bile duct also gets involved, i.e. ascending cholangitis, will get an increased ALP
How can Fibrate medication lead to gallstone formation?
Blocks Cholesterol —7alphahydroxylase —>Bile Acids
= decreases cholesterol solubility = precipitation/stone
Tx for porcelain gallbladder (calcified edges due to chronic cholecystitis)
Take it out! Cholecystectomy as prophylaxis due to high conversion rates to gallbladder carcinoma
Pancreatic adenocarcinoma: good or bad?
death within a year!!!! very aggressve.
Common at pancreatic head = obstructive jaundice
CA 19-9 (also can have CEA)
Risk factors for Pancreatic Adenocarcinoma
Tobacco, chornic pancreatitis, diabetes, age over 50, jewish/african american males
Abdominal pain radiating to back Wt loss (malabsorption) Migratory thrombophlebitis (Trousseau) Obstructive jaundice with palpable, nontender gallbladder (Courvoisier sign)
Pancreatic Adenocarcinoma
2 names to associate with Pancreatic Adenocarcinoma
Trousseau syndrome (migratory thrombophlebitis) and Courvousier sign (palpable, nontender gall bladder with obstructive jaundice –> pruritis, pale stool, dark urine)
Redness and tenderness of the extremities
Migratory thrombophlebitis –> Troussea syndrome = indication of Visceral Cancer
(considered a paraneoplastic syndrome of hypercoagubility in pts with cancer)