GI Flashcards
Most common cause of Pseudomembranous colitis
C.difficile
Terminal ileum lumpy why?
Correlation?
Peyers patches:- lymphoid follicles/nodules
Crohns ileitis with structure: thicked wall and peyers patches
Define diverticula versus pseudo diverticula
Diverticula:- Mucosa penetrates the muscle layer
Pseudo:- Defective wall
Stomach parts describe with cell tyoes
- Cardia: have the esophagic sphincter
- Fundus and body:- no histologic difference, make acid
- short gastric pits, gland is 2/3 mucosal, parietal and chief cells - Antrum:- No pink mucin (1/2 glands of mucosal)
- Pyloris: more flat, theres are pyloric junction before the duodenum
H and E in stomach and in ulcers
Blue for nuclei which takes H and E for cytoplasm/mucin in cytoplasm
- tortuousity: hyperplasia
- erosion of stomach
- fibrin (pink) and neutrophils:- PUS (due to sloughing)
H.Pylori Sequela
-Incites duodenal and gastric ulcer,
-intestinal metaplasia/dysplasia/then neoplasia
Sequela:
-Gastric Ulcer, Metaplasia, Carcinoma,, Lymphoma
- Gastric ulcer (indent with smooth edges not heaped up, benign)
-Intestinal Metaplasia
- Carcinoma (e.g. signet cell adenocarcinoma or Linitis Plastica- See mucin in center and nuclei pushed into periphery,)
-lymphoma (if switch from polyclonal to monoclonal..proliferative small round blue cells or B cell lymphocytes that efface architecture)..also MALTOMA
-KISSING ULCERS (not pathognomic)
Intestinal metaplasia describe
Goblet cells are INTENSTINAL NOT GASTRIC ORGAN
Paneth cells native to intestines
When you find this in the stomach it is a sign of METAPLASIA
Signet ring cell seen in
Linitis Plastica..THICK FOLDS., leather bottle stomach
Substance P is a capsaicin senstive neuron T or F
Describe sequence
IN RESPONSE TO INJURY
Sub P secreting neuron and CGRP activate NO (hence vasodilation)which activates COX-1 hence PGI2 which inhibits neutrophil activation
Which gender is less prone to duodenal ulcer
Females of child bearing age
CGRP in mucosa greater in females, FGI2 metabolite greater as well. Sex differences in mucosal defense may be partly due to estrogen (CGRP mice with ovaries removed, can be replaced with estrogen, reverses ulcer)
Mucoid cap..Describe how its formed
Bicarb, mucus, exuded plasma and cell debris: gelatinous cap in response to injury.
-Cells from outer epithelium send lamellopodia projections to seal off..allow regeneration of epithelial layer
Acute gastropathy
Chronic Gastropathy
Acute: Little inflammation, some erosion. due to stress gastritis, NSAID gastropathy, alcoholic gastritis (Tend to be hemorrhagic)
Chronic: autoimmune as with Pernicious anemia and inflammation as with H.pylori
Stress gastritis
- Vasoconstriction
- Hypo perfusion
- Cytokines
HPylori Colonization
- Superficial Diffuse Antral Gastritis (CHronic gastritis with neutrophils). Can lead to Increased gastrin and HCl, then Duodenal ulcer (BUT H.P is not in duodenum)
- Multifocal Pangastritis
- Chronic atrophic gastritis with intestinal metaplasia (Similar to pernicious anemia)
- Then lead to gastric carcinoma
- Can lead to gastric ulcer - MALT
- MALToma
Where in which H-Pylori chooses 1, 2 or 3 is very geographically based. Likely strain related
Gastric versus Duodenal Ulcers Trends
-gastric
appetite reduced, older, weight loss, low acid…
-duodenal
appetite ok, younger, normal, increased acid
NB Gastric ulcers tend to be related to atrophic gastritis
Indications for endoscopy..other tests
age>= 55 years…
if less do serology which is very sensitive! C-diff antigen test or breath test
Gastric vs duodenal..clinical assessment
- Assess aspirin status
- if YES, stop, do serology if yes treat and protect..if no, just protect
- if NO, check for H.Pylori, if not do fasting gastrin
IF WITH ENDOSCOPE, ulcer seen? -acid suppresed, mucosal protection NO BIOPSY duodenal ulcer -Send blood for serology, if pos, eradicate, if negative fastin serum gastrin -Re endoscope 8-12 wks
Pharmacology of Ulcers..Side effects etc
-Acid suppresion
1) Buffer (not bicarb but use antaacid..mg
2) Histamine receptor blocker on parietal cell (cimetidine, ranitidine, famotidine/nizavadine). Competes with creatinine for tubulous secretion. hence Cr goes up slightly..Side effect of C is diarrhea, etc gynectomastia, oligospermia..slightly..second generation dont have these side effects
3) Acetylcholine receptors
BTW:- Enterochromaffin cells paracrine secretion of histamine
4) Somatostatin analog subcutaneously. TURNS EVERYTHING OFF, as well as PROSTAGLANDINS..BUT IV! and side effects are like ulcer
5) Mucosal protection:-(sulcrafate)
Forms of Budesonide (an oral glucocorticoid for IBD)
Ileal disease is Crohns (pH 5.2)
Colonic release is ulcerative colitis ( at the ileocecal junction)
Immunosuppresive agents for induction and maintenance of remission in IBD
- are weight based
- Azathioprine/6-MP
- Crohns and UC
- dose dependent liver injury and leukopenia, dose independent infx and pancreatitis
- MTX
- only Crohns
- Teratogenic, hepatic fibrosis, interstitial pneumonitis, transaminitis
Biologics(anti TNF alpha:- fc/IgG1). Name them and side effects
- Chimeric monoclonal antibody: infliximab/remicade (crohns)
- Human monoclonal:- Adalimumab/humira (crohns)
- Human monoclonal:- Golimunab (UC)
- Humanized Fab1 fragment:- Certolizumab pegol
Side effects:- NHL lymphoma, TB infx, infusions rxn, Hepatosplenic T cell lymphoma in young males (HSTCL), skin cancer, autoimmune (SLE, vasculitis, psoriasis), demyelinating diseases and heart failure
Cyclosporin
Steroid refractory UC. Bridge to 6-MP
Esophageal Cancers
- Etiology
- Pathogenesis
- Predisposing Cancer
- Adenocarcinoma (young white males)
- Mid upper esophagus:- SCC (young black females?)
Smoking, Alcohol, Nitrosmines, Se/Mo deficiencies
-Pathogenisis
-Squamous (Dysplasia to Carcinoma)
-Adeno (metaplasia to dysplasia)
-Predisposing
- Achalasia (likely myenteric problem, stuff stays longer in esophagus)
-Barrets
-Corrosive Esophagitis
-Diverticula (Zankers:- outpouching in upper esophagus, increased contact with carcinogen)
-Esophageal web
-Familial (tylosis palmaris and plantaris)
Precursor to endocrine tumor
Autoimmune gastritis can lead to endocrine/carcinoid tumor
Enterochromaffin cell hyperplasia from gastritis.
Upper GI carcinomas and lymphomas
-SCC
-Adenocarcinoma (Lichins Plastica with Signet Cell carcinoma:- antral mucinous cells invade the mucosa)
-Lymphoma
-MALT common in stomach, associated with H.Pylori,
- Mantle cell lymphoma is a lymphomatous polyposis. Most common in small bowel
-Small Intestine, associated with celiac disease (poly clonal intraepithelial lymphocytes become monoclonal)
(Lymphoepithelial lesion!!! stain with keratin, characteristic in lymphomas)
Carcinoid Tumors location
Other neuroendocrine tumors
Small intestine and appendix
- If they go into the liver, patients can have carcinoid syndrome
- Tumor is beneath the epithelium
- Nest of cells, normal nuclei. Chromagranin/synaptophysin are neuroendocrine cell stain. Dense core granules on electromicroscopy
Distinguish tumors of GI tract
-Carcinomas (Intraepithelial, can be from the gland or squamous cell)
DONT INVOLVE THE SURFACE EPITHELIUM
-Lymphoma (lymphocytic infiltrates)
-Neuroendocrine tumor
-Stromal tumors (GIST from interstitial cajal cells)..It is mesenchymal so looks white and fibrous. Spindly nuclei. Can be epitheliod when high grade and not look as epitheliod. Cell with a cross (mitosis). DO C-KIT STAIN (tell you if its tyrosine kinase responsive?). RESPOND TO GLEEVEC (IMATINIB)
Esophageal cancer Symptoms
- SVC
- phrenic nerve paralysis
- aortoesophageal fistula
- TEF
- Horners due to stellate ganglion involvement
- atrophy of hand intrinsics due to T1 involvement
Virchow lymph node
Sister Mary Joseph
Krukenberg
Bloomer’s Shelf
Virchows:-internal thoracic duct comes from the right, crosses over to drain at the left subclavian..Virchows node occurs at the left neck
Sister Mary Joseph:- Cells exfoliate off gastric cancer (down falsiform ligament, down round ligament:- umbilical)
Krukenberg Tumor:- Ovary
Bloomers Shelf:- (peritoneal reflection, shelf)
Small bowel Tumors
-Adenocarcinoma
-Lymphoma
-Stromal
-Carcinoid (flushing, diarrhea, wheezing, right heart valve lesions, 5Ht/serotonin, the outcome of the break down of this product by the liver affects the tricuspid and pulmonary valves)
MOST COMMON TUMOR is METs from Metastatic Melanoma
Colorectal cancer Symptoms
-Hemorrhoid (5 and 7 o clock) Veins draining there Can be blocked by rectal cancer -Pencil like stool due to blockage -Tenesmus (rectal cancer involves lining of rectum, can involves sphincter muscles, hence need to defecate but no stool..similar to urinary frequency..transmural/muscularis propria)
Hepatic failure with rectal cancer
rectal cancer can restrict Strictures capsule?? clarify
- Rectal cancer lymphadenopathy
- Rectal cancer sounds
- Lymph can be obstructed, takes a different route, inguinal node palpable..hardly Virchows
- High pitched sounds, moments of silence interspaced..With sounds, there’s pain
Dysplasia in Colon
nuclei size, n/c ratio, hyperchromasia, pencil shaped
-takes up space of mucin
low grade:- nuclei still perpendicular, some uniformity
high grade:- axis not oriented well, rounded and tilted
-Adenoma (villous polyps)are precursors to colon cancer
-All are removed!!!
Only time in GI we care about low/high grade are
-inflammatory bowel disease
-barretts esophagues
Adenoma types
Pedunculated ADENOMA (best type to have): TIP is dysplastic, stalk is ok.
- Intramucosal carcinoma- still not metastatic as long as its taken out
- Transition to carcinoma (shows necrosis with more atypic nuclei, VERY glandular villi, extracellular mucin which tracts through the wall)
- When its invasive, MALIGNANT polyps
On polyps (Serrated- no dysplasia/ adenoma types have dysplasia)
-Adenomatous (adenoma):- displasia from the beginning
-Hyperplastic:- this is ok
-Sessile serrated:- no dysplasia but has broad crypt base, not as blue. also sawtooth
-Serrated adenoma (sawtooth but with dysplasia)
Serrated-no blue as with the adenomas, filed with lots of mucin
Adenocarcinoma of the colorectum
- look ulcerous
- Invade submucosa
Pediatric Growth
First calories head, next height, next weight
- Caloric insuffiency (weight drops, height is ok)
- Intrauterine insult (head, height nad weight low)
- acquired hypothyroidism (height and weight drops, but height drops faster, head is ok)
Cirrhosis, always comes with abnormal physical exam?
No! So will need a biopsy in such a case..physical signs are muscle wasting, ascites
Cirrhosis
Portal HTN…variceal hemorrhage
Liver Insufficiency…encephalopathy and jaundice
NB there is splanchnic vasodilatation, also occurs systemically, hence increased portal hypertension.
Portal pressure HVPG an independent predictor of decompensation in cirrhosis
Drugs for cirrhosis, varices and variceal bleeding
Vasoconstrictors like non selective beta blocker (nadolol, propranolol)…decrease flow through portal vein, but increased portal venous resistance with overall slight decrease in portal pressure of 35%… Beta blockers used in varices or ligation…extrahepatic action…in acute bleed, use somatostatin a strong IV vasopressive agent..in recurrent bleeds use both ligation and Betablockers.
Vasodilators like simvastatin use with caution (vasodilation occurs after collaterals have been formed)..intrahepatic action
Combination of both is carvedilol..main effect is b2 effect and less flow into the portal blood flow..50%
Endoscopic therapy such as ligation , sclerotherapy
TIPS Trans jugular intra hepatic portosystemic shunt…deviate flow through liver, hepatic vein and IJV..problem with encephalopathy.
Relationship between serum ascites albumin or SAAG gradient and HVAG.
Good correlation…saag of 1.1 correlates with 11, the cut off for sinusoidal cause of ascites hence cirrhosis. But total protein is normal compared to cardiac ascites and peritoneal malignancy…serum BNP ON THE OTHER HAND helps diagnose cardiac ascites.
Ascites drugs, treatment, complications and their treatments
Drain
TIPS
spironolactone first, can add furosemide
Complications are usually spontaneous peritonitis, empyemas and bacteremia…. For SBP give albumin! Cefurotaxime, ceftriaxone, betalactams, NO AMINOGLYCOSIDES
Hepatorenal syndrome is the worst complication! Melt score involves bilirubin, creatinine and INR.. This is due to intense splanchnic vasodilatation leading to low effective arterial blood volume and activation of RAAS, hence renal vasoconstriction….severe! Transplant is the main solution
Cholestasis versus jaundice
Jaundice is hyperbilirunemia
Cholestatis is elevation in everything including bile acids…bile flow reduced, bile salts retained, bilirubin and cholesterol retained, increased alk phos.
Liver biopsy with bile plus in bile canaliculi
Clinical feature of cholestasis
Itching from bike salts retention
Increased cholesterol wi xanthimas
Target cells and schisocytes with buildup of bile in rbcs
Alk phos
5 nucleotidase
Gamma glutamyl transferase
Steatorhea, Vit ADEK MALABSORPTION .E more common in children than adults
What forms micelles
Bile acid and phospholipid, through bile acid transporter and the flippase…are both ABC superfamily transporters hence need ATP
MDR3 mutation and polymorphisms
Cholestatis of pregnancy
PFIC has three different presentation
Cholangitis
- Charcots triad
- Raynauds pentad
Charcot:- fever, chills and jaundice
Raynaud:- Charcot+hypotension and (another feature of shock)
Cholangiocarcinoma
Gets worse as you ascend the bile duct Some causes -Clonorchis parasite -Sclerosing Cholangitis -Constant gall stones
Pancreatic cancer
1) Severe weight loss. Other symptoms depend on site
- Head (painless jaundice, gastric outlet obstruction with nausea and vomiting)
- Body & Tail
COURVOISERS LAW
In presence of jaundice a palpable gall bladder is unlikely due to stone!!! (Increase in pressure due to obstruction, gall bladder takes up pressure and is palpable, intrahepatic biliary system -hence likely pancreatic cancer. On the other hand takes up the pressure when there is obstruction in gall bladder due to stone)
For head pancreatic cancer
Whipple Procedure:- pancreaticoduodenectomy
removal of the distal segment (antrum) of the stomach; the first and second portions of the duodenum; the head of the pancreas; the common bile duct; and the gallbladder.
The basic concept behind the pancreaticoduodenectomy is that the head of the pancreas and the duodenum share the same arterial blood supply (the gastroduodenal artery). These arteries run through the head of the pancreas, so that both organs must be removed if the single blood supply is severed.
Reconstruction consists of attaching the pancreas to the jejunum (pancreaticojejunostomy) and attaching the hepatic duct to the jejunum (hepaticojejunostomy) to allow digestive juices and bile respectively to flow into the gastrointestinal tract and attaching the stomach to the jejunum (gastrojejunostomy) to allow food to pass through.
Acinar Cell Carcinoma
Lipase Hypersecretion syndrome!!! (hence subcutaneous fat necrosis and paniculitis)
Tends to happen more in kids
Cystic neoplasms of the pancreas
-Mucinous- TEND TO BE MALIGNANT. Especially the main duct IPMN compared to side branch IPMN (intraductal papillary mucinous neoplasm)
Another type is mucinous cystic types which have the classic spindle like ovarian stroma cells.
ALL are lined by columnar cells
-Serous- USUALLY BENIGN
Cystadenoma (very vascular)- body and tail. Lined by cuboidal cells
-Solid and papillary epithelial neoplasm
-Cystic neuroendocrine tumors (islets!!!)
