What is a good general approach to looking at an abdominal plain film?

- Technical assessment: name, position, penetrance

- Bones: ribs, spine, pelvis (ex; ppl with Chron's often have sacroillitis), look for pagets, metastasos

- Solid organs: liver, spleen, kidneys (T12 to L3), bladder, Psoas *look at the margins in between

- GI tract gas pattern: fluid levels will not appear on supine films. Large bowel is about 6cm dilated, small bowel 3 vm. Most common cause of large bowel obstruction is ca, small bowel adhesions.

- Calcifications: vascular, lymph, kidney

- Free air: under the diaphragm could mean perforation (upright CXR is the best)

- Forgein bodies

What are symptoms of pancreatic cancer? How about risk factors?

- low appetite

- weight loss

- fatigue

-abdominal pain

- diarrhea

- steatorrhea

- jaundice

- unusual bloating/belching.

- Risk factors: age, fam hx, smoking, chronic pancreatitis big time, DM, obesity, partial gastrectomy, cholecystectomy. H pylori

The doctor says Heather, go do a physical exam for this woman who we think has pancreatic ca, what would you look for?

- Palpable non-tender gallbladder is a big one

- Virchow's node may be enlarged (metastasis)

- Pancreatic panniculitis (inflammation of fat under the skin)

- Sister Mary Joseph node: node bulging into the umbilicus due to metastasis

- Hepatomegally

- jaundice (if the tumor obstructs the bile duct)

How would you work someone up if you're suspecting pancreatic cancer based on signs and symptoms.

- start with an abdominal U/S, then do a CT which will be more precise and is better at looking at the pancreas

- he says you can do ERCP but don't go to it first cause it's not great for distal tumors.

- if a mass is detected, do an EU/S guided biopsy

What is the general prognosis of somepne with pancreatic ca? What surgical procedure can sometimes be done? What are the chemo names to know?

- less than 20%

- In whipple, they remove the lower portion of the stomach, the duodenum, then portion of the pancreas involved, and then reconnect them.

- Attach jejumun to the stomach, the pancreas, and the common hepatic duct

- Gemcitabine, 5-FU

What is ECOG performance?

- it's a prognostic marker (in this case for someone with a recurent secondary). Chemo is not helpful in ECOG 3-4.

0 = no symptoms

1 = strenuous activity restricted

2 = symptoms, but up and about more than 50% of waking hours

3 = confined to bed/chair more than 50% of waking hours

4 = bed bound.

What are S/s of hepatocellular carcinoma?

- B symtpms, early satiety

- 80% caused by chronic Hep B and C

What are hepatocellular carcinoma risk factors?

- Hep B and C

- HH

- alcohol

- chronic liv dis/ cirrhosis

- aflatoxin (fungus toxin

- microcystin (blue green algae)

- betel nut

- NAFLD

- A-1 antitripsin

How would one diagnose hepatocellular carcinoma?

- look for specific physical findings: like ascites, encephalopathy

- AFP level over 400 mg/ml is diagnostic.

- so do all of their LFTs and LEs

- I would do serology for Hep as well, U/S of the liver

- do a CT or infused MRI, if you do not see arterial hypervascularity AND venous or delayed phase washout, in which case you could diagnose it right away, then do a biopsy and do another CT or MRI.

- Prognosticate with Chil-Turcotte-Pugh classes, which look at bilirubin, albumin, INR, ascites and encephalopathy

How do you treat someone with hepatocellular carcinoma?

- resection, but you need enough residual functional liver.

- 5 year survival is about 50% give or take 10%

- For someone who is higher stageand cannot undergo sx but not necessarily terminal, they can do TACE (trans-catheter arterial chemoembolization) and tx with Sorafenib.

What makes the stomach distend after you eat? What causes it's peristaltic contractions?

- vagus tone does the relaxation through NO and VIP (vasoactive intestinal peptide) then the bolus remains in the stomach for about 40-60 mins.

- the stomach has a pacemaker in the longitudinal muscle of the greater curvature which, in the right environment including a distensing force (air or food), CCK and cortisol, will cause peristatic contractions at a rate of about 3/min

- Trituration is what the stomach does to grind the food against the closed pylorus. Then particles must be smaller than 1-2mm to get through.

What are "housekeeping" contractions of the GIT?

- They are called MMCs, or migrating motor complexes, and they happen abotu once every hour or a bit longer, and they push all of whatever is left in the gut down, the wave goes well into the small intestine.

- this is good for moving along undigestible materials and also assuring sterilization.

- ppl with scleroderma can lack this, and sometimes they get small bowel bacterial overgrowth because of it.

What is the motor in the small bowel like in a fasting state? In a fed state?

- there are a series of well organized MMCs.

- in a fed state it is more disorganized.

- all movements of the small bowel are sortof regulated by the "slow wave", which Dr. Najeeb talked about. They are electrical stimulations of the bowel that do not result in contraction unless there are other signals to do so (like distension or chemical stimulation), they happen about 12/min.

What is gastroparesis? What causes it? How do you treat it?

- delayed emptying of a solid meal which causes N/V, pain, satiety and bloating, anorexia and weight loss.

- impaired fundal tone, antral hypomotility, antroduodenal incorrdination, gastric pacemaker dysrhythmia, excessive inhibitory fbk by KKC or somatostatin.

- 25% is caused by DM, 50% is idiopathic (maybe post viral), 10% post gastric sx, 10% collagen vascular disease, 5% intestinal pseudo-obstruction. Other: infiltrative, Parkinson's, drugs

- diet, supplemental feeding, exercise, pro-kinetids METOCLOPROMIDE, DOMPERIDONE, anti-emetics, Ghrelin (stimulates gastric contraction)

How much water gets secreted into the proximal jejunum, and how much ends up being excreted in stool? How much can be absorbed by the colon?

- 9 L

- 100 cc

- 5 L/day

How do you calculate stool osmolar gap?

Stool OG = 2 (Na + K)

N = < 50

How do tight junctions change as you move from the small to the large intestine? What do the crypts do vs. what the villi do?

- they become less permeable and are more efficient in absorbing water.

- crypts secrete, villi absorb.

How does Cl secretion work? How does Cholera work?

- the basolateral transporter carries 2 Cl anions into the cell along with one Na and one K. Cl then moves through a channel in the apical membrane down it's electrochemical gradient.

- Cholera toxin binds to the epithelial cells and irreversibly stimulates cyclic AMP production. That blocks electroneural Na absorption from villous cells and stimulates Cl secretion from crypt cells. This results in excess NaCl in the lumen and diarrhea.

- The toxin does not affect Na coulpled nutrient (glucose) transport, therefore, providing a rehydration solution is effective in treating this. 

What 3 tests should we do to diagnose celiac disease?

- IgA antibodies to Tissue Transglutaminase

- Anti-endomysial Abs

- IgA level (to identify false negatives)

- on endoscopy you see scalloped mucosa

- Histology shows intraepithelial lymphocytosis, villous atrophy with crypt hyperplasia, lamina propria expansion with mononuclear cells

PR gives you a case which shows duodenal mucosa with villous atrophy, crypt hyperplasia and intraepithelial lymphocytosis, and you super think it's celiac. But then it asks you for a DDx...

- Tropical sprue (it's often found in tropical regions, has the same histological things, cause is unknown, they think it may be infectious)

*difference is that celiac is most definately caused by autoimmunity.

- Giardiasis

- Bacterial overgrowth syndrome

- Cow's milk intolerance

- Chron's disease

- Viral infections

- Drug effects.

Giardiasis

- most common parasitic infection in humans

- fecal oral

- diarrhea, abdominal pain and malabsorption, some ppl are asymptomatic

Whipple disease

- rare, caused by Tropheryma whippeli

- weird extraintestinal symtpms other than the diarrhea, wt loss and malabsorption are:

- fever

- anemia

- lymphadenopathy, arthritis, pleurisis, endocarditis, CNS

- can diagnose by histology

What are pseudomembranes?

- they're a layered mixture of fibrin, PMNs and mucin which coats the luminal surface of the colon in people infected with C diff, where the C diff toxin causes loss of tight junctions, cytokine release and cell death.

- You can get something similar with E coli infection also, they mention especially E.coli 0157:H7. *also remember that's the one that can cause hemolytic uremic syndrome!

Outline some major differences between Crohn's and UC. 

Chron's:
Typically transmural, regional enteritis affecting anywhere in the GIT. Skip lesions, stricturing, fistulas, creeping fat. Can see transmural lymphoid aggregates and even granuloma formation. 

UC:

Severe ulcerating inflam dis limited to colon and extends only into the mucosa and submucosa. Continuous, no skip lesions and no small bowel disease.

What's the diff between dysplasia and carcinoma of the bowel?

- first of all, this is in an IBD lecture because chronic inflam leads to genomicay unstable epithelium with progression to neoplasia.

Dysplasia: Premalignant state with neoplastic epithelium confined by a basement membrane (in this case or the muscularis mucosa).

Carcinoma: Malignant state where the neoplastic epithelium has breached the basement membrane and has the capacity to induce metastases.