GI- upper GI Flashcards
(194 cards)
1
Q
Gastrin
1) where is it produced and by what cells?
2) what is secretion stimulated by
3) what inhibits secretion
4) target cells
5) response to hormone
6) How does Omeprazole (PPIs) work
A
1) G cells in stomach ANTRUM
2) amino acids, vagal input (acetylcholine), calcium, ETOH, antral distention, pH>3.0
3) pH
2
Q
Somatostatin
1) where is it produced and by what cells?
2) what is secretion stimulated by
3) target cells
4) response to hormone
5) How does Octreotide work and when to use
A
1) produced by D (somatostatin) cells in the stomach ANTRUM
2) acid in duodenum
3) many, it is the great inhibitor!
4) inhibits gastrin and HCl release; inhibits release of insulin, glucagon, secretin and motilin. Decreases pancreatic and biliary output
5) Somatostatin analogue. Can be used to decrease pancreatic fistula output
3
Q
CCK
1) where is it produced and by what cells?
2) what is secretion stimulated by
3) response to hormone
A
1) produced by I cells of the DUODENUM
2) amino acids and fatty acid chains
3) gallbladder contraction, relaxation of sphincter of Oddi, increases pancreatic enzyme secretion
4
Q
Secretin
1) where is it produced and by what cells?
2) what is secretion stimulated by
3) what inhibits secretion
4) response to hormone
A
1) S cells of DUODENUM
2) fat, bile, pH4.0, gastrin
4) increased pancreatic HCO3- release, inhibits gastrin release (this is reversed in pts with gastrinoma), and inhibits HCl release
- high pancreatic duct output-> increased HCO3-, decreased Cl-
- slow pancreatic duct output-> increased Cl-, decreased HCO3- (carbonic anhydrase in duct exchanges HCO3- for Cl-
5
Q
Vasoactive intestinal peptide
1) where is it produced and by what cells?
2) what is secretion stimulated by
3) response to hormone
A
1) produced by cells in gut and pancreas
2) fat, acetylcholine
3) increased intestinal secretion (water and electrolytes) and motility
6
Q
Glucagon
1) where is it produced and by what cells?
2) what is secretion stimulated by
3) what inhibits secretion
4) response to hormone
A
1) mainly alpha cells of pancreas
2) stimulated by decreased glucose, increased aa’s, acetylcholine
3) inhibited by increased glucose, increased insulin, somatostatin
4) glycogenolysis, gluconeogenesis, lipolysis, ketogenesis, decreased gastric acid secretion, decreased GI motility, relaxes sphincter of Oddi.
7
Q
Insulin
1) where is it produced and by what cells?
2) what is secretion stimulated by
3) what inhibits secretion
4) response to hormone
A
1) beta cells of the pancreas
2) glucose, glucagons, CCK
3) somatostatin
4) cellular glucose uptake, promotes protein synthesis
8
Q
pancreatic polypeptide
1) secreted by what cells?
2) secretion stimulated by?
3) response to hormone
A
1) islet cells in pancreas
2) food, vagal stimulation, other GI hormones
3) decreased pancreatic and gallbladder secretion
9
Q
Motilin
1) where is it produced and by what cells?
2) what is secretion stimulated by
3) what inhibits secretion
4) response to hormone and what drug acts on it’s receptor to stimulate motility
A
1) intestinal cells of gut
2) duodenal acid, food, vagus input
3) somatostatin, secretin, pancreatic polypeptide, duodenal fat
4) increased intestinal motility (small bowel, phase III peristalsis)-> erythromycin acts on this receptor
10
Q
1) Bombesin (Gastrin-releasing peptide) actions
2) Peptide YY- where is it released from and actions
3) what organ mediates anorexia
4) what is the order/timeframe of bowel recovery from surgery
A
1) increases intestinal motor activity, increases pancreatic enzyme secretion, increases gastric acid secretion
2) released from terminal ileum following fatty meal-> inhibits acid secretion and stomach contraction, inhibits gallbladder contraction and pancreatic secretion
3) hypothalamus
4) Small bowel fnc returns within 24 hours
stomach in 48 hours and large bowel in 3-5 days
11
Q
Esophagus anatomy 1) layers of the esophageal wall 2) muscle in a- upper 1/3 of esophagus b- middle and lower 2/3 of esophagus 3) blood supply to cervical esophagus 4) blood supply to thoracic esophagus 5) blood supply to abdominal esophagus 6) venous drainage
A
1) mucosa (squamous epithelium), submucosa, and muscularis propria (longitudinal muscle layer); NO serosa
2) a- striated muscle; b-smooth muscle
3) inferior thyroid artery
4) vessels directly off the aorta
5) left gastric and inferior phrenic arteries
6) hemi-azygous and azygous veins in chest
12
Q
Esophagus anatomy
1) where do lymphatics drain
2) where do the right and left vagus nerves travel and what do they supply
3) where does the thoracic duct travel and insert
4) MC site of esophageal perforation (usually with EGD)
5) cause of aspiration with brainstem stroke
A
1) upper 2/3 drain cephalad; lower 1/3 caudad
2) -Right vagus- travels on posterior stomach as it exits chest and becomes celiac plexus. Also has criminal nerve of Grassi which can cause persistently high acid levels postop if left undivided after vagotomy
- Left vagus- travels on anterior stomach. goes to liver and biliary tree
3) Travels from right to left at T4-5 as it ascends in the mediastinum. Inserts into left subclavian vein
4) cricopharyngeus muscle
5) failure of cricopharyngeus muscle to relax
13
Q
Upper esophageal sphincter
1) distance from incisors
2) muscle
3) nerve innervation
4) normal EUS pressure at rest
5) normal EUS pressure with food bolus
A
1) 15cm
2) cricopharyngeus muscle (circular muscle, prevents air swallowing)
3) recurrent laryngeal nerve
4) 60 mmHg
5) 15mmHg
14
Q
Lower esophageal sphincter
1) distance from incisors
2) what is the resting state
3) nl LES pressure at rest
4) nl LES pressure with food bolus
A
1) 40cm
2) normally contracted at resting state (prevents reflux). relaxation mediated by inhibitory neurons. Anatomic zone of high pressure but NOT an anatomic sphincter
3) 15mmHg
4) 0 mmHg
15
Q
Anatomic areas of esophageal narrowing
A
at cricopharyngeus muscle, compression by the left mainstem bronchus at aortic arch, and diaphragm
16
Q
Stages of swallowing
1) what initiates it
2) primary peristalsis- what initiates
3) secondary peristalsis- what initiates
4) Tertiary peristalsis
5) resting state of UES and LES bw meals
A
1) CNS
2) occurs with food bolus and swallow initiation
3) occurs with incomplete emptying and esophageal distention, propagating waves
4) non-propagating, non-peristalsing (dysfunctional)
5) contracted
17
Q
Swallowing mechanism
A
soft palate occludes nasopharynx, larynx rises and airway opening is blocked by epiglottis, cricopharyngeus relazes, pharyngeal traction moves food into esophagus.LES relaxes soon after initiation of swallow (vagus mediated)
18
Q
Which side should you approach from in surgery for repair of
1) cervical esphagus
2) upper 2/3 thoracic esophagus
3) lower 1/3 thoracic esophagus
A
1) left
2) right (avoids aorta)
3) left (left-sided course in this region)
19
Q
Hiccoughs
1) causes
2) what nerves are part of the reflex arc
A
1) gastric distention, temperature changes, ETOH, tobacco
2) vagus, phrenic, sympathetic chain T6-12
20
Q
Esophageal dysfunction
1) primary causes
2) secondary causes
3) best test for heartburn
4) best test for dysphagia or odynophagia
5) best test for meat impaction
A
1) achalasia, diffuse esophageal spasm, nutcracker esophagus
2) GERD (most common), scleroderma
3) endoscopy (can visualize esophagitis)
4) barium swallow (better at picking up masses)
5) endoscopy (dx and rx)
21
Q
Pharyngoesophageal disorders
1) In what part of swallowing is the prbm?
2) causes
3) T/F- liquids are worse than solids for these disorders
4) Plummer-Vinson syndrome- components of syndrome and rx
A
1) trouble in transferring food from mouth to esophagus
2) MC neuromuscular disease- myasthenia gravis, muscular dystrophy, stroke
3) True
4) upper esophageal web, Fe-deficient anemia
rx- dilation, Fe; screen for oral CA
22
Q
Esophageal Diverticula 1) Zenker's Diverticulum a- what causes it b- is it true or false diverticulum c- location d-symptoms e-dx f-rx
A
1) a) increased pressure during swallowing 2/2 failure of cricopharyngeus to relax
b) false diverticulum located posteriorly
c- between the pharyngeal constrictors and cricopharyngeus
d- upper esophageal dysphagia, choking, halitosis
e- barium swallow studies, manometry, risk for perf with EGD and Zenker’s
f-cricopharyngeal myotomy, Zenker’s itself can either be resected or suspended. L cervical incision
-L cervical incision, leave drains in, get esophogram on POD#1
23
Q
Esophageal Traction Diverticulum
1) True or False diverticulum
2) cause
3) location
4) sx
5) rx
A
1) true diverticulum
2) inflammation, granulomatous disease, tumor
3) usually in mid-esophagus and lies lateral
4) regurgitation of undigested food, dysphagia
5) excision and primary closure if symptomatic, may need palliative therapy (ie- XRT) if due to invasive CA. if asx, leave alone
24
Q
Esophageal Epiphrenic diverticulum
1) what disorders are associated
2) location
3) sx
4) dx
5) rx
A
1) esophageal motility disorders (ie-achalasia)
2) in distal 10cm of esophagus
3) most are asx. can have dysphagea and regurgitation
4) esophagram and esophageal manometry
5) rx- diverticulectomy and esophageal myotomy on the side opposite the diverticulum if sx
25
Achalasia
1) sx
2) cause/pathophys
3) manometry findings
4) barium swallow findings
5) rx
6) what infection can produce similar symptoms
1) dysphagia, regurg, weight loss, respiratory symptoms
2) failure of LES to relax and lack of peristalsis after food bolus 2/2 neuronal degeneration in muscle wall
3) Increased LES pressure, incomplete LES relaxation. NO peristalsis
4) birds beak. tortuous dilated esophagus and epiphrenic diverticula
5) balloon dilatation of LES-> effective in 80%. Nitrates, Ca-channel blockers.
- If above fails do Heller myotomy (left thoracotomy, myotomy of LOWER esophagus ONLY) plus partial Nissen funduplication
6) T. cruzi parasite
26
Diffuse esophageal Spasm
1) sx
2) manometry findings
3) rx
1) Chest Pain!, dysphagia, psychiatric history
2) strong non-peristaltic unorganized contractions; LES relaxes normally
3) Ca-channel blockers, nitrates. Heller Myotomy (myotomy of upper and lower esophagus) if meds fail but less effective than for acholasia
27
Nutcracker esophagus
1) sx
2) Manometry findings
3) rx
1) Chest Pain!, dysphagia
2) high-amplitude peristaltic contractions; LES relaxes normally
3) Ca-channel blocker, nitrates. Heller myotomy if those fail of upper and lower esophagus, but less effective than for acholasia
28
Scleroderma leading to dysphagea
1) pathophysiology
2) rx
1) fibrous replacement of esophageal smooth muscle->dysphagia and loss of LES tone with MASSIVE REFLUX and STRICTURES
2) esophagectomy usual if severe
29
GERD
1) what is normal anatomic protection from GERD
2) pathophys of GERD
3) sx
4) empiric rx
5) diagnostic studies
6) surgical indications
7) Nissen
a- steps of operation
b-what is the paraesophageal membrane and extension of
c- key maneuver for wrap is identification of?
d-complications
8) approach for Belsey procedure
9) Collis gastroplasty- when to use it and how it is done
1) need LES competence, normal esophageal body, normal gastric reservoir
2) increased acid exposure to esophagus from loss of gastroesophageal barrier
3) heartburn sx 30-60min after meal, worse lying down, asthma symptoms (cough), choking, aspiration
4) empiric PPI (omeprazole 99% effective) for 3-4 weeks. If fails do diagnostic studies.
5) pH probe (best test), endoscopy, histology, manometry (resting LES esophagus (neo-esophagus)
30
Hiatal Hernia
1) Describe type I-IV
2) which type usually needs repair 2/2 high risk of incarceration
3) how to repair
4) Hernia associated with Schatzki's ring and treatment
1) Type I- sliding hernia from dilation of hiatus (MC); often associated with GERD
Type II- paraesophageal. hole in diaphragm beside esophagus, normal GE jnction. sx- CP, early satiety, dysphageia
Type III- combined I and II
Type IV- stomach in chest + another organ (colon/spleen)
2) Type II paraesophageal
3) Nissen + resect hernia
4) ring of tissue in lower esophagus-> esophageal narroing. Associated with sliding hiatal hernia (Type I), rx-dilation of the ring and PPI usually sufficient. Do not resects
31
Barrett's Esophagus
1) cellular change that occurs
2) cause
3) how much does its presence increase CA risk
4) what is indication for esophagectomy
5) treatment and followup
1) squamous metaplasia to columnar epithelium
2) long-standing exposure to gastric reflux
3) increases cancer risk by 50 times (adenocarcinoma)
4) Severe Barret;s dysplasia is indication for esophagectomy
5) Treat uncomplicated like GERD (PPI or Nissen). Surgery will decrease esophagitis and further metaplasia but will not prevent malignancy or cause regression of the columnar lining.
- Need careful f/u with EGD for lifetime. Even after Nissen
32
Esophageal Cancer
1) T/F: esophageal tumors are almost always malignant but with late invasion of nodes
2) How does it spread
3) risk factors
4) diagnosis
5) best test for determining resectability and what factors prevent resection
6) MC type of cancer overall
- where is adenoCA usually located and where does it met
- what about squamous cell cancer
7) MC benign esophageal tumor
1) False, almost always malignant with early nodal invasion
2) submucosal lymphatic spread
3) ETOH, smoking, achalasia, caustic injury, nitrosamines
4) Esophagram (best test for dysphagia)
5) CT chest and abdomen
- unresectable if hoarseness (RLN invasion), Horner's syndrome (brachial plexus invasion), phrenic nerve invasion, malignant pleural effusion, malignant fistula, airway invasion, vertebral invasion, nodal disease outside the area of resection (ie-supraclavicular or celiac nodes (M1 dz))
6) Adenocarcinoma is #1. Found in lower 1/3 of esophagus, mets to liver MC
- Squamous cell CA usually in upper 2/3 of esophagus, lung mets MC
7) Leiomyoma
33
Esophageal CA treatment
1) role of pre-op Chemo-XRT
2) What Chemo agents are used
3) Esophagectomy
a-mortality and cure rates
b- what is primary blood supply to stomach after replacing esophagus
c-Describe the diff bw the Transhiatal approach, Ivor Lewis and 3-Hole esophagectomy techniques
d-what additional procedure do you need with all of the above
4) when is colonic interposition a good choice and what blood supply does it depend on
5) what is needed after esophagectomy to r/o leak and when to do it
6) Rx of postop strictures
7) Malignant fistulas- how to rx and prognosis
1) can downstage tumors and make resectable
2) 5-FU and Cisplatin (for node + disease or use pre-op to shrink tumors)
3) a-5% mortality from surgery. 20% cure rate
b-Right gastroepiploic artery (have to divide the left gastric and short gastrics
c-Transhiatal- abdominal and neck incisions. bluntly dissect thoracic esophagus (has dec mortality from leaks with cervical anastamosis)
-Ivor Lewis- Abd incision and R thoracotomy.-> exposes all of intrathoracic esophagus-> intrathoracic anastamosis
-3-Hole: abdominal, thoracic and cervical incisions
d- pyloromyotomy
4)choice in young pts when you want to preserve gastric function. need 3 anastamoses. blood supply depends on colon marginal vessels
5) contrast study on POD7
6) dilate
7) can palliate with stent, most die within 3 mo from aspiration
34
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Leiomyoma
1) where is it located
2) dx
3) Biopsy technique
4) rx
Esophageal polyps
5) how common
6) location
7) rx
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1) in muscularis propria, usually in lower 2/3 of esophagus (smooth muscle cells)
2) esophagram #1, EUS, CT scan (to r/o CA)
3) Do NOT biopsy bc can for scar and make later resection difficult
4) rx if >5cm or symptomatic with excision (enucleation) via thoracotomy
5) 2nd MC benign lesion after leiomyoma
6) usually cervical esophagus
7) if small- resect with endoscopy; if larger-cervical incision
35
Caustic esophageal injury
1) role of NG tube, induced vomiting and drinking water to flush it out in treatment
2) Diff in necrosis from alkali and acid injury and which is worse/most likely to cause CA
3) How to determine severity/follow injury
4) Treatment if
a- Primary burn (hyperemia)
b- secondary burn (ulcerations, exudate and sloughing)
c-tertiary burn (deep ulcers, charring and lumen narrowing)
d- caustic esophageal perforation
1) DON'T do any of these-NO NGT, NO vomiting, NOTHING to drink
2)Alkali-> deep liquifaction necrosis (Worse injury and more likely to cause CA). Ie-Drano
Acid-> coagulation necrosis, mostly gastric injury
3) Do endoscopy to assess lesion except if suspected perforation. Do NOT go past a site of severe injury. Follow with serial exams and plain films
4) a-obseve and conservative therapy (IVFs, spitting, abx, po intake after 3-4days, may need future serial dilation for strictures (usually cervical).
b-prolonged observation and conservative therapy. Unless Esophagectomy indicated (Sepsis, peritonitis, mediastinits, free air, mediastinal or stomach wall air, crepitance, contrast extravasation, pneumothorax, large effusion)
c- same as seconday burn. Most need esophagectomy. Don't restore alimentary tract until pt recovers from caustic injury
d-esophagectomy (NOT repaired 2/2 extensive damage)
36
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Esophageal Perforation
1) MCC
2) MC location
3) sx
4) Dx
5) Criteria for nonsurgical management and what does conservative therapy consist of
6) Repair of Non-contained perforations
a- if diagnosed in
```
1) endoscopy
2) at cricopharyngeaus muscle in cervical esoph
3) dysphagia, tachycardia, pain
4) CXR initially for free air. Then Gastrografin swallow followed by barrium swallow
5) contained perforation by contrast. self-draining. no systemic effects
6) a- primary repair with drains via longitudinal myotomy to see full extent of injury. Consider intercostal muscle flaps to cover repair
b- If in Neck- Just place drains (no esophagectomy)
-If in Chest: need 1) resection (esophagectomy or cervical esophagectomy) or 2) exclusion and diversion (cervical esophagectomy, staple across distal esophagus, washout mediastinum, place chest tubes and do late esophagectomy at time of gastric replacement=when pt fully recovers)
7) pts with severe intrinsic dz (burned out esophagus from achalasia or esophageal CA)
37
Boerhaave's syndrome
1) classic presentation
2) MC site of perforation
3) what is Hartmann's sign
4) Dx
5) Tx
6) prognosis
1) forceful vomiting then chest pain.
2) in Left lateral wall of esophagus, 3-5cm above GE junction
3) mediastinal crunching on auscultation
4) Gastrografin swallow
5) same as for esophageal perforation
6) highest mortality of all perforations- survival improves with early dx and rx
38
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Stomach
1) Stomach transit time
2) where does peristalsis occur
3) what nerves sense gastroduodenal pain
4) Blood supply and branches
a- branches of celiac trunk
b- supply to greater curvature
c-supply to lesser curvature
d- supply to pylorus
```
1) 3-4 hours
2) distally in antrum only
3) afferent sympathetic fibers of T5-10
4) a- splenic (left gastroepiploic and short gastric are branches, Common hepatic (gastroduodenal and Right gastric are branches) and Left gastric
b- right (branch of gastroduodenal) and left gastroepiploics and short gastrics
c- right and left gastrics
d-gastroduodenal artery
39
Stomach
1) what cells line mucosa
2) what do cardia glands secrete
3) what do chief cells release and role in digestion
4) what do parietal cells release
5) what stimulates H+ release
6) inhibitors of parietal cells
7) role of intrinsic factor
1) simple columnar epithelium
2) mucus
3) pepsinogen (1st enzyme in proteolysis)
4) H+ and intrinsic factor
5) Acetylcholine (Vagus nerve), gastrin (from G cells in antrum), and histamine (from mast cells)
6) somatostatin, prostaglandins (PGE1), secretin, CCK
7) binds B12 and complex is reabsorbed in the terminal ileum
40
H+ release- describe the pathway leading to release for
1) Acetylcholine
2) Gastrin
3) Histamine
4) final common pathway
5) at what part of the pathway do PPIs work like Omeprazole
1 and 2) Activate phospholipase leasing to inc Ca-> Ca-calmodulin activates phosphorylase kinase-> inc H+ release
3) activates adenylate cyclase-> cAMP-> protein Kinase A-> H+ release
4) Phosphorylase kinase and Protein Kinase A phosphorylate H+/K+ ATPase channels to increase H+ secretion and K+ absorption
5) block H+/K+ ATPase channels
41
Stomach
1) Antrum and pylorus glands
a- name the secreting cells found here and what they release
b- name the 2 other types of secreting glands here and their function
2) what inhibits G-cells
3) what stimulates G-cells
4) where are Brunner's glands and what do they secrete
5) when are somatostatin, CCK and secretin released
1) a- G cells-> gastrin release (why antrectomy is helpful for ulcer disease) and D-cells- secrete somatostatin. inhibit gastrin and acid release
b- Mucus and HCO3- secreting glands- protect stomach from acid
2) H+ in duodenum
3) amino acids, acetylcholine
4) In duodenum, secrete alkaline mucus
5) with antral and duodenal acidification
42
Stomach
1) causes of rapid gastric emptying
2) causes of delayed gastric emptying
3) What are Trichobezoars made of and Tx
4) what are Phytobezoars made of and Tx
5) What is a Dieulafoy's ulcer
6) what is Menetrier's disease
1) previous surgery (#1), ulcers
2) diabetes, opiates, anticholinergics, hypothyroidism
3) made of hair. hard to pull out. Rx- EGD generally inadequate so likely need gastrostomy and removal
4) made of fiber (seen in DM with poor gastric emptying). rx- enzymes, EGD, diet changes
5) vascular malformation (can bleed)
6) mucous cell hyperplasia (inc rugal folds)
43
Gastric Volvulus
1) what hernia is it associated with
2) type of volvulus
3) rx
1) type II (paraesophageal) hernia
2) usually organoaxial volvulus
3) reduction and Nissen
44
Mallory-Weiss Tear
1) cause and presentation
2) Dx/rx (and MC location)
1) 2/2 forceful vomiting-> hematemesis-> bleeding stops spontaneously
2) EGD with hemo-clips. tear is usually on lesser curvature, near GE jnc. If continued bleeding may need gastrostomy and oversewing of the vessel
45
Vagotomies
1) Effect of Truncal and Proximal Vagotomies on gastric emptying of solids and liquids
2) what about if you add a pyloroplasty to truncal vagotomy
3) Other effects of truncal vagotomy
a- gastric effects
b-nongastric effects
4) MC problem after vagotomy and cause
1) Both-> increase liquid emptying (vagally-mediated receptive relaxation is removed-> increased gastric pressure-> inc liquid emptying
For Solids
-Truncal vagotomy divides vagal trunks at level of esophagus-> dec emptying of solids
-Proximal Vagotomy (aka- Highly Selective)-> divides individual fibers that supply the gastric fundus only-> nl emptying of solids
2) then you will have increased solid emptying
3) a- decreases acid output by 90%, inc gastrin, gastrin cell hyperplasia
b- decreases exocrine pancreas fnc (digestive), dec postprandial bile flow, inc gallbladder volumes, dec release of vagally-mediated hormones
4) diarrhea (40% get) 2/2 sustained MMCs (migrating motor complexes) that force bile acids into the colon
46
Upper GI bleed
1) risk factors
2) Dx/Rx
3) what test to get if slow bleeding and hard to localize
4) biggest risk factor for rebleed at time of EGD
5) highest risk factor for mortality with non-variceal UGI bleed
6) Cause and Rx in pt with liver failure
1) previous UGI bleed, PUD, NSAIDs, smoking, liver disease, esophageal varices, splenic vein thrombosis, sepsis, burn injuries, trauma, severe vomiting
2) EGD, potential rx with hemo-clips, epi-injection or cautery. If ulcer get bx for H. Pylori-> rx with omeprazole and abx
3) tagged RBC scan
4) #1- spurtung blood vessel (60% chance), #2 visible blood vessel (40% chance), #3 diffuse oozing (30% chance)
5) continued or re-bleeding
6) MC esophageal varices. Do EGD with variceal bands or sclerotherapy. TIPS if that fails
47
Duodenal ulcers
1) T/F: MC peptic ulcer
2) what sex is it MC in
3) MC location- which ulcers perforate and which bleed (from what artery)
4) sx
5) dx
6) rx
7) what does H. pylori triple therapy consist of
1) True; 2) male;
3) 1st part of duodenum, usually anterior. Anterior ulcers perforate; posterior ulcers bleed from the gastroduodenal artery
4) epigastric pain radiating to back, abates with eating but recurs 30min later
5) EGD
6) PPI, triple therapy for H. pylori
7) Omeprazole, clarithromycin and amoxicillin. +/- Bismuth salts
48
Duodenal Ulcers
1) what is Zollinger-Ellison syndrome components
2) Surgical indications for rx
3) Surgical optons and how to reconstruct after antrectomy
- which has the lowest ulcer recurrence
- which has the lowest mortality
1) gastic acid hypersecretion, peptic ulcers and gastrinoma
2) Perforation, protracted bleeding after EGD therapy), Obstruction, Intractability despite medical therapy, inability to rule out cancer (ulcer remains despite treatment)
3) a)Proximal vagotomy- lowest complications, no need for antral or pylorus procedure, 10-15% ulcer recurrence, lowest mortality (0.1%)
b)Truncal vagotomy and pyloroplasty- 5-10% ulcer recurrence, 1% mortality
c) Truncal vagotomy and antrectomy-1-2% ulcer recurrence (lowest rate), 2% mortality
RECONSTRUCTION: Roux-en-Y gastro-jejunostomy is best bc less dumping syndrome and relfux gastritis compared to Billroth I (gastroduodenal anastomosis) and Billroth II (gastrojejunal anastamosis)
49
Duodenal Ulcers- complications
1) MC complication
2) what constitutes major bleeding
3) Rx of duodenal bleed
4) rx of duodenal obstruction 2/2 ulcer
5) rx of perforation
6) Intractability with escalating doses of PPI- next step
1) bleed
2) >6units in 24 hours or pt remains hypotensive despite transfusion
3) EGD- clips, epi, cauterize. If fails-> OR-> duodenotomy and GDA ligation (avoid hitting common bile duct posteriorly); if pt has been on PPI also need acid-reducing surgery
4) PPI and serial dilation 1st. If fails-> antrectomy and truncal vagotomy (best), also get bx to r/o CA
5) Graham patch (omentum over perf) + acid-reducing surgery if pt has been on PPI
6) >3mo PPI without relief based on EGD mucosal findings (not sx)-> acid reducing therapy
50
GASTRIC ULCERS
1) risk factors
2) MC location
3) T/F: hemorrhage is associated with higher mortality than with duodenal ulcers
4) Best test for H. Pylori
5) describe the location and whether it is due to high acid secretion vs. decreased mucosal protection for Type I-V peptic ulcers
6) surgical treatment if indicated
1) older male, tobacco, ETOH, NSAIDs, H. pylori, uremia, stress (burns, sepsis and trauma), steroids, chemotherapy
2) 80% on lesser curvature of the stomach
3) true
4) biopsy with histo examination from antrum. CLO test (rapid urease test)- detects urease released from H. Pylori
5) type I- lesser curve, low along stomach body (decreased mucosal protection)
type II- 2 ulcers (lesser curve and duodenal)- high acid secretion (like duodenal ulcers)
type III- pre-pyloric ulcer- high acid secretion
type IV- lesser curve, high along cardia. decreased mucosal protection.
Type V- ulcer 2/2 NSAIDS
6) truncal vagotomy and antrectomy best (try to include ulcer with resection=extended antrectomy) otherwise separate ulcer excision bc of high risk of gastric CA. omental patch and ligation of bleeding vessels poor options 2/2 high recurrence of sx and risk of gastric CA in ulcer
51
```
Stress gastritis
1) timeframe for occurance
2) rx
Chronic gastritis
3) location of Type A and B
4) which type is associated with pernicious anemia and autoimmune disease
5) which type is associated with H. pylori
6) rx
```
1) 3-10d after event, lesions appear in fundus first
2) PPI
3) Type A is fundus, Type B is antral
4) type A
5) Type B
6) PPI
52
Gastric CA
1) MC location
2) sx
3) risk factors
4) risk of CA with adenomatous polyps and rx
5) what is krukenberg tumor
6) what is Virchow's nodes
1) antrum has 40%
2) pain unrelieved by eating, weight loss
3) adenomatous polyps, tobacco, previous gastric operations, intestinal metaplasia, atrophic gastritis, pernicious anemia, type A blood, nitrosamines
4) 15% risk. Tx- endoscopic resection
5) mets to ovaries
6) mets to supraclavicular node
53
Gastric CA
1) Intestinal-type gastric CA- who gets it and surgical rx
2) diffuse gastric cancer (linitis plastica)-
a- who is at risk
b- spread
c-prognosis compared to intestinal-type gastric CA
d- surgical rx
3) use of chemo and what drugs
4) what is c/i for resection
5) palliative option
1) high-risk populations, older men, japan (rare in US). surgical rx- subtotal gastrectomy (need 10-cm margins)
2) a- low-risk populations, women, MC type in US
b- diffuse lymphatic invasion, no glands
c- less favorable prognosis (25% 5-yr survival)
d- total gastrectomy bc of diffuse nature
3) poor response but can try 5-fu, doxorubicin, mitomycin C
4) metastatic dz outside of area of resection
5) if obstructed-> stent proximal lesions, bypass distal lesions with gastrojejunostomy
if low/moderate bleeding/pain-> XRT
if above fail can consider palliative gastrectomy
54
Gastrointestinal Stromal Tumors (GIST)
1) benign or malignant?
2) US findings
3) Dx- what stain?
4) indications of malignancy
5) rx
1) MC benign gastric neoplasm, although can be malignant
2) hypoechoic with smooth edges
3) bx- C-Kit positive
4) malignant if >5cm or >5mitoses/50HPF
5) rx- resection with 1-cm margins; chemo with imatinib (Gleevec, tyrosine kinase inhibitor) if malignant
55
Mucosa-Associated Lymphoid Tissue Lymphoma (MALT lymphoma)
1) what is it cause by
2) rx
3) MC location
1) H. pylori infection, usually regress after rx
2) H. pylori triple therapy (clarithromycin, amoxicillin and PPI) and surveillance. If doesn't regress, do XRT
3) stomach MC location
56
Gastric Lymphomas
1) MC type
2) Dx
3) rx
4) when is surgery indicated
5) overall 5-yr survival
1) non-Hodgkin's lymphoma (B cell). Stomach is MC location for extranodal lymphoma
2) EGD with bx
3) chemo and XRT.
4) surgery for complications, possibly indicated for stage I disease (tumor confined to stomach mucosa) and then only partial resection is indicated
5) 50%
57
Morbid Obesity
1) what 4 criteria must be met for bariatric surgery
2) bariatric surgery operative mortality
3) what comorbidities get better after surgery
1) -BMI> 40 or >35 with coexisting comorbidities
- failure of nonsurgical methods of weight reduction
- Psychological stability
- Absence of drug and alcohol abuse.
2) 1%
3) DM, HLD, sleep apnea, HTN, urinary incontinence, GERD, venous stasis ulcers, pseudotumor cerebri, joint pain, migrains, depression, polycystic ovarian syndrome, nonalcoholic fatty liver disease
58
Roux-en-Y gastric bypass
1) compare to gastric banding
2) risk factors
3) what other surgery should you consider performing during the operation
4) failure rate due to high carbohydrate snacking
5) Leak: a) signs, b) MC cause, c) dx, d) rx
6) Marginal ulcers a)how many get b) rx
7) rx of stenosis
1) better weight loss
2) marginal ulcers, leak, necrosis, B12 deficiency (intrinsic factor needs acidic environment to bind B12), iron-def anemia (bypasses duodenum where Fe absorbed), gallstones (from rapid weight loss)
3) cholecystectomy if stones present.
4) 10%
5) a) inc RR and HR, abd pain, fever, inc WBC;
b) ischemia; c) UGI; d)if early leak (not contained)-> re-op. if late leek (likely contained)-> perc drain, abx
6) 10%. rx with PPI
7) serial dilation
59
Roux en Y gastric bypass complications
1) dilation of excluded stomach postop
a) symptoms
b) dx
c) rx
2) SBO rx
3) Jejunoilial bypass pts- why don't we do these operations anymore and what should you do if a pt has one
1) a) hiccoughs, large stomach bubble
b) AXR; c) G-tube
2) surgical emergency in these pts 2/2 high risk of small bowel herniation, strangulation, infarction and necrosis. rx- surgical exploration
3) associated with liver cirrhosis, kidney stones and osteoporosis (dec Ca). convert to roux-en-y gastric bypass
60
Postgastrectomy complications
1) Dumping syndrome
a) when does it occur
b) cause
c) describe the 2 phases
d) rx
1) a) after gastrectomy or vagotomy and pyloroplasty
b) rapid entering of carbohydrates into small bowel
c) phase 1: hyperosmotic load-> fluid shift into bowel (hypotension, diarrhea, dizziness)
Phase 2: hypoglycemia from reactive inc in insulin and dec in glucose (rarely occurs)
d) 90% resolve with medical rx and diet changes- small, low-fat, low-carb, high protein meals. no liquids with meals, no lying down after meals, octreotide
-if need surgery can convert Billroth to roux-en-y or inc gastric reservoir (jejunal pouch) or inc emptying time (reversed jejunal loop)
61
Post Gastrectomy complications: Alkaline reflux gastritis
1) sx
2) dx
3) rx including surgical option
1) postprandial epigastric pain associated with N/V. pain not relived with vomiting.
2) evidence of bile reflux into stomach, histo evidence of gastritis
3) PPI, chloestyramine, metoclopramide. surgical options (rarely needed) include conversion of billroth to roux-en-y gastrojejunostomy
62
Postgastrectomy complications: Chronic gastric Atony= Delayed gastric emptying
a) sx
b) dx
c) rx including surgical options
a) N/V, pain, early satiety
b) gastric emptying study
c) metoclopramide (Reglan), prokinetics (erythromycin)
Surgical option is near total gastrectomy with roux en-Y
63
Effect of small gastric remnant
1) sx
2) dx
3) rx including surgical option
1) early satiety (actually want this for gastric bypass patients)
2) EGD
3) small meals or jejunal pouch construction
64
Post Gastrectomy complication: blind loop syndrome
1) what surgeries do you get it with?
2) symptoms
3) cause
4) dx
5) rx
1) Billroth II or Roux-en-Y
2) pain, steatorrhea (bacterial deconjugation of bile), B12 deficiency (bacteria use it up), malabsorption
3) poor motility -> stasis in afferent limb-> bacterial overgrowth (E. Coli, GNRs)
4) EGD of afferent limb with aspirate and culture for organsims
5) tetracycline and flagyl, metoclopramide to improve motility. surgical option: reanastamosis with shorter (40-cm) afferent limb
65
Post Gastrectomy Complication: afferent-loop obstruction
1) what surgeries do you get it with?
2) symptoms
3) cause and which limb is the afferent
4) dx
5) rx
1) Billroth II or Roux-en-Y
2) RUQ pain, steatorrhea, nonbilious vomiting, pain relieved with bilious emesis
3) caused by mechanichal obstruction of afferent limb (the one . risk factors include long afferent limb with billroth II or Roux-en-Y: the limb that carries the bile towards the anastamosis= stomach remnant limb or Y limb of roux en Y)
4) CT scan
5) balloon dilation may be possible. surgical options are reanastomosis with shorter (40cm) afferent limb to relieve obstruction.
66
Post Gastrectomy efferent-loop obstruction
1) which limb is the efferent-limb
2) sx
3) dx
4) rx
1) efferent= exit (limb from the gastrojejunostomy to the jejunojejunostomy anastomosis)
2) N/V/abd pain
3) UGI, EGD
4) balloon dilation. or surgery to identify site of obstruction and relieve it
67
Post-vagotomy diarrhea
1) mechanism
2) rx
1) 2/2 non-conjucated bile salts in the colon-> osmotic diarrhea. Caused by sustained postprandial organized MMCs
2) cholestyramine, octreotide. Or reverses interposition jejunal graft
68
1) treatment of duodenal stump blowout
| 2) PEG complications
1) place lateral duodenostomy tube and drains
| 2) PEG- insert into liver or colon
69
Liver
1) Hepatic artery variants for
a- Right hepatic artery
b- Left hepatic artery
2) falciform ligament- where is it, what embryologic remnant does it carry
3) ligamentum teres location
4) what line separates R and L liver lobes
1) a- right hepatic artery off SMA (#1 variant) courses behind pancreas, posterolateral to CBD
b-left hepatic artery off left gastric artery (~20%)- found in gastrohepatic ligament medially
2) separates medial and lateral segments of the left lobe. attaches to anterior abdominal wall, extends to umbilicus and carries remnant of umbilical vein
3) carries the obliterated umbilical vein to the undersurface of the liver, extends from the falciform ligament
4) draw line from middle of gallbladder fossa to IVC (portal fissure or Cantlie's line)
70
1) What is Glisson's capsule?
2) where is Bare area on liver that doesn't have capsule?
3) where does the portal triad enter the liver
4) under which segments does the gallbladder lie
1) peritoneum that covers liver
2) posterior-superior surface
3 and 4) Segments IV and V
71
1) What are Kupffer cells
2) What makes up the portal triad and where do they lie in relation to each other (ie- posterior, lateral, etc)? What do they come together into
3) what is the Pringle maneuver and what type of bleeding doesn't it stop
4) Foramen of winslow is the entrance into what space? Define the anterior posterior inferior and superior boundaries
1) liver macrophages
2) Common Bile duct (lateral), portal vein (posterior) and proper hepatic artery (medial) all come together in the hepatoduodenal ligament (porta hepatis)
3) porta hepatis clamping. doesn't stop hepatic vein bleeding
4) entrance into lesser sac.
- Anterior-Portal triad
- Posterior- IVC
- Inferior- duodenum
- superior-liver
72
1) what 2 veins make up the portal vein
2) how many portal veins are in the liver? how much (%) of blood flow does it provide to the liver?
3) segments supplied by left vs right protal vein
4) what is the arterial blood supply to the liver?
5) where does the middle hepatic artery MC a branch of?
6) what are most primary and secondary liver tumors supplied by?
7) what are the hepatic veins and where do they drain?
1) superior mesenteric vein joins splenic vein (no valves) and inferior mesenteric vein enters splenic vein
2) 2 in liver. provides 2/3 of hepatic blood flow
3) Left- seg II, III, IV; Right- seg V, VI, VII, VIII
4) right, left and middle hepatic arteries, follows the hepatic vein system below.
5) left hepatic artery
6) hepatic artery
7) left hepatic vein (seg II, III, superior IV), middle hep vein (seg V and inferior IV), right (VI, VII, VIII)
73
1) what does the middle hepatic vein branch off of?
2) what does the accessory right hepatic vein drain
3) where do the inferior phrenic veins drain
4) caudate lobe arterial and venous supply
1) comes off left hepatic vein in 80% before going into IVC, other 20% goes directly into IVC
2) medial aspect of right lobe directly to IVC
3) directly into IVC
4) receives separate right and left portal and arterial blood flow. drains directly into IVC via separate hepatic veins
74
1) where is alkaline phosphatase located
2) where does nutrient uptake occur in the liver
3) what is the usual energy source for the liver and how is it obtained
4) where is glucose stored and in what form? what happens to excess glucose
5) where is urea synthesized
1) canicular membrane
2) sinusoidal membrane
3) ketones
4) it is converted to glycogen and stored in the liver. excess converted to fat
5) liver
75
1) what transcription factors are not made in the liver
2) what types of vitamins does the liver store
3) what are the MC problems associated with hepatic resection
4) which hepatocytes are most sensitive to ischemia
5) how much of liver can you safely resect
1) vWF and VIII (made in endothelium)
2) fat-soluble vitamins. B12 is the only water-soluble vitamin stored in the liver
3) bleeding and bile leak
4) central lobular (acinar zone III)
5) 75%
76
Bilirubin
1) breakdown product of? (chain of breakdown to it)
2) what is it conjugated to in the liver and effect of conjugation
3) where does breakdown of conjugated bilirubin occur? and what breaks it down?
4) what happens to free bilirubin in the intestine?
5) what turns urine dark like cocacola?
1) hemoglobin (Hgb-> heme-> biliverdin-> bilirubin)
2) glucuronic acid (glucuronyl transferase)-> improves water solubility-> actively secreted into bile
3) broken down in terminal ileum by bacteria
4) reabsorbed, converted to urobilinogen and released into urine as urobilin (yellow color)
5) excess urobilinogen
77
Bile
1) what comprises bile?
2) what are bile salts/acids made of?
3) what are bile salts conjugated to?
4) a) primary bile acids (salts)
b) secondary bile acids (salts)
5) what is main biliary phospholipid
6) role of Bile
1) bile salts (85%), proteins, phospholipids (lecithin), cholesterol, and bilirubin
2) cholesterol
3) taurine or glycine (improves water solubility)
4) a- cholic and chenodeoxycholic
b-deoxycholic and lithocholic (dehydroxylated primary bile acids by bacteria in gut)
5) lecithin
6) solubilizes cholesterol and emulsifies fats in the intestine, forming micelles which enter enterocytes by fusing with membrane
78
Jaundice
1) at what level of bili does it occur
2) first place it is evidence
3) maximum bilirubin is 30 unless patient has what?
4) causes of elevated un-conjugated bili
5) causes of elevated
1) >2.5
2) under tongue
3) underlying renal disease, hemolysis or bile duct-hepatic vein fistula
4) prehepatic causes (hemolysis, hepatic deficiencies of uptake or conjugation
5) secretion defects into bile ducts, excretion defects into GI tract (stones, strictures, tumor
79
Hyperbilirubinemia Syndromes- what is the defect and have type of bili is high in the following:
1) Gilbert's disease
2) Crigler-Najjar disease
3) Physiologic jaundice of newborn
4) Rotor's syndrome
5) Dubin-Johnson Syndrome
1) high unconjugated bili. Defect in glycuronyl transferase
2) high unconjugated bili. inability to conjugate 2/2 severe deficiency of glucuronyl transferase (Life-threatening dz)
3) high unconjugated bili. immature glucuronyl transferase
4) high conjugated bili (deficiency in storage ability)
5) high conjugated bili. Deficiency in secretion ability
80
Viral hepatitis
1) which hepatitis viral agents can cause acute hepatitis
2) which types can cause fulminant hepatic failure
3) which types can cause chronic hepatitis and hepatoma (HCC)
4) which type rarely has serious consequences
5) which type is not an RNA virus
6) which type is a cofactor for hepatitis B/worsens prognosis?
7) which type causes fulminant hepatic failure in pregnancy
8) which can have long incubation period and is MC viral cause for liver txpt
9) FOr hep B- what Ab is elevated in first 6 months? then what takes over?
10) what are the antibody profiles for
a) pt with HBV vaccination, never infected
b) pt with h/o HBV infection, recovery and subsequent immunity
1) all
2) Hep B, D, and E more common
3) HBV and HCV and Hep D
4) Hep A
5) HBV (DNA)
6) Hep D
7) Hep E
8) HCV
9) Anti-HBcore-IgM. then IgG takes over
10) a-Pt will have Anti-HBsurface-IgG only
b- Anti-HBcore-IgG, Anti-HBsurface IgG. No HB surface antigens
81
Liver failure
1) MCC
2) best indicator of synthetic fnc in pt with cirrhosis
3) mortality and rx of acute liver failure
1) cirrhosis (palpable liver, jaundice, ascites)
2) prothrombin time (PT)
3) 80% mortality. consider urgent liver txplt if King's College criteria met
82
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What are King's College Criteria of Poor Prognostic Indicators for
1) Acetaninophen-Induced ALF (acute liver failure)
a-pH
b-INR
c-Creatinine
d-encephalopathy grade
2) Non-Acetaminophen-Induced ALF
a-INR
b-or 3 of which other factors
```
1) a- Arterial pH6.5, Cr>3.4 mg/dL, grade III/IV encephalopathy
2) a-INR>6.5 or and 3 of the following:
b- age 40, drug toxicity or undetermined etiology, jaundice>7 days before encephalopathy, INR>3.5 bili>17mg/dL
83
Hepatic encephalopathy
1) mechanism of liver failure as a cause
2) other causes
3) treatment
4) what type of food should you limit
5) role of abx
6) role of Neomycin and rifaximine
1) lier can't metabolize-> build up of ammonia, mercantanes and false neurotransmitters
2) GI bleed, infection (SBP), electrolyte imbalance
3) lactulose- cathartic that gets rid of bacteria in gut and acidifies colon (preventing NH3 uptake by converting it to ammonium). titrate to 2-3BM/day
4) limit protein intake. Branched-chain amino acids are metabolized by skeletal muscle and may help
5) only give if infectious source
6) get rid of ammonia-producing bacteria from gut
84
Mechanism of cirrhosis
hepatocyte destruction-> fibrosis and scarring of liver-> increased hepatic pressure-> portal venous congestion-> lymphatic overload-> leaking of splanchnic and hepatic lymph into peritoneum-> ascites
85
Ascites treatment
1) conservative treatment
2) paracentesis for ascites- what should you replace with and ratio for replacement
3) surgical treatment
1) water restriction 1.5-1L/day, decreased NaCl intake, diuretics (spironolactone counteracts hyperaldosteronism seen with liver failure)
2) replace with albumin 1g for every 100cc removed
3) TIPS
86
Sontaneous Bacterial Peritonitis
1) when to use prophylactic abx to prevent
2) what abx for ppx
3) symptoms and lab findings
4) MC pathogens
5) risk factors
6) treatment
1) if previous SBP or current UGI bleed
2) norfloxacin
3) fever, abd pain, PMNs> 250 in fluid, positive cultures
4) E.Coli (#1), pneumococci, streptococci. MC monoorganism. if not, worry about bowel perf
5) prior SBP, UGI bleed (Variceal hemorrhage), low-protein ascites
6) 3rd gen cephalosporin. pt's usually respond within 48 hours
87
Why is aldosterone elevated with liver failure
2/2 impaired hepatic metabolism and impaired GFR
88
Hepatorenal syndrome
1) lab findings
2) treatment
1) same lab findings as prerenal azotemia (progressive renal failure)
2) no good therapy other than liver txplt. Stop diuretics, give volume.
89
what is asterixis
neuro change in liver failure, sign that liver failure is progressing
90
Postpartum liver failure with ascites
1) cause
2) dx
3) rx
1) from hepatic vein thrombosis, has an infectious component
2) SMA arteriogram with venous phase contrast
3) heparin and abx
91
Esophageal varices
1) treatment of bleed
2) role of propranolol
3) treatment of refractory variceal bleeding
1) banding and sclerotherapy (95% effective), Vasopressin (splanchnic artery constriction) and octreotide (decreased portal pressure by decreased blood flow) can be used to temporize
2) can help prevent re-bleed. no role in acute bleed
3) TIPS
92
Portal HTN
1) causes of presinusoidal obstruction
2) causes of sinusoidal obstruction
3) causes of post-sinusoidal obstruction
4) normal portal vein pressure
5) what veins serve as collaterals bw the portal vein and the systemic venous system of the lower esophagus (azygous vein)
1) schistosomiasis, congential hepatic fibrosis, portal vein thrombosis (50% of portal HTN in children)
2) cirrhosis
3) Budd-CHiari syndrome (hepatic vein occlusive dz), constrictive pericarditis, CHF
4) 12 mmHg
5) coronary veins
93
TIPS
1) indications
2) end-result
3) mechanism of procedure
4) complications
1) protracted bleeding, progression of coagulopathy, visceral hypoperfusion or refractory ascites
2) allows anterograde flow
3) catheter passed into hepatic vein via jugular vein and expandable metal stent placed from hepatic vein through the liver tissue into a major portal vein branch
4) dev't of encephalopathy
94
Plenorenal shunt
1) when can you use it/indications
2) contraindications
3) what veins do you ligate
4) risks and benefits
1) Child's A Cirrhotics who present with just bleeding (rarely used anymore). Childs B and C must get TIPS.
2) pts with refractory ascites (can worsen ascites)
3) left adrenal, left gonadal, inferior mesenteric and coronary veins and pancreatic branches of splenic vein
4) less risk of encephalopathy but worsens ascites
95
Child-Pugh Score in Liver failure
1) what does it correlate with?
2) components and how to determine class
1) mortality after open shunt placement. A=2% mortality; b=10% mortality with shunt, c= 50% mortality
2) Albumin, Bilirubin, encephalopathy, ascites, INR (1-3 pts for each). A is 5-6 pts. B is 7-9 pts, C is 10+ pts
96
Portal HTN in kids
1) MCC
2) T/F: it is the MCC of massive hematemesis in children
1) extra-hepatic portal vein thrombosis
| 2) true
97
Budd-Chiari syndrome
1) what is occluded?
2) symptoms
3) dx
4) rx
1) hepatic veins or IVC
2) RUQ pain, hepatosplenomegaly, ascites, fulminant hepatic failure, muscle wasting and variceal bleeding.
3) angiogram with venous phase, CT angio; liver bx shows sinusoidal dilatation, congestion and centrilobular congestion
4) porta-caval sunt (needs to connect to IVC above obstruction
98
Splenic Vein thrombosis
1) type of varices seen
2) MCC
3) tx
1) isolated gastric varices without elevation of pressure in the rest of the portal system
2) pancreatitis
3) if bleed-> do splenectomy
99
```
Liver Abscesses
1) Amebic
a-where is primary infection and how does it get to liver
b- signs of liver infection (sx and labs)
c- risk factors
d-MC associated infection
e- abscess culture results
f-dx
g-rx
```
1) a-colon (amebic colitis)-> reaches liver via portal vein
b-F/C/RUQ pain/jaundice/increase in R lobe of liver, inc LFTs, inc WBCs
c-travel to mexico, ETOH, fecal-oral transmission
d-Entamoeba histolytica (90% have infection)
e- often sterile, only peripheral rim has protozoa
f- CT characteristics
g- Flagyl. Aspirate only if refractory; surgery only if free rupture.
100
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Liver abscesses
2)Hydatid cyst
a-infectious agent
b- who are carriers, who exposes humans
c- when should you aspirate it
d- CT findings
e- other diagnostic tests
f- when do you need pre-op ERCP
g-treatment
```
1)a-Echinococcus
b-sheep are carriers, dogs expose humans
c- never! can leak and cause anaphylactic shock
d- ectocyst (calcified) and endocyst (double-walled)
e- Positive Casoni skin test, positive Echinococcus serology
f- jaundice, inc LFTs or cholangitis to check for communication with the biliary system
g- pre-op albendazole for 2 weeks then surgical removal (intra-op can inject cyst with alcohol to kill organisms and then aspirate out), need to remove all of cyst wall and don't spill contents!
101
```
Liver Abscesses
1) Schistosomiasis
a) signs/sx
b- site of primary infection
c- rx
```
1) a-maculopapular rash, inc eosinophils, can cause variceal bleeding, petechiae, ulcers and fine granulation tissue in sigmoid colon (primary infection site=b)
c-Praziquantel and control of variceal bleeding
102
```
Liver abscesses
1) Pyogenic abscess
a- T/F: 2nd most common abscess
b- sx
c- #1 organism/cause
d- dx
e- rx
```
1) False. MC (80% of all abscesses)
b-F/C/weight loss, RUQ pain, inc LFTs, Inc WBCs, sepsis, inc in R lobe
c- E. Coli, MC 2/2 to contiguous infection from biliary tract. Can occur following bacteremia from diverticulitis or appendicitis
d- aspiration
e-CT-guided drainage and abx. Surgeical drainage if unstable and cont signs of sepsis
103
```
Liver Tumors
1) Hepatic adnomas
a- risk factors
b- sx/risks
c- malignant or benign
d- MC side of liver
e- sx
f-dx
g-rx
```
1) a- women, steroid use, OCPs
b- 20% risk of significant bleed, 80% of symptomatic.
c- Benign but Can become malignant
d- Right
e- pain, inc LFTs, dec BP (from rupture), palpable mass
f-no Kupffer cells in adenomas-> no uptake on sulfur colloid scan (cold)
g- if asx- stop OCPs. if no regression, need surgery
if sx- tumore resection for bleeding and malignancy risk. embolization if multiple and unresectable
104
```
Liver TUmors
2) Focal nodular hyperplasia
a- characteristic appearance
b- malignant or benign
c-dx
d-rx
```
2) a- central stellate scar
b- benign, no malig potential
c- abdominal CT. Has kupffer cells so will take up sulfur colloid on liver scar. MRI/CT show hypervascular tumor
d- no resection. conservative
105
Liver TUmor
1) MC benign hepatic tumor
2) MC malignant hepatic tumor
3) MC cancer world-wide
1) hemangioma
2) mets 20:1 primary
3) hepatocellular CA
106
```
Liver tumor
1) Hemangima
a- MC sex
b- dx
c-rx
d- rare complication
```
1) a- females
b- MRI and CT show peripheral to central enhancement
c- conservative unless symptomatic, then surgery + or - preop embolization
d- consumptive coagulopathy (Kasabach-Merritt syndrome) and CHF. usually seen in kids
107
Liver Tumors
1) solitary cysts
a- who gets them and where
b- rx
1) a- congenital, women, right lobe, walls have charactersitic thickened blue hugh
b- nothing
108
Hepatocellular CA (hepatoma)
1) risk factors
2) T/F: Pt's with primary biliary cirrhosis and Wilson's disease are at higher risk of getting HCC
3) what 3 types have the best prognosis
4) what hormone level do you check for
5) 5-year survival with resection
1) #1 is Hep B, Hep C, ETOH, hemochromatosis, alpha-1-antitrypsin deficiency, primary sclerosing cholangitis, aflatoxins, hepatic adenoma, steroids, pesticides
2) FALSE- they aren't risk factors
3) Clear cell, lymphocyte infiltrative and fibrolamellar types
4) AFP, correlates with tumor size
5) 30%
109
1) risk factors for Hepatic Sarcoma and prognosis
2) tx of isolated colon CA mets to liver
3) diff in vascularity of primary vs metastatic liver tumors
1) PVC, Thorotrast, arsenic-> rapidly fatal
2) resect if can leave enough liver for the patient to survive. 35% 5-year survival rate after resection for cure.
3) primary tumors are hypervascular. Mets are hypovascular
110
Biliary system
1) triangle of Calot- borders and what is found inside
2) arterial supply to hepatic and common bile duct and their location for consideration in ERCP
3) where do cystic veins drain
4) where are lymphatics located
5) where do parasympathetic fibers come from?
6) sympathetic fibers?
1) lateral- cystic duct, medial CBD, superior-liver. cystic artery (branches off R hepatic) is found here
2) RIght hepatic (lateral) and retroduodenal branches of gastroduodenal artery (medial) at 9- and 3-o'clock position so make ERCP spincterotomy at 11-o'clock.
3) right branch of portal vein
4) right side of CBD
5) left (anterior) trunk of vagus
6) T7-T10 *splanchnic and celiac ganglions
111
Biliary system
1) type of cells in gallbladder mucosa
2) type of cells in gallbladder submucosa
3) T/F: CBD and common hepatic duct have no peristalsis
4) How does gallbladder fill?
a- what contracts sphincter
b-what relaxes it?
1) columnar epithelium
2) none- no submucosa
3) true
4) contraction of sphincter of oddi at the ampulla of Vater
a- morphine
b- Glucagon
112
Normal size of
1) Common bile duct b4 and after chole
2) Gallbladder wall
3) pancreatic duct
1) b4: <4mm
113
1) effect of cholecystectomy on total bile salt pools
2) where are highest [ ] of CCK and secretin cells
3) What are Rokitansky-Aschoff sinuses
4) where are ducts of luschka
1) decreased total bile salt pools
2) duodenum
3) epithelial invaginations in the gallbladder wall, formed from increased gallbladder pressure
4) in gallbladder fossa, can leak after cholecystectomy
114
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1) Bile excretion:
a- what increases excretion
b- what decreases excretion
2) What causes gallbladder contraction
3) what are the essential functions of bile
4) function of gallbladder
```
1) a- CCK, secretin, and vagal input
b- somatostatin, sympathetic stimulation
2) CCK causes constant, steady, tonic contraction
3) fat soluble vitamin absorption, essential fat absorption, bilirubin and cholesterol excretion
4) forms concentrated bile by active resorption of NaCl and water
115
1) Where does active resorption of conjugated bile salts occur
2) where does passive resorption of nonconjugated bile salts occur
3) when is postprandial gallbladder emptying maximum
4) what cells secrete bile
5) what is responisble for the color of bile
6) what is the breakdown product of conjugated bili in gut that gives stool brown color?
7) what gives urine its yellow color?
1) terminal ileum (50%)
2) small intestine (45%) and colon (5%)
3) at 2 hours (80%)
4) hepatocytes and bile canalicular cells
5) 2/2 conjugated bili
6) stercobilin
7) urobilinogen (coverted form of resorbed conjugated bili breakdown products)
116
1) what is the rate limiting step in cholesterol synthesis and what is the chain of events for bile salt synthesis
2) what % of gallstones are radiopaque
3) what % of the population has stones
1) HMG CoA resuctase is RLS in cholesterol synth;
HMG CoA-> (HMG CoA reductase)-> cholesterol-> 7-alpha-hydroxylase)-> bile salts (acids)
2) 10%
3) 10%
117
1) what type of stones are most common worldwide
2) what is MC type of stone in US
3)a- what are nonpigmented stones made of
b- causes of nonpigmented stones
c-where they are found
4) 3 types of pigmented stones
1) pigmented stones
2) nonpigmented (cholesterol) stones
3) a-cholesterol; b- stasis, calcium nucleation and increased water reabsorpiton from GB, also caused by decreased lecithin and bile salts; c- almost exclusively in GB
4) calcium bilirubinate stones, black stones (hemolysis, cirrhosis), brown stones (primary CBD stones)
118
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Pigmented stones
1) Calcium bilirubinate stones- cause
2) Black stones
a-cause
b- factors for develpment
c-where they form
d- rx
3) Brown stones
a- who gets them and where
b- cause (MC)
c- what else should you check for in patients with these stones
d- rx
```
1) caused by solubilization of unconjugated bilirubin with precipitation
2) a-hemolytic d/o, cirrhosis, ileal resection (loss of bile salts)
b- increased bili load, decreased hepatic function, and bile stasis-> get calcium bilirubinate stones
c-gallbladder
d-chole if sx
3)a-Asians, primary CBD stones, formed in ducts
b- Infection (E. Coli) produces beta-glucuronidase which deconjugates bili-> formation of calcium bilirubinate
c-ampullary stenosis, duodenal diverticula, abnl sphincter of oddi
d- biliary drainage procedure (ie- sphincteroplasty)
119
Cholecystitis
1) etiology
2) what labs are elevated
3) def of suppurative cholecystitis
4) MC organsim
5) US findings
6) what can you get if US unclear to further dilineate
7) HIDA results that indicate cholecystectomy after CCK-CS test
1) obstruction of cystic duct by a gallstone
2) Alk phos and WBCs
3) frank purulence in the gallbladder-> can be associated with sepsis and shock
4) E. Coli (#1), Klebsiella, Enterococcus
5) stones- hyperechoic focus, posterior shadowing, movement of focus with change in posn. acute cholecystitis- gallstones, gallbladder wall thickening >4mm, pericholecystic fluid
6) HIDA- technetium taken up by liver and excreted in biliary tract. can use CCK choleschintigraphy with it to detect cholecystitis (shows contraction)
7) gallbladder not seen (stone in cystic duct), takes >60 minutes to empty (chronic cholecysitis), EF
120
1) risk factors for gallstones
2) best initial evaluation test for jaundice or RUQ pain
3) Indications for immediate ERCP
4) indications for pre-op ERCP
5) what % of pts underging cholecystectomy will have a retained CBD stone
1) Age >40, female, obese, pregnant, rapid weight loss, vagotomy, TPN and ileal resection (pigmented stones)
2) Ultrasound
3) signs that CBD stone is present- jaundice, cholangitis, US shows stone in CBD.
4) if any of the following are persistently high for >24hours- AST or ALT >200, bilirubin>4, or amylase or lipase >1000
5)
121
1) rx for cholecystitis
a- in otherwise healthy pt
b- in pt who are v ill and can't tolerate surgery
2) best rx for late common bile duct stone
3) ERCP risks
1) a-cholecystectomy
b- cholecystostomy tube
2) ERCP with sphincterotomy
3) bleeding, pancreatitis, perforation
122
1) causes of air in biliary system
2) MC route for bacterial infection of bile
3) highest incidence of positive bile cx occurs with what?
1) previous ERCP and sphincterotomy (MC), cholangitis or erosion of the biliary system into the duodenum (ie-gallstone ileus)
2) dissemination from portal system (NOT retrograde through sphincter of oddi)
3) postop strictures (usually E. coli, polymicrobial)
123
Acalculous cholecystis
1) MC precipitating event
2) primary pathology
3) US findings
4) HIDA findings
5) rx
1) after severe burns, prolonged TPN, trauma or major surgery
2) bile stasis (narcotics, fasting), leading to distention and ischemia. Also have inc viscosity 2/2 dehydration, ileus and transfusion
3) sludge, GB wall thickening, and pericholecystic fluid
4) positive HIDA
5) cholecystectomy, perc drainage if too unstable
124
Emphysematous gallbladder disease
1) MC infectious source
2) what comorbidity increases risk
3) sx
4) rx
1) clostridia perfringens
2) DM
3) severe, rapid-onset abdominal pain, nausea, vomiting and sepsis. Can see gas in GB wall on XR
4) emergent cholecystectomy or perc drainage if pt too unstable
125
Gallstone Ileus
1) pathophysiology
2) XR findings
3) MC site of obstruction
4) rx
1) fistula bw GB and duodenum that releases stone, causing small bowel obstruction. seen in elderly
2) air in biliary system- pneumobilia
3) terminal ileum
4) remove stone through enterotomy proximal to obstruction. cholecystectomy and fistula resection if pt can tolerate (if old and frail, leave fistula)
126
CBD injury- intraop injury-type of repair based on size of injury
if <50% can likely do primary repair. if more will need hepaticojejunostomy or choledochojejunostomy
127
Workup of persistent N/V or jaundice following lap chole
| -management of bile leak
get US to look for fluid collection.
- if present, may be bile leak-> perc drain into collection. If bilious, get ERCP-> sphincterotomy and stent if 2/2 cystic duct remnant leak, small injuries to hepatic or CBD or duct of luschka. larger lesions need hepaticojejunostomy or choledochojejunostomy
- if not present and hepatic ducts dilated-> complete CBD transection-> initial manatement with PTC tube, then:
- hepaticojejunostomy for lesions with early sx 7d
128
Management of sepsis following lap chole
fluid resusctation and stabilize. Get US to look for dilated intrahepatic ducts or fluid collections. May be 2/2 complete transection of the CBP and cholangitis
129
Management of anastamotic leak following transplantation or hepaticojejunostomy for bile leak
perc drainage of fluid collection followed by ERCP with temporary stent (leak will heal)
130
Bile duct strictures
1) MC cause
2) other causes
3) sx
4) Dx
5) rx
1) Ischemia following lap chole
2) chronic pancreatitis, gallbladder CA, bile duct CA
3) sepsis, cholangitis, jaundice
4) MRCP (magnetic resonance cholangiopancreatography) defines anatomy and looks for mass-> if CA not ruled out need ERCP with brush biopsies
5) if 2/2 ischemia or chronic pancreatitis-> choledochojejunostomy
if CA- appropriate wu for CA
131
hemobilia
1) cause
2) sx/presentation
3) dx
4) rx
1) MC with trauma or percutaneous instrumentation to liver (ie- PTC tube) -> fistula bw bile duct and hepatic arterial system (MC)
2) UGI bleed, jaundice and RUQ pain
3) angiogram
4) angioembolization, operation if that fails
132
1) MC CA of biliary tract
1) gallbladder CA
133
Gallbladder adenocarcinoma
1) MC site of mets
2) porcelain gallbladder rx
3) 1st nodes for spread
4) 1st areas for direct spread
5) sx
6) rx
7) prognosis
1) liver
2) cholecystectomy bc 15% CA
3) cystic duct nodes (right side)
4) liver seg IV and V
5) jaundice 1st (bile duct invasion with obstruction) then RUQ pain
6) If no muscle involved-> cholecystectomy
if in muscle but not beyond-> wedge resection of seg IVb and V
if beyond muscle but resectable-> formal resection of seg IVb and V
*laparoscopic approach contraindicated for GB CA
7) 5% overall 5-yr survival
134
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Cholangiocarcinoma (bile duct CA)
1) risk factors
2) sx
3) labs
4) Dx
5) rx
a-c) 3 types/areas and rx for each
6) prognosis
```
1) elderly, males, C. Sinensis infection, ulcerative colitis, choledochal cysts, primary sclerosing cholangitis, chronic bile duct infection
2) early- painless jaundice; late- weight loss, pruritis
3) inc bili and alk phos
4) MRCP to define anatomy and look for mass
5) consider surgery if no distant mets and tumor resectable.
a- upper 1/3 (Klatskin tumor)- MC, worse prognosis, usually unresetable but can try lobectomy and stenting of c/l bile duct if localized to 1 lobe
b- middle 1/3=> hepaticojejunostomy
c- lower 1/3=> whipple
6) 20% 5-yr survival
135
Choledochal cysts
1) who gets them
2) what % are extrahepatic
3) CA risk
4) symptoms
5) cause
6) MC type
7) rx
8) where are type IV cysts? what about type V?
1) asian, females
2) 90%
3) 15% cholangiocarcinoma risk
4) older pts- episodic pain, fever, jaundice, cholangitis. infants- biliary atresia like sx
5) abnormal reflux of pancreatic enzymes during uterine development
6) type I- fusiform or saccular dilatation of extrahepatic ducts (v. dilated)
7) cyst excision with hepatico jejunostomy and cholecystectomy usual
8) Type IV- partially intrahepatic. V-totally intrahepatic. (need partial liver resection or TXP)
136
Primary Sclerosing Cholangitis
1) who gets it
2) associated diseases
3) sx
4) pathophysiology
5) complications
6) rx
7) does it get better after colon rsxn in Crohn's pts?
1) Men in 4th-5th decade
2) ulcerative colitis, pancreatitis, DM
3) jaundice, fatigue, pruritis (from bile acids), weight loss, RUQ pain
4) get multiple strictures in hepatic ducts-> portal HTN and hepatic failure 2/2 progressive fibrosis of intrahepatic and extrahepatic ducts
5) cirrhosis, cholangiocarcinoma
6) liver TXP long term, PTC tube drainage, choledochojejunostomy or balloon dilatation of dominant strictures may relieve sx. Cholestyramine can decrease pruritis (dec bile acids). UDCA (ursodeoxycholic acid) can dec sx (dec bile acids) and improve liver enzymes.
7) no, doesn't get better
137
Primary Biliary Cirrhosis
1) who gets it
2) pathophysiology
3) symptoms
4) what lab test should you check for (Ab test)
5) CA risk
6) rx
1) women, medium-sized hepatic ducts
2) cholestasis-> cirrhosis-> portal HTN
3) jaundice, fatigue, pruritus, xanthomas
4) antimicrobial Ab
5) no CA risk
6) liver TXP
138
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Cholangitis
1) cause
2_ Charcot's triad
3) Reynold's pentad
4) MC organisms
5) At what pressure does colovenous reflux occur and what is the result?
6) Dx
7) late complications of cholangitis
8) rx
```
1) obstruction of bile duct: stone, indwelling tube, stricture, neoplasm, choledochal cysts, duodenal diverticula
2) fever, RUQ pain, Jaundice
3) Charcot's + AMS and shock (suggests sepsis)
4) E. Coli #1, and Klebsiella
5) >200mmHg-> systemic bacteremia
6) inc AST/ALT/bili/Alk Phos and WBCs. US-dilated CBD if 2/2 obstruction
7) stricture and hepatic abscess. renal failure is #1 erious complication related to sepsis
8) IVF and abx initially. Emergent ERCP with sphincterotomy and stone extraction. If this fails, place PTC tube to decompress the biliary system
- if due to infected PTC tube, change the PTC tube.
139
Causes of shock following lap chole
1) within 1st 24hrs
2) after 1st 24hrs
1) hemorrhagic shock from clip that fell off cystic artery
| 2) septic shock from accidental clip on CBD with subsequent cholangitis
140
adenomyomatosis
1) what is it
2) rx
1) thickened nodule of mucosa and muscle associated with Rokitansky-Aschoff sinus. Not premalignant. Doesn't cause stones, can cause RUQ pain
2) cholecystectomy
141
Granular cell myoblastoma
1) benign or malignant
2) sx
3) rx
1) benign neurectoderm tumor of gallbladder
2) can occur in biliary tract with signs of cholecystitis
3) cholecystectomy
142
1) Cholesterolosis- what is it
2) Gallbladder polyps- which are concerning for malignancy and rx
3) effect of ceftriaxone on GB
4) what is delta bilirubin's t1/2
1) speckled cholesterol deposits on GB
2) >1cm concerning for malignancy. Also more likely to be malignant in pts>60yo. rx-chole
3) can cause GB sludging and cholestatic jaundice
4) bound to albumin covalently, T1/2 18days, may take a while to clear after long-standing jaundice
143
1) Mirizzi Syndrome- what is it, causes and treatment
| 2) indications for asymptomatic cholecystectomy
1) compression of the common hepatic duct by 1) a stone in the gallbladder infundibulum or 2) inflammation from GB or cystic duct extending to the contiguous hepatic duct-> hepatic duct stricture. rx- cholecystectomy. may need hepaticojejunostomy if stricture
2) liver TXP or gastric bypass (if stones are present)
144
1) relation of superior mesenteric vein and superior mesenteric artery
2) what is the kocher maneuver?
3) where is the uncinate process of the pancreas
4) where do the SMV and SMA lay in relation to the pancreas
5) where does the portal vein run in relation to the pancreas
1) SMV is anterior to SMA
2) Mobilization of the duodenum to expose head of the pancreas over IVC over Aorta
3) rests on aorta, behind SMV
4) behind the neck of the pancreas
5) forms from the SMV and splenic vein behind the neck of the pancreas
145
Pancreatic Blood Supply
1) to the head of pancreas
2) to body of pancreas
3) to tail of pancreas
1) superior (off GDA) and inferior (off SMA) pancreaticoduodenal arteries (anterior and posterior branches for each)
2) great, inferior and caudal pancreatic arteries off of the splenic artery
3) splenic, gastroepiploic and dorsal pancreatic arteries
146
Pancreas
1) venous drainage to where?
2) what nodes does the lymph drain to?
3) what do pancreatic ductal cells secrete?
4) what do pancreatic acinar cells secrete?
1) portal system
2) celiac and SMA nodes
3) secrete HCO3- solution (have carbonic anhydrase)
4) secrete digestive enzymes
147
Exocrine function of the pancreas
1) what enzymes are secreted
2) what is the only pancreatic enzyme secreted in active form
1) amylase, lipase, trypsinogen, chymotrypsinogen, carboxypeptidase, HCO3-
2) amylase- hydrolyzes alpha 1-4 linkages of glucose chains
148
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Endocrine function of the pancreas
1) what cells produce:
a- glucagon
b-insulin
c-somatostatin
d- pancreatic polypeptide
e- vasoactive intestinal peptide (VIP) and serotonin
2) which cells receive the majority of blood supply related to size
```
```
1) a- Alpha cells
b- Beta cells (at center of islets)
c- Delta cells
d- PP or F cells
e- Islet cells
2) islet cells, then goes to acinar cells
```
149
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1) Enterokinase
a- where is it released
b- action
2) action of Trypsin
3) action of secretin (and where is it released)
4) of CCK (and where is it released)
5) of acetylcholine
6) of somatostatin
7) of glucagons
```
1) a- duodenum
b- activates trypsinogen to trypsin
2) activates other pancreatic enzymes including trypsinogen
3) inc HCO3- mostly (duodenum)
4) inc pancreatic enzymes mostly (duodenum)
5) inc HCO- and enzymes
6,7) inhibits exocrine fnc
150
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Embryology of Pancreas
1) Ventral pancreatic bud
a- what duct is it connected to
b- path of migration
c- what parts of pancreas does it form
2) Dorsal pancreatic bud
a- what parts of pancreas does it form
b- what duct does it contain
3) Duct of wirsung- what does it merge with
4) Duct of santorini- what does it drain into
```
1) a- duct of wirsung
b- migrates posteriorly to the right and clockwise to fuse with dorsal bud
c- uncinate and inferior portion of the head
2) a- body, tail and superior aspect of the pancreatic head
b- duct of Santorini
3) merges with CBD before draining into duodenum
4) small accessory pancreatic duct that drains directly into the duodenum
151
Annular pancreas
1) embryologic abnormality
2) appearance on XR
3) symptoms
4) associated syndrome
5) treatment
1) forms from the ventral pancreatic bud from failure of clockwise rotation-> 2nd portion of duodenum trapped in pancreatic band
2) double-bubble on AXR
3) pancreatic obstruction- N/V, abd pain
4) duodenojejunostomy or duodenoduodenostomy, possible sphincteroplasty (Don't resect the pancreas!)
152
Pancreas Divisum
1) embryologic abnormality
2) sx
3) Dx
4) rx
1, 2) failed fusion of the pancreatic ducts-> can get pancreatitis from duct of Santorini (accessory duct) stenosis
3) ERCP- minor papilla will show long and large duct of santorini; major papilla will show short duct of wirsung
4) ERCP with sphincteroplasty. open sphincterotomy if that fails
153
Heterotopic pancreas
1) MC location
2) sx
3) rx
1) in duodenum
2) usually asx
3) only if sx, resect
154
Pancreatitis
1) causes
2) mortality for a- pancreatitis; b- hemorrhagic pancreatitis
3) Diagnostic workup required
4) rx
5) what pain medication to avoid and why
1) ETOH and gallstones (MC); others- ERCP, trauma, hyperlipidemia, hypercalcemia, viral infection, meds (azathiprine, furosemide, steroids, cimetidine, lamivudine)
* gallstones obstruct ampula-> impaired extrusion of zymogen granules and activation of degraded enzymes-> pancreatic autodigestion
* ETOH-> auto-activation of enzymes while still in pancreas
2) a-10%, b- 50%
3) RUQ US to check for stones and CBD dilation, and abdominal CT to check for complications (necrotic pancreas doesn't take up contrast)
4) NPO, IVF, ERCP if retained CBD stone with sphincterotomy and stone extraction, chole once recovered on same admission
- can give abx for stones, severe pancreatitis, failure to improve or suspected infection.
5) Morphine- can contract sphincter of oddi and worsen attack
155
Signs of hemorrhagic Pancreatitis, describe:
1) Grey Turner sign
2) Cullen's sign
3) Fox's sign
1) flank ecchymosis
2) periumbilical ecchymosis
3) inguinal ecchymosis
156
Pancreatic necrosis
1) what % become necrotic
2) what to do if sterile necrosis
3) rx for infected necrosis
4) rx of pancreatic abscesses
5) rx if gas in necrotic pancreas
1) 15%
2) leave it alone!
3) if fever, sepsis, positive blood cx-> cx pancreatic fluid to diagnose. Rx- surgical debridement
4) surgical debridement
5) open debridement (infected necrosis or abscess)
157
Pancreatitis
1) Leading cause of death
2) when to operate
3) Most imp risk factor for necrotizing pancreatitis
4) Cause of ARDS in pancreatitis
5) Cause of Coagulopathy
6) cause of Pancreatic fat necrosis
7) what are other things that can cause mild inc in amylase and lipase
1) infection (usually GNR)
2) if infection or abscess
3) obesity
4) related to release of phospholipases
5) related to release of proteases
6) related to release of phospholipases
7) cholecystitis, perfed ulcer, sialoadenitis, small bowel obstruction and intestinal infarction
158
Pancreatic Pseudocyst
1) MC in patients with what type of pancreatitis
2) what should you worry about in a pt with cyst not associated with pancreatitis
3) sx
4) location (MC)
5) rx
1) chronic pancreatitis
2) r/o CA (mucinous cystadenocarcinoma)
3) pain, fever, weight loss, bowel obstruction from compression
4) head of pancreas (non-epithelialized sac= PSEUDO- cyst)
5) most resolve spontaneously, esp if rx with expectent management for 3 months (allows pseudocyst to mature if cystogastrostomy required)
- Surgery only for continued symptoms (cystogastrostomy, open or percutaneous)
- or for growing pseudocyst (resection to r/o CA)
159
Pancreatic Pseudocyst
1) complications
2) rx of incidental cysts not associated with pancreatitis
3) what type of cysts have extremely low malignancy risk and can be followed
1) infection of cyst, portal or splenic vein thrombosis
2) resect 2/2 concern for intraductal papillary-mucinous neoplasms (IPMNs) or mucinous cystadenocarcinoma) unless cyst is purely serous and non-complex
3) non-complex, purely serous cystadenomas
160
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Pancreatic Fistulas
1) rx
a- medical management
b- what inc chance of spontaneous closure
c- what if medical management fails
```
1) most close spontaenously (esp if low output <200cc/day) . allow drainage, NPO, TPN, octreotide
- if failure to resolve with medical management can try ERCP, sphincterotomy and pancreatic stent placement (fistula will usually close, then remove stent)
161
Pancreatitis- Associated pleural effusion (or Ascites)
1) cause
2) rx
3) dx
1) retroperitoneal leakage of pancreatic fluid from the pancreatic duct or pseudocyst (not a pancreatic-pleural fistula).
2) majority close on their own,. Do thoracentesis (or paracentesis) followed by conservative Rx (NPO, TPN and octreotide- follow pancreatic fistula pathway... ie ERCP if not resolving.
3) elevated amylase in the fluid
162
Chronic pancreatitis
1) pathology of cells
2) MC causes
3) MC sx
4) Are endocrine or exocrine functions preserved?
5) complication and rx
6) Dx
7) rx
1) irreversible parenchymal fibrosis
2) ETOH (MC), then idiopathic
3) pain, anorexia, weight loss, malabsorption, steatorrhea, recurrent acute pancreatitis
4) endocrine function preserved (Islet cells preserved). Exocrine fnc decreased-> give pancrelipase
5) can cause malabsorption of fat-soluble viatmins- rx c pancrelipase
6) Abd CT- shrunken pancreas c calcifications
US- pancreatic ducts >4mm, cysts, atrophy; or ERCP (very sensitive)
163
1) what does a chain of lake appearance of pancreatic duct suggest
2) rx of chronic pancreatitis
3) surgical indications
1) advanced disease (alt seg of dilation and stenosis in duct)
2) supportive incl pain control and nutritional support (pancrelipase)
3) pain interferes with quality of life, nutrition abnormalities, addiction to narcotics, failure to ro CA, biliary obstruction
164
Surgical options for chronic pancreatitis
1) Puestow procedure- describe procedure and who it works for
2) Distal pancreatic resection- when to do
3) when to do a Whipple
4) Beger-Frey- describe procedure and when to do it
5) when to do bilateral thoracoscopic splanchnicectomy or celiac ganglionectomy
6) rx if common bile duct stricture causing CBD dilation
1) pancreaticojejunostomy, for enlarged ducts>8mm. open along main pancreatic durct and drain into the jejunum
2) if normal or small ducts and only distal portion of gland affected
3) if only head is affected with small or normal ducts
4) Duodenal preserving head "core out"- for normal or mall ducts with isolated pancreatic head enlargement
5) for pain relief
6) hepaticojejunostomy or choledochojejunostomy for pain, jaundice, progressive cirrhosis or cholangitis (make sure stricture isn't CA)
165
Spleniv vein thrombosis
1) MCC
2) common complication
3) rx
1) chronic pancreatitis
2) can get bleeding from isolated gastric varices that form as collaterals
3) splenectomy if isolated bleeding gastric varices
166
Pancreatic insufficiency
1) causes
2) which function is insufficeint, exocrine or endocrine
3) sx
4) dx
5) rx
1) chronic pancreatitis or after total pancreatectomy (over 90% of function must be lost)
2) exocrine function
3) malabsorption, steatorrhea
4) fecal fat testing
5) high-carbohydrate, high-protein, low-fat diet. Pancreatic enzymes (Pancrease)
167
Workup for Jaundice
1) 1st test
2) test if CBD stones and no mass
3) test if no CBD stones and no mass
4) test if mass
1) Ultrasound
2) ERCP-> allows for stone extraction
3) MRCP
4) MRCP
168
Pancreatic adenocarcinoma
1) who gets it/risk factors
2) sx
3) prognosis
4) serum marker for pancreatic CA
5) MC mutation, what type of gene is it and function
6) what type of spread occurs first
1) Males, 6th-7th decades of life
2) weight loss (MC), jaundice, pain
3) 20% 5-year survival with resection
4) CA 19-9
5) p16 mutation (tumor suppressor)- binds cyclin complexes
6) lymphatic
169
Pancreatic Adenocarcinoma
1) MC location
2) what mets indicate unresectable disease
3) what type has most cures
4) other more favorable prognosis CA of the pancreatic duct
5) when to get a bx
1) ductal adenoCA (90%), head (70%)
2) invasion of portal vein, SMV or retroperitoneum at time of diagnosis, mets to peritoneum, liver, or omentum or celiac of SMA noral system (nodal systems outside area of resection)
3) pts with pancreatic head disease
4) papillary or mucinous cyst-adenocarcinoma
5) only if pt appears to have mets to confirm dx. if resectable and no mets in pancreas, will take out regardless so don't need bx.
170
1) best test for differentiating dilated ducts 2/2 chronic pancreatitis vs CA
2) what sign might you see on CT
1) MRCP- signs of CA= duct with irregular narrowing, displacement, destruction, vessel involvement
2) double duct sign for pancreatic head tumors (dilation of both the pancreatic duct and CBD
171
1) rx for uncresectable pancreatic CA
2) complications from Whipple and rx
3) rx of bleeding after whipple or other pancreatic surgery
4) postop chemo-XRT after whipple for pancreatic CA- when to use it and what chemo agent
5) what is non-met pancreatic CA prognosis related to
1) palliation with biliary stents of hepaticojejunostomy (for biliary obstruction) gastrojejunostomy (for duodenal obstruction) and celiac plexus ablation (for pain)
2) delayed gastric emptying #1 (tx- metoclopramide), fistula (rx-conservative), leak (rx- drains and rx like fistula), marginal ulceration (rx- PPI)
3) angio for embolization
4) All post op patients should get it. Gemcitabine
5) nodal invasion and ability to get a clear margin
172
Non-functional endocrine tumors
1) what % are malignant
2) course compared to pancreatic adenoCA
3) rx
4) MC site of mets
1) 90% malignant. Non-functional are 1/3 of pancreatic endocrine neoplasms
2) more indolent and protracted course
3) resect. mets preclude resection. 5-FU and streptozocin may be effective.
4) liver
173
Functional Endocrine pancreatic tumors
1) when to use octreotide
2) MC tumors in pancreatic head
3) 1st site of mets
4) MC islet cell tumor of the pancreas
5) MC islet cell tumor in MEN-1 patients
1) effective for insulinoma, glucagonoma, gastrinoma, VIPoma
2) gastrinoma and somatostatinoma
3) liver
4) insulinoma
5) gastrinoma (Zollinger-Ellison syndrome)
174
Insulinoma
1) Whipple's triad of symptoms
2) malignant or benign?
3) Dx
4) rx
1) fasting hypoglycemia (0.4 after fasting; increased C peptide and proinsulin (if not elevated suspect Munchausen's syndrome)
4) enucleate if 2cm. If mets- 5-FU and streptozocin. Octreotide.
175
Gastrinoma
1) % malignant? %multiple?
2) % spontaneous?
3) MC location
4) sx
5) dx
6) rx
7) what to do if you can't find the tumor in the OR
8) single-best test for localizing tumor
1) 50%, 50%
2) 75%, 25% MEN-1
3) gastrinoma triangle: CBD, neck of pancreas and 3rd portion of duodenum
4) refractory or complicated ulcer disease and diarrhea (improved with PPI)
5) serum gastrin >200, 1,000s is diagnostic. Secretin stimulation test for ZES patients: increased gastrin (>200); normal patients: decreased gastrin
6) enucleation if 2cm
- if malignant disease-> excise suspicious nodes
- Duodenal tumor- resect with primary closure, may need whipple if extensive
- Debulking can improve sx
7) if can't find tumor-> duodenostomy and look inside duodenum (15% of microgastrinomas are there
8) octreotide scan
176
Glucagonoma
1) sx
2) dx
3) benign or malignant
4) MC location
5) how to treat skin rash
1) DM, stomatitis, dermatitis (rash- necrolytic migratory erythema), weight loss
2) fasting glucagon level
3) most are malignant
4) distal pancreas
5) zinc, amino acids or fatty acids
177
VIPoma (Verner-Morrison syndrome)
1) sx
2) dx
3) benign or malignant
4) MC location
5) rx
1) very rare- cause DM, gallstones, steatorrhea, hypochlorhydria
2) fasting somatostatin level
3) most are malignant
4) head of pancreas
5) cholecystectomy with resection.
178
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Spleen Anatomy and Physiology
1) location of splenic vein in relation to splenic artery
2) function of spleen
3) % that is read pulp and fnc
a- what is pitting
b-what is culling
c- what are howell-jolly bodies
d- what are heinz bodies
4) % that is white pulp and fnc
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1) splenic vein is posterior and inferior to the splenic artery
2) antigen-processing center for macrophages and largest producer of IgM
3) 85% red pulp- acts as filter for aged or damaged RBCs
a-removal of abnormalities in RBC membrane
b- removal of less deformable RBCs
c- nuclear remnants
d- hemoglobin
4) 15% white pulp- immunologic function, contains lymphocytes and macs. Major site of bacterial clearance that lacks preexisting Abs, site of removal of poorly opsonized bacteria, particles and cellular debris. Ag processing occurs with interaction bw macs and helper T cells
179
function of the following
1) Tuftsin
2) Properdin
3) Hematopoeisis- where/when does it occur
4) T/F: Spleen is a reservoir for platelets
5) MC location of accessory spleen
1) an opsonin, facilitates phagocytosis and is produced in Spleen
2) activates alternate complement pathway & produced in spleen
3) occurs in spleen before birth and in conditions such as myloid dysplasia
4) true
5) 20% of ppl have it. MC at splenic hilum
180
1) indications for splenectomy
2) MC non-traumatic condition requiring splenectomy
3) vaccines needed before splenectomy (or after if emergent)
1) idiopathic thrombocytopenic purpura (ITP) far greater than for thrombotic thrombocytopenic purpura (TTP), trauma with significant bleed
2) idiopathic thrombocytopenic purpura (ITP)
3) Pneumovax, H. Flu, Meningococcus
181
Idiopathic thombocytopenic purpura (ITP)
1) etiologies
2) cause/pathophysiology
3) sx
4) T/F: spleen is abnormal in these patients
5) who should you avoid splenectomy in?
6) rx
7) indications for splenectomy and how soon before surgery to give platelets
1) drugs, viruses, etc
2) caused by anti-platelet Ab (IgG)-> bind platelets-> decreased platelets
3) petechiae, gingival bleeding, bruising, soft tissue ecchymosis
4) false- spleen is normal
5) in children removes IgG production and source of phagocytosis. 80% cure rate. give platelets 1hour before surgery.
182
Thrombotic thrombocytopenic purpura (TTP)
1) etiologies
2) pathophysiology
3) sx
4) rx
5) MCC of death
1) medical reactions, infections, inflammation, autoimmune disease
2) loss of platelet inhibition-> thrombosis and infarction-> profound thombocytopenia
3) purpura, fever, mental status changes, renal dysfunction, hematuria, hemolytic anemia
4) 80% respond to medical therapy- plasmapherisis 1st. If doesn't work, try immunosuppression. splenectomy rarely indicated
5) intracerebral hemorrhage or acute renal failure
183
Post-Splenectomy Sepsis syndrome
1) % risk after splenctomy and who has increased risk
2) causative bugs
3) pathophysiology
4) how to prevent
5) time frame for when it occurs
1) 0.1% risk. higher in children and pt with splenectomy for hemolytic disorders or malignancy
2) S. pneumonia is #1; H. flu, N. meningitidis
3) 2/2 to specific lac of immunity (IgM) to capsulated bacteria
4) pre-splenectomy vaccinations, try to wait until at least 5yo for children to allow Ab formation and so child can get fully immunized. Children <10yo should be given ppx abx for 6months (controversial)
5) MC within 2 years postop
184
Definition of hypersplenism: 3 required components
1) Decrease in circulating cell count of RBC, plt and or leukocytes
2) normal compensatory hematopoietic responses present in bone marrow
3) correction of cytopenia by splenectomy
* with or without splenomegaly
185
Hemolytic Anemias
1) types with membrane protein defects and the associated defecit
2) types without membrane protein defects
3) MC congenital hemolytic anemia requiring splenectomy
1) Spherocytosis- spectrin deficit-> deforms RBCs and leads to splenic sequestration (hypersplenism)
Elliptocytosis- spectrin and protein 4.1 deficit
2) Pyruvate kinase deficiency, G6PD deficiency, Warm-Ab-type acquired immune hemolytic anemia, sickle cell anemia, Betal thalassemia
3) Spherocytosis
186
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Hemolytic anemias
1) Spherocytosis
a- defect
b-complications/sx
c-rx
2) G6PD deficiency
a- precipitators
b- rx
3) rx of warm Ab- type acquired immune hemolytic anemia
4) Sickle cell
a) pathophysiology
b-effect on spleen
5) a- Beta Thalassemia (MC thalasemia)
a- pathophys
b- 2 types
c- sx
d- rx and prognosis
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1) a- spectrin deficit (membrane protein)
b- pigmented stones, anemia, reticulocytosis, jaundice, splenomegaly
c- splenectomy and cholecystectomy, curative. try to give immunizations first and do after age 5yo.
2) a- infection, certain drugs (ie-sulfa), fava beans
b- splenectomy usually not required.
3) splenectomy
4) a-HgbA is replaced with HgbS-> spleen usually autoinfarcts and splenectomy not required
5) a-2/2 persistent HgbF
b- Major- both chains affected, minor- 1 chain, asx
c- pallor, retarded body growth, head enlargement
d) medical rx: blood transfusions and iron chelators (deferoxamine, deferiprone). Splenectomy if splenomegaly may dec hemolysis and sx. Most die in teens 2/2 hemolysis
187
Hodgkins disease
1) difference between type A and type B
2) What cell type do you see on pathology
3) which type has best and worst prognosis
4) MC type
5) rx
6) MCC of chylous ascites
1) type A= asx; B= sx (fever, night sweats, weight loss)-> unfavorable prognosis
2) Reed-Sternberg cells
3) Lymphocyte predominant= best prog; lymphocyte depleted= worst prog
4) Nodular sclerosing
5) chemo
6) lymphoma
188
Describe Stage I-IV of Hodgkin's disease
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I= 1area or 2 contigous areas on same side of diaphragm
II= 2 non-contiguous areas on same side
III= involved on each side of diaphragm
IV= liver, bone, lung or any other non-lymphoid tissue except spleen
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189
Non-Hodgkin's lymphoma
1) prognosis related to Hodgkins
2) MC type
3) rx
1) worse prog
2) 90% are B cell lymphomas
3) chemo (generally systemic at time of dx)
190
Other conditions affecting spleen
1) Rx of hairy cell leukemia
2) causes of spontaneous splenic rupture
3) Cause of splenosis
4) cells seen in hyposplenism
5) MCC of splenic artery or vein thrombosis
1) rarely need splenectomy
2) mononucleosis, malaria, sepsis, sarcoid, leukemia, polycythemia vera
3) trauma-> splenic implants
4) howell-jolly bodies
5) pancreatitis
191
Other conditions affecting spleen
1) Post splenectomy changes in RBC, WBC, Platelets.
2) post splenectomy rx of platelets >1 x10^6
3) #1 splenic tumor and benign splenic tumor
4) rx of hemangioma
5) #1 malignant splenic tumor
1) all increased
2) ASA
3) hemangioma
4) if sx-> splenectomy
5) non-hodgkin's lymphoma
192
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Other conditions affecting spleen
1) rx of splenic cysts
2) Sarcoidosis of spleen
a- labs
b- rx
3) what is felty's syndrome and rx
4) rx of splenic abscess
5) rx of echinococcal splenic cyst
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1) surgery if sx or >10cm
2) a-anemia, dec platelets
b- splenectomy for symptomatic splenomegaly
3) rheumatoid arthritis, hepatomegaly, splenomegaly. rx- splenectomy for symptomatic splenomegaly
4) splenectomy bc bleeding risk with percutaneous drainage)
5) spelenctomy
193
Post splenectomy blood smear
1) erythrocyte products seen and what from
2) platelet product seen
3) leukocyte product seen
1) howell-Jolly bodies (nuclear fragments), Heinz bodies (Hgb deposits), Pappenheimer bodies (iron deposits), Target cells, Spur cells (acanthocytes
2) transient thrombocytosis
3) transient leukocytosis, persistent lymphocytosis, and monocytosis
194
Guidelines for prevention of postsplenic sepsis
1) when to vaccinate
2) who gets abx prophylaxis
3) T/F: early abx treatment for signs of infection is one.
4) what should all post splenectomy patients wear
1) 10-14 days prior at least for pneumococcal vaccine. if urgent, wait until POD14 or later. High risk pts get meningococal and H. flu vaccines as well (immunosuppresed and kids
