GIT Flashcards
Identify the source action and regulation of Intrinsic factor
From Parietal cells
Facilitates Vit B12 absorption
Identify the source action and regulation of Gastric acid
Parietal cells
Lowers pH to optimal range for pepsin function
Release is stimulated by histamine, Ach, gastrin
and inhibited by PG, somatostatin, GIP
Identify the source action and regulation of Pepsin
From Chief cells
Facilitates Protein digestion
Release is stimulated by vagal input and local acid
Identify the source action and regulation of Cholecystokinin (CCK)
From I cells of duodenum and jejunum
Increases GB contraction and Pancreatic secretion. Decreases gastric emptying.
Release is stimulated by increased presence of fatty acids and amino acids
Identify the source action and regulation of Cholecystokinin (CCK)
From I cells of duodenum and jejunum
Increases GB contraction and Pancreatic secretion. Decreases gastric emptying.
Release is stimulated by increased presence of fatty acids and amino acids/ monoglycerides in the duodenum
Identify the source action and regulation of Somatostatin
From D cells in pancreatic islets , GI mucosa
Inhibits release of ALL GI hormones
Release stimulated by acid and inhibited by vagus
In Cholelithiasis , pain worsen after eating fatty foods due to?
Increased secretion of Cholesystokinin
Alkaline pancreatic juice in duodenum neutralizes gastric acid, allowing pancreatic enzymes to function.
Secretin
Very inhibitory hormones- Anti GH
Somatostatin
This GI secretion is used to treat VIPomas and carcinoid tumors
Somatostatin
Destruction of this GI secretion will result in Pernicious anemia
Intrinsic factor
Inadequacy of this GI secretion predisposes to a high risk of Salmonella
Gastric Acid
Pesin by H+
Pepsinogen
This part of GI wall decreases diameter
Circular muscle (think circle)
This part of GI tract shortens a segment
Longitudinal muscle (think length)
Structure of the wall of GI tract
Epithelial cells- For secretion or absorption
Muscularis mucosa
Circular muscle- reduce diameter
Longitudinal muscle- shortening of a segment
Submucosal plexus (Meissner’s plexus and myenteric plexus)- Comprise the enteric nervous system, coordinate motility, secretory and endocrine functions of GIT
These cells of GI tract are responsible for absorption and secretion
Epithelial cells
This part of GI tract wall Comprise the enteric nervous system, coordinate motility, secretory and endocrine functions of GIT.
Submucosal plexus (Meissner’s plexus and myenteric plexus)
Describe the Intrinsic Innervation (enteric nervous system)
100 millions neurons
Coordinate information from PNS and SNS to GIT
Uses local reflexes to relay information within GIT
Controls most functions e.g. motility and secretion even in the absence of extrinsic innervation - “ Gut brain”
Myenteric plexus (Auerbach’s plexus)- Controls Motility
Submucosal plexus ( Meissner’s plexus)- Controls Secretion and blood flow
This Coordinates information from PNS and SNS to GIT and Uses local reflexes to relay information within GIT
Intrinsic Innervation (enteric nervous system)
Controls Motility
Myenteric plexus (Auerbach’s plexus)
Controls Secretion and blood flow
Submucosal plexus ( Meissner’s plexus)
Four “official” GI hormones are
gastrin
cholecystokinin (CCK)
secretin
glucose-dependent insulinotropic peptide (GIP).
GI hormones release from endocrine cells of GI mucosa into _________________, enter ________________ and have physiological actions on target tissues.
portal circulation
general circulation
Gastrin
Is released in response to meal from G cells of the gastric antrum.
Increases H+ secretion by gastric parietal cells and Stimulates growth of gastric mucosa – trophic action.
Release is stimulated by small peptides and amino acids esp. phenylalanine and tryptophan; Distension of stomach and; Vagal stimulation
Release is Inhibited by Acid [H+] in the lumen of stomach (-ve feedback)
Release of Gastrin is stimulated by?
Small peptides and amino acids esp. phenylalanine and tryptophan.
Distension of stomach
Vagal stimulation
Occurs when gastrin is secreted by non-beta-cells of pancreas resulting in hypertrophy of gastric mucosa
Zollinger-Ellison syndrome (gastrinoma)
What are the actions of Cholecystokinin (CCK)
Stimulates contraction of GB , relaxation of sphincter of Oddi leading to ejection of bile.
Stimulates pancreatic enzyme secretion.
Potentiate secretin-induced stimulation of pancreatic HCO3 secretion.
Stimulates growth of exocrine pancreas.
Inhibits gastric emptying. Thus fatty meal stimulates CCK, which slows gastric emptying. Therefore , fatty meal hangs around in stomach for longer time to allow more time for intestinal digestion & absorption
Release of Cholecystokinin (CCK) is stimulated by
Fatty acids and monoglycerides in duodenum
Nature’s antacid
Secretin
Actions of secretin are?
Stimulates pancreatic HCO3 , this in turn neutralizes H+ in the intestinal lumen
Stimulates HCO3 and H2O secretion by the liver, and increases bile production
Inhibit H+ secretion by gastric parietal cells
Secretin is released by
S cells of duodenum
Release of secretin is stimulated by?
H+ in the lumen of the duodenum
the principle stimulus for delivery of pancreatic enzymes and bile into small intestine
CCK
Name 2 Neurocrine “neurotransmitters” Synthesized in neurons in GIT, diffuse across the synaptic cleft to target cell (+ or - )
VIP
Enkephalins
Vasoactive intestinal peptide
Is released from neurons in mucosa and smooth muscle of GIT
Produces relaxation of GI muscle, including LES
Stimulates pancreatic HCO3 and inhibit gastric H+ (like secretin)
Is secreted by pancreatic islet cell tumor and is presumed to mediate pancreatic cholera
Enkaphalins
Are released from nerves in mucosa and smooth muscle of GIT
Stimulates contraction of GI smooth muscles
Inhibit intestinal secretion and fluid and electrolytes.
Therefore, opiates are used in the treatment of diarrhea
This GI neurotransmitter is presumed to mediate pancreatic cholera
VIP (Vasoactive intestinal peptide)
This GI neurotransmitter is Produces relaxation of GI muscle, including LES
VIP (Vasoactive intestinal peptide)
1/3 of the upper GIT is made of?
Striated muscles
Lower 2/3 of upper GIT is made of?
smooth muscles
High LES pressure during swallowing
Achalasia
Low LES pressure during swallowing
GERD
Segmentation contractions
In small intestine
mixes the chyme
Peristaltic contractions
Moves the chyme in caudal direction
GI smooth muscles are contractile tissues except
upper 1/3 of esophagus and external anal sphincter
Circular muscle contraction
Decrease diameter
Longitudinal muscle contraction
Decrease length
Phasic contractions are
periodic contraction and relaxation
Tonic contractions occur in
LES and ext. and internal anal sphincter
GI motility is Lowest in ________ and highest in_________
the stomach
duodenum
Swallowing is coordinated in?
the medulla
Nerves involved in swallowing are?
Vagus and glossopharyngeal nerve
Describe the swallowing process
Nasopharynx closes, breathing is inhibited
Laryngeal muscles contract and close the glottis
UES relaxes and peristalsis propels food down to stomach
Intra-esophageal pressure = intrathoracic pressure
This drug increases gastric Motility
Neostigmine
These drugs decrease gastric tone and motility
atropine, meperidine and epinephrine
Gastric contraction increases by ____________ stimulation and decreases by _____________ stimulation
vagal stimulation
sympathetic stimulation
Receiving area in gastric motility
Fundus and proximal body relax to accommodate meal
Contraction of this area mixes the food and propels it into the duodenum
Caudad stomach
Small intestine motility is coordinated by
enteric NS
Small intestine is how long
4 meter
Characteristics of Small intestine motility
4 m long tube
Parasympathetic NS stimulate and sympathetic NS decrease it
Mixing of intestinal contents (chyme)
Propulsion of chyme toward large intestine
Is coordinated by the enteric NS
Characteristics of Large intestine motility
Water is absorbed in proximal colon, mass movements propel it into the rectum
Defecation happens when
External anal sphincter relaxes, smooth muscle of rectum contracts
Gastrocolic reflex
Presence of food in stomach increase motility of colon
Increased stretch by food lead to parasympathetic stimulation
Describe IBS
Occurs during stress
Constipation due to increased segmentation contraction
Diarrhea due to decreased segmentation contraction
Vomiting is
A wave of reverse peristalsis
UES close – retching
UES open – vomiting
Medullary VC stimulated by?
Tickling throat
Gastric distension
vestibular stimulation ( motion sickness)
CTZ in fourth ventricle is stimulated by
emetics, radiation and vestibular stimulation.
Vomiting will cause which acid base disturbance
Metabolic alkalosis
Droperidol is antiemetic by blocking dopamine receptors and may cause extrapyramidal symptoms. Treatment for extrapyramidal symptoms is
Benztropine
Extrapyramidal symptoms
These symptoms include dystonia (continuous spasms and muscle contractions), akathisia (may manifest as motor restlessness), parkinsonism (characteristic symptoms such as rigidity), bradykinesia (slowness of movement), tremor, and tardive dyskinesia (irregular, jerky movements).
Contraindicated in parkinson disease
Droperidol
Antiemetic of choice for parkinson’s
Ondansetron
Characteristics of Metoclopramide
Increases LES and gastric motility, decreases tone of pyloric sphincter, relax duodenum
No effect on gastric pH
Increases action of Sux by inhibiting plasma AchEsterase
This drug is used in emesis linked to chemotherapy
Ondansetron (Zofran)
Ondansetron (Zofran) characteristics
Used in emesis linked with chemotherapy
5-HT3 receptor blocker (5-hydroxytryptamine or serotonin)
Drug of choice for Parkinson’s
S/E headache
The absence of the colonic enteric nervous system, results in constriction of the involved segment, marked dilatation and accumulation of intestinal proximal to constriction , and severe constipation.
Megacolon (Hirschsprung’s disease)
Disorders of Swallowing(Dysphagia)
CVA (stroke) / cranial nerves damage
Aspiration - UES and pharyngeal contractions are not coordinated
Secondary peristalsis is still functional
Muscular diseases - myasthenia gravis, polio, botulism
Anesthesia - aspiration of stomach contents will cause aspiration pneumonitis (Mendelson syndrome)
Mendelson syndrome
aspiration of stomach contents leading to aspiration pneumonitis
Features of CVA (stroke) / cranial nerves damage dysphagia
Aspiration because UES and pharyngeal contractions are not coordinated.
Secondary peristalsis is still functional.
The orad region of the stomach includes ____________ whereas the caudad region includes the _____________
the fundus and the upper body
lower body and the antrum
Parietal cells (body)
Found in the stomach body
Are stimulated by Gastrin, Vagal stimulation, Histamine.
Secrete HCL and intrinsic factor
HCl kills bacteria, breaks down food and convert pepsinogen to pepsin
Intrinsic factor aid vitamin B12 absorption
Chief cell (Body)
Found in the stomach body
The secrete pepsinogen which breaks down to pepsin
Secretion is by Vagal stimulation
G cells (Antrum)
Found in the Antrum of the stomach
They secrete gastrin which is responsible for stimulating HCl secretion
Secretion is stimulated by vagal vis GRP and inhibited by somatostatin and H+ in stomach
Mucous cells (Antrum)
Found in the antrum of the stomach
Its a lubricant that protects the surface from H+
Secreted by vagal stimulation
Identify 3 types of Gastric cells responsible for gastric secretions
Parietal cells (body) ; secretes HCl and IF Chief cells ( body); secretes pepsinogen G cells (antrum); secretes gastrin
Mechanism of gastric H+ secretion
Parietal cells secretes HCl into the lumen and absorb HCO3
In parietal cell; CO2 +H2O –> H+ + HCO3- catalysed by CA
H+ is secreted into the lumen of the stomach , by H+ - K+ pump (H+, K+ -ATPase). Cl- is secreted along with H+; thus the secretion product of parietal cell is HCl
This drug inhibit the H+, K+ - ATPase and blocks H+ secretion
Omeprazole
What is Alkaline tide? Where this HCO3 goes?
Refers to a condition, normally encountered after eating a meal, where during the production of hydrochloric acid by parietal cells in the stomach, the parietal cells secrete bicarbonate ions across their basolateral membranes and into the blood, causing a temporary increase in pH.
This drug will cause S/E of hypergastrinemia WHY?
Omeprazole
Inhibition of HCl secretion will reduce the concentration of H+ ions in the stomach thereby eliminating the inhibition on Gastrin secretion leading to hypergastrinemia.
What are the 4 mechanism of stumulation of gastric H+ secretion
Vagal stimulation
Histamine
Gastrin
Histamine potentiation of actions of Ach and gastrin
Describe gastric H+ secretion via Vagal stimulation
Directly by vagus nerve (Muscarinic M3)
Indirectly by stimulating G cells which produce gastrin. Gastrin then stimulates H+ secretion. The neurotransmitter is GRP (not Ach)
Atropine inhibit direct pathway only.
Vagotomy eliminates both direct and indirect pathways
Describe gastric H+ secretion via Vagal stimulation
Directly by vagus nerve (Muscarinic M3)
Indirectly by stimulating G cells which produce gastrin. Gastrin then stimulates H+ secretion. The neurotransmitter is GRP (not Ach)
Atropine inhibit direct pathway only.
Vagotomy eliminates both direct and indirect pathways
Describe gastric H+ secretion via histamine
Is released from mast cells in the gastric mucosa
Stimulates H+ secretion by activating H2 receptors on the parietal cell membrane
Histamine potentiate the actions of Ach and gastrin
Describe gastric H+ secretion via gastrin
Is released in response to eating meal (small peptide, distension of the stomach , vagal stimulation)
Stimulates H+ secretion
This drug inhibit H+ secretion by blocking the stimulatory effect of histamine
H2 receptors blockers like cimetidine
This drug inhibit direct pathway of vagal stimulation gastric H+ secretion but has no effect in the indirect pathway
Atropine
What are the mechanisms of inhibition of Gastric H+ secretion in the stomach
Low pH <3 in stomach- inhibit gastrin secretion
Chyme in duodenum- Inhibits H+ secretion both directly and via GIP ( released by fatty acids in the duodenum) and secretin ( released by H+ in the duodenum)
Prostaglandins- inhibit H+ secretion
Name 3 pathophysiologic conditions of gastric HCl
Gastric ulcers
Duodenal ulcers
Zollinger-Ellison syndrome
Gastric ulcers
If the normal protective barrier (of mucus and HCO3) of the stomach is damaged, the presence of H+ and pepsin may injure gastric mucosa
Helicobacter pylori has high Urease activity and converts urea to NH3 , which damages the gastric mucosa.
H+ secretion is decresed, not increased (as might be assumed)
Gastrin level are increased ( by -ve feedback ) in patients with gastric ulcer because of lower-than-normal H+ secretion.
Duodenal ulcers
Are more common than gastric ulcer
H+ secretion is higher than normal and is responsible , along with pepsin , for damaging the duodenal mucosa
Gastrin levels in response to a meal are higher than normal.
Parietal cell mass is increased because of trophic effect of gastrin
Gastrin secreting tumor
Gastrinoma - Zollinger-Ellison syndrome
Pathophysiology of Gastrinoma (Zollinger-Ellison syndrome)
Non-beta cell tumor of pancreas (80%) or G-cell tumors in duodenum (10-15%)
Continually secretes large amount of gastrin into blood
Markedly high acid secretion leads to ulcers
20% associated with MEN I
H+ secretion continues unabated because the gastrin secreted by pancreatic tumor cells is not subject to -ve feedback inhibition by H+
Constant stimulation of hyperplastic mucosa
Symptoms of Gastrinoma (Zollinger-Ellison syndrome)
Secretory diarrhea because gastrin inactivates lots of digestive enzymes leading to malabsorption.
Weight loss.
Steatorrhea (fatty diarrhea) because pancreatic enzymes are inactivated by very high acid.
Very severe ulcers, ulcers with complications, ulcers are located on atypical places !
Diagnosis of Gastrinoma (Zollinger-Ellison syndrome)
High fastening gastrin level (normal < 100 picogram/ml)
Secretin stimulation test
CT to see the tumor
Treatment of Gastrinoma (Zollinger-Ellison syndrome)
Medical vs. Surgical
Secretin stimulation test
low gastrin levels after IV secretin indicate normal test
High gastrin levels after IV secretin indicate ZE syndrome
Steatorhea in ZE syndrome is due to?
The low pH inactivates pancreatic lipase and causes bile salts to precipitate. The result is steatorrhea.
Hypokalemia in ZE syndrome is due to?
Hypokalemia results from loss of GI secretions in stool.
Bile contains
bile salt
phospholipids
bile pigment ( bilirubin)
water (97%)
Describe emulsification
It’s an important step in fat digestion
Bile salts; have both hydrophobic and hydrophilic portions. In aqueous solution, bile salts orient themselves around droplets of lipid and keep the lipid droplets dispersed ( emulsification)
Bile solubilize lipids in _______ for absorption
micelles
Describe the process of bile formation
Primary bile acids (cholic acid and chenodeoxycholic acid) are synthesized from cholesterol by hepatocytes
Intestinal bacteria convert primary bile acids to secondary bile acids
The bile acids are conjugated with glycine or taurine to form bile salts
During interdigestive period, the GB is relaxed, the sphincter of Oddi is closed and the GB fills with bile
Bile is concentrated in GB by water absorption
Contraction of the bladder can be stimulated by?
CCK
Ach
CCK is released in response to?
peptide and fatty acids in the duodenum
Bile is recirculates to liver through?
terminal ileum
What is the cause of prolonged PT after ileal resection
After ileal resection , bile salts are not recirculated to the liver, but are excreted in feces. The bile acid pool is thereby depleted and fat absorption is impaired, resulting steatorrhea (fatty diarrhea). This results in malabsorption of fat soluble vitamins ADEK. Lack of vitamin K results in the inability of the liver to make vitamin k dependent factor 1972
Primary bile acids are?
cholic acid and chenodeoxycholic acid
Secondary bile acids are?
Deoxycholic acid
Lithocholic acid
primary bile salts are converted to secondary bile salts by?
Intestinal bacteria
Lactose intolerance
Result from the absence of brush border lastase and the inability to hydrolyze lactose into glucose for absorption
Non-absorbed lactose and H2O remain in the lumen and causes osmotic diarrhea
Carbohydrate digestion and absorption
Only monosaccharides are absorbed
Digestive enzymes: alpha amylase, maltase, sucrase, lactase
Na+/glucose cotransport- SGLT-1
Fructose by facilitated diffusion
Identify the 4 Pancreatic proteases responsible for protein digestion? What happens to these enzymes after completion of digestion?
Trypsin
chymotrypsin
elastase
carboxypeptidases
After digestive job is done, the pancreatic enzymes degraded and reabsorbed
Optimal pH for Pepsin is
1-3
Denaturation of pepsin will occur at what pH?
> 5
If intestinal pH is >5, as HCO3- is secreted in pancreatic juice then inactivation of pepsin will occur
Endopeptidases and Exopeptidases are responsible for?
Protein digestion
Absorption of proteins is via?
Na+ cotransport
Absorb as AA ,dipeptides and tripeptides
Lipid digestion in the Stomach
In stomach, mixing breaks lipid into droplets to increase surface area for digestion by pancreatic enzymes.
CCK slows gastric emptying. Thus , delivery of lipids from stomach to duodenum is slowed to allow adequate time for digestion and absorption in the intestine.
Lipid digestion in the Small intestine
Bile acids emulsify lipids , increasing surface area for digestion.
Pancreatic lipase hydrolyze lipid to FA , monoglyceride, cholesterol.
The hydrophobic products of lipid digestion are solubilized in micelles by bile acids for absorption.
In the intestinal cells, the products of lipid digestion are re-estereified to TG, cholesterol and phospholipids and with apoprotein form Chylomicrons
Chylomicrons are big molecules , so they transferred to lymph vessels and added to bloodstream via the thoracic duct
Malabsorption of lipids—Steatorrhea may be due to?
Pancreatic disease (pancreatitis, cystic fibrosis)
Hypersecretion of gastrin
Bacterial overgrowth
Tropical sprue: low number of intestinal cells
Failure to synthesize apoprotein B , which lead to the inability to form chylomicrons-abetalipoproteinemia
This condition will leads to a depletion of bile acid pool because of the bile acids do not recirculate to the liver
Ileal resection
Steatorrhea due Low number of intestinal cells.
Tropical sprue
Failure to synthesize apoprotein B, which lead to the inability to form chylomicrons-
abetalipoproteinemia
This condition will lead to deconjugation of bile acids and their “early” absorption in the upper small intestine thereby depleting them before they reach small intestine to aid in lipid absorption
Bacterial overgrowth
Presentation of a patient with malabsorption of lipids
Failure to grow in infancy Fatty, pale stools Frothy stools Foul smelling stools Protruding abdomen Mental retardation/developmental delay Dyspraxia, evident by age ten Muscle weakness Slurred speech Scoliosis (curvature of the spine) Progressive decreased vision Balance and coordination problems Retinitis Pigmentosa
Big molecules that are transferred to lymph vessels and added to bloodstream via the thoracic duct
Chylomicrons
Sodium moves into the intestinal cells by
Passive diffusion
Na+ - glucose cotransport– most important
Na+ - H+ exchange
Absorption of K+
Passive diffusion
Secreted in colon
In diarrhea, K+ secretion by the colon is increased because of flow rate leading to Hypokalemia
____________ increases Na+ reabsorption and K+ secretion in small intestine and colon (just like kidneys
Aldosterone
This condition causes diarrhea by stimulating Cl- secretion via cAMP causing opening of Cl- channels. Na+ and H2O follow Cl- into the lumen and lead to secretory diarrhea.
Vibrio cholerae (cholera toxin)
Some strains of E.Coli
Vitamins absorption
Fat soluble vitamins ( A, D, E, K)
Are incorporated into micelles and absorbed along with other lipids
Water soluble vitamins - By Na+ cotransport
Vit B12 is absorbed in terminal ileum and requires IF
Gastrectomy causes loss of parietal cells which are source of IF leading to Pernicious Anemia
Ca++ absorption
Depend upon active Vit D
Rickets in children and osteomalacia in adults
Iron absorption
Is absorbed as heme iron (iron bound to Hb) or as free Fe++.
In the intestinal cells heme iron is degraded, free Fe++ binds to apoferritin and is transported into the blood.
Free Fe++ circulates in the blood bound to transferrin.
Iron deficiency is the MCC of anemia.
Diseases that result in decreased absorption even when food is well digested are often classified as
Sprue
Non tropical sprue
also called celiac disease
allergic to gluten (wheat, rye)
destroys microvilli and sometimes villi “bald intestine”
Tropical sprue
- bacterium (?)
- treated with antibacterial agents
What are the 4 indications of splenectomy
Trauma
Idiopathic thrombocytopenic purpura ITP
Thrombotic thrombocytopenic purpura TTP
Hypersplenism
Post-splenectomy problems
Thrombocytosis- no treatment if < 1,000,000
Sepsis
More common in children
Vaccinate for pneumococcus , hemophilus
Prophylactic antibodies in children
Hypersplenism
Spleen removes one or more cell lines of blood (RBC,WBC, platelets)
Primary hypersplenism is rare
MC due to portal venous hypertension
Other causes- lymphoma, leukemia, lupus, mononucleosis, hemolytic anemia, thalasemia, sarcoidosis, Gaucher’s disease, malaria
Treatment based on underlying cause
Most common cause of hypersplenism is?
portal venous hypertension
Causes of hypersplenism
portal venous hypertension lymphoma leukemia lupus mononucleosis hemolytic anemia thalasemia sarcoidosis Gaucher’s disease malaria
Thrombotic thrombocytopenic purpura (TTP)
Capillary blocked by platelet deposits.
Fever , hemolytic anemia , renal failure, low platelets ( used up in forming clumps in body).
Idiopathic thrombocytopenic purpura (ITP)
Most frequent hematologic indication for Splenectomy.
Excess platelet removal and destruction by spleen.
Bleeding with minor trauma.
Childhood form- following URI; self-limiting
What is the treatment for TTP
Plasmapheresis
Steroids
FFP
Aspirin
Splenectomy for refractory patients has some improvement
Treatment of ITP
Avoid trauma ( sports)
Steroids
Splenectomy
Spleen trauma
Abdominal /LUQ pain, shoulder pain (due to irritation of diaphragm), hypotension
Dx- peritoneal lavage, CT
Treatment of spleen trauma
Avoid Splenectomy if possible
Splenorrhaphy (repair) with mesh, sutures
Protrusion of portion of stomach to thoracic cavity
Hiatus hernia
Hiatus hernia
Protrusion of portion of stomach to thoracic cavity
Sliding 30%
Severe reflux
Surgical repair
Acute Pancreatitis
Pancreatic enzymes are activated in pancreas rather than in intestinal lumen.
What are the causes of acute pancreatitis
Hypercalcemia/Hyperlipidemia
Trauma (iatrogenic- post ERCP)
Drugs e.g. fursemide, sulfa, estrogen, thiazide
Infection
ETOH and gallstones
______________ account for > 90% of cases of acute pancreatitis
ETOH and gallstones
What are the signs and symptoms of acute pancreatitis
Severe epigastric pain to back; increases post-prandial
Peritoneal signs, N/V causing dehydration
Grey-Turner sign
Cullen sign
Pulmonary finding- ARDS (due to elastase)
superficial edema with bruising in the subcutaneous fatty tissue around the peri-umbilical region.
Cullen sign
bruising of the flanks, the part of the body between the last rib and the top of the hip. The bruising appears as a blue discoloration.
Grey-Turner sign
Lab findings in acute pancreatitis
Markedly high amylase, lipase, hypocalcemia , hyperglycemia
CT
ERCP
Ranson’s criteria*
Extrahepatic complication of acute pancreatitis is?
SHOCK due to loss of lots of fluid “ internal burn”
Pleural effusion, ARDS
ARF (third spacing)
DIC
Pseudocyst is a complication of acute pancreatitis and which may?
Bleed Obstruct Infected Leak: ascites, pleural effusion Needs drainage
Name 3 complications of acute pancreatitis
- Big swollen pancreas
- Extrahepatic
- Pseudocyst which may bleed, obstruct infect or leak causing ascitis and pleural effusions that need drainage
Management of acute pancreatitis involves
NPO and NG suction- put the pancreas to rest. “deactivate the gland”
IV hydration- massive volume depletion
Pain meds
Remove the stones!!
ERCP
Etiology of chronic pancreatitis
Mostly due to ETOH, never from gall stones
Pancreatic duct obstruction
Idiopathic
What are the signs and symptoms of chronic pancreatitis
Pain, Pain, Pain
Steatorrhea
DM
Malabsroption
What are the diagnostic tests of chronic pancreatitis
X-ray: calcification of pancreas
Sono
ERCP
Treatment therapy for chronic pancreatitis (6)
- No alcohol
- Narcotics
- Celiac axis block
- Medium chain FA
- Pancreatic enzyme supplements
- Gastric acid secretion suppression
What are the anesthetic considerations for chronic pancreatitis
- Acute abdomen
- Rule out diabetes
- Electrolyte disorders
- Hypocalcemia
- Hypomagnesemia
- Hypokalemia
- Hypochloremia
- Blood coag profile
- Kidney profile
- Pulmonary assessment
- CVS assessment
Tumor of neuroendocrine cells of GIT (90%), most commonly the Stomach, ileum and appendix.
Carcinoid tumor
Carcinoid tumors secrete_______ causing carcinoid syndrome
Serotonin
Also cause markedly high levels of bradykinin, prostaglandins, kallikrein and histamine
Markedly high levels of bradykinin, prostaglandins, kallikrein and histamine in carcinoid tumors will cause
Skin flushing Watery diarrhea and abdominal pain Bronchospasm Valvular lesions Large swings in BP SVT
High levels of 5-HIAA (5-hydroxyondoleacetic acid) in urine indicates
Carcinoid tumor
During anesthesia for a patient with carcinoid tumor, avoid____?
Hypotension
Catecholamine
Histamine-releasing drugs e.g. morphine, atracurium
Treatment for carcinoid tumors includes this drug.
octeroids (somatostatin analogue)
Ischemia in 2 of 3 mesenteric vessels: Celiac axis, SMA, IMA
Abdominal angina
Symptoms of Abdominal angina
Post-prandial pain
Sitophobia
Weight loss
Diagnostic tests of abdominal angina
H&P
Angiogram
Treatment of abdominal angina
Revascularization
Ischemia of SMA
Mesenteric Ischemia
Mesenteric Ischemia is usually due to?
Usually non-occlusive- low flow (CHF, hypotention) vs. occlusive (embolus in A.fib; thrombus)
Severe abdominal pain out of proportion to physical finding
Mesenteric Ischemia
Lab/ diagnostic findings in Ischemia of the SMA
High K+
Lactic acidosis
Leukocytosis
“Thumbprinting” on barium enema
Mesenteric angiography
This condition predisposes to a risk of intestinal gangrene
Mesenteric Ischemia
Ischemia of IMA
Ischemic Colitis
Ischemic Colitis is usually due to?
Usually non-occlusive- low flow (CHF, hypotention) and with small vessel disease (therefore angiogram not helpful)
Can occur after AAA repair and IMA damage
What are the sigs and symptoms of ischemic colitis
Painless bleeding
Typical colitis- bloody diarrhea, pain
Acute left sided abdominal finding
Most commonly in “watershed” areas- splenic flexure and rectosigmoid
Treatment of pseudomembranous colitis
D/C offending antibiotics
Metronidazole
Oral vancomycin
Antibiotic associated colitis
Overgrowth of C. diff
Pseudomembranous Colitis
Signs and symptoms of Pseudomembranous Colitis
Watery diarrhea
Abdominal cramp
Toxic megacolon
Pathophysiology of Pseudomembranous colitis.
Yellowish plaque-like lesions in colon. Caused by an exotoxin produced by Clostridium difficile that inhibits a signal transduction protein, leading to death of enterocytes.
Daily bile production =
1200ml
Bile vomitus is ____________ while gastric vomitus is ______
alkaline
acidic
Liver acts as a blood reservoir holding _____ ml
500 ml
(Increased liver size in CHF). Sympathetic stimulation results expulsion of blood from liver
When BG is high, _________ occurs, when BG is low ,_________ occurs and glucose is released into the blood from the liver
glycogenesis
glycogenolysis
Functions of the liver
Converts non-carbohydrates to glucose.
Oxidizes fatty acids to produce ATP.
Synthesizes lipoproteins, phospholipids, and cholesterol.
Converts carbohydrates and proteins into fats.
Formation of all clotting factors except III & vWF (and IV ‘Calcium’).
Deaminates amino acids.
Synthesizes plasma proteins and amino acids.
Converts some amino acids to other amino acids.
Stores glycogen, vitamins A, D, B12 and iron.
Phagocytosis of worn out RBCs and foreign substances. Kupffer cells (tissue macrophage) are blood cleaner – kill 99% bacteria from gut.
Can regenerates itself
Produces urea in order to remove NH3 (from hepatic deamination process and from bacterial production in the gut)*
Insulin clearance
Detoxification of drugs , poisons, hormones
Detoxification of drugs , poisons, hormones by the liver
Toxic substances are presented to liver via portal circulation
Liver modifies these substances by “first pass metabolism”
Phase I reactions are catalyzed by cytochrome P-450 enzymes. Important in metabolism of anesthetics These are followed by Phase II reactions that conjugate the substances. Once conjugated the substance can be easily excreted
Tolerance develops due to induction of P-450 by various drugs
Phase II reactions slow down in old age.
___________ reactions slow down in old age.
Phase II
REVIEW IMAGES IN SLIDES 52-62 SECOND PPT. Memorize slide 75
REVIEW IMAGES IN SLIDES 52-62 SECOND PPT
Site of Portal-systemic Anastomosis
Esophagus - esophageal varices
Umbilicus -caput medusae
Rectum - internal hemorrhoids
Portal-systemic Anastomosis
Varices of gut, butt and caput (medusae) are commonly seen in portal hypertension (high back up pressure)
May cause life-threatening bleeding
Portocaval shunt (connecting portal vein and IVC) is inserted to relieve portal hypertension
25-30 % of cardiac output
Blood Supply of Liver
Liver receive blood from
hepatic artery (25%) and from hepatic portal vein (75%)
Oxygen supply is 50:50
Normal portal vein pressure =
9 mmHg
Cirrhosis has high resistance to blood flow, therefore low _________.
portal blood flow
Liver blood circulation pathway
Blood enters via hepatic artery (25%) and hepatic portal vein (75%)
In liver, hepatic artery and portal vein divide and subdivide finally into interlobular vessels.
Interlobular vessels open into hepatic sinusoids.
Thus, hepatic arterial blood mixes with portal venous blood in the sinusoids and flow between hepatocytes.
Hepatic sinusoids drain into interlobular veins which join to form central vein -> hepatic vein -> IVC ->systemic circulation
Hepatic blood flow depends on
Driving pressure (MAP- hepatic venous pressure)
Intrahepatic vascular resistance
Metabolic demand
All volatile anesthetics _______ hepatic blood flow
decrease
bilirubin is conjugated with glucuronic acid in the liver by?
enzyme UDP glucuronyl transferase.
LFT: Bilirubin
N= 0.5 mg/dl. Elevated in obstructive & hemolytic jaundice
LFT: Alkaline phosphatase
Raises with biliary tract obstruction , hepatocellular damage
Elevated in osteoblastic bone activity
LFT: Gama-Glutamyl transpeptidase (GGT)
GGT levels are parallel those of Alk phos
LFT: SGOT , SGPT (AST,ALT)
Elevated in hepatocellular injury due to leakage ( hepatitis, ischemia)
SGOT in heart , muscle and kidney
LFT: GST (Glutathione S-transferase)
More sensitive marker of hepatocellular damage
LFT: 5ˈ nucleotidase activity
Most sensitive marker of hepatocellular damage
LFT: LDH
High in hepatocellular damage
LFT: Albumin
Hepatic injury causes low production
This LFT raises with biliary tract obstruction
Alkaline phosphatase
Best indicator of hepatocellular dysfunction ( not making Prothrombin)
PT prolongation
Last liver function to fail
Ammonia conversion to urea
Glucose production ( hypoglycemia is sign of worst prognosis)
What are the effects of anesthesia to hepatic function
Decreased Blood flow and Drug metabolism
Increased Biliary pressure
Postoperative jaundice- Resorption of large hematoma or hemolysis after transfusion
Causes of Hyperbilirubinemia
Massive hemolysis with rapid release of bilirubin.
Decrease excretion (e.g. liver damage or bile duct obstruction).
Normal level of free bilirubin=
0.5 mg/dl
bilirubin > 1.5 mg/dl
jaundice
Van den Bergh test
Differentiates between hemolytic jaundice and obstructive jaundice
High unconjugated (free) bilirubin in blood
hemolytic jaundice
Liver has no time to conjugate due to excessive production of bilirubin in spleen.
High conjugated bilirubin in blood
Obstructive jaundice
Obstruction is past hepatocytes therefore more conjugated bilirubin
In Obstructive jaundice, obstruction may be due to?
Gall stones
Cancer of head of pancreas
Damage of hepatic cells e.g. in hepatitis
-ve urobilinogen in urine and no stercobilin in stool “ clay color stool” indicate?
total obstruction of bile flow
high conjugated bilirubin in urine indicates
severe biliary obstruction
Sign and symptoms of viral hepatitis
- Dark urine
- Fatigue
- Anorexia
- Fever
- Emesis
- Headache
- Abdominal discomfort
- Light-colored stool
- Pruritus
- Jaundice
- Tender hepatomegaly
Hepatitis A Virus (HAV)
Fecal-oral route, water born, shellfish, gays , IV drug abuser
Short incubation period (3 wk)
Course: cholestatic (high bilirubin) or hepatocellular (high transaminase)
No carriers, not chronic (doesn’t hurt but taste bad!)
Dx: HAV IgM
Exposure: immunize human Ig
Hepatitis B Virus (HBV)
DNA virus
Parenteral , skin poppers, vertical (mother to neonate) and sexual (50%)
Long incubation period (3 mo)
HBsAg + , HBcAb +
Carriers , lead to chronic
Predispose to cancer
Exposure: vaccine+HBIG
Dx: HBsAg; HBcAb- IgM; HBeAg
Hepatitis B Virus (HBV)
DNA virus
Parenteral , skin poppers, vertical (mother to neonate) and sexual (50%)
Long incubation period (3 mo)
HBsAg + , HBcAb +
Carriers , lead to chronic
Predispose to cancer
Exposure: vaccine+HBIG
Dx: HBsAg; HBcAb- IgM; HBeAg
Hepatitis C Virus (HCV)
Skin poppers (60%)
Sexual
Before 90’s – blood transfusion
Carriers
Predispose to cancer, cirrhosis and chronic hepatitis
HDVs
Defective virus
Requires co-infection with HBV
More severe course- fulminant hepatitis
More prevalent in IV drug abuser, hemophiliacs
IgM antibody to HAV; best test to detect active hepatitis A
IgM HAVAb
HBsAg
Antigen found on surface of HBV, indicates active state; Appears before the symptoms, persists 3-4 months , disappears when virus clear. If persistent for > 6 months- carrier state
Antibody to ABsAg, appears a few weeks after the disappearance of the antigen and indicates recovery and vaccination (immunity)
HBsAb
Antigen associated with core of HBV
HBcAg
Antibody to HBcAg; Only marker during window period. Appears 4 weeks after the appearance of HBsAg, is present during acute illness and can remain elevated for years
HBcAb
HBeAg
A second different antigenic determinant in the HBV core. Important indicator of infectivity ( transmissibility) BEware!
Antibody to ‘e’ antigen; indicates low transmissibility
HBeAb
These drugs can cause acute hepatitis
INH
Methyldopa
These drugs can cause Cholestasis
Chlorpromazine
Erythromycin
Estrogen
These drugs can cause Fatty liver
Steroids, alcohol (MCC), tetracycline
Acetaminophen overdose
Dose related
Reduced glutathione stores
Can be severe , fatal
Sky high transaminases- in thousands !
Severe toxicity with low dose = ETOH
Treatment :N-Acetylcysteine
Rare, often fatal childhood hepatoencephalopathy
Reye’s syndrome
Reye’s syndrome Findings
Fatty liver
Hypoglycemia “ominous sign”
Coma
Associated with viral infection (VZV, influenza B) and salicylates; thus aspirin is no longer recommended for children (use acetaminophen with caution!)
Why should babies not receive baby aspirin.
It is associated with reye’s syndrome.
Chronic alcoholism is characterized by
Thrombocytopenia
Leukopenia
Megaloblastic anemia- Due to dietary deficiency of folate (and thiamine).
MAC elevated in sober and decreased in intoxicated patients.
Bleeding due to sick liver
Bleeding due to sick liver can be treated by
Platelet transfusion
Vit K
FFP
Cryo
Delirim Tremens -DTs
Alcohol withdrawal syndrome
After 24-96 hrs cessation of drinking
Restlessness, confusion, agitation and hallucinations
Treatment: Long acting benzo, Antipsychotic
ALCOHOLIC HEPATITIS
Most common drug induced hepatitis
Low portal blood flow (due to high resistance).
Oxygen delivery depends on hepatic artery blood flow
Avoid hypotension during anesthesia
Clinical : fever, tachycardia, jaundice , RUQ symptoms
Lab: SGOT (AST) to SGPT (ALT) ratio is greater than 1.5 (AST>ALT)
SGOT (AST) to SGPT (ALT) >1.5
ALCOHOLIC HEPATITIS
General characteristics of fatty liver
Disease of fat people, reversed by weight loss
Common cause of asymptomatic LFT abnormalities
Microvesicular fat vs. macrovesicular fat
Chronic Hep B
Persistence of LFT’s abnormalities > 6 months
Sx: asymptomatic carrier vs chronic active disease
Prognosis: cirrhosis and hepatoma
Tx: alpha-interferon
Chronic Hepatitis C
Frequent progression to chronic hepatitis and cancer (20X)
Tx: alpha-interferon
Chronic Autoimmune hepatitis
Typically disease of women
May be hirsute, Cushinoid
Dx: Anti smooth muscle antibody
Tx: immune suppression : steroid
Anesthetic consideration in Hepatitis
Less anesthetic is needed
Aspiration precaution must be implemented
Increase risk of surgical bleeding
Brain less tolerant to hypoxia
Decrease neurotransmitter uptake => increase levels of catecholamine
Copper overload creating copper accumulation in liver, brain, cornea
Wilson’s disease
Elevated ceruloplasmin; Low serum copper
Wilson’s disease
Keyser-Fleischer ring at rim of cornea
Wilson’s disease
D-penicillamine
treatment for wilson’s disease
Features of Wilson’s disease
Copper overload creating copper accumulation in liver, brain, cornea
Elevated ceruloplasmin; Low serum copper
Asymptomatic
Chronic active hepatitis , fulminant hepatic failure
Neuropsychiatric; dementia
RTA
Keyser-Fleischer ring at rim of
cornea
Hemochromatosis
Hyper-absorption and deposition of iron in many organs
Secondary to multiple blood transfusion
Elevated ferritin and % Fe sat
Hyper-absorption and deposition of iron in many organs
Hemochromatosis
Clinical features of Hemochromatosis
Liver diseases => cirrhosis => hepatoma
DM ( ‘Bronze’ diabetes)
Arthropathy
Cardiomyopathy
Impotence ( due to pituitary dysfunction “hypo pit”)
Treatment of hemochromatosis
Repeated phlebotomy, deferoxamine
This patient has enough in the body to set off metal detectors
hemochromatosis
Iron~50 g
alpha 1-Antitrypsin deficiency
Autosomal recessive
High trypsin level; a proteolytic substance
Rare syndrome of progressive cirrhosis
With or without pulmonary disease
alpha 1-Antitrypsin deficiency
Autosomal recessive
High trypsin level; a proteolytic substance
Rare syndrome of progressive cirrhosis
With or without pulmonary disease
Findings of alpha 1-Antitrypsin deficiency
Emphysema
Neonatal hepatitis; chronic hepatitis in adults
Cirrhosis and hepatoma
Low alpha-1 antitrypsin level is diagnostic for?
alpha 1-Antitrypsin deficiency
Treatment for alpha 1-Antitrypsin deficiency
Treatment of complication
Hepatoma surveillance
Liver transplant for end-stage liver disease
Diffuse fibrosis of liver that destroys normal architecture. Widespread nodule formation in the liver.
Liver cirrhosis
Distortion of liver anatomy in Liver cirrhosis
causes?
Decreased blood flow leading to portal hypertension and back streaming.
Liver failure.
Causes of Liver cirrhosis (9)
Ethyl alcohol EOH (MCC) HBV HCV PBC (Primary biliary cirrhosis) CHF Autoimmune hemochromatosis Wilson’s disease Alpha 1 antitrypsin deficiency
Differentiate between micronodular and macronodular in liver Cirrhosis
Micronodular: nodules < 3 mm, uniform size. Due to metabolic insult (e.g. alcohol)
Macronodular: nodules > 3 mm, varied size. Due to significant liver injury, leading to hepatic necrosis (e.g. post-infectious or drug induced hepatitis). Increased risk of hepatocellular Ca.
Effects of portal hypertension (low BF through liver)
Bleeding from esophageal and gastric varices => hematemesis, melena
Splenomegaly, cardiomyopathy Caput medusae (distension of abdominal wall veins)
L albumin => ascites => decrease FRC
Due to excessive hydrostatic pressure liver “sweating” occurs. Also due to low albumin
Abdominal distention, shifting dullness (+ve)
Testicular atrophy
Hemorrhoids, esophageal varices “back stream”
Effects of liver cell failure
Bleeding tendency (Low prothrombin). Major cause of morbidity and mortality.
Hepatic encephalopathy (due to High NH3)
Scleral icterus
Fetor hepaticus (bad breath like corpse)
Spider navi
Gynecomastia, Loss of sexual hair (due to decreased breakdown of estrogen)
Jaundice
Liver “flap” : coarse hand tremor
Anemia ,low PO2
Impair protein synthesis => increase third spacing => Increase effect of protein bound drugs e.g. barbiturates
Hepatic encephalopathy => coma
Treatment of cirrhosis
Lactulose (lactic acid) converts NH3 to NH4+ that is poorly absorbed and thus excreted (Base+ Acid => ionized form)
Gut sterilization by neomycin enema kills intestinal bacteria responsible for NH3 production
Protein restricted diet
Maintain BP to maintain hepatic artery blood flow
BP should be maintained in liver cirrhosis to maintain hepatic artery blood flow because
Oxygen supply largely depends on hepatic artery blood flow as portal blood flow decreased in cirrhosis.
Remember portal vein supplies 50% 02 same as hepatic artery
Anesthetic consideration for a patient with liver cirrhosis
High dose of non-depolarizing NM blockers is needed (due to increase volume of distribution)
Sux toxicity due to deficient plasma cholinesterase
Mnemonic AC, 9H in liver cirrhosis refers to?
Ascites Coagulopathy Hypoalbuminemia Portal Hypertension Hyperammonnemia Hepatic encephalopathy Hepatorenal syndrome Hypoglycemia Hyperbilirubinemia/jaundice Hyperestrinism Hepatocellular carcinoma
High pressure in portal vein ( >10 mmHg)
Portal Hypertension
Most common cause of portal hypertension is?
Alcoholic cirrhosis (Fibrosis in liver, high resistance to portal vein)
Patient with portal hypertension is Prone to massive bleeding because?
Backward pressure => congestive splenomegaly => platelet sequestration => thrombocytopenia
Impaired coag factor production
drugs for treatment for portal hypertension
Propranolol
Vasopressin +NTG
Treatment of portal hypertension
Endoscopic sclerotherapy
Banding
Portocaval shunt
Encephalopathy is an Adverse effect of portocaval shunt because?
Blood is bypassing the liver, no detoxification.
Portal hypertension Risk factor bleeding
variceal size
endoscopic stigmata
Preoperative Anesthetic considerations for a patient with portal hypertension
Wait till normalization of LFTs
LFT, Lytes, HBsAg
High PT => Give Vit K and FFP
Intraoperative Anesthetic considerations for a patient with portal hypertension
Inhalation A. are preferable to IV A. => Isoflurane is agent of choice for maintaining hepatic blood flow.
Avoid decrease in hepatic blood flow (low O2 delivery) due to: Hypotension; Excessive sympathetic activation; High mean airway pressure.
Regional anesthesia is useful in advanced liver disease
Greater loading dose and smaller maintenance doses of muscle relaxant
Gall stones Form when
solubilization bile acids and lecithin are overwhelmed by increased cholesterol and/or bilirubin. OR “too much water absorption”
Risk factors for gallstones (4 F’s)
Female
Fat
Fertile
Forty
Gall stones May present with Charcot’s triad which is?
Epigastric/RUQ pain radiating to shoulder
Fever
Jaundice
Describe Three types of Gall stones
Cholesterol stones: MC,associated with obesity, Chron’s disease, C.fibrosis, advanced age, estrogen, multiparity, rapid weight loss and Native American origin
Mixed stones: have both cholesterol and pigment component.
Pigment stones: seen in pt with chronic RBC hemolysis, alcoholic cirrhosis, advanced age, and biliary infection
Cholesterol stones are most commonly associated with?
obesity Chron’s disease C.fibrosis advanced age estrogen multiparity rapid weight loss Native American origin
Diagnosis and treatment of gallstones
Dx with sono
Tx with cholecystectomy
Physiological jaundice of newborn
During 1st week
High unconjugated bilirubin
No clinical importance
Due to deficiency of glucuronyl transferase in the immature liver; in primies
Tx: Phototherapy
Prehepatic hepatic dysfunction lab findings and causes
Bilirubin: High unconjugated
Aminotransferase: Normal
Alkaline phosphatase: Normal
Causes: Hemolysis, Hematoma resorption, Bilirubin overload from whole blood transfusion
Intrahepatic (Hepatocelluar) hepatic dysfunction lab findings and causes
Bilirubin: High conjugated
Aminotransferase: Markedly high
Alkaline phosphatase: Normal or slightly high
Causes: Viral, Drugs, Sepsis, Hypoxemia, Cirrhosis
Posthepatic (cholestatic) hepatic dysfunction lab findings and causes
Bilirubin: High conjugated
Aminotransferase: Normal or slightly high
Alkaline phosphatase: Markedly high
Causes: Stones, Sepsis
Most common Congenital Hyperbilirubinemia
Gilbert syndrome
Congenital Hyperbilirubinemia marked by low uptake of bilirubin by liver cells and decreased activity of glucuronyl transferase
Gilbert syndrome
Severe form of Congenital Hyperbilirubinemia marked by early death and damage to basal ganglia.
Grigler-Najjar syndrome
Congenital Hyperbilirubinemia marked by Defective bilirubin transport
Dubin-Johnson syndrome
Compare the pathophysiology of Primary Biliary Cirrhosis and Primary sclerosing Cholangitis
PBC: Autoimmune reaction leading to Destruction of microscopic biliary ductules.
PSC: Idiopathic intra or extra hepatic bile duct fibrosis leading to stricturing that cause obstruction
Compare the presentation of Primary Biliary Cirrhosis and Primary sclerosing Cholangitis
PBC: Middle-age women, Pruritus (high bile salts) , jaundice, dark urine, light stool, hepatosplenomegaly, Vit ADEK deficiency .
PSC: Pruritus (high bile salts) jaundice, dark urine, light stool, hepatosplenomegaly
Compare the labs of Primary Biliary Cirrhosis and Primary sclerosing Cholangitis
PBC: High conjugated bilirubin, high Alk P, high cholesterol
PSC: High conjugated bilirubin and Alk P
Compare the treatment of Primary Biliary Cirrhosis and Primary sclerosing Cholangitis
PBC: Liver transplant
PSC: ERCP
Compare the diagnosis of Primary Biliary Cirrhosis and Primary sclerosing Cholangitis
PBC: Elevated Anti-mitochondrial antibodies; Liver biopsy to confirm diagnosis
PSC: Associated with ulcerative colitis; US
peptic ulcer desease
Pain Greater with meals: weight loss
Helicobacter pylori infection in 70%; NSAID (inhibit PG secretion)
Due to low mucosal protection against gastric acid
High in smokers, ETOH, stress ‘type A’ personality
