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208 Cards in this Set

  • Front
  • Back
Source of salivary secretions
Parotid (most serous), submandibular, submaxillary, and sublingual glands (most mucinous)
Products contained in saliva (fct)
(1) alpha amylase (begins starch digestion); inactivated by low pH in stomach
(2) bicarbonate (neutralizes oral bacterial acids, maintains dental health)
(3) mucins (glycoproteins) lubricate food
(4) antibacterial secretory products
(5) growth factors promote epithelial renewal
Salivary glands secretion innervations
Sympathetic (T1-T3) and parasympathetic (facial, glossopharyngeal n)
Slow flow (hypotonic)
High flow (isotonic)
Gastrin
(a) source
(b) action
(c) stimulus
(d) inhibition
(e) notes
(a) G cells (antrum of stomach)
(b) incr H+ secr, growth of gastric mucosa, gastric motility
Also incr pepsinogen (chief) and histamine (ECL)
(c) Incr by stomach distension, aa;s, peptides, vagal stim
(d) Decr by stomach pH<1.5
(e) incr in Zollinger Ellison syndrome. Phenylalanine and tryptophan potent stimulators
Cholecystokinin
(a) source
(b) action
(c) stimulus
(d) inhibition
(e) notes
(a) I cells (duodenum and jejunum)
(b) incr pancreatic secr, incr gallbladder contr
Decr gastric emptyin
(c) incr by fatty acids, amino acids
(d) n/a
(e) in cholelithiasis, pain worsens after fatty food ingestion due to incr CCK
Secretin
(a) source
(b) action
(c) stimulus
(d) inhibition
(e) notes
(a) S cells (duodenum)
(b) incr pancreatic HCO3, bile secretion
Decr gastric acid secretion
(c) incr by FA in duodenum
(d) n/a
(f) incr HCO3 neutralizes fastric acid in duodenum, allowing pancreatic enzymes to fct
Somatostatin
(a) source
(b) action
(c) stimulus
(d) inhibition
(e) notes
(a) D cells (pancreatic islets, GI mucosa)
(b) decr gastric acid and pepsinogen secretion, pancreatic and small int fluid secretion, GB contraction, insulin and glucagon release
(c) incr by acid
(d) decr by vagal stimulation
(e) inhibitory hormone; antigrowth effects (digestion and absorption of substances needed for growth); used to treat VIPoma and carcinoid tumors
Glucose-dependent insulinotropic peptide (GIP)
(a) source
(b) action
(c) stimulus
(d) inhibition
(e) notes
(a) K cells (duodenum, jejunum)
(b) exocrine: decr H+ secretion
Endocrine: incr insulin release
(c) incr by FA, aa, oral glucose
(d) n/a
(e) an oral glucose load is used more rapidly than the equivalent give by IV
Vasoactive intestinal peptide
(a) source
(b) action
(c) stimulus
(d) inhibition
(e) notes
(a) parasympathetic ganglia in sphincters, GB, small intestine
(b) incr intestinal water and electrolyte secretion, incr relaxation of intestinal smooth muscle and sphincters
(c) incr by distention and vagal stim
Decr by adrenergic output
(d) VIPoma-non alpha or beta islet cell pancreatic tumor that secretes VIP and causes copius diarrhea
Nitric oxide
(a) source
(b) action
(c) stimulus
(d) inhibition
(e) notes
(a) n/a
(b) incr smooth muscle relaxation, including LES
(c) n/a
(d)n/a
(e) loss of NO secretion implicated in incr LES tone in achalasia
Motilin
(a) source
(b) action
(c) stimulus
(d) inhibition
(e) notes
(a) small intestine
(b) produces MMC's
(c) incr in fasting state
(d) n/a
(e) n/a
Histamine
(a) source
(b) action
(c) stimulus
(d) inhibition
(e) notes
(a) enterochromaffin cells
(b) incr gastric acid secretion (directly and potentiates gastrin and vagal stimulation)
(c) gastrin, ach
(d) n/a
(e) n/a
GRP
(a) source
(b) action
(c) stimulus
(d) inhibition
(e) notes
(a) vagal nerve endings
(b) stimulates gastrin release from G cells
(c) cephalic stimulation, gastric distension
(d) n/a
(e) n/a
Pancreatic polypeptide
(a) source
(b) action
(c) stimulus
(d) inhibition
(e) notes
(a) F cells of pancreas, small intestine
(b) protein, fat, glucose in lumen
(c) n/a
(d) decr pancreatic secretion
(e) n/a
Enteroglucagon
(a) source
(b) action
(c) stimulus
(d) inhibition
(e) notes
(a) L cells of intestine
(b) decr gastric/pancreatic secretions
Incr insulin release
(c) n/a
(d) n/a
(e) n/a
Intrinsic factor
(a) source
(b) action
(c) regulation
(d) notes
(a) parietal cells (stomach-body/fundus)
(b) vitB12 binding protein (required fro B12 uptake in terminal ileum)
(c) n/a
(d) autoimmune destruction of parietal cells causing chronic gastritis and pernicious anemia
Gastric acid
(a) source
(b) action
(c) regulation
(d) Notes
(a) parietal cells (stomach)
(b) decr stomach pH
(c) incr by histamine, Ach, gastrin
Decr by stomatostatin, Gip, prostaglandin secretion
(d) gastrinoma: gastrin secreting tumor that causes continuous high levels of acid secretion and ulcers
Pepsinogen
(a) source
(b) action
(c) regulation
(d) notes
(a) chief cells (stomach-body/fundus)
(b) protein digestion
(c) incr by vagal stimulation, local acid
(d) inactive pepsinogen (goes to active by H+)
Bicarbonate
(a) source
(b) action
(c) regulation
(d) notes
(a) mucosal cells (stomach, duodenum, Brunner's glands)
(b) neutralizes acid, prevents autodigestion
(c) incr by secretin
(d) bicarb trapped in mucus that covers gastric epithelium
Leukoplakia
(a) description
(b) complictions
(c) predisposing factors
(a) white plaques on oral mucosa (hyperkeratosis)
(b) 10% have epithelial dysplasia (precancerous)
(c) smoking, tobacco, alcohol abuse, chronic friction, irritants
Erythroplakia
(a) description
(b) complications
(a) flat, smooth, red lesion in oral cavity
(b) high risk of malignant transformation (atypical epithelial cells)
Hair leukoplakia description
Wrinkled surface, patched on side rather than middle of tongue; no malignant transformation
Lichen planus
White reticular lesions on buccal mucosa/tongue
Benign tumors of oral cavity
Hemaniogoma, hamartoma, fibroma, lipoma, adenoma, papilloma, neurofibroma, nevi
SCC of oral cavity
(a) peak age
(b) risk factors
(c) common site
(a) 40-70
(b) tobacco, alcohol, esp together
(c) lower lip (but floor and tongue also)
Achalasia
(a) pathophys
(b) symptoms
(c) etiology
(d) diagnosis
(e) increase risk for?
(a) failure of Les to relax due to loss of myenteric (Auerbach's) plexus; high LES opening pressure
(b) dysphagia, regurg, aspiration, chest pain
(c) idiopathic; secondary to Chagas or malignancy
(d) barium sloww: bird's beak
(e) esophageal carcinoma
Esophageal varices
Related to portal HTN; painless bleeding of submucosal veins in lower 1/3 of esophagus
Mallory-Weiss syndrome
Painful mucosal lacerations at GE jct due to severe vomiting; found in alcoholics/bulimics
Boerhaave syndrome
Transmural esophageal rupture due to violent retching
Sliding hernia
GE jct above diaphragm (assoc w/reflux); 90% of stomach hernias
Paraesoageal hernia
Gastic cardia above diaphragm; at risk for strangulation and infarction
Schatszki rings
Mucosal rings at squamocolumnar jct below aortic arch
Tracheoesophageal fistula
-usually esoph blind pouch w/fistula b/w lower eso and trachea
-assoc w/other congenital malformations
Esophageal strictures assoc w/?
Lye ingestion
Esophagitis associated w?
Reflux, infection (HSV-1, CMV, Candida, chemical ingestion
Plummer Vinson Syndrome
Triad: dysphagia (esophageal web), glossitis, iron deficiency anemia
Zenker diverticula
(a) location
(b) symptoms
(a) jct of pharynx and esophagus in elderly men
(b) dysphagia, regurg of undigested food soon after ingestion
Esophageal Diverticula
Protrusion of 1+ layer of pharyngeal or esophageal wall
Traction diverticula
True diverticula in mid esophagus; usually asypmtomatic
Barrett's esophagus
(a) describe
(b) cause
(c) incr risk for?
(a) glandular metaplasia; replacement of nonkeratinized stratified squamous w/intestinal epithelium
(b) GERD
(c) esophageal adenocarcinoma
Risk factors for esophageal cancer
Alcohol/achalasia
Barrett's
Cigarettes
Diverticuli
Esophageal web
Esophagitis
Familial
Portion of esophagus mainly affected by squamous cell? Adenocarcinoma?
Upper/middle 1/3: squamous
Lower 1/3: SCC
Celiac sprue
(a) pathophys
(b) pathology
(c) incr risk of?
(d) screening
(a) Abs to gluten (gliadin) in wheat and grains
(b) atrophy of villi in jejunum (small bowel only; mainly jejunum); lymphocytes in lamina propria
(c) neoplasm esp lymphoma
(d) tissue transflutaminase
Tropical sprue
(a) etiology
(b) pathology
(a) unknown; prob infectious (resopnds to antibiotics)
(b) smilar to celiac but can affect whole bowel
Whipple's disease
(a) etiology
(b) pathology
(c) symptoms
(d) epidemiology
(a) infx w/Tropheryma whippelii (G+ bacilli)
(b) PAS positive macs in lamina propria, mesenteric nodes
(c) malabsorption, arthralgias, cardiac and neuro sx
(d) older men
Disaccharidase deficiency
(a) most common
(b) path
(c) symptoms
(d) etiology
(a) lactase deficiency
(b) normal appearing villi
(c) osmotic diarrhea
(d) can be self limited if following villi injury (viral diarrhea)
Pancreatic insufficiency
(a) etiologies
(b) effect
(a) CF, obstructing cancer, chronic pancreatitis
(b) malabsorption of fat and fatsoluble vitamins
Dermititis herpetiformis (associated with what GI disease)?
Celiac sprue
Acute gastritis
(a) describe
(b) etiologies
(c) symptoms
(a) disruption of mucosal barrier; inflammation
(b) stress, NSAIDs, uremia, alcohol, burns, brain injury
Cushing's ulcers
Caused by CNS trauma (incr vagal stimulation, incr Ach, incr acid)
Curling's ulcer
Caused by burns (incr plasma volume, sloughing of fastric mucosa)
Chronic gastritis Type A
(a) location
(b) associations
(a) fundus/body of stomach
(b) autoimmune disorder characterized by autoabs to parietal cells, pernicious anemia, or achlorhydria
Chronic gastritis Type B
(a) location
(b) etiology
(c) incr risk for?
(a) antrum
(b) H pylori
(c) incr risk of MALTomas
Menetrier's disease
(a) describe
(b) sx
(c) incr risk for?
(d) pathology
(a) gastric hypertrophy
(b) protein loss, incr mucous cells
(c) precancerous
(d) rugae so hypertrophied they look like gyri
Stomach cancer
(a) type
(b) behavior
(c) risk factors
(d) histology
(e) presentation
(a) almost always adenocarcinoma
(b) aggressive; spread to LN/Liver
(c) nitroasmines (smoked foods), pernicious anemia/achlorhydria, type A blood, chronic gastritis, genetic predisposition
(d) 50% in antrum and pylorus;
(e) usually asymptomatic until late; mayy have acanthosis nigricans; Virchow's node
Virchow's node
Involvement of left supraclavicular node by mets from stomach (most common site of met)
Linitis plastica
Infiltrating gastric carcinoma (fibrous response)
Krukenberg's tumor
Bilateral mets to ovaries (abundent signet rings)
Gastric ulcer
(a) symptoms
(b) epidemiology
(c) etiologies
(d) risk for future malignancy
(a) epigastric pain can be greater w/meals (wt loss)
(b) often in older pts
(c) H pylori infx in 70%; chronic NSAIDs also implicated; due to decr mucosal protection against gastric acid
(d) rarely do become malignant
Duodenal ulcer
(a) etiology/sx
(b) associations
(c) appearance
(d) complications
(a) incr acid secretion or decr protection; pain decr w/meals-wt gain
(b) 100% have H pylori infx
(c) clean, "punched out" margins; hypertrophy of Brunner's glands
(d) bleeding, penetration into pancreas, perforation, obstruction (not intrinsically cancerous)
Pyloric stenosis
(a) describe
(b) classic case
(c) treatment
(a) congenital hypertrophy of pyloric muscle
(b) firstborn boy, projectile vomiting 3-4wks after birth; assoc w/olive mass in epigastric region
(c) surgical
Ischemic bowel disease
(a) etiology/most common artery
(b) epidemiology
(c) symptoms
(a) thrombosis/embolism of SMA (50%); venous thrombosis for 25%; commonly occurs at splenic flexture
(b) >60YO
(c) abdominal pain, n/v
Duodenal atresia
(a) describe
(b) presentation
(c) associations
(a) congenital absence of region of bowel
(b) polyhydramnios, obstruction, bile stained vomiting in neonate; "double bubble" due to failure of recanalization
(c) down's syndrome
Intussusception
(a) epidemiology
(b) cause
(c) complications
(a) usually infants
(b) telescoping of 1 bowel segment into distal segment;; often due to mass
(c) can compromise blood supply
Volvulus
(a) describe
(b) complications
(c) common location
(d) peak age
(a) twisting of bnowel around it's mesentery
(b) obstruction, infarction
(c) sigmoid colon common; redundant mesentery
(d) elderly
GI lymphoma
(a) most common type
(b) at risk population?
(a) usually NHL, large cell, diffuse
(b) immunosuppressed
MALToma
(a) histo
(b) outcome
(c) associations?
(d) treatment
(a) often follicular
(b) follow a more benign course than other GI lymphomas
(c) h pylori
(d) may regress after Ab therapy
Appendicitis
(a) epidemiology
(b) presentation
(c) complications
(d) differential
(a) all age groups
(b) diffuse periumbilical pain; n/v/f
(c) perforation (peritonitis)
(d) diverticulitis (elderly), ectopic pregnancy (use beta hCG to rule out)
Chron's disease
(a) possible etiology
(b) distribution
(c) gross morphology
(d) microscopic morphology
(e) complications
(f) intestinal manifestation
(g) extraintestinal manifestation
(h) genetic history
(i) cancer risk
Chron's disease
(a) possible etiology: postinfectious
(b) distribution: anywhere in Gi; typically terminal ileum; skip lesions common
(c) gross morphology; transmural inflammation; creeping fat, "string sign" on barium swallow; cobblestone
(d) microscopic morphology: noncaseating granulmonas and lymphoid aggregates
(e) complications: linear ulcers, strictures, fistulas, perianal dz, malabsorption, nutritional depletion
(f) intestinal manifestation; diarrhea that may or may not be bloody
(g) extraintestinal manifestation: immunologic disorders, migratory polyarthritis, erythema nodosum; ankylosing spondylitis; uveitis; immunological disorders
(h) genetic history; fam hx of any type of IBD assoc w/incr risk
(i) cancer risk: slight
Ulcerative colitis
Chron's disease
(a) possible etiology
(b) distribution
(c) gross morphology
(d) microscopic morphology
(e) complications
(f) intestinal manifestation
(g) extraintestinal manifestation
(h) genetic history
(i) cancer risk
Ulcerative colitis
(a) possible etiology: autoimmune
(b) distribution: continuous always w/rectal involvement
(c) gross morphology: mucosal/submucosal inflammation onlyl pseudopolyps; "lead pipe" appearance on imaging
(d) microscopic morphology: crypt abscesses and ulcers, bleeding
(e) complications; severe stenosis, toxic megacolon, colorectal carcinoma
(f) intestinal manifestation; bloody diarrhea
(g) extraintestinal manifestation; pyoderma gangrenosum, primary sclerosing cholangitis
(h) genetic history; fam hx of any type of IBD incr risk
(i) cancer risk; 5-25%
Treatment for Chron's
Corticosteroids, infliximab
Treatment for UC
Sulfasalazine, inflixamab, colectomy
Diverticulum
(a) describe
(b) most common location
(a) blind pouch popping out of alimentary tract communicates w/lumen of gut; most acquired
(b) sigmoid colon
True diverticulum
All 3 gut layers outpouch
False diverticulum
Only mucosa and submucosa outpouch; usually acquired. Occur esp where vasa recta perforate muscularis externa
Diverticulosis
(a) describe
(b) cause
(c) associated with?
(d) common location
(e) epidemiology/presentation
(a) many diverticula
(b) incr intraluminal pressure w/focal weakness in wall
(c) low fiber diet
(d) sigmoid colon
(e) ~50% >60YO; usually asymptomatic or vague disconfort and/or painless rectal bleeding
Diverticulitis
(a) describe
(b) presentation
(c) complications
(d) treatment
(a) inflammation of diverticula
(b) LLQ pain, fever, leukocytosis
(c) perforation (peritonitis, abscess, bowel stenosis; fsitula w/bladder)
(d) antibiotics
Meckel's diverticulum
(a) cause
(b) complication
(c) five 2's
(a) persistance of vitelline duct or yolk stalk; most common congenital anomaly of GI tract
(b) may contain ectopic acid secreting gastric mucosa; can cause bleedingk, instussusception, volvulus, obstruction near terminal ileum
(c) 2in; 2ft from ileocoecal valve; 2% of population; commonly prsents in first 2yr of life; may have 2 types of epithlia (gastric/panc)
Hirschprung's disease
(a) etiology
(b) presentation
(c) risk incr w/what genetic condition?
(a) congenital megacolon; failure of neural crest cell migration (lack of both plexi)
(b) chronic constipation early; usually failure to pass meconium
(c) risk incr w/Down syndrome
Meconium ileus
Meconium plug obstructs intestine preventing stool passage at birth; CF
Necrotizing enterocolitis
Necrosis of intestinal mucosa and possible perforation; neonates; can involve entire Gi
Intestinal adhesion
(a) describe
(b) cause
(a) acute bowel obstruction; have well demarcated necrotic zones
(b) commonly from recent surgery
Angiodysplasia
(a) describe
(b) location
(c) epidemiology/presentation
(a) tortuous dilation of vessels leading to bleeding
(b) usually cecum and asc colon
(c) older patients/lowe rintestinal bleeding
Imperforate anus
Failure of perforation of the membrane that separates endodermal hindgut from ectodermal anal dimple
Majority of colonic polyps; usually location
90% benign hyperplastic hamartomas; often rectosigmoid
Significance of villous morphology of polyp
More likely to be malignant
Tubular adenoma
(a) gross
(b) epidemiology
(a) pedunculated; 75% of adenomatous polyps
(b) sporadic or familial; avg age of onset 60; usually in left colon
Villous adenoma
(a) gross
(b) risk of malignancy
(a) largest, least common; usually sessile
(b) 1/3 cancerous
Peutz Jehger's syndrome
(a) inheritence
(b) presentation
(c) incr risk of?
(a) audosomal dominant benign polyposis syndrome
(b) hamartomatous polyps in colon and small intestine; hyperpigmented buccal mucosa, lips, hands, genitalia
(c) incr risk of CRC and other visceral malignancies
Turcot syndrome
Colonic polyps assoc w/brain tumors
Gardner Syndrome
Colon polyps assoc w/desmoid tumors risk of colon cancer nearly 100%
Difference in left sided vs right sided colorectal cancer?
Left (obstruction
Right (bleed)
Risk factors for colorectal cancer
Villous adenomas
Chronic IBD (espUC)
Incr age
FAP
HNPCC
Past medical Hx or Fam Hx
Tumor marker for CRC
CEA
Majority of CRC (type)
Adenocarcinoma (98%)
Squamous in anal region and assoc w/papilloma viruses
Family Adenomatous polyposis
(a) inheritence
(b) gene/chromosome
(c) presentation
(d) risk for cancer
(a) AD
(b) APC c5q
(c) thousands of polyps; pancolonic; always involve rectum
(d) virtually 100%
HNPCC/Lynch syndrome
(a) mutation
(b) site of Gi tract involvement
(c) risk for cancer
(a) DNA mismatch repair genes
(b) proximal colon always involved
(c) 80%
Carcinoid tumor
(a) most common site
(b) EM
(c) classic symptoms
(a) small intestinal tumor of endocrine cells
(b) dense core bodies
(c) wheezing; right sided heart murmurs; diarrhea; flushing (due to serotonin)
Only if met outside of GI due to serotonin inactivation by liver 1st pass metabolism
Micronodular cirrhosis most often due to?
Metabolic insult (alcohol, hemochromatosis, wilson's)
Macronodular (>3cm) cirrhosis most often to? Incr risk for?
Significant liver injury leading to hepatic necrosis (post infection, drug induced).
Incr risk for HCC
Major diagnostic use of aminotransferases (AST/ALT)?
Viral hepatitis (ALT>AST)
Alcoholic hepatitis (AST>ALT)
MI (AST)
Major diagnostic use of GGT (gamma glutamyl transpeptidase)
Various liver diseases (incr w/heavy alcohol consumption)
Major diagnostic use of alkaline phosphatase
Obstructive liver disease (HCC)
Bone disease
Bile duct disease
Major diagnostic use of amylase
Acute pancreatitis, mumps
Major diagnostic use of lipase
Actue pancreatitis
Major diagnostic use of ceruplasmin
Wilson's disease (decr)
Reye's syndrome
(a) epidemiology
(b) findings
(c) etiology
(a) fatal childhood hepatoencephalopathy
(b) fatty liver (microvescicular change); hypoglycemia; coma
(c) assoc w/viral infx (esp VZV influenza B) treated w/salicylates
3 major stages of alcoholic liver disease
Hepatic steatosis
Alcoholic hepatitis
Alcoholic cirrhosis
Hepatic steatosis
Short term change assoc w/minor alcohol intake; macrovesicular fatty change
Alcholic hepatitis histology
Sustained long term consumption
Swollen necrotic hepatocytes w/neutrophilic infiltration
Mallory bodies present
AST>ALT (>1,5)
Alcoholic cirhossis
(a) appearance
(b) location of damage
(b) symptoms
(a) micronodular, irregularly shrunken liver w/hobnail appearance
(b) sclerosis around central vein (Zone III)
(c) manifestations of chronic liver disease
Leading etiologies of cirrhosis
hepC and alcohoism
Leading causes of intrahepatic portal HTN
Most common cause usually secondary to cirrhosis; also schistosomiasis; sarcoid
Leading causes posthepatic portal HTN
Right sided heart failure, Budd Chiari syndrome
Leading cause of prehepatic portal HTN
Portal vein obstruction
Clinical manifestations of portal HTN
Ascites
Varices (hrmorrhoids, esophageal, caput medusae)
Encephalopathy
Splenomegaly
Gynecomastia (impaired estrogen metabolism)
Gonadal atrophy
Amenorrhea
Spider angiomata
Palmar erythema
Atelectasis
Nutmeg liver
Backup of blood into liver; usually right sided heart failure or Budd chiari
Mottled like nutmeg
Centrolobular congestion and necrosis can result in cardiac cirrhosis
Primary Sclerosing cholangitis
(a) presentation
(b) associated w?
(c) predisposition for?
(d) imaging appearance
(e) diagnosis (LFT)
Concentric "onion skin" bile duct fibrosis
(a) chronic fibrosing inflammatory disease of extrahepatic and larger intrahepatic bile ducts
(b) IBD
(c) predisposition for cholangiocarcinoma; can lead to secondary biliary cirrhosis
(d) "beading" on ERCP; alternating strictures and dilation
(e) incr ALP
Budd chiari syndrome
(a) describe
(b) presentation
(c) associated with?
(a) occlusion of IVC or hepatic veins w/centrilobular congestion and necrosis leading to congestive liver disease
(b) HSM, ascites, abd pain, liver failure; NO JVD!
(c) pvera-pregnancy-HCC
Hepatocellular jaundice
(a) composition of hyperbilirubinemia
(b) urine bilirubin
(c) urine urobilinogen
(a) composition of hyperbilirubinemia: conjugated/unconjugated
(b) urine bilirubin: high
(c) urine urobilinogen: normal or low
Obstructive jaundice
(a) composition of hyperbilirubinemia
(b) urine bilirubin
(c) urine urobilinogen
(a) composition of hyperbilirubinemia: conjugated
(b) urine bilirubin: incr
(c) urine urobilinogen: decr
Hemolytic jaundice
(a) composition of hyperbilirubinemia
(b) urine bilirubin
(c) urine urobilinogen
(a) composition of hyperbilirubinemia: unconjugated
(b) urine bilirubin: absent (no color)
(c) urine urobilinogen: incr
Hemochromatosis
(a) classic triad; other sx
(b) cause
(c) blood chemistry (ferritin, iron, TIBC, transferrin)
(d) MHC association
(e) treatment
Hemosiderin/iron deposition in tissues
(a) triad: cirrhosis, diabetes mellitus, skin pigmentation
CHF, incr risk of HCC, arrythmias, gonadal insuff, arthropathy
(b) primary (autosomal recessive) or due to multiple blood transfusions
(c) incr ferritin, incr iron, decr TIBC, incr transferrin sat
(d) HLA A3
(e) repeated phlebotomy, deferoxime
Wilson's disease
AR inherited disease; inability to excrete copper and failure of copper to enter circulation as ceruloplasmin (copper accumulation)
Wilson's disease presentation
Rarely before 6
Asterixis
Basal ganglia defeneration (Parkinsonism)
Ceruploplasmin low, cirrhosis, corneal deposits, copper accumulation, carcinoma, choreiform movements
Dementia
Hemolytic anemia
Weakness, fevers, angiomas, eventually portal HTN
Labs for wilson's disease
Low serum ceruloplasmin, incr urinary copper excretion
Liver cell adenoma
(a) incr risk w?
Benign mass
May rupture
Incr risk with anabolic steroid/oral contraceptive use
Nodular hyperplasia
(a) appearance
(b) histology
(a) solitary nodule w/fibrous capsule and bile ductules
(b) stellate fibrous core present; nodular regenerative hyperplasia (normal hepatocytes w/loss of architecture)
Cholangiocarcinoma
(a) associations?
(b) clinical
(c) spread
(a) assoc w/primary sclerosing cholangitis
(b) wt loss, jaundice, pruritis
(c) metastatsize via hematogenous/lymphatic spread
Hepatoblastoma
(a) epidemiology
(b) presentation
(a) rare, malignant neoplasm of children
(b) hepatomegaly, n/v/d, wt loss, elevated AFP
Hepatocellular carcinoma
(a) epidemiology
(b) associations
(c) clinical
(d) markers
(a) 90% of primary liver neoplasms
(b) cirrhosis, HCV, HBV
(c) tender hepatomegaly, ascites, wt loss, fever, polycythemia, hypoglycemia
(d) AFP present in 50-90% of cases
Acute viral hepatitis
(a) clinical
(b) labs
(a) malaise, anorexia, fever, nausea, upper abd pain, hepatomegaly
(b) elevated liver enzymes
Chronic hepatitis
(a) etiologies
(b) histology
(a) HBV, HCV, drug toxicity, Wilson's, alcohol, alpha 1 antitrypsin deficiency, autoimmune hep (b) chronic inflammation w/hepatocyte destruction, cirrhosis, liver failure
Fulminant hep
(a) presentation
(b) etiology
(c) pathology
(a) massive hepatic necrosis and progressive hepatic dysfct
(b) HBV, HCV, HDV, HEV, chloroform, carbon tetrachloride, certain mushrooms, aceaminophen overdose
(c) progressive shrinkage of liver
Pyogenic liver abscesses (main cause and route of infx)
E coli
Klebs
Strep
Staph
Ascending cholangitis most common cause
Parasitic liver abscesses (presentation)
Entamoeba (thick, brown abscess fluid)
Ascaris lumbricoides (can block bile ducts, eosinophilia, verminous abscesses)
Parasitic infx
Schistosomiasis; splenomegaly, portal HTN, ascites
Amebias; Entamoeba histolytica, bloody diarrhea, pain, fever, jaundice, hepatomegaly
Extrahepatic biliary atresia
(a) etiology
(b) presentation
(a) incomplete recanalization
(b) within first weekso f life: jaundice, dark urine, light stools, HSM
Intrahepatic biliary atresia
(a) etiology
(b) association
(c) presentation
(a) diminished number of bile ducts
(b) sometimes assoc w/alpha 1 antitrypsin def
(c) infancy; cholestasis, pruritis, growth retardation, incr serum lipids, icterus
Gilbert's syndrome
(a) labs
(b) clinical presentation
(c) precipitating factor
(a) elevated unconjugated bilirubin w/out overt hemolysis; decr UDP glucuronyl transferase or decr bilirubin uptake
(b) asymptomatic
(c) stress
Crigler Najjar syndrome type I
(a) cause
(b) presentation
(c) treatment
(a) AR; completely absence of glucuronyl transferase
(b) present early; incr unconjugated bilirubin; kernicterus (brain deposition), jaundice
(c) plasmapheresis and phototherapy; death within a few years
Crigler Najjar syndrome type II
(a) cause
(b) presentation
(c) treatment
(a) AD w/mild deficiency of glucuronyl transferase
(b) no kerniecterus but incr unconjugated bilirubin
(c) phenobarbital (incr liver enzyme synth)
Dubin Johnson Syndrome
(a) cause
(b) presentation
(a) defective liver excretion of biirubin due to impaired transport
(b) liver is black; benign
Rotor's syndrome
Asymptomatic similar to Dubin Johnson but no pigmented liver
Problem/result
(a) Gilbert's
(b) Crigler Najjar
(c) dubin johnson
(a) Gilbert's: impaired bilirubin uptake; increased unconjugated bilirubin
(b) Crigler Najjar: problem with bilirubin conjugation; increased unconjugated bilirubinemia
(c) dubin johnson; problem with excretion of conjugated bilirubin; incr conjugated bilirubinemia
Cholestasis
(a) general presentation
(b) intrahepatic causes
(c) extrahepatic causes
(a) impaired excretion of bilirubin; chalky stool
(b) viral hep, cirrhosis, drug tox
(c) gallstones, carcinoma of bile duct, ampulla of vater or head of pancreas
Primary biliary sclerosis
(a) describe
(b) presentation
(c) serum markers
(d) associations
(a) intrahepatic autoimmune disorder
(b) severe obstructive jaundice; steatorrhea, pruritis, hypercholesterolemia (xanthoma); fatigue and pruritis
(c) incr ALP, incr AMA
(d) scleroderma, CREST
Secondary biliary sclerosis
(a) cause/presentation
(b) complications
(c) serum markers
(a) extrahepatic biliary obstruction; incr pressure in intrahepatic ducts causing injury/fibrosis; often presents w/jaundice
(b) ascending cholangitis, bile, stasis
(c) incr ALP, incr conjugated bilirubin
General cause of gallstones
Solubilizing bile acids and lecithin are overwhelmed by incr cholesterol and/or bilirubin
2 types of stones
Cholesterol
Pigmented
Cholesterol stones
(a) appearance on imaging
(b) risk factors
(a) radiolucent w/calcifications-accounts for 80% of stones
(b) obesity, chron's, cystic fibrosis, advanced age, clofibrate, estrogens, multiparity, rapid weight loss, native american origin
Pigment stones
(a) appearance on imaging
(b) cause
(a) radioopaque
(b) chronic RBC hemolysis, alcoholic cirrhosis, advanced age, biliary infx
Complications of gallstones
Ascending cholangitis, acute pancreatitis, bile stasis, cholecystitis, biliary colic, fistula b/w GB abd small intestine
Biliary colic
Gallstones interfere with bile flow causing bile duct contraction
Charcot's traid of cholangitis
Jaundice, fever, RUQ pain
If gallstone obstructs ileocecal valve, what can be seen on imaging?
Air
Diagnosis of gallstones?
Ultrasound
Treatment of gallstones
Cholecystectomy
Cholelithiasis in a young person; think?
Hereditary spherocytosis, sickle cell, or other chronic hemolytic process
Carcinoma of gallbladder
(a) symptoms/epidemiology
(b) pathology
(c) prognosis
(d) risk factors
(a) primarily in elderly; dull abdominal pain, mass, wt loss, anorexia (present late)
(b) typically involves fundus and neck; 90% adenocarcinomas
(c) poor
(d) cholelithiasis, cholecystitis, porcelain gallbladder
Carcinoma of bile ducts (cholangiocarcinoma)
(a) associated with gallstones?
(b) epidemiology
(c) symptoms
(d) risk factors
(a) no
(b) M>F; elderly more frequent
(c) obstructive jaundice
(d) chronic inflammation, infections, ulcerative cholitis
Define acute pancreatitis
Autodigestion of pancreas by enzymes
Causes of acute pancreatitis
Gallstones, ethanol, trauma, steroids, mumps, autoimmune disease/biliary tract diseases, scorpion sting, hypercalcemia/hyperlipidemia, drugs (sulfas)
Clinical presentation of acute pancreatitis
Epigastric abdominal pain radiating to back, anorexia, nausea,
Labs in acute pancreatitis
Elevated amylase, lipase (higher specificity), leukocytosis
Complications of acute pancreatitis
DIC
ARDS (pancreatic enzymes on lung tissue)
Diffuse fat necrosis
Hypocalcemia (Ca collects in pancreatic calcium soap deposits)
Pseudocyst formation
Hemorrhage
Infection
Gross description of acute pancreatitis
Gray areas of destruction, white areas of fat necrosis, red areas of hemorrhage
Chronic pancreatitis complications/presentation
Repeated episodes of mild pancreatitis can lead to damage; may lead to pancreatic insufficiency (steatorrhea, fat soluble vitamin deficiency, DM, pseudocyst formation)
Pancreatic pseudocyst
Possible sequelae of pancreatitis or trauma; fibrous capsule; no epithelial lining or direct communication with ducts
Cystic fibrosis
(a) inheritance
(b) gene defect
(c) presentation
(d) outcome
(a) AR
(b) CFTR chloride transport defective; thick mucus secretion and high sodium and chloride levels in sweat
(c) present with meconium ileus, steatorrhea, pulmonary infx (usually pseudomonas)
(d) mean survivial 20YO; usually due to pulmonary infx
Pancreatic adenocarcinoma: risk factors
Smoking, high fat diet, chemical exposure
Presentation of pancreatic adenocarcinoma
(1) abdominal pain radiating to back
(2) wt loss due to malabsorption and anorexia
(3) migratory thrombophlebitis (redness and tenderness on palpation of extremities-Trousseau's syndrome)
(4) obstructive jaundice w/palpable gallbladder (Courcoisier's sign)
Tumor markers for pancreatic adenocarcinoma
CEA and CA199
Most common place for pancreatic adenocarcinoma
Pancreatic head (may compress bile duct and cause obstructive jaundice)
Dysentery; poultry/domestic animals, water
MCC/pathogenesis/treatment
-Campy/invades epithelium/only treat severe cases (erythromycin)
-Salmonella/penetrates lamina propria causing PMN response and prostaglanding synthe which stim cAMP/severe cases only
Dysentery: no animal reservoir; fecal/oral transmission; musocal ulcerations
MCC/treatment
Shigella/fluoros TMPSMX for severe cases
Dysentery: pseudoappendicitis; arthritis; milk/domestic animals/fecal oral
Yersinia, heat stable enterotoxin; treat only severe cases (aminoglycosides, TMPSMX)
Dysentery: antibiotic use: MCC/treatment
C diff, metronidazole
Dysentery: food/water, fecal oral (G- rod, lactose fermenter
E coli
Dysentery; flask like lesions, extraintestinal abscesses (liver): MCC/treatment
Entameoba histolytica (mebendizol)
Watery diarrhea: day care, water, fecal oral, microvilli blunted: mCC/treatment
Rotavirus/supportive
Watery diarrhea: older kids/adults; blunting of microvilli
Norwalk virus/supportive
Watery diarrhea: nosocomial (young kids, IC)
Adenovirus 40/41
Watery diarrhea: rice water stools: MCC, treatment
Vibrio cholerae; oral rehydration, tetracycline shortens symptoms
Watery diarrhea: raw or undercooked fish
Vibrio parahaeomolyticus (treatment not indicated)
Watery diarrhea: undercooked fruits/veggies
ETEC
Watery diarrhea, children, AIDS
Crypsosporidium (intracellular brush border)
Watery diarrhea: day care, camping, beavers, dogs
Giardia (metronidazole)
Diarrhea: ham, potato salad, cream pastries: MCC, pathogenesis
Diarrhea and vomiting
Staph aureus
Heat stabile enterotoxin in food
Recovery without treatment
Vomiting followed by diarrhea: fried rice
B cereus
Recovery without treatment
Cimetidine
(a) mechanism
(b) clinical use
(c) toxicity
(a) reversible block of histamine H2 receptors causes decr H+ secretion by parietal cells
(b) peptic ulcer; gastritis; mild esophageal reflux
(c) Potently inhibits P450
Antiandrogen effects (prolactin release, gynocomastia, impotence, decr libido in males)
Decr renal excretion of creatinine
Can cross BBB (confusion, dizziness, HA)
Ranitidine
(a) mechanism
(b) clinical use
(c) toxicity
(a) reversible block of histamine H2 receptors causes decr H+ secretion by parietal cells
(b) peptic ulcer; gastritis; mild esophageal reflux
(c) decr renal excretion of creatinine
Famotidine
(a) mechanism
(b) clinical use
(a) reversible block of histamine H2 receptors causes decr H+ secretion by parietal cells
(b) peptic ulcer; gastritis; mild esophageal reflux
Nizatidine
(a) mechanism
(b) clinical use
(a) reversible block of histamine H2 receptors causes decr H+ secretion by parietal cells
(b) peptic ulcer; gastritis; mild esophageal reflux
Omeprazole, Lansoprazole
(a) mnechanism
(b) clinical use
(a) irreversibly inhibit H/K ATPase in stomach parietal cells
(b) Peptic ulcer, gastritis, esophageal reflux, ZE syndrome
Bismuth, sucralfate
(a) mechanism
(b) clinical use
(a) bind ulcer base providing physical protection, allow HCo3- secretion to reestablish pH gradient in mucous layer
(b) incr ulcer healing, traveler's diarrhea
Misoprostol
(a) mechanism
(b) clinical use
(c) toxicity
(a) PGE1 analogue. Incr production and secretion of gastric mucous barrier; decr acid production
(b) prevention of NSAID induced peptic ulcers; maintenance of patent ductus arteriosus; also used to induce labor
(c) diarrhea; contraindicated in childbearing potential (abrotifacient)
Triple therapy of H pylori
Metronidazole
Amoxicillin
Bismuth
Pirenzepine
(a) mechanism
(b) clinical use
(c) toxicity
(a) block M1 receptors on ECL1 cells (decr histamine secretion) and M3 receptors on parietal cells (decr H+ secretion)
(b) peptic ulcer (rarely used)
(c) tachycardia, dry mouth, difficulty focusing eyes
Propantheline
(a) mechanism
(b) clinical use
(c) toxicity
(a) block M1 receptors on ECL1 cells (decr histamine secretion) and M3 receptors on parietal cells (decr H+ secretion)
(b) peptic ulcer (rarely used)
(c) tachycardia, dry mouth, difficulty focusing eyes
Major antacids
Aluminum hydroxide
Magnesium hydroxide
Calcium carbonate
Overuse of aluminum hydroxide side effects:
Constipation and hypophopshatemia
Proximal muscle weakness
Osteodystrophy
Seizures
Overuse of magnesium hydroxide side effects:
Diarrhea
Hyporeflexia
Hypotension
Cardiac arrest
Overuse of calcium carbonate side effects:
Hypercalcemia, rebound acid incr
Infliximab
(a) mechanism
(b) clinical use
(c) toxicity
(a) a monoclonal antibody to TNF, proinflammatory cytokine
(b) chronic's disease, rheumatoid arthritis
(c) respiratory infection (incl reactivation of latent TB), fever, hypotension
Sulfazalazine
(a) mechanism
(b) clinical use
(c) toxicity
(a) a combo of sulfapyridine (antibacterial) and mesalaine (anti inflammatory); activated by colonic bacteria
(b) ulcerative colitis; Chron's disease
(c) malaise, nausea, sulfonamide toxicity, reversbile oligospermia
Ondansetron
(a) mechanism
(b) clinical use
(c) toxicity
(a) 5-HT3 antagonist; powerful central acting antiemetic
(b) control of vomiting postop and in patients undergoing cancer chemotherapy
Metoclopramide
(a) mechanism
(b) clinical use
(c) toxicity
(a) D2 receptor antagonist. Incr resting tone, contractility, LES tone; does not influence colon transport time.
(b) diabetic and post surgery gastroparesis
(c) incr parkinsonian effects; drug interaction w/digoxin and diabetic agents; contraindicated in patients with small bowel obstruction