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137 Cards in this Set
- Front
- Back
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Retroperitoneal structures
(I DAP DAK) |
IVC
Duodenum Aorta Pancreas Descending Colon Ascending Colon Kidney |
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GI ligament that is derived from the fetal umbilical vein
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Falciform ligament
(attaches liver to anterior wall) |
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GI ligament that separates the left greater and lesser sacs
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Gastrosplenic
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This section of small intestine houses Brunner glands
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Duodenum
(all have crypts) |
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This section of small instestine houses Peyer's patches
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Ileum
(all have crypts) |
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Celiac trunk anastomoses
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-Left and right gastroepiplocis
-Left and right gastrics |
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Branches of the Celiac trunk
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common hepatic, splenic, left gastric
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Other collateral anastomeses (4 of them)
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-superior and inferior epigastric
-superior and inferior pancreaticoduodenl -middle and left colic -superiror and middle rectal |
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3 sites portal portal hypertension anastomoses
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- esophagus
-umbilicus (caput) -rectum (internal hemorrhoids) |
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Hernia protruding through DEEP inguinal ring, SUPERFICIAL (external) inguinal ring, and into the scrotum.
Where is this hernia's location? Seen in infants due to failure of what? |
- Indirect hernia
- lateral to inferior epigastric vessels - processus vaginalis |
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Hernia protruding through SUPERFICIAL (external) inguinal ring only.
This exit space is also know as? What is the location of this hernia? |
- Direct hernia
- Hasselach's triangle - medial to inferior epigastric vessels |
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This nerve can be damage during parathyroid surgery.
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VII: facial
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Lost of the Myenteric (Auebach's) plexus in the Lower Esophagus Sphincter.
What can cause this and what does it look like on xray? |
Achalasia
Chaga's and bird's beak on barium sallow |
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Heartburn that increase on lying down. With Nocturnal cough and dyspnea.
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-GERD
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Mucosal laceration due to serve vomiting
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Mallory-Weiss
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Gastritis
What are the 3 main causes of Acute gastritis and their mechanism. |
1. NSAIDS,
2. Curling- burns decrease plasma leads to mucosa sloughing off 3. Cushings- brain damage leads to increased vagal tone leads to increased Hcl |
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The two main types of chronic gastritis and their associations.
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Type A- Autoimmune, Anemia, Achlorydria (affects the body)
Type B- Bacteria: H. polyi (affects the antrum) |
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An infection that is similar to Celiac Sprue that is typically seen in travelers.
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Tropical Sprue
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What are the 4 salivary secretions?
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amylase, Bicarb, mucin, GF
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Triad: glossitis, dysphagia (due to a web), iron deficiency
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Plummer-Vinson syndrome
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These organisms can cause esophagitis
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- CMV, HSV-1, Candida
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Painless esophageal bleeding due to portal hypertension
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-Esophageal varices
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Mallory-Weiss & Boerhaave Syndrome are associated with what two groups of people?
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Alcoholics and Bulimics
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Tearing of the esophagus due retching
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Boerhaave Syndrome
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Gram positive, PAS-positive, leads to cardiac and neurologic problems
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Whipple's disease
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Celiac Sprue
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Auto-antibodies to gluten/gliadin
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Digestive tract histology
-Esophagus |
nonkeratinized stratified squamous epithelium
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Digestive tract histology
-stomach |
gastric glands
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GI blood supply to the Foregut (stomach to proximal duodenum)
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Celiac
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GI blood supply to midgut (distal duodenum to proximal 2/3 of transverse colon)
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Superior mesenteric artery (SMA)
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Gi blood supply to hindgut (distal 1/3 of transverse colon to rectum)
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Inferior mesenteric artery (IMA)
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Barrett's esophagus
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-Glandular metaplasia
-nonkeratinized stratified to-> columnar - associated with esophagitis, ulcers, increase of cancer |
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Esophageal cancer
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-progressive dysphagia (solids->liquid)
-Causes: Achalasia, Barrett's, Cigarettes, Zenker's diverticuli, Plummer-Vision |
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Menetrier's disease
-Cause: ? -Characteristics: ? |
Cause: protein loss leads to gastric hypertrophy
Characteristics: parietal cell hypertrophy; -rugae enlarge and can look like brain gyri; -diarrhea w/no ulcers |
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Stomach Cancer
-Cause: ? -Characteristics: ? |
-Cause: nitrosamines (smoked foods); type A blood
-Characteristics: Signet ring cells -acanthosis nigricans |
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-Pain great w/ meals; weight loss (doesn't want to eat)
- 70%- H. pylori - chronic NSAID use -due to decrease mucosal (cancerous) |
Gastric Ulcer
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- decrease pain w/ meals; weight gain
- 100%- H. pylori - increased acid secretion or decreased mucosal -(non-cancerous) |
Duodenal Ulcer
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Etiology: intestinal bacteria
Location: terminal ileum, colon; skip lesions (no rectal) Macro morphology: transmural, cobblestone, fat walls, Micro morphology: noncaseating granulomas Manifestations: Diarrhea may or may not be bloody |
Crohn's disease
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Etiology: autoimmune
Location: colon (always rectum) Macro morphology: 2 walls layers; pseudopolyps; lead pipe appearance Micro morphology: bleeding (no granulomas); HLA-B27 Manifestations: bloody diarrhea |
Ulcerative colitis
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What may proceed appendicitis in a child?
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lymphoid hyperplasia after viral infection
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What may proceed appendicitis in an adult?
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obstruction; fecalith
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What must be ruled out from appendicitis?
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diverticulitis (elderly); ectopic pregnancy(beta-HCG)
(will always see neutrophils for appendicitis) |
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-blind pouch protruding from tract; "false"
-Most often in sigmoid colon (esphagus, stomach, duodenum) |
Diverticulum
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- Multiple diverticula; caused by increase pressure
- associated with low-fiber - most often in sigmoid colon |
Diverticulosis
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- inflammation of diverticula causing LLQ pain
& - Rx: ? |
Diverticulitis
Rx: antibiotics |
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Herniation at the junction of the pharynx and esophagus; false diverticulum
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Zenker's diverticulum
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- Persistence of vitelline duct (yolk stalk)
- following the rules of two's |
Meckel's diverticulum
2- inches long; ft from ileocecal; % of pop.; types of tissue |
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-jelly stool, can be caused by adenovirus, usually in children
-telescoping of the bowel, may lead to infarc |
Intussusception
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- twisting of bowel; leading to infarction
- mostly in cecum and sigmoid colon - mostly in eldery |
Volvulus
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- lack of ganglion cells
-due to failure of neural crest cell migration -fails to pass meconium; increase risk in Downs |
Hirschsprung's (congenital megacolon)
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- bilious vomiting early in life
- double bubble - failure to recanalize; associated is Downs |
Duodenal atresia
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-necrosis of intestinal (colon)
- in premies (due to low immune) w/1st food |
Necrotizing enterocolitis
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- Black pigment in colon caused by laxative abuse
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Melanosis Coli
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-reduction of blood flow
-pain after eating; caused by atherosclerosis |
Ischemic colitis
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- Masses protruding into gut lumen -> saw tooth appearance
- Often in the rectosigmoid - 90% are non-neoplastic (adenomatous are precancerous) |
Colonic polyps
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- Most common non-neoplastic polyp in colon
- 50% found in rectosigmoid |
Hyperplastic polyp
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- Most sporadic lesions in children (<5 years old)
- 80% in rectum |
Juvenile polyp
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- Autosomal-dominant syndrome featuring multiple nonmalignant hamartomas
- hyperpigmented mouth -associated w/increase risk of colorectal cancer (CRC) |
Peutz-Jeghers
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- Autosomal-dominant mutation of APC gene on chromosome 5q
- thousands of polyps; rectum always involved - 100% lead to CRC |
Familial adenomatous polyposis (FAP)
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- Familial adenomatous polyposis (FAP) plus bone and soft tissue tumors
- retinal hyperplasia |
Gardner's syndrome
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- Familial adenomatous polyposis (FAP) plus malignant CNS tumor
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Turcot's syndrome
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- Autosomal-dominant mutation of DNA mismatch repair genes
- proximal colon always involved - 80% progress to CRC |
Hereditary nonpolyposis colorectal cancer
(HNPCC/Lynch syndrome) |
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Presentation of distal (left) colorectal cancer?
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obstruction, colicky pain, hematochezia
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Presentation of proximal (right) colorectal cancer
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dull pain, iron deficiency, fatigue
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How to diagnose colorectal cancer?
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Apple core lesion with barium x-ray; CEA tumor maker
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- Tumor of neuroendocrine cells
- Classic symptoms: wheezing, right side heart murmurs, diarrhea, flushing - appendix, ileum, and rectum most common sites |
Carcinoid tumor
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(liver cell failure)
Micronodular nodule size? |
<3 mm; uniform in size
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(liver cell failure)
Micronodular cause? |
metabolic insult (ie.- alcohol, hemochromatosis, wilson's disease)
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(liver cell failure)
Macronodular nodule size? |
>3 mm; varied size
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(liver cell failure)
Macronodular cause? |
Hepatic necrosis (ie.- postinfection or drug-induced hepatitis)
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Markers of GI pathology
ALT>AST |
Viral hepatitis
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Markers of GI pathology
AST>ALT |
Alcohol hepatitis
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Markers of GI pathology
GGT (gama-glutamyl transpeptidase) |
Various live diseases
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Markers of GI pathology
Amylase |
acute pancreatitis, mumps
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Markers of GI pathology
Lipase |
acute pancreatitis
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Reye's syndrome is associated with what viruses?
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VZV and influ B
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Hepatic steatosis
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Alcoholic liver disease
-short term change -fatty changes; reversible with cessation |
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Alcoholic hepatitis
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Alcoholic liver disease
-requires sustained, long-term consumption - swollen -Mallory bodies (intracytoplasmic eosinophilic) |
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Alcoholic cirrhosis
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Alcoholic liver disease
- final and irreversible - shrunken liver w/hobnail appearance |
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Hepatocellular carcinoma/hepatoma has increase incidence with what?
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- hepatitis B & C
- alcohol cirrhosis - aflatoxin in peanuts - wilson's disease - hemochromatosis - alpha 1- antitrypsin deficiency |
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Nutmeg liver is cause by?
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back up of blood to the liver
(right-sided heart failure & Budd-Chiari syndrome) |
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- Occlusion of IVC or hepatic veins
- no JVD seen - may develop varices and visible veins of abs or back |
Budd-Chiari syndrome (Type I)
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Budd-Chiari syndrome (Type I) is associated with what?
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- hypercoagulable state
- polycythemia vera - pregnancy - hepatocellular carcinoma |
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- Misfolded gene product protein accumulates in hepatocellular ER
- PAS- positive globules in liver - codominant trait (chromosome 17 PiZZ) |
alpha 1- antitrypsin deficiency
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Physiologic neonatal jaundice
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immature UDP-glucuronyl transferase
(can't conjugate bilirubin) |
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What is the treatment for physiologic neonatal jaundice?
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Phototherapy
(converts UCB to water-soluble form) |
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Type of jaundice and hyperbilirubinemia?
Urine bilirubin- increased Urine urobilinogen- normal/decrease |
Jaundice: Hepatocellular
Hyperbilirubinemia: Conjugated/unconjugated |
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Type of jaundice and hyperbilirubinemia?
Urine bilirubin- increased Urine urobilinogen- decrease |
Jaundice: Obstruction
Hyperbilirubinemia: Conjugated |
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Type of jaundice and hyperbilirubinemia?
Urine bilirubin- decrease (absent) Urine urobilinogen- increase |
Jaundice: Hemolytic
Hyperbilirubinemia: Unconjugated |
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Gilbert's syndrome deficiency in what?
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Mildly decreased UDP-glucuronyl transferase or decrease bilirubin uptake
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Crigler-Najjar syndrome type I deficiency in what?
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absent UDP-glucuronyl transferase
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Dubin-Johnson syndrome deficiency in what?
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Defect in liver excretion of conjugated bilirubin
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- Elevated unconjugated bilirubin without overt hemolysis.
- Asymptomatic - Bilirubin increases with fasting and stress - Mildly decrease UDP-glucuronyl transferase and bilirubin liver uptake |
Gilbert's syndrome
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- findings: kernicterus (bilirubin in brain), increased unconjugated bilirubin
-presents early in life,Pts dies within a few years - absent UDP-glucuronyl transferase |
Crigler-Najjar syndrome type I
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Crigler-Najjar syndrome type II responds well to what medication?
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phenobarbital
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- conjugated hyperbilirubinemia
- benign - black liver |
Dubin-Johnson syndrome
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- inadequate hepatic copper excretion
- copper accumulation in live, brain, cornea, kidneys, and joints - Basal ganglia degeneration (Parkinson's like) - Ceruloplasmin decreases, cirrhosis, Kayser-Fleischer rings, dementia |
Wilson's disease
(hepatolenticular degeneration) |
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- Associated w/ HLA-A3
- Cirrhosis - Diabetes mellitus - skin pigmentation (Bronze Diabetes) |
Hemochromatosis
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Hemochromatosis results in what?
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CHF and increase risk of hepatocellular carcinoma
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What can cause Hemochromatosis?
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1- autosomal recessive
2- chronic transfusion (ie anemias) |
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Treatment of hereditary Hemochromatosis is what?
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phlebotomy and deferoxamine
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Presentation: jaundice, light stools, hepatosplenomegaly
Labs: increased conjugated bilirubin; increased cholesterol; increased ALP Pathophys: extrahepatic biliary obstruction (gallstone, cancer of the head of the pancreas) |
Secondary Biliary Cirrhosis
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Presentation: jaundice, light stools, hepatosplenomegaly
Labs: increased conjugated bilirubin; increased cholesterol; increased ALP Pathophys: mitochondrial antibodies (IgM); autoimmune; associated w/ CREST |
Primary Biliary Cirrhosis
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Presentation: jaundice, light stools, hepatosplenomegaly
Labs: increased conjugated bilirubin; increased cholesterol; increased ALP Pathophys: "onion skin" bile duct fibrosis; associated w/ulcerative colitis |
Primary Sclerosing Cholangitis
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What are the causes of cholelithasis (gallstones)?
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- increased cholesterol and/or bilirubin
- decreased bile salts |
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- radiolucent
- associated w/ obesity, age, native american's |
cholesterol stone (cholelithasis)
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- radiopaque
- seen in Pts w/ chronic hemolysis, cirrhosis, and biliary infection |
Pigment stone (cholelithasis)
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Autodigestion of the pancreas by pancreatic enzymes is caused by what?
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Gallstones
Ethanol Trauma Steroids Mumps Autoimmune Scorpion Hyper-calcemia/lipidemia ERCP Drugs (sulfa) |
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Acute pancreatitis can lead to what condition(s)?
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DIC and ARDS
calcium soap deposits |
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- CEA and CA-19 tumor markers
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Pancreatic adenocarcinoma
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- presents with: ab pain radiates to back
weight loss redness and tenderness on extremities obstructive jaundice |
Pancreatic adenocarcinoma
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Cimetidine, ranitidine, famotidine, nizatidine
Mechanism: ? Clinical use: ? Toxicity: ? |
Mechanism: H2 blockers; decreases H+ secretion
Clinical use: peptic ulcer, gastritis, mild esophageal reflux Toxicity: *Cimetidine* P450 inhibitor; gynecomastia and impotence; crosses BBB and placenta (cimetidine & ranitidine renal eliminated) |
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Omeprazole, lansoprazole
Mechanism: ? Clinical use: ? Toxicity: ? |
Mechanism: Irreversibly inhibits H+/K+ ATPase (proton pump inhibitor)
Clinical use: peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison Toxicity: N/A |
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Bismuth, sucralfate
Mechanism: ? Clinical use: ? Toxicity: ? |
Mechanism: bind to ulcer base, physical protection
Clinical use: increase ulcer healing and traveler's diarrhea Toxicity: N/A |
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Misoprostol
Mechanism: ? Clinical use: ? Toxicity: ? |
Mechanism: PGE1 analog; increase mucous barrier & decreases acid production
Clinical use: Prevention of NSAID ulcers; maintain PDA; induces labor Toxicity: Diarrhea; don't use in possible pregnant Pts |
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Pirenzepine, propantheline
Mechanism: ? Clinical use: ? Toxicity: ? |
Mechanism: M1 receptor blocker on ECL (decrease histamine); M3 receptor blocker (decrease HCL)
Clinical use: Peptic ulcers (rarely used) Toxicity: Tachycardia, dry mouth, blurry eyes |
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Antacid use: Over use of this can cause?
Aluminum hydroxide |
constipation and hypophosphatemia (osteodystrophy)
proximal muscle weakness seizures |
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Antacid use: Over use of this can cause?
Magnesium hydroxide |
diarrhea
Hyporeflexia hypotension cardiac arrest |
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Antacid use: Over use of this can cause?
Calcium carbonate |
hypercalcemia and rebound acid
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Infliximab
Mechanism: ? Clinical use: ? Toxicity: ? |
Mechanism: monoclonal antibody to TNF, proinflammatory
Clinical use: Crohn's disease, rheumatoid arthritis Toxicity: Respiratory infection (reactive TB), fever, hypotension |
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Sulfasalazine
Mechanism: ? Clinical use: ? Toxicity: ? |
Mechanism: sulfapyridine+5-aminosalicylic acid (anti-inflammatory)
Clinical use: Ulcerative colitis, Crohn's disease Toxicity: Malaise, nausea, sulfonamide toxicity |
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Ondansetron
Mechanism: ? Clinical use: ? Toxicity: ? |
Mechanism: 5-HT3 antagonist (central acting)
Clinical use: PostOp vomiting & chemo treatments Toxicity: Headache, constipation |
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Metoclopramide
Mechanism: ? Clinical use: ? Toxicity: ? |
Mechanism: D2 receptor antagonist (increases tone, LES)
Clinical use: diabetics and post-surgery Toxicity: parkinson-like, drug interaction w/digitoxin (don't use in Pts w/small bowel obstructions) |
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Gastrin source?
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G cells (stomach)
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Cholecystokinin (CCK) source?
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I cells (duodenum)
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Secretin source?
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S cells (duodenum)
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Somatostatin source?
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D cells (pancreas)
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Glucose-dependent insulinotropic peptide (GIP) source?
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K cells (duodenum, jejunum)
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Vasoactive intestinal polypeptide (VIP) source?
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sphincters, gallbladder, small intestine
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Motilin source?
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Small intestine
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GI Hormone?
Action - increases H+ secretion - increases growth of gastric mucosa - increases grastic motility |
Gastrin
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GI Hormone?
Action - increases pancreatic secretion - gallbladder contraction - decreases gastric emptying - relaxes sphincter of Oddo |
Cholecystokinin (CCK)
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GI Hormone?
Action - increases pancreatic HCO3 secretions - decreases gastric acid secretion - increase bile secretion |
Secretin
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GI Hormone?
Action - decreases acid and pepsinogen secretion - decreases pancreatic and intestinal secretion - decreases gallbladder contractions - decreases insulin and glucagon |
Somatostatin
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GI Hormone?
Action - decrease gastric H+ secretion - increase insulin realease |
Glucose-dependent insulinotropic peptide (GIP)
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GI Hormone?
- increases intestinal water and electrolyte secretion - relaxes smooth muscle of the intestine |
Vasoactive intestinal polypeptide (VIP)
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GI Hormone?
Action - produces migrating of motor complexes (MMCs) |
Motilin
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