Term
| List the retroperitoneal structures. |
|
Definition
Gastric structures that lack a mesentery ad non-GI structures
Damage can cause blood/gas in retroperitoneal space
SAD PUCKER
1) Suprarenal (adrenal) gland
2) Aorta and IVC
3) Duodenum (2,3 and 4th parts)
4) Pancreas (except tail)
5) Ureters
6) Colon (descending and ascending)
7) Kidneys
8) Esophagus (lower 2/3)
9) Rectum (upper 2/3) |
|
|
Term
What are the key contents and structures connected by each of the following ligaments?
1) Falciform
2) Hepatoduodenal
3) Gastrohepatic
4) Gastrocolic
5) Gastrosplenic
6) Splenorenal |
|
Definition
1) Liver to anterior body wall
- Contains ligamentum teres, which is derived from fetal umbilical vein.
2) Liver to duodenum (connects greater and lesser sacs)
- Contains portal triad: HA, CBD, PV
3) Stomach (lesser curvature) to liver
- Contains gastric arteries
- cut during surgery to access lesser sac
4) Greater curvature and transverse colon
- Gastroepiploic arters (part of greater omentum)
5) Greater curvature to spleen
- Contains short gastric arteries and separates left greater/lesser sacs.
6) Spleen to posterior abdominal wall
- Splenic artery and vein. |
|
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Term
| What are the 4 basic layers of the gut wall (inside to outside) and the important structures located in each? |
|
Definition
1) Mucosa
- Epithelium (absorption)
- Lamina propria (support and immune)
- Muscularis mucosa (motility)
2) Submucosa
- Meissner's secretory plexus
3) Muscularis externa
- Myenteric (aurbach's) motility plexus (in between muscle layers)
- Circular and longitudinal smooth muscle layers
4) Serosa/adventisia |
|
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Term
| How do the basal electric rhythms (slow waves) differ between the stomach, duodenum and ileum? |
|
Definition
Slow waves come from ICCs
1) Stomach is slowest (3 w/min)
2) Duodenum is fastest (12 w/min)
3) Ileum (8 w/min) |
|
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Term
What are the key characteristic histological features of each of the following GI organs?
1) Esophagus
2) Stomach
3) Duodenum
4) Jejunum
5) Ileum
6) Colon |
|
Definition
1) Non-keratinized stratified squamous empithelium
2) Gastric pits and glands
3) Villi and microvilli (absorption) with Brunner's glands (submucosa) and crypts of Lieberkuhn.
4) Plicase circulares and crypts of Lieberkuhn.
5) Peyer's patches (LP and submucosa), plicae circulares (proximal ileum) and crypts of Lieberkuhn.
- Largest number of goblet cells with
6) Crypts but NO VILI |
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Term
| What are the major branches of the abdominal aorta (top to bottom)? |
|
Definition
Arteries supplying GI structures branch anteriorly, while those supplying non-GI structures branch laterally.
1) Left and right inferior phrenic (Diaphragm)
2) Celiac trunk (T12)
3) SMA (L1)
4) L/R renal and suprarenal arteries (L1)
5) Testicular arteries (L2)
6) IMA (L3)
7) Bifurcation into common iliacs (L4) |
|
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Term
What is the 1) embryonic origin, 2) parasympathetic innervation and 3) structures supplied by each of the following branches of the abdominal aorta?
A) Celiac
B) SMA
C) IMA |
|
Definition
A) T12
- Foregut
- Vagus
- Stomach to proximal duodenum; liver, gallbladder, pancreas, spleen (mesoderm)
B) L1
- Midgut
- Vagus
- Distal duodenum,to proximal 2/3 of transverse colon
C) L3
- Hindgut
- Pelvic
- Distal 1/3 transverse colon, to upper portion of rectum; - splenic flexure is "watershed region" |
|
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Term
| What are the major branches of the celiac trunk and what structures do they supply? |
|
Definition
Celiac trunk (foregut/T12) supplies stomach through proximal duodenum, spleen, pancreas, gallbladder and liver.
1) Common hepatic
- GIves off hepatic artery proper, which gives rise to right gastric and L/R hepatic arteries
.
- Gives off gastroduodenal as well, which branches into right gastro-omental artery (also called gastroepiploic artery ) and superior pancreaticoduodenal artery
2) Splenic (in splenorenal ligament)
- Spleen
- Dorsal pancreatic
- Short gastric (poor anastomoses if SA is blocked)
3) Left gastric
- left stomach
- gives of esophageal branch |
|
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Term
| What are the 4 compensatory anastamotic systems that can compensate in cases of abdominal aorta blockage? |
|
Definition
1) Superior epigastric (internal thoracic/mammary) with Inferior epigastric (external iliac)
2) Superior pancreaticoduodenal (celiac) with inferior pancreaticoduodenal (SMA)
3) Middle colic (SMA) with left colic (IMA)
4) Superior rectal (IMA) with middle rectal (interal ileac) |
|
|
Term
Why might you see each of the following clinical signs?
1. Esophageal varices
2. Caput medusae
3. Internal hemorrhoids |
|
Definition
"Portal hypertension causes problems in the butt, the gut, and caput."
Dilation of portosystemic anastomoses, which can be solved with TIPS procedure to relieve portal hypertension (connection/stent between portal vein and hepatic vein)
Portal (left) and Systemic (right)
1. Left gastric and Esophogeal at esophagus
2. Paraumbilical, and superficial and inferior epigastric and Umbilicus
3. Superior rectal and middle/inferior rectal and Rectum |
|
|
Term
| What is the source, action, regulation and associated clinical features of each the gastric hormone Gastrin? |
|
Definition
1) G cells (antrum of stomach)
2) Increase gastric H+ secretion, mucosal growth and motility
3a) Increased by stomach distention/alkalization, amino acids (Phenylalanine and Tryptophan), peptides, vagal stimulation
3b) Decreased by pH<1.5
4) Increased in Zollinger-Ellison syndrome (gastric secreting tumor) |
|
|
Term
What is the major diagnostic use of each of the following plasma markers of liver and pancreas function?
1) AST/ALT
2) GGT
3) ALP
4) Amylase
5) Lipase
6) Ceruloplasmin |
|
Definition
1) Viral hepatitis (ALT>AST)
Alcoholic hepatitis (AST>ALT)
2) Increased with heavy alcohol use
- If ALP is elevated but GGT is normal, it is extra-hepatic (bone)
3) Obstructive liver disease (HCC), bone disease, bile duct disease (cholestasis)
4) Acute pancreatitis, mumps
5) Acute pancreatitis
6) Decreased in Wilson's (copper accumulation) |
|
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Term
Child presents with hypoglycemia, vomiting, hepatomegaly after a recent viral infection (influenza B) that was treated and subsided.
Imaging reveals fatty liver.
What question should you ask the mother initially about his viral infection treatment? What is the mechanism of this condition? |
|
Definition
Don't give Aspirin to CHILDREN!
Reye's syndrome- also see mitochondrial abnormalities,
1) Influenza B or VZV treated with salicilates
2) Salicilate (aspirin) metabolites decrease B-oxidation by reversible inhibition of mitochondrial enzyme |
|
|
Term
| What are the 3 major stages of Alcoholic liver disease? |
|
Definition
1) Hepatic steatosis
- short-term fatty change with moderate intake
- macrovesicular change that can be reversed with cessation
2) Alcoholic hepatitis (AST>ALT :1.5)
- Sustained long-term intake
- Swollen and necrotic hepatocytes with PMN infiltrate and MALLORY BODIES (eosinophillic inclusions)
3) Alcoholic cirrhosis
- Final, irreversible form, with micronodular, irregularly shrunken liver with "hobnail" appearance.
- Sclerosis around central vein (zone III) and jaundice/hypoalbuminemia |
|
|
Term
Patient presents with jaundice, tender hepatomegaly, ascites, polycythemia and hypoglycemia.
You run labs and find elevated AFP levels
What are the most common diseases associated with this condition? |
|
Definition
HCC- commonly spread hematogenously and may lead to Budd-Chiari (occlusion of IVC or hepatic veins producing CHF)
1) HBV/HCV
2) Wilson's (copper)
3) Hemachromatosis (iron retention)
4) a1 anti-trypsin deficiency
5) Alcoholic cirrhosis
6) Toxins (aflatoxin from Aspergillus) |
|
|
Term
| Why might you see "nutmeg liver" and why is it worrisome? |
|
Definition
1) Backup of blood into liver caused by CHF or Budd-chiari (occluded IVC or hepatic veins)
2) May lead to centrilobular congestion and necrosis leading to cardiac cirrhosis. |
|
|
Term
| How can labs help you tell between Hepatocellular, obstructive and hemolytic causes of jaundice? |
|
Definition
1) Hepatocellular
- Mixed hyperbilirubinemia with increased urine bilirubin and normal/decreased urine urobilinogen
2) Obstructive
- Direct hyperbilirubinemia with increased urine bilirubin and decreased urobilinogen (reduced bilirubin in intestine by bacteria)
3) Indirect hyperbilirubinemia with absent urine bilirubin (acholuria) and increased urine urobilinogen |
|
|
Term
| What is the cause for physiological neonatal jaundice? |
|
Definition
1) Immature UDPGT leads to increased indirect bilirubin
2) Jaundice (indirect) can lead to kernicterus, unless you use PHOTOTHERAPY |
|
|
Term
| Why do you get emphysema and cirrhosis in alpha-1 antitrypsin deficiency? |
|
Definition
Also a risk for HCC, because of cirrhosis
1) Mis-folded protease inhibitor accumulates in hepatocellular ER (cirrhosis with PAS-positive globules in liver).
2) Protease dominance in lung decreases elastic tissue and leads to panacinar emphysema. |
|
|
Term
| Describe the 3 common causes of Hereditary hyperbilirubinemia. What are the clinical consequences of each? |
|
Definition
Gilbert (uptake= unconjugated)
CNS1 (conjugation= unconjugated)
Dubin-Johnson and Rotor (excretion= conjugated)
1) Gilbert
- Mildly decreased UDP-GT or decreased uptake
- Elevated indirect bilirubin without overt hemolysis (increases with fast and stress)
- No clinical consequences
2) Crigler-Najjar syndrome type 1
- Absent UDP-GT (die in few years because of kernicterus do to indirect bilrubin deposition in brain)
- Treat immediately with plasmapheresis and phototherapy
**Type II is less ever and responds to phenobarbital (increase enzyme synthesis)
3) Dubin-Johnson
- Conjugated hyperbilirubinemia because of defective liver excretion (grossly black liver)
- Benign
**Rotor's syndrome is similar but even milder and does not cause black liver** |
|
|
Term
| What is the pathophysiology and treatment of Wilson's disease? |
|
Definition
AR disease of copper excretion (Copper is Hella BAD)
C (Ceruloplasmin decrease, cirrhosis, corneal deposits, carcinoma)
H (Hemolytic anemia)
B (Bassal ganglia- "PD-like"
A (asterixis)
D (Dementia, Dyskinesia, Dysarthria)
1) Poor hepatic copper excretion and failure of copper to enter circulation as ceruloplasmin
- Accumulates in liver, brain, kidneys, cornea and joints
2) Penicillamine |
|
|
Term
Diabetic patient presents in liver failure. You notice a "bronze" color to their skin.
On PE, you discover ascites, elevated JVP and hepatomegaly.
On biopsy, you discover evidence of micronodular cirrhosis.
What is going on and how would you treat? |
|
Definition
Skin pigmentation + Cirrhosis + Diabetes= Hemochromatosis, which often leads to CHF and increased risk of HCC
**HLA-A3 association**
1) Can be primary (AR) or secondary to chronic transfusion therapy (B-thalassemia)
- Increased ferritin, iron, decreased TIBC and increases transferrin saturation.
2) Treat with phlebotomy and deferoxamine |
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|
Term
50 year old women presents with Pruritis, jaundice, dark urine, light stools and hepatomegaly.
Labs reveal conjugated hyperbilirubinemia, hypercholesterolemia and increased ALP
What is on your differential and how might you proceed? |
|
Definition
Cholestatic picture
- Secondary Biliary Cirrhosis, PBC and PSC
You should order serum antibodies.
anti-AMA fits PBC (association with other autoimmune)
anti-pANCA and hyper IgM fits PSC (IBD association)
- If neither is positive, you might think extrahepatic obstruction like gallstone, stricture, carcinoma of pancreas head, ect.) |
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|
Term
45 year old pregnant women presents with jaundice, fever and RUQ pain.
When she breathes in during deep palpation of abdomen she winces.
Would could be going on and how would you narrow down your diagnosis? |
|
Definition
Charcot's triad of cholangitis and she has at least 3 of 4 risk factors for gallstones (Female, Fat, Fertile (pregnant), Forty)
- This sounds like ascending cholangitis, secondary to Gallstones, which are caused by increased cholesterol and/or bilirubin, decreased bile salts and gallbladder stasis.
Could be 1) cholesterol (radioluscent) stones or 2) pigment stones (radiopaque) so order radionuclide biliary scan and ultrasound -treat with cholecystectomy.
1) Cholesterol associated with obesity, CD, CF, age, estrogens, native american descent
2) Pigment stones seen with chronic hemolysis (bilirubin), alcoholic cirrhosis, advanced age and biliary infection (Black with hemolysis or Brown with infection)
- Increased cholesterol |
|
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Term
| What are the major branches of the superior mesenteric artery and what structures do they supply? |
|
Definition
SMA (L1/midgut) supplying the distal duodenum to proximal 2/3 of transverse colon
1) Inferior pancreaticoduodenal
- When abdominal aorta blockage is present, this artery will anastomose with the superior pacreaticoduodenal (Celiac trunk)
2) Intestinal arteries (jejunum and illeum)
3) Ileocolic (ilium, cecum and appendix)
4) Right colic (ascending colon)
5) Middle colic (transverse colon)
- In aorta block, anastomoses with left colic artery (IMA) |
|
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Term
| What are the major branches of the Inferior mesenteric artery and what structures do they supply? |
|
Definition
IMA (hindgut, L3) supplies distal 1/3 transverse colon, to upper portion of rectum; - splenic flexure is "watershed region"
1) Left colic artery (descending colon)
- Anastomoses with middle colic (SMA) during aorta blockage
2) Sigmoid arteries (sigmoid colon)
3) Superior rectal (upper rectum)
- Anastamoses with middle rectal (internal iliac) during aorta blockage |
|
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Term
| What is the "pectinate" or dentate line an what happens above and below it? |
|
Definition
Line formed where endoderm (hindgut) and ectoderm meet, dividing the upper 2/3 (supplied by superior rectal artery from IMA) and lower 1/3 of the anal canal (middle and inferior rectal arteries from internal iliac)
1) Above= Painless internal hemorrhoids & adenocarcinoma
- Supplied by superior rectal artery (IMA)
- Drained by superior rectal vein off of IMV
*Portosystemic anastamosis that forms internal hemorrhoids during portal HTN*
2) Below= Painful external hemorrhoids and squamous cell cancer
- Supplied by inferior rectal artery (Internal pudendal off off internal iliac)
- Drained by inferior rectal vein..internal pudendal vein...internal iliac vein....IVC |
|
|
Term
| Why types of hemorrhoids are painless and why? |
|
Definition
1) Internal hemhorroids (above pectinate line) receive visceral innervation and are therefore NOT painful.
- They are seen in portal HTN, at sight of porto-systemic anastamosis between superior rectal vein and middle/inferior rectal veins.
2) External hemorrhoids (Below pectinate line) receive somatic innervation (inferior rectal branch of pudendal nerve) and are therefore painful |
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Term
| Describe the basic zonal anatomy of the liver. |
|
Definition
Dual blood supply (Hepatic artery and Portal vein)
Zone 1 (periportal):
- Receives most oxygenated blood for incoming portal triads and performs oxidative functions like gluconeogenesis, beta oxidation and cholesterol synthesis
- 1st by viral hepatitis
Zone 2 (intermediate):
Zone 3 (pericentral/centrilobular)
- Glycolysis, lipogenesis and cytochrome P-450-based drug detoxification
- 1st affected by Ischemia, toxic injury and Alcoholic hepatitis (congestion build up behind central vein in hepatic vein) |
|
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Term
| Which zone of the liver are affected by alcoholic and viral hepatitis, respectively, and why? |
|
Definition
1) Zone 1 (periporta) gets hit by Viral
- Receives most oxygenated blood for incoming portal triads and performs oxidative functions like gluconeogenesis, beta oxidation and cholesterol synthesis
2) Zone 3 (centrilobular) gets hit by Alcohol
- Glycolysis, lipogenesis (fatty liver) and cytochrome P-450-based drug detoxification |
|
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Term
| Describe the basic anatomy of a liver lobule. |
|
Definition
Hexagonal arrangements of cords of hepatocytes radiating outward from a central vein and separated from each other by radiating capillary sinusoids.
1) Central vein receives from from capillary sinusoids and drains in the hepatic vein (and on to the IVC)
- Kuppfer cell (macrophages) are found in sinusoids)
2) Portal triads at edges of lobules with hepatic artery (oxygenated blood), portal vein (nutrient-rich blood) and bile duct |
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Term
| Describe the anatomical organization of the biliary tract beginning at the liver and ending in the small intestine. |
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Definition
Liver
- Left and Right hepatic ducts collect bile from liver, forming the common hepatic duct
Gallbladder
- The common hepatic duct and cystic duct (from gallbladder) combine to form the Common bile duct
Duodenum
- Common bile duct and main pancreatic duct join at the Ampulla of vater, which empties into the dueodenum (delivering bile acids)
*gallstone at ampulla can block bile and pancreatic ducts** |
|
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Term
| Why can a tumor at the head of the pancreas cause biliary obstruction? |
|
Definition
| Tumor can block common bile duct at entry point to duodenum at the ampulla of vater |
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Term
You are trying to place a Foley catheter and are concerned about the organization of the femoral region.
What structures are in the femoral triangle and sheath, respectively? Where do femoral hernias occur in relation to these structure? |
|
Definition
NAVEL- Nerve, artery, vein, empty, lymphatics (lateral to medial)
1) Triangle: Nerve, artery and vein (venous near penis)
2) Sheath: Fascial tube 3-4 cm below inguinal ligament that contains vein, artery and canal (deep inguinal lymph nodes), but NOT the nerve
3) Femoral hernias occur at the femoral ring which lies medial to the femoral vein and surrounds the lymphatics |
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|
Term
| Describe the anatomy of the inguinal canal. Where do indirect and direct inguinal hernias occur? |
|
Definition
Indirect hernias occur Laterally to Direct hernias
- Indirect occur at internal inguinal ring in parietal peritoneum.
- Direct hernias occur in the abdominal wall, medially to the internal inguinal ring
Inner to outer
1) Superficial inguinal ring
- Inguinal ligament is penetrated medially at the superficial inguinal ring by the Spermatic Chord (External spermatic fascia, cremasteric fascia and internal spermatic fascia)
2) Deep inguinal ring
- After passing through internal obliques, the spermatic chord penetrates the transversus abdominus in the deep inguinal ring.
- Medially, you find rectus abdominus overlying the pyramidal muscles and the conjoined tendon.
3) Internal Inguinal ring
- Parietal peritoneum is penetrated laterally by the spermatic cord |
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Term
Hernias are protrusions of peritoneum through openings at site of weakness.
Describe the location and nature of the diaphragmatic hernia types. |
|
Definition
Abdominal structures enter thorax, most commonly through hiatal hernias, where the stomach herniates upward through the esophageal hiatus of the diaphragm (T10).
1) "Sliding" hiatal hernias are most common, where the GE junction is displaced "hourglass stomach"
2) "Paraesophogeal" hernias occur when GE junction is normal, and the fundus protrudes into the thorax. |
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|
Term
Hernias are protrusions of peritoneum through openings at site of weakness.
Describe the location and nature of the inguinal hernia types. |
|
Definition
1) Indirect- Goes through INternal (deep) inguinal ring, external (superficial) inguinal ring and INto the scrotum
- Enters internal inguinal ring lateral to inferior epigastric artery (more common in males and infants, with failure of processes vaginalis closure-hydrocele)
2) Direct
- Protrudes through inguinal (Hesselbach's) triangle and bulges directly through abdominal wall medial to inferior epigastric artery
- passes through superficial inguinal ring ONLY and covered by external spermatic fascia (older men) |
|
|
Term
| What is Hesselbach's triangle and what is its relevance? |
|
Definition
Comprised of 1) Inferior epigastric artery, 2) lateral border of rectus abdominus and the 3) Inguinal ligament.
This triangle forms the anatomical borders through which Direct inguinal hernias protrude, covered by external spermatic fascia, to exit through the abdominal wall medial to the inferior epigastric artery. |
|
|
Term
| Where do femoral hernias occur in relation to inuinal hernias? |
|
Definition
Femoral= Women Inguinal= Male (direct is older than indirect)
1) Femoral hernias protrude below the inguinal ligament through the femoral canal below and lateral to the pubic tubercle.
- They pass through the femoral ring, which lies medially tot the femoral vein in the femoral sheath (can obstruct lymphatics)
2) Inguinal hernias pass through the inguinal (Poupart's ligament), either laterally (indirect) or medial (direct) to the inferior epigastric artery off of the femoral artery |
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|
Term
Which type of hernia is described in each of the following?
1) Occurs in infants as a result of defective development of the pleuroperitoneal membrane
2) Most common cause of bowel incarceration
3) Passes in between inferior epigastric artery, lateral border of rectus abdominus and inguinal ligament in older men
4) Occurs in infants owing to failure of processus vaginalis to close (can form hydrocele) |
|
Definition
1) Hiatal diaphragmatic hernias, where stomach passes through esophageal hiatus and into the thorax (T10)
2) Femoral hernia (women > men)
- Below inguinal ligament and below and lateral to the pubic tubercle
3) Direct inguinal through Hesselbach's triangle
4) Indirect inguinal hernia (lateral to inferior epigastric artery) |
|
|
Term
| Which amino acids are potent stimulators of gastrin release in the antrum? |
|
Definition
G-cells release gastrin in response to Phe and Trp
Remember, Phe can become catecholamines and Trp can become Niacin (B6-mediated) and 5-HT |
|
|
Term
| Describe the regulation and action of CCK |
|
Definition
Released from I cells in the duodenum and Jejunum in response to fatty acids and amino acids.
"Its time to digest, so stop emptying and start chewing it up"
1) Acts on neural muscarininc pathways to cause pancreatic secretions (pancreatic liase)
2) Increases gallbladder contractions (bile acids)
3) Decreases gastric emptying
4) Relaxes sphincter of Oddi (controls ampulla of vater) |
|
|
Term
| When/why is secretion released? |
|
Definition
Neutralize it so that the pancreas can do its thing.
- Secreted from S cells of the duodenum in response to acid and fatty acids in the duodenum.
- Increases pancreatic HCO3- secretion
- Decreases gastric acid secretion
- Increases bile secretion |
|
|
Term
| When/why is Somatostatin released? |
|
Definition
Released from D cells (pancreatic islets and GI mucosa) in response to acid (suppressed by vagal stimulation)
Anti-GH effects (stops digestione and absorption of substances needed for growth)
- Stops acid and pepsinogen secretion in stomach
- Stops pancreatic and small intestine fluid secretion
- Stops gallbladder contraction
- Stops insulin and glucagon release |
|
|
Term
| Describe the regulation and action of Glucose-dependent insulinotropic peptide (GIP) |
|
Definition
GIP released from K cells in the duodenum and jejunum in response to fatty acids, amino acids and oral glucose
**oral glucose load is used more rapidly than IV**
1) Exocrine: decreases H+ secretion
2) Endocrine: Increases insulin release |
|
|
Term
| Describe the regulation and action of Vasoactive intestinal polypeptide (VIP) |
|
Definition
A Motility factor
Released by parasympathetic ganglia in sphincters, gallbladder and small intestine in response to stomach distention and vagal stimulation.
- Inhibited by adrenergic input
1) Increases intestinal water and electrolyte secretion
2) Relaxation of intestinal smooth muscle and sphincters
**VIPomas are non-apha, non-beta islet cell pancreatic tumors that secrete VIP and cause copious diarrhea** |
|
|
Term
| Which type of islet cell tumor would produce copious diarrhea? |
|
Definition
|
|
Term
| What is the pathophysiological mechanisms of achalasia |
|
Definition
| Increased lower esophageal tone due to loss of NO secretion, which is important for smooth muscle relaxation. |
|
|
Term
| What are Migrating motor complexes (MMCs) and hwo do they occur? |
|
Definition
| Motilin binds to motilin receptors in small intestine in the fasting state and ccause contractions to clear it out. |
|
|
Term
What is the source and action of each of the following secretory products?
1) Intrinsic factor
2) Gastric acid
3) Pepsin
4) HCO3- |
|
Definition
1) Produced by parietal cells (stomach)
- Binds B12 and allows it be taken up in illeum
- Autoimmune destruction of parietal cells can cause chronic gastritis and pernicious anemia.
2) Produced by parietal cells (stomach)
- Decreases stomach pH in response to histamine, ACh and gastrin (G cells)
- Inhibited by somatostatin, GIP and prostaglandins
3) Released from chief cells (stomach)
- Activated form pepsinogen by H+ from parietal cells
- Protein digestion in response to vagal stimulation and/or local acid
4) Mucosal cells (stomach, duodenum, salivary glands and pancreas) and Brunner's glands (Duodenum)
- Neutralizes acid in response to secretin release from duodenal S cells |
|
|
Term
| Where is HCO3- found in mucosal cells? |
|
Definition
Trapped in mucus that covers gastric epithelium
Produced by cells in stomach, duodenum (also by brunner's glands), salivary glands and pancreas |
|
|
Term
| PUD is often associated with MEN-1 syndrome. Why? |
|
Definition
| Zollinger-Ellison syndrome often involves pancreatic gastrinomas, which secrete high levels of gastrin that stimulates parietal cells of the stomach to produce H+ |
|
|
Term
Which GI hormones are produced by each of the following cell types?
1) G cells in the antrum of the stomach
2) I cells (duodenum and jejunum)
3) S cells (duodenum)
4) D cells (pancreatic islets and GI mucosa0
5) K cells (duodenum and jejunum) |
|
Definition
1) Gastrin, which increases H+ secretion by parietal cells and growth/motility of gastric mucosa
2) CCK, which increases pancreatic and gallbladder secretions in response to fatty acids and amino acids
3) Secretin, which causes pancreatic HCO3- release in response to acid or fatty acids in the duodenal lumen
4) Somatostatin, which inhibits glucagon/insulin release, decreases gallbladder contractions and pancreatic fluid secretions (opposite of GIP and VIP)
5) GIP increases gastric H+ secretion and insulin release in response to fatty acids, amino acids and oral glucose |
|
|
Term
| Where is saliva produced and what does it contain? |
|
Definition
Parotid, submandibular and sublinguial glands stimulated by sympathetic and parasympathetic activity.
Hypotonic due to absorption, unless high flow rates make it isotonic
1) Amylase- Digest apha 1,6 starch
2) HCO3- Neutralizes bacterial acids
3) Mucins- lubricaiton |
|
|
Term
Where are each of the following GI secretory cells found?
1) Parietal cells
2) Chief cells
3) Enteroendocrine cells (APUD)
4) G cells
5) Mucous cells |
|
Definition
Stomach regions: Cardia, Body/fundus, Antrum, ending in pyloric sphincter to the duodenum.
Innervation by Vagus nerve, which stimulates post-synaptic cholinergic neurons in body (stimulate parietal cells) and GRP neurons in antrum (stimulate gastrin release to circulation)
1) Body/fundus: secrete gastric acid (HCl) and intrinsic factor in response to histamine (H2 receptor), acetylcholine (M3 receptors) and gastrin (CCK2 receptors)
2) Body (below parietal): Release Pepsinogen, which is activated to pepsin by H+
3) Mostly in duodenum/jejunum, except G cells, which are found in antrum with Mucous cells
- I, K, S, D cells
4) Stomach antrum- Release gastrin in response stomach distension and alkalization (inhibited by acid), binding ECL cells, which release histamine and bind parietal cells to release H+
5) Antrum of stomach- Secrete HCO3- containing mucous |
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Term
| Why does Atropine only block gastric acid secretion partially? |
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Definition
The Vagus nerve stimulates 2 groups of neurons, which both contribute to acid release.
1) ACh neurons that stimulate parietal cells in the body via M3 receptors (this is inhibited by atropine)
2) GRP neurons that stimulate G cells in antrum (these are fine) to release Gastrin to stimulate ECL (histamine) cells in circulation (MOST IMPORTANT) and directly stimulating parietal cells (CCKb receptor)
** The H2 receptors can be inhibited by Cimetidine, but there is no inhibitor of the CCKb receptor that is useful** |
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Term
| How does Omeprazole act on the gastric parietal cell? |
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Definition
| Inhibits H+/K+ ATPase, which normally releases H+ in exchange for K+. |
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Term
| How is acid generated in parietal cells? |
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Definition
Variety of mechanisms.
H+ is generated from H2O and CO2 via CA (HCO3- is removed by HCO3/Cl transporter ("alkaline tide")
1) ACh via M3 receptor from vagus
- Gq (GPCR) activates IP3/Ca2+ signaling, which activates the H/K ATPase (inhibited by PPis)
2) Gastrin binding to CCKb receptor
- Same mechanisms as 1
3) Histamine binding to H2 receptor (inhibited by Cimetidine)
- cAMP/PKA activates H+/K+ ATPase
- cAMP is Inhibited by Gi (GPCR), which is stimulated by Prostaglandins/misoprostol and Somatostatin |
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Term
| Where are Brunner's glands found and what do they secrete? |
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Definition
Secrete alkaline mucus in duodenum, to neutralize acid contents entering from stomach
**Hypertrophy seen in PUD** |
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Term
| What enzymes are contained in pancreatic secretions into the common bile duct? |
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Definition
Isotonic fluid (low flow= high Cl-, high flow= high HCO3-)
1) alpha amylase- starch digestion (secreted in inactive form)
2) Lipase, phospholipase A, colipase- fat digestion
3) Proteases (trypsin, chymotrypsin, elastase, carboxypeptidase) secreted as zymogens
4) Trypsinogen- converted to active form by enterokinase/enteropeptidase from duodenal mucosa and then activates other pancreatic enzymes |
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Term
| How are carbohydrates digested and absorbed? What is the rate limiting step? |
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Definition
RSL is brush border disaccharidases
1) Begins with salivary amylase, which hydrolyzes alpha-1,4 linkages to yield disacccharides (maltose and alpha-lmit dextrins)
2) Pancreatic lipase in duodenum hydrolyzes starch to oligosaccharides and disaccharides
3) Brush border oligosaccharide hydrolases (RLS) produce monosaccharides that can be absorbed
4) Glucose (SGLT1), galactose (SGLT1) and fructose (GLUT5) are absorbed by enterocytes and then ALL are transported to blood via GLUT-2
**SGLT1 is Na+ dependent** |
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Term
| What is the D-xylose test and why is it used? |
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Definition
| Absorption test to distinguish between GI mucosal damage and other forms of malabsorption. |
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Term
| Where are iron, folate and B12 absorbed, respectively? |
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Definition
1) Iron= duodenum
2) Folate= jejunum
3) B12= illeum, along with BA , and requires intrinsic factor |
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Term
| What are "Peyer's patches" and what is their function? |
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Definition
IgA mucosal immunity and antigen sampling
-Un-encapsulated lymphoid tissue found in lamina proprio and submucosa of small intestine (illeum)
- M cells sample antigen and transport them to B cells in Peyer's patches, which differentiate into IgA-secreting plasma cells.
- IgA receives protective secretory component and is then transported across epithelium to gut to deal with intraluminal antigen |
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Term
| What are the major components of bile and what is its function? |
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Definition
Bile composed of bile salts (acids conjugated to glycine or taurine, making them water soluble), cholesterol, bilirubin, water and ions
1) Digestion and absorption of lipids and fat-soluble vitamins
2) Cholesterol excretion (body's only means of excreting it)
3) Anti-microbial activity (membrane disruption) |
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Term
| Describe the major steps of heme metabolism that occur in macrophages, bloodstream, liver and gut, respectively. |
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Definition
Produces bilirubin (removed from blood by liver, conjugated with glucuronate and excreted in bile) and Porphyrin..
1) Macrophages in the spleen break RBCs down to Heme, and then to unconjugated bilirubin
2) Unconjugated bilirubin (indirect, water insoluble) is carried in blood by albumin to the liver
3) Enters liver and is conjugated via Uridine glucuronyl transferase (UGT) to a water soluble form
4) Conjugated bilirubin leaves liver and enters gut, where bacteria act on it to produce Urobilinogen, 20% of which goes to the kidney/recycle and 80% is excreted in feces as Stercobilin, which gives color.
5) of 20% that is kept, 10% is excreted in urine (color) and 90% is recycled enterohepatically to the liver. |
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Term
| Describe the parasympathetic innervation os the GI tract. |
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Definition
Parasympathetics are generally excitatory here.
- Carried by vagus (esophagus, stomach, pancreas and upper large intestine) and pelvic nerves (lower large intestine, rectum and anus)
- Nerves synapse in myenteric (between muscle layers) and submucosal plexuses (between muscularis mucosa and circular muscle)
- Post-ganglionics send information to smooth muscle, secretory cells and endocrine cells |
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Term
| Describe the sympathetic and enteric innervation of the GI tract. |
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Definition
1) Sympathetics
- Inhibitory signals from T8-L2 that synapse in prevertebral ganglia and then leave to synapse in myenteric and submucosal plexuses
2) Intrinsic (enteric)
- Local reflexes to relay information
- Myenteric (Aurbach) for motility
- Submucosal (Meisner) for secretion and BF |
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Term
| What kinds of neoplasms can be found in the salivary glands and which ones are dangerous? |
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Definition
Usually benign and in the parotid (benign is pleomorphic adenoma and malignant is epidermoid carcinoma).
1) Pleomorphic adenoma (MOST common)
2) Warthin's tumor
- Salivary tissue trapped in a lymph node and surrounded by lymphatic tissue
3) Mucoepidermoid carcinoma (most common malignant) |
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Term
Patient presents complaining of a "lump in their throat," but you can't find anything radiologically.
What is this called? |
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Definition
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Term
Patient complains of progressive dysphagia for solids and liquids.
A barium wallow shows a dilated esophagus with an area of distal stenosis that looks like a "birds beak."
What is going on and what are you worried about? |
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Definition
1) Achalasia from loss of Myenteric (Aurbach) plexus, where the LES cannot relax (vs. dysphagia for solids only in the case of an obstruction).
With high pressure opening of LES and discoordinated motility you get dysphagia.
- Can be primary or secondary to Chagas disease (t. cruzi)
2) Increased risk of esophageal carcinoma |
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Term
| Why might you be concerned if a patient has dysphagia and telangiectasias? |
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Definition
2 parts of CREST
1) Calcinosis
2) Raynaud's
3) Esophageal dysmotility (dysphagia)
4) Sclerodactyly
5) Telangiectasia |
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Term
What esophageal pathology is described by each of the following?
1) Presents as heartburn and regurgitation upon lying down (sometimes with dyspnea or a nocturnal cough)
2) Painless bleeding of submucosal veins in lower 1/3 of esophagus
3) Painful reflux associated with punched-out ulcers
4) Painful reflux associated with linear ulcers
5) Painful reflux associated with white pseudomembranes |
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Definition
1) GERD
2) Esophageal varices (portal hypertension backing up into portosystemic anatamosis between left gastric and esophageal veins)
3) Esophagitis from HSV-1
4) Esophagitis from CMV
5) Esophagitis from candida |
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Term
Which of the following is not a known cause of esophagitis?
1) HSV-1
2) CMV
3) Aspergillus
4) Candida |
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Definition
3- Aspergilliosis may cause lung cavitations post-TB or infections in immunocompromised patients, but it is not typically found in the esophagus
1) HSV-1 (Punched-out ulcers)
2) CMV (Linear ulcers)
4) Candida (Pseudomembranes) |
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Term
| What are Mallory-Weiss tears and how do they relate to Boerhaave syndrome? |
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Definition
1) Mucosal lacerations at the GE junction due to severe vomiting with hematemeis (Alcoholics and Bulemia)
2) Boerhaave syndrome is a transmural esophageal rupture due to violent retching "Been-Heaving syndrome" |
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Term
| Why might a patient presents with esophageal strictures? |
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Definition
| Lye ingestion (window cleaners) and Acid reflux |
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Term
| What are the 3 primary features of Plummer-Vinson syndrome? |
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Definition
Occurs in people with chronic iron deficiency and can be treated with iron or upper endoscopy for webs.
1) Dysphagia (esophageal webs in upper or middle)
2) Iron deficiency
3) Glossitis |
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Term
| What is the pathophysiology and risk factors underlying Barret's esophagus? |
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Definition
Look out for adenocarcinoma of distal esophagus
1) Risk factors: Esophagitis and Ulcers
2) Pathophysiology
- Glandular metaplasia (columnar) in place of non-keratinized stratified squamous epithelium in the distal esophagus (GE junction)
- Line between metaplasia and squamous epithelium is Z line, and it location of carcinoma. |
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Term
Patient presents with progressive dysphagia for solids and then for liquids, along with weakness and significant weight loss.
They are a smoker and a heavy drinker.
What could be going on? |
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Definition
Dysphagia and weight loss sound like Esophageal cancer.
In world, squamous > adenocarcinoma
In US, adenocarcinoma > squamous.
- Smoking and Alcohol are risk factors for Squamous, which occurs in the upper 2/3 of the esophagus
- Adenocarcinoma is associated with Barrett's metaplasia from chronic GERD. |
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Term
Which of the following is NOT a risk factor for squamous cell esophageal cancer?
1) Smoking
2) Achalasia
3) Alcohol
4) GERD
5) Esophageal webs
6) Zenker's Diverticulosis |
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Definition
4- Chronic GERD is associated with Barrett's esophagus, which is associated with ADENOcarcinoma (most common cause in US)
1- Chronic inflammation
2- Chagas disease and primary loss of aurbach's plexus
3- Chronic inflammation
5- Iron deficiency (Plummer vinson)
6- False diverticulum (not involving all layers of esophagus) located in the pharynx just above the upper esophageal junction |
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Term
There are numerous malabsorption syndromes, each of which can cause diarrhea, steathorrea, weight loss and weakness.
Which syndrome is described by each of the following?
1) Infectious malabsorption syndrome that affects entire small bowel, and that can be treated with antibiotics
2) Arthralgias, cardiac and neurological symptoms with foamy, PAS-positive macrophages in the intestinal lamina propria and mesenteric nodes
3) Autoantibodies to gliadin in wheat and other grains, affecting the duodenum and proximal jejunum
4) Milk intolerance with normal-appearing villi and osmotic diarrhea
5) Early childhood presentation with neurological manifestations and fat accumulation in enterocytes due to chylomicron deficiency
6) Child with cystic fibrosis with increased neutral fats in stool |
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Definition
These Will Cause Devastating Absorption Problems
1) Tropical Sprue
2) Whipple's diseases: Tropheryma whippelii (gram +)
- Foamy Whipped cream in a CAN
3) Celiac sprue
4) Lactase Disaccharidase deficiency
- Located at tips of vili, so self-limited cases can occur following infection
5) Abetalipoproteinemia (AR)
- No ApoB48 (Chylomicrons) or ApoB100 (VLDL)
6) Pancreatis insufficiency due to CF (can be due to cancer and chronic pancreatitis as well)
- ADEK issues |
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Term
Patient presents complaining of diarrhea, steatorrhea and weight loss. He recently had a viral infection, but has otherwise been healthy.
Administration fo lactose produces the symptoms, and glucose rises only 10 mg/dL
What happened? |
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Definition
Self-limited lactose intolerance following viral infection.
Lactase is located at tips of intestinal villi (Dissacharidase), and viral infections can transiently deplete it.
The Lactose intolerance test was + (load and glucose response) |
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Term
People of northern european descent tend to be particularly sensitive to wheat and other grains (often gives them fatty diarrhea and a rash).
What is the pathophysiology of this condition and what are these patients at risk for? |
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Definition
Celiac sprue:
1) Anti-gliadin Ab and anti-TTG (Screening) Ab cause blunting of villi and crypt hyperplasia, with lymphocytes in the lamina propria of the distal duodenum and proximal jejunum
- Decreased mucosal absorption primarily affecting jejunum (Folate deficiency)
- Rash is dermatitis herpetiformis (prurutiic papulovesicular rash on extensor surfaces)
2) Risk of T-cell lymphoma |
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Term
| Why might you get a megaloblastic anemia with celiac sprue? |
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Definition
Anti-gliadin and anti-TTG antibodies damage mucosal surface of distal duodenum and jejunum, where folate is absorbed.
Folate deficiency causes a megaloblastic anemia.
Watch out for T-cell lymphoma! |
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Term
| What are the differences in etiology and presentation between acute and chronic gastritis? |
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Definition
Acute= Erosive from drugs, trauma and toxins
Chronic= Autoimmune (A) or Bacteria (B)
1) Acute= Erosive
- Stress, NSAIDS, alcohol, uremia, burns (Curling ulcer) and brain (Cushion's ulcer) injury
- Disruption of mucosal barrier produces inflammation
2) Chronic= Non-erosive
- Type A (fundus/body): Autoimmune with anti-parietal cell Ab, pernicious Anemia and Achlorhydria
- Type B (Antrum): Most common- caused by H. pylori with increased risk of MALT lymphoma |
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Term
| Why do patients with severe burns often get erosive gastritis and what is this called? |
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Definition
Acute gastritis from burns= Curling ulcer (curling iron)
- Decreased plasma volume leads to sloughing of gastric mucosa |
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Term
| Why do patients with brain injuries often get erosive gastritis and what is this called? |
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Definition
Acute gastritis with brain injury= Cushion Ulcer
- Increased vagal stimulation leads to increased ACh and increased H+ production, producing ulcerations |
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Term
| Why do patients with RA and alcoholics often get acute gastritis? |
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Definition
Alcohol and NSAIDS are major factors
- NSAID's inhibit COX 1/2 and COX-1 mediated PGE1 synthesis, which is protective against stomach ulcers. |
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Term
| Which types of chronic gastritis affect the body/fundus and which types affect the antrum? |
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Definition
1) Type A/Body-fundus= Parietal/chief cells
- Autoimmune Pernicious Anemia with Achlorhydria
- Associated with other autoimmune conditions
2) Type B/Antrum= G cells and Mucous cells
- H. pylori bacterial infections with risk of MALT lymphoma |
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Term
What disease is associated with gastric hypertrophy (look like "brain gyri") and protein loss, parietal cell atrophy and increased mucosal cells?
What are the worrisome complications? |
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Definition
Menetrier's disease- Massive mucosal secretions causing protein loss
- Post-prandial epigastric pain and weight loss
- No good treatments, but gastrectomy and high-protein diet
- Pre-cancerous |
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Term
| What is the most common type of stomach cancer and where does it metastasize? |
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Definition
Gastric Adenocarcinoma can be
- Intestinal (looks liek colonic adenocarcinoma)
- Diffuse (signet ring cells (linitus plastica)
1) Virchow node: Left supraclavicular node (Virchow's node)
2) Krukenberg: Bilerateral ovaries with abundant mucus and signet rings
3) Sister Mary Joseph's nodule: Subcutaneous peri-umbilical metastasis |
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Term
| What are the major risk factors for gastric carcinoma? |
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Definition
Adenocarcinoma is MOST common (intestinal or diffuse) with early local spread and metastasis
**Look for acanthosis nigricans; brown to black, poorly defined, velvety hyperpigmentation of the skin**
1) Dietary nitrosamines (smoked foods)
2) Achlorhydria
3) Chronic gastritis (Autoimmune or H. pylori)
4) Type A blood |
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Term
| What is a patient with type A blood who loves smoked foods at particularly high risk for? |
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Definition
Gastric adenocarcinoma
Type A blood and Nitrosamines are 2 of 4 risk factors (with Chronic gastritis and Achlorhydria) |
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Term
What type of gastric adenocarcinoma metastasis is described by each of the following?
1) Left supraclavicular lymph node
2) Bilateral ovarian mets with mucus and signet ring cells
3) Sub-Q peri-umbilical met |
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Definition
1) Virchow's node
2) Krukenberg's tumor
3) Sister Mary Joseph's nodule |
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Term
| How can you differentiate between gastric and duodenal ulcers in PUD clinically? |
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Definition
Both are associated with H. pylori (duodenal 100% vs. gastric 70%)
1) Gastric has increased pain with meals (weight loss) and cancer risk: they tend to hemorrhage, but not perforate
- Less mucosal protection against gastric acid and association with NSAID use
2) Duodenal has less pain with meals (weight gain) and no cancer risk: Perforate (anterior) and Hemorrhage (posterior)
- Due to increased Gastric acid secretion (ZE syndrome) or deceased mucosal protein, with Brunner gland hypertrophy.
- Clean "punched out" margins |
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Term
| Why is it important to ask a patient with suspected PUD whether the pain gets better or worse with meals? |
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Definition
If it gets better, it is likely Duodenal ulcers, which have no cancer risk
If it gets worse, it is Gastric ulcers, which have cancer risk |
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Term
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Definition
If H. pylori associated (almost always true, in gastric and duodenal), give triple therapy.
1) PPi (Omeprazole)
2) Clarithromycin
3) Amoxicillin (if PCN allergic, give Metronidazole) |
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Term
| What are the important complications of Ulcers? |
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Definition
Hemorrhage, Perforation and Cancer
1) Gastric
- Cancer and Hemorrhage
2) Duodenal
- Hemorrhage (posterior) and Perforation (anterior) |
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Term
Crohn's and UC are the major forms of IBD. Which is described by each of the following?
1) Autoimmune cause
2) Affects any portion of GI tract, but mostly hits terminal illeum and colon, with "skip lesions" and "rectal sparing"
3) Transmural inflammation with "Cobblestone mucosa" and "creeping fat"
4) Non-caseating granulomas and lymphoid aggregates (Th1)
5) Complications include malnutrition, sclerosing cholangitis, toxic megacolon and colorectal carcinoma that is worse with R-sided of pancolitis |
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Definition
1) UC
2) CD
3) CD
4) CD
5) UC |
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Term
Crohn's and UC are the major forms of IBD. Which is described by each of the following?
1) Caused by disordered response to intestinal bacteria
2) Crypt abscesses and ulcers, with bleeding and non granulomas (Th2)
3) Pyoderma gangrenosum and PSC association
4) Migratory polyarthritis, erythema nodosum, immunologic disorders and kidney stones
5) Treated with Corticosteroids and infliximab |
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Definition
1) CD
2) UC
3) UC
4) CD
5) CD (UC is also hit with infliximab, but with ASA and 6-MP |
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Term
Crohn's and UC are the major forms of IBD. Which is described by each of the following?
1) Complications include strictures, fistulas, perianal disease, malabsorption and colorectal cancer
2) Can be associated with bloody or non-bloody diarrhea
3) Mucosal and submucosal inflammation only, with friable mucosal pseudopolyps and freely hanging mesentery
4) "lead pipe" appearance of colon on imaging, with no haustra
5) "String sign" on barium swallow x-ray, with linear ulcers, fissures and fistulas
6) Continuous colon lesions with rectal involvement |
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Definition
1) CD
2) CD
3) UC
4) UC
5) CD
6) UC |
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Term
Crohn's and UC are the major forms of IBD. Which is described by each of the following?
1) Cobblestone mucosa with creeping fat and bowel wall thickening ("String sign")
2) Colitis with rectal involvement
3) Treated with ASA (sulfsalazine) and 6-MP
4) Polyarthritis and erythema nodosum
5) Ankylosing spondylitis and Uveitis |
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Definition
1) CD
2) UC
3) UC
4) UC
5) BOTH (seronegative polyarthritis) |
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Term
Patient presents with alternating diarrhea and constipation. You treat their symptoms only.
What are the critical features of IBS? |
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Definition
Recurrent abdominal pain with >=2 of
1) Pain improves with defectation
2) Change in stool frequency
3) Change in appearance of stool
You can only treat symptomatically |
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Term
What is the most common cause of emergent abdominal surgery in children?
What are the most common causes of this issue in children and adults? |
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Definition
Appendicitis
1) Kids
- lymphoid hyperplasia after viral infection
2) Adults- Obstruction, fecalith |
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Term
Patient presents with nausea fever and localized pain at a point 1/3 the distance from the ASIS to the umbilicus.
He says the pain began the day before, and it was more diffuse around his "belly button"
What is on your differential and what are you worried about? |
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Definition
Diffuse peri-umbilical pain that spreads to McBurney's point, in the context of Nausea and fever suggests Apendicitis.
Must also consider Diverticulitis (elderly) and Ectopic pregnancy (beta-hCG to rule out) |
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Term
| Where is the most common location of Diverticular disease and what is the difference between a "True" and "False" Diverticulum? |
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Definition
Blind pouches protruding from alimentary tract of Sigmoid colon associated with low fiber diets
They are common in adults >60 and are often asymptomatic, but may cause vague discomfort and/or painless rectal bleeding (hematochezia)
1) True- All 3 gut walls including muscularis externa (Meckels)
2) False: Diverticulum or pseudodiverticulum including only the mucosa and submucosa
**Occur especially where vasa recta perforate muscularis externa** |
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Term
What is the most common cause of LLQ pain with fever and leukocytosis?
What are the important complications? |
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Definition
Diverticulitis ("left-sided appendicitis) with worry for Perforation: Give antibiotics
- Peritonitis
- Abscess formation
- Bowel stenosis
- Colovesical fistula (bladder and colon) calle Pneumaturia |
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Term
Patient presents with halitosis, dysphagia and signs of GI obstruction (solids, but not liquids).
What is Zenker's diverticulum and why is it worriesome? |
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Definition
False diverticulum (mucosa and submucosa only) with mucosal herniation at Pharyngoesophageal junction that puts patients at risk for Squamous cell esophageal cancer.
**Halitosis due to trapped food particles** |
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Term
What is the most common congenital anomaly of the GI tract?
What are the typical presenting symptoms? |
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Definition
Meckel's (true) Diverticulum due to persistence of Vitelline duct or yolk sack at the level of the umbilicus
Presents with melena, RLQ pain and is associated with Intussusception, volvulus or obstruction near the terminal ileum
five "2's"
- 2 inches long
- 2 feet from illeocecal valve
- 2% of population
- first 2 years of life
- may have 2 types of epithelia (gastric/pancreatic) |
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Term
1 year old child is experiencing RLQ pain and his stool as dark, brownish blood in it.
How do you diagnose the likely congenital anomaly? |
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Definition
Meckel's (True) Diverticulum from persistent vitelline duct/yolk sac
Pertechnetate study for ectopic uptake. The scan detects gastric mucosa; since approximately 50% of symptomatic Meckel's diverticula have ectopic gastric or pancreatic cells contained within the |
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Term
Common complications of Meckel's diverticulum are Intussusception and Volvulus.
What are these and how do they differ? |
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Definition
1) Intussusception- more common in kids
- "telescoping" of 1 bowel segment into distal segment, commonly at ileocecal junction
- Currant jelly stool and compromise blood supply (Abdominal emergency)
2) Volvulus (more common in elderly
- Twisting of portion of bowel around its mesentery (obstruction and infarction risk)
- Occurs at cecum and sigmoid colon, where there is redundant mesentery |
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Term
| Where do most cases of intestinal volvulus occur and why? |
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Definition
| Occurs in elderly at cecum and sigmoid colon, where there is redundant mesentery |
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Term
What is the pathophysiological basis of the condition that presents with chronic constipation early in life and a dilated portion of colon on imaging?
What chromosomal anomaly is associated? |
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Definition
Hirschsprung's disease causing congenital megacolon because of lack of ganglion cells (Aurbach and Meissner) from FAILURE OF NEURAL CREST MIGRATION
- constricted segment with dilation proximally
Associated with Down's syndrome |
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Term
Which intestinal disorder is described by each of the following?
1) Causes bilious vomiting with proximal stomach distention ("double bubble") due to failure of re-canalization of small bowel (associated with trisomy 21)
2) Obstructive plugs in the intestine that prevent stool passage at birth in CF patients
3) Necrosis of intestinal mucosa and possible perforation, usually involving the colon in infants (especially pre-mes)
4) Excruciating pain after eating with weight loss in the elderly, but only minor pain to palpation of abdomen
5) Acute bowel obstruction following recent surgery
6) Tortuous dilation of vessels in cecum, terminal ileum and/or ascending colon, leading to bleeding in older patients |
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Definition
1) Duodenal atresia
2) Meconium illeus
- baby can't pass poo composed up stuff from in utero
3) Necrotizing enterocolitis
4) Ischemic colitis- affects the splenic flexure and distal colon
5) Adhesions with well-demarcated necrotic zones
6) Angiodysplasia- confirmed by angio |
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Term
| What are the major types of colonic polyps and which ones are most commonly cancerous? |
|
Definition
Usually asymptomatic masses protruding into gut lumen with a "sawtooth" appearance (90% benign, can cause melena, diarrhea, partial obstruction)
- Can be tubular or villous
- Colorectal Cancerous risk increases with size, villous histology and degree of epithelial dysplasia
1) Hyperplastic
- most common non-malignant
- recto-sigmoid junction
2) Juvenile (benign if single)
- Sporadic lesions in <5 years old, mostly in rectum
- Only risk of adenocarcnoma in Juvenile polyposis syndrome with multiple polyps
3) Peutz-Jeghers (benign if single)
- AD syndrome featuring multiple nonmalignant hamartomas throughout GI tract, along with hyper-pigmented mouth, lips, hands, genitalia
- Increased risk of CRC and other visceral malignancies |
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Term
True or False:
Colorectal cancer is most common in young individuals with a family h/x |
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Definition
False! Usually >50
- 25% have family h/x
- 3rd most common cancer and 3rd most deadly |
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Term
There are multiple genetic syndromes associated with colorectal cancer. What are the critical characteristics of each of the following?
1) Familial adenomatous polyposis (FAP)
2) Gardner's syndrome
3) Turcot's syndrome
4) Hereditatry nonpolyposis colorectal cancer (HNPCC/Lynch syndrome) |
|
Definition
CRC most commonly presents at Rectosigmoid junction
FAP= APC gene (5q) and pan-colon
HNPCC= DNA repair gene and proximal colon
1) AD mutation in APC gene on chromosome 5q
- 2-hit hypothesis with 100% progression to CRC
- Pan-colonic (always involving rectum)
2) FAP + osseous and soft tissue tumors (congenital hypertrophy of the retinal pigment epithelium)
3) FAP + malignant CNS tumor
4) AD mutation in DNA mismatch repair genes
- 80% progress to CRC
- Always involve proximal colon |
|
|
Term
Which of the following is NOT a primary risk factor for colorectal cancer?
1) IBD
2) Streptococcus bovis
3) Tobacco
4) Jevenile polyposis syndrome
5) Heliobacter pylori
6) Peutz-Jeghers syndrome |
|
Definition
5- This is a risk factor for MALT lymphoma and gastric carcinoma, but not CRC
CRC is associated with villous polyps, multiple polyp syndromes, tobacco, strep and IBD |
|
|
Term
| What are the 3 most common presentations of CRC (location and pattern)? |
|
Definition
Rectosigmoid> Ascending >Descending
Ascending- exophytic mass, iron deficiency and weight loss
Descending- Infiltrating mass, partial obstruction, colicky pain and hematochezia. |
|
|
Term
| What groups of people are at particular risk for developing colorectal cancer? |
|
Definition
Iron deficiency anemia in males (>50) and post-menopausal females raises suspicion
Screen > 50 with stool occult blood test and colonoscopy |
|
|
Term
Why might you see an "apple core" like lesion on a barium enema x-ray.
What tumor marker is associated? |
|
Definition
Colorectal cancer- CEA marker
Rectosigmoid> ascending > descending |
|
|
Term
| What are the 2 molecular pathways that lead to the development of colorectal cancer? |
|
Definition
Remember, sporadic is MOST common
1) Microsatellite instability (15%)
- Unstable DNA repeat regions with repair defect (HNPCC/Lynch)
2) ABC/beta catenin (chromosomal instability-85%)
- mutations in APC prevent phosphorylation/ubiquination of beta-catenin, which leads to uncontrolled growth.
- Loss of APC in normal colon leads to increased risk, which can be sent into Adenoma by KRAS mutations (unregulated intracellular signal transduction) and finally into carcinoma by P53 mutations |
|
|
Term
| Why might a patient present with wheezing, right-sided heart murmurs, diarrhea and flushing? |
|
Definition
Metastatic Carcinoid tumor from small intestine, rectum or appendix
**local tumors do not cause Carcinoid syndrome, because the liver metabolizes 5-HT** |
|
|
Term
| What are carcinoid tumors and where are they commonly found? |
|
Definition
Neuroendocrine tumors (50% of small bowel tumors) most commonly found in illeum, but also in rectum and appendix.
- Produce 5-HT, which is metabolized locally by liver (portal circulation), but can cause Carcinoid syndrome in cases of metastasis (diarrhea, flushing, right side heart murmors and wheezing). |
|
|
Term
Cirrhosis occurs when diffuse fibrosis and nodular generation destroys the normal architecture of the liver.
Which porto-systemic shunts partially alleviate portal hypertension that occurs?
What about are the most common complications of Cirrhosis? |
|
Definition
Caused by viral hepatitis, alcohol (60-70%), biliary diesease and hemochromatosis.
1) Shunts
- Esophageal varices
- Hemorrhoids
- Caput medussa
2) Complications
- Risk of HCC |
|
|
Term
Patient presents complaining of hemorrhoids and hematemesis.
On PE, you note scleral icterus, spider nevi and gynecomastia, as well as a "Flapping" tremor.
What is on your differential? |
|
Definition
Cirrhosis
- Hemorrhoids and Hematemesis (esophageal varices) are compensatory shunts.
1) Alcohol (60-70%)
2) Viral hepatitis
3) Hemochromatosis
4) Biliary disease |
|
|
Term
| What are the major signs of portal hypertension that are seen in cirrhosis? |
|
Definition
1) Esophageal varices
- Cause hematemesis and melena
2) Peptic ulcers
3) Splenomegaly
4) Ascites and caput medusae
5) Hemorrhoids |
|
|
Term
| Why are palmar erythema, spider angiomas and Gynecomastia common in Cirrhosis? |
|
Definition
| All arise because of sex hormone imbalance, with excess conversion of androstenedione to estrogen |
|
|
Term
Which of the following is not characteristic of cirrhosis?
1) Palmar erythema
2) Asterixis
3) Ankle edema
4) Dermatidis herpetiformes
5) Ascites
6) Hemorrhoids |
|
Definition
|
|
Term
Numerous plasma markers are associated with liver and pancreas pathology. Interpret the meaning of elevation in each of the following.
1) AST/ALT
2) GGT
3) Alkaline phosphatase
4) Amylase
5) Lipase
6) Ceruloplasmin (decrease) |
|
Definition
1) Viral hepatitis (ALT> AST) or Alcoholic hepatitis (AST >ALT)
2) Increased with heavy alcohol consumption and other liver diseases
3) Obstructive liver disease (HCC), bone disease, bile duct disease
4) Acute pancreatitis, mumps
5) Acute pancreatitis
6) Wilson's disease |
|
|
Term
Young child who recently had the chickenpox presents with nausea/vomiting and hepatomegaly.
He is hypoglycemic and you document a microvesicular fatty change in his liver.
You are worried he will fall into a fatal coma.
What is Reye's syndrome? |
|
Definition
Rare (often fatal) Childhood hepatoenencephalopathy from aspirin
- Viral infection (VZV or influenza B) that has been treated with salicylates, where asprin metabolites decrease Beta-oxidation by reversible inhibition of mitochondrial enzymes. |
|
|
Term
| Describe the major stages of alcoholic liver disease. |
|
Definition
1) Hepatic steatosis
- short-term change with moderate intake, where macrovesicular fatty change can be reversed with cessation
2) Alcoholic hepaititis (AST> ALT with elevated GGT)
- Requires sustained, long-term consumption
- Swollen and necrotic hepatocytes with PMN infiltrate and Mallory bodies (intra-cytoplasmic eosinophilic inclusions)
3) Cirrhosis
- Final, irreversible form
- Micronodular, irregularly shrunken liver with "hobnail" appearance and sclerosis around the central evein |
|
|
Term
Patient presents with jaundice, tender hepatomegaly, ascites, hypoglycemia and polycythemia.
You are worried that their cirrhosis may have progressed to cancer.
What are the major risk factors for HCC and is it diagnosed? |
|
Definition
Increased AFP levels and biopsy
**Budd-Chiari occlusion of hepatic vein is common complication**
- Hep B/C
- Wilson's disease (copper)
- Hemachromatosis (iron)
- A-1-antitrypsin deficiency
- Alcoholic cirrhosis
- Aspergillus (aflatoxin) |
|
|
Term
| Which fungus is associated with hepatocellular carcinoma? |
|
Definition
| Aspergillus flavus and Aspergillus parasiticus (45 degree angled septate hyphae) produce aflatoxin |
|
|
Term
| How does Hepatocellular carcinoma spread? |
|
Definition
| Hematogenously- may lead to hepatic vein obstruction (Budd-chiari) |
|
|
Term
Which of the following is NOT associated with hepatocellular cancer?
1) Apergillus flavus
2) Alpha-1 anti-trypsin deficiency
3) B12 deficiency
4) Wilson's disease
5) Hemochromatosis
6) Hepatitis B |
|
Definition
| 3- This is associated with neurological symptoms like subacute demyelination of spinal cord. |
|
|
Term
| What is the name of the common benign liver tumor that occurs in ages 30-50, where biopsies are contraindicated due to hemorrhage risk? |
|
Definition
|
|
Term
| What is the pathophysiology underlying the "nutmeg" liver that can be seen in RHF? |
|
Definition
Backup of blood into liver in RHF and Budd-Chiari syndrome
- Centrilobular congestion and necrosis can result in cardiac cirrhosis, eventually. |
|
|
Term
Patients with congestive liver disease may present with absent JVD, varices and visible abdominal/back veins.
What is "Budd chiari syndrome" and what conditions is it associated with? |
|
Definition
Occlusion of IVC or hepatic veins with centrilobular liver congestion and necrosis, leading to congestive liver disease
- Hypercoagulable states
- P. vera
- Pregnancy
- HCC |
|
|
Term
| What are the 2 major clinical consequences of alpha 1 anti-trypsin deficiency? |
|
Definition
Misfolded protein aggregates in hepatocellular ER
1) Cirrhosis with PAS-positive globules in liver
2) Pan-acinar emphysema |
|
|
Term
| What are the possible causes of Juandice of the skin or sclerae? |
|
Definition
Elevated bilirubin
1) Direct hepato-cellular injury
- direct/indirect hyperbilirubinemia
- high urine biliruibin and low urobilinogen
2) Obstruction to bile flow
- Direct hyperbilirubinemia
3) Hemolysis
- Indirect hemoglobuinemia
- No urine bilirubin, with increased urobilinogen |
|
|
Term
Biliary obstruction is a common cause of jaundice.
Why does it occur. What are urine bilirubin and urine urobilinogen levels? |
|
Definition
Direct hyperbilirubinemia with high urine bilirubin and low urine urobilnogen.
RBCs are broken down to unconjugated bilirubin, which is sent to liver for conjugation and then to the bile duct to be secreted into the duodenum.
In this case, conjugation is fine, but you can't deliver the conjugated bilirubin to the small intestine, so it cannot be processed by bacteria to Urobilinogen.
Bilirubin in bile backs up and spills into urine, but it is NOT processed to urobilinogen, so Urine bilirubin is high and urine bilinogen is low.
The hyperbilirubinemia is direct, because it is conjugated and water soluble. |
|
|
Term
Hemolysis is a common cause of jaundice.
Why does it occur. What are urine bilirubin and urine urobilinogen levels? |
|
Definition
Indirect hyperbilirubinemia
Bilirubin metabolism: RBCs are broken down to unconjugated bilirubin, which is sent to liver for conjugation and then to the bile duct to be secreted into the duodenum, where it is processed by bacteria to urobilinogen.
With hemolysis, you are sending a TON of unconjugated bilirubin to the liver, and much of it cannot get conjugated.
Under NORMAL conditions, no bilirubin should be in urine, but since more conjugated bilirubin is being processed by bacteria, urine urobilinogen is high. |
|
|
Term
Viral hepatitis is a common cause of jaundice.
Why does it occur. What are urine bilirubin and urine urobilinogen levels? |
|
Definition
Mixed direct/indirect hyperbilirubinemia.
Bilirubin metabolism: RBCs are broken down to unconjugated bilirubin, which is sent to liver for conjugation and then to the bile duct to be secreted into the duodenum, where it is processed by bacteria to urobilinogen.
With primary liver injury, conjugation is disrupted, but the stuff that is spills into urine (high urine bilirubin)
The urine urobilinogen levels are normal/low, since less conjugated bilirubin is being successfully sent through the bile duct to the small intestine for bacterial processing. |
|
|
Term
| Why are neonates jaundiced under normal conditions? |
|
Definition
At birth, immature UDP-glucuronyl transferase is not able to conjugate bilirubin very well.
The unconjugated bilirubin causes jaundice/kernicterus.
Treat with phototherapy (converts UCB to water-soluble form) |
|
|
Term
Describe the pathophysiology and clinical relevance of the following hereditary hyperbilirubinemias.
1) Gilbert's syndrome
2) Crigler-Najar syndrome, type 1
3) Dubin-Johnson syndrome |
|
Definition
Gilbert= Uptake (benign)
Crigler-Najjar- Conjugation (lethal)
Dubin-Johnson- Excretion (benign)
1) Mild decrease in UDP-glucuronyl transferase or decrease in bilirubin uptake
- Asymptomatic with unconjugated hyperbilirubinemia in absense of hemolysis that increases with stress/fasting
2) Absent UDP-glucuronyl transferase
- Presents early in life and patients die in first few years
- Jaundice, kernicterus (bilirubin in the brain) and unconjugated hyperbilirubinemia
- Treat with plasmapheresis and phototherapy
3) Conjugated hyperbilirubinemia due to defective liver excretion (black liver). Benign.
** Rotor's syndrome is similar, but even milder and does not cause black liver. |
|
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Term
There are many causes of hyperbilirubinemia. Which is described by each of the following?
1) Direct hyperbilirubinemia with black liver due to difficulty with conjugated bilirubin excretion
2) Direct hyperbilirubinemia with pink liver due to difficulty with conjugated bilirubin excretion
3) Indirect hyperbilirubinemia presenting early in life, with kernicterus, jaundice and early death
4) Asymptomatic indirect hyperbilirubinemia due to low UDP-glucoryonyltransferase and/or deficient bilirubin hepatic uptake.
5) Neonatal jaundice due to immature conjugation enzyme |
|
Definition
1) Dubin-Johnson syndrome= Excretion issue
- Benign
2) Rotor's syndrome- Less severe DJS
3) Crigler-Najjar type 1
- Absent UDP glucouronyltransferase treated with plasmapheresis and phototherapy
4) Gilbert's syndrome
5) Physiological jaundice of newborn
- Immature UDP-glucuronyl transferase cannot conjugate bilirubin well, so treat with phototherapy |
|
|
Term
| What is the difference between Crigler-Najjar type 1 and type 2 |
|
Definition
Type 1 is more severe and can only be treated with phototherapy and plasmapheresis
Type 2 responds to phenobarbital, which increases liver enzyme synthesis |
|
|
Term
| What are the typical symptoms/signs of hepatolenticular degeneration? |
|
Definition
Wilson's disease- AR condition with inadequate hepatic copper excretion
- treated with Penicillamine
Copper is Hella BAD
- Cerulosplasmin (decrease), Cirrhosis, Corneal deposits (Kayser-Fleischer rings, golden-brown rings in cornea), Copper accumulation, Carcinoma (HCC)
- Hemolytic anemia
- Basal ganglia degeneration (parkinsonian)
- Asterixis
- Dementia, Dyskineasia, Dysarthria |
|
|
Term
| How do you treat a patient that presents with parkinsonian symptoms, asterixis, hemolytic anemia and low ceruloplasmin levels? |
|
Definition
| AR Wilson's treated with Penicillamine, which is a copper chelator that allows for urinary excretion. |
|
|
Term
Which of the following is NOT seen in Wilson's disease?
1) Low ceruloplasmin levels
2) Asterixis
3) Dementia
4) Corneal deposits
5) Dysarthria
6) Megaloblastic anemia |
|
Definition
6- You see a hemolytic anemia, not megaloblastic
Copper is Hella BAD
- Cerulosplasmin (decrease), Cirrhosis, Corneal deposits (Kayser-Fleischer rings, golden-brown rings in cornea), Copper accumulation, Carcinoma (HCC)
- Hemolytic anemia
- Basal ganglia degeneration (parkinsonian)
- Asterixis
- Dementia, Dyskineasia, Dysarthria |
|
|
Term
| What is/are the classic presentation and complications of Hemochromatosis? |
|
Definition
Hemochromatosis Can Cause Deposits
- Hemosiderin deposits that can be primary (AR) or secondary to chronic transfusion therapy (beta-thalassemia major)
1) Triad: micronodular Cirrhosis, Diabetes and skin pigmentation
2) Complications: CHF, testiuclar atrophy in males and a risk of HCC |
|
|
Term
Which of the following iron study results fits Hemochromatosis?
1) High TIBC, low ferritin, low serum iron
2) Low TIBC, high ferritin, high serum iron
3) low TIBC, high ferritin, low serum iron
4) Low TIBC, normal ferritin, high serum iron |
|
Definition
Risk of CHF, testicular atrophy and HCC
4- There is more iron and stored iron (ferritin), which means there is less "free binding sites" (TIBC).
1- Iron deficiency anemia
3- ACD
4- Unclear |
|
|
Term
Which of the following regarding hemochromatosis is FALSE
1) Associated with HLA-A3
2) Treated with phlebotomy and deferoxamine
3) Autosomal dominant assocation
4) Can cause testicular atrophy and CHF
5) Associated with diabetes mellitus |
|
Definition
3- It is autosomal recessive or secondary to transfusions (beta thalasemia)
1) True
2) True: Defeoxamine is a chelator
4) True: Also risk of HCC
5) True (bronze diabetes): also associated with skin pigmentation and cirrhosis |
|
|
Term
Biliary tract diseases often present with Pruritis, jaundice, dark urine, light stools and hepatosplenomegaly.
Which disease of the biliary tract is associated with each of the following ?
1) Extrahepatic biliary obstruction that can be complicated by ascending cholangitis
2) Autoimmune reaction inovling lymphocytic infiltrate and granulomas
3) Concentric "onion skin" bile duct fibrosis producing alternating strictures and dilation with "Beading" of intra- and extra-hepatic bile ducts on ERCP |
|
Definition
All have increased conjugated bilirubin (dark urine), increased cholesterol (pruritis is from bile acids in skin) and increased ALP
1) Secondary biliary cirrhosis
- Gallstones, biliary strictures, chronic pancreatitis and carcinoma of the head of the pancreas can all increase pressure in the intrahepatic ducts, leading to fibrosis and bile stasis.
2) PBC
- Incrased serum anti-mitochondrial antibodies (including IgM)
- Associated with other syndromes (CREST, RA, celiac)
3) PSC
- Hypergammaglobulinemia (IgM) with UC association
- Can lead to secondary biliary cirrhosis. |
|
|
Term
| What are the major differences between primary sclerosis cholangitis and primary biliary cirrhosis? |
|
Definition
Both present with pruritis, dark urine, light stool and hepatosplenomegaly.
1) PSC
- IBD-associated
- More in men (UC association)
- Diagnosis by ERCP, beaded appearance
2) PBC
- Autoimmune (associated with RA and CREST)
- 90% in women
- anti-mitochondrial antibody
- diagnosis on biopsy with lymphocytic infiltrate and granulomas |
|
|
Term
| Why might you give a patient with PSC cholestryamine? |
|
Definition
| Pruritis in PBC and PSC is due to bile acid deposition in skin from excess cholesterol, so the bile acid sequestrate will treat this. |
|
|
Term
There are 2 major types of gallstones (cholelithiasis)
What are the critical features of each and what are the major risk factors for Cholelithiasis? |
|
Definition
1) Risk factors (4 F's)
- Female, Fat, Fertile, Forty
- Older, obese pregnant women get em'
2a) Cholesterol (80%)
- Radioluscent stones associated with obesity, CD, CF, advanced age, estrogens, mutiparity, rapid weight loss and native American descent.
2b) Pigment stones
- Radiopaque
- Chronic hemolysis, alcoholic cirrhosis, advanced age and biliary infection
- Black (hemolysis), Brown (infection) |
|
|
Term
Patient presents with fever, jaundice and RUQ pain.
There is evidence of inspiratory arrest on deep palpation due to pain.
Which of the following is NOT associated with the most common cause of these symptoms?
1) Native american descent
2) Female gender
3) Older age
4) Chronic hemolysis
5) Pregnancy (multiparity)
6) Crohn's disease |
|
Definition
Fever, Jaundice and RUQ pain is Charcot's triad
4- This is characteristic of Pigment stones (black in hemolysis and brown in infection)
The most common cause of cholelithiasis is cholesterol stones.
Cholesterol stones are associated with
- Radioluscent stones
- obesity
- CD
- CF
- Advanced age
- Estrogens
- Multiparity
- Rapid weight loss
- Native American descent. |
|
|
Term
What are the most common causes of pigment stones?
Why do pigment/cholesterol stones cause biliary colic? |
|
Definition
1) Chronic hemolysis (Black) or Biliary Infection (Brown) in alcoholics and older patients
2) Pain due to neurohormonal activation (by CCK after meal) and contraction of bile duct, which may push the stone into the cystic duct (diabetics may NOT show pain). |
|
|
Term
| What are the common complications of cholelithiasis? |
|
Definition
Diagnose with radionuclide biliary scan and ultrasoun, and Treat with cholecystectomy
1) Cholecystitis (most common)
2) Ascending cholangitis and bile stasis
3) Acute pancreatitis
4) Biliary colic
5) Gallbladder-intestinal fistula |
|
|
Term
| Why are some gallstone "pigment stones" black and others brown? |
|
Definition
Pigement stones consist of bilirubin and calcium salts that are found in bile (vs. cholesterol, which are more common and due to cholesterol supersaturation)
1) Black= Calcium + bilirubin
- Stasis or chronic hemolysis
2) Brown= calcium salts of unconjugated bilirubin with small amounts of cholesterol and protein
- Infection |
|
|
Term
| How can gallstones cause air to enter the biliary tree? |
|
Definition
IF stones cause fistula to form between gallbladder and small intestine, air may enter the biliary tree.
If the stone obstructs the ileocecal valve (gallstone illeus), air can be seen in the tree on imaging. |
|
|
Term
What is the most common cause of cholecystitis?
Why might ALP be elevated? |
|
Definition
1) Inflammation of gallbladder from Gallstones (more rarely, you can see ischemia or CMV)
2) Alkaline phosphatase would be high if the duct becomes involved (ascending cholangitis) |
|
|
Term
| What are the major causes of severe epigastric abdominal pain radiating to the back in the context of anorexia and nausea. |
|
Definition
Acute pancreatitis- auto-digestion of the pancreas by pancreatic enzymes
GET SMASHED
1) Gallstones
2) Ethanol
3) Trauma
4) Steroids
5) Mumps
6) Autoimmune
7) Scorpion
8) Hypercalcemia/hypertriglyceridemia
9) ERCP
10) Drugs (sulfa) |
|
|
Term
Patient presents with elevated amylase and lipase levels
Which of the following DOES NOT cause acute pancreatitis?
1) 5-FU
2) Gallstones
3) Smoking
4) Hypercalcemia
5) ERCP
6) Mumps |
|
Definition
3- Alcohol, but not smoking is associated
GET SMASHED
1) Gallstones
2) Ethanol
3) Trauma
4) Steroids
5) Mumps
6) Autoimmune
7) Scorpion
8) Hypercalcemia/hypertriglyceridemia
9) ERCP
10) Drugs (sulfa) |
|
|
Term
True or False:
Lipase levels are a more specific indicator of acute pancreatitis than Amylase levels. |
|
Definition
|
|
Term
Which of the following is NOT a complication normally associated with acute pancreatitis?
1) DIC
2) ARDS
3) Pancreatic adenocarcinoma
4) Fat necrosis
5) Hypocalcemia
6) Pseudocyst formation |
|
Definition
3- This is CHRONIC pancreatitis
Hypocalcemia occurs because of calcium-soap deposits |
|
|
Term
True or False:
Acute pancreatitis is associated with smoking and alcohol |
|
Definition
False: Acute= Alcohol
Chronic= BOTH
Chronic pancreatitis leads to steatorrhea, fat-soluble vitamin deficiency, diabetes and increased risk of pancreatic adenocarcinoma. |
|
|
Term
| What are the risk factors and prognosis associated with pancreatic adenocarcinoma? |
|
Definition
CA 19-0 and CEA (less specific) tumor marks1) Risk
Most often in head, where it causes painless, obstructive jaundice
- Tobacco (but not EtOH)
- Chronic pancreatitis (>20 years)
- Age > 50
- Jewish and AA males
2) Average 6 months or less- usually already metastasized at presentation |
|
|
Term
Patient presents with abdominal pain radiating to the back. She has lost significant amounts of weight and there is redness and tenderness on palpation of her extremities.
Her gallbladder is also palpable
What markers are associated with this condition and what is the prognosis? |
|
Definition
Pancreatic adenocarcinoma: 6 months or less and look for CA 19-9 and CEA (less specific) markers
Presenting symptoms:
- Migratory thrombophlebitis (Trousseu's syndrome)
- Courvoisier's sign of obstructive jaundice.
- Pain in correct distribution and weight loss |
|
|
Term
| Which forms of pancreatic disease are associated with smoking and/or alcohol? |
|
Definition
1) Acute= Alcohol only
2) Chronic= BOTH
3) Adenocarcinoma= Smoking only
- but associated with chronic pancreatitis, which is associated with smoking |
|
|
Term
Where do each of the following agents work and by what mechanism?
1) Octreotide
2) PPis
3) Antacids
4) Sucralfate and Bismuth salts
5) Misoprostol |
|
Definition
1) Somatostatin analogue that inhibits ECL histamine release (prevents parietal cell stimulation)
2) Inhibit H/K ATPase in parietal cells
3) Inhibit H+
4) Bind ulcer base, providing physical protection and allowing HCO3- secretion to reestablish pH
5) PGE1 analog that increases production and secretion of gastric mucous barrier, with decreased acid production |
|
|
Term
| Why might you use Cimetidine and how does it work? What side effects are concerning? |
|
Definition
H2 blockers- CimeTIDINE, Ranitidine, Famotidine, Nizatidine
1) Reversible block of H2 receptors on parietal cells to reduce H+ secretion
2) PUD, gastritis, mild esophageal reflux
3) P-450 inhibitor (other H2 blockers have less side effects)
- anti-androgenic effects (prolactin release, gynectomastia, impotence and decreased libido in males)
- Cross BBB (confusion, dizziness, headache)
- Decrease renal excretion of creatinine |
|
|
Term
| Why might you use Lansoprazole and how does it work? What side effects are concerning? |
|
Definition
Lansoprazole and Omeprazole are PPis
1) Irreversibly inhibit H+/K+ ATPase in parietal cells
2) PUD, gastritis, reflux, ZE syndrome
3) Pernicious anemia with long-term use |
|
|
Term
| Why might you use Sucralfate and how does it work? |
|
Definition
Sucralfate and Bismuth are anti-ulcer drugs
1) Bind ulcer base and provide physical protection, allowing HCO3 secretion to reestablish pH gradient in mucous layer
2) Ulcer healing and traveler's diarrhea |
|
|
Term
| Why might you use Misoprostol and how does it work? Who should it not be used in? |
|
Definition
1) PGE1 analog that increases production and secretion of gastric mucous barrier (decrease acid production)
2) Prevent NSAID-induced peptic ulcers, Maintain PDA, Induce labor
3) Women of childbearing potential (Abortifacient)
- can also cause diarrhea |
|
|
Term
| Why might you use Octreotide and how does it work? What side effects are concerning? |
|
Definition
1) Long-acting somatostatin analog that inhibits ECL histamine release
2) Acute variceal bleeds, acromegaly, VIPoma and carcinoid tumors
3) Nausea, cramps, steatorrhea |
|
|
Term
| What are the available types of antacids and what are the important side effects to keep in mind? |
|
Definition
All can affect other drugs (tetracyclines) by altering gastric and urinary pH or by delaying gastric emptying.
**All can cause hypokalemia**
1) Aluminum hydroxide: Constipation and hypophosphatemia; proximal muscle weakness, osteodystrophy and seizures
2) Magnesium hydroxide: Diarrhea, hyporeflexia, hypotension, cardiac arrest
3) Calcium carbonate- Hypercalcemia and rebound acidemia |
|
|
Term
| There are a number of osmotic laxatives available. What are they, how do they work and what toxicities are associated with their use? |
|
Definition
1) MgOH, Mg citrate, polyethylene glycol, lactulose
2) Osmotic load to draw water out
**lactulose also treats hepatic encephalopathy since glut flora degrade it into metabolites that promote nitrogen excretion as NH4+
3) Diarrhea, dehydration; abused by bulimics |
|
|
Term
| Which osmotic laxative is useful in treating hepatic encephalopathy and why? |
|
Definition
Lactulose
Gut flora degrade it to lactic acid and acetic acid, which promote nitrogen excretion as NH4+ |
|
|
Term
What is infliximab and why is it used?
What is the major worry with its use? |
|
Definition
1) anti-TNF antibody used in CD and RA
2) Watch out for infection (reactivation TB), fever and hypotension |
|
|
Term
| Sulfasalazine is often given to treat UC and CD. How does it work and what are the associated toxicities? |
|
Definition
1) Combination of sulfapyridine (antibacterial) and 5-aminosalicyclic acid (anti-inflammatory), which is activated by colonic bacteria
2) Malaise, nausea, sulfonamide toxicity, reversible oligospermia |
|
|
Term
Ondansetron is an anti-emetic agent
How does it work and when should it be used? |
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Definition
1) Ondansetron is a 5-HT3 antagonist that acts as a powerful central-acting anti-emetic to control vomiting
2) Post-operativeley and in patients undergoing chemo.
**can cause headache and constipation** |
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Term
| What is the mechanism and utility of Metoclopramide? Who should NOT receive it? |
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Definition
1) Metaclopramide inhibits D2 receptors,
, increasing resting tone, contractility, LES tone and motility
2) Given for diabetic and post-surgery gastroparesis
3) PD effects and can interact with digoxin and diabetic agents
- Don't give to patients with small bowel obstruction or PD |
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