Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
279 Cards in this Set
- Front
- Back
Enzyme co-factor for insulin action
|
Chromium
|
|
Inhibits Vitamin K (anticoagulant)
|
Warfarin (Coumadin)
|
|
most widespread micronutrient deficiency in the world
|
iodine-- goiters and cretinism (kids), hypothyroidism
|
|
Role: Connective tissue/collagen formation, promotion of iron absorption by keeping iron in the absorbable state (ferrous Fe2+)
|
Vitamin C/Ascorbic Acid
|
|
micronutrient synthesized in the liver from trypthophan
|
Niacin (Vitamin B3)
|
|
Cofactor for folate function
|
Cobalamine (Vitamin B12)
|
|
2 things absorbed in the terminal ileum
|
bile acids and vitamin B12 (cobalamine)
|
|
1. Acute: papilledema, bulging fontanelles, vertigo, diplopia, skin exfoliation
2. Chronic: anorexia, headache, dry skin, hair loss, hepatosplenomegaly |
Vitamin A/Retinol excess
|
|
Role: increase intestinal absorption of calcium and phosphorus, increase renal reabsorption of calcium
|
Vitamin D (Ergocalciferol)
|
|
1. decreased calcium absorption from small intestine
2. decreased reabsorption of calcium from the kidneys 3. stimulates PTH release 4. PTH- increases calcium absorption from the gut but also leaches it from bones |
Vitamin D (Ergocalciferol) deficiency
|
|
seen in granulomatous disease: sarcoidosis, lymphoma
|
1,25 dihydroxyvitamin D excess--> hypercalcemia
|
|
1. increased calcium reabsorption from the gut
2. hypercalcemia-stones, moans, psychological overtones 3. hypercalcuria (stones) |
vitamin D excess
|
|
Excess Sx:
1. dec platelet aggregation 2. interferes with vitamin K metabolism (don’t use with warfarin—too much anticoag effect) |
Vitamin E (alpha tocopherol) excess
|
|
Zollinger Ellison syndrome
|
gastrinoma- tumor that secretes gastrin causing parietal cells to release HCl and intrinsic factor-- this leads to high levels of acid secretion and peptic ulcer disease.
|
|
Functions of Cholecystokinin
|
1. Gallbladder contraction
2. sphincter of Oddi relaxation 3. delayed/dec gastric emptying 4. stimulation of pancreatic acinar cells |
|
Stimulants of CCK release
|
fatty acids and protein- CCK-releasing peptide and monitor peptide (panc acinar cells)
|
|
Why does eating fatty foods potentially make the pain of cholelithiasis worse?
|
Fatty foods stimulate the release of CCK which stimulates the contraction of the gallbladder
|
|
Where is CCK released from?
|
I cells of the duodenum
|
|
Where is secretin released from and what are it's function.
|
Released from S cells of duodenum
1. Stimulates the release of HCO3- (bicarb) from pancreatic ductular cells. Water follows. This allows pancreatic enzymes to flow into duodenum and function (alkaline pH) 2. decreases gastric acid secretion 3. increases bile secretion |
|
What stimulates the release of secretin?
|
The entry of acid from the stomach along with food
|
|
Where is somatostatin released from?
|
D cells in the antrum of the stomach and pancreatic islets (delta cells--endocrine-release somatostatin into blood)
|
|
What are the functions of somatostatin?
|
Turns everything off...
1. dec gastric acid (parietal cells) and pepsinogen (chief cells) secretion 2. dec pancreatic and small intestine fluid secretion 3. dec gallbladder contraction 4. dec insulin and glucagon release |
|
What is a type of synthetic somatostatin and what is it used for?
|
Octreotide/Sandostatin
1. carcinoid tumors 2. VIPomas 3. esophageal varices-- GI hemorrhage 4. chronic pancreatitis |
|
What is GIP and what are its endocrine and exocrine functions?
|
Glucose dependent Insulinotropic Peptide stimulated by oral glucose load
endocrine: increase insulin release- pull glucose intracellular exocrine: decrease gastric H+ secretion |
|
What is VIP and what does it do?
|
Vasoactive Intestinal Peptide- relaxation of intestinal sphincter and smooth muscle, increase intestinal water and electrolyte secretion
VIPoma-- massive diarrhea (relaxation + H20 and lytes secretion) |
|
What is motilin and what does it do? What can stimulate it?
|
Motilin is secreted by the small intestine during the fasting state. It produces Migrating Motor Complexes to clear the gut of undigested food (less than size of nickel). Stimulated by erythromycin-- can clear gut of blood prior to scope.
|
|
What is intrinsic factor? What does it do and where it is release from?
|
secreted by parietal cells of the stomach (in addition to HCl), it is a vitamin B12 binding protein needed for the absorption of vit b12 in the terminal ileum
|
|
What is autoimmune gastritis what does it lead to?
|
autoimmune destruction of gastric parietal cells-- less HCl, but high gastrin levels, lack of intrinsic factor--> pernicious anemia (macrocytic)
|
|
What stimulates gastric acid secretion in the stomach? What inhibits it?
|
stimulate HCl release: gastrin (g cells in antrum), ACh, histamine (ECL cells)
inhibit HCl release from parietal cells: somatostatin, glucose dependent insulinotropic peptide (GIP), prostaglandin, secretin |
|
What is pepsinogen? Where is it released?
|
Pepsinogen is released from gastric chief cells-- it cleaved by H+ to its active form= pepsin--degrades protein (not nearly as important as pancreatic proteinases)
|
|
Where is Bicarb (HCO3-) produced/released in the GI tract? What is its purpose?
|
pumped out by pancreatic ductular cells (secretin), brunners gland of duodenum, mucus that covers gastric epithelium (protects epithelium from damage from acid)
Neutralizes acid and prevents autodigestion of pancreatic enzymes (only work in alkaline env) |
|
What pancreatic enzyme is secreted in its active form?
|
amylase
|
|
what characteristic histological feature do you see with Hep B infection?
|
"ground glass" hepatocytes--> HBsAg
|
|
What activates trypsinogen and where is it located?
|
enteropeptidase/enterokinase on the intestinal brush border
|
|
How must carbohydrates be absorbed?
|
As monosaccharides (glucose, galactose, fructose)
|
|
How is glucose absorbed into enterocytes?
|
Via the Sodium-Glucose-Galactose co-transporter (SGLT-1) -- so when someone is dehydrated you should give sodium glucose in 1:1 concentrations.
|
|
How is fructose absorbed by enterocytes?
|
By facilitated diffusion (GLUT-5)
|
|
Plummer Vinson Syndrome
|
Triad of
1. dysphagia from esophageal webs 2. glossitis 3. iron deficiency anemia |
|
Risk Factors for Esophageal Cancer
|
ABCDEF
Alcohol/Achalasia Barret's esophagus from GERD (LES) Cigarrettes Diverticuli (Zenker's above the upper eso sphincter) Esophageal web (plummer-vinson syndrome), esophagitis Famlial |
|
most common type of esophageal cancer worldwide and where found in the esophagus?
|
squamous cell carcinoma, in the upper and middle esophagus
|
|
most common type of esophageal cancer in the U.S. and where found in the esophagus?
|
adenocarcinoma in the lower 1/3 of esophagus. Barret's (intestinal metaplasia is risk factor)
|
|
celiac sprue
|
autoantibodies to gliadin (in wheat, barley, rye)-- causes 1. blunting of villi in the proximal small bowel
2. massive malabsorption and diarrhea 3. lymphocytes in the lamina propria in the epithelium 4. crypt hyperplasia Blood test- alpha1 gliadin and tissue transglutaminase (TTG) Treatment- gluten free diet associated with dermatitis herpetiformis at slightly increased risk for T cell lymphoma |
|
disease associated with dermatitis herpetiformis
|
celiac sprue
|
|
Acute gastritis (erosive)
|
disruption of the mucosal barrier--> inflammation
Causes: 1. stress 2. NSAIDs (block PGE2-- which stimulates mucous production) 3. burns = Curling ulcer-- dec plasma volume--> sloughing of gastric mucosa 4. brain = Cushing's ulcer-- inc vagal stimulation--> inc ACh--> in parietal cell H+ secretion |
|
Chronic gastritis (nonerosive)
Type A- body of stomach |
two types: A (body) and B (antrum), AB Pairing to help remember
A (Body)- Autoimmune gastritis-attacks parietal cells--> Achlohydria, pernicious Anemia (lack of intrinsic factor) |
|
chronic gastritis
Type B- antrum of the stomach |
caused by H. pylori Bacterium infection--affects Antrum
increased risk for MALT lymphoma |
|
Menetrier's disease
|
gastric hypertrophy with protein loss, parietal cell atrophy, and inc mucous cells--precancerous condition. Rugae of the stomach are so hypertrophied they look like the gyri of the brain
|
|
common features of gastric adenocarcinoma
|
1. signet rings (looks like class ring) and 2, acanthosis nigricans (dark brown/black hyperpigmentation of the skin that is also associated with endocrine dysfunction--DM, hypothyroid etc)
|
|
things associated with stomach cancer
|
1. nitrosamines (smoked foods)
2. chronic gastritis 3. achlorhydria (lack of stomach acid) |
|
linitis plastica
|
thickened leathery appearance of the stomach when gastric adenocarcinoma is diffusively infiltrative ("leather bottle")
|
|
virchow's node
|
gastric adenocarcinoma mets to the left supraclavicular node
|
|
krukenberg's tumor
|
gastric adenocarcinoma with bilateral mets to the ovaries- abundant mucus and signets rings
|
|
compare and contrast gastric ulcers and duodenal ulcers
|
Gastric ulcer- pain is Greater with meals, 70% caused by H. pylori infection, chronic NSAID use also implicated (block PGE2--dec mucus production/protection)
Duodenal ulcer- pain Decreases with meals--> weight gain, almost 100% caused by H. pylori infection. See hypertrophy of Brunner's gland (secrete alkaline mucus), clean punched out margins (bleeding, perforation, penetration of pancreas, and obstruction can occur) |
|
crohn's disease
|
granulomas,
skip lesions-seen as cobblestoning on imaging, transmural inflammation, fistulas and fissures creeping fat/mesentery-from trans inflam, smoking, rectal sparing, |
|
extraintestinal manifestations of crohn's
|
1. migratory polyartheritis,
2. erythema nodosum (inflammation of fat cells on the skin--causing nodules often on the shins), 3. ankylosing spondylitis (cannot extend or flex spine), 4.uveitis, 5. immunologic disorders |
|
ulcerative colitis
|
-continuous inflammation of the colon always involving the rectum
-only mucosal and submucosal inflammation -pseudopolyps, ulcers, bleeding -increased risk for colorectal cancer, severe stenosis, toxic megacolon -"lead pipe" appearance on imaging- major continuous inflammation |
|
extraintestinal manifestations of ulcerative colitis
|
1. primary sclerosing cholangitis (alternating areas of stricture and dilatation intra and extrahepatic bile ducts-- cholestasis)
2. pyoderma gangrenosum (tissue becomes necrotic forming deep ulcers--usually on the legs)--can also be seen in crohns though |
|
appendicitis presentation
|
periumbical pain (visceral-- non localizing) that then localizes the RLQ- McBurneys point. Can perforate-- peritonitis
rule out diverticulitis and ectopic pregnancy |
|
diverticulum
(true vs false) |
blind outpouching of the GI tract
true- involves all layers of the gut wall false- involves only mucosa and submucosal layers, often where vasa recta penetrate muscularis propria/externa |
|
diverticulosus
|
many diverticuli, often asymptomatic or vague discomfort
-very common (50% of ppl over 60) -arise from increased intraluminal pressure, low fiber diet-hard stools - most common in sigmoid colon |
|
diverticulitis
|
-inflammation of diverticula causing LLQ pain, fever, leukocytosis
-may perforate-- peritonitis, abscess formation, or bowel stenosis - give Abx - may cause bright red blood per rectum, colovesical fistula (colon to bladder-->pneumaturia) |
|
Zenker's diverticulum
|
false diverticulum located above the upper esophageal sphincter. presents with halitosis (trapped food), regurgitation of undigested food, dysphagia, obstruction
|
|
Meckel's diverticulum
|
persistence of the vitelline duct or yolk sac,
may contain acid-secreting gastric mucosa or pancreatic tissue can cause bleeding, volvulus, intussusception, or obstruction near the terminal ileum the 5 twos 1. 2 inches long 2. 2 feet from ileocecal valve 3. 2% of population 4. often present within first 2 years 5. may have 2 types of epithelia (gastric, pancreatic) |
|
most common congenital anomaly of the GI tract
|
Meckel's diverticulum
|
|
possible outcomes of Meckel's diverticulum
|
bleeding, volvulus, intussusception, or obstruction near the terminal ileum
|
|
intussusception
|
telescoping of 1 bowel segment into a distal segment
can compromise blood supply often due to intraluminal mass or stricture causing one part to get stuck and the other to slide inside it usually seen in infants--constipation |
|
volvulus
|
twisting of portion of the bowel around its mesentery/stalk
can lead to obstruction and infarction may occur at sigmoid colon cuz of redundant mesentery usually in elderly |
|
Hirschsprung's disease
|
congenital megacolon characterized by lack of myenteric/Auerbach's plexus in segment of bowel
due to failure of neural crest cells to migrate presents as chronic constipation early in life (failure to pass meconium) dilated portion of the colon proximal to aganglionic segment involves rectum pts with Down syndrome at inc risk |
|
duodenal atresia
|
causes early bilious vomiting with proximal stomach distention = "double bubble"
Associated with down's syndrome |
|
meconium ileus
|
in cystic fibrosis, meconium plug obstructs intestine, preventing stool passage at birth
|
|
necrotizing enterocolitis
|
necrosis of intestinal mucosa and possible perforation
colon usually involves but can involve entire GI tract in neonates- more often in preemies |
|
ischemic colitis
|
reduction in intestinal blood flow causes ischemia
commonly occurs at the splenic flexure--watershed region/border zone typically seen in elderly |
|
adhesion
|
acute bowel obstruction
usually after surgery can cause well demarcated necrotic zones |
|
angiodysplasia
|
tortuous dilation of vessels--> bleeding
most often seen in cecum and ascending colon more common in elderly |
|
colonic polyps
which type is most likely to be malignant? |
90% are benign hyperplastic hamartomas, not neoplasms--remove them anyway
grow into the intestinal lumen- can be flat (sessile) or pedunculated (on stalk) The more villous (colon does not usually have villi--only small bowel, since villi are for absorption) |
|
Colorectal cancer
gene involved |
3rd most common cancer
most are sporadic (APC gene mutation) |
|
presentation of right sided vs left sided CRC
|
right bleeds- Iron deficiency in man over 50 is CRC until proven otherwise
left obstructs (lumen is more narrow on the left) |
|
risk factors for CRC
|
1. age
2. villous adenomas 3. chronic IBD, esp ulcerative colitis 4. family hx 5. FAP (100% chance of developing CRC) 6. HNPCC (80% develop CRC) |
|
CRC screening
|
all people over 50 unless hereditary condition--then earlier
stool occult blood and colonoscopy |
|
FAP (familial adenomatous polyposis)
gene involved, presentation, and other cancers |
thousands of polyps throughout entire colon
always involved the rectum--carpeted (100% risk of developing CRC)-- do colectomy gene: APC at risk for duodenal and thyroid cancer (many die from duodenal ca if colon removed) |
|
Gardener's syndrome
|
FAP with osseous and soft tissue tumors, retinal hyperplasia
SODD sebaceous cyts osteomas dental caries desmoid tumors |
|
Turcott's syndrome
|
FAP with possible brain involvement (glioma, medulloblastoma)
TURcott = TURban |
|
HNPCC = Hereditary Non-Polyposus Colorectal Cancer = Lynch syndrome
presentation, gene, other cancers |
80% go onto develop CRC
proximal colon always involved gene= DNA mismatch repair genes other cancers: esop's gu ENDOMETRIAL, stomach, ovarian, pancreas, genitourinary |
|
Peutz Jegher Syndrome
inheritance pattern? presentation, other cancers at risk for? |
Autosomal Dominant
benign polyposis syndrome hyperpigmentation macules on oral mucosa, hands and feet (mucocutaneous lesions-abnormal freckling) other cancers- colon, breast, lung, pancreas, ovary, uterus, stomach Risk: intussusception |
|
Carcinoid tumor
|
tumor of endocrine cells
50% of small bowel tumors most common in small intestine often produce 5-HT which can lead to carcinoid syndrome-- right sided valvular disease, wheezing, flushing, diarrhea. carcinoid syndrome only happens if there are mets outside the GI tract (otherwise liver metabolizes excess 5-HT) met is often in liver |
|
Carcinoid syndrome
|
carcinoid tumor produces 5-HT--leading to...
flushing wheezing diarrhea right sided valvular disease |
|
small bowel adenocarcinoma
where does it usually occur? risk factors? presentation? |
usually in the duodenum
risk factors: IBD, HNPCC, FAP, celiac, Peutz Jegher, juvenille polyposis present: obstruction--> jaundice, blood loss |
|
cirrhosis
histology? presentation? |
histo: diffuse fibrous bands/septae and regenerative nodules
presentation: portal HTN--> esophageal varices (hematemesis), caput medusa (umbilical veins), internal hemorrhoids (painless) jaundice, sceral icterus, ascites, edema, asterexis (arms outstretched, hand's flap) hyperestrogen state- spider angiomata, gynecomastia, testicular atrophy |
|
Measurements of Liver Function (3)
|
1. albumin
2. bilirubin 3. prothrombin time (INR) - liver makes clotting factors |
|
TIPS
|
transjugular intrahepatic portosystemic shunt (relieves portal HTN but may exacerbate encephalopathy if present)
|
|
micronodular cirrhosis
|
nodules <3 mm uniform in size
due to metabolic insult: alcohol, hemachromatosis, wilson's dz |
|
macronodular cirrhosis
|
nodules > 3mm varied in size
usually due to significant liver injury leading to hepatic necrosis (post-infectious or drug induced hepatitis) inc risk for HCC |
|
LFTs: AST and ALT
when elevated? which is elevated more when? |
viral hepatitis (ALT > AST) more liver specific
alcoholic hepatitis (AST > ALT) ratio > 2:1 S= sauced Myocardial infarction (AST) |
|
Markers of cholestasis
what else could cause these elevations? |
Alkaline Phosphatase (ALP)- bone, bile duct dz, obstructive liver dz,
Gamma Glutamyl Transpeptidase- (GGT)- liver dz, heavy EtOH |
|
Markers of acute pancreatitis
|
Amylase- up in 2 hrs peaks quickly
Lipase- up in 4 hrs-- stays elevated longer, best marker |
|
Labs indicating Wilson's dz
|
low serum ceruloplasmin, high serum and urine copper
|
|
Reye's syndrome
presentation, cause, histo |
rare, often fatal childhood hepatoencephalopathy
present: hypoglycemia, coma histo: microvesicular steatosis (drug) cause: virus (esp VZV or influ B) treated with aspirin/salicylates |
|
hepatic steatosis
histo? |
short-term change with moderate alcohol intake
macrovesicular fat, reversible |
|
alcoholic hepatitis
histo? |
requires sustained, long term consumption of alcohol
Mallory bodies- intracytoplasmic eosinophilic inclusions), chickenwire fibrosis in zone 3 (near central vein) |
|
alcoholic cirrhosis
|
irreversible
micronodular, irregularly shrunken liver sclerosis around the central vein (EtOH in zone 3) (drugs and bugs in zone 1 around portal vein) |
|
Hepatocellular carcinoma (HCC)
risk factors? |
chronic Hep B or C
alcoholic cirrhosis NASH Wilson's hemochromatosis alpha-1-antritrypsin deficiency aflatoxin in peanuts! |
|
HCC findings
|
1. hypoglycemia
2. tender hepatomegaly 3. ascites 4. polycythemia (inc HCT--lost fluid from circ due to low albumin) |
|
What may be elevated in HCC?
|
50% of the time alpha-fetoprotein levels are elevated
|
|
Nutmeg liver
cause? |
blood backing up into liver caused by right sided heart failure or Budd-chiari syndrome
liver appears mottled like nutmeg-- if persists centilobular congestion and necrosis may occur |
|
Budd-Chiari syndrome
what is it? what is it associated with? |
clot in hepatic vein or IVC leading to centrilobular congestion and necrosis--congestive liver disease (ascites, hepatomegaly, portal HTN)
associations: pregnancy, polycythemia vera, HCC |
|
alpha1- antitrypsin deficiency
histo? |
misfolded protein accumulates in the liver (PAS positive globules) (protease inhibitor of neutrophil elastase)-- there is no inhibition of neutrophil elastase so lungs are destroyed-- emphysema
|
|
PAS positive globules seen in the liver
|
alpha-1-antitrypsin deficiency
|
|
Gilbert's syndrome
|
hereditary hyperbilirubinemia- 30% less less UGT1A1 to conjugate bilirubin. Asymptomatic--but may have jaundice and scleral icterus with stress, dehydration or fasting
|
|
Criggler-Najjar Syndrome Type I
|
absence of UDP glucoronyl transferase (UGT)-- cannot conjugate bilirubin. unconjugated hyperbilirubinemia.
Findings: jaundice, kernicterus (bilirubin deposition in the brain)- will die without liver transplant tx: plasmaphoresis and light therapy |
|
what can be given to increase liver synthesis of UGT1A1 ?
|
phenobarbital (good tx for Criggler Najjar type 2-- less severe than type 1- with 70% reduction in UGT1a1 levels.
|
|
what drug is metabolized by UGT1A1 and can have impaired metabolism with Gilbert or Criggler Najjar
|
Irinotecan- chemotherapy drug
|
|
Dubin Johnson syndrome
|
hereditary conjugated hyperbilirubinemia-- can conjugate bilirubin but not excrete it into bile ductules--leads to grossly black liver (pigmented) . benign
|
|
Rotor syndrome
|
similar to dubin-johnson syndrome- hereditary caonjugated hyperbilirubinemia-- milder and no liver pigmentation
|
|
Wilson's disease
aka? characterized by? tx? |
copper accumulation in brain, kidneys, liver, joints, cornea
characterized by ABCD: Asterexis Basal ganglia degeneration- movement disorder (parkinsonian) Cirrhosis, dec ceruloplasmin, corneal deposits (Kaiser-Fleysher rings), chorea, copper accumulation, Carcinoma (HCC) Dementia tx: penicillamine (copper chelation) |
|
hemochromatosis
gene? sx? |
accumulation of iron because of continuous absorption-defect in HFE gene
Sx: dilated cardiomyopathy-CHF deposition in pituitary-- melanin-bronze discoloration of skin, and dec gonadotropins-- testicular atrophy, gynecomastia deposition in the pancreas- diabetes increased risk for HCC tx: repeated phlebotomy |
|
causes of acute pancreatitis
|
IGET SMASHeD
Idiopathic Gallstones Ethanol Trauma Steroids Mumps Autoimmune dz Scorpion bite Hypercalcemia, hyperlipidemia, hypothermia e Drugs-steroids, sulfazalazine, a , NSAIDs, diuretics, DII (HIV drug) |
|
primary sclerosing cholangitis
ERCP? histo? lab findings? associations? |
inflammation and fibrosis of intra and extrahepatic bile ducts
ERCP: beading of bile ducts--alternating areas of strictures and dilatations histo: onion skinning- thick layers of collagen deposition around bile ducts lab: inc ALP and/or GGT assoc: ulcerative colitis in 80% |
|
Abdominal Zones, names and blood supply
1. foregut = 2. midgut = 3. hindgut = |
1. foregut= epigastrium- celiac artery- stomach--> ampulla of vater in D2
2. midgut = periumbilical- superior mesenteric artery- ampulla of vater--> proximal 2/3 of transverse colon 3. hindgut- hypogastrium/suprapubic- inferior mesenteric artery- distal 1/3 of transverse colon--> rectum above pectinate line |
|
pain derived by the autonomic nervous system that is midline and generalizes to a zone but it is not focal-- due to wall tension, dull cramping
|
visceral pain
|
|
pain at site of origin, sharp, severe, persistent, due to acute pH or temperature changes
somatic nervous system |
parietal pain
|
|
referred pain
left shoulder |
left diaphragm irritation-- spleen
esophagus heart |
|
referred pain
right shoulder |
right diaphragm irritation -liver, gallbladder, duodenum
|
|
referred pain, right subscapular
|
biliary tree
|
|
referred pain, flank
|
kidney, pancreas
|
|
referred pain, groin
|
ureters, bladder
|
|
retroperitoneal structures
|
SAD PUCKER
* S = Suprarenal glands (aka the adrenal glands) * A = Aorta/IVC * D = Duodenum (second and third segments [some also include the fourth segment] ) * P = Pancreas (tail is intraperitoneal) * U = Ureters * C = Colon (only the ascending and descending branches) * K = Kidneys * E = Esophagus * R = Rectum |
|
causes of upper GI bleeds
|
peptic ulcer eroding into vessels
(duodenal ulcer can erode into gastroduodenal artery--huge bleed) esophageal/gastric varices Mallory-Weiss tear- tear of mucosa at gastroesophageal junction (retching-alcohol) esophagitis |
|
causes of lower GI bleeding
|
1. colon cancer (occult bleeding)
2. internal hemarrhoids (painless) 3. external hemarrhoids (painful) 4. ulcerative colitis 5. diverticular bleeding- not associated with diverticulitis 6. infections- bloody diarrhea- shigella etc |
|
what is the largest lymphoid organ in the body?
|
GI tract (peyer's patches - ileum has more than jejunum)
|
|
name the layers of the GI tube
|
lumen--> epithelium--> lamina propria--> muscularis mucosa--> submucosa (messeners plexus)--> muscularis externa/propria circular--> myenteric plexus of Auerbach--> longitudinal--> serosa
|
|
what type of muscle is the upper 1/3 of the esophagus? the rest of the GI tract?
|
striated muscle
smooth muscle |
|
what part of the GI tract lacks serosa? what is a consequence of this?
|
esophagus- esophageal cancers (adenocarcinoma) can spread easily to other retroperitoneal structures
|
|
what is the pain purpose of crypts? villi?
small bowel has which? large bowel has which? |
crypts--> secretion
villi--> absorption small bowel has crypts and villi large bowel only has crypts-- goblet cells-secreting mucin |
|
Describe the innervation of the GI tract
|
SNS- inhibitory
PNS- excitatory ENS- enteric nervous system- main driver of GI tract- myenteric plexus of Auerbach--controls smooth muscle contractions |
|
Achalasia
sx? etiology? appearance on imaging? what disease can mimic this? |
sx: dysphagia
lack of inhibitory neurons of myenteric plexus of Auerbach at the lower esophageal sphincter-- LES cannot relax to allow for passage of food (sticks in chest) imaging- bird beak or rat's tail sign mimic: Chagas disease |
|
pacemaker cells of the GI track (located between circular and longitudinal muscle layers)-- receive innervation from myenteric plexus of Auerbach?
|
interstitial cells of Cajal
|
|
Basal Electrical Rhythm (BER)
relative rates of stomach and duodenum |
rhythmic wave of partial depolarization- uncoordinated/ slow waves of contraction within the GI tract
stomach (3/min) duodenum (12/min) |
|
peristalsis
|
coordinated contraction and relaxations of the smooth muscles of GI tract- pushing food along
-controlled by enteric nervous system |
|
oropharyngeal dysphagia
description? signs? causes? |
dysfunction in swallowing at the level of the pharynx, mouth-- usually under voluntary control-- epiglottis covering trachea, palate rising to protect nasopharynx
frequently see aspiration and repeated episodes of pneumonia signs: aspiration pneumonia, nasal regurg, drooling, facial droop etc causes: stroke, parkinson's, myasthenia gravis (autoimmune- blocking ACh receptors at motor end plate), ALS (degeneration of motor neurons) |
|
esophageal dysphagia
causes? |
dysfunction in the esophagus
causes: achalasia, strictures, rings/webs, esophagitis, connective tissue disease (i.e. scleroderma) |
|
gastroesophageal reflux disease
sx: possible causes? consequence? when is it worse and why? |
reflux of gastric contents into esophagus
SX: heartburn/retrosternal burning, dysphagia, worse at night cause: may have more relaxation of the LES than other people (pregnancy, progesterone), or may have more acidic stomach juices (caffeine/coffee), may eat things that induce relaxation of the LES (chocolate, mint, alcohol) 2. hiatal hernias-sliding of GE jxn consequence: 10% get Barrett's esophagus-- intestinal metaplasia (which can go onto to become esophageal adenocarcinoma in 10%) WORSE: at night when lying flat-- decreased peristalsis/gastric emptying, gravity, dec saliva production |
|
esophageal dysphagia: motility vs mechanical/structural, signs
|
motility- trouble with both liquids and solids (achalasia)
mechanical/structural (strictures etc)-- trouble with solids > liquids |
|
TX for GERD
|
1. H2 blockers (-dine) -
histamine is released by ECL cells of the stomach and stimulates parietal cell release of HCl 2. Proton Pump Inhibitors- i.e. omeprazole- must take before meal because proton pumps are only induced by presence of food 3. antacids- tums |
|
normal epithelium of the esophagus?
|
squamous cell epithelium
|
|
2 types of hiatal hernias
|
1. sliding hiatal hernia- GE jxn slides back and forth through diaphragm hiatus (20% of people have it- normally asx, but can get GERD)
2. paraesophageal hernia- cardia, part of stomach herniates through the diaphragmatic hiatus but the GE jxn remains below diaphragm |
|
what radiological test exposes patient to the most radiation and thus should be avoided in pregnant women?
|
CT
|
|
what do the gastric chief cells secrete?
|
pepsinogen and gastric lipase
|
|
What activates trypsinogen so that it can become trypsin and activate all other pancreatic enzymes?
|
enteropeptidase on the brush border of the duodenum
|
|
what is the most common benign liver lesion?
at risk for? tx? |
cavernous hemangioma
at risk for rupture: hemoperitoneum tx: none, do not biopsy |
|
focal nodular hyperplasia
related to? characteristic histo lesion? |
benign liver lesion
related to congenital malformation of portal vein branches that leads to increased hepatic artery flow-- arterial enhancement with quick venous washout histo: central fibrous scar |
|
what liver lesion are females on contraceptives at risk for?
why are these risky? functioning hepatocytes? histo characteristic? tx? |
adenoma (estrogen dependent)
risk: they can rupture--> hemoperitoneum (especially during pregnancy) hepatocytes are non-functional histo characteristic: naked/unaccompanied arteriole tx: stop birth control and resect tumor as it may transform into HCC |
|
common benign liver lesion that may be related to ADPKD
appearance on CT? tx? |
liver cysts
round fluid filled cysts tx: nothing |
|
what is the most common cause of hepatocellular carcinoma worldwide?
|
chronic hepatitis B infection (especially if maternally transmitted)
|
|
Risk factors for HCC?
|
cirrhosis (alcohol, chronic hep b or c)
hemochromatosis) |
|
presentation of HCC?
|
right upper quadrant pain, may refer to right shoulder, weight loss, decompensation of liver disease
|
|
malignancy symptoms?
|
fatigue, unintended weightloss, night sweats, low grade fever, anorexia ,diarrhea
|
|
What cancers are likely to metastasize to the liver?
|
Cancers Sometimes Penetrate Benign Livers
Colon > Stomach > Pancreas > Breast > Lung |
|
lactulose is used to treat? mechanism?
|
hepatic encephalopathy
mech: undigestable--causes diarrhea and traps nitrogen as NH4+ (must be excreted since it is charged and cannot be absorbed) |
|
rifaxamine
used to tx? |
travelers diarrhea and hepatic encephalopathy
mech: kills colonic bacteria that produce nitrogenous wastes |
|
mechanism of ascites?
|
loss of albumin
decreased ECV- revs up RAAS |
|
drugs to treat portal HTN
|
octreotide- blocks splanchnic vasodilation
non-specific Beta blockers- blocks vasodilation of the gut (propanolol, nadolol) |
|
side effect of ribavirin?
|
hemolytic anemia
|
|
what is the goal of HBV treatment?
|
decreased HBV DNA and HBV Surface Antigen
|
|
what is used to treat HBV?
|
pegylated interferon and lamuvidine (nucleoside analogue--reverse transcriptase inhibitor)
|
|
what is unique about HBV? (the type of virus it is)
|
DNA virus that uses an RNA intermediate to replicate (needs a reverse transcriptase)
|
|
what is the goal of HCV treatment?
|
eradication of the virus
|
|
markers of cholestasis?
|
ALP- alkaline phosphatase-- also elevated with bone resorption
GGT- gamma glutamyl transpeptidase |
|
manifestations of cholestasis?
|
jaundice, pruritis, steatorrhea, vitamin D, A, K, E deficiency
|
|
primary biliary cirrhosis
who is most often affected? lab test? |
affected: middle aged women
lab test: anti-mitochondrial antibodies |
|
primary sclerosing cholangitis
associated with? appearance on ERCP? |
associated with ulcerative colitis
ERCP: alternating strictures and dilations |
|
large gallstones are most likely to cause what?
|
cholecystitis
|
|
double duct sign is clue for?
|
pancreatic cancer in head of pancreas- obstructing pancreatic duct and common bile duct
|
|
what causes secondary biliary cirrhosis?
in kids? |
prolonged obstruction of extrahepatic ducts
kids-- biliary atresia |
|
what can you give reduce jaundice in person with Criggler-Najjar Type II? why?
|
phenobarbital-- induces UGT1A1-- conjugated bilirubin
|
|
Extraintestinal manifestations of Inflammatory Bowel Disease
|
CHEATS-
cholangitis (UC > CD) Hematologic- iron deficiency anemia- malabsorption (CD > UC) Eyes- uveitis-- A- artheritis + ankylosing spondylitis T Skin- erythema nodosum (CD) and pyoderma gangrenosum (UC) |
|
hartnup disease
|
decreased absorption of tryptophan- decreased hepaticc synthesis of niacin (vit B3) from tryptophan--> pellagra
|
|
mechanism of methotrexate?
|
inhibits DNA synthesis by disrupting folate metabolism- must give folate supplement
|
|
what is the hallmark histologic feature of primary sclerosing cholangitis?
|
onion-skinning-- fibrosis around the bile ducts- but still have nice cuboidal epithelium
|
|
patients with PSC are at increased risk for?
|
cholangiocarcinoma and Colorectal carcinoma
|
|
histology of primary biliary cirrhosis?
|
squished bile ducts with abnormal epithelium and vague granulomas (inflammatory infiltrates)
|
|
what is the best test for cholelithiasis?
|
ultrasound
|
|
pseudocyst
|
pancreatic cyst filled with pancreatic juices after acute pancreatitis- no epithelial lining
|
|
murphy's sign
|
have pt breathe in- palpate liver- if they have cholecystitis they will stop breathing in when the liver edge hits your hand because it hurts so bad
|
|
If a stone is lodged in the cystic duct, will you see jaundice?
|
No- the stone is not blocking passage of bile from the liver so bilirubin is still being excrete in the bile
|
|
gallstone ileus
|
gallstone erodes through the gallbladder into the duodenum and causes obstruction- usually at the ileocecal valve
|
|
ascending cholangitis
|
stone in the common bile duct causes infection
|
|
what size stones are most likely to cause acute pancreatitis?
|
small stones because they are able to make their way through the cystic duct into the common bile duct and obstruct outflow of pancreatic enzymes/juices
|
|
risk factors for gallstones?
|
four F's
Fat Female Forty Fertile |
|
2 types of gallstones? which is most common?
|
cholesterol and pigmented
most common = cholesterol overall most common is mixed |
|
what are pigmented stones made out of?
two types of pigmented gallstones? where are each formed? what are they associated with? |
calcium and unconjugated bilirubin
black pigmented- formed in gall bladder- hemolysis brown stone- formed outside of the gall bladder due to infection |
|
what does bacteria do to bilirubin
|
unconjugates it
|
|
courvosier's sign
|
palpable gall bladder with painless jaundice-- usually do pancreatic malignancy obstructing the common bile duct
|
|
porcelain gallbladder
what is it? what does it increase risk for? |
calcification of the gallbladder that increases risk of developing gallbladder adenocarcinoma
|
|
kernicterus
|
unconjugated bilirubin is fat soluble and can cross the BBB leading to mental status changes
|
|
risk factors for cholangiocarcinoma
|
blockage, primary sclerosing cholangitis, chronic infection
|
|
klatskin tumor
|
cholangiocarcinoma arising from the confluence of the hepatic ducts- will not see gallbladder dilation since it is upstream from gallbladder
|
|
what is the difference between small bowel and colonic mesenteric ischemia?
|
small bowel- usually from embolus in the background of atherosclerotic disease-- develops suddenly, pain with eating (intestinal angina), occult bleeding (obvious bleeding is late- bad sign- necrosis), periumbilical pain, do angiography
colonic ischemia- usually in older people, atherosclerosis or unknown mechanism, obvious blood in stool, non-painful or suprapubic pain, often in watershed regions, do colonoscopy to look for source |
|
where do emboli get lodged in mesenteric ischemia?
|
distal superior mesenteric artery (angle and diameter)
|
|
how do drugs cause ischemic colitis? what drugs do this?
|
vasospasm
drugs: triptans (for migraines), cocaine (blocks reuptake of NE), pseudoephedrine (a 1 agonist), birth control |
|
Describe HCO3- secretion from the ductular cells of the pancreas.
what stimulates it? What drives it? |
Cl- is pumped out through CFTR and this creates gradient for it to be pumped back in in exchange for HCO3-
|
|
Describe cystic fibrosis in the context of the GI tract/pancreas etc.
|
CFTR channels are defective so Cl- cannot be pumped out into the lumen creating a gradient for an antiporter whereby Cl- is reabsorbed and HCO3- is pumped out with water and Na+ following. There is plugging of the pancreatic ducts leading to pancreatic insufficiency-- acinar cells are working but enzymes are not making it into the duodenum.
|
|
what stimulates release of secretin?
where is it released from? |
gastric acid stimulates release
released from S cells of duodenum |
|
how long is the small bowel?
how long is the large bowel? |
small bowel: 20 ft- 6m
large bowel: 5 ft- 1.5 m |
|
What are paneth cells? where are they located?
|
cells with eosinophilic granules contain lysosyme- contribute to host defense
|
|
describe the vascular supply of the rectum. why is this relevant for cancer mets?
|
the upper rectum is supplied by the IMA and drained by the IMV so mets from this part of the rectum will go to the liver through portal circulation.
the lower rectum is supplied by the inferior rectal artery off of the internal iliac artery and drained by iliac vein into the IVC so mets will go through heart to lungs |
|
What is the major stimulatory neurotransmitter of the GI tract?
inhibitory neurotransmitters? |
stimulate: ACh (contraction)
inhibit: Vasoactive Intestinal Peptide, NO (relaxation) |
|
what is contracted and what is relaxed during flatulence?
pooping? |
flatulence: internal and external anal sphincters relax, puberectalis contracts
pooping: internal, external anal sphincters and puborectalis muscle all relax |
|
what are essential fatty acids?
|
must be obtained from diet- linolenic and linoleic acid
|
|
what are micelles necessary for?
what is required to make micelles? |
digestion of cholesterol, fat soluble vitamins (D, A, K, E) and some LCFA
required: bile salts |
|
what creates greater fat malabsorption and subsequent steatorrhea, lack of pancreatic lipase? lack of bile salts?
|
lack of pancreatic lipase-- only can digest 30% of fats
with no bile salts-- can still digest 60% of fats |
|
discuss the differences in fat absorption for SCFA and MCFA vs LCFA, cholesterol and fat soluble vitamins
|
SCFA and MFCA- portal venous sx
others: emulsion droplet--> micelles--> absorption-->re-esterification--> packaging with apoproteins to make chylomicrons--> lymphatics--> venous circ via thoracic duct into subclavian |
|
what electrolytes are involved in absorption?
secretion? |
absorption: water follows Na+ IN
secretion: water follows Cl- out |
|
how does cholera toxin work?
|
stimulates Cl- secretion from CFTR, water follows--> secretory diarrhea
|
|
what is the normal osmolality of stool?
|
290mOsm/kg water
|
|
how do you calculate the stool osmotic gap?
if gap is high what does this mean? |
290 - (Na+ + K+) x 2
high gap (>50)-- there are ions that are unaccounted for (like lactose, polyethylene glycol, sorbitol) causing water to be drawn into lumen |
|
what kind of diarrhea do bile acids cause?
|
secretory- they are an irritant-- do not draw water in (not an ion)
|
|
which requires further digestion in cells: proteins or monosaccharides?
|
proteins
|
|
what breaks down disaccharides?
|
brush border enzymes- isomaltase (can break 1,6 glycosidic bond, which amylase cannot),
lactase, etc |
|
hydrogen breath test
|
test for lactose intolerance-- if cannot digest lactose it gets to the colon and the bacteria ferment it producing H+ and CO2 gas
|
|
which enzyme is not affected by celiac sprue/blunting of brush border?
|
amylase-- secreted in its active form- does not need to be activated by trypsin which requires enteropeptidase
|
|
risk factors for esophageal cancers
|
Achalasia
Barrett's Cigarettes Diverticula (Zenker's) Esophagitis, Esophageal webs (Plummer Vinson Syndrome) Familial |
|
bethanecol
|
ACh analogue- prokinetic
resists breakdown by AChesterase SE: cholinergic: SLUDGE |
|
metochlopramide
|
anti-emetic and prokinetic
dopamine receptor antagonist and ACh agonist SE: extrapyramidal tardive dyskinesia, dystonia |
|
prochloperazine, chlorpromazine
|
dopamine antagonists
|
|
what kind of receptors are located in the Chemoreceptor trigger zone of the area postrema? what is significant about this area?
|
histamine, dopamine, serotonin, opiod
this area is responsible for vomitting in response to toxins in the blood-- lacks BBB |
|
ondansetron
|
anti-emetic
serotonin antagonist good for chemo, pregnancy and post op |
|
benadryl, diphenhidramine
|
anti-histamine (H1)- anti-emetic good for motion sickness
SE: anti-cholinergic- mad, red, blind, dry |
|
scopolamine
|
muscarinic antagonist-- use to treat SLUDGE and good for motion sickness
|
|
glucagon
|
inhibits smooth muscle contraction- used to relax GI tract before endo
|
|
erosions vs ulcers
|
erosions are more shallow
ulcers penetrate the muscularis mucosa |
|
protective factors for the stomach
|
mucous, HCO3-, prostaglandins, blood flow, cell turnover
|
|
damaging factors to the stomach
|
smoking, NSAIDS, alcohol, H. pylori, acid
|
|
misoprostol
SE: |
prostoglandin analogue used to induce mucous cells to produce mucus, bicarb and phospholipid--protection against ulcers
ALSO decreases acid production SE: induces uterine contractions and closes PDA- do not give to pregnant women |
|
sucralfate
|
bind to ulcer surface--> physical protection
use: traveler's diarrhea, ulcers |
|
bismuth
|
bind to ulcer surface-- physical protection against stomach acid
use: traveler's diarrhea, gastric ulcers |
|
triple therapy for H. Pylori infection
|
Please MAke Tummy Better
PPI, Metronidazole, amoxicillin or tetracycline, Bismuth |
|
H. pylori
gram, motility, associated conditions? where does it take up residence>? what does it produce? how can it be tested? |
gram negative, spiral shaped, flagella (crawls under mucous layer of stomach)
can cause chronic gastritis, increased risk of gastric cancer, gastric and duodenal ulcers prevalence is 50% reside: in stomach- can only survive on gastric mucosa produces urease: breaks down urea to ammonia-- base that is protective against stomach acid test: urease breath test- radiolabeled urea is given, if bacteria present they break it down to ammonia and CO2 which is exhaled (labeled), also stool Ag, serology |
|
H. pylori can affect antrum or body of stomach- how does it differ in terms of acid production?
|
antrum- destroys D cells that make somatostatin-- less inhibition of gastrin and parietal cells- more acid
body- destroys parietal cells- less acid |
|
risk factors for gastric adenocarcinoma
where does it occur? |
nitrosamines, nitrates (smoked foods), achlorhydria, H. pylori
antrum of the stomach (usually from intestinal metaplasia) |
|
B cell lymphoma or T Cell lymphoma- which is related to celiacs, which to H pylori
|
b cell MALT- h pylori
t cell MALT- celiac |
|
high gastrin levels, but low gastric acid
(may be seen with hashimoto's thyroiditis etc) |
autoimmune gastritis
|
|
acute necrotizing colitis of premature, low birth weight babies-- affects the terminal ileum and ascending colon
|
necrotizing entercolitis
|
|
GI ulcer related to head trauma
|
Cushing's ulcer (need to cushion the brain)
|
|
GI ulcer related to burns
|
curling's ulcer (curling irons burn you)
|
|
Boerhaave's syndrome
|
complete esophageal rupture
|
|
differential for microcytic anemia
|
TAILS: thalassemia
Anemia of Chronic Disease Iron Deficiency Lead poisoning Sideoblastic anemia- cannot incorporate iron into Hb |
|
Antacids
Calcium, Mg, Al mech? SE? |
increases pH, binds pepsin,
Ca- kidney stones, rebound high acidity Mg- diarrhea- Must go to bathroom Aluminum- a minimum amount of poop |
|
H2 blockers
|
-tidine
cimetidine etc |
|
PPIs
|
-prazoles
must be taken before meals because the K+/H+ ATPase pump is only present when parietal cells are stimulated |
|
test for carbohydrate malabsorption
|
fecal pH- if carbs are not absorbed they are fermented by colonic bacteria producing acid- lower pH
hydrogen breath test- radiolabeled - fermentation- gets into blood-breathed out |
|
if you find alpha-1-antitrypsin in the stool, what other protein may be there too?
|
albumin
|
|
fetal duodenal atresia can cause what during pregnancy? after birth?
|
during pregnancy- polyhydramnios- fetus cannot swallow amniotic fluid so it spits it out- increased levels of fluid
after birth- repeated vomitting |
|
gastric inhibitory peptide.
released from? function? |
K cells of the duodedum
delays gastric emptying by closing the pyloric sphincter, decreases release of gastrin |
|
tropical sprue
where found? what deficiency associated? tx? |
where: SE Asia
deficiency: vitamin b12 and folate tx: tetracycline |
|
causes of macrocytic anemia
|
vitamin B12, folate deficiency, lack of intrinsic factor
|
|
how do intestinal bacteria relate to
vitamin K, folate, vitamin B12, and bile salts? |
bacteria synthesize vitamin K and folate- decreased PT with bacterial overgrowth
digest vitamin B12 and deconjugate bile salts |
|
whipples disease
presentation? histology? |
males (8:1), arthralgia, weight loss, diarrhea, abdominal pain, lymphadenopathy
histo: PAS positive macrophages(containing bacteria) in lamina propria |
|
what gene is associated with spontaneous CRC?
|
APC gene
|
|
difference between adenoma and adenocarcinoma
|
adenocarcinoma- invasion into or beyond muscularis mucosa
|
|
what determines prognosis of stomach cancer?
|
depth of invasion
|
|
What is FAP? inheritance pattern?
what gene is associated? what is risk of CRC? What other cancers are associated? |
Familial Adenomatous Polyposis
Autosomal Dominant APC gene 100% risk of CRC duodenal, thyroid |
|
What are FAP variants?
|
Gardner's syndrome- FAP with
Sebaceous cysts Osteomas Dentition abnormalities Desmoid tumors Turcott- Turban-- FAP with brain cancers/CNS tumors |
|
hyperplastic colon polyps
incidence, tx, histo? |
most common benign polyps in the colon
incidence: 50% of people over 60 have them tx: must remove for potential malignant transformation histo: star shaped pattern |
|
HNPCC most commonly presents in which part of the colon?
|
R> L
|
|
cowden's syndrome
inheritance pattern? where on body? other cancers? |
autosomal dominant
hamartomas on skin (may appear like acne) and in GI tract other cancers: thyroid and breast |
|
diverticulosis complications
|
diverticulitis- inflammation/blockage
diverticular bleeding (not associated with diverticulitis) |
|
complications of diverticulitis
|
abscess, fistula, obstruction, perforation
always operate when pt can |
|
treatment for acute diverticulitis- then later?
|
bowel rest then high fiber diet
|
|
what can be given for pain related to pancreatitis?
|
uncoated pancreatic enzymes + acid suppression- active in the duodenum and break down CCK-RP--not as much CCK stimulus of exocrine pancreas
|
|
what can be given for malabsorption related to pancreatitis?
|
pancreatic enzymes either uncoated or coated
|
|
treatment of acute pancreatitis
|
fluids, fluids, fluids for third spacing
octreotide |
|
chronic vs acute colitis
edema, crypts, metaplasia? |
acute- edema, straight crypts, no metaplasia, PMNs in lamina propria
chronic colitis- no edema, distorted crypts, metaplasia, lymphocytes in crypts |
|
microscopic colitis
colonoscopy? presentation? types? distinguishing features? associations |
scope: appears normal
presentation: watery diarrhea types: lymphocytic (intraepithelial lymphocytes), collagenous (mallory trichome stain, subepithelial collagen band) associations: NSAIDs, PPIs, SSRI |
|
acute systemic complications of pancreatitis
|
ARDS/SIRS
shock renal failure DIC |
|
most common cause of acute and chronic pancreatitis?
|
alcohol
|
|
how might chronic alcoholism lead to pancreatitis?
|
concretions develop in ducts that lead to partial obstruction
|
|
new onset diabetes in someone > 50
palpable gallbladder and painless jaundice |
pancreatic cancer
|
|
tumor marker elevated in pancreatic cancer
|
CA19-9
|
|
treatment of diverticulitis
|
2 ABx: metronidazole and ciprofloxacin
bowel rest in short term |