How is Metabolic Syndrome defined and how does it relate to Diabetes Mellitus Type II?
Met Synd: obesity, HTN, hyperglycemia, hyperlipidemia, hypocholesteremia; Inc. risk of insulin resistance, lipotoxicity--> DM-II
Describe the pathogenesis of H. pylori infection.
ingestion--> antrum(no invasion)--> urease VF-->inflammation--> mucosal damage--> acute gastritis
Explain how motor and sensory abnormalities can provoke symptoms of IBS.
Visceral hypersensitivity (distention); Visceral mesenteric nerves respond to distention and serotonin&bradykinin; histamine activates pain fibers
Compare and contrast Metformin and liraglutide (MOA)
Metformin: activates AMP-activated protein kinase--> decreased gluconeogenesis/insulin sensitivity; Liraglutide (GLP-1 receptor agonist) --> insulin release
Describe the relationship between gut flora and IBS, including how it relates to use of probiotics.
Dysbiosis (high ratio Firmicutes :Bacteroidetes, few Lactobacilli &Bifidobacteria-> activation gut immune system-->inflammation; attempt to restore symbiosis
Describe how the effects of NSAIDs, alcohol, cigarette smoke, and stress lead to the development of gastritis.
Decrease mucosal lining in stomach--> cells exposed to acid--> cell damage--> inflammation
What are the most common causative agents of traveler's diarrhea?
Enterotoxigenic Escherichia coli (ETEC), Campylobacter jejuni, Shigella spp., Salmonella spp., other E. coli strains
Differentiate between acute pancreatitis, chronic pancreatitis, and exocrine pancreatic insufficiency (EPI).
Pancreatitis: auto-digestion; Acute: enzymes prematurely activated/ Chronic: persistent inflammation; EPI: not making pancreatic enzymes (treat w/ pancrelipase)
Compare normal movement of ions and nutrients across intestinal epithelium to that of secretory diarrhea.
Water is absorbed on osmotic gradient; water follows solute. Secretory diarrhea: solute (such as Cl-) secreted into lumen--> water follows--> diarrhea
Describe the role of the lower esophageal sphincter and list factors that affect its functioning.
control entry of bolus--> stomach & prevent gastric contents from entering esophagus; RF: truncal obesity, nicotine,
Explain the pathophysiological effects of Enterotoxigenic Escherichia coli (ETEC) AB toxins in the stomach and intestinal tract.
increases cAMP--> upregulate CFTR and NKCCI cotransporter crypt cells--> secrete Cl- into lumen--> H2O and Na follow--> watery diarrhea
What are the signs, symptoms, and risk factors for acute pancreatitis?
N/V, tachycardia, fever, abdominal pain worse after eating, upper abdominal pain (radiates to back), ecchymosis; RF: alcohol, smoking, obesity, FHx
List recommended lifestyle approaches for people with IBS.
incr. fluids, fiber, exercise; avoid FODMAPs, alcohol, coffee, spicy & fatty food; manage stress; regular meal pattern; squatting for defecation
What is the relationship between insulin resistance, leptin, ghrelin, and incretins (GLP-1, GIP)?
Leptin inhibits insulin/insulin stimulates leptin; Ghrelin stim. appetite & gastric emptying; Incretins stim. insulin; insulin resistance= ++ insulin & ++hunger
What are some alarm (red flag) symptoms for esophagogastroduodenoscopy?
Dyspepsia: weight loss, iron-deficiency anemia, GI bleeding, persistent vomiting, dysphagia, epigastric mass
Characterize H. pylori (structure, physiology, mode of transmission).
Gram-, urease+, flagellum, oxidase+, curved helico rod, ingestion--> gastric antrum
Compare/contrast normal pancreatic enzyme function to pancreatitis.
trypsin --> activates zymogens prematurely (in pancreas instead of in stomach)--> autodigestion of the pancreas-> high amylase + lipase=pancreatitis
What are potential long-term risks of prolonged gastric acid suppression?
increased risk of acid-labile bacterial infection; pepsinogen can't convert to pepsin--> poor digestion
What is the MOA, indications, and an example of a proton-pump inhibitor?
irreversibly block H+/K+ ATPase enzyme--> prevents movement of H+ ions; Indication: ++gastric acid; Omeprazole
Describe the MOA of loperamide and bismuth compounds.
Loperamide: binds peripheral mu in enteric NS--> slow colonic transit (no BBB); Bismuth: salicylate inhibits intestinal prostaglandin and Cl- secretion
Describe the major motor patterns that occur in the small intestines and colon during FED and FASTED conditions.
Fed: motility mix contents to absorb nutrients; isolated contraction->segmentation->peristalsis; Fasted: MMC, I-quiescence II-contractions III-rapid propulsions
Explain the role of alcohol in pancreatitis.
Primary acinar cell injury = Increased calcium flux ---> activation of trypsinogen by trypsin and generation of free radicals --> Acinar injury
Relate positive behavioral modifications to their affect on the LES and GERD.
Weightloss (decreased pressure), avoid cigarettes (they relax LES), avoid alcohol (reduces LES tone), stay upright after meals/don't eat late
Which hormones play important roles in maintenance of normoglycemia in FED and FASTING states?
Fed state-insulin= promoting glucose uptake by its target organs; Fasting-glucagon= mobilizes hepatic glucose