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UNIT 5 SIGS cases 1-3
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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
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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
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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
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Compare and contrast Metformin and liraglutide (MOA)
Metformin: activates AMP-activated protein kinase--> decreased gluconeogenesis/insulin sensitivity; Liraglutide (GLP-1 receptor agonist) --> insulin release
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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
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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)
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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
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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
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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
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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
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Describe the pathogenesis of H. pylori infection.
ingestion--> antrum(no invasion)--> urease VF-->inflammation--> mucosal damage--> acute gastritis
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Characterize H. pylori (structure, physiology, mode of transmission).
Gram-, urease+, flagellum, oxidase+, curved helico rod, ingestion--> gastric antrum
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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
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What are some alarm (red flag) symptoms for esophagogastroduodenoscopy?
Dyspepsia: weight loss, iron-deficiency anemia, GI bleeding, persistent vomiting, dysphagia, epigastric mass
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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
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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,
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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
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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
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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
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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
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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
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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
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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
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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
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