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food-drug interactions
warfarin can interact with proteins/high k value in formula
monitor inr and consider dose adjustment
phenytoin absorption reduces greatly
hold feeds +- 2 hours
fluoroquinolones can bind to divalent cations in formula
hold feeds +- 2 hours
fluoroquinolones get absorbed in duodenum
admin iv, dont give through tube in pts that terminate in jejunum
macro and micronutrients composition of total enteral nutrition
macronutrients
dextrose 3.4 kcal/g
amino acids 4 kcal/g
lipids
emulsion 10 kcal/g
dietary 9 kcal/g
micronutrients
electrolytes
vitamins
trace minerals
diagnostic for gerd
if there are any alarm sx or age >60, go straight to endoscopy
we are concerned about more malignant underlying causes
if no alarm sx or age <60, can start with an h.pylori test
→ treatment! be my tummy protector, or ppi trial if no improvement
→ ppi trial
typical gerd sx
heartburn, dysphagia
try qd ppi trial for 8 weeks
extra-esophageal sx
hoarseness, chronic cough, asthma
try bid ppi trial for 12 weeks
atypical sx
chest pain, dyspepsia, nausea, bloating, belching
just scope em
mild, infrequent gerd tx
antacids, h2ras
mild-moderate gerd tx
otc ppi for two weeks
severe gerd or erosive esophagitis
rx ppi for 8 weeks
nsaid induced pud
treat duo ulcers for 4 weeks, gastric for 8
can do with ppi, h2ra, or sucralfate
h pylori testing
invasive aka endoscopic tests
can get biopsy sample to do histology, culture, etc
non invasive aka non endoscopic
ab testing → does not tell you if the infection is active or in the past
urea breath test
fecal antigen test
dyspepsia alarm symptoms
dysphagia
odynophagia
upper gi bleed → blood in vomit or stool
unexplained weight loss
when to refer to pcp for gerd
after two weeks
otc ppis
omeprazole, esomeprazole, lansoprazole
rx ppis
pantoprazole, rabeprazole, dexlansoprazole
portal triad
proper hepatic artery
hepatic portal vein
splenic vein
sup mes
inf mes
common bile duct
sketch path of biliary tree
cystic duct brings bile from gallbladder
the l/r hepatic ducts drain bile from the liver
form the common hepatic duct
common hepatic duct and cystic duct join to form common bile duct
when the main pancreatic duct joins it, forms hepatopancreatic ampulla
contains pancreatic juices and bile
terminates into major duodenal papilla
gallstone in cystic duct
still able to secrete bile
no jaundice
gallstone in common bile duct
block all sources of bile and most likely cause jaundice
gallstone in hepatopancreatic ampulla
pancreatitis plus blockage of bile and jaundice
phases of acid secretion
basal
cephalic
gastric
food in stomach is sensed by mechanoreceptors → activate vagus
protein broken down into aa’s by pepsin are sensed by gastrin cells that sample lumen
releases gastrin
intestine
pancreatic exocrine secretions
carbs broken down by alpha-amylase
fats broken down by lipases
proteins broken down by proteases, like pepsin
nucleic acids broken down by nucleases
macronutrient maldigestion
can lead to fatty diarrhea
get those orange rings due to water insoluble vitamins like vitamin a
pancreatic exocrine insufficiency → not enough enzymes for digestion of smth
bile salt deficiency
inactivation of pancreatic lipases
inherited enzyme deficiency
macronutrient malabsorption
small bowel mucosal disease
structural abnormality → eg damage to villi preventing absorption
rapid transit → moves through the gi tract too fast to get reabsorbed
general liver function
synthetic function
clearance and protection
storage of vitamins and iron
exocrine function
metabolic function
hepatocellular injury abs
lfts → enzymes leaking from cells
cholestatic liver injury
interruption of normal bile secretion or drainage
can be a mechanical obstruction like a gallstone or tumor
look for increase alkaline phosphatase, bilirubin (gets excreted into bile)
synthetic capacity labs
PT/INR, probs best markers of liver function
albumin
acute liver injury
coagulopathy → increased risk of bleed, bruising, increased INR and PT
production of vit k dependent coag factors decreases
encephalopathy
cant process blood and remove toxins like ammonia
no pre-exiting liver dx
portal htn
loss of sinusoidal caps due to fibrosis
they try to defend themselves via endothelina but that increases R and engorges the vessels
pressure gradient greatly increases and prevents blood flow through liver
hepato-renal syndrome
kidney injury secondary to liver disease
drop in ecv due to vasodilation causese drop in blood flow to other organs such as kidneys to protect liver and brain
renal artery vasocontriction
spontaneous bacterial peritonitis
infection in peritoneal space in pts with ascites
watch for wbc count
hrs-aki
an aki in the context of advanced liver dx
increase in scr >0.3 mg/dl over 48 hr or increase more than 50% over 1 week
gotta meet a shit ton of criteria, like a diagnosis of exclusion
cirrhosis with ascites
aki diagnosis
no improvement in scr with volume challenge, gotta make sure the pts not hypovolemic
lack of shock
no nephrotoxin
no structural kidney dx
glp-1 agonists
slows gastric emptying and decreases food intake to increase satiety
Semaglutide
12.4% tbwl reater than placebo at one year
Liraglutide
5.6% tbwl greater than placebo at one year
Tirzepatide
17.8% tbwl reater than placebo at 72 weeks
Sympathomimetics
stimulate anorexic signaling and suppress appetite
Phentermine
short term use 3 months only
4.4% tbwl greater than placebo
Phentermine/Topiramate
topiramate suppresses appetite and enhances satiety
8.6-9.4% tbwl greater than placebo at one year
Buproprion/Naltrexone
dopa/ne reuptake inhibitor and opioid antagonist
regulates appetite and reward system
4.22-5.2% tbwl greater than placebo at one year
Orlistat
reduces absorption of dietary fat by inhibiting lipases
take before fat containing meals
4% tbwl greater than placebo at one year
post-bariatric surgery
monitor more often
try liquid over solid
crushable ir crushes er
consider non-po routes if possible
vitamin a
teratogenic at high doses
decreases bone mineral density
vitamin e
increased mortality from hemorrhagic stroke