diet/nutrition Flashcards by Lux Smith

diet for CHF

2g Na
low fat
fluid restriction

avoid ETOH soups and sodas

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diet for COPD

high calorie
MVI w/mineral
low carb
hight fat

avoid: carbs

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dysplipdemia

avoid

Fat
cholesterol
Na

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hypertriglycerdiema

increase intake of omega-3FFA
weight reduction
limit carbs

avoid :
Fat
cholesterol
Na

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afibb diet

consistent K

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renal disease

reduce protein

if on dialyses increase protein

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ECL

enterochrommafin cells

respond to gastrin and make histamine

they are down regulated by somatistatin

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inhibition in the cephalic phase

loss of appetite via depression or stress causes lack of stimulatory input from the PSNS
from the cerebral cortex

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inhibitory effects that occur in the gastric phase

excessive acidity of less than 2 inhibits g cells

also emotional upset will trigger SNS and overide PSNS controls

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what are the inhibitory effects that can occur in the intestinal phase

Distention of the DUODENUM

and distention under the presence of fatty and acidic food

enterogastric reflex is about slowing it down what’s going on in the stomach so the SI can absorb stuff

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two things that stimulate gastric phase

stomach distension and food chemicals (peptides and caffeine) and rising pH

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intestinal hormones that inhibit intestinal phase

secretin

gastric inhibitory peptide

CCK- stimulates pancreas

vasoactive intestinal peptide

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protein stimulates

peptidase

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excessive distention and acidity

will activate entero gastric reflex which will inhibit the stomach and slow stuff down

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redness swelling and irritation in the lining of the stomach are known as

GASTRITIS

loss of mucous layer
PG
failure to turnover epithelial cells
imbalance in these protective factors

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pharmodynamics of NSAIDs as they relate to the AC

carboxcylic acid
not ionized

can become ionized and trapped within epithelial cells causing damage

systemic effects through PG are major thing though

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what layer of the stomach involves PG production through what intermediate

gastric and duodenal mucosa convert PGH2 from precursor arachidonic acid into PG and throboxane

PGE2 protects the stomach through reduced acid and increased bicarb

inhibition of this pathway

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gastritis on steroids

pud

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Describe PUD

break in the mucosal linging of the esophagus stomach or duodenum

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ulcers are defined as

breaks in the mucosal surface >5mm with depth to the submucosa

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what accounts for the majority of FU

H pylori and NSAIDS

pylori stimulates gastrin release and leads to mucosal damage and increased gastric emptying

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RF for PUD

H pylori 
advanced age
smoking
ETOH
NSAID
severe illness or trauma

most impair healing

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h pylori pathyphys with PUD

pancreas can’t make enough bicarb to keep up

urease hydrolyzes urea and forms ammonia which buffers acids

flagells and mucolytic enzymes help facilitate movement

and further break down

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CM of PUD

dyspepsia 80-90% but need more than that
(less than 25% have PUD with this symptom)

nausea and vomitingf
PE may show mild localized epigastric pain to deep palpation

hunger like pain
dull and achy

1/2 get relief with antacids or eating but depends on the pt

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PUD PE

localized epigastric pain to deep palpation fecal occult blood is positive in 1/3 pts with PUD

PUD dx and treatment

usually make a clinical diagnoses based on sxs look at use of pain medication look at alcohol use put on PPI and don't go any further don't send for an endoscopy

MCC of esophageal cancer

squamous cell found in upper 1/3 peaks in 50-70's

risk factors for SCC

``` etobacco ETOH hot beverages AA men ``` decreased incidence with coffee and NSAIDS

adenocarcinoma is seen in

younger patients obese caucasions M/c in lower 1/3 usually a complication of GERD and comes from barrett's esophagus

CM of esophageal neoplasm

dysphagia to solid food increasing to fluids weight loss chest pain hypercalcemia in pts with SCC (due to PTH)

PPI warning because

old people -alzheimers | cardiac events

when to use H2 for peptic ulcers

allergies

what to do with a positive h pylori?

if you have a positive test you should probably do something about it

gastrin secreting tumor

zollinger ellison syndrome

zollinger ellison syndrome | where do we see it

MC in duodenal wall second most common in pancrease few found in lymph nodes greater than 66% malignancy

gastrIn in stimulated by

food gastric distention vagal stimualtion elevated pH

Gastrin is inhibited by

somatostatin (D cells) acid pH but not in sollinger ellison syndrome

tx for zollinger ellis

usually you treat for PUD if they keep getting reoccurring ulcer symptoms go looking

dx for zollinger

fasting gastrin test can measure gastrin with IV secretin imaging for tumor could have occult blood and anemia

definition of diarrhea

increase in frequency fluidity and volume 3 or more daily can make a diagnosis if more than their norm normal range 3 a week to 3 a day

three major mechanisms of diarrhea

osmotic secretory motility

causes of diarrhea

infection- MC (viruses like norovirus) toxic dietary

osmotic diarrhea

introduction of nonabsorbable substance in the intestine that draws out excess water

casues of osmotic diarrhea

lactose intolerance pancreatic enzymes deficiencies because they make the meal absorbable mannitol (non-absorbable sugar)

bacteria is the cause of what proportion of diarrhea

<10%

inflammatory diarrhea mostly caused by

e coli | fecal oral

inflammatory diarrhea is characterized by

blood and pus in the stool maybe a fever blood because breakdown of mucosa

diarrhea without inflammatory process

secretory seen as excessive mucosal secretion of fluid and electrolytes can still be infectious

causes of secretory diarrhea

bacterial endotoxin from e coli (incapulsated so no inflammation, just dumping) neoplasms pancreatic insufficiency

small volume diarrhea

overflow diarrhea | little bit squeezing past hard stool

cholerae physiology

chlorae attached to the lining of the colon (requiring appropriate proteins) exotoxin causes hypersecretion of water and chloride ions leading to severe dehydration

cholerae comes from

contaminated food and water

motility diarrhea

not what's in it it's the function that is disturbed

diarrhea that causes fistula formation

motility

systemic effects of prolonged diarrhea

fever and bloody stools can caused IBD steatorrhea is a common sign of malabsorption

what are the risks of bleeding for diverticulitis

age greater than 60 HTN atherosclerosis regular NSAID use most of the time bleeding stops with

what are macronutrients

provide energy lipids proteins carbs

what are micronutrients

DO NOT provide energy minerals and vitamins

simple carbs consist of

maltose sucrose lactose

complex carbs consist of

starches cellulous glycogen

diets for dyslipidemia

avoid trans fat limit saturated fat focus on mono and poly fats (liqud at room)

kidney disease diet

low sodium phosphorus restriction (dairy) fluid restriction - no DARK sodas reduce protein low potassium don't want hyperkalemia and death also want to reduce magnesium

CHF diet

promote high K foods on diuretics control with A afibb low sodium fluid restriction limit alcohol low fat DASH

cirrhosis diet

``` protein control fluid restriction low sodium avoid alcohol small frequent calorically dense ```

what disease would you NEVER want restrictions in diet

Cystic fibrosis

pacreatic diet

NPO

seizure diet

carb restirction

diet for diverticulitis

low fiber

GERD diet

portion control

cancer diet

food safety and microbial diet (unpasturized foods)

prengnacy diet

energy: 300 additional folate iron calcium

when would you want to do a parenteral nutrition

non functional GIT short term PPN (peripheral) long term TPN (total)