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NURS 6200: Pharmacology & Nutrition

Exam 1
3 Phases of Drug Interaction: Basics of Pharmacology
1) Pharmaceutical: Goal is to get the drug in solution (dissolved in liquid) so the
GI can absorb it.
- Mostly talking about PO meds
- Liquid meds already dissolved
- Parenteral meds (Injected meds: IM, IV, SQ) have NO pharmaceutical phase!
2 Parts: 1) Disintegration: break tablet up; increase surface area 2) Dissolution of smaller particles allows for absorption
Special Considerations: Alter Bioavailability: Amount/percent of administered drug that is actually available
- Acidic environment  absorption
- Young and Old have less acid = slower absorption
- Enteric coating prevent stomach acid working (no disintegration)  alkaline pH of SI causes disintegration
- Food can interfere; some require empty stomach = pay attention!
- Drugs can irritate the GI AD-ME
2) Pharmacokinetics: Drug movement to target & start acting
A) Absorption: Getting drug from GI into plasma/body fluids
- Protein-bound drugs (insulin, hormones) would get destroyed
in stomach – must be injected, not ingested
- Lipid-soluble absorbed by SI
- Exercise  absorption
- First-Pass Metabolism: Meds absorbed in GI pass through liver
and get metabolized  amount of drug (bioavailability)
B) Distribution: Drug available to body fluids & tissues
- Influenced by blood flow - Protein-binding effect
- Affinity for the tissues - Volume of drug determined by dose size and concentration of drug!
Some drugs bound to protein (Albumin)
- Drug bound to protein NOT active
- Only free (unbound) drug is available to do its job
- As free drug used/metabolized  bound drug released; free to function
Special Consideration:
Blood Brain Barrier – only lipid soluble drugs have a chance to get
Pregnancy: lipid soluble and insoluble drugs can get across placenta
Drugs can get into breast milk too
C) Metabolism: Drug inactivation: chemically changing it
Mostly by Liver  enzymes change drugs & made water soluble
 excreted by kidneys
* Kidney and Liver problems affect metabolism rates*
If decreased  possible toxicity (Too much active drug available)
Measured by Half Life: Time it
takes for ½ the dose to be
metabolized AND eliminated
(Eg. 650mg dose of aspirin)
D) Elimination: Drug/metabolite
leaves body
- Mostly kidney job
- Can be lungs, feces, sweat, milk, saliva
- Complication pH & kidney disease  measure renal function:
 w/ (CLcr) creatinine clearance: compare lvls in blood:urine
 Glomerular Filtration Rate (GFR): better test (costs more): less renal function means lower dose for patient
3) Pharmacodynamics: The way drugs affect the body
 Drug Response: relationship btwn minimal vs. maximal amount of drug dose needed to produce the primary response
- Primary: desirable  goal/hope for drug
- Secondary: can be desirable or not Eg: Diphenhydramine
 Onset of action: time it takes to reach the minimum effective concentration (MEC) after a Primary: antihistamine
drug is administered Secondary: CNS depressant
• Peak action: occurs when the drug reaches its highest blood or plasma concentration
• Duration of action: length of time the drug has a pharmacologic effect

Classes of drug activity:

1) Stimulate cell activity, normal function (agonist)
2) Depresses normal cell activity (antagonist)
3) Replace a non-functioning normal activity (agonist)
4) Interfere with or irritate normal function (antagonist)

Drug agonists: stimulate the

function of a chemical
messenger – mimic it and cause
increased response
Drug antagonist: block receptor
for a molecule; prevent signaling

 Therapeutic index (TI): estimates the margin of safety of a drug through the
use of a ratio that measures the effective (therapeutic) dose (ED) in
50% of people (ED50) & the lethal dose (LD) in 50% of people (LD50)

*The closer the ratio is to 1

the greater the danger of toxicity*

Peak drug level: Highest plasma concentration of drug at a specific time • Tolerance: decreased responsiveness to drug
• Indicates the rate of absorption • Tachyphylaxis: rapid decrease in response to the drug
• Blood sample should be drawn at the proposed peak time Common for narcotics, barbiturates, laxatives, & psychotropics
Trough drug level: Lowest plasma concentration of a drug
• Measures the rate at which drug is eliminated
• Trough levels drawn immediately before the next dose of drug is given
Pain & Inflammation Management Agents
Inflammation: Response to tissue injury & infection
S&S: erythema, edema, heat, pain, loss of function
- Histamines: First mediators present  cause
arteriole dilation and  capillary permeability
- Bradykinins  capillary permeability & pain
- Prostaglandins  capillary permeability,
vasodilate, pain and fever

- COX enzyme: Cyclooxygenase needed to activate

prostaglandins COX1 and COX2:
COX1 = protects stomach lining COX2 = reduce pain
Cox inhibitors stop inflammation from happening!
Anti-inflammatory Drugs:
1) NSAIDS: Non-steroidal Anti-inflammatory drugs
Mode of Action (MOA): stop prostaglandin production, analgesic (lower pain), antipyretic
(lower fever), inhibit platelet aggregation, mimic corticosteroids
A) First Generation: Block COX1 and COX2
- Salicylates: Aspirin Therapeutic range: 15-30mg/dL; Toxic >30mg/dL
Anticoagulant ( bleeding & bruises), possible gastric problems and ulcers,
Hypoglycemia w/ oral antidiabetic meds
Side effects: Tinnitus, fatigue, gastric pain & ulcers, thrombocytopenia,
hepatotoxic, No 3rd trimester preggers, not for kids w/ flu  Reye Syndrome
- Para-Chlorobenzoic Acid: sodium & water retention: Indomethocin, Sulindac
- Phenylacetic acid Derivatives: Diclofenac acid, Ketoralac  INJECTABLE NSAID
- Propionic Acid: end in -en (Ibuprofen (Motrin & Advil)
increase bleeding, tinnitus, gastric distress  take w/ food
- Fenamates: STRONG NSAID; end in -mates, for chronic arthritis; NO if Hx of ulcer
- Oxicam: cream/gel – wash hands
B) Second Generation: Selective COX2 Inhibitor  Celecoxib  protects stomach lining by not blocking COX1

2) Corticosteroids: end in “-sone”

Physiologic dose: normal endocrine function
Pharmacologic dose: reduce inflammation, many side effects
*Must be tapered off of these*

3) DMARDS: Disease Modifying Antirheumatic Drugs

Immunosuppressive  Azathioprine
Immune modulators: Interleukin 1 antagonist/TNF blocker  disrupt inflammation process/delay disease  used for RA
Antimalarial drugs: second line of defense for RA – combed w/ NSAIDs
- May suppress inflammation: Cyclophosphamide, methotrexate  can be used for cancer patients too

4) Anti-gout: Gout = defect in purine metabolism  deposits uric acid crystals – avoid organ meats, sardines, beer, liver
Colchicine, take w/ food  renal, GI, heart problems not a good candidate
Toxicity due to narrow therapeutic range!
Allopurinol – blocks uric acid production
Probenecid: Uricosuric  pee out more uric acid

Pain Management: Pain is 5th vital sign; people have different pain toleranceNon-opioid & opioid analgesics
Acute pain – 1 time, or short term pain with obvious cause  changes in vital sign, anxiety, distress
Chronic – on going, long-lasting people  no VS changes, feel pain, depression
Up to 75% of patients have unrelieved pain – assess, intervene, and reassess!
1) NSAIDS to treat mild to moderate pain. Inhibit COX1 and/r COX2  anti-inflammatory & antipyretic
- Can result in tinnitus, GI problems, Reyes Syndrome in children, decrease platelet aggregation
E.g. aspirin, ibuprofen (advil, motrin), naproxen

2) Acetaminophen – Tylenol NOT NSAID: antipyretic, analgesic

Block prostaglandin synthesis: stops pain different way than NSAIDS
Can cause rash, hepatotoxicity, thrombocytopenia, limit to 4g/day 
if overdose use “Mucomyst”

3) Opioids: Morphine binds opioid receptors  suppress pain impulse

- For moderate-severe pain; act on CNS – can overdose cause CNS
depression and RR rates drop dangerously low
- Also cause constipation, urine retention, antitussive

- Meperidol – 1st synthetic opioid; choice or preggers but not for older
adults. No antitussive property

- Hydromorphone = Dilaudid; synthetic – 6x stronger than morphine Combo drugs: hydrocodone & ibuprofen
Can cause hallucinations; allergies to it acetaminophen & codeine
- Fentanyl drip or patches – give more potent dose that morphine

PCA – Patient-Controlled Analgesia: loading dose given, programmed to respond to press of button to administer
additional doses. Lock out time to prevent addiction and overdose. If used = produces constant analgesic levels

4) Adjuvants: additives to an opioid & nonopioid pain treatment: anticonvulsants,

antidepressants, local anesthetics, etc.
- Nalbuphine – has opioid agonist and antagonist function by  pain threshold

Naloxone = Narcan  opioid antagonist to reverse overdose or resp. depression

- must monitor overdose patient continuously: Vitals, bleeding, n&v

Addiction: biological need for a substance to achieve emotional and physical state
Associated with tolerance; need larger doses to achieve same result

Headache care: Migraine severe headache: often on single side, sometimes with aura, n&v, photophobia – can last DAYS
More common in women; cause: inflammation and dilation of blood vessel and/or serotonin imbalance
Triggers: cheese, chocolate, red wine
Prevention: beta blockers (end in -olol), anticonvulsants: Depakote & gabapentin, TCAs
Management: Analgesics (caffeine & acetaminophen), opioids, migranal, SSRIs
Imatrex (Sumatriptan): causes cranial vessels to vasoconstrict
Side effects: dizzy, drowsy, cramps, dysrhythmias, thromboembolism, heart attack, stroke

Endocrine Agents
Hormones: messengers that control and regulate activity or target
tissues – bind to target receptors to activate response
- Lipid soluble: steroids and thyroid hormones – bind to
proteins in plasma for travel; cross cell membrane of target
tissue  receptor is inside the cell
- Water-soluble: insulin, GH, prolactin – circulate freely in
plasma – receptors are ON surface of target tissue

Negative feedback (like thermostat); most common for of regulation

Pituitary: “master” gland  releases hormones to stimulate other glands to make their hormones
- Ant Pit: 80% of gland. Connected to Hypothalamus via portal system of capillaries
Trophic hormones produced: GH, ACTH, TSH, FSH, LH, prolactin
- Post Pit: Nerve tissue that extends down from Hypothalamus – extension of Hypothalamus!
Hormones: ADH, oxytocin
Hormone Dysregulation Treatment Side Effects
Anterior Pituitary
Growth Hormone Low GH Somatrem, Somatropin
High GH Bromocriptine, Octreotide (Sandostatin)
TSH Low TSH Thyrotropin (Thytropar)
ACTH Low ACTH Corticotropin (Acthar) – stimulates adrenal Diagnose adrenal gland disorders
cortex to make cortisol! Treat adrenal gland insufficiency
Anti-inflammatory for allergic rxn
Posterior Pituitary
ADH Low ADH Vasopressin – acts like ADH  retain water & Na Treatment for diabetes insipidus
Monitor cardiac: BP, HR, ECG –
possible hypernatremia/hypokalemia
Possible water toxicity too
No booze!
High ADH Demeclocyline – makes you pee Treatment for SIADH & hyponatremia

Produces T3 (Triiodothyronine), T4 (thyroxine), calcitonin – T4 is
most abundant produced, but T3 is more potent.

- T4 is converted to T3 in the blood; both require iodine for

synthesis; affect metabolism, caloric needs, O2 consumption,
carb and lipid metabolism, growth and development, brain

- Calcitonin – made by C cells when Ca levels are high  stops

bone leeching, inc. Ca storage, inc. excretion of Ca and PO4
Disorder Dysregulation Treatment Side Effects
Hypothyroid Levothyroxine (Synthroid) Thyrotoxicosis, MI, severe renal disease
raise T3 & T4 *Interactions with MOST things
- For Hashimoto’s, goiter  Increased cardiac insufficiency with epinephrine
• Increased effects of anticoagulants, TCAs, vasopressors, decongestants
• Decreased effects of antidiabetics, digitalis
• Decreased absorption with cholestyramine, colestipol
Take by self in morning 30 min before other drugs
Hyperthyroid - Surgical removal, Treat thyrotoxicosis
radioactive Iodine, anti- Interactions:
thyroid drugs • Increase effect of anticoagulants
- Propylthiouracil (PTU) & • Decrease effect of antidiabetics
methimazole (Tapazole) • Digoxin & lithium increase action of thyroid drugs
• Phenytoin increases T3 level
Cause Ca to be leeched from bone when levels are low  stimulate osteoclast activity
PTH promotes Ca absorption from GI, activates renal conversion of Vit D to calcitriol (active version of Vit D)
Disorder Dysregulation Treatment Effect
Hypoparathyroid Calcitriol Treat rickets  increases serum Ca
Hyperparathyroid Calcitonin Treat Paget’s disease  too much Ca in serum/not enough in bones
Adrenal: Cortex regulates Sugar, Salt, Sex
Sugar: glucocorticoids (cortisol)
• Promote sodium retention, potassium
Salt: Mineralocorticoids (aldosterone)
• Secretes aldosterone
• Promotes sodium & water retention
• Controlled by RAAS
Sex: Androgens

Corticotropin (Acthar), cosyntropin  drugs used to test adrenal and pituitary function/dysfunction
Disorder Dysregulation Treatment Effect
Hypocortisol – Prednisone – suppress • Increased effect w/ barbiturates, phenytoin, rifampin, ephedrine,
Addison’s inflammation, replace cortisol • Decreased effects of aspirin, anticonvulsants, INH, antidiabetics
Hypercortisol - Mitotane – suppress cortisol Hypoglycemia, weakness, fatigue, tachycardia
Hypo Hydrocortisone, Salt retention
fludrocortisone (oral med) –
helps retain salt
Insulin causes drop in BG  b/c glucose leaves bloodstream
and goes into cells
Insulin causes liver and muscle cells: 1) undergo
Glycogenesis: to take in glucose and store it as glycogen. 2)
prevents Gluconeogenesis: form new glucose from other
sources 3) store fat 4) increase protein production

Glucagon also made by pancreas  released when BG low:

1) stimulates breakdown of glycogen: Glucogenolysis and 2)
Make glucose from other, source: Gluconeogenesis, 3)
stops glucose transport into cells. (GH, cortisol, epinephrine
also have same effect – make glucose available in the

Type 1 - Diabetes mellitus (T1D) – hyperglycemia
from abnormal insulin production, broken insulin
use, both
Type 2 – Late-onset – (T2D) AKA Non-insulin-
dependent diabetes mellitus (NIDDM)
Gestational – during pregnancy; often resolves

Other – disease influence development of diabetes

T1D require life-long insulin treatment

T2D may/may not

Basal-bolus – multiple daily insulin

injections/or pump. Frequent monitoring
of BG
Use rapid and short-acting insulins
before meal w/ intermediate or long-
acting 1-2 times a day

Mealtime insulin AKA bolus: timing

rapid/short acting to coincide w/ meals

Long acting – no mixing

Short & Intermediate can be mixed – clear before cloudy
- Injections should be rotated within the same site via SQ injection; absorption rates different – abdomen fastest
Insulin needles for single injections, pens w/ insulin cartridges inject yourself
Pumps: continuous SQ infusion, use rapid-acting insulin to deliver basal rate; at meals user programs amount of insulin
to give
Complications: lack of insulin, infection at site, higher risk for DKA, hypoglycemia, allergic reaction,
lipodystrophy (lose subcut. Fat from constant injections to same site), hypertrophy, Somogyi Effect

Side effects: Hypoglycemia – “Cold and & Clammy gets some candy”  follow rule of 15 if sugar is low & patient awake
Hyperglycemia – “High & Dry”; diabetic symptoms

Oral Antidiabetics: Used for T2D only

improve mechanisms to make body do better at
making insulin
Work on 1) insulin resistance, 2) decreased
insulin production, 3) increased hepatic glucose
a) Metformin: first line treatment for T2D
 different forms for different release
Reduces liver production of glucose, enhances
insulin sensitivity
Metformin not for people with kidney disease,
liver or heart failure, or alcohol drinkers
b) Sulfonylureas, Meglitinides, Glucagon-
like Peptie-1 Receptor Agonist – increase
insulin production by pancreas
c) Alpha glucosidase inhibitors (starch
blockers) – taken with first bite of food
d) Thiazolidinediones for insulin resistance
– given with meals– not for people with heart disease, liver disease!

Nutrition across the lifespan

Pregnancy: successful outcomes: viable birthweight, no defect, long-term health for infant and mother
- Metabolic changes for mom: BMR 15-20% & use fat as fuel – ketoacidosis: good fat, not visceral (organ) fat
- Physiologic: blood volume doubles – can cause hemodilution
-  GFR – can cause BP problems pre-eclampsia can lead to eclampsia  deadly and MUST lead to delivery of baby
- GI motility smooth muscle relaxes = constipation, delayed emptying, heartburn results
- Needs to gain weight for higher nutritional needs: fluid volume, more support tissues, support fetus and placenta
Not enough weight gain: low birth weight and small gestational age = want baby at least 5.5lbs
Suggested Gain for body mass index (BMI):
• Normal BMI (18.5 to 24.9): 25 to 35 pounds
• Underweight BMI (<18.5): 28 to 40 pounds
• Overweight BMI (25 to 29.9): 15 to 25 pounds
• Obese BMI (>30): 11 to 20 pounds
INCREASE ENERGY INPUT! extra 340 kcal/day during second trimester and 452 kcal/day during third trimester
• Protein Recommended Dietary Allowance (RDA): 71 g/day for adolescents and adults
• Vitamin and mineral supplementation use prenatal type multivitamin-mineral supplement
*Excessive preformed vitamin A or vitamin D can cause birth defects*
– Folate to prevent neural tube defects! RDA increases to 600 μg/day
– Iron (ferrous): RDA increases to 30 mg/day necessary beginning in second trimester
– Calcium Adequate Intake (AI): 1000 mg for pregnant adult women; 1300 mg for pregnant adolescents
• Baby uses Ca+ in blood stream, mom must replace from bones and teeth
need to have high Ca+ levels to prevent bone tissue loss
• Alcohol Fetal alcohol syndrome (FAS)/fetal alcohol spectrum disorder (FASD); causes specific anatomic
and central nervous system defects; no safe level
Risk Factors:
1) Foodborne illness: High risk for infections from Listeria monocytogenes, Salmonella species, and Toxoplasma gondii
2) Maternal age
– Risk factors for adolescents Lactation: breastfeeding increase BMR of
- Growth pattern of mother; psychologic maturity breastfeeding mother, also helps return
- Older mothers have longer medical history, risk of gestational diabetes uterus to pre-pregnant size, reduced
3) Lack of economic resources; delay in medical care ovarian and breast cancer risk, cheaper!

Infant Needs: First year- breast milk/formula all that is needed!

1) Protein: needs highest during first 4 months; 1.6g/kg/day for second 6
• Excess protein affects renal solute load
2) Vitamins and mineral supplementation provided by breast milk/formulas
Iron: fetal iron stores depleted by age 4 months  breast
milk/formula provides:
Vit D: needs supplements, fluoride not needed until 6months
Vit K: given shortly after birth
3) Introduce new foods 1 at a time starting @ 6months; start with veg  don’t introduce sugars until after veg
- Don’t give fake juice/water and milk everything pasteurized!
4) Congenital defects: cleft palate, heart problems, etc. may compromise ability to get nutrition  NG tube, TPN for low
birth weight  worry about failure to thrive = can’t gain weight – lots of
emotional, growth, physical problems result
5) PKU – can’t have stuff w/ phenylalanine in it (sorry diet soda) – causes seizures,
mental disabilities, stunt growth

Childhood: 1-12years: growth fluctuations = changes in dietary needs

Protein and k/cal needs increase w/ age

Lead poisoning impacts learning!

Age Group Dietary needs Milestones Things to watch
Toddler (1-3yo) Energy: 1300kcal - Self-feeding - Consistency
Protein: 16g - Choice - Control portion size
Milk 2-3cup/day - watch allergies - Try new foods
Fruit 1 tbsp per year of age - Offer low-fat foods
¼ of adult serving for bread
4-6yo Energy: 1800kcal - Independence - Hunger and appetite may vary
Protein: 24g - New foods still - Food jags (Eg. chicky nugs only)

7-12yo – school Energy: 2000-2200kcal - Puberty changes needs - Peer influence

age & puberty!! Protein: 28-46g - Growth spirts - Healthy snack options
Ca increased from 800mg to
1300mg by 13yo
Need more Fe and Zn
13-19yo – Energy: m = 2300-2900kcal - Requirements vary based - Diet-related disorders
Adolescence f = 220kcal on activity, size, etc. - Eating disorders
Protein: m = 45-59g - Self-responsibility  - Need physical & emotional support
F = 45g - Watch influence of fast food
For adolescents: high-energy needs for sports, Ca for bone mineralization, MUST EDUCATE
nutrition needs increase! Goals: maintain current weight while continue to
Eating disorders and poor nutrition neg. impact growth and development, grow in size (slim down)
sexual maturity Develop healthy lifestyle & maintain it
Fe deficiency: b/c of poverty, poor diet, lead poisoning  Fe-deficient Anemia neg. impacts learning
Obesity among kids and adolescents – lots of causes
Associated with T2D, HTN, CVD, GERD, sleep apnea – poor nutrition

Adulthood: aging reduces energy and dietary needs

Age Group Dietary needs Milestones Things to watch
20s and 30s 2900kcal for men; 58-63g protein - Establish food patterns - Food affects childbearing
220kcal for women; 46-50g protein - Responsible for self - Food affects health
Ca and P needs decline
Women watch Ca and Fe
Men may need Fe supplement if vegan
40s and 50s Kcal needs decline - Positive diet habits and - Nutrient dense diets
Lean body mass replaced by fat exercise promote health - Low-fat & high-fiber
2300kcal = m, 1900kcal = f
Women need less Fe (no menses)
60-80s Same as 40-50s but need more Vit D! - Access to food and - Watch for ETOH abuse
Digestion and absorption decrease prepared meals needs Disorientation and fluid,
Dental health may decline monitoring dehydration balance!
Need B12 supplements - Micronutrients and - Memory/dementia
Constipation from slow GI protein needs - Access to foods

Nutrition Assessment & Patient Care

Genetics and environment influence disease!
Prenatal diet affects long-term health of child:
placental insufficiency, maternal malnutrition, intrauterine growth restriction (IUGR)  impair fetal growth
IUGR leads to HTN, CVD, T2D in adults
Nutrition Team: ID patient needs and work to help patients

Dietetic technicians,
Registered dietician- registered (DTR) - take
nutritionist (RDN) - do histories, collect info, work
Doctor - writes orders directly w/ patient, provide
assessment & ID needs of
patient basic info
Medical Nutrition Therapy: legal term for pre-renal failure,
diabetic patients that get treatment from RDN under Medicare

Malnutrition: Imbalanced nutrition or intake; can be over OR

Hospitalization: durable power of attorney – authorize
another adult to make decisions if person can’t
Primary: inadequate intake of nutrients, undernutrition
Secondary: caused by disease or some other impact
Types of Secondary Malnutrition:
- Starvation-related: chronic starvation w/out any inflammation

- Chronic disease-related: Chronic mild-moderate inflammation

- Acute disease: Injury-related too w/ acute & severe


Once Admitted a patient must get:

1) Nutrition screening w/in 48hrs – ID if malnutrition, or risk, personnel involved, referrals necessary if problems
- Screening can be done by nurse, RD, DTRs, physicians, etc.
- Cultural considerations for patients in hospital: food choices, and timing and sequence of meals, determine who shops
for food (patient or other), patient vegan (or special diet), allergies, other issues

2) If signs nutrition risk  refer RD for Nutrition Assessment

Assessment Steps:
A – anthropometric: Simple – height (stadiometer for babies), weight, head circumference, skinfold thickness  BMI
Healthy BMI: 18.5-24.9kg/m2
B – biochemical: Blood tests for CBC, protein, albumin, etc. Limitations b/c no single test; use serial measurements
Pay attention to albumin, if <3.0 = could be inflammation; indicator of morbidity, mortality, disease severity
C – clinical: medical Hx, social Hx, physical exam
D – dietary: Intake assessment – what did you eat the last 24hr, food record, kilocalorie counts

Interventions for at risk and malnourished – weights, lab results, feeding schedules and modes
Meds: many drugs decrease GI absorption, interact w/ drugs, create toxic response
Dietary supplements and herbal remedies should also be considered!! – alter bioavailability, metabolism
Examples: antihypertensives and antianxiety meds cause weight

Drugs that impact appetite:

Appetite stimulants: antidepressants, steroids
Appetite suppressants: antidepressant fluoxetine,
amphetamines, anti-ADHD meds
ETOH has deficiency risks b/c ETOH suppressed appetite and
interacts with nutrients; limit drinks
Drugs that alter taste: lots do – lithium may produce metallic
Drugs that impact food/nutrients
Anti-ulcer agents  Vit B12 absorption
Anticonvulsants  metabolism of folate, Vit D & K increased
Foods that may impact drugs
1) Foods high in Vit K  counteract warfarin/heparin
2) Diabetic meds interact with insulin
3) High fiber diets, and St. John’s Wart blocks digoxin  cardiac patients that need to slow heart rate, not good!
4) Grapefruit leads to greater side effects of meds: higher trans-aminase  leads to faster bioavailability
- Calcium-channel blockers
- Statin drugs
- Anxiety/Depression meds

Food related issues

Attain a nutritional status: gain, lose, maintain  modifications can involve (Quantitative) # of meals, time between
meals, snack frequencies, number of calories (Qualitative) types of meals, meal choice

Diet orders: right diet, right time, right textures & nutrients  depends on dietary needs and orders

Types of diets: ordered by physician usually

1) Regular/general – basic diet  whatever the dieticians of hospital use: maintain optimal nutrition – well
2) Diet as tolerated: allow for progression after procedure (ice  clear liquid  full liquid, etc. after surgery)
3) Clear liquid diet: inadequate for energy, low in everything but water: water, juice, jello. Careful w/
caffeine (diuretic)
No more than 8-24hr at a time!
If post-op – no orange or red jello b/c it might look like blood – be sure patient not bleed to death on food
4) Full liquid: liquid at room temp can’t see them – creamy soups; ice cream, shakes – for patients with difficulty
swallowing. Can provide full nutrition.
5) Mechanically altered – chopped, smashed, ground/puree food – lightly seasoned, decent fiber
6) Low sodium, low fiber, high fiber, vegetarian, allergy free, dysphagia diets (those prone to aspirate) – thicken
liquid, - - nectar, honey, pudding levels!!

Food safety: Food poisoning – norovirus, salmonella, s. aureus,

clostridium, campylobacter --. Safe serve to teach proper cooking
temps, storage, cross contamination, etc.

Cultural and/or religious pref: know patterns of populations

- Muslim preferences: no pork; halal. no coffee, tea, ETOH, fasting
- Jewish preferences: Keep it kosher: No pork or fish w/ scales,
dairy and meat must be separate

Oral: start of GI tract – technically enteral nutrition – usually means tube feeding’; GI has to be working!!
- Tube feedings for when patient is unable/unwilling to consume appropriate amount of nutrition
- Maintains gut integrity
- Indicated for us when 5 days or longer malnourished, reduced oral intake, dysphagia, short gut syndrome, etc.
Non-oral (enteral): through tubes but use rest of GI
A) Types of enteral feedings
1) Standard Intact: require normal functioning GI: high kcal, blenderized food, milk-based
2) Special: GI not functioning properly
Administrations of enteral feedings (i.e., continuous)
- Continuous
- Intermittent
- Bolus
Duration: How long will patient need feeding
- Short-term non-surgical tube placement
- Long-term = surgical placement

Safe administration: tube placement must be documented and

- Wash hands!
- Medications

Complications of enteral feedings

a. Diarrhea
b. Tube displacement and/or obstruction
c. Aspiration wrong placement
d. Metabolic issues: dehydration, over-hydration
e. Fluids/electrolytes

B) Parenteral nutrition: IV food administered; rest the GI tract for rested, lack of movement
- Use large vein  Central Parenteral Nutrition (CPN) aka Total Parenteral Nutrition (TPN)
- Must be isotonic, limited in kilocalories, for short-term nutritional support
- Contain simple molecules: dextrose, amino acids, essential fatty acids, electrolytes, vitamins
- Complications: Pneumothorax, Infection, Embolus

C) Transitional feeding enteral mixed with parenteral; wean patient off of TPN; check swallowing

Nutrition for disorders of the liver, gallbladder & pancreas

Liver: needed for digestion: sugar, amino acids, fatty acids
enter liver for storage; when needed these broken down for
Excretes cholesterol and bile
Blood is filtered: for toxic metabolites, converts ammonia to
urea  excreted via kidneys

1) Hepatitis: inflammation of liver

HepA (fecal-oral) poor sanitation, food, handwashing
HepB: (sexual transmission, body fluid swap)
HepC  can lead to cirrhosis: no dietary recommendations
HepD: coinfection with HepC: IV drug use, no dietary recs.

Diets: Adequate nutrition; no ETOH: small frequent feedings w/ 40% carbs,

proteins, low fat. 2500-300mL of fluid a day. VitB12, thiamine, Zinc, VitC

2) Non-alcoholic fatty liver (NASH/NAFLD): not from ETOH  diet-related;

Can cause Hepatic fibrosis; fat plus scarring  damages hepatocytes
Once cirrhosis can’t reverse: portal hypertension results – lower blood supply
result  esophageal varicies, ascities, encephalopathy (toxic ammonia build
up from lack of access to liver for metabolism by liver)
- Treat with antibiotics, lactulose to bind ammonia and excrete = lots of acid diarrhea
- Diet: 0.8g/kg protein, high-calorie intake to prevent protein breakdown, Na restriction, I&O restricted (deal w/ ascities)
3) Liver Transplant
- Diets vary post-transplant: TPN, tube-feeding
- Watch the ideal weight; lots of excess water to throw off measurements
- After transplant: healthy-well balanced; prevent HTN, weight gain, diabetes  may cause failure again!

Gallbladder diseases: Forty, Fat, Female, Fertile, Fair (skin) are risk factors for gallstones
- food diets contribute to gallbladder problems
- Follow low-fat diet: nothing fried, creamy, etc.
- After surgery: clear liquids  low fat diet  stay away from fatty foods!

Pancreas: pancreatitis
Acute pancreatitis inflammation from a cause: gallbladder disease, genetics, ETOH use
- Fats are problem for digestion = cause pain
- Reduce symptoms: parenteral feeds to give GI a break  can cause malnourishment
- If enteral feeding = LOW fat feeds; usually NJ tube – bypass the pancreas, tube in jejunum
- May need to change eating habits; 6 small meals, no ETOH, low fat!
Nutrition for diabetes mellitus
American Diabetes Association – idk, it’s a thing

Client teaching: need life-long diet and exercise changes: SELF MANAGEMENT!
Type 1: insulin and sugar control
a. Exercise – Don’t exercise when blood glucose levels are really high (>250) or ketones in blood
- measure BG before, during, after exercise  Eat sugar is BG is low!
b. Control and monitor BG levels!! Reduces microvascular problems

Type 2: diet and exercise, oral anti-diabetics and insulin if

can’t be weight-controlled

Special considerations:
1) sickness often comes with elevated blood glucose
- If can’t deal with solid foods, may need liquid nutrition
- May need to replace fluid volume if n&v
- gastroparesis may occur

2) Once started on insulin may result in weight gain

- Some patients may restrict their insulin to lose weight

3) Metabolic Syndrome: high sugar, high LDL, low HDL, big waist, hypertension  can lead to T2D
Management across the lifespan
-assess knowledge, compliance, and willingness to change if needed
- Include family members in discussion

1) Gestational DM: usually resolves after birth  may cause baby to

be larger and lead to sooner delivery
If a diabetic becomes pregnant: watch BG regularly  excellent
glycemic control is needed Weight loss NOT recommended!

2) T2D in young: increasing 30-fold since 1994; more common in

females. Decrease carbs, increase exercise
- Attempt to normalize BG and A1c

3) T2D in elderly: macro and microvascular problems; higher risk for

cardiovascular disease! - A1c should be ~7%