Nutrion

examples of micronutrients

vitamins, minerals

macronutrients

carbs, proteins, fats

what is a cal

energy req to raise 1kg of water by 1 degree celcius

* proteins & carbs (4 Cal/g); fats (9); 
* If not used => stored for later use (>90% as ‘fat’)

where does digestion take place?

* Duodenum, jejunum, ileum; large intestine (water)

malnutrition

* lack of food or ineffective utilization of food for body needs
* >40 nutrients required for normal function
* = or > BMR required for adequate energy
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* Causes: poverty, neglect, acute or chronic illness, mental health, elderly

Failure to Thrive

* Inadequate nutrition to support growth & development
* Organic vs Non-organic causes:

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* Organic: ‘cachexia’ d/t pathology (e.g. cardiac; GI disease; cancer,…)
* Cachexia: accelerated BMR, high cytokines affecting normal hunger triggers = low appetite
* Non-organic: poverty, neglect (child abuse)
* Neglect: most predominant type of child abuse in N.America

organic FTT

* ‘cachexia’ d/t pathology (e.g. cardiac; GI disease; cancer,…)
* Cachexia: accelerated BMR, high cytokines affecting normal hunger triggers = low appetite

non-organic FTT

* poverty, neglect (child abuse)
* Neglect: most predominant type of child abuse in N.America

TX FTT

* Treat the cause; increase calories per mL; hydrate; vitamins & minerals

Kwashiorkor FTT

* Develops in children whose diets are deficient in protein
* 6 mon to 3 yrs
* subcutaneous fat is preserved
* oedema is present
* enlarged fatty liver
* ribs are not very prominent
* lethargic
* muscle wasting mild or absent
* poor appetite
* needs PROTEIN

Marasmus FTT

* Deficiency of proteins and calories
* common in infants under 1yr
* subcutaneous fat is not preserved
* oedema is absent
* no fatty liver
* ribs are prominent
* severe muscle wasting
* voracious feeder
* needs cals + proteins + carbs

Enteral nutrition

* PO; Feeding tubes: NG, NJ, G-tube
* Preparations: 
* Polymeric (protein, lipid, carb) = intact nutrients, high calorie
* E.g. Pediasure; Ensure
* Oligomeric (easily digestible components: amino acids, peptides, ….) = hydrolyzed nutrients
* Specialized (if organ disease present)

Enteral nutrition timing

* Bolus (mimics normal meals) & Intermittent (like bolus but at a slower infusion, e.g. 30-60min)
* Continuous (ideal for recovery; avoids dumping syndrome = osmotic shift)

Parenteral nutrition

TPN. IV=> central line

* Goal: increase nutritional intake;

supply nutritional spectrum

* s/e: fluid overload; infection;

Electrolyte imbalances; hyperglycemia;

GI dysfunction

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when does re-feeding syndrome occur

post nutritional starvation

what happens during starvation

* Body shift to alternate hormonal and metabolic pathways for energy use
* Stored fat => fatty acids => main energy source => rise in serum ketones
* low gluconeogenesis (no glucose)
* Depletion of: intracellular minerals (to preserve serum concentrations) e.g. Phosphorus, Potassium, Mg,… & Vitamins
* Reduced organ function (e.g. renal, liver,..)

What happens during refeeding

* Glucose surge => Insulin secretion => mineral shift into cells (low plasma levels!) => water shift (osmosis) into cells + normal metabolism non-functional => massive hemostatic changes

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re-feeding guidelines

* Assess all baseline minerals, vitamins
* SUPPLEMENT with Vitamins (Thiamine, B-complex vitamins) & trace elements immediately
* SLOW refeeding (50% of energy requirements max & build)
* SLOW rehydration

root reflex

Responsive infant to tactile stimulation of the cheek or lips; causes infant to turn toward the stimulus and open mouth

suck reflex

Involves tongue protrusion and retraction in preparation for receipt of liquid stimulated by contact to the upper lip

how long should breastfeeding be exclusive

X 6 months, then in with diet upto 2yrs

* What are the pharmacokinetics regarding Vitamin D, in the human body?

Vitamin D is absorbed from the diet or synthesized in the skin when exposed to sunlight. It is then transported in the bloodstream and distributed to various tissues in the body, where it is converted to its active form. Vitamin D is primarily excreted in the bile and feces, and excessive intake of vitamin D supplements can lead to toxicity.

* What is the significance of Vitamin D?

* What is the significance of Vitamin D?
* Helps the body absorb and use calcium and phosphorus
* Essential for the development and maintenance of strong bones and teeth
* Regulates the immune system
* May reduce the risk of certain chronic diseases, including osteoporosis, some cancers, and autoimmune disorders
* May be important for muscle function, cardiovascular health, and cognitive function

what will a vit D deficiency in adults cause

* Osteoporosis : fragile bones d/t increased bone resorption
* most common cause: menopause (hormone changes – low estrogen)
* other causes: thyroid hormone deficiency, age, genetics, very high ETOH or caffeine intake

TX of vit d deficiency

* Vitamin D & Calcium
* Biphosphonates: 
* Alendronate (Fosamax); Risedronate (Actonel)
* suppress osteoclast activity => decrease rate of bone resorption

vit meds

* Vitamin D with Calcium


* Calcium gluconate (IV or PO), Ca acetate, Ca citrate


* Calcitriol (Calcijex)
* Active Vitamin D3, PO
* If vit D deficiency; if at risk d/t GI/liver/renal dysfunction

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* Note: Vitamin D can be overdosed (lipid soluble)

S&S: fatigue, GI pain, N&V, renal changes

Vit C

Antioxidant; tissue repair; immuno logic; collagen production

if deficient=scurvy

Vit A (retinol)

visual pigments (phototransduction); epithelial cells synthesis

if deficient= avitaminosis

Vit K 1 & 2

Blood clotting co-factor;

Bone building (‘osteocalcin’ synthesis)

K2: GI synthesis

K1: eggs, cheese, cooked: spinach, asparagus, broccoli 

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Vit B 12

erythrocyte maturation; cellular metabolism; CNS fx

if deficient= Cobalamin

Female lactation hormones stimulation

* Prolactin (anterior pituitary gland) =>  milk synthesis
* Oxytocin (posterior pituitary gland) => milk excretion ‘let-down’ & ejection

breastmilk

* Colostrum: 1-3 days post delivery; highly immunologic (IgA), EGF, low in lactose 
* Transitional milk: 3-14 days post delivery; lactose, protein, fat
* Mature milk: foremilk (higher in free water, lower calorie & fat) & hindmilk

how much fat is in breastmilk

56%, and cals =70/100mL

what does breast milk contain

* Fatty acids essential to brain development (Omega 3: DHA, ARA)
* Amino acids
* Carbohydrates: Lactose
* Essential minerals, vitamins, trace elements…..
* Free water
* Immunity components
* Iron: bioavailability upto 100%

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* Low in Vitamin D => supplement

why do we need iron

* Essential for normal cell function, mitochondrial energy production; Hgb synthesis
* >60% used for hemoglobin synthesis (RBC’s = Hgb)

normal levels of iron in body

* 1-2 mg/day (adult); 0.27 mg/day
* normal losses 1-2 mg/day (adult); 0.27 mg/day

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Iron kinetics

* protein bound
* unbound = toxic

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* Transferrin protein (in blood) 
* Ferritin & hemosiderin proteins (within cells)
* Stored in the liver as Ferritin

sources of iron

* Fetal iron liver stores in 3rd trimester of gestation - adequate til 6 months
* Iron recycled - from old RBCs
* Dietary iron - replaces losses !

what is the average amt of iron reqt in older children

10mg/day

highest demand during rapid growth times

how much iron in breast milk

* = 0.35 mg/L
* reqt is 0.27mg/day

where is heme iron (20%) found

meat, poultry, fish

where is non-heme (5%) iron found?

legumes, veggies, fruits, grains, nuts, eggs, tofu

inducers for iron

protein, Vit c

inhibitors for iron

calcium

popeyes spinach rant

* Spinach does contain iron
* Iron does increase energy – it allows for normal cellular function & Hgb synthesis 
* Spinach contains non-heme iron which does not absorb as readily
* Spinach also contains inhibitors to absorption: oxalate, tannins which decrease bioavailability

contradictions to breastfeeding

* Infection
* HIV
* Active herpes on nipples
* Toxic substances, e.g.
* drug abuse
* drugs which pass into breastmilk 
* as a rule: not high Vd drugs, not highly lipophilic drugs, short t1/2 is best (allows for drug clearance prior to next breastmilk synthesis)

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Infant:

* Galactosemia
* Lactose intolerance

Galactose: monosaccharide (can’t be broken down)

Primary source: metabolized lactose (via ‘Leloir pathway’ (Lactose =>Galactose + Glucose)Other sources: synthesized in cells

* Present in dairy & some protein products & breastmilk
* milk, cheese, butter, yogurt, ice cream
* Whey, Cassein protein supplements
* additive in prepared foods & drugs

Galactosemia

* Metabolic disorder (inherited autosomal recessive)
* Gene testing available for prenatal dx; neonatal screen test if suspected
* Deficient hepatic enzyme, GALT  (galactose-phosphate uridyltransferase)
* =>alternate metabolism => active toxic metabolites (e.g. galactitol)

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* S&S: vomiting, poor weight gain, fatigue, hypoglycemia
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* Complications: 
* FTT 
* Hypoglycemia = > brain damage
* Other damage – eyes (cataracts), liver (jaundice, bleeding disorders)
* e-coli sepsis (opportunistic d/t high galactose – non-metabolized sugar)

TX for Galactosemia

* Soy protein isolate formula with Calcium supplements
* Stop milk (human or animal) intake
* Diet restricted in galactose and lactose
* Tx associated symptoms
* If liver damage
* Phototherapy for bilirubin (inability to conjugate bilirubin)
* Vitamin K; FFP for bleeding
* Antibiotics for opportunistic infection/sepsis

Lactose intolerance

* Lactase enzyme deficiency (brush border of duodenum) 
* Inability to hydrolyze lactose (disaccharide)
* varying degrees of deficiency

Types of Lactose intolerance

* congenital intolerance: autosomal recessive trait
* primary intolerance: decreasing levels of lactase with age (post 2 yrs of age common)
* Note: secondary intolerance associated with other illnesses: e.g. Crohn’s disease flare-up, acute gastroenteritis, ….

S&S of lactose intolerance

* Unabsorbed lactose:
* => osmotic fluid shift into intestine => watery stool
* => fermentation by colonic bacteria => gas, bloating
* abdominal bloating/cramping, flatulence, diarrhea

TX for lactose intolerance

* stop milk intake (human or dairy); avoid milk & milk products
* Lactose free formula
* Soy formula (2nd choice)

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* Lactase enzyme medication
* E.g. Lactaid (not in infants)

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Lactose intolerance testing

* Breath test: hydrogen gas concentration high post-lactose ingestion
* Lab test: milk tolerance (500 mL of milk = serum glucose measurement, if low then indicative of lactose malabsorption)

Wellness check 2 week visit

* feeding q 2-3 hrs
* Breastfeeding duration 20-30 min
* Formula volume 70-100 mL/feed
* No bottle propping=>  EAR INFECTIONs

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* Needs: 90 cal/kg/day

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* Void: q 1-3 hrs
* Stool: upto 6/24 hrs
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* Iron:
* Fetal iron stores utilized 
* Iron in breastmilk + formulas fortified

wellness checks at 6 months

* Breastfeeding continued (or formula) 
* Start solid foods at 6 months
* NO cow’s milk (ideal start @ 12 months)
* 1st Baby cereals & vegetables/fruits

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* Needs: 100 cal/kg/day
* Void: 6/24 hrs
* Iron:
* supplementation required after 6 mo

Expected G&D by 1yr of age

* Brain = 2/3 of adult size
* Head circumference = 47 cm (0.5cm growth/month)
* Myelination of nervous system nearly complete (full at 2 yrs)

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* Birth weight approx. tripled
* Begins walking


* Language: single words, babbling, imitates sound

when is cow milk rec

* At > 2yrs of age: recommended intake is 2 cups /day
* Helps meet Vit D requirements

issues with too much cow milk

* Interferes with iron absorption (d/t Calcium) => secondary anemia
* displaces other foods from diet (fill up on milk)

Erythrocyte production

* Adults: Bone marrow of flat bones (pelvis, ribs, sternum)
* Utero: Endothelial cells 1st, then in liver & spleen
* Production elements: iron, Vit B12, folate
* Stimulus: Cytokine hormone Erythropoietin (EPO), produced in kidneys

erythrocyte elimination

* spleen, liver, bone marrow
* iron & amino acids = recycled (*some iron fecally excreted*)
* heme (=>bilirubin) = biliary excretion

erythrocyte fx

* Oxygen transport in plasma - on hemoglobin
* Acid-base balance
* Requires glucose for its function

Anemia

impaired o2 carrying capacity

=>hypoxemia => hypoxia

* Low Hgb or low RBCs

causes of anemia

* Low production: low EPO (e.g renal disease); low RBCs (e.g. bone marrow disease); low Iron 
* Losses: haemorrhage = loss of RBCs; hemolysis = destruction of RBCs (e.g. Sickle cell anemia)

serum iron

transferrin

ferritin

iron stores- plasma ferritin is in trace amounts, but proportional to stored ferritin

hematocrit

RBC vol

MCHC

amt of Hgb per RBC

Iron supplements: PO ferrous salts

Ferrous sulfate; Ferrous fumarate; Ferrous gluconate 

* Dosage in elemental (available) iron
* Bioavailability = 90%
* patient-based amount recommendations (e.g. peds vs adults)
* avoid Calcium with intake

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* Side effects: 
* GI pains, constipation (decreased peristalsis), drug-drug-food interaction

Iron by injection

Iv or IM admin

* Iron Dextran
* calculate based on lean body weight & Hgb
* If hemorrhage replacement: Iron mg = mL (blood loss) x Hct
* Monoferric (Monofer, Venofer)
* better absorption - lower risk of free iron OD

Iron poisoning

* Excess of iron ingested
* accidental OD at home or medication error
* acute event = medical emergency
* Effects seen in hours, peak in 2-3 days

S&S:

* **Vomiting & GI pain** d/t intestinal hemorrhage => intestinal mucosa damage + intestinal osmotic fluid shift => hemorrhage & hypovolemia
* **Cardiac & CNS** abnormalities d/t mitochondrial damage (no ATP production; altered Ca cellular transport) => cardiac arrhythmias, cardiogenic shock, altered LOC

TX for iron poisoning

* excretion
* evacuation of bowel
* IV administration of Deferoxamine (Desferal) - chelates (binds) iron to form non-reactive complexes

Acute hemorrhagic anemia

* sudden loss d/t acute injury/surgical bleed/childbirth
* 10-30% of blood volume loss = symptoms
* ⇒compensatory mechanisms, hypotension, shock

TX hemorrhagic anemia

* Blood products: PRBCs (packed red blood cells)
* if Hgb

Allergic transfusion reaction of PRBC

* **IV vein redness/pain**
* **Flushed face**
* VS changes 
* tachycardia, hypotension, dyspnea
* Headache
* Chills/Fever
* Urticaria 
* Back pain
* renal pain d/t hemolyzed RBCs
* N&V

TX for blood transfusion allergy

* Antihistamines
* Glucocorticoids: e.g. hydrocortisone
* Epinephrine 
* O2
* Intubation?
* NS
* Hemolysis of RBC’s => renal injury
* NS & diuretics enhance renal perfusion & fx
* VS - monitor

Allergy review

* ALLERGY: allergen-IgE binding = mast cell degranulation => Histamine
* pro/inflammatory: cytokines, complement, leukotrienes, bradykinins, PAF, NO,…

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* ⇒ANAPHYLAXIS: rapidly progressing systemic response, life threatening


* severe immune-mediated vasodilation & bronchoconstriction
* => respiratory compromise, declining SBP
* S&S are variable: urticaria, SOB, tachycardia, declining BP, soft tissue edema: angioedema, laryngeal edema; anxiety, change in LOC; GI symptoms

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=> Anaphylactic shock: hypoperfusion & fluid shift => circulatory collapse

* Upto 35% of volume loss within 10 min!

Hunger hypothalamic stimulation via:

Hypothalmic peptides

Ghrelin (from an empty stomach)

\+dopamine continues to stimulate appetite

=> hypothalmic secretion of thyroid & adreno-cortcoids:

metabolism, utilization of food stuff

satiety

CNS receives inhibitory signals:

GI: CCK from duodenum + Pyy + GLP-1

Insulin

Lipid metabolism byproducts (ketones)

**Leptin (from adipose tissue cells)**

keto diet

high lipid & protein ingestion

limit carbs

Based on hunger inhibitory mechanisms:

Quick satiety due to CKKs inhibitory mechanisms:

* CKK released w/ protein/fat presence in duodenum
* lipid biotransformation byproduct (ketones) inhibitory mechanism

Risk for keto acidosis

can low iron decrease hunger

yes

cal use

used immediately as glucose (carbs) or converted into glucose as needed (lipids biotransformed via lipolysis into glycerol => glucose & fatty acids

\-Pyruvate in krebs cycle

note: most organs req insulin for cellular glucose transport

Excess nutrients stored as glycogen (stacked glucose molecules) & triglyercides (adipose)=> weight gain

what organs DONT need insulin for cellular glucose transport

liver, brain, RBCs

BAT

brown adipose tissue

thermogenic organ, for insulation

highest % in term infants => declines

Synthesis: myogenic origin

more similar to skeletal muscle than to WAT

WAT

white adipose tissue

\-SC (SAT) & Visceral (VaT)

* synthesis from pre-adipocytes
* highest % in : obesity, females, elderly

Adipose cells: triglycerides & organelles

Adipose cell energy fx

uptake of excess nutrients

=> biotransformation into triglycerides (3 fatty acids & glycerol)

stores triglycerides

\-release: biotransforms triglycerides into components => 3 fatty acids & glycerol

what hormone controls where fat is stored in the body

estrogen and testosterone

WAT is an endocrine organ:

energy storage. stores >90%. of bodys ‘energy cache’

synthesis & secretion of : leptin (satiety regulation)

adiponectin

cytokines (interleukins, growth factor)

leptin

satiety hormone

BUT IF HIGH WAT=> decreased leptin BBB distribution & receptor binding (resistance)

=> INCREASED hunger signaling

Risk of: arthritis, osteoarthritis, joint deformity, back pain

Adiponectin hormone

homeostasis protective:

* suppresses fatty acid influx into the liver & increases fatty acid oxidation
* Enhances insulin fx
* anti-inflammatory (decreased cytokine & Tcell proliferation

IF HIGH WAT=> decreased adiponectin synthesis & secretion

* increased fatty acid deposition
* insulin resistance
* inflammation (BW- high c reactive protein)

Risk of: pro-inflammatory diseases, cardiac disease, cholecystitis, hyperglycemia & DM 2

cytokine proteins

pro-inflammatory mediators

synthesis in adipose tissue

IF HIGH WAT => Increased lvls due to increased numbers of cytokine synthesizing adipose cells

risk of : inflammatory disease states; atherosclerosis; metabolic alterations leading too insulin resistance

firmicutes

higher in obese pts= higher digestion= > higher absorption of fats

Bacteroidetes

higher in lean pts= lower fat absorption

ass patho for obesity

* depression
* impaired wound healing
* obstructive sleep apnea
* hypercholesterolemua, dyslipidemia (atherosclerosis; cAD, HTN, CVA)
* gastric reflux
* cholecystitis
* metabolic: DM II , hypothyroidism
* urinary incontinence
* arthritis
* osteoarthritis

Drug interactions: lipophillic drugs -increased t1/2 & decreased elimination

Cholecystitis (gallbladder inflammation)

* high fat/ cholesterol intake'
* low oxidation of fatty acids (dt low adiponectin fx)
* pro-inflammatory state dt obesity

Cholecytectomy

surgical excision of gallbladder

* preop & post op pain management
* incision ass/
* risk of clot formation
* Obesity complications

Osteoarthritis (degenerative disorder of articular cartilage)

wear and tear arthritis

fewer joints affected than in RA

risk factors: mechanical stress, obesity, age, gender

what cartilages changes occur during OA

decreased proteoglycans & collagen

=> pro-inflammatory mediator release → further destruction of tissues

=> increased inflammation & increased cartilage tissue destruction => bone to bone articulating surface pain

TX: NSAIDS, glucorticoids

dm II

relative insulin deficiency

NOT autoimmune beta cell destruction

\-strong lifestyle link

strong genetic link

Main causes: increased tissue resistance

(low adiponectin) high cytokines

* insufficient production

DM II tx

Oral antidiabetic agents

Increase beta cell insulin release: drug class **Sulfonylureas**

* Glyburide
* hypoglycemia

Decrease hepatic glucose release: drug class **biguanides**

* metformin

Increase cellular blood glucose uptake: drug class **Thiazolidinediones**

* rosiglitazone
* wt gain

Increase glucose excretion: drug class **SGLT2** inhibitors

* sanagliflozin

Slow GI absorption & centrally decrease appetite: drug class **GL1 receptor agonists**

* dulaglutide, SC injection