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SUM '20 - Pharm II > Week 3 Nutrition Vitamins & Herbs > Flashcards

Week 3 Nutrition Vitamins & Herbs Flashcards

1
Q

Enteral Nutrition:

A

Providing nourishment to a patient delivered directly into the GI tract.

(NG; Nasointestinal tube, Gastrostomy Tube, Jejunostomy Tube)

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2
Q

Parenteral Nutrition:

A

Delivery of nutrients directly into the venous circulation

Peripheral vein or Central Vein

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3
Q

Total Parenteral Nutrition (TPN):

A

used when the only source of nutrition supply is via the parenteral route.

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4
Q

what do you do with TPN during the surgical period?

A

TPN should be continued during the peri-op period

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5
Q

Enteral nutrition should be D/C’ed

A

~ 6 hours before surgery

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6
Q

if a pt was receiving enteral feeding and they have high residuals or it’s an emergent case, what would we do?

A
  • full stomach = RSI

- if not emergent, may want to wait?

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7
Q

prior to surgery, in pts receiving nutritional support, we should ensure we have what on them prior to surgery?

A

blood glucose

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8
Q

_ supplies all the essential inorganic and organic nutritional elements necessary

A

to maintain optimal body composition.

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9
Q

Alimentation by the GI tract (enteral nutrition) is preferred to what ? why?

A
  • IV alimentation (parenteral nutrition)

- because it is more physiologic

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10
Q

Enteral Nutrition does what two things:

A
  1. Nutrients that stimulate trophic factors (gastrin, cholecystokinin, bombesin) released from the lumen maintaining gut integrity
  2. Maintains absorptive activity of the small intestine
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11
Q

Nutrients that stimulate trophic factors are released from the lumen to maintain gut integrity.

what are these trophic factors?

A

“BCG”

  • bombesin – “BOMB”
  • cholecystokinin — “CHOLE”
  • gastrin, , “GAS”
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12
Q

These factors (trophic) reduce the translocation of bacteria from the GI tract and promote development of IgA-producing immunocytes which reside in the

A

gut associated lymphoid tissue (GALT)

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13
Q

what is more important than the amt of nutrition provided?

A

the ROUTE.

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14
Q

Enteral protein intake in injured pts correlates with

A

outcome

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15
Q

Even if caloric and nitrogen requirements can’t be met with luminal nutrition what should be done?

A

the enteral route should be used unless contraindicated.

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16
Q

enteral route contraindications:

A
  1. Bowel obstruction
  2. Inadequate bowel surface area
  3. Intractable diarrhea
  4. Short gut syndrome*
  5. Circulatory shock
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17
Q

why do we care (anesthesia) about the use of enteral feedings?

A
  • electrolytes

- hydration status

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18
Q

If it is contraindicated and the pt is not malnourished or severely stressed, then parenteral nutrition is not necessary for the first week following surgery or ICU admission b/c …

A

it has not been shown to be of benefit

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19
Q

what technique(s) has not been shown to improve outcomes to meet nutritional requirements in pts?

A

Simultaneous enteral and parenteral routes

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20
Q

Indications For Use of Nutritional Support

Table 36-1 pg 717:

A
  • well nourished, minimally stressed pts unable to eat for 7-10 days.
  • major elective surgery in severely malnourished
  • major trauma (blunt, penetrating, head injuries)
  • burns
  • hepatic dysfunction
  • renal dysfunction
  • BM transplant recipients undergoing intense chemo
  • pts unable to eat/absorb nutrients for an indefinite period of time (neuro, pharyngeal, short bowl)
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21
Q

tpn is indicated in the well nourished, minimally stressed pts unable to eat for ___.

A
  • 7-10 days.
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22
Q

Patients who are not expected to resume adequate oral feedings within 7-10 days of surgery should begin nutritional support within

A

2-4 days postop and within 1-2 days if they are in ICU.

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23
Q

Severe Injuries; burns; and those pts with sepsis often are hypermetabolic may benefit from nutritional support within

A

24-48 hours of admission.

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24
Q

Severe Burns:

Energy requirements

A

may double

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25
Q

Severe Burns:

Protein requirements

A

may triple

** very important. d/t loss of albumin.

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26
Q

in burn pts, the increased loss of albumin impacts us(anesthesia) how?

A
  • lost of protein
  • less protein for meds to bind to
  • increases r/o toxicity (doses need to adjust)
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27
Q

Major Uncomplicated Elective Surgery:

Increase in basal metabolic rate occurs soon after the surgery but is less than (%)?

A

10%

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28
Q

Providing glucose solutions in postop period is sufficient – about what amount/day?

A

(~ 500 kcal/day)

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29
Q

Stressed Patients in order to remain in nitrogen and energy equilibrium.

Minimally Stressed pts (ca/kg and g/kg for protein):

A

25-30 ca/kg and 1 g/kg of protein daily

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30
Q

Stressed Patients in order to remain in nitrogen and energy equilibrium:

Moderately to Severely Stressed: (cal/kg)

A

Resuscitated first and then started on a hypocaloric regimen (20 cal/kg) until stress response abates

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31
Q

what route is preferred nutritionally speaking?

A

enteral nutrition

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32
Q

Early Nutrition Support is Proactive Therapy. what has been shown to be of benefit to early nutritional support? (4)

A
  • Reduce disease severity
  • Diminish complications
  • Decrease length of stay in ICU
  • Favorably impact pt outcome after severe injury
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33
Q

Carbohydrates can be a source of:

% calories and osmolarity effects

A
  • 90% of the calories.

- increases the osmolarity of these solutions.

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34
Q

Fat an be a source of:

calories and osmolarity effects

A
  • Fat has a higher caloric density than carbohydrates

- DOES NOT increase the osmolarity of the formula as much as carbohydrates

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35
Q

Formulas containing a normal range of fat content ~ 30% are preferred unless:

A

Maldigestion
Malabsorption
Still may try medium chain triglycerides

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36
Q

entreral formulas containing ______, specifically when administered to pts w/burns, reduced hospital and icu LOS, primarily through a reduction in _____.

A
  • glutamine
  • infection

pg 717.

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37
Q

Selection of a formula that provides sufficient total nitrogen as protein or amino acids is essential for all patients.

recommendation for g/protein per kg/day?

A

(1-1.5 g protein per kg/day)

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38
Q

Enteral Feedings are stopped for:

A 
c/o bloating or distention
High gastric residuals (200 – 250 ml)
Diarrhea
Reduced passage
Absence of flatus
Do not stop feedings for gastric residual volume of less than 500 ml in absence of other signs/symptoms

*surgeons preference on residuals

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39
Q

a danger with enteral feedings?

what to do to prevent?

A

Pulmonary aspiration is always a danger with enteral tube feedings:

Maintain in semi-sitting position (HOB > 30 degrees) ; semi-fowlers

In pts at highest risk of aspiration the feeding tube should be placed through the pylorus

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40
Q

In pts at highest risk of aspiration the feeding tube should be placed

A

through the pylorus

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41
Q

Short Term parenteral therapy:

A
  • 3-5 days in pts without nutritional deficits
  • Glucose solutions (5%, to 10%) with supplemental Na+, chloride, and other electrolytes are commonly administered for short-term therapy
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42
Q

Approx ______grams of glucose maintains brain and erythrocyte metabolism and decreases protein catabolism from skeletal muscles and viscera

A

150 g

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43
Q

Approx 150 g of glucose maintains

A
  • brain and erythrocyte metabolism

- decreases protein catabolism from skeletal muscles and viscera

44
Q

concerns/things we should do with Long Term TPN:

A
  1. labs should be measured periodically during use:
    - Serum electrolytes,
    - blood glucose and
    - BUN
    - Hepatic and Renal functions are recommended by less frequent
  2. Infections: Catheter related sepsis is one of the most common and is associated with significant morbidity.
  3. Mechanical: pneumothorax and thrombosis for catheters left in for extended periods of time
45
Q

metabolic complications of parenteral nutrition:

Early Complications
See Table 36-2

A
  • Vol overload
  • Hyperglycemia
  • Hyperchloremic acidosis
  • Hypophoshatemia (refeeding syndrome)
  • Hypokalemia
  • Hypomagnesemia

“VHHHHH” — “V-5H’s”

46
Q

metabolic complications of parenteral nutrition:

Late Complications
See Table 36-2

A
  • Hepatic steatosis
  • Hepatic chlestasis
  • Metabolic bone disease
  • Trace mineral deficiency
  • Vitamin deficiency

“MTV-HH” …. MTV-H.appy H.hour

47
Q

one of the most common and is associated with significant morbidity.

A

Catheter related sepsis

48
Q

mechanical complications of parenteral therapy:

A

pneumothorax and thrombosis

-from catheters left in for extended periods of time

49
Q

What is best source of vitamins and healthy persons consuming an adequate balanced diet will not benefit from supplemental vitamins.

A

Food

50
Q

Use of _____ vitamin are discouraged and should not be used as a substitute for vitamin rich foods

A

megadose

51
Q

Those most likely not to eat balanced diets include:

A

Alcoholics
Malabsorbtion syndromes
Elderly
Economically disadvantaged

Amee (like Amy)

52
Q

vit b complexes solubility?

A

water soluble

53
Q

deficiency in this vitamin can lead to teratogenicity, hepatotoxicty, and cerebral edema

A

vitamin A

54
Q

Vit K is responsible for:

A

synthesis of clotting factors VII, IX, X (7, 9, 10)

55
Q

night blindness results from deficiency of

A

vitamin a

56
Q

magaloblastic anemia and peripheral neuropathies are associated with deficiency in what ?

A

vitamin b12 (pantothenic acid)

57
Q

name the fat soluble vitamins

A

DEAK

58
Q

Vitamin A is stored where in a healthy person?

A

liver

59
Q

Important for retina, integrity of mucosal and epithelial surfaces, bone development and growth, reproduction and embryonic development

A

vitamin A

60
Q

Symptoms of Deficiency of Vitamin A:

A

Early s/s can be overlooked:
-skin lesions (follicular hyperkeratosis) and infections are early signs

  • Increase in pulmonary infections and keratinization of epithelial cells as mucous in bronchial epithelial decrease
  • Urinary calculi are frequent as well as reproductive abnormalities
61
Q

Most vit A deficiencies occur in

A

infants and children

62
Q

Most recognizable manifestation of vitamin A deficiency is

A

is night blindness (nyctalopia)

63
Q

less than ___ micrograms/dL are at risk of vitamin a deficiency

A

less than 20 micrograms/dL

64
Q

HYPERVITAMINOSIS A -

Toxic syndrome from excessive ingestion of vitamin A particularly in children
Typically from overzealous prophylactic use of Vitamin A.

diagnostic plasma level=
Tx?

A

Diagnostic is plasma concentration of
> 300 mcg/dL

Treatment: withdrawal of vitamin source.

S/S should dissipate in 7 days

65
Q

Early Signs of Vit. A Intoxication:

A

Irritability
Vomiting
Dermatitis

Fatigue, myalgia, loss of body hair, diplopia, nystagmus*, gingivitis, stomatitis, and lymphadenopathy have been observed.

Hepatosplenomegaly accompanied by cirrhosis of the liver, portal vein hypertension and ascites.

66
Q

Hypervitaminosis A may also mimic a brain tumor with what s/s?

A

Intracranial pressure and neurologic symptoms including papilledema may mimic brain tumor

-Diagnosis is confirmed by radiologic demonstration of hyperostosis underlying tender swellings on the extremities and the occipital region of the head.

Plasma alkaline phosphatase concentrations are increased, reflecting osteoblastic activity.

67
Q

(in vit A deficiencies) Hypercalcemia may occur due to bone destruction. Bone grow in length but not in thickness.

What might this lead to?

A
  • weaker bones
  • more prone to break
  • if have bone dx makes your bones brittle
  • osteogenesis imperfecta
68
Q

Vit D comes in 2 forms. What are they and how do we get it?

A
  1. D2 comes from diet and
  2. D3 is synthesized in the skin by UV light’s action on 7-dehydrocholesterol

D2 and D3 are metabolically inert and require two chemical reactions to acquire activity (read on pg 727)

69
Q

Calcitriol primary function is to

A

maintain calcium and phosphorous homeostasis.

70
Q

Calcium levels are maintained through 3 mechanisms:

A
  1. Absorption of calcium in the duodenum and jejunum
  2. Release of calcium from bone
  3. Increase uptake of calcium in the distal tubule of the kidney
71
Q

calcium is inversely relational to

A

phosphate

72
Q

Low levels of Phosphate: calcitriol increases

A
  • its absorption in the small intestine or
73
Q

when phosphate levels are high calcitriol acts on

A
  • osteocytes to release fibroblast growth factor 23

- which increases loss of phosphorous in the renal distal tubule.

74
Q

Vit. D Deficiency: Results in decreased plasma concentrations of calcium and phosphate ions, with the subsequent stimulation of

A

parathyroid hormone secretion.

75
Q

In Adults, Anticonvulsant therapy with PHENYTOIN increases target organ resistance to vitamin D resulting in an increase incidence

A

of rickets and osteomalacia

76
Q

Parathyroid hormone acts to restore plasma calcium concentrations at the expense of

A

bone calcium

77
Q

Vit. D Deficiency In infants and children: failure to mineralize newly formed osteoid tissue and cartilage thus causes

A

soft bone formation and weight bearing causing deformities known as rickets

78
Q

anticonvulsant medication associated with vit D deficiency

A

phenytoin

79
Q

Hypervitaminosis D Manifests as :

A 
hypercalcemia, 
skeletal muscle weakness, 
fatigue,
headache, and 
vomiting
80
Q

tx of vit D toxicity:

A

stop vitamin D

  • increase fluid intake
  • administer corticosteriods
81
Q

Early impairment of renal function from hypercalcemia manifests as:

A
  • polyuria,
  • polydipsia,
  • proteinuria, and
  • decreased urine concentration ability
82
Q

epidemiologic studies have provided evidence of an inverse relationship b/w CAD and antioxidant intake (Vit E inparticular). This association has been attributed to the finding that antioxidants prevent oxidation of lipids in LDL’s. It is proposed that oxidation of lipids in LDL (lipid peroxidation) initiates the process of .

A

atherogenesis

pg 728

83
Q

vit E requirements may be increased in individuals exposed to high oxygen environments or in those receiving

A
  • therapeutic dose of iron or

- large doses of thyroid hormone replacement.

84
Q

required for normal blood clotting

A

vitamin k

85
Q

forms of vitamin K are:

A
  1. Vit K1: phytonadione

2. Vit K2

86
Q

is the only natural form of Vitamin K available for therapeutic use

A

Phytonadione (Vitamin K1): variety of food contain K1 and

87
Q

what vitamin is synthesized by gram positive bacteria in GI tract

A

Vitamin K2:

88
Q

what % of Vit K is synthesized and what % is required in diet?

A

50:50

Synthesis of vitamin K provides approx. 50% of estimated daily requirement of vitamin K the other 50% supplied by diet

89
Q

Vitamin K accumulates in the

A

Liver, Lung and spleen but

90
Q

what’s needed to absorb vit k?

A

-adequate bile salts

absorbed in the GI tract

91
Q

can we store vitamin k?

A

significant amounts are not stored in the body for prolonged periods of time

92
Q

MOA of Vitamin K

A

vit k functions as an essential cofactor for teh hepatic microsomal enzyme that converts Glutamic acid residues to Y(gamma)-carboxyglutamic acid residues in Factors II, VII, IX, and X.

the acid residues make it possible for these coagulation factors to bind to Ca adn attach to phospholipid surfaces for clot formation.

93
Q

clinical uses of phytonadione

A
  • preferred drug to tx hypoprothrombinemia (neonate)

- reversal of oral anticoagulants

94
Q

clinical use of menadione

A
  • same actions as phytonadione.
  • water soluble salts do not require bile salts for systemic absorption after PO administration.

**this is important when malabsorption of vit K is due to Biliary obstruction

95
Q

vitamin k supplementation is indicated in pts receiving prolonged

A

TPN

especially if abx are concomitantly administered

96
Q

in non emergent reversal of oral anticoagulants, what is the preferred method of phytonadione administration?

why?

A

Oral and IM

  • less likely than IV to casue SE’s
  • even large doses are ineffective against heparin induced anticoagulation
97
Q

IV injections of phytonadione may cause:

A

life threatening allergic reactions

  • hypotension
  • bronchospasm

IM injection may cause local hemorrhage in hypoprothrombinemic pts.

98
Q

in neonates, doses of phytonadione greater than 1 mg may cause

A

hemolytic anemia

– increase the plasma concentration of unbound bilirubin thus increasing risk of kernicterus.

99
Q

the occurrence of hemolytic anemia in some neonates reflects a deficiency of

A

glycolytic enzymes

100
Q

vit k activity is assessed by monitoring

A

PT - prothrombin time

101
Q

menadione is not used in

A

hemorrhagic disease of the neonate

102
Q

large amts of menadione or phytonadione may depress

A

liver function

*esp in the presence of liver dx

103
Q

Estimated 25% of pts use alternative therapies characterized as

A

dietary supplements.

104
Q

the most serious SE’s associated with dietary supplements include:

A
  • CV instability
  • Bleeding tendency
  • Delayed awakening from anesthesia
105
Q

ephedra (ma huang) is a stimulant common in many weight loss products, decongestans and bronchodilators.

Structurally like sympathomimetic amphetamine.

Serious adverse reactions include:

A 
HTN
Cardiac arrhythmias
Prolonged QTc
MI
CVA
death

**chances of AR are estimated to be 100-fold greater than any other supplement or herbal remedy.

— reason for FDA ban

106
Q

Warfarin interactions:

A

-ginseng - decreases effects

effects may be enhanced

  • ginkgo
  • garlic
  • ginger
107
Q

supplements that may delay awakening from anesthesia

A

valerian
kava-kava
-st.jonhs wort (possibly)

by prolonging sedative effects of anesthetic drugs

SUM '20 - Pharm II (30 decks)

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