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DEMS > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

How are proteins broken down in gut

A

by specific peptidases

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2
Q

How are proteins broken down in tissues

A

in peripheral tissues, glutamine accepts N from other amino acids and then goes to the liver/kidney where it become glutamate then alphaKG, this is catalyzed by glutamate DH (minor pathway= arginine and production of NO)

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3
Q

Issues with metabolism of proteins containing branched chain

A

require special enzymes: defect: maple syrup urine disease

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4
Q

What makes an amino acid glucogenic vs ketogenic

A

used as substrates for gluconeo vs acetyl coA which then goes through krebs and can make ATP via this cycle or be used for ketone synth

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5
Q

Flow of nitrogen from an amino acid to urea

A

Nitrogen can be put onto glutamate by transamination and then become either ammonia or be moved onto asp (asp will also enter the urea cycle by combining carbamoyl phosphate)

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6
Q

post translational modifcation of aminos

A

oh-pro, oh-lys, gamma carboxyglutamate

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7
Q

Scurvy

A

reduced collagen synthesis due to lack of vit c which is co-factor for lysyl oh-lase

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8
Q

co-factors: enzymes/diseases

Scuvy, glytamyl carboxylase, aminotransferases

A

Vit-c for lysyl oh-lase, Glu to gamma carboxyglutamate is (vik-k) dependent and involved in clotting, aminotransferases: B6 (pyridoxal phosphate)

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9
Q

protein degradation: intracellular paths(2)

A

Ubq-proteasome

lysosomal pathway

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10
Q

transamination

A

occurs via aminotransferases, converts one a-keto acid to its corresponding aa to another a-keto and its aa

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11
Q

Pepsinogen cleave by ___

A

Hcl

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12
Q

Pepsin is a __peptidase

A

endo

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13
Q

Trypsin is cleaved by __

A

enteropeptidase

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14
Q

Most zymogens are cleaved by __

A

trypsin

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15
Q

Ubq-proteasome is an ATP (in/dependent)means of breaking down proteins

A

dependent (b/c x-linking protein to ubq)

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16
Q

Entry points for N in urea cycle (2)

A

Aspartate, free ammonia

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17
Q

What is the Keq of transamination

A

1, reversible

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18
Q

Direction of transamination depends on __

A

[] of substrates

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19
Q

where does urea cycle occur?

A

conversion of ornithine to citrulline occurs in mitochondrion, everything else occurs outside in cytosol

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20
Q

regulated step of urea cycle

A

formation of carbamoyl phosphate by carbamoyl phosphatase synthetase I

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21
Q

Control points of urea cycle

A

carbamoyl phosphate synthetase I in MITOCHONDRIA (note that II is in cytosol)
allosteric (+) n-acetylglutamate (the only one!) indirect indication that a lot of substrate is coming b/c it is made from glu

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22
Q

means of ammonia transport in the blood

A

most tissues use glutamine often “holds” two ammonia groups, muscles instead uses alanine (b/c of pyruvate buildup which can be converted to alanine)

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23
Q

difference b/w ketogenic and glucogenic AA’s

A

produces pyruvate or TCA cycle intermediates, keto: acetyl coA or acetoacetate is produced

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24
Q

MSUD: what is the pathology caused by? how to tx?

A

buildup of leucine, valine, isoleucine products b/c branched chain DH complex is deficient… but only need to exclude leucine b/c it is neurotoxic

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25
Q

Thyroid chem

A

Thyroid hormone, T4=4 iodines hooked onto 2 tyr (t3 is 3)

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26
Q

Sulfur containing AA

A

met, cys

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27
Q

Biologic utility of Cys in regard to its oxidative state (alone or with glutathione)

A

Cys forms disulfide bridges when oxidized, in its free form when it is reduced
when GSH is present, it acts as a chaperone to ensure that correct disulfide bridges form

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28
Q

Describe Met metabolism, its relation to SAM, and energy provided by SAM

A

SAM=S-adenosylmethionine, SAM is major methyl donor and can store energy like ATP
Met becomes SAM when it is activated by ATP, methyl group is then able to move and be donated to other molecules (eventually becomes homocysteine)
Note that you can go from homocys to met backwards using THF
i.e. NE to epi

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29
Q

hyperhomosystinemia

A

Elevated levels of homocysteine and low levels of cysteine b/c homcys can’t be converted into cys, due to low levels of folate, B6 (tx with b6, b12, folate) cysteine an essential AA b/c it can’t be made from Met w/o these AA’s

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30
Q

homocystinuria signs

A

Mental retardation, osteoporosis, vascular disease result from defect of CBS (cystathione B synthase) (can’t convert homocyst to cystathione)

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31
Q

cysteinuria

A

kidney stones, due to defective renal transporter cysteine, ornithine, lysine and arg crystallize in urine, use acetazolamide to make cys more soluble

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32
Q

Biologically important molecules derived from Trp

A

Metabolized into Pyruvate, Acetyl CoA,
BH4 required as a cofactor
1. serotonin 2. melatonin 3. niacin

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33
Q

Lead poisoning affects which enzymes

A

d-aminolevulinate dehyrdratase and ferrochelatase

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34
Q

Lead poisoning affects which enzymes

A

d-aminolevulinate dehyrdratase and ferrochelatase

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35
Q

Steps of heme degradation

A

heme, biliverdin, bilirubin, bilirubindiglucuronide, urobilinogen, stercobilin

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36
Q

what is conjungated bilirubin, where is it made

A

bilidiglucuronide, liver

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37
Q

where is stercobilin made

A

intestine

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38
Q

what is the limiting step in jaundice

A

bilirubin glycuronyltransferase cannot convert bilirubin to bili diglucuronide fast enough

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39
Q

Signs of lead poisoning?

A

LEAD: Lead lines on gingiva, Encephalopathy/erythrocyte basophlic stippling, Abdominal colic/sideroblastic Anemia, wrist and foot Drop

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40
Q

Signs of lead poisoning?

A

LEAD: Lead lines on gingiva, Encephalopathy/erythrocyte basophlic stippling, Abdominal colic/sideroblastic Anemia, wrist and foot Drop

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41
Q

sources of atoms in purine and pyrimidine bases, key cofactors, source of energy involved in de novo synthesis

A 
Atoms: 
N sources: Glutamine, Glycine, Asp, THF 
C: CO2
co-factors: AMP, GMP 
Energy:
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42
Q

key differences b/w purine and pyrimidine synth

A

Pyrimidines (purines)

  1. base ring is synthesized then attached to the ribose
  2. initial nucleotide product is UMP (IMP)
  3. UMP converted to C as a triphosphate (IMP converted to A, G as a ?)
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43
Q

key regulated steps and feedback loops: purine and pyrimidine synth

A

purine: glutamine phosphoribosyl pyrophosphate amidotransferase (first N added to PRPP) activated by: PRPP, (-) AMP, GMP, IMP
Pyrimidine: carbamoyl phosphate synthetase II (activated by PRPP and inhibited by UTP)

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44
Q

ribose to deoxyribose enzyme, regulation and substrates

A

ribonucleotide reductase, (-) dATP

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45
Q

Major difference b/w carbamoyl phosphatase used in urea cycle vs in pyrimidine synthesis

A

urea: CPS I: located in mitochondrial matrix, N source=ammonia, Activated by N-acetyl glutamate
pyr: CPS II: located in cytosol, gamma amide group of glutamine, activated by: ATP, inhibited by UTP

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46
Q

Gout: enzyme target for tx

A

usually a defect of decreased excretion, tx with allopurinol that blocks xanthine oxidase and increases amounts of soluble precursors

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47
Q

SCID: enzyme deficient

A

adenosine deaminase (ADA), thus we get buildup of dATP which then leads inhibition of ribonucleotide reductase

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48
Q

Lesch-Nyhan: enzyme deficient

A

deficiency of HGPRT (active in purine salvage)

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49
Q

How 5-FU (and similar) inhibit nucleotide synth

A

targets thymidylate synthase and folate metabolism

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50
Q

Acycylovir

A

targets viral DNA pol and reverse transcriptase

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51
Q

Acroparesthesia, renal failure, proteinuria, angiokeratomas

A

Fabry

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52
Q

Bone pain, hepatosplenomegaly

A

Gaucher

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53
Q

Short stature, hepatosplenomegaly, coarse facial features

A

Hunter

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54
Q

Short stature, hepatosplenomegaly, coarse facial features, corneal clouding

A

Hurler

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55
Q

Cherry red spot, hepatosplenomegaly, foam cells

A

Niemann Pick

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56
Q

severe LVH, high voltage EKG, muscle weakness, sleep apnea

A

Pompe

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57
Q

cherry red spot, increased startle

A

Tay Sachs

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58
Q

muscle cramping, myoglobinuria

A

McArdle

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59
Q

Inheritance of LSDs

A

autosomal recessive except for fabry and hunter which are x-linked

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60
Q

special issues with feeding pt with resp failure

A

resp: careful of overfeeding b/c more co2 will be produced and more ventilation will be needed however, underfeeding will lead to further resp muscle weakness

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61
Q

When to feed?

A

10-14 days for prev healthy
5-7 days if undernourished and minimal medical illness
3-5 days if undernourished and severe illness
(shorter in infants and children b/c lower stores)

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62
Q

special issues feeding patient with liver failure

A

Liver: limit protein, salt, and h20 intake (prevent ammonia production and increased fluid retention)

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63
Q

special issues feeding patient with renal failure

A

renal: limit dietary protein (to prevent BUN levels from rising due to protein catabolism)

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64
Q

special issues feeding pt with cardiac failure

A

cardiac: restrict sat fat, Na, fat (restrict overload, restrict energy in overwt pts)

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65
Q

special issues feeding patient with diabetes

A

diabetes: restrict carbs, also could keep diet similar to home diet to avoid changing meds so often

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66
Q

Difference b/w cysteine and cystine

A

cystEine is reduced, cystine is oxidized

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67
Q

which amino acid derivative is associated with vascular disease?

A

homocysteine

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68
Q

newborn screening criteria

A

Wilson-junger

  • should be public health concern
  • should have a pre-clinical phase
  • should be treatable
  • test should be acceptable to population
  • natural hx adequately understood
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69
Q

succinylacetone in urine

A

tyrosinemia

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70
Q

palmarplantar hyperkeratosis

A

present in tyrosinemia type II

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71
Q

homocysteinuria (duplicate, consolidate)

A

looks exactly like marfans

pectus carinatum, myopia, scoliosis, lens dislocation (can’t metabolize met, homocysteine), can tx with b6 and betaine

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72
Q

most common UCD

A

ornithin carbamylase deficiency
NO METABOLITE to check for on newborn screening
ammonia is very volatile
dx metabolite: orotic acid

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73
Q

at birth: cerebral edema, lethargy, anorexia, hypothermia

A

urea cycle disorder

74
Q

ehrlenmeyer flask deformity of femur

A

gaucher’s disease finding

75
Q

order of symptomatology in fabry

A
  1. acroparesthesia
  2. temp intolerance
  3. angiokeratoma

later: renal failure

76
Q

Conditions that place patient at risk for nutritional deficiency

A

Young/old
Underweight or recent loss of >10% body wt
Obese with central adiposity/insulin resistance
Protracted losses
Hyper metabolic state
Chronic use of substance with anti-nutrient/catabolic
Marginalized circumstances

77
Q

4 components of nutrition assessment

A
  1. History
  2. Anthropometrics
  3. Exam: clinical signs
  4. Labs/Biochemical changes/levels
78
Q

nutrient requirement/analysis and how these releated to RDA’s

A

EAR: estimated average requirement (adequacy in 50% of people in a life stage or gender GROUP, used as a starting point for RDA
RDA: meets requirements for nearly all INDIVIDUALS

79
Q

BMI calculation

A

weight in kg/ht in m^2

80
Q

how to initiative and implement dietary and lifestyle counseling

A

start convo
structure encounter (assess, advise, agree, assist, arrange)
use small steps
use resources

81
Q

key messages behind Dietary Guidelines (DG) (5)

A
  1. healthy eating pattern
  2. variety, nturient density, amount
  3. limit calories from added sugars and reduce sodium intake
  4. healthier food and beverage choices
  5. Healthy eating patterns for all
82
Q

Anorexia nervosa

A
  1. restrictive
  2. binge/purge
    Highest mortality rate of any psychiatric disorder
    temperament issues are inherited
83
Q

Vit A: biochem fxn, physiologic metabolic role, dietary source, charac of deficiency

A

Vision, carrying signal from retina to brain
preformed:liver, dairy, egg
precursor: orange/yellow veg
Night blindness, xerophthalmia

84
Q

Vit D: biochem fxn, physiologic metabolic role, dietary source

A

maintains intra/extra cellular Ca w/in range
precursor: dehyrocholesterol in skin
D3: fish oil, egg yolk, fortified milk/formula

85
Q

Toxicity clinical features: Vitamin A

A

Vit A: retinol, vomiting, increased intracranial pressure, headache, bone pain

86
Q

Lab findings of deficiency/insufficiency

A

Vit A: serum retinol

87
Q

Bitot’s spot indicates

A

Vit A deficiency: heaped up cornea (generally lots of vitamin a flattens the epithelium)

88
Q

Risk of vit D toxicity

A

granulomatous disease (i.e. sarcoid where these actually activate vit D), vomiting, seizures, naphrocalcinosis, soft tissue calcification (moans, groans, kidney stones)

89
Q

Vit E: biochem fxn, physiologic metabolic role, dietary source, charac of deficiency

A

antioxidant, free radical scavenger, cell memb stabilization
Diet: Polyunsatured veg oil, wheat germ
Charac of def: Neurologic degeneration, hemolytic anemia, speniocerebellar ataxia, hemolytic anemia

90
Q

Vit K: biochem fxn, physiologic metabolic role, dietary source, charac of deficiency

A

Carboxylation, coagulation
Source: leafy veg, fuits, seeds, synth by intestinal bacteria
prolonged coag time, hemorrhagic dis of newborn

91
Q

Risk of vitamin a deficiency/toxicity

A 
low intake(refugee, autistic child w/ restricted diet), fat malab (liver/pancreas), increased requirements (metab/nutrient), drug interactions
tox: too much preformed vit A retinol
92
Q

Toxicity A clinical features

A

Vit A only PRE-formed (not beta carotene): vomiting, increased intracranial pressure, headache, bone pain

93
Q

Vitamin A and D: Lab findings of deficiency/insufficiency

A

Vit A: serum retinol, retinol bp

Vit D: serum 25(OH)vit D <20 ng/ml, rickets at <11 ng/ml (infants exclusively breastfed should get 400 IU per day, adults 600, 800 IU elderly)

94
Q

Risk of vit E deficiency, tox

A

prematurity, fat malab, short gut

tox: low risk coagulopathy with large dose b/c inhibits vit K

95
Q

Risk of vit K deficiency, tox

A

def: newborns, breastfed infants, malab, chronic antibiotic use, WORST CASE: hemorrhagic disease of newborn
tox: none?

96
Q

Vit B1: function, source, deficiency finding

A

coenzyme TPP, source: whole grains, lean pork, legumes

def: Beri beri (dry, wet, cerebral)

97
Q

other name for b1

A

thiamin

98
Q

B1: high risk of def/tox in

A

alcoholics, refeeding, bariatric, nations with hi reliance on refined rice

99
Q

B2: function, source, deficiency finding

A

FAD, FMN
source: liver, wheat germ, milk
increased vascularization of conj, cheliosis, angular stomatitis, oral-ocular-genital synd

100
Q

B2: high risk of def/tox in

A

women/infants, Ocps (sub-clinical), eating disorders, chronic dis
tox: none

101
Q

other name for b2

A

riboflavin

102
Q

b3: function, source

A

NAD, NADP
source: meat, peanut butter, legume, trp is precursor (diet w/ liberal milk/eggs likely to allow for conversion if preformed is insufficient)

103
Q

b3 deficiency finding /tox findings:

A 
def signs: Pellagra, 4D's: dermatitis, dementia, diarrhea, death 
tox: vasodilation and flushing
104
Q

b3 def risk:

A

poor intake, corn as staple, malab, etohism, cirrhosis, shunting (excessive serotonin prod will shunt trp away and lead to deficiency), isoniazid, hartnup dis

105
Q

other name for b3

A

niacin

106
Q

folate: function, source, deficiency finding

A

1 carbon transfers ie nucleic acid synth, homocys to met conversion

source: foliage
def: NTDs, macrocytic anemia, increased plasma homocysteine

107
Q

folate def/tox high risk

A

def: pregnant women, goat’s milk consumption w/o supplementation, dilantin, sulfalazine, chronic hemolytic anemia/blood loss
tox: none

108
Q

other name for b12

A

cobalamin

109
Q

folate: function, source, deficiency finding

A

1 carbon transfers ie nucleic acid synth, homocys to met conversion

source: foliage
def: NTDs, macrocytic anemia, increased plasma homocysteine

110
Q

b12: function, source, deficiency finding

A

fxn: 1-c transfers, metabolism of odd-# chain FA’s, re-form THF from methylfolate, isomerization of methylmalonyl coA to succinyl coA
source: animal products only!

111
Q

b12 risk for def/tox

A

most commonly inadequate absorption, pernicious anemia, gastric atrophy, stomach/ileum resection, strict vegan, auto-immune conditions
tox: none

112
Q

evaluation for deficiency of b12

A

elevated methylmalonic acid in deficiency

113
Q

vit c: function, source, deficiency finding

A

fxn: antioxidant/reducting agent, collagen synth, reduction Fe3+ to Fe2, NE synth
source: fruits, veggies
def: scurvy, petechiae, bleeding gums, anemia, bruising

114
Q

vit c: risk for def/tox

A

diets lacking in fruits/veggies, low income, smokers, infants fed cow’s milk w/o supplementation

115
Q

vit c also known as

A

ascorbic acid

116
Q

Iron: function, source, factors affecting bioavail

A

oxygen transport in blood, electron transport enzymes
Source: heme: cellular animal protein
non-heme: legumes, nuts, whole grains
factors affecting bioavail: dietary factors may form insoluble complexes, phytate, tannins, phosphate, oxalate, ascorbic acid increases reduced form which is more absorbable, interaction with Zn or Cu decreases absorption

117
Q

Iron: homeostasis, differences in homeostasis b/w trace minerals

A

regulation occurs at intestine, once absorbed retained very well

118
Q

Iron: etiology/consequences of deficiency, prevalence

A

MOST common nutrient def globally, infants > 6mo, premature infants, adolescents, pregnant somen, chronic infections, bariatric surg, RARE in men or post-menopausal women (may be bleeding)

119
Q

Iron: toxicity

A

pro-oxidant, medicinal doses (1-2 gm may be fatal)

120
Q

Zn: function, source, factors affecting bioavail

A

growth and prolif +immmune fxn, (regulation of gene exp, structural roles and membrane stability, metalloenzymes)

source: animal products
bioavail: absorb impaired by phytate, absorb does NOT increase in cases of deficiency

121
Q

Zn: homeostasis, differences in homeostasis b/w trace minerals

A

Absorption from diet, excretion for reg. pool

122
Q

Zn: etiology/consequences of deficiency, prevalence

A

same as iron plus GI/illness diarrhea, wounds/burns (b/c needed for synth of new tissue)
deficiency consequences; growth delay, stunting, dermatitis (acrodermatitis enteropathica)

123
Q

Zn: function, source, factors affecting bioavail

A

growth and prolif +immmune fxn, (regulation of gene exp, structural roles and membrane stability, metalloenzymes)

source: animal products
bioavail: absorb impaired by phytate, absorb does NOT increase in cases of deficiency

124
Q

Zn: etiology/consequences of deficiency, prevalence

A

same as iron plus GI/illness diarrhea, wounds/burns (b/c needed for synth of new tissue)
deficiency consequences; growth delay, stunting, dermatitis
prevalence: widespread esp in those that have diet rich in phytate

125
Q

severe dermatitis, growth failure, diarrhea

A

acrodermatitis enterohepathica (mutation in enterocyte Zn transporter that is fatal if un-tx)

126
Q

Zn: toxicity

A

low, can lower HDL cholesterol, impair Fe and Cu absorption

127
Q

Iodine: deficiency consequences

A

hypothyroidism, goiter, spontaneous abortion, deafness, cretinism, mental retardation

128
Q

Malnutrition: biological causes, clinical consequences

A

SAM/Marasmus: simple starvation, energy deficiency, fat and muscle wasting
Kwashiorkor: protein deficiency, edematous PEM, related more to metabolic stress and inflammation

129
Q

tx approaches to PEM

A
  1. resolve life threatening cond: restore circulation, give K avoid Na, avoid hypoglycemia
  2. Restore nutritional status without abruptly disrupting homeostasis: small, frequent feeds q<4hr, protein and fat
  3. Ensuring nutritional rehab, AFTER edema resolves
130
Q

Malnutrition: biological causes, clinical consequences

A

SAM/Marasmus: simple starvation, energy deficiency, wt loss, fat and muscle wasting, diarrhea
Kwashiorkor: protein deficiency, edema, psych impairment,, anorexia, assoc infection

131
Q

energy/substrate metabolism in short and long term

A

?

132
Q

pathophys and adaptive responses to Kwashiorkor

A

Kwashiorkor: failure of adaptie rsponse of protein sparing that is normally seen in fasting
response; hypoalbuminemia, increased memb perm, impaired Na/K homeostatis, hypotransferrinemia, immune impairment

133
Q

ID physical exam findings in kwashiorkor vs marasmus

A

?

134
Q

pathophys and adaptive responses to Marasmus:

A

“normal response”

reduction in energy expenditure, increased mobilization of body fat, muscle catabolism, impaired GI tract fxn

135
Q

flaky paint skin lesions, moon facies, flag sign

A

kwashiorkor

136
Q

Def of Obesity: BMI and waist circumference

A

overwt: 25-29 kg/m^2, >30 obese

waist cirumference: 35 in women, 40 in men

137
Q

medical probs associated with obesity

A

DM2, dyslipidemia, CAD, sleep apnea, NAFLD

138
Q

metabolic syndrome using AHA/NCEP definition

A 
abdominal obesity plus 3 of 5: 
waist circumference >102cm men or >88cm women
TG's: > 150*
HDL: <40 men, <50 women*
BP; >130/85*
fasting blood gluc: >100* 
*or on drug tx fo this problem
139
Q

Steps in clinical eval of obese patient

A
  1. measure degree of adiposity
  2. assess other existing risk factor for CVD
  3. screen for complications of obesity
  4. asses for dietary, behavioral, and social factors contributing
  5. assess readiness for tx
140
Q

Role of diet, phys activity and behavioral changes in obesity tx

A

must have diet AND phys act b/c body will adapt

141
Q

people first language for describing patient with obesity

A

patient with obesity is patient first rather than “obese patient”

142
Q

amount of phys activity recommended to maintain general health to prevent wt gain, to prvetn wt regain

A

to prevent regain: 30 mins strenouos activity and 60 mins moderate physical activity (or more b/c threshold is increased in wt reduced people)

143
Q

Behaviors that individuals in Nat Wt control reg report help them to maintain a reduced weight

A
  1. moderately low fat, high carb diet
  2. frequent self-monitoring
  3. eating breakfast
  4. large amounts of physical activity
  5. Limiting TV viewing
144
Q

Roles of HT (arcuate nucleus)

A

Stim: neurons that prod NPY, AgRP promote feeding, neurons that prod alpha-MSH, CART promote satiety

145
Q

Role of VMN

A

stim: feeding cessation
lesion: voracious feeding (oppose it of lateral HT)

146
Q

Role of Lat HT/PVN

A

stim: voracious eating lesion: aphagia
Peptides MCH and orexins are expressed here and induce feeding
(opposite of VMN)

147
Q

Mech used to promote and inhibit food intake

A

NPY/AfRP promote feeding while alpha-MSH/CART promote satiety

148
Q

Predict impact of knocking out POMC

A

Animal will eat more, use less energy (decreased catabolism)

149
Q

Knocking out NPY

A

animal will eat less, increase its energy expenditure (decrease anabolism)

150
Q

Role of peripheral hormones from GI tract in regulation of food intake

A

Ghrelin: increases anabolism, decreased catabolism

Lepin, Insulin: decreased anabolism, increased catbolism

151
Q

Roles of brain reward and environmental cues

A

opoid agonsim: increased feeding

serotonin agonism: activation of POMC and wt loss

152
Q

Definitions and classification of childhood weight status, including use of BMI

A

BMI for age and sex >95% is obese

85th-94th %ile is overweight

153
Q

Describe current demographics of child overweight/obesity

A

17% of children ages 2-19 are obese

30% of U.S. children are overweight or obese

154
Q

co-morbidities assoc with childhood obesity

A

obstructive sleep apnea, obesity hypoventilation syndrome, PCOS, metabolic syndrome, hyper/dys lipidemia, hypertension

155
Q

Key assessments of peds obesity: diet, phys act, fam hx, ROS, PE, labs

A 
diet: 
phys act: 1+ hour of play per day 
fam hx: obesity, CVD, DM2
PE: HTN, acanthosis nigricans, acne, striae, organomegaly
labs: obese
156
Q

Essential Tx principles

A

“Prevention plus”: use motivational interviewing, involve the family, clean up the environment

157
Q

Phentermine: MOA, side effects

A

structurally similar to amphetamine, increases NE levels, acts centrally to increase satiety and thus decrease intake
5-8% wt loss, only approved for 3 months
Side effects: nervousness, difficulty sleeping, headache, dry mouth, increase in BP/pulse

158
Q

Orlistat: MOA, side effects

A

Pancreatic lipase inhibitor, blocks absorption of 1/3 of dietary fat
side effects: oily stools, urgency
5% weight loss

159
Q

lorcaserin: MOA, side effects

A

selective serotonin 2c receptor agonist

Side effects: LEAST of all wt loss drugs, previous iterations had cardiac valve issues, this one theoretically does not

160
Q

Phentermine/topiramate: MOA/Side effects

A

MOA: phentermine acts similarly to amphetamines, top: blocks VG dependent NaC, increases GABA activity by allosteric binding to GABA-a-rec

Side effects; dry mouth, paresthesias, insomnia, dizziness, anxiety, irritability, disturbance of attention, birth defects with topiramate

161
Q

Naltrexone/bupropion: MOA, SE

A

MOA: opioid receptor antagonsim, NE reuptake inhibition
SE: SI BLACK BOX WARNING, lowering of seizure threshold, increased pulse/BP,

162
Q

liraglutide: MOA/SE

A

GLP-1 agonist

SE: nausea (also is an injection which people don’t like)

163
Q

Pro cons of gastric bypass, sleeve gasrectomy, laparacoptic banding , ileal bypass (Roux en y)

A

lap band least effective, BPD most

Band: subject to mechanical failure or slippage

Sleeve: doesn’t need adjustment, doesn’t have vitamin deficiencies that you get with the roux en y

Biliary pancreatic diversion: greatest weight loss but highest risk of nutritional deficiencies

164
Q

Vitamin deficiencies

A

Thiamine (Wernicke korsakoff), D, iron, B12

165
Q

Pro cons of gastric bypass, sleeve gasrectomy, laparacoptic banding , ileal bypass (Roux en y)

A

Pros: lap band least effective, BPD most
DM2 may resolve with all types of surgery

Cons: Band: subject to mechanical failure or slippage

Sleeve: doesn’t need adjustment, doesn’t have vitamin deficiencies that you get with the roux en y

Biliary pancreatic diversion: greatest weight loss but highest risk of nutritional deficiencies

166
Q

Pharm pts, vs surgical patients

A

Pharm: >30 BMI or >27w/ comorbidities
Surg: >40 BMI or >35 with comorbidities

167
Q

Vitamin deficiencies with bariatric surgery

A

Thiamine (Wernicke korsakoff), D, iron, B12

168
Q

Key elements of effective behavior change counseling

A
  • behavior change must come from pt
  • must see reason to change
  • pt must feel confident in ability to adopt new behavior
  • demonstrate empathy
169
Q

List stages of change/typical responses

A 
pre-contemplative 
Contemplative 
Planning 
Action 
Manitenance 
Relapse 
Identification
170
Q

primary goal of motivational inteviewing

A

examination and resolution of ambivalence

171
Q

Values-based

A

find core values, relate core value to the behavior that you think should be adressed

172
Q

health-belief model

A

behavior change occurs when sees the need for change, has believes tx proposed are effective, needs a compelling case and know that they can perform what is being proposed

173
Q

Situations where CBT may be appropriate

A

cases where behavior might be unconconscious or helpful

174
Q

6 mo old breastfed infant, vomiting, ophthalmoplegia, CHF

A

thiamin

175
Q

5 year old child, only eat burgers w/ bun and milk, now limping and refusing to walk

A

scurvy

176
Q

Alcoholic, found down, AMS, anemic

A

Folate deficiency

177
Q

Obese adolescent s/p bariatic surgery, can’t walk, falls down

A

thiamin

178
Q

adult, low SES, chronic diarrhea/malab, rash on arms, hands, neck

A

niacin

179
Q

SCFE

A

Slipped capital femoral epiphysis, a manifestation of obesity that presents with hip, groin or knee pain with leg held in external rotation, more likely to progress to bilat dis in obese

180
Q

Blount’s Disease

A

repeated injury to medial tibial growth plate, often painless and less obvious than SCFE

DEMS (5 decks)

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