Exam 3 Flashcards
1
Q
How are proteins broken down in gut
A
by specific peptidases
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)
3
Q
Issues with metabolism of proteins containing branched chain
A
require special enzymes: defect: maple syrup urine disease
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
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)
6
Q
post translational modifcation of aminos
A
oh-pro, oh-lys, gamma carboxyglutamate
7
Q
Scurvy
A
reduced collagen synthesis due to lack of vit c which is co-factor for lysyl oh-lase
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)
9
Q
protein degradation: intracellular paths(2)
A
Ubq-proteasome
lysosomal pathway
10
Q
transamination
A
occurs via aminotransferases, converts one a-keto acid to its corresponding aa to another a-keto and its aa
11
Q
Pepsinogen cleave by ___
A
Hcl
12
Q
Pepsin is a __peptidase
A
endo
13
Q
Trypsin is cleaved by __
A
enteropeptidase
14
Q
Most zymogens are cleaved by __
A
trypsin
15
Q
Ubq-proteasome is an ATP (in/dependent)means of breaking down proteins
A
dependent (b/c x-linking protein to ubq)
16
Q
Entry points for N in urea cycle (2)
A
Aspartate, free ammonia
17
Q
What is the Keq of transamination
A
1, reversible
18
Q
Direction of transamination depends on __
A
[] of substrates
19
Q
where does urea cycle occur?
A
conversion of ornithine to citrulline occurs in mitochondrion, everything else occurs outside in cytosol
20
Q
regulated step of urea cycle
A
formation of carbamoyl phosphate by carbamoyl phosphatase synthetase I
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
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)
23
Q
difference b/w ketogenic and glucogenic AA’s
A
produces pyruvate or TCA cycle intermediates, keto: acetyl coA or acetoacetate is produced
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
25
Thyroid chem
Thyroid hormone, T4=4 iodines hooked onto 2 tyr (t3 is 3)
26
Sulfur containing AA
met, cys
27
Biologic utility of Cys in regard to its oxidative state (alone or with glutathione)
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
28
Describe Met metabolism, its relation to SAM, and energy provided by SAM
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
29
hyperhomosystinemia
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
30
homocystinuria signs
Mental retardation, osteoporosis, vascular disease result from defect of CBS (cystathione B synthase) (can't convert homocyst to cystathione)
31
cysteinuria
kidney stones, due to defective renal transporter cysteine, ornithine, lysine and arg crystallize in urine, use acetazolamide to make cys more soluble
32
Biologically important molecules derived from Trp
Metabolized into Pyruvate, Acetyl CoA,
BH4 required as a cofactor
1. serotonin 2. melatonin 3. niacin
33
Lead poisoning affects which enzymes
d-aminolevulinate dehyrdratase and ferrochelatase
34
Lead poisoning affects which enzymes
d-aminolevulinate dehyrdratase and ferrochelatase
35
Steps of heme degradation
heme, biliverdin, bilirubin, bilirubindiglucuronide, urobilinogen, stercobilin
36
what is conjungated bilirubin, where is it made
bilidiglucuronide, liver
37
where is stercobilin made
intestine
38
what is the limiting step in jaundice
bilirubin glycuronyltransferase cannot convert bilirubin to bili diglucuronide fast enough
39
Signs of lead poisoning?
LEAD: Lead lines on gingiva, Encephalopathy/erythrocyte basophlic stippling, Abdominal colic/sideroblastic Anemia, wrist and foot Drop
40
Signs of lead poisoning?
LEAD: Lead lines on gingiva, Encephalopathy/erythrocyte basophlic stippling, Abdominal colic/sideroblastic Anemia, wrist and foot Drop
41
sources of atoms in purine and pyrimidine bases, key cofactors, source of energy involved in de novo synthesis
```
Atoms:
N sources: Glutamine, Glycine, Asp, THF
C: CO2
co-factors: AMP, GMP
Energy:
```
42
key differences b/w purine and pyrimidine synth
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 ?)
43
key regulated steps and feedback loops: purine and pyrimidine synth
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)
44
ribose to deoxyribose enzyme, regulation and substrates
ribonucleotide reductase, (-) dATP
45
Major difference b/w carbamoyl phosphatase used in urea cycle vs in pyrimidine synthesis
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
46
Gout: enzyme target for tx
usually a defect of decreased excretion, tx with allopurinol that blocks xanthine oxidase and increases amounts of soluble precursors
47
SCID: enzyme deficient
adenosine deaminase (ADA), thus we get buildup of dATP which then leads inhibition of ribonucleotide reductase
48
Lesch-Nyhan: enzyme deficient
deficiency of HGPRT (active in purine salvage)
49
How 5-FU (and similar) inhibit nucleotide synth
targets thymidylate synthase and folate metabolism
50
Acycylovir
targets viral DNA pol and reverse transcriptase
51
Acroparesthesia, renal failure, proteinuria, angiokeratomas
Fabry
52
Bone pain, hepatosplenomegaly
Gaucher
53
Short stature, hepatosplenomegaly, coarse facial features
Hunter
54
Short stature, hepatosplenomegaly, coarse facial features, corneal clouding
Hurler
55
Cherry red spot, hepatosplenomegaly, foam cells
Niemann Pick
56
severe LVH, high voltage EKG, muscle weakness, sleep apnea
Pompe
57
cherry red spot, increased startle
Tay Sachs
58
muscle cramping, myoglobinuria
McArdle
59
Inheritance of LSDs
autosomal recessive except for fabry and hunter which are x-linked
60
special issues with feeding pt with resp failure
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
61
When to feed?
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)
62
special issues feeding patient with liver failure
Liver: limit protein, salt, and h20 intake (prevent ammonia production and increased fluid retention)
63
special issues feeding patient with renal failure
renal: limit dietary protein (to prevent BUN levels from rising due to protein catabolism)
64
special issues feeding pt with cardiac failure
cardiac: restrict sat fat, Na, fat (restrict overload, restrict energy in overwt pts)
65
special issues feeding patient with diabetes
diabetes: restrict carbs, also could keep diet similar to home diet to avoid changing meds so often
66
Difference b/w cysteine and cystine
cystEine is reduced, cystine is oxidized
67
which amino acid derivative is associated with vascular disease?
homocysteine
68
newborn screening criteria
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
69
succinylacetone in urine
tyrosinemia
70
palmarplantar hyperkeratosis
present in tyrosinemia type II
71
homocysteinuria (duplicate, consolidate)
looks exactly like marfans
| pectus carinatum, myopia, scoliosis, lens dislocation (can't metabolize met, homocysteine), can tx with b6 and betaine
72
most common UCD
ornithin carbamylase deficiency
NO METABOLITE to check for on newborn screening
ammonia is very volatile
dx metabolite: orotic acid
73
at birth: cerebral edema, lethargy, anorexia, hypothermia
urea cycle disorder
74
ehrlenmeyer flask deformity of femur
gaucher's disease finding
75
order of symptomatology in fabry
1. acroparesthesia
2. temp intolerance
3. angiokeratoma
later: renal failure
76
Conditions that place patient at risk for nutritional deficiency
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
4 components of nutrition assessment
1. History
2. Anthropometrics
3. Exam: clinical signs
4. Labs/Biochemical changes/levels
78
nutrient requirement/analysis and how these releated to RDA's
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
BMI calculation
weight in kg/ht in m^2
80
how to initiative and implement dietary and lifestyle counseling
start convo
structure encounter (assess, advise, agree, assist, arrange)
use small steps
use resources
81
key messages behind Dietary Guidelines (DG) (5)
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
Anorexia nervosa
1. restrictive
2. binge/purge
Highest mortality rate of any psychiatric disorder
temperament issues are inherited
83
Vit A: biochem fxn, physiologic metabolic role, dietary source, charac of deficiency
Vision, carrying signal from retina to brain
preformed:liver, dairy, egg
precursor: orange/yellow veg
Night blindness, xerophthalmia
84
Vit D: biochem fxn, physiologic metabolic role, dietary source
maintains intra/extra cellular Ca w/in range
precursor: dehyrocholesterol in skin
D3: fish oil, egg yolk, fortified milk/formula
85
Toxicity clinical features: Vitamin A
Vit A: retinol, vomiting, increased intracranial pressure, headache, bone pain
86
Lab findings of deficiency/insufficiency
Vit A: serum retinol
87
Bitot's spot indicates
Vit A deficiency: heaped up cornea (generally lots of vitamin a flattens the epithelium)
88
Risk of vit D toxicity
granulomatous disease (i.e. sarcoid where these actually activate vit D), vomiting, seizures, naphrocalcinosis, soft tissue calcification (moans, groans, kidney stones)
89
Vit E: biochem fxn, physiologic metabolic role, dietary source, charac of deficiency
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
Vit K: biochem fxn, physiologic metabolic role, dietary source, charac of deficiency
Carboxylation, coagulation
Source: leafy veg, fuits, seeds, synth by intestinal bacteria
prolonged coag time, hemorrhagic dis of newborn
91
Risk of vitamin a deficiency/toxicity
```
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
Toxicity A clinical features
Vit A only PRE-formed (not beta carotene): vomiting, increased intracranial pressure, headache, bone pain
93
Vitamin A and D: Lab findings of deficiency/insufficiency
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
Risk of vit E deficiency, tox
prematurity, fat malab, short gut
| tox: low risk coagulopathy with large dose b/c inhibits vit K
95
Risk of vit K deficiency, tox
def: newborns, breastfed infants, malab, chronic antibiotic use, WORST CASE: hemorrhagic disease of newborn
tox: none?
96
Vit B1: function, source, deficiency finding
coenzyme TPP, source: whole grains, lean pork, legumes
| def: Beri beri (dry, wet, cerebral)
97
other name for b1
thiamin
98
B1: high risk of def/tox in
alcoholics, refeeding, bariatric, nations with hi reliance on refined rice
99
B2: function, source, deficiency finding
FAD, FMN
source: liver, wheat germ, milk
increased vascularization of conj, cheliosis, angular stomatitis, oral-ocular-genital synd
100
B2: high risk of def/tox in
women/infants, Ocps (sub-clinical), eating disorders, chronic dis
tox: none
101
other name for b2
riboflavin
102
b3: function, source
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
b3 deficiency finding /tox findings:
```
def signs: Pellagra, 4D's: dermatitis, dementia, diarrhea, death
tox: vasodilation and flushing
```
104
b3 def risk:
poor intake, corn as staple, malab, etohism, cirrhosis, shunting (excessive serotonin prod will shunt trp away and lead to deficiency), isoniazid, hartnup dis
105
other name for b3
niacin
106
folate: function, source, deficiency finding
1 carbon transfers ie nucleic acid synth, homocys to met conversion
source: foliage
def: NTDs, macrocytic anemia, increased plasma homocysteine
107
folate def/tox high risk
def: pregnant women, goat's milk consumption w/o supplementation, dilantin, sulfalazine, chronic hemolytic anemia/blood loss
tox: none
108
other name for b12
cobalamin
109
folate: function, source, deficiency finding
1 carbon transfers ie nucleic acid synth, homocys to met conversion
source: foliage
def: NTDs, macrocytic anemia, increased plasma homocysteine
110
b12: function, source, deficiency finding
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
b12 risk for def/tox
most commonly inadequate absorption, pernicious anemia, gastric atrophy, stomach/ileum resection, strict vegan, auto-immune conditions
tox: none
112
evaluation for deficiency of b12
elevated methylmalonic acid in deficiency
113
vit c: function, source, deficiency finding
fxn: antioxidant/reducting agent, collagen synth, reduction Fe3+ to Fe2, NE synth
source: fruits, veggies
def: scurvy, petechiae, bleeding gums, anemia, bruising
114
vit c: risk for def/tox
diets lacking in fruits/veggies, low income, smokers, infants fed cow's milk w/o supplementation
115
vit c also known as
ascorbic acid
116
Iron: function, source, factors affecting bioavail
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
Iron: homeostasis, differences in homeostasis b/w trace minerals
regulation occurs at intestine, once absorbed retained very well
118
Iron: etiology/consequences of deficiency, prevalence
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
Iron: toxicity
pro-oxidant, medicinal doses (1-2 gm may be fatal)
120
Zn: function, source, factors affecting bioavail
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
Zn: homeostasis, differences in homeostasis b/w trace minerals
Absorption from diet, excretion for reg. pool
122
Zn: etiology/consequences of deficiency, prevalence
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
Zn: function, source, factors affecting bioavail
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
Zn: etiology/consequences of deficiency, prevalence
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
severe dermatitis, growth failure, diarrhea
acrodermatitis enterohepathica (mutation in enterocyte Zn transporter that is fatal if un-tx)
126
Zn: toxicity
low, can lower HDL cholesterol, impair Fe and Cu absorption
127
Iodine: deficiency consequences
hypothyroidism, goiter, spontaneous abortion, deafness, cretinism, mental retardation
128
Malnutrition: biological causes, clinical consequences
SAM/Marasmus: simple starvation, energy deficiency, fat and muscle wasting
Kwashiorkor: protein deficiency, edematous PEM, related more to metabolic stress and inflammation
129
tx approaches to PEM
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
Malnutrition: biological causes, clinical consequences
SAM/Marasmus: simple starvation, energy deficiency, wt loss, fat and muscle wasting, diarrhea
Kwashiorkor: protein deficiency, edema, psych impairment,, anorexia, assoc infection
131
energy/substrate metabolism in short and long term
?
132
pathophys and adaptive responses to Kwashiorkor
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
ID physical exam findings in kwashiorkor vs marasmus
?
134
pathophys and adaptive responses to Marasmus:
"normal response"
| reduction in energy expenditure, increased mobilization of body fat, muscle catabolism, impaired GI tract fxn
135
flaky paint skin lesions, moon facies, flag sign
kwashiorkor
136
Def of Obesity: BMI and waist circumference
overwt: 25-29 kg/m^2, >30 obese
| waist cirumference: 35 in women, 40 in men
137
medical probs associated with obesity
DM2, dyslipidemia, CAD, sleep apnea, NAFLD
138
metabolic syndrome using AHA/NCEP definition
```
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
Steps in clinical eval of obese patient
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
Role of diet, phys activity and behavioral changes in obesity tx
must have diet AND phys act b/c body will adapt
141
people first language for describing patient with obesity
patient with obesity is patient first rather than "obese patient"
142
amount of phys activity recommended to maintain general health to prevent wt gain, to prvetn wt regain
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
Behaviors that individuals in Nat Wt control reg report help them to maintain a reduced weight
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
Roles of HT (arcuate nucleus)
Stim: neurons that prod NPY, AgRP promote feeding, neurons that prod alpha-MSH, CART promote satiety
145
Role of VMN
stim: feeding cessation
lesion: voracious feeding (oppose it of lateral HT)
146
Role of Lat HT/PVN
stim: voracious eating lesion: aphagia
Peptides MCH and orexins are expressed here and induce feeding
(opposite of VMN)
147
Mech used to promote and inhibit food intake
NPY/AfRP promote feeding while alpha-MSH/CART promote satiety
148
Predict impact of knocking out POMC
Animal will eat more, use less energy (decreased catabolism)
149
Knocking out NPY
animal will eat less, increase its energy expenditure (decrease anabolism)
150
Role of peripheral hormones from GI tract in regulation of food intake
Ghrelin: increases anabolism, decreased catabolism
| Lepin, Insulin: decreased anabolism, increased catbolism
151
Roles of brain reward and environmental cues
opoid agonsim: increased feeding
| serotonin agonism: activation of POMC and wt loss
152
Definitions and classification of childhood weight status, including use of BMI
BMI for age and sex >95% is obese
| 85th-94th %ile is overweight
153
Describe current demographics of child overweight/obesity
17% of children ages 2-19 are obese
| 30% of U.S. children are overweight or obese
154
co-morbidities assoc with childhood obesity
obstructive sleep apnea, obesity hypoventilation syndrome, PCOS, metabolic syndrome, hyper/dys lipidemia, hypertension
155
Key assessments of peds obesity: diet, phys act, fam hx, ROS, PE, labs
```
diet:
phys act: 1+ hour of play per day
fam hx: obesity, CVD, DM2
PE: HTN, acanthosis nigricans, acne, striae, organomegaly
labs: obese
```
156
Essential Tx principles
"Prevention plus": use motivational interviewing, involve the family, clean up the environment
157
Phentermine: MOA, side effects
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
Orlistat: MOA, side effects
Pancreatic lipase inhibitor, blocks absorption of 1/3 of dietary fat
side effects: oily stools, urgency
5% weight loss
159
lorcaserin: MOA, side effects
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
Phentermine/topiramate: MOA/Side effects
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
Naltrexone/bupropion: MOA, SE
MOA: opioid receptor antagonsim, NE reuptake inhibition
SE: SI BLACK BOX WARNING, lowering of seizure threshold, increased pulse/BP,
162
liraglutide: MOA/SE
GLP-1 agonist
| SE: nausea (also is an injection which people don't like)
163
Pro cons of gastric bypass, sleeve gasrectomy, laparacoptic banding , ileal bypass (Roux en y)
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
Vitamin deficiencies
Thiamine (Wernicke korsakoff), D, iron, B12
165
Pro cons of gastric bypass, sleeve gasrectomy, laparacoptic banding , ileal bypass (Roux en y)
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
Pharm pts, vs surgical patients
Pharm: >30 BMI or >27w/ comorbidities
Surg: >40 BMI or >35 with comorbidities
167
Vitamin deficiencies with bariatric surgery
Thiamine (Wernicke korsakoff), D, iron, B12
168
Key elements of effective behavior change counseling
- behavior change must come from pt
- must see reason to change
- pt must feel confident in ability to adopt new behavior
- demonstrate empathy
169
List stages of change/typical responses
```
pre-contemplative
Contemplative
Planning
Action
Manitenance
Relapse
Identification
```
170
primary goal of motivational inteviewing
examination and resolution of ambivalence
171
Values-based
find core values, relate core value to the behavior that you think should be adressed
172
health-belief model
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
Situations where CBT may be appropriate
cases where behavior might be unconconscious or helpful
174
6 mo old breastfed infant, vomiting, ophthalmoplegia, CHF
thiamin
175
5 year old child, only eat burgers w/ bun and milk, now limping and refusing to walk
scurvy
176
Alcoholic, found down, AMS, anemic
Folate deficiency
177
Obese adolescent s/p bariatic surgery, can't walk, falls down
thiamin
178
adult, low SES, chronic diarrhea/malab, rash on arms, hands, neck
niacin
179
SCFE
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
Blount's Disease
repeated injury to medial tibial growth plate, often painless and less obvious than SCFE
