SCAT MAN

with dr byrd

whats a comordbiity? is obesity a comorbidity

comob: associated with a disease state, not necessarily a complication

NO obesity is a chorinc disase (a state in itself)

management of dumping syndrome

avoid high sugar, high osmolar food

drinking fluids separately from meals

acarbose— prevent carb absorption

which glp specifically for OSA

tirzepatide

do bariatric pts have shorter or longer onset of action

shorter— can have increased absorption bc less stomach preventive factors

what happens to ER formulations in gastric bypass

reduced bioavailablity bc less stomach to travel through

etiology of obesity

genetics— fat distribution

epigenetics

obesity-promoting culture

pharm agents for binge eating disorder

topiramate

GLP-1 agonists

SSRIs

lisdexamfetamine is only FDA approved choice

what guideline defined obesity as a disease

2017-18 ASBP obesity algorithm

ama definition of a disease

1. An impairment of the normal functioning of some aspect of the body

2. • Characteristic signs or symptoms

3. • Harm or morbidity

what is morbidity

affecting quality of life— ex other disease, limited activities

how does endocrine and immune function in adipose normally work

adipose tissue..

1. Safely stores excess energy as triglycerides

2. Releases hormones called adipokines

3. Helps regulate appetite, insulin sensitivity, inflammation, and lipid metabolism

what does masld mean

fatty liver

what are s/s of sick fat disease

Endocrine/metabolic:

‒ Elevated blood glucose

‒ Elevated blood pressure

‒ Dyslipidemia

‒ Other metabolic diseases

what is fat mass disease associated with

negative effects of fat distribution on other organs

• joints

• tissue compression—sleep apnea, gerd, etc

what is sick fat disease also called/what associated iwth

• Adiposopathy

• adipose tissue dysfunction

• metabolic/endocrine

when fat cells grow too large, store fat in the wrong places, and release harmful stress signals and swelling chemicals

examples of metabolic manifestations ofo adiposopathy

• HTN

• hyperlipidemia

• hyperglcyemia

• CKD (kidney)

• cholelithiasis— gallstones

• gout

• etc

what is VAT fat

visceral adipose tissue

• in the abdomen— around organs

what is the metabolically active (sick) fat— secretes hormones

VAT

• “apple” more metabolically active

what is SCAT fat

subQ tissue— behind arms, on stomach , hips

women specific manifestations of adiposopathy

hirsutism

acne

pos

thrombosis

pre-eclampsia

men manifestations of adiposopathy

hypoandrogenemia

ed

what is bmi classification for obesity

over 30 kg/M²

what is range for pre-obesity BMI

from 25 to 30 kg/m²

what is BMI equation

wt (kg)/ ht (m²)

what is anoterh term for pre-obesity

overweight

what is wc

waist circumference

what is WC risk for men

40 in (102 cm)

what is WC risk in women

35 in (88 cm)

what effect does modest wt loss have on abdominal fat

5-10% wt loss can reduce visceral fat by 30%

what is goal for pt wt loss

• 5-10% wt loss over 3-6 months

• 1-2 lbs/wk

• 500-700 kcal/day

where is sensory and hormone cues for hunger controlled?

hypothalamus

examples of drugs that can increase body weight

anticonvulsants— carbamazepine, gabapentin

antidep— ssris, tcas

atypicals— clozapine, olanzapine, quetiapine, risperidone

conventional antipsychotics— haloperidol

DM medications— TZDs, sulfonylureas, insulin

hormones— corticosteriods, estrogens

which wt loss meds work on la brain

phentermine/topiramate

bupropion/naltrexone

tirzepatide

orforglipron, liraglutide, semaglutide

what wt loss meds work on the gut

orlistat

tirzepatide

lira/sema, orforglipron

how long use phentermine

short-term! up to 12 weeks

how else besides BMI 30 is qualification for obesity drug treatment

bmi with 27 AND a comorbidity

• HTN, hypertriglycemia

• but can be like sleep apnea, ckd, etc

phentermine ad eff

Overstimulation, palpitations, insomnia, hypertension and tachycardia

• think like excess catecholamines

warnings for phentermine

risk of abuse and dependance

phentermine CI

cardiovascular dz, glaucoma, hyperthyroid, pregnancy/breastfeeding

orlistat moa

blocks gastric/pancreatic lipases— makes eaten fat pass through stool unabsorbed

orlistat ad eff

• flatus

• fecal urgency

• fatty/oily stool

  • many variations of this

which antidep worst offender in wt gain

mirtazapine

what is counseling for orlistat in regard to meals and vitamins

• take within 1 hour of fatty meal

• must take fat soluble vitamins w/in 2 hours

orlistat possible drug inx

levothryozine

oral contraceptives

fat soluble meds— gabapentins, lamotringe, valproic acid, amiodarone

warfarin

cyclosporine

what are two brand names of orlistat? which is OTC?1

• Alli (otc)— 60 mg

• Xenical 120

what was OG glp for obesity

liraglutide

what is foundayo generic

orforglipron

phentermine and topiramate is it just wt loss

no wt management

phentermine and topiramate what do women need to do

use birth contorl per rems

what happens when women on phentermine and topiramate concieve

baby has cleft palate

phentermine and topiramate cna you immiedate start

no taper on AND OFF

phentermine and topiramate what to monitor

metabolic acidosis, hypokalemia, elevation in SCr

Naltrexone/bupropion MOA

• bupropion— keep more DA, NE in the brain

• block mu-opioid— stops craving/reward system

who should not have phentermine

HTN, dependance risk, CV disease, increases intraocular pressure

Naltrexone/bupropion ad ef

• constip, n, v, d

• dizz, headache

• dry mouth

Naltrexone/bupropion CI

• seizure disorderes BA/AN

• chronic opioid use

what is the CYP inx for Naltrexone/bupropion

CYP2B6— ticlopidine; clopidogrel

GLP-1 MOA

• upreg POMC/CART neurons to increase satiety

  • Downreg NPY/AgRP neurons to decrease hunger

which phent formulation cna be chronic

phen w/ topiramate

how does liraglutide:saxenda dose compare to victoza dose

saxenda is 3 mg dose

• victoza is 1.2-1.8 mg dose

general concerns for GLP-1s

gall bladder AEs, pancreatitis, thyriod cancer

how does semaglutide:wegovy dose compare ot ozempci

2.4mg and 7mg high dose vs 2 mg ozempic dose

• po doses range form 1.5 to 9 mg, high dose is 25 mg

which GLP-1 ag has approval for obesity+ASCVD and MASH

semaglutide (wegovy)

main GLP ad eff ACTUALLY

nausea, constip, dia

what makes orgorlipron different

oral NON-PEPTIDE

• not SNAC dependant

what is SNAC

• Sodium N-(8-[2-hydroxybenzoyl]amino) caprylate. It is an absorption enhancer formulated in the tablet.

• raises pH locally (makes stomach basic to make it more dissolveable)

• has to land on stomach lining— must take on empty stomach

what is MASH

from fatty liver to inflammed liver

• from MASVL to MASH to cirrohis

• metabolic dysfunction-associated steatohepatitis.

ozempic pill counseling

• before first meal

• 4 oz of water

• 30 min before you eat

so does NOT apply to foundayo

foundayo is wt loss more than injectable (wegovy)

less loss than wegovy

why is tirezpatide (zepbound) differenct

gip/glp-1 agonist

• most effective— wt loss up to 15-21%

which glp-1 approved for sleep apnea

zepbound (tirzepatide)

which glp-1 also approved for MASH

semaglutide hw

which glp-1 for obese teens approved

semaglutide (12+)

plenity how is this treatment different

DEVICE for wt loss

how does plenity work

• swallow capsules with water before meals to work a large gel that makes you feel full

• just a matrix of cellulose and citric acid

how to take plenity

• 3 cap; 20 min before lunch/dinner

• taken with bottle of water (16 oz)

• available OTC

what is CKM

cardiovascular-kidney-metabolic syndrome

what does CKM mean

that CV disease, kidney disease and metabolic disorders (ie obesity and diabetes) are all related

• “CKM syndrome is a health disorder due to connections among heart disease, kidney disease, diabetes, and obesity, leading to poor health outcomes.”

what is stage 0 for ckm

no risk factors

stage 1 for ckm what does this mean

• excess/dysfunctional adipose tissue

• overweight/prediabetes

• fasting bg above 100, a1c between 5.7-6.4

  • bmi 25

stage 2 of ckm

metabolic risk factors, CKD, or both

• HTN— 130/80 and above or on meds

• hyper tri— 150 mg/dL

• T2D— a1c over 6/5%; fasting BG over 126

stage 3 of CKM

subclinical CVD in CKM

• “pre heart failure”

• there are some plaques but can’t stent

• high Ca, biomarkers, but no like storke yet

prevent score of 20% or above

stage 4 CKM

clincal CVD

• heart fail, stroke, PAD

• stage 4b is kidney failure (eGFR less than 15)

what does COR mean

how much evidence supports the guideline

• ex 2a is good, but not as strongly supported as 1a

what does LOE or level of evidence

the NEXT a means randomized controlled trial

what is bmi “cut off” for glp-1 meds

BMI of 27 (with comorbiditiies— stage 1-3 CKM— which can lit just be overweight or prediabetes)

are low or high glycemic index foods pref

low glycemic— small spike in BG over time— “sustained release”

is whole-foods or micronutrients approach better

per T Colin Campbell there are more holistic benefits with whole foods (durp)

what are rec for stage 4 (HF, stroke, ASCVD, Afib)

intensive behavioral thearpy

GLP-1 (if BMI over 27)

rec for stage 1-3 CKM

lifestyle fs

• secondary is GLP-1 (b-nr level) if bmi over 27

when are GLP-1s cost effective

• stage 4 CKM (pts with ASCVD)

• bc naltrex/wellbbutrin and phentermine is damaging to heart

• GLP-1s very good for heart

  • if GLP-1s dont work do surgery (if BMI over 30)

when is there harm (ranked level 3) for bupropion and phentermine

stage 4 CKM— stimulation and increase BP and heart rate

when is there no “just lifestyle” trial CKM wise

just stage 4

what is premise for low carb diet

carb restriction lowers insulin level, body burns stored fat for energy

which diet used for epilepsy

ketogenic (low carb)

what is the goal of ketogenic diet

put body in state of ketosis to switch from glucose to fat burning

example of low glycemic index

brown rice, oat, whole wheat, beans, chia seeds

what happens when body is in ketosis

• elevated ketones in blood/urine

  • ketones produced by liver as emergency energy

    • causes body to start burning fat instead of using glucose

what are benefits of keto diet

reduce risk of seizure

• short term wt loss, increased BG, decreased TG, and increased HDL

downsides of keto diet— short term

GI intolerance, weakness, headaches, exercise intolerance, keto-flu