Obesity Flashcards

1
Q

What is the definition and occurance of obestiy

A
  • Excessive accumulation of (white) fat tissue
  • Energy intake > utilization
  • Overweight ca/fe: ideal body weight +15-30%
  • Obese ca/fe: ideal body weight + >30%
  • Occurrence of obesity ca/fe: 20-45%
  • Endocrine disease: <1% of obese ca/fe
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2
Q

What is the two-component model

A
A technique of masuring body composition based on two components:
🔺Fat Mass (FM)
- Energy reserve (fat)
- Homogeneous composition 
- Water and potassium free
🔺 Fat Free Mass (FFM)
- Health state
- Constant ratio of components (minerals, ec/ic water, glycogen)
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3
Q

What are different methods/modles we can use to describe body composition and nutritional status?

A
  • Body weight (change)
  • Body Condition Score (BCS)
  • Cachexia Score (sick animals) = Muscle Condition Score (MCS)
  • Morphometric measurements
  • Bioelectrical Impedance Analysis (BIA)
  • Dual Energy X-ray Absorptiometry (DEXA) (Most specific- density of both soft tissues and bone - osteopor.!)
  • (Densitometry, CT/MRI, whole body potassium )
  • (Chemical analysis of dead body) most accurate but can only be done in dead…
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4
Q

What does the body weight measure inform us about?

A
  • No information on body composition
  • Modified by dehydration or fluid accumulation
  • Scale: exact, same (Should be appropriate for the size of patient)
  • Monitor changes! (Most imp thing of bwt! Growth, decr: fat accumulation or loss (or other))
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5
Q

What does the body condition scoring (BCS) inform us about?

A
  • 1…3…5 or 1…5…9 - charts
  • Most practical (Very important, valuble - should be part of basic values!)
    BUT:
  • Subjective
  • Investigator-to-investigator variance
  • Body composition is only estimated
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6
Q

What are the basic causes of obesity

A
  • lower Basic Metabolic Rate (BMR)
  • lower Physical activity
  • higher Energy intake
    We rarely have them alone! May influence eachother
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7
Q

Describe the possible backgrounds of decreased BMR

A
  • Breed, genetic factors (retriever, beagle, spaniel, dachshund…)
  • Gender:
    The female ffm is lower than the male ffm, so the female bmr is lower too as their energy demand is lower.
    ➡️ in most spp female is more predisp to develope obesity
  • Neutering decr the BMR
  • Aging decrease the energy demand/BMR
    ➡️ Ca: 7-12 years = esp prone to obesity
  • Hypothyroidism decr. BMR
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8
Q

Describe the connection between neutering and obesity

A

🔺Neutered dogs: prevalence of obesity 2x!!!
- BMR ⬇️
- Appetite ⬆️
- Physical activity ⬇️
🔺 Fe: castrated Male can dev most severe obesity!
Indoor neut. (diff in dog - female)
🔺 Energy demand 30% ⬇️ (must red. Intake!)
🔺 2-3 body weight and BCS
monitoring in the year following neutering!

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9
Q

Describe the connection btw hypothyroidism and obesity

A
  • Especially if the breed is predisposed to both (Eg. Beagles)
  • FM increase, FFM normal!
  • BMR decrease, physical activity decrease (lethargy)
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10
Q

What are causes of decreased physical activity

A
🔺Indoor lifestyle 
- Room dog: 31% 
- Garden dog: 23%
🔺Aging (Painful joint, bone diseases also a factor)
🔺Owner's lifestyle
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11
Q

Describe higher energy intake as cause of obesity

A

🔺 Polyphagia (pathology, hormones, drugs)
- Cushing’s syndrome!!, stress, (acromegaly)
- Medications: glucocorticoids, progestins, antiepileptics (phenobarbital)
🔺 Calories (fat and carbohydrates) in food ⬆️
- eg. Diet wrong proportion of nutrients, right amount of food.
🔺 Feeding problem/error
- Too big/frequent doses or ad libitum feeding
- Treats, “snacking” at family meals
- Competing for food, more pets in the family
- More family members are feeding
- Feeding ≠ love, voracity ≠ health, snacks ≠ boredom killing

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12
Q

What is the connection bwt Cushing’s syndrome and obesity

A
  • higher fat mass, lower(!) Fat free mass

- Abdominal size increase/pot belly, muscle weakness (decr. Activity contr more to problem aswell!)

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13
Q

Describe the connection betweein higher calorie/fat content of food and obesity

A
🔺 The energy concentration of fat is highest
🔺 Satiety 
- Fat ☹️
- Carbohydrate 🙂
- Protein/amino acid 🙂
🔺 Utilization/digestebility of energy content (monogastric) 
- Fat 98%
- Carbohydrate 94% 
- Protein 77%
🔺 Fat supplement: palatability ⬆️
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14
Q

How might obesity be a health risk?

A

🔺Physical
🔺 Endocrinologic and metabolic
🔺 Other

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15
Q

How does the physical consequences of obesity influence the health?

A

🔺 Increased load on joints/bones
- Ca: cruciate ligament rupture, discopathy
🔺 Tracheal collapse (ca)
🔺 Heatstroke (ca) (more “insulation”/fat tissue

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16
Q

How does the Endocrinologic and metabolic consequences of obesity influence the health?

A

🔺 Hypoxia in cell groups of fat deposits
🔺 Fat stores produce inflammatory mediators (adipokins which are released:)
🔺 TNF-α ⬆️, IL-6 ⬆️, leptin ⬆️, CRP , adiponectin ⬇️!! (Benefitial, reduce inflamm, decr insulin resistance)
- Chronic systemic inflammation (➡️ osteoarthritis)
- Hypertension (ca), atherosclerosis
- Insulin resistanceðtype-2 DM (fe! ca?)
🔺 Hyperlipidemia (TG ⬆️, cholesterol ⬆️)
- Pancreatitis
- Liver lipidosis (fe esp!)

17
Q

Explain the connection between obesitas and hypertension

A

🔺 Circulating volume ⬆️, cause:
- adipokine release ➡️ RAA system activation ➡️ renal water retention
🔺 Peripheral resistance of blood vessels ⬆️, cause:
- Endothelial dysfunction
- Adipokins ⬆️ (inflamm mediators)

18
Q

Mention the other risk factors we might see in connection to obesity

A
  • Ca-oxalateurolithiasis (ca)
  • Other urinary tract diseases
  • Heart disease (ca)
  • Kidney disease (ca)
  • Incontinence (ca)?
  • Tumors
  • Reproductive problems
19
Q

How does obesity increase the incidence of heart disease?

A

🔺Most common: myocardial hypertrophy
- Circulating volume incr ➡️ Preload increase
- Hypertension ➡️ Afterload increase
- adipokins ➡️ Myocardial hypertrophy and fibrosis
- ➡️ Coronary calcification
➡️➡️➡️ DECREASED LEFT VENTRICLE FUNCTION

20
Q

Describe the connection btw obesity and nephropathy

A

Release of adipokins➡️ RAAS activated ➡️ Hypertension

➡️ increased GFR ➡️ Glomerulus expands, Bowman’s capsule is tight ➡️Glomerulosclerosis

21
Q

What are the main points in the treatment of obesity

A
  • Diet
  • Increase physical activity
  • Treatment of hormonal disease
  • Medication support? No longer available
22
Q

How do you approach starting a weight loosing diet?

A

🔺 Body weight (BW) – ideal body weight (IBW) – target body weight (TBW)
🔺 optimal body weight loss: 1-2% /week, 4-8% /month
🔺 Calorie intake ⬇️
- (40-)60% of target body weight maintenance energy demand
(set if lower if:)
- female: -15%
- Neutered: -15%
Don’t be drastic: rather too little than too muc!
- Hunger ➡️ behavior ➡️ owner gives up
- Excessive FFM ⬇️
- Increased risk of relapse (BMR ⬇️)
- Liver lipidosis (fe) due to fat mobilisation

23
Q

How do you modify the nutrient proportion correctly while decreasing caloric intake?

A

🔺 Fat/calorie ratio ⬇️
- Fat: max. 25% of ME content (25-30g fat/Mcal ME)
🔺 Fiber ⬆️ (not too much!)
- Water soluble:
gastric emptying ⬇️, nutrient absorption ⬇️
- Insoluble: passage ⬆️
- Palatability ⬇️ but satiety⬆️ (full stomach)
- (Stool quantity ⬆️, frequency ⬆️)
- (Flatulence, diarrhea)
🔺 (Water ⬆️, air ⬆️) to increase volume!
🔺 Protein-to-calorie ratio ⬆️ (higher protein)
- Target body weight protein requirement
- FFM↔️, FM⬇️
- Protein energy is utilized worse
- Satiety ⬆️
🔺After ideal weight is met, we switch to maintenance diet

24
Q

Things to add to a weight loss diet?

A

🔺 Vitamin/mineral supplementation +/-
➡️ Bc diet low in fat, fat soluble vits need to be absorbed in presence of fat!
🔺 Potentially slimming additives
➡️ Chitosan, green tea extract, L-carnitine, ginseng saponins, chromium, conjugated linoleic acid (t10, c12-CLA) … etc.

25
Q

How does physical activity affect the FFM?

A

Either it stays the same or it might increase (mm building)