5.06 Evaluation and Management of Obesity and Disorders of Lipoprotein Metabolism Flashcards
In evaluating obesity, what 5 major factors should you consider?
Ready For CHangE
- The px’s Readiness to adopt lifestyle changes
- Fitness lvl
- Comorbid conditions
- Focused obesity-related History
- physical Examination to determine the degree and type of obesity
For obesity-focused hx, can ask these q’s
-
slide
Screen for presence of 2’ causes
Drug use
- DM, steroids, psychotropic agents, mood stabilizers, antidepressants
- Weight gain due to peripheral edema
Review current diet (food diary) and PA
An important predictor of all-cause mortality independent of BMI and body composition. This is reported by questionnaire or measured by what test?
Physical fitness!
-measured by a maximal treadmill exercise test
What is one metabolic event?
One metabolic event is defined as the amount of oxygen consumed while sitting at rest and is equal to:
= (3.5 mL oxygen per kg body weight)(minute) or 3.5 mL oxygen per kg body weight per minute
It represents a simple practical and easily understood procedure for objectively expressing the energy cost of PA as a multiple of the resting metabolic rate.
- The evaluation of obesity-associated comorbid conditions should be based on which 3 factors?
- Initial screening would including which 3 tests?
- Who are px who are at v high absolute risk?
- Evaluation based on: Presentation of Symptoms, Risk Factors, and Index of Suspicion
(RIP) - Initial screening:
Fasting lipid panel, FBG, BP determination - Px at v high absolute risk: established CHD, presence of other atherosclerotic dses such as peripheral arterial dse, abdominal aortic aneurysm, and symptomatic carotid artery dse; type 2 DM; sleep apnea
- Obesity Markers that provides an estimate of body fat and is related to risk of dse
- Formula for #1.
- Body Mass Index (BMI)
2. weight (kg) / [height (m)]^2 OR weight (lbs) / height (inches)
Obesity Marker: BMI
- Asia-Pacific region have (lower or higher) values for BMI classification? Explain.
- BMI classification WHO
- BMI classification Asia Pacific
- Lower values because they have lower BMI thresholds for overweight and obesity since this population appears to be at risk at lower body weights for glucose and lipid abnormalities
- BMI classification WHO
Underweight: (x, 18.5)
Healthy weight: [18.5, 24.9]
Overweight: [25, 29.9] - dse risk: increased
Obesity class I: [30, 34.9] - dse risk: high
Obesity class II: [35, 39.9] - dse risk: very high
Extreme obesity (class III): [40, x) - dse risk: extremely high - BMI classification Asia Pacific
Underweight: (x, 18.5) - risk of co-morbidities: low (but inc risk of other clinical problems)
Normal range: [18.5, 22.9] - risk of co-morb: average
Overweight: [23, x)
-At risk: [23, 24.9] - risk of co-morb: inc
-Obese I: [25, 29.9] - risk of co-morb: moderate
-Obese II: [30, x) - risk of co-morb: severe
Obesity Markers: Waist Circumference and Waist-Hip Ratio
- Importance
- Waist circumference is a surrogate for?
- How to measure waist circumference?
- WC for Filipinos?
- Excess abdominal fat, assessed by measurement of WC and WHR, is independently associated with higher risk for DM and CVD
- Surrogate for visceral adipose tissue
- To measure WC:
- Locate the upper hip bone and top R iliac crest. Place a measuring tape in a horizontal plane around the abdomen at the level of the iliac crest. Before reading the tape measure, ensure that the tape is snug, but does not compress the skin, and is parallel to the floor. The measurement is made at the end of expiration. - South Asians:
Men: > 90 cm (>35 inches)
Women: > 80 cm (>31.5 inches)
Readiness of a px to do lifestyle changes for obesity can be viewed as a balance of which two opposing forces?
Motivation and Resistance
Cholesterol Metabolism
Video
What does the lipid panel contain?
Total cholesterol, HDL, LDL, VLDL, TG
Thus it will tell the type of abn or dyslipidemia present in the px e.g. high LDL, low HDL, or high TG BUT always consider a 2’ cause.
T or F. For px w/ dyslipidemia, always consider a 1’ cause.
F F F!!! Always consider a 2’ cause and tx that first then check for improvement. If no improvement, try to look for another 2’ cause or consider a 1’ cause.
Chylomicron metabolism
Let us discuss chylomicron metab. Some of your CMs carry dietary TGs, cholesterol, and fat-sol vits from small intestines to peripheral tissues. Your extrahepatic tissues. And TGs account for 90% of lipids in a CM. So the process begins w/ the CMs receiving apo E and apo C from your HDL. The CMs goes to your extrahepatic tissues where apo C activates your LPL. This enzyme breaks down your TGs to FAs for use as an energy source in the muscle or for storage in adipose tissues. The glycerol component is transported back to the liver while the Apo A and C are returned to the HDL for reuse later while the CM remnant is taken up by the liver assisted by apo E.
Familial Chylomicronemia Syndrome
- What is it?
- Mode of inheritance?
- Give the 4 possible disorders with the affected gene, affected lipid, presentation, mode of inheritance, and prevalence
- When is this present
- Manifestation in the eyes
- Manifestation as severe abdominal pain
- Manifestation in the skin
- Manifestation in the liver
- Lab findings:
- plasma VLDL, CM, fasting TG, fasting cholesterol - Clinical Diagnosis
- Main goal and treatment
- Group of disorders producing elevated TGs due to mutations in enzymes of co-factors
- Autosomal recessive
3.
a. Lipoprotein lipase deficiency - most common
-Mutation: LPL (LPL)
-Lipid/s affected: CM, VLDL
-Presentation: Eruptive xanthomas, hepatosplenomegaly, pancreatitis
-Mode of Inheritance: AR
-Prevalence: ~1/1,000,000
b. Familiar apoC-II deficiency
- co-factor for LPL
- Mutation: ApoC-II (APOC2)
- Lipid/s affected: CM, LDL
- Presentation: Eruptive xanthomas, hepatosplenomegaly, pancreatitis
- Mode of Inheritance: AR
- Prevalence: x < 1/1,000,000
c. ApoA-V deficiency
- facilitates association of VLDL and CM w/ LPL and promotes hydrolysis of TG
- Mutation: ApoA-V (APOA5)
- Lipid/s affected: CM, VLDL
- Presentation: Eruptive xanthomas, hepatosplenomegaly, pancreatitis
- Mode of Inheritance: AR
- Prevalence: x < 1/1,000,000
d. GPIHBP1 deficiency
- Required for transport and tethering of LPL to the endothelial luminal surface
- Mutation: GPIHBP1
- Lipid/s affected: CM
- Presentation: Eruptive xanthomas & pancreatitis
- Mode of Inheritance: AR
- Prevalence: x < 1/1,000,000
- Present in adulthood or childhood
- Lipemia retinalis - retinal blood vessels are opalescent
- Acute pancreatitis
- Eruptive xanthomas - small, yellowish white papules, often appear in clusters on the back, buttocks, and extensor surfaces of the arms and legs.
- Hepatosplenomegaly due to the uptake of circulating CMs by reticuloendothelial cells in the liver and spleen
- Lab findings:
VLDL: elevated plasma lvls
CM: chylomicronemia predominates
Fasting TG are almost invariably > 1000 mg/dL
Fasting cholesterol: usually elevated but to a much lesser degree
Note: If you look at the fasting plasma, it’s turbid. And if left at 4 deg C for a few hrs, the CM float to the top and form a creamy supernatant. - Clinical Diagnosis: Severe persistent hypertriglyceridemia in the setting of acute pancreatitis.
- Main goal: TG < 500 mg/dL
Tx: Dietary fat restriction (as little as 15 g/day) w/ fat-soluble vitamin supplementation. Fish oils modestly effective. Fibrates may be tried.
T or F. Premature CHD is generally a feature of familial chylomicronemia syndromes.
F F F!! NOT generally a feature.
