Obesity - Exam 5 Flashcards
Healthy weight is classified as a BMI of:
18.5-24.9
BMI formula:
BMI = wt in kg / (ht in m)^2
OR
BMI = (wt in lbs/ ht in inches^2) x 703
A person’s degree of obesity is defined using _
BMI
Overwt is defined by a BMI of=
25-29kg/m^2
Obesity is defined by a BMI of=
30kg/m^2
Class I obese BMI:
30-34.9kg/m^2
Class II obese BMI:
35-39.9kg/m^2
Class III obese BMI:
> 40kg/m^2
Lean body mass in obese pts is _ % which accounts for extra muscle needed to carry the weight.
30%
-so this means LBW is 30% higher than IBW
Lean body wt (LBW) =
IBW x 1.3
male IBW = Ht in cm -100
female IBW = Ht in cm -105
What kind of organ is adipose tissue? What does it secrete?
Endocrine; proteins
What are the main functions of adipose tissue?
- Reservoir of energy
- Maintain heat insulatio
What results from liver fat metabolism?
Fatty acids –> energy
Triglycerides from carbohydrates and proteins
Phospholipid and cholesterol synthesis
Why is fat a good insulator?
Fatty acid chains in fat cells shorten with long-term cold exposure –> becomes more unsatruated –> does not get metabolized because only liquid fat can be metabolized
T/F All cells contain some saturated fats made by the liver
False, UNsaturated
Fat cells arise from modified _
fibroblasts
Mechanism of obesity (physical change) children vs adults
Children become obese due to increased fat cell #
Adults become obese due to enlarged fat cells
Apple body hip/waist ratio associated with comorbidities in men and women?
0.85 men < x (nagelhout)
0.92 women < x (nagelhout)
> 1.0 (men/women) bad
Waist circumference associated with increased comorbidities?
> 40 in men
35 in women
Waist:Hip ratio is calculated by dividing the _ waist measurement by the _, and is taken while the pt is _
narrowest
broadest
standing
pear body hip/waist ratio associated with comorbidities?
<0.76
What’s better, pear (gynecoid) or apple (android), why?
Pear (gynoid)
Fat stores in gynecoid do not release FFAs (they are metabolically static)
Android fat stores release FFAs –> to liver –> LDL/VDL creation
Which body system is the primary cause of morbidity and mortality associated with obesity?
CV
-HTN
-Ischemic heart disease
-CHF
CO goes up by how much per kg of fat?
0.1 L/min
How to assess for abdominal obesity?
Waist:Hip ratio
Underweight BMI:
<18.5
Normal BMI:
18.5-24.9
Overweight BMI:
25-29.9
Obese (Class I) BMI::
30-34.9
Obese (Class II) BMI:
35-39.9
Obese (Class III) BMI:
> 40
_ fat distribution is metabolically static and proposed to work as energy deposits for pregnancy and lactation
gynoid/pear
_ fat distribution is metabolically active regarding free fatty acid release
Android/apple
It is possible that hyper_ alone may cause HTN
hyperinsulinemia
Adipocytes are known to produce and store several inflammatory mediators such as: (4 items)
-leptin
-TNF-alpha
-monocyte chemotactic protein
-IL-6
Number one cause of morbidity and mortality associated with obesity:
cardiovascular disease
For every 13.5kg of fat gained, an estimated _ miles of neovascularization is created to provide blood flow rate of - mL/100g of tissue
25 miles
2-3mL/100g
increases CO by 0.1L/min per kg of fat gained
Cardiovascular changes with obesity (non-specific pathologies, not physical changes)
Increased CO
Increased O2 consumption
Increased CO2 production
Increased blood volume
How much does BP increase per 10% increase in body weight
6.5 mmHg per 10% body weight increase
How does obesity activate RAAS?
Fat compresses the kidney, stimulating the sympathetic nervous system , also impairs sodium excretion
What is hypercholesterolemia?
> 240 mg/dL
How do respiratory parameters change with obesity?
Decreased:
FRC
ERV
TLC
Increased:
Dead space
CO2 retention
(Restrictive lung disease)
What is the relationship between BMI and FRC?
FRC exponentially decreases
Respiratory changes in obesity lead to what risk factors cardiovascularly?
Chronic hypoxia –> polycythemia –> CAD/Stroke
Definition of OSA?
apnea during sleep longer than 10 seconds despite ventilatory efforts, 5+ more times/hr of sleep, decrease in SpO2 > 4%
What is hypoapnea?
50% reduction in airflow for 10 seconds, 15 + times during an hour of sleep
5-15 mild
15-30 moderate
Which muscles dilate/contract the pharyngeal airway?
Intrapharyngeal –> contract/collapse
Pharyngeal –> dilate
What keeps your airway open as you sleep?
Tensor muscles via CNS
Pathophysiology of sleep apnea?
Multifactorial causes (neural, physical obstruction, mechanical issues) –> Upper airway collapse –> pharyngeal dilator muscle activity surge –> hyperventilation –> decreased CO2 –> decreased respiratory drive –> repeat
Increased vagal tone is associated with…(increased/decreased OSA?)
increased OSA
Gold standard OSA diagnosis
Overnight PSG
What is Pickwickian syndrome?
AKA Obesity hypoventilation syndrome (OHS)
-Most severe form of OSA
-Hypercapnia (sleep-disordered breathing not due to other syndromes)
-NO respiratory effort
-Hypersomnolence during the day
-Cyanosis-induced polycythemia
-Respiratory acidosis (Pa CO2 > 45)
-Pulmonary HTN
-R sd HF
-Dependent edema
-Obesity (BMI > 30)
Which component of CO causes its increase in obese individuals: HR, SV, or both?
SV
-this causes cardiomegaly, bivent hypertrophy, and atrial and biventricular dilation -> HTN -> CHF
Factors influencing increase in HTN with obesity:
-increased blood viscosity
-altered catecholamine kinetics
-increased estrogen concentration
-hyperinsulinemia
-elevated mineralcorticoids
-abnormal sodium reabsorption
-RAAS activation
-increased SNS activity
Thoracic _ (kyphosis/lordosis) and lumbar _ (kyphosis/lordosis) result in impaired _ movement and fixation of the thorax in an _ (inspiratory/expiratory) position
Thoracic KYPHOSIS
Lumbar LORDOSIS
rib
inspiratory
Chronically elevated CO precedes increased _ (right/left) sd heart pressures and _ (right/left) vent hypertrophy
left
left
Skeletal changes from obesity such as kyphosis and lordosis cause a _ (increase/decrease) in chest wall, lung, parenchyma, and pulmonary compliance of about 35%
decrease
Which 2 factors regarding obesity cause an increase in myocardial O2 consumption?
-metabolic needs of fat tissue
-greater mechanical WOB
Which factors cause increases CO2 production and retention in obese pts?
-reduced respiratory muscle efficiency
-decreased ventilation
Reductions in chest wall and lung compliance in obese pts cause a _ pattern of breathing
restrictive
In obese pts, lung inflation is _ causing a decrease in FRC to _ than closing capacity.
inhibited
less
Premature airway closure in obese pts causes: (5 items)
-increased CO2 retention
-increased dead space
-VQ mismatch
-shunting
-hypoxemia
EXTREME obesity is associated with reductions in which 3 respiratory parameters?
-FRC
-expiratory reserve volume (ERV)
-total lung capacity
(also decreasing vital capacity)
Rapid, shallow breathing seen with obese pts is characteristic of _ lung disease. These patterns will eventually burn out, causing a _ in CNS responsiveness to chronic hypoxia. This leads to _ventilation and respiratory _ (alkalosis/acidosis)
restrictive
decrease
hypoventilation
acidosis
Recurrent hypoxemia leads to secondary _
polycythemia
-increases risk for CAD and CVA
Apnea is the cessation of airflow at the nose/mouth for > _ sec
10 sec
Hypoponea characteristics:
-50% drop in airflow for 10 sec
-happens 15+ times / hr of sleep
-assoc with snoring and 4% decrease in O2
OSA is diagnosed by _ using an apnea-hypopnea index (AHI)
polysomnography (PSG)
-AHI is # of abnormal respiratory events during sleep
Minimum DIAGNOSTIC criteria for OSA:
AHI of 10
WITH
symptoms of excessive daytime sleepiness
Diagnostic criteria for OSA per the American Academy of Sleep Medicine
Mild OSA:
Moderate OSA:
Severe OSA:
Mild: 5-15 AHI
Mod: 15-30 AHI
Severe: >30 AHI
Minimum MEDICARE criteria for OSA:
-AHI of 15
OR
-AHI of 5 WITH 2 comorbidities
T/F CAD is a risk factor for obesity
false, it is independent
Genetic factors involved with obesity:
-Prader Willi Syndrome
-Baret Biedl Syndrome
-Obesity “hormone” LEPTIN (not enough -> overeating)
Diseases that can CAUSE obesity:
cushings, PCOS, hypothyroidism
T/F FRC is directly proportional to BMI
false
INVERSELY (increased obesity = decreased FRC)
Physical factors related to OSA that increase as obesity increases:
-BMI > 30
-abdominal fat distribution
-neck girth (men >17inches ^2, women >16inches^2)
The site of upper airway obstruction is usually the _
pharynx
Patho of OSA:
1.While awake, patency is maintained by mediation of contraction of the _ muscles in the CNS
2. Then, _ muscles oppose the neg inspiratory forces that collapse them
3. While asleep, these muscles relax and cause the soft-walled _ to collapse between the _ and _
4. The resulting hypoventilation triggers a surge of _ dilator muscle activity, which opens the airway then causing _.
5. _ reverses the hypercarbia, which reduces the _ drive to breathe again. This is a vicious cycle.
- tensor
- dilator
- oropharynx, uvula, epiglottis
- pharyngeal, hyperventilation
5.Hyperventilation, CNS
this causes fluctuating hypercarbia and hypoxia, poor sleep, and triggers adrenergic output with each cycle
HR abnormalities associated with OSA:
-bradycardia
-sinus node dysfunction
-asystole
_ or more clinically significant apneic episodes per hr or > _ episodes per night cause hypoxia, hypercapnia, systemic and pulmonary _, and cardiac _
5 times/hr or 30 times /night
systemic and pulm HTN
cardiac arrhythmias