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Cardiopulmonary > Obesity > Flashcards

Obesity Flashcards

1
Q

Normal BMI

A

18.5-25

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2
Q

Overweight BMI

A

25-30

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3
Q

Obese class 1 BMI

A

30-35

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4
Q

Obese class 2 BMI

A

35-40

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5
Q

Obese class 3 BMI

A

40+

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6
Q

Prevalence of obesity/overweight in adults

A

71.6%

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7
Q

The Cost of Obesity

A

21% of annual medical costs in the United States. Around $149 billion a year

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8
Q

Contributing Factors to obesity

A

Genetic, epigenetic, and societal/environmental factors, Early childhood food experiences, social network

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9
Q

Genetic factors to obesity

A

Several genes have been identified and there are several genetic syndromes associated with obesity

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10
Q

How impairments in executive function affects obesity

A

the ability to engage in goal‐oriented behaviors, self‐regulation, and working memory are common in obesity.

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11
Q

Early childhood experiences and obesity

A

influence preferences towards food choices and eating habits/behaviors.
These preferences for foods may even develop in utero (“Prenatal and Postnatal Flavor Learning”) and during breast feeding as breast milk is flavored by maternal dietary intake.
Parental eating behaviors influence those of their children.
Activity habits also tend to develop in adolescence.

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12
Q

Social network and obesity

A

A person’s chances of becoming obese increase by 57% if they had another friend
become obese and 40% if a spouse became obese.

Peer groups even as early as childhood tend to organize around people with similar activity patterns and people tend to model our activity around our least fit friend

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13
Q

Social economic status and obesity

A

Higher rates of obesity observed in patients of lower SES
Financial burden of lifestyle interventions may be a significant factor influencing adherence for many patients (Travel, co-payments, equipment, gym memberships)
Lower access to green recreational spaces and team sports in childhood.
School programs for health/physical education and athletics have been cut.

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14
Q

White adipose tissue

A

Lipid storage and undergoes pathological expansion during obesity

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15
Q

Brown adipose tissue

A

Thermogenic, large amounts of mitchondria, dissipate large amounts of chemical energy as heat, defends core body temperature in cold weather
Contributes to energy expenditure

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16
Q

adipose tissue in Visceral/Intra-abdominal

A

Produce more pro-inflamatory cytokines; tumor necrosis factor-alpha (TNF-α) and
interleukin-6 (IL-6) and less adiponectin
Increased sympathetic activity
Strongly lined to cardiovascular disease, type 2 diabetes and various other condition

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17
Q 
Adipose tissue is a type of \_\_\_\_ cell 
A. autocrine
B. paracrine
C. endocrine 
D. All of the above
A

D

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18
Q

Adipose tissue produces

A

Produces adipose-derived cytokines Adipokines
Also produces ANG-2 and ROS, changes to
Leptin sensitivity and signaling

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19
Q

Adipokines

A

some are beneficial (adiponectin) while some are pathogenic and induce atherogenesis, insulin resistance, inflammation and endothelial dysfunction

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20
Q

Obesity and affects of adipokines and adiponectin

A

abnormal production of pro-inflammatory adipokines and reduction in adiponectin

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21
Q

ET-1 is a vasodilator or vasoconstrictor?

A

Vasoconstrictor

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22
Q

Nitric oxide is a vasodilator or vasoconstrictor?

A

vasodilator

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23
Q

adiponectin function

A

increases NO bioavailability

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24
Q

Perivascular Adipose Tissue (PVAT)

A

Vascular homeostasis is maintained by the opposite action of endothelium-derived relaxing and contracting factors, mainly nitric oxide (NO) and endothelin (ET)-1.

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25
Q

Obesity and PVAT

A

Obese patients also have lower levels of adiponectin compared to healthy and greater production or pro-inflammatory adipokines (TNF-α, IL-6 etc)
TNF-α reduces NO bio-availability in obese patients and thus NO’s effect on ET-1
May also increase ROS and Angiontensin-2 production in obesity

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26
Q

Coronary PVAT

A

Altered contractile effects of obese coronary PVAT are related to differences in smooth muscle responsiveness between obese and lean coronary arteries. They have primary effects of increased vascular tone and impaired relaxation

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27
Q

Atherosclerotic plaques

A

have been shown to occur predominantly in epicardial coronary arteries that are encased in PVAT

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28
Q

myosteatosis

A

which is the presence of intermuscular and intramuscular adipose tissue
Myosteatosis induces pathological changes to skeletal muscle structure and insulin signaling pathways into the muscle
Myosteastosis is induced with obesity.

29
Q

Implications of Obesity on Muscle

A

Reduction in anabolic hormones such as insulin-like growth factor-1 (IGF-1) and Testosterone
Obesity results in an increased secretion and expression of Myostatin.

30
Q

The Obesity Paradox

A

Although obesity is a cardiovascular risk factor in epidemiological studies, an “obesity paradox” exists in which obese patients are associated with more favorable prognosis compared to lean patients among cohorts of cardiac patients.

31
Q

BMI and CVD

A

BMI may be a less accurate reflection of CVD risk within individuals.

32
Q

Cardiorespiratory fitness

A

more closely linked to mortality risk in populations exhibiting an obesity paradox
CRF “neutralizes” the obesity paradox

33
Q

Clinical implications on obesity paradox

A

Strategies to reduce mortality risk in such populations should emphasize preserving or increasing CRF and LM more than weight loss alone

34
Q

More Reliable Way to Measure Obesity

A

waist and hip measurement

35
Q

Waist circumference measurement for increased risks

A

Men: >94cm (37inches)
Women: >80cm (31 inches)

36
Q

Waist to hip ratio for increased risks

A

Men: 0.9
Women: 0.85

37
Q

Bariatric Surgery

A

Indicated for individuals BMI >40 kg/m2
Weight loss often more dramatic and sustained than medical management. Reduces comorbidities like diabetes, hyperlipidemia and hypertension

38
Q

Obesity significantly associated with more functional difficulty:

A 
Moderate-Vigorous activities
Lifting/Carrying groceries
Walking 1 or more flights of stairs
Bending/kneeling
Walking 1 or more blocks
Bathing or dressing
Increased Fall Risk
39
Q

Realistic goal for weight loss in obese patients

A

5%–15%. Even a 5% reduction in body weight, and weight loss takes time (4-6 months for most programs)

40
Q

moderate intensity aerobic exercise training (AET)

A

Strong evidence to support this mode for weight loss. Goal is around 225–300 minutes per week.

41
Q

High intensity interval training (HIT)

A

may be an effective alternative mode of exercise training for obese individuals
When compared to moderate intensity AET, HIT has similar outcomes, shorter training durations, and higher levels of enjoyment in obese individuals

42
Q

Role of Physical Therapy

A

Education

Goal Setting

Exercise prescription either with or without bariatric surgery.

Addressing any barriers to movement and exercise

43
Q

Assessments for exercise capacity

A

6MWT, 2 Min Step Test, incremental shuttle walking test (ISWT), or Cardiopulmonary Exercise Testing (CPET)

44
Q

Assessments Strength and Mobility

A

Hand-held dynamometry, 30 sec chair rise test, 5 time sit to stand, TUG

45
Q

Goals and intentions for treatment

A

Weight loss/Energy balance

Improving cardiorespiratory fitness

Improving functional mobility

Improving body composition (Lean/Fat-Free Mass)

Improving strength and mobility

46
Q

How to keep patients going

A

Pick an activity or exercise that they enjoy!
Develop a Social Team
Add in activity to daily routine

47
Q

Patient adherence and consistency

A

The primary factor that predicts a successful response to a weight loss program is patient adherence.
Pick something that moves you and healthy food you like to eat.

48
Q

effect of diabetes on the body

A

Endothelial and vascular smooth muscle cell function propensity to
thrombosis
Contributes to atherosclerosis and its complications.
Hyperglycemia decreases endothelium-derived NO
Increased synthesis of vasoconstrictor prostanoids and endothelin-1
Increased activated platelets, increased coagulation factors (factor VII, vWF and tissue factor ) and inhibited pathways for fibrinolysis

49
Q

Non-diabetic

A

At physiological levels, insulin regulates vascular homeostasis by maintaining the balance of endothelial derived NO and ET-1

50
Q

Insulin resistance

A

In patients with insulin resistance, this relationship become paradoxical and P13K is selectively reduced allowing ET-1 production to be unopposed.
In addition to vasoconstriction ET-1 has other adverse effects on vascular health.

51
Q

Advanced glycation end-products (AGE) Also known as “glycotoxins”

A

The formation of AGEs is a part of normal metabolism. But in Diabetic patients, AGEs is excessively high resulting in Increased ROS, increased arterial stiffness, impaired wound healing, increases
in diastolic pressure, retinopathy, neuropathy.

52
Q

Signs and Symptoms of diabetes

A 
Frequent Urination
Excessive Thirst
Extreme fatigue
Vision Changes (Blurry)
Feelings of hunger
Cuts/bruises that are slow to heal
Weight loss (DM 2)
Polyneuropathy
53
Q

Diabetic Polyneuropathy sensory

A

usually insidious in onset and showing a stocking-and-glove distribution in the distal extremities

54
Q

Diabetic Polyneuropathy motor

A

Distal, proximal, or more focal weakness, sometimes occurring along with sensory neuropathy (i.e., sensorimotor neuropathy)

55
Q

Diabetic Polyneuropathy autonomic

A

Neuropathy that may involve the cardiovascular, gastrointestinal, and genitourinary systems and the sweat glands

56
Q

Primary risk factor for type II Diabetes. need 3/5

A 
Large waist circumference/abdominal obesity
Elevated triglycerides
Low HDL
Hypertension
Elevated blood glucose level (fasting)
57
Q

Increased level of C-reactive protein (CRP) causes

A

Increases risk of atherosclerosis and HTN

58
Q

Type 1 Diabetes

A

Onset generally 6-13 y/o but can also occur in adults

Beta cells in Islets of Langerhans fail to produce sufficient insulin

59
Q

Type 2 Diabetes

A

Onset generally >40 y/o

Hallmark: insulin resistance

60
Q

Hypoglycemia

A

Glucose Levels ~ <70mg/dl for DM

61
Q

Hypoglycemia early symptoms

A 
Palpitations
Fatigue
Pale skin
Shakiness and incoordination
Anxiety
Sweating
Hunger
Irritability
Tingling sensation around the mouth
Weakness
62
Q

Hypoglycemia severe symptoms

A 
Confusion,
Abnormal behavior
Inability to complete routine tasks
Visual disturbances (blurred vision)
Seizures
Loss of consciousness
63
Q

Hyperglycemia

A

Often Asymptomatic <200mg/dl

64
Q

Hyperglycemia early symptoms

A 
Frequent urination
Increased thirst
Blurred vision
Fatigue
Headache
65
Q

Hyperglycemia Severe Symptoms

A 
Nausea and vomiting
Shortness of breath
Dry mouth
Weakness
Confusion
Coma
Abdominal pain
Fruity-smelling breath
Presence of Ketones
66
Q

Ketoacidosis

A

Caused by metabolism of fats and proteins which produce ketones
More common in DM1 than DM2

67
Q

Ketoacidosis early symptoms

A

Increased Thirst
Dry mouth
Frequent or more frequent urination
Glucose Levels >240mg/dl

68
Q

Ketoacidosis Severe Symptoms

A 
Dry or flushed skin
Nausea, vomiting, or abdominal pain
Difficulty breathing
Fruity odor on breath
A hard time paying attention, or
confusion
May eventually lead to coma
69
Q

Exercise for the Diabetic Patient benefits

A

Exercise increases glucose uptake during AND after exercise

Increased insulin- INDEPENDENT glucose uptake (1-3 hours)

Increased insulin SENSITIVITY lasts hours to days

Cardiopulmonary (7 decks)

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