Week 11 Flashcards
1
Q
What is obesity?
A
a complex multifactorial chronic disease with a complex etiology
2
Q
Most simply defined, what is the etiology of obesity?
A
a long-term energy imbalance between consumed calories and expended calories
3
Q
Obesity is typically characterized by a BMI of at least…
A
30kg/m2
4
Q
Obesity is a risk factor for many chronic diseases such as…
A
T2DM, CVD, osteoarthritis, 13 types of cancer, chronic kidney disease etc.
5
Q
Are there example populations in which the obesity epidemic has been reversed by public health measures?
A
No
6
Q
The rising obesity prevelance is driven mainly by…
A
changes in global food system (processed food more readily available & more affordable)
- combined with other local environmental factors
7
Q
There are variations in obesity within a population due to…
A
interactions between environment and individual factors (e.g. genetics)
7
Q
What are the two main factors matter when diagnosing obesity?
A
the location of excess adipose tissue and metabolic health
8
Q
Why does the location of excess adipose tissue matter when diagnosing obesity?
A
visceral adiposity is associated with chronic disease risk
9
Q
Why does metabolic health matter in the diagnosis of obesity?
A
- adipose tissue is an endocrine organ that can impact metabolism & inflammtory status
- look at blood glucose, lipid levels & blood pressure to determine metabolic health
- can also measure blood inflammatory measure
10
Q
How is increased adiposity linked to T2DM?
A
adipose tissue has endocrine/signaling functions → produce adipose-derived cytokines (adipokines) and other cytokines lead to insulin resistance
11
Q
What are the cytokines secreted in obesity? What do they do?
A
- adiponectin (protective effects): insulin-sensitizing, anti-inflammatory; levels decrease in obesity
- leptin (pro-inflammatory): regulation of food intake, metabolic rate; obesity induces leptin receptor resistance; levels increase in obesity
- others: TNF-alpha, IL-6 etc. → all pro-inflammatory
12
Q
What is the result of the cytokines released from adipose signalling function?
A
- chronic systemic inflammation
- increased circulating free fatty acids → insulin resistance → Type II diabetes
13
Q
What is the treatment goal of obesity?
A
weight loss
**should this be the goal?
14
Q
What are the treatment modalities of obesity?
A
- multimodal lifestyle interventions that include dietary modification, increase PA, behaviour modification
- pharmacotherapy: drugs that aim to reduce food intake e.g. by decreasing hunger, slow gastic emptying, reduce absorption of fat
- medical devices:
→ intragastic ballons
→ vagus nerve blocker (specific to GI area); suppresses neural communication between stomach and brain - bariatric surgery
15
Q
What are the 5 main factors of metabolic syndrome?
A
- visceral obesity
- low HDL-cholesterol
- high triglycerides
- insulin resistance
- hypertension
16
Q
What is the very effective treatment (cure?) for metabolic syndrome?
A
diet and exercise
17
Q
What is the typical progression of MetS?
A
genetic predisposition + behavioural factors → accumulated body fat → develop MetS → greatly increased risk for a progression to multiple chronic diseases (type 2 diabetes, CVD, etc)
18
Q
What is metabolic obesity?
A
normal weight, metabolic markers in the blood
19
Q
What does it mean to have metabolically unhealthy obesity?
A
high BMI and metabolic markers in the blood
20
Q
What does it mean to have metabolically healthy obesity?
A
high BMI e.g. higher BF% but no metabolic markers
21
Q
What is a neoplasm?
A
- tumor
- cellular growth that no longer responds to normal genetic control (dividing outside of regular mitotic signals
- deprives other cells of nutrients & metabolism
22
Q
What do the characteristics of each tumor depend on?
A
- type of cell from which tumor arose
- unique structure and growth pattern
23
Q
What are benign tumors?
A
- typically differentiated cells
- replicate at higher rate than normal
- expands within a capsule, no spread
24
What are malignant tumors?
- more often cells are abnormal- poorly differentiated, nonfunctional, disorganized
- rapid uncontrolled replication
- can infiltrate other tissues and blood vessels, break away, spread to distant regions
25
What are the types of abnormal cell growth that may develop into cancer?
hyperplasia, atypia, metaplasia, dysplasia
26
What is hyperplasia?
cells are dividing at a rate faster than normal
27
What is atypia?
cells are slightly abnormal
28
What is metaplasia?
change in cell type in a particular area
29
What is dysplasia?
cells are abnormal, they are growing faster than normal & not arranged like normal cells
30
What is meant by carcinoma in situ?
cells very abnormal but have not grown into nearby tissue
31
Give an example of the normal progression of abnormal cell growth that has progressed to cancer.
normal mucosa → hyperplasia → dysplasia → carcinoma in situ → invasive carcinoma
32
What are the two factors involved in cancer classification?
1. based on location where the cancer first developed
2. based on type of tissue
33
What is a carcinoma?
cancer with epithelial origin
- cancer of the lining of organs etc.
- 80-90% of cancers
34
What is a sarcoma?
cancer with supportive and connective tissue origin
- e.g. bones, tendons, cartilage, muscle, fat
35
What is melanoma?
cancer of melanocytes (skin pigment cells)
36
What is myeloma?
cancer of plasma cells
37
What is leukemia?
cancer of white blood cells
38
What is lymphoma?
cancer that develops within the lymphatic system
39
What is carcinogenesis?
the process by which normal cells are transformed into cancer cells
40
What are the risk factors for the etiology of carcinogenesis?
multifactorial → lead to changes in gene expression
- genetics and age
- environment (e.g. viruses, smoking, UV, other radiation, chemical exposure
- lifestyle (diet, activity status, stress)
- biological factors (chronic inflammation, hormones, obesity)
41
Describe the steps in the multistage model of carcinogenesis
initiation: exposure to one or multiple carcinogens causes first DNA change → promotion: exposure to promoters lead to changes in the cell that 'promote' the cancer phenotype
progression: changes to regulation of growth leads to malignant tumor growth, invasiveness and matastasis
42
Tumors create their own ______________
microenvironment
43
What are the hallmarks of cancer?
- cells lack mitotic control and normal homeostatic function/cell communication
- altered cell membranes and surface antigens
- cells do not properly adhere to each other (they secrete enzymes that break down proteins of the extracellular matrix. enables them to break off from the tissue mass and spread.
- secrete growth factors that stimulate development of new capillaries (promoting angiogenesis)
44
What are the three core local effects of malignant tumors?
pain, obstruction, inflammation & necrosis of surrounding healthy tissue → loss of normal function
45
Describe the pain associated with the local effects of a malignant tumor
- often absent until later stages, when tumor is well advanced
- depends on type and location of tumor
- can be due to: ischemia, blood or fluid collecting in the area, inflammation, infection, physical compression
46
Describe the obstruction associated with the local effect of malignant tumors
- due to tumor compression
- can be a reason to maintain treatment during late stages (palliative treatment)
47
How can tumors cause obstruction?
- tumor can compress a passageway or duct, from the inside or due to growth around a structure
48
What are the 5 main systemic effects of malignant tumors?
fatigue, weight loss and cachexia, edema, bleeding, paraneoplastic syndromes
49
Why is fatigue a systemic effect of malignant tumors?
inflammatory process, stress, anemia
50
Why is weight loss and cachexia (tissue wasting) a systemic effect of malignant tumors?
due to lack of appetite, fatigue, pain, stress, increased metabolic demands due to cancer
51
Why is edema a systemic effect of malignant tumors?
inflammatory response causes fluid buildup within body cavities
52
Why is bleeding a systemic effect of malignant tumors?
if tumor erodes blood vessels
53
What are the sytemic paraneoplastic syndromes associated with malignant tumors?
tumor cells can secrete substances that affect neurologic function, blood clotting, hormone levels
54
What are the ways malignant tumors can spread?
tissue invasion, metastasis, seeding
55
Describe tissue invasion as a way of malignant tumors spreading
local spread
- tumor cells grow in adjacent tissue e.g. invasive carcinoma of the cervix
56
Describe metastasis as a way of malignant tumors spreading
spread to distant sites
- via blood and/or lymphatic system
- liver and lungs are common sites of metastasis
57
Describe seeding as a way of malignant tumors spreading
spread of tumor cells within body fluid or along membranes within a body cavity
58
What is involved in the detection and diagnosis of cancer?
- warning signs
- routing screening and self-examination
- blood tests
- X-ray, ultrasound, CT, MRI
- histologic and cytological exams (biopy)
59
Why is grading and staging of cancer used?
- described the extent of the disease
- provides a basis for treatment and prognosis
60
What does grading of cancer mean?
grading describe the appearance & behaviour of the cancer cells
e.g. Grade 1-4; atypical (grade 1) → poorly differentiated or aggressive (grade 4)
61
What does staging of cancer mean?
describes the size and extent of spread
e.g. stage 1 generally small, localized, easy to treat, good prognosis vs. stage 4 distant spread, difficult to treat, poorer prognosis
62
What is the TNM staging system?
- size of primary tumor (T)
- involvement of lymph nodes (N)
- spread (metastasis) of tumor (M)
63
cancer treatment can be....
curative or palliative
64
What are the three main types of treatment for cancer?
surgery, radiation, chemotherapy
65
What is radiation therapy?
- delivered externally or implanted within tumor tissue (brachytherapy)
- radiation causes mutations that kill the tumor cells and damages the surrounding blood vessels
66
What is chemotherapy
- cancer types are matches to specific drug treatment
- use an optimal combination of drugs to effectively target different points in the tumor cell cycle
67
What is personalized oncogenomics?
analyzes the cancer genome in order to determine the best treatment for the individual
68
What is a prognosis?
he predicted or expected course and outcome of a disease or injury, including the likelihood of recovery or recurrence.
- varies depending on type and staging of cancer
- a "cure" is defined as 5 years without recurrence after treatment
69
What are the two main ways to prevent cancer?
healthy choices and informed decisions
70
What are some examples of healthy choices in the prevention of cancer?
- live smoke-free
- be sun-safe
- have a healthy body
- eat well
- move more, sit less
- limit alcohol
71
What are some examples of informed decisions in the prevention of cancer?
- be aware of your family history
- understand medication risks
- get vaccinated
- work safety
- know your environment
- be informed
72
What should we know about exercise & cancer prevention?
- lot of research supporting regular physical activity as effective primary prevention (effective dose? lifelong exercise vs. critical stages in life? target at initiation vs. promotion vs. progression?)
- linked to the effect of exercise on immune function
73
What should we know about exercising with cancer?
- regular PA is linked to reduced cancer recurrence and improved survival
- evidence supporting effectiveness in decreasing common side-effects of cancer
- both aerobic & resistance exercise considered safe and effective
- Ok during active treatment
- prescription with individual limits, modify as needed
