Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

(OMS1) MOD Exam 2 > Chapter 9: Environmental and Nutritional Diseases > Flashcards

Chapter 9: Environmental and Nutritional Diseases Flashcards

1
Q

What is the leading causes of death in developed countries?

What is the leading cause of death in developing countries?

What are the 3 preventable leading cause of death in kids <5yo?

A

ischemic heart disease and cerebral vascular disease

Infectiious disease

pneumnia, diarrhea, malaria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Generally, what trends have we observed in diseases that are increasing?

A

Cardiovascular disease

Cancer

HIV/AIDs and TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Generally, what trends have we observed in diseases that are decreasing?

A

Neonatal conditions

Diarrhea

Lower respiratory infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 3 categories of emerging infectious diseases?

A

newly evolved strains (drug resistant TB)

strains that “jumped” to human population (HIV)

pathogens with increased incidence (dengue in southern US due to warming)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are some negative impacts on human health suffered from climate change?

A

Air pollution/heatwaves –> Cardiovascular, cerebrovascular and respiratory dzs

Floods/disruption of clean water supplies –> Gastroenteritis, cholera & foodborne/waterborne infectious dzs

Disrupted crop production –> malnutrition

Increased temps, extreme weather –> Malaria, dengue fever (vector borne infectious disease(

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are xenobiotics?

How do they enter and how are they metabolized in the body?

A

exogenous chemicals absorbed into the body

most are lipophilic and able to penetrate into the basement membrane

either metabolized to inactive (detoxification) or activated to form toxic metabolites (needs to be repaired so they don’t cause damage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the role of cytochrome P450?

A

detoxifies xenobiotics or convert them to active compounds, activity decreased by malnutrition

both tyeps of rxn produce ROS (like CCl3- from CCl4 metabolism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How are humans exposed to pollutants?

A

air, water, soil > skin, lungs and GI tract > bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What population is most vulnerable to air pollution?

A

people with preexisting pulmonary or cardiac diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pollutant:

Ozone

Populations at risk?

A

Healthy children

Healthy adults

Atheletes

Outdoor workers

Asthmatics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pollutant:

Ozone

Effects on healthy adults/chilrden?

A

Decreased lung function

Increased airway reactivity

Lung inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pollutant:

Ozone

Effects on Athletes, outdoor workers, asthmatics?

A

Decreased exercise capacity

Increased hospitalizations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pollutant:

Sulfur Dioxide

Populations at risk?

A

Healthy adults

Individuals with chronic lung disease

Asthmatics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Pollutant:

Sulfur Dioxide

Effect on healthy adults?

A

Increased respiratory symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pollutant:

Sulfur Dioxide

Effect on Individuals with chronic lung disease?

A

Increased mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pollutant:

Sulfur Dioxide

Effect on Asthmatics?

A

Increased hospitalization

Decreased lung function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is ozone toxic?

A

ozone gets damaged by CFCs, resulting in free radicals > injure respiratory epithelium and type 1 alveolar cells > release of inflammatory mediators. usually leads to mild symtpoms but more dangerous for patients with asthma or emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why is sulfur dioxide toxic?

A

combines with ozone and particulate matter = withce’s brew (often made by industrial plants)

sulfuric acid & sulfuric trioxide causees burning sensation in nose & throat, SOB and asthma attacks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why is particulate matter (soot) so dangerous to inhale?

A

*THEY ENTER THE ALVEOLI –> which causes the release of inflammatory mediators

Induces pulmonary inflammation and secondary CV effects

Fine or Ultrafine particles less than 10microm in diameter are the most harmful since they are so small and can travel further into the alveoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the major hallmark for carbon monoxide poisoning?

A

Cherry red color of the skin and mucous membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe carbon monoxide’s characteristics as a gas

A

Nonirritating

Colorless

Tasteless

Odorless

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are some notable situations where a person is suceptible to chronic CO poisoning?

A

Working in tunnels

Underground garages

Highway toll booths

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are some notable situations where a person is suceptible to acute CO poisoning?

A

In small, closed garage w/ running car (can produce sufficient CO to cause death in 5 minutes)

Mine fires

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does CO poisoning ultimatley kill?

A

Kills by inducing CNS depression and widespread ischemic changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What anatomic structures are affected by CO poisoning?

A

Basal ganglia

Lenticular nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What would you expect to see on a patient who dies rapidly of CO poisoning?

How about a patient who dies but survived longer?

A

no morphologic changes

edematous, pnctate hemorrhages and hypoxia induced neuronal changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

If your patient recovers from CO poisoning, what would you expect to be lasting effects?

A

Memory, vision, hearing and speech impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

With 60-70% CO saturation of Hb, what happens?

If Hb is saturated 20-30% with CO, what happens?

A

Unconsciousness <5 minutes

systemic hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is unique about a CO poisoned brain vs a normal brain?

A

CO posioned brain has increased detail in anatomical structures

petechial hemorrhages seen 24-48 hours after exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How does a CO poisoned brain appear under the microscope?

A

appearance of dead red neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Which CNS cell types are particularly vulnerable to CO poisioning?

A

Neurons (especially Sommer’s in hippocampus and Purkinje’s in the cerebellum)

Oligodendrocytes

Astrocytes

Endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are examples of indoor air pollution?

A
  • Wood smoke
  • Bioaerosols (pet dander, fungi, molds)
  • Radon (from uranium)
  • Formaldehyde
  • Sick building syndrome (fungal mold develop from poor ventilation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Lead

What are it’s effects on the human body?

A

Hematologic

Skeletal

Neurologic

GI

Renal

TOXICITIES!!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Where is lead frequently found by children?

A

Flaking lead paint and soil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Where are common places for adults to encounter lead during occupational exposure?

A

Battery manufacturing

Pigments

Car radiators

Tin cans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Where does lead primarily deposit in the human body?

How long does it stay there?

A

Bone & Developing teeth

20-30 years!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Low levels of lead in the body lead to in children?

A

Subtle deficits in…

  • Intellect
  • Behavioral problems
  • Hyperactivity
  • Poor organizatinoal skills in kids
  • Brain damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Low levels of lead causes what symptoms in adults?

A

CNS disturbances

Wrist drop

Foot drop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is a hallmark finding in the bones to indicate lead poisoning?

A

“Lead lines”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the major morpholigcal features you will see in a patient with lead posioning?

A

Hypochromic microcytic anemia

Basophilic stippling

Ring sideroblasts (red cell precursors with iron laden mT due to inhibitioin of ferrochelatase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is “lead colic”?

A

Extremely severe and poorly localized abdominal pain caused by lead poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What effect does lead poisoning have on the kidney?

A

proximal tubule damage leading to fibrosis and renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is this showing?

A

Lead lines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is this showing?

A

Lead lines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is this?

A

Ringed Sideroblast

Associated with sideroblastic anemia due to excess IRON in mitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Classification of anemia

What are the lab values for:

MCV

MCH

That would allow a microcytic anemia diagnosis?

A

[average RBC size] MCV <80 fL

[hemoglobin amount per RBC] MCH <27 pg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Histologically speaking…

How big should a RBC be?

A

A RBC should be about the same size as the nucleus of a normal lymphocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is this?

A

Microcytic/hypochromic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is this?

A

Basophilic stippling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are three major metals that are enviornmental pollutants?

A

Mercury

Arsenic

Cadmium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What disease is related to mercury poisoining?

A

Minamata disease:

Cerebral palsy, deafness, blindness, mental retardation and major CNS defects in children exposed in utero (brain atrophy worse in kids than adults)

52
Q

How is mercury toxic?

What is the major protective substance against mercury in the body?

A
  • binds to sulfhydryl groups and damage the developing CNS and kidney (lipid soluble so it accumulates easily there)
  • Glutathione
53
Q

What disease is related to cadmium poisoning?

A

“Itai-Itai” (ouch-ouch)

Oseoporosis and osteomalacia w/ renal disease, increased risk for lung cancer

54
Q

What are visual indicators that someone has had arsenic poisoning?

A

Hyperpigmentation

Hyperkeratosis

(increased risk of lung, bladder and skin cancer)

“MEES lines” in the nails

55
Q

What are examples of organic solvents?

A

Chloroform

Carbon Tetrachloride

56
Q

What happens if you get exposed to large quantities of arsenic?

What happens 2-8 weeks post exposure to arsenic?

A

GI, CV and CNS issues

neuropathy, parasthesia, numbness, pain

57
Q

What toxins lead to heart disease?

What toxins lead to lung cancer?

What toxins lead to COPD?

A

CO, lead

Radon, arsenic

cadmium

58
Q

What toxins lead to peripheral neuropathies?

What toxins lead to ataxia?

What toxins lead to renal toxicity?

A

mercury, lead, arsenic

mercury

mercury

59
Q

What toxins lead to infertility and teratogenesis?

What toxins lead to leukemia?

What toxins lead to liver angiosarcoma?

A

lead and mercury

benzene

vinyl chloride

60
Q

What can prolonged exposure of chloroform and carbon tetrachloride do to the human body?

A

CNS depression

Coma

61
Q

ASSOCIATE: Occupational exposure of rubber workers to …

A

Benzene and 1,3-butadiene

62
Q

What is the effect of benzene/1,3-butadiene on these rubber workers?

A

Marrow aplasia

HUGE RISK for acute myeloid leukemia

63
Q

What do polycyclic hydrocarbons lead to?

A

lung, bladder and scrotal cancers

exposed from fossil fuel combustion and chimney sweeps

64
Q

What do organochlorines lead to?

A

examples: PCB, dioxin and DDT that disrupt hormonal balance by targeting steroid activity

PCB and dioxin lead to chloracne: acne, hyperpigmentation, hyperkertaosis in face and behind ears, also liver and CNS problems (what the Ukrainian president got)

65
Q

What do mineral dusts like abestos, silica and beryllium lead to?

A

pneumonoconioses, abestosis and ferruginous bodies

66
Q

Asbestosis leads to?

A

Mesothelioma ; black lung

67
Q

What are furrungious bodies?

A

Asbestos fibers coated in iron

68
Q

Vinyl chloride leads to?

A

Angiosarcomas in liver

69
Q

What is bisphenol A?

A

BPA

Lines almost all food bottles and cans

*Is a potential endocrine disruptor

70
Q

What is this?

A

Aplastic anemia

71
Q

Name the disease

A

Mesothelioma

72
Q

Name the disease

A

Black lung from abestosis

73
Q

Tobacco accounts for ___% of lung cancers

A

90%

74
Q

How do you calculate pack years?

A

Pack years = average number of cigarette packs smoked/day (x) # years smoking

the higher the pack years athe worse the odds

75
Q

Describe the benefits of cessation of smoking for a smoker

A

Within 5 years, cessation of smoking improves mortality and decreases risk of death from cardiovascular disease

Lung cancer mortality drops by 21% w/in 5 years

76
Q

Even if you quit smoking, the excess risk of smoking persists…

A

For 30 years

77
Q

How do tobacco agents cause disease?

A

irritate the tracheobronchial mucosa > inflammation and mucus production (production)

smoke causes recrutiment of leuks to the lung > increase elastase > emphysema

78
Q

Abestos workers and uranium miners are at higher risk for?

Tobacco used with alcohol increases the risk of?

Tobacco smoking with HTN and hypercholesterolemia increases the risk of?

A

lung cancer

laryngeal and oral cancers (multiplicative)

MI (multiplicative)

79
Q

Cigarette smokers are at an increased risk of:

A

Emphysema

Bronchitis

ALL forms of cancer

COPD

MI

Atherosclerosis

80
Q

Maternal smoking poses in increased risk of?

A

Spontaneous abortions

Preterm births

Intrauterine growth redardation

81
Q

What risks does passive smoke expsoure have?

A

1.3x risk of lung cancer, increased risk of CAD, fatal MI and asthma in children

82
Q

What are the 3 ways alcohol is metabolized to acetaldehyde?

After it gets converted to acetaldehyde, what happens?

A

Microsomes: by CYP2E1

Cytosol: Alcohol dehydrogenase/ADH

Peroxisomes: Catalse

-ALDH (acetaldehyde dehydrogenase) convert it to acetic acid

83
Q

What happens when you consume high amoutns of alcohol?

A

competes with CYP2E1 substrates and delays catabolism of the drugs = potentiate the depressant effect of drugs

84
Q

Why do alcoholics get fatty liver?

A

alcohol metabolism requires NAD+ > NADH = NAD+ is depleted.

NAD+ is required for FA oxidation so FA accumulates in the liver

85
Q

What conditions are characteristic of alcoholism?

A

steatosis, cirrhosis, alcoholic cerebellar degeneration, esophageal varices that could rupture and lead to death

86
Q

What are the ACUTE adverse effects of EtOH?

A
  • Steatosis (fatty liver)
  • CNS effects (depressant)

gastritis

ulceration

*reversible if etoh is stopped

87
Q

What are the CHRONIC adverse effects of EtOH?

A

Liver: steatosis, alcoholic hepatitis, cirrhosis, portal hypertension, hepatocellular carcinoma

Thiamine deficiency: peripheral neuropathies, Wernicke-Korsakoff syndrome

Fetal alcohol syndrome: microcephaly, facial anomalies and growth anomalies

Alcoholic cardioomyopathy= dilated congestive cardiomyopathy

Cancer: especially breast, esophagus and laryngeal (due to acetaldehyde)

Malnutrition - VITAMIN B!!!

88
Q

Child presents with microcephaly, epicanthal folds, flat face, low nasal bridge, smooth philtrum and underdeveloped jaw. What is the most likely dx?

A

Fetal alcohol syndrome

89
Q

Thiamine deficiency secondary to alcohol use results in what neuro issues?

A
  1. Wernicke encephalopathy: psychotic symptoms and opthalmoplegia (eye muscle paralysis), also hemorrhage and nerosis in the mammillary bodies
  2. Untreated WE >>> Korsakoff’s: irreversible + confabulation
  3. cerebellar dysfunction: ataxic gait nystagmus, atrophy of anterior vermis
90
Q

Discoloration of the skin in this image is caused by?

A

Adverse drug reaction to Antibiotic = Minocycline

iron and melanin pigments seen under microscope

91
Q

What are the pathological effects of these drugs?

Anticoagulants

Anabolic steroids

A

Bleeding (Warfarin inhibits Vit K and dabigatran inhibits thrombin)

gonadal changes, psych issues, increased risk of MI

92
Q

What are the pathologic effects of oral contraceptives?

A

increased risk of cervical cancer, DVT and PE

2x increase in CAD in <35 yo who smoke

hepatic adenoma - rare, benign (usually older patient with prolonged OC use)

93
Q

What are you at an increased risk of aquiring with acetaminophen?

A

Liver failure

Centrilobar necrosis

94
Q

How is APAP metabolized?

A

95% of the time: Phase II enzymes detoxify it > urine excretion

5% of the time: CYP2E1 turns it to NAPQ = 2 outcomes:

  1. ) conjugation with GSH (glutathione) = excretion
  2. ) lipid peroxidation and protein adducts = liver failure and necrosis
95
Q

What is a typical presentation of APAP overdose commonly seen in teens attempting suicide?

A

Initial effect: none

Some tme later: liver failure (reversed if treated at hospital, 30% mortality rate for those untreated)

96
Q

What are you at increased risk of aquiring w/ aspirin?

A

salicylate poisoning of CNS (nausea, coma); chronic effects (salicylism (HA, dizz, tinnitus, bleeding,

Analgesic nephropathy

97
Q

What are the profound risks with opiate intake?

A

Respiratory depression

Arrhythmia

Cardiac arrest

“Foamy mouth”

Pulmonary edema

Infections (endocarditis in R heart valves from bacterial penetration from injecting opiate)

98
Q

What are the risks associated with methamphetamine use?

A

violent behavior, confusion, psychotic sx, hallucinations

99
Q

What are the risks associated with Marijuana use?

A

increase HR, angina in pts with COD, cognitive and motor impairments, carcinogen exposure

100
Q

What are the major complications associated with cocaine use?

A

Tachycardia

HTN

Peripheral vasoconstriction

101
Q

What risks are associated with huffing/glue sniffing?

What are the risks associated with bath salts?

A

MRI brain damage ranging from mild - severe dementia

agitation, psychosis, MI and suicide

102
Q

What are the cardiovascular, obstetrical and cerebral effects of cocaine?

A

CV: coronary artery vasoconstriction + platelet aggregation + thrombus = myocardial ischemia

legal arrythmias that can occur even in low doses

OB: decreased blood flow to placenta leading to fetal hypoxia & spontaneous abortion

Cerebral: hyperpyrexia and seizures

103
Q

What is the rule of nines?

A

Percentage of body surface covered in burns

104
Q

What factors contribute to the extent of burn damage?

How are burns usually managed?

A

depth of the burn, % of body surface burned, internal injuries (inhalation, heat that can “cook” organs)

Tx: fluid and electrolytes, infection control

105
Q

Describe the differences b/w burn classifications

A

1st degree= superficial, only epidermis (red)

2nd degree = epidermis and dermis = blisters

3rd degree = full thickness, extend into the subq tissue , can not hurt due to nerve damage

106
Q

What are the major complications associated with thermal injuries?

A
  1. Shock: if burn >20% of body surface, fluid shifts to interstitium leading to generalized and pulmonary edema

also hypermetabolic state from excess heat loss and need nutritional support

  1. Sepsis: burns colonized by Pseudomonas aeruginosa, MRSA, candida
  2. Respiratory insufficiency: noxious gas inhalation + heat affects airway within 24-48 hours
  3. Hypertrophic scars: from excessive collagen deposition
107
Q

What are some defining features of fire damage?

A

soot in airway + thermal injury of airway from heat

pugilistic stance of burnt body (muscle contractures due to heat), also firm internal organs from “cooking”

108
Q

What is malignant hyperthermia?

A

“Heat-stroke-like” from lack of sweating

Rise in core body temp and muscle contractions

In response to ANESTHETICS (if patient has RYR1 gene)

109
Q

What are the effects of hypothermia?

A

<90F tempt, LOC, brady, Afib

110
Q

How does electrical injury present?

A

a. burns
b. vfib or cardiorespiratory failure
c. lightning injury (presents with lichtenberg figures that are transient)

111
Q

What is a curie?

What is a Gray?

What is a Sievert?

A

unit for radiation emitted

unit for energy absorbed

Eq dose = absorbed dose (gray) x biologic effectiveness of radiation

112
Q

What are the end effects of ionizing radiation molecularly?

A

cell death, teratogenesis and carcinogenesis

113
Q

What is the morphology of ionizing radiation damage?

A

swelling, giant cells with pleomorphic (>1) nuclei,

enodthelial proliferation, hyalinazation and intimal thickening (leading to narrowing of vessel lumen), interstitial collagen (leading to scarring & contractions)

*looks similar to malignant cells

114
Q

What cancers are at risk of developing from radiation exposure?

What are “second cancers”?

A

leukemias, thyroid, breast, lung, also birth defects

OTHER cancers develop in indivuduals who received radiation therapy for an initial cancer (AML, myelodysplastic syndrome)

115
Q

How is the brain affected by ionizing radiation?

A

Brain is affect at high doses and injured in less time compared to other tissues

116
Q

What is primary and secondary dietary insufficiency?

A

Primary: missing from diet

Secondary: malabsorption, excess loss or increase need

117
Q

What is protein energy malnutrition?

A

causes death in infants and nursing home patients

symptoms: SubQ fat depletion, wasting of quads and deltoids, ankle or sacral edema
- increased risk fo infection, sepsis, imparied wound healing and death after surgery in bedridden patients

118
Q

Marasmus vs Kwashiorkor vs Cachexia

A

Marasmus: normal serum albumin, muscle proteins and fat used as fuel leading to really thin extremities

Kwashiokor: hypoabuminemia leading to edema, fatty liver, normal extremities

Cachexia: complication of AIDS or cancer, extreme weight loss and muscle wasting

119
Q

What induces cachexia?

A

TNF and tumor binds to receptor on muscle cells, activates NF-KB

leads to ubiquitinylation and proteolysis of myofibrils

120
Q

Anorexia nervosa vs. Bulimia

What are both diseases susceptible to?

A

Anorexia: self induced starvation, amenorrhea, decrease thyroid hormone, decrease bone density (eventual osteoporosis)

Bulimia: binge/purge, leading to hypokalemia > arrythmia, pulmonary aspiration of gastric contents, esophageal and gastric rupture

arrythmia and death due to hypokalemia

121
Q

What does obesity increase the risk of?

A

Type 2 DM, dyslipidemia, CVD, HTN, cancer

122
Q

How do you measure risks from obesity?

A

BMI >25 (overweight) and BMI > 30 (obese)

Central obesity - trunk/abdominal accumulation of fat (higher risk for disease)

123
Q

What are the consequences of obesity?

A

Metabolic syndrome

CAD

non-alcoholic fatty liver dz

cholelithiasis

osteoarthritis

124
Q

What is hypoventilation/pickwickian syndrome?

A

hypersomnolence from increased intra-abdominal pressure when sleeping leading to sleep apnea, polycythemia and cor pulmonale (right sided heart failure)

125
Q

How does obesity increase cancer risk?

A

insulin resistance = hyperinsulinemia leading to IGF-1 production, which is a mitogen

obesity = increase estrogen

proinflammatory state associated with obesity also carcinogenic

126
Q

What cancers are these correlated to?

Aflatoxin

Nitrosamines and Nitrosamides

animal fat and low fiber

total dietary fat

A

hepatocellular carcinoma

gastric carcinoma

colon cancer

breast cancer

127
Q

What are some examples of anticarcinogens?

A

Vit C, E, B-carotenes and selenium

(OMS1) MOD Exam 2 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions