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Hannah MOD > chapter 9 environmental nutritional disorders > Flashcards

chapter 9 environmental nutritional disorders Flashcards

1
Q

The Global Burden of Disease (GBD) measures what? by what unit?

A

estimates the burden imposed by environmental disease including communicable and nutritional diseases.

-applying the DALY metric (disability adjusted life year) which is a sum of years of life lost due to premature mortality and years of life lost to disability in a population

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2
Q

___ is the single leading cause of health loss (defined as morbidity and premature death)

A

undernutrition

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3
Q

on a worldwide basis there was a dramatic increase in mortality due to _____

A

HIV/AIDS and associated infections

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4
Q

___ and ___ are the leading cause of death in developed countries

A

ischemic heart disease, and cerebrovascular disease (CVD)

-main risk factors associated with loss of healthy life: smoking, HTN, obesity, high CHO, alcohol abuse

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5
Q

in developing countries 5 out of 10 leading causes of death are

A

infectious disease

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6
Q

in the postnatal period, about 50% of all deaths in children younger than 5 are attributed to what 3 conditions? are they preventable or not?

A

pneumonia, diarrheal disease, malaria
all preventable

Please Make Developments

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7
Q

categories of emerging (recently increased or could reasonablely increase in the near future) infectious disease

A
  1. dz caused by newly evolved strains/organisms (resistant drugs)
  2. dz caused by pathogen “jumping” into human species
    (HIV)
  3. dz always present but have shown recent increase in incidence ( dengue fever due to warming climate)
    **risk to spread to southern US
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8
Q

principal culprit in global warming

A

rising atmospheric level of greenhouse gases

  • particularly CO2 from burning fossil fuels, ozone, and methane
  • these gases with water vapor produce green house effect by absorbing and re-emmiting infrared energy radiated from earth surface that would normally be lost in space

-increases also from deforestation and decrease in attendant decrease in carbon fixation by plants

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9
Q

health impacts of climate change will depend on what 3 things

A
  1. extent/rapidability
  2. nature/ severity of consequences
  3. our ability to mitigate the damage
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10
Q

the negative impact associated with climate change is the increased incidence of what diseases

A
  1. cardiovascular, cerebrovascular, respiratory (worsened by heat waves and air pollution)
  2. gastroenteritis, cholera, food/waterborne dz (contamination following weather disasters)
  3. vector-borne infectious diesase like malaria and dengue fever (increased temp, crop failure, extreme weather)
  4. malnutrition (disrupted crop production)
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11
Q

define toxicology

A

distribution, effects, and mechanism of action of toxic agents
-studies effects of physical agents such radiation and heat
“ science of poisons”

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12
Q

define poison

A
  • *strictly dependent on dosage

- not straightforward

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13
Q

define xenobiotic

A

exogenous chemicals in the environment (air, water, food, soil) that may be absorbed into the body (inhalation, ingestion, skin contact)

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14
Q

how do most drugs and solvents enter cells

A

-most solvents and drugs are lipophilic. transport in the blood is facilitated by lipoproteins. lipophilic nature allows transport through the plasma membrane

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15
Q

how do solvents, drugs, and xenobiotics affect cells after entering them

A

most are metabolized to a inactive water-soluble product (detoxification) or activated to form toxic metabolites

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16
Q

what are the 2 phases associated with xenobiotics metabolism into nontoxic products or active toxic compounds. what is the most important enzyme associated

A

phase 1: chemical undergo hydrolysis, oxidation, or reduction
phase 2: products of phase 1 metabolized into water soluble compounds via glucuronidation, sulfation, methylation, and conjugation with glutathione.
*enzymes that catalyze biottransformation of xenobiotics and drugs = drug metabolizing enzymes

  • Cyt P-450 = most important phase 1 catalyst located mainly in ER of liver (also skin, lungs, GI, etc)
  • heme containing enzyme
  • may produce ROS as byproduct in both detoxifying and toxic metabolite reactions
  • participate in metabolism of: acetaminophen, barbiturates, warfarin, anticonvulsants, and alcohol
  • fasting or starvation can decrease CYP activity
  • variation of activity among individuals
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17
Q

air pollution is especially hazardous to people with ____

A

preexisting pulmonary or cardiac disease

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18
Q

outdoor air pollutants

A

ozone, nitrogen dioxide, sulfur dioxide, acid aerosols, particulates

***O -S N A P

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19
Q

how is good ozone produced and what is its function

A
  • interaction of UV radiation and Oxygen in the stratosphere and naturally accumulates 10-30 miles above earth surface
  • this layer protects life on earth by absorbing UV radiation emitted by the sun
  • can be destroyed by air pollutants
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20
Q

what is bad ozone and what is its effects

A

“ground level ozone” or ozone that accumulates in the lower atmosphere instead of the stratosphere = most dangerous air pollutant

  • formed by rxn of nitrogen oxides and volatile organic compounds in presence of sunlight
  • ozone toxicity is mediated by free radical production that damage epithelial cells along respiratory tract and type 1 alveolar cells
  • healthy individuals= upper respiratory tract inflammation and mild symptoms of decreased lung function, chest discomfort, increased airway reactivity, and lung inflammation
  • athletes, outdoor workers, asthmatics or those with emphysema = decreased exercise capacity, increased hospitalizations
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21
Q

what is the effects of the outdoor air pollutant sulfur dioxide and how is it made

A
  • produced by plants burning coal and oil, copper smelting, and paper mill by product
  • combines with ozone = witches brew
  • converted into sulfuric acid or sulfur trioxide = nose/throat burning, dyspnea, asthma attacks
  • increased respiratory symptpms, mortality, hospitalizations, and decreases lung function
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22
Q

what is “soot”

A

particulate matter that is a known outdoor air pollutant
-imp cause of mortality and morbidity related to pulmonary inflammation and secondary cardiovascular effects
-ultrafine particles
-readily inhaled in alveoli releasing lots of inflammatory mediators
(> 10 micrometers = less damaging bc removed in nose or trapped in mucous)

*only air pollutant that increases risk of attacks with heart disease patients

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23
Q

a non irritating colorless tasteless odorless gas produced when there is incomplete oxidation of hydrocarbons that kills its victims by CNS depression and widespread ischemic change.

A

carbon monoxide

  • 200x greater infinity for O2 than Hgb
  • generalized cherry-red color of skin and mucous membranes
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24
Q

what are the effects of carbon monoxide poisoning

A
  • acute toxicity in 5 minutes and can lead to coma or death
  • affects the basal ganglia and lenticular nuclei via ischemic changes
  • long exposure and survival = brain edematous. punctate hemorrhage, hypoxia-induced neuronal changes
  • if pt recovers = impaired memory, vision, hearing, speech
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25
Q

indoor air pollutant

A

wood smoke, bioaersols, radon, formaldehyde, sick building syndrome (multiple indoor pollutants + poor ventilation)

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26
Q

radioactive gas derived from uranium widely present in soil and in homes and can cause lung cancer in long term high exposure

A

radon

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27
Q

what are the metals associated as environmental pollutants

A

lead, mercury, arsenic, cadmium

*CALM

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28
Q

what metal is readily absorbed and binds to sulfhydrol groups in proteins and affects calcium metabolism. and what major effects does it have?

A

LEAD

  • effects lead to hematologic, skeletal, neurologic, gastrointestinal, and renal toxicities
  • most absorbed lead is incorporated into bones and developing teeth, and competes with calcium, and half life of 20-30 years in bone
  • low levels = neuro impairments (drop in IQ), behavioral problems, hyperactivity, blindness. toxcity affects brain development
  • in adults mainly causes peripheral neuropathies = wrist drop (affected extenosors) and foot drop ( perineal muscle paralysis)
  • encephalopathy in kids
  • LEAD LINES in gums and radio dense in bone X-rays
  • = heme deficiency and HYPOCHROMIC MICROCYTIC ANEMIA with basophilic stippling and ring sideroblasts (iron laden mitochondria)
  • lead colic = severe poorly localized ab pain
  • possible renal failure
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29
Q

classification of microcytic hypo chromic anemia

A

MCV <80 [volume]

MCH < 27 [Hgb]

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30
Q

describe mercury toxicity

A

-binds to sulhydryl groups and damages CNS of developing brains and kidneys
-sources: contaminated fish, mercury vapors, and in dental amalgams
= minamata dz = cerebral palsy, deafness, blindness, retardation,
**major CNS defects in children exposed in utero

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31
Q

which metals bind to sulfhydryl groups in proteins

A

lead and mercury

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32
Q

effects of arsenic poisoning

A
  • interferes with cell metabolism
  • affects GI, nervous system, skin, heart
  • sources: naturally in soil and water, wood preservatives, herbicides, herbal medicines
  • 2-8 wks post exposure, sensorimotor neuropathy, parathesisa,, numbness pain (neuro signs)
  • chronic exposure - skin changes (hyperpigmentation and hyperkeratosis) , respiratory disease
  • increased cancer risk of lungs, bladder, skin (palms and soles)
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33
Q

effects of cadmium toxicity

A
  • toxic to kidneys and lungs
  • uncertain mechanism that causes ROS production
  • source: nickel-cadmium batteries, soil and plants contamination, MOST IMP = food
  • alveolar epithelial cell necrosis = obstructive lung dz
  • renal tubular damage –> end-stage renal disease
  • skeletal abnormalities associated with calcium loss
  • itai-itai = postmenopausal dz, combo of osteoporosis and osteomalacia associated with renal dz
  • increased risk of lung cancer
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34
Q

what are MEES lines and where are they seen

A

-hyperkeratonisis which is a sign of arsenic poisoning

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35
Q

6 important occupational health exposures

A
  1. formaldehyde - respiratory irritation
  2. ammonia- respiratory irritation
  3. asbestos- lung cancer
  4. arsenic -lung cancer
  5. uranium -lung cancer
  6. benzene - leukemia
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36
Q

occupational exposure of rubber workers to the organic solvent benzene and 1,3 butadiene increases risk of

A

leukemia

-dose dependent marrow aplasia and increased risk of acute myeloid leukemia

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37
Q

what organochlorines disrupt hormone balance by being anti-estrogenic and anti-androgenic

A

DDT and PCB

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38
Q

what occupational exposures are linked with increase in lung cancer

A

radon, asbestos, silica, bis ether, nickel, arsenic, chromium, mustard gas, uranium
BAR CAN SUM

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39
Q

what occupational exposures are linked with increase in fibrosis of respiratory system

A

silica, asbestos, cobalt

SAC

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40
Q

which metal exposure can lead to ataxic gait

A

mercury

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41
Q

vinyl chloride exposure affects what

A

GI tract –> liver angiosarcoma

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42
Q

what metal exposure leads to chronic obstructive lung disease

A

cadmium

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43
Q

organic solvents such as chloroform and carbon tetrachloride have what effects

A

CNS depression, comma, dizziness, confusion

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44
Q

____ most potent carcinogens released during combustion of fossil fuels (coal and gas), and industrial exposure is linked to lung and bladder cancer. is present in soot which was said to be cause of scrotal cancer in chimney sweeps

A

polycyclic hydrocarbons

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45
Q

what causes folliculitis and dermatosis disorder known as chloracne (acne, cysts, hyperpigmentation, hyperkeratinosis) and liver and CNS problems

A

PCB and dioxins

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46
Q

what causes chronic nonneoplastic lung dz called pneumoconiosis

A

-inhalation of mineral dusts:
coal dust, silica, asbestos beryllium
(CABS)

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47
Q

what leads to mesothelioma , black lung and increases risk of cancer

A

asbestos

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48
Q

what are ferruginous bodies

A

asbestos fibers coated in iron and calcium ( seen in vascular mesenchymal tumors)

Blue stains on histo slide

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49
Q

___ is a potential endocrine disruptor linked to heart disease in adults and endocrine effects in infants

A

BPA

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50
Q

what is the leading exogenous cause of cancer and 90% of all lung cancers

A

tabacco

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51
Q

how to find pack years of smokers

A

avg number of packs smoke/day x numbers of years smoking

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52
Q

cessation of smoking greatly decreases risk of mortality and death by CVD dz in __ years. lung cancer mortality decreases ___ in ___ years, but the excess risk persists for 30

A

5 years

21% in 5 years

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53
Q

___ is not a direct cause of tobacco related dz (even though found in tobacco leaves) but is strongly addictive

A

nicotine

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54
Q

which country is the worlds largest producer and consumer of cigarettes

A

CHINA

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55
Q

what components of tabbacco smoke have carcinogenesis effects

A

tar , polycyclic aromatic hydrocarbons, benzopyrene , nitrosamine
T P B N (brother, please try now)

56
Q

what component of tobacco smoking have effects related to ganglionic stimulation and depression with tumor promotion

A

nicotine

57
Q

what components of tobacco smoking have tumor promotion effects

A

nicotine and phenol

58
Q

what components of tobacco smoking cause mucosal irritation

A

phenol, formaldehyde, nitrogen oxides

59
Q

what components of tobacco smoking have cilia toxicity effects

A

formaldehyde and nitrogen oxides

60
Q

what components of tobacco smoking impairs O2 transport and utilization

A

carbon monoxide

61
Q

agents in smoke have direct irritant effect on the tracheobronchial mucosa, which is

A

producing inflammation and increased mucus production on tracheobronchial mucosa

62
Q

how does smoking relate to emphysema

A

-inflammation of lungs leads to recruitment of leukocytes and increases local elastase production and subsuqeunt injury to lung tissue –> emphysema

63
Q

___ and phase II enzymes increase water solubility of some carcinogens and facilitate excretion

A

CYP (cytochrome P450)

64
Q

10x increased incidence of lung carcinoma in ___ and ___ who smoke tabacco

A

asbestos workers and uranium miners

A U stop smoking

65
Q

combo interaction of tobacco and alcohol lead to increased incidence of _____

A

laryngeal and oral cancers

66
Q

besides lung cancer, smoking is linked to what other malignant and nonmalignant disorders?

A
  • esophagus, pancreas, bladder, kidney, cervix, and bone marrow cancer
  • common nonmalignant diseases: emphysema, chronic bronchitis, COPD
  • highly linked to atherosclerosis and MIs (heart attacks)
67
Q

maternal smoking increases the risk of

A

spontaneous abortions, preterm birth, and intrauterine growth retardation (IUGR)

68
Q

does alcohol or drugs kill more people per year

A 
alcohol, 
10 mill chronic alcoholics in US 
-50% death from drunk driving, and alcohol related suicides/ homicides
-common death cause = liver cirrhosis 
-3.2% of deaths worldwide
69
Q

how is alcohol metabolized

A

ethanol is absorbed unaltered in the stomach and smalll intestine, then distributed to all tissues and fluids of the body in direct proportion to the blood level

  • *therefore amount that is exhaled is proportional to the blood level (breathilizers)
  • oxidized to actealdehyde in liver by alcohol dehydrogenase (ADH) in cytosol
  • ALDH converts acetaldehyde to acetate in mitochondria
  • acetate is used in mitochondrial respiratory chain
  • also induces CYP2e1 (some ROS production) and high levels of EtOH can compete with drug catabolism which potentates its depressants effects of narcotics, sedatives, and psychoactive drugs CNS
70
Q

__ is legal limit of alcohol in blood and for a standard person it takes ____ amount of drinks. ___ causes drowsiness and ___ causes stupor

A 
80mg/dl 
3 drinks 
200 mg/dl  = drowsiness 
300 = stupor
>300 = coma or possible respiratory distress
71
Q

where does the specifics of alcohol metabolism take place,

A

ADH in cytosol
CYP2e1 in ER
catalase in peroxisomes

72
Q

alcohol metabolism produces a lot of ___ as a by product and increases in this causes

A

NADH + H
increased NADH is linked to increased lactic acid and steatosis (bc no NAD which is needed for fatty acid oxidation and conversion of lactate –> pyruvate)

73
Q

what are the effects of acute alcoholism

A

mainly CNS effects (depressant, affects high brain first)
may induce hepatic and gastric changes (some fat droplets in liver = fatty change/steatosis; acute gastritis and ulceration)
if lower medullary centers are depressed, respiratory distress my occur
*reversible if alcohol intake is discontinued

74
Q

what are the effects of chronic alcoholism? including specifics of organ effects

A
  • shortened life span due to damage of the liver, GI tract, CNS, heart, and pancreas
  • liver: steatosis, hepatitis, cirrhosis
  • GI: bleeding from ulcers or varies
  • malnutrition: thamine B1 def: peripheral neuropathy and wernicke korsakoffs, CNS atrophy
  • cardiomyopathy: dilated congestive cardiomyopathy, HTN , and decreased HDL increases risk of coronary heart dz
  • acute and chronic pancreatitis
  • increase in incidence of oral, esophageal, liver and breast cancer
75
Q

cirrhosis (seen mainly in alcoholics) is associated with what risks

A

pulmonary HTN,

increased risk of hepatocellular carcinoma

76
Q

what occurs if mother drinks alcohol in pregnancy

A

fetal alcohol syndrome

  • microcephaly, growth retardation, facial anomalies, decreased mental function
  • most harmful in first trimester
77
Q

alcohol and hypothermia

A

alcohol causes blood vessels on skin surface to dilate which increases blood flow and heat loss. it makes you feel warm, but yet it is actually making your internal temperature colder and can lead to hypothermia if not careful

78
Q

minocycline adverse drug reaction

A

skin discoloration

79
Q

drug induced hypersensitivity reactions most commonly present as ____.

A

skin rashes

80
Q

risk: benefit consensus for menopausal hormone therapy (MHT)

A

most common type consists of estrogen and progesterone together

  • estrogen therapy alone increases risk of uterine cancer and is only used in women with hysterectomy, which also helps decrease risk of breast cancer
  • after 5-6 years combo of both increases risk of breast cancer, stroke, venous thromboembolism (DVT an PE).
  • MHT can help <60 yo women protection against heart disease, not older women
  • don’t use long term for chronic disease prevention
81
Q

risk benefit consensus to oral contraceptive use

A

risks
-increase risk of cervical cancer, thromboembolism, older women who smoke increased heart disease risk , benign hepatic adenoma (esp in older OC use women)

benefit
-protect against endometrial and ovarian cancer , and obvi avoiding unwanted pregnancy

82
Q

adverse affects of anabolic steroids

A

stunted growth, acne, gynecomastia, testicular atrophy, psychiatric issues and increase risk of MI

female facial hair and menstrual changes

83
Q

how does acetominophen detoxification produce liver damage

A

95% is detoxed with phase 2 enzymes and excreted in urine with no toxicity

5% activates CYP2e1 to metabolize it to NAPQI (usually conjugated with glutathione and produces no toxicity, but in large amounts of acetaminophen it can accumulate non conjugated NAPQI which leads to heptocellular injury by binding to proteins and causing membrane/mitochondira; dysfunction and depleting GSH increases risk of ROS injury—-> centrilobular necrosis of hepatocyte and liver failure
**lower threshold for chronic alcoholics

84
Q

metabolic and hematologic effects of aspirin overdose

A
  • acute saliycyte overdose–> respiratory alkalosis–> metabolic acidosis (accumulate pyruvate and lactate)–> inhibits krebs cycle–> metabolic acidoses increases non-ionized form which enters brain and causes effects from nausea–> coma
  • chronic overdoes (salicylism)–> HA, dizziness, tinnitus, bleeding (from decreased coag and GI ulcers), coma, tubulointerstitial nephritis–>renal papillary necrosis–> analgesic nephropathy
85
Q

presentation for cocaine

A

psychomotor stimulant

  • dopamine transport antagonist, and adrenaline rey-take
  • tachycardia, HTN, peripheral vasoconstriction
  • CA vasocontriciton –> myocardial ischemia
  • lethal arrhythmia (not dose related effects)
  • hyperprexia (high fever)
86
Q

risk of cocaine use while pregnant

A

acute decreases in placenta blood flow –> fetal hypoxia and spontaneous abortion. or possible neuro impairment

87
Q

presentation of opiates (heroin, oxycodone)

A 
-sudden death (not OD related) by:
respiratory depression 
arrthymia 
cardiac arrest 
pulmonary edema
  • risk of endocarditis in right heart valve, and other places.
  • septic emboli from endocarditis
  • lung granulomas
  • viral hepatitis
  • cutaneous lesions (absences, cellulitis, ulceration)
  • kidney amyloidosis and glomerulisclerosis –> proteinuria and nephrotic syndrome
88
Q

presentation of long term methamphetamines users

A

violent behaviors , confusion, psychotic sx (paranoia and hallucinations)

89
Q

presentation of MDMA (ecstasy)

A
  • euphoira and hallucination for 4-6 hours

- if spiked with meth or cocaine it can increase CNS effects

90
Q

risk/presenations of marijuana

A

increase heart rate, increase or decreased blood pressure,

  • CAD pt can have angina
  • cognitive and psychomotor impairment with continued use
  • carcinogens in smoke –> laryngitis, pharyngitis, bronchitis, hoarseness
91
Q

clinical significance of burn injuries depends on

A

depth of burn
% of body surface covered by burn (rule of nines)
internal injuries (inhalation of toxic fumes and heat)

92
Q

how to treat burn injuries

A

fluid and electrolyte management with infection control q

93
Q

burn classification

A

1st degree: superficial; epidermis [redness swelling]
2nd : partial thickness; epidermis and dermis [redness and blistering]
3rd: full thickness; extension into hypodermis and subq tissue [numbness, infection risk, lead to scarring or possible loss of function/sensation]

94
Q

complication of burns >20% over body

A

shock from:
rapid shift of body fluids into interstitial compartments
(hypovolemic shock)
-sx: edema, (pulm edema can be severe)

95
Q

greatest life threats to burn victims

A
  1. shock -development of hyper metabolic state –> heat loss and need for nutritional support

sepsis- pseudomonas aeurgnoisa, MRSA (staph aureus), candida infections

respiratory insufficiency - with in 1-2 days leads to injury to airway and lungs from direct heat on mouth nose and upper airway

96
Q

t/f hypertrophic scarring is common in burn victims bc of donor graft and original burn leads to excessive college deposition

A

true

97
Q

what is a heat like stroke rise in core body temp and muscle contractors in response to common anesthetics (RYR1 gene associated)

A

malignant hyperthermia

  • heat cramps, heat exhaustion, heat stroke
  • also sustained contraction of skeletal muscle exacerbates hyperthermia and leads to muscle necrosis ( rnhabdomylosis)
98
Q

dinintergrations per second of a radionuclide (radioisotope). expression of amount of radiation emitted by a source

A

Curie (Ci)

99
Q

what is the name of the unit that expresses the energy absorbed by the target tissue per unit mass

A

Gray (Gy)

100
Q

the equivalent dose for radiation effects to make a uniform measure of biologic dose effects

A

Sievert (Sv)

101
Q

main determinant effects of ionizing radiation

A
  1. rate of delivery -fractioned> at once
  2. field size: high doses to small fields> small doses to large fields
  3. cell proliferation. quiescent cells (neurons and muscle cells) > rapidly dividing cells bc DNA damage
  4. O2 effects and hypoxia (poorly vascularized with low O2 are less sensitive to radiation effects bc ROS formation/damage )
  5. vascular damage (can cause occlusion)
102
Q

3 main biologic effects of radiation

A

cell death, fetus/germ cell teratomas, carcinogensis

DUE TO DNA DAMAGE

103
Q

Morphologic effects of radiation on DNA and blood vessels

A

DNA
-ds-DNA breaks, mitotic spindle affected (aneuploidy/polyploidy), nuclear/cytoplasmic swelling , chromatin clumping, giant cells with multiple/pleomorphic nuclei,

vascular

  • interstiital fibrosis –> scarring and contraction
  • endothelial cell swelling/vacuolation, necrosis,
  • cell proliferation, collagen hyalinization, intimacy thickening, narrowing lumen
104
Q

tumors associated with radiation

A

leukemia and solid tumors
thyroid cancer
birth defects
acute myeloid leukemia/ mylodyplastic syndrome

105
Q

common sites of fibrosis after radiation

A

head neck: lungs and salivary glands

prostate/rectum/cervix: colorectal and pelvic areas

106
Q

primary vs secondary dietary insufficiency

A

primary (missing from diet)

secondary (malabsorption, impaired use, excess loss)

107
Q

how are albumin levels affected in marasmus

A

no affect bc small effect on visceral compartment vs somatic

-no edema like kwasiworker

108
Q

enlarged fatty liver
skin lesions (alternating hyper/hypopigmentation = flaky paint look)
loss of hair color
apathy, listlessness, loss of appetite

A

kwasiworkers

109
Q

mortality from cachexia is bc

A

diaphragm atrophy and other respiratory muscles

110
Q

cause of cachexia

A

mediators secreted by tumors :
proteolysis inducing factor = protein loss in urine from skeletal m. breakdown from NF-kB and ubiquitin proteasome pathway
lipid mobilizing factor increase FA ox and TNF and IL-6

111
Q

electrolyte imbalance (hypokalemia–>arrthymia)
pulmonary aspiration of gastric contents
esophageal and gastric rupture
complication of ?

A

bulimia

hypokalemia and sudden death cardiac arthymia is complication of both bulimia and aneoxeria

112
Q

function of vitamin A and effect of def

A

component of visual pigment
maintain specialized epithelia (skin)
maintain infection resistance

def- night blindness, squamous metaplasia of respiratory epithelium , infection vulnerability

sx: pitot spots , pulm infections,

113
Q

presentation of vitamin A toxicity

A

acute: HA, dizziness, vomiting, stupor, blurred vision (psuedotumor cerebri)
chronic: wt loss, anexoria, nausea, vomiting, bone/joint pain. bone resorption and fractures . teratogenic in pregnancy

114
Q

function of vitamin D

A

intestinal calcium absorption, renal calcium reabsorption, PTH regulator for calcium homestasis , mineralization of bone

115
Q

frontal bossing , squared head, rachitic rosary, pigeon breast, lumbar lordosis, bowing of legs

A

rickets seen in vitamin D def

116
Q

vitamin D helps clear what infection

A

TB

117
Q

effects of vitamin C def

A

impaired collagen fxn: poor vessel support =bleeding, inadequate synthesis of asteroids, impaired wound healing

118
Q

what vitamin deficiency results in spinocerebellar degeneration

A

vitamin E

119
Q

what vitamin deficiency results in pellagra (dementia, dermatitis, diarrhea)

A

vitamin B3, niacin

120
Q

what deficiency results in megaloblastic pernicious anemia and degeneration of posterolateral spinal cord tracks

A

B12

121
Q

folate deficiency results in

A

megaloblastic anemia and neural tube defects

122
Q

what deficiency results in poor wound healing, depressed immune response, depressed mental function, impaired night vision, and rash called acrodermatitis enteropathica (eyes, mouth, nose, and anus)

A

zinc

123
Q

function of adiponectin

A

adiponectin (from adipose)

  • FA oxidation “fat burning”
  • decrease gluconeogensis
  • increases insulin sensitivity
124
Q

how is leptin effects different from PYY

A

both act to decease appetite.

  • leptin activates catabolic pathway to increase energy expediture and create feeling of satiety
  • PYY opposes ghrelin and decreases energy intake

disorder of PYY = hyperphagia

125
Q

what characterizes metabolic syndrome

A
  • visceral adiposity
  • insulin resistance glucose intolerance
  • HTN
  • hyperinsulenmia/triglycerides
  • low HDL
  • mostly due to obesity
126
Q

what has high association with non-alcoholic fatty liver disease

A

obesity

127
Q

what is pickwickian syndrome

A

aka “hypoventilation syndrome”

  • respiratory defects in obese people
  • results in hypersomnolence (excess sleepiness) from associated sleep apnea, polycythemia, and right sided heart failure (cor pulmonale)
128
Q

marked _____ predisposes development of osteoarthritis (degenerative joint disease)

A

adiposity

129
Q

t/f obesity increases the steroid hormones estrogen and androgens

A

true

decreases SHBG production

130
Q

___ is a controller of energy balance and energy metabolism

A

adipocytes

131
Q

adipocytes and chronic inflammation

A

adipose tissue produces cytokines (TNF, IL-6, IL-1, IL-18) which creates a chronic inflammatory state marked by high levels of circulating C-reactive protein

132
Q

role of IGF in cancer

A

increased in free IGF-1 from obese state increases activity of RAS pathway to promote growth of normal and neoplastic cells

133
Q

an exogenous carcinogen associated with cancer with TP53 gene mutation

A

aflatoxin and hepatocellular carcinoma

134
Q

an endogenous production of ___ and ___ has association to gastric carcinomas

A

nitriasmides and nitrosamines

135
Q

what dietary components contribute to colon cancer

A

high animal fat and low fiber

136
Q

anti carcinogenic vitamins with antioxidant properties

A

vitamin C, E, B-carotenes, and selenium

Hannah MOD (6 decks)

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