Chapter 9 Flashcards
What is GBD?
global burden disease is the burden caused by environmental diseases has on us , like communicable and nutrional diseases
What is DALY
disability adjusted life year
the sum of years of life lost d/t premature mortality and disease
What global health trend do we see with AIDS from 1990-2010
increase in the mortalitiy d/t AIDS and HIV.
maybe because people do not see them as a disease killing illness
what is health loss
what is the single leading cause of health loss
health loss => morbidity and premature death
undernutrition
What are the leading causes of death in developed countries?
Ischemic heart disease and cerebrovascular disease
Postnatally, what are the 3 conditions that are preventable that cause deaths in children under 5 y/o?
1) Pneumonia
2) Diarrheal diseases
3) Malaria
In developing nations, 5/10 leading causes of death are due to what?
What are they?
infectious diseases
- Respiratory diseases
- HIV/AIDS
- Diearrheal disease
- Tb
- Maleria
We are seeing a increase in lifes lost due to what dieases
Cardiovascular
HIV/AIDS/TB
Cancer
We are seeing a decrease in lifes lost due to what dieases
Neonatal conditions
Diarrheal, lower respiratory infections and other common infectious diseases
What emerging infectious diseases are coming up?
- New strains and organisms (multi-drug resistant TB)
- Diseases that previously affected other species but now affect humans (HIV)
- Diseases caused by an increase in pathogens (dengue fever related to climate change)
what is poised to be the global leading cause of environmental disease?
why
climate change
it is increasing diseases
what diseases are being worsened by heat and air pollution?
- Cardiovascular
- cerebrovascular
- respiratory diseases
what disease are being worsened by rising sea levels that are increasing flood and contaminating our waters
GI problems: gastroentertitis, cholera, food/waterborn infectious diseases
What diseases are being caused by increased temperature, crop failures and extreme weather variation?
give 2 examples
vector-born illnesses (maleria and dengue fever)
What is being caused by changed in local climate that disrupt crop production?
malnutrition
What is toxicology
distribution, effects and MOA of toxins
poisons
all substances are poisons; dose dependent
what are xenobiotics?
exogenous substances (food, air, water soil) taken in via inhaling, ingesting, skin contact that can be detoxified and excreted from the body OR nmetabolized into reactive metabolites that cause damage via CYP P450
how does xenobiotics make ROS
by both detoxing and metabolizing them into reactive metobolites
What are the phases of detoxification of xenobiotics
- Phase I: chemicals undergo hydrolysis, oxidation, or reduction (by CYP 450)
Phase II: often metabolized to WATER SOLUBE compounds through glucuronidation, sulfation, methylation, and conjugation w/ glutathione
Xenobiotics are metabolized by what?
Cause what?
- CYP-450 system in ER of liver
- Either detoxification or conversion into active compounds that cause cell injury –> ROS
What are the inducers of CYP? (mnemonic)
SHADE
Smoking
Hormones
Alcohol
Drugs
Enviornmental chemicals
What decreases CYP activity?
Fasting and/or starvation
detoxification involves metabolism that forms what?
inactive water-soluble substances
how do most drugs and solvents enter cells
lipophilic and carried in blood by lipoproteins
Pollutants in the air, water an d soil are absorbed how?
Where do they act
lungs, GI tract and skin
They can act at the site of absorption or the organs they are stored and metabolized to
EPA puts limits on what? (6)
sulfure dioxide ozone CO particulate matter nitrogen dioxide AND LEAD
name imp outdoor air pollutants
- ozone (O3)
- sulfur dioxide
- CO
- particulate matter
what is ozone made and where does it accumulate
UV + O2 in the stratosphere and accumulates in ozone layer
prupose of ozone
in the last 35 years, what has happaned
protect us from harmful UVC
last 35 yrs, stratosphere has been shrinking d/t chlorforocarbons
what is ground level ozone toxicity?
ozone makes free radicals => damage epithelial cells in respiratory tract and type 1 alveolar => decreased lung function and chest discomfort
Exposure to ozone is more dangerous to ppl with
- asthma
2. emphysema`
Population at risk (PAR): ozone
healthy adults and children =>
athletes, outdoor workers, asthmatics=>
healthy adults and children => decreased lung function, increased
airway reactivity, lung inflammation
• athletes, outdoor workers, asthmatics=> decreased exercise capacity, increase
hospitalization
What makes sulfur dioxide
power plants that burn fossil fules, copper melting and paper mills
what creates witches brew
sulfur dioxide
ozone
particulate matter
sulfur dioxide (sulfuric acid and sulfur trioxide)
PAR: heathy adults =>
Individuals with chronic lung dz =>
Asthmatics =>
heathy adults => increased respiratory problems
- Individuals with chronic lung dz => increased mortality
- Asthmatics => decreased lung function and increased hospitilation
Particulate matter (soot) causes what?
What makes soot?
pulmonary inflammation and secondary cardiovascular effects
coal and oil-fired pwer plants
Which size particles are the most harmful?
What happens when inhaled?
- Fine or ultrafine particles less than 10 μm in diameter
- Readily inhaled into alveoli where they are phagocytosed => inflammatory mediators
what are features of CO and when are they made
Carbon monoxide is a nonirritating, odorless, tasteless, and colorless gas
made when there is
incomplete oxidation of hydrocarbons
acute CO toxicity
usually quickly converted to CO2, but in small confined areas we make enough to cause coma or death in 5 min
Chronic CO poisoning occurs when working where
underground tunnels, parking gararages or highway booths
CO binds to Hb with ____ more affinity
____ saturation causes hypoxia
_____ saturation xauses unconscious or coma
200x
20-30
60-70
how does CO kill
what areas does it affect most
depress CNS and ischemia
basal ganglia and lenticular nuclei
Chronic poisoning by CO=> CO on hemoglobin (carboxyhemoglobin) is very stabl. chronic low levels of CO
can rise to dangerous levels.
but is is removed when the RBCs are recycled
• The slowly rising levels of bound CO can make ischemic changes in the CNS,
especially in the basal ganglia and the lenticular nuclei
People can typically recover after taking the CO source away, but they can have what problems
perm mem loss
vision/hearing loss
speech loss
Acute poisoning by CO is marked by which characteristic morphology?
Cherry-red color of the skin and mucous membranes
if death occurs rapidly with CO, will morpholopical changes be seen?
What will they be
no, must last a while
edema
puntuate hemorrhages
hypoxia induced neuronal changes
- List pollutants associated with indoor air pollution
- Wood smoke (polycyclic hydrocarbons)
- Bioaerosols
- Radon: radioactive gas from uranium
- Formaldehyde from building materials
- Sick building syndrome many indoor pollutants d/t poor ventilation
Lead is a readily absorbed metal that binds to what?
Interferes with?
Leads to what kind of toxicities?
binds to sulfhydral groups and interferes with Ca2+ metabolism
- Leads to: hematologic, skeletal, neurologic, GI, and renal toxicities
Most absorbed lead is incorporated into?
Competes with?
- Bones and teeth
- Competes with calcium
High levels of lead cause CNS disturbances in both adult and children, but what condition is predominant in adults?
Peripheral neuropathies (foot drop and wrist drop)
Lead inhibits the activity of what 2 enzymes involved in heme synthesis?
Causes what type of anemia?
- δ-aminolevulinic acid dehydratase and Ferrochelatase
- Microcytic hypochromic anemia (& mild hemolysis)
What morphological blood and bone marrow changes are present in lead poisoning?
Histological findings?
Ring sideroblasts —> RBCprecursors w/ iron-laden mitochondria that are detected with Prussian blue stain
- Punctate basophilic stippling of the red cells
low levels of lead in kids cause
IQ defects
hyperactivity
poor organization skulls
brain damage
high levels of lead in others
Sensory/motor/intellectual and psychological impairments, learning disabilities, slowed
psychomotor development, blindness. In severe cases: psychoses, seizures and coma.
•
Severe cases: brain edema, demyelination of cerebral and cerebellum WM, necrosis of
cortical neurons
lead poisoning occurs mostly in
kids
adults absorb less than 15%
what causes nerotoxic effects of lead
inhibiting NT that Ca2+ dysreg causes
lead lines occur where
epiphyses of bone (radiodense)
gums (hyperpigmented)
how does lead affect healing of fractures
abdomdomen
kidneys
inhibits healing of fractures
lead colic: severe, poorly localized abdominal pain
damage proximal tubules.
if chronic rnal damage => intertersitial fibrosis
saturine gout => decrease uric acid secretion
Mercury mostly affects what organs?
CNS (developing brain)
Kidney
3 kinds of mercury?
Which one is the brain most susceptible to and why?
- Metallic mercury
- methyl mercury (organic)
- mercuric chloride (inorganic)
developing brain is most susceptible to methyl mercury
Which type of mercury causes tremors, gingivitis, and bizzare behavior when inhaled from dental amalgams?
MAD HATTER
metallic mercy
What type of mercury infected fish in the Minamata and Agano river?
merthyl mercury
What is minimata disease?
Mercury poisining that leads to:
- cerebral palsy
- deafness/blindness
- MR
- CNS defecfts in fetuses
What is the main protective mechanism from mercury induced damage to the CNS?
intracellular glutathoine, a sulfhydral donor
Arsenic affects what organs most commonly?
GI tract
Nervous System
Skin
Heart
Arsenic trioxide
is a frontline treatment for?
Acute promyelocytic leukemia
neurological effects caused by arensic poisoning are usually what?
sensorimotor neuropath: paresthesia, numbness and pain
chronic exposure to arsenic increases the risk for cancers of the lungs, bladder, and skin.
what will the skin cancer look like
(multiple
tumors on palms and soles of feet)
Cadmium is toxic to what systems?
Due to increased production of?
- Kidneys and Lungs
- Increased production of ROS, thus, not directly toxic
The principal toxic effects of excess cadmium take the form of what diseases?
Due to?
- Obstructive lung disease caused by necrosis of alveolar epithelial cells
- Renal tubular damage that may progress to end-stage renal disease
what is the most important source of cadmium?
food
what is itai itai (ouch-ouch) disease)
when post-menopausal Japanese women drink cadmium-containing water, causes
osteoporosis + osteomalacia assx with RENAL disease
What are examples of organic solvents
- chloroform
- carbon tetrachloride
- benzene
- 1,3 butadiene in rubber workser
chloroform and carbon tetrachloride cause what
at acute and chronic levels
acute: dizziness and confusion => CNS
depression, coma
chronic: lower levels toxic to liver and kidneys
benzene and 1,3-
butadiene in rubber
workers=>
stop differentiation of HPC in
BM => marrow aplasia and increase risk of
acute myeloid leukemia (AML)
What are the most potent carcinogenes and how are they made
what do they cause?
polycylic hydrocarbons
fossil fuels
lung and bladder cancer
what are Organochlorines
examples
synthetic lipophillic products that do not degrade
pestacides (DDT) and nonpestacides (PCB and dioxin)
how do most organochlorines work?
disrupt hormonal balance d.t antiestrogenic and antiandrogenic activity
Dioxins and PCBs can cause what skin disorder?
Affect CYPs how?
- Folliculitis and a dermatosis known as chloracne, characterized by acne, cyst formation, hyperpigmentation, and hyperkeratosis of face and behind ears
- Induce CYPs, may shown abnormal drug metabolism
mineral dusts include what
coal dust
silica
asbestos
berrylium
what do mineral dusts cause?
pneumoconiosis, a chronic,
nonneoplastic lung disease
asbestors causes what
when is risk increased
when asbestos fibers become covered with iron and Ca2+, what are they callled
mesothelioma
when you smoke
ferrougous bodies
** vinyl chloride can cause what UNCOMMON TUMOR
hepatic angiosarcoma
BPA, used in food and water containers, does what
what population is more prone to ir
disrupts endocrine system, most often in babies bc they drink out of bottles
Organophosphates can cause parylsis of DIAPRAGM and death. how?
inhibit ACh-ase=> increase ACh levels in body
• _____ is the leading exogenous cause of human cancers, yet the most preventable COD
tobacco
In US, smoking is responsible for ______ deaths
____ of all deaths in ppl who smoke are d/t lung cancer
> 400,000
1/3
_____ of lung cancers are due to tobacco smoke
90%
When you stop smoking, Overall mortality and risk of death from CV decreases within ___ years.
When you stop smoking, lung cancer mortality decreases by ___% within ___ years, but you are still at high risk for____years.
5 years
21%
5 years
30 years
_____% of nonsmokers are alive at age 70, but only _____% of smokers are.
o Difference in survival between smokers and non-smokers is ____years.
75%
50%
7.5 years
Tobacco decreases overall survival through _______ effect?
How is this expressed?
dose-dependent effect
packs-years: average packs a day * years of smoking
Which components of cigarette smoke are potent carcinogens and are directly involved in the development of lung cancer?
Polycyclic hydrocarbons
Nitrosamines
Other: tar, benzo[a]pyrene
what component of tobacco smoke causes ganglionic stimulation and depression
and promotes tumor formation?
nicotene
what components of tobacco
promote tumor production causes mucosal irritation?
phenol
formaldehyde
NO
what causes tobacco smoke to impair O2 transport and utilization?
CO
Tobacco and alcohol have a multiplicative interaction and can cause increase risk of what cancers?
laryngeal and oral cancers
Agents in smoke irritate the tracheobronchial mucosa => cause inflammation and increased mucus
production (bronchitis) => metaplasia, which can then cause
squamous cell cancer
____ workers and ____ miners who smoke have a 10-fold higher chance of lung carcinomas
asbestos
uranium
what cancers are assx with smoking?
eso pancrease bladder kidney cervix BM
how is cig smoking correlated with MI
athersclerosis => MI
smoking + HTN + hyper cholesoltema => multiplicative effect of MI
Maternal smoking can cause what?
spontaneous abortion
preterm births
low birth weight
is nicotene a carcinogene
no
is passive smoking bad?
yes: assx with 30-60k cardiac deaths
1. 3x risk of lung cancer if living in a smokers home
Worldwide, alcohol kills _______ people a year (___% of all deaths)
- 8 million
- 2 of all deaths
more widespread than other substances and cuases more deaths
how does alcohol goes to all tissues and fluids in the body
in direct proportion to the blood level.
it is absorbed UNALTERED in stomach and small Intestine
EtOH is metabolized into acetylaldehyde in 3 ways
where? and using what enzyme ?
star the most imporatnt
- in the cytsol of the liver cell via alcohol dehydrogenase**
- ER (microsome) of the liver cell via CYPS (CYP2E1)
- In the peroxisome (via catalse)
After we convert alcohol => acetylaldehyde, what does it become?
go to mT and converted to acetate/acetic acid via (ALDH: acetyladehyde DH), which can be used in mT resp chain
What is the direct, and toxic, product of alcohol oxidation?
Acetaldehyde
Oxidation of ethanol by ADH (alcohol dehydrogenase) takes place in the?
cytosol
The cytochrome P-450 system and its CYP2E1 isoform are located?
In the ER (microsome)
What is the main cause of accumulation of fat in liver of alcoholics and lactic acidosis?
low NAD
in the mT,
NAD=> NADH, which decreases levels of NAD and increases lactic acid levels and steastosis
_____ is the main agent associated with alcohol induced laryngeal and esophageal cancer
acetylaldehydr
Those with one ______ allele (in 50% of azns)=>
higher risk of developing ESO cancer.
one ALDH2*2
affects of acute alcoholism
CNS (Depressant)
hepatic steatosis
acute gastritis and ulceration
what is the main site of chronic alcoholism?
what does it cause
these are assx with increased risk of what
liver
alocholic hepatitis and cirrhosis,
which are assx with portal HTN and increased risk of hepatocellular
How does chronic alcoholism affect CNS
what does it cause
thiamine (vit B1) deficiency
peripheral neuropathy
wernicke-korsakoff syndrome
chronic alocholism can lead to an ataxic gait, how?
atrophy the superior vermis of cerebellum
how is alcochol good
20-30 (250mL) win a day=> protect against CAD by increasing HDL, which inhibits platelet aggregation and lower finbrinogen levels
alcohol can cause hypothermia.
whaaaat and how?!
dilates superficial blood vessels
MHT: give menopausal pt estrogen + progesterone
• Early in menopause=> alleviates menopausal sx (hot flashes) and reduces chances of fractures (because reduces osteoporosis),
but what happen if this is given over a prolonged pd of time?
increase risk of breast cancer and thromboembolism => stroke
thus, good for a little, not for a long time
Does menopausal hormonal therapy protect women older or younger than 60?
and of what
women younger than 60 from MI and CAD
no protections for grandmas
oral contraceptives and cancers
breast cancer?
endometrial and ovarian cancers?
cervical cancer?
no increase risk for BC
protect against endometrial and ovarian
increase risk in cervical, especially in those who have HPV
oral contraceptives and thrombembolism
3-6x increase risk for venous thrombosis pulmonary embolism, especially in smokers
oral contraceptive and CVD risk in those younger than 30YO
no increase risk, unless pt is a smoker
older patients who have been taking prolonged oral contraceptives have an increased risk for what tumor
a rare benign tumor- hepatic adenoma
do anabolic steroids increase risk for MI
yes
how is acetominophin detoxified
At therapeutic dosages, 95% of acetaminophen is detoxified by phase II hepatic enzymes and
excreted in our urine as glucuronate or sulfate conjugates, NOT causing toxicity
- Remaining 5% is metabolized by CPY2E1 into NAPQ, a highly reactive metabolite.
- Before it can cause harm, it is conjugated by glutathione (GSH)
• if overdosed, all glutathione is used => NAPQ causes protein adducts and lipid peroxidation
=> centrilobular necrosis => liver failure
Toxicity can occur in lower doses in alcoholics because alcohol induces ____ in the ____
CYP2E in the liver
how do we tx acetominophin overdose
can be treated in the first 12 hours by giving N-acetylcysteine to increase glutathoine levels
acetominophin causes Causes ___% of unintentional OD and ___% of acute liver failure
50%
50%
In serious overdoses of acetaminophen, how does liver failure occur?
Beginning with centrilobular necrosis that may extend to entire lobules
*Liver transplantation will be the only hope for survival
Acute salicylate (aspirin) overdose causes what acid-base shift, due to?
Followed by?
- Alkalosis as a consequence of stimulation of the respiratory center in the medulla (ASA is an acid)
- Followed by metabolic acidosis which forms salicyclates that diffuse into the brain and cause nausea and a coma
johnny took 3g of aspirin (acetylsalicyclic acid) a day for long periods of time. what does he have?
what sx will he show
chronic salicyclism
HA, dizziness, tinnitus, bleeding, coma, analgesic nephropahy
______ occurs when you take aspirin + acetominophin together for many
years
analgesic nephropathy, Tubulointerstitial nephritis w/ renal papillary necrosis
what causes bleeding when you have Chronic (salicylism
thromboxane A2 and cyclooxygenase is blocked => no platelets aggregate
what factors of burn are of clinical significance?
depth,
% of body it covers,
internal injuries caused by inhaling fumes and heat,
efficacy of burn treatment
how do we classify burns?
1st degree: superficial (epidermis): PAIN, REDNESS AND SWELLING
2nd degree: partial thickness (epideris and dermis): REDNESS AND BLISTERING
3rd degree: full thickness(into subcutaneous tissue): NUMBESS BC NERVES ARE DMGED, SCARS, LOF
what 2 things should people pay attention to when treating burns?
management of fluid and electrolytes
controlling the infection
what do we want to monitor burn patients for, because they are the greatest threates to life?
in ones over 20%
sepsis
hypovolemic shock
respiratory insuffiency
how do burn pts develop hypovolemix show
fluid shifts into interstial compartment at the burn site and systemically d/t [systemic inflammatory response syndrome] => hypovolemic show
can cause pulmonary edema
what is malignant hyperthermia?
it pt sweating?
inherited mutation in RYR1 that causes a heat stroke like RAISE in core temperature when a anesthetic is given
pt is not sweating
Total body irradiation will cause cells to look like CANCER cells. what are the feaures
form giant cells
nuclear/cytoplasmic swelling
form mitotic figures
Major morphological consequences of total body irradiation
- interstitial fibrosis in lungs
- fibrosis of GI tract
- Atrophy and fibrosis of gonads
An important pathophysiologic effect of burns is the development of what state?
Hypermetabolic state associated with excess heat loss and increased need for nutritional support
*Estimated that when >40% of body surface is burned the RMR may double
–
what cancers are assx with ioizing radiation
- leukemias
- THYROID tumors
AML is a 2nd cancer that can occur
Which tissues are extremely vulnerable to radiation?
Tissue with high rate of cell division:
- Gonads
- Bone marrow
- Lymphoid tissue
- Mucosa of GI tract
as we increase levels of total body radiation, what do we affect
acute radiation syndrome, which affects
hematopoetic (lymphocytes 1st, then bone marrow) => small bowel=> BRAIN
0-1 Sv of total body radiation
NO EFECTS
1-2 Sv=> affects _______ in 1 day- 1 week
o Signs and symptoms:
o lethal?
lymphocytes
granulocytopenia/ lymphopenia
not lethal
2-10 Sv=> affects _______ in 2-6 weeks
o Signs and symptoms:
o lethal?
bone marrow
leukopenia, hair loss and vomitting, hemorrhave
variable: 0-80%
10-20 Sv=> affects _______ in 5-14 days
o Signs and symptoms:
o lethal?
small bowel
D/V, fever amd electrolyte imbalance
100% yes
> 50 Sv=> affects _______ in 1-4 hours
o Signs and symptoms:
o lethal?
brain
ataxia, coma, convulse, vomit
100%
what is malnurition
Malnutrition (Protein energy malnutrition (PEM)) occurs when we do not eat enough protein/calories or when
we have a problem digesting/absorbing proteins
Kwashiokor: ____ deprivation is more than ____ deprivation
protein deprivation is MORE
Kwashiokor: protein deprivation is more than calorie deprivation
bb will have
protein loss in vsiceral comparment: hypoalbunemia => edema => look big
vit deficiency
fattty liver
immune def , with 2nd
marasmis occurs when
weight of bb falls below 60% of normal height, sex and age
marasmis will look
skinny
muscle loss
growth reatdation
marismus bbs albumin levels will be what
normal bc they loose proteins from somatic compartment (skeletal mycsle)
thus, emaciated extremeties and anemia
what is it called when when the diet is lacking one or all food sources (carbohydrates,
proteins, and/or lipids)
primary malnutrition
what is it called when malabsorption, impaired utilization or storage, excess loss, or increased
need for nutrients
secobndary malnutrition
What is the main site of injury from 1-2 Sv ionizing radiation?
2-10 Sv?
10-20 Sv?
> 50 Sv?
1-2 Sv = Lymphocytes
2-10 Sv = Bone marrow
10-20 Sv = Small bowel
> 50 Sv = Brain
Which mediators secreted by tumors and during chronic inflammatory reactions contribute to development of Cachexia?
- Proteolysis-inducing factor: excreted in urine of weight-losing patients w/ pancreatic, breast, colon, and other cancers
- Lipid-mobilizing factor: increases fatty acid oxidation and proinflammatory cytokines, such as TNF and IL-6
Proteolysis-inducing factor and proinflammatory cytokines cause skeletal muscle breakdown in cachexia through what path
NF-kB induced activation of the ubiquitin proteasome pathwa
anorexia causes
amenorrhea**
decrease in thyroid hormone
decrease in bone densirty
Bulimia: causes what
- hypokalemia: electrolyte imbalance => <3 problems, r
2. rupture of ESO and gastric bc we are throwin up
what is a complication of both anorexia and bullimeia?
cardiac arrhythmia and sudden death d/t hypokalemia
Adipose tissue makes afferent signals that influence the activity of the hypothalamus, which is THE regulator of appetite and satiety. These signals decrease food intake by inhibiting _____ circuits and
enhance NRG expenditure by activating ____ circuits.
- Leptin: ____
- Insulin: _____
- Ghrelin: ___
- PYY: ____
anabolic
catabolic
adipocytes
pancreatic B cells
stomach
intestines
Pro-inflammatory state assx with obesity can be ______
carcinogenic
what is the main driver of metabolic syndromes
obsesity
high IGF-1: hyperinsulinema, glucose intolerance
what is pickwickian syndrome
occurs in obese pts
hypoventiliation and hypersomnolence (super sleepy) at night and day,
associated assx with sleep apnea and right sided <3 failure (cor pulmonale)
obsity increases risk for what cancers
eso pancrease colon rectum breast endometrium kidney thyroid gb
Aflaxtoxin => _____ carcinoma
Nitrosamines and nitrosamides => _____ carcinomas
High animal fat and low fiber => _____ cancer
- Vit C and E, B-carotenes and selenium => _______ properties
- Total dietary fat => increases ____ cancer
- Omega3FA => ___ lower risk of CV?
hepatocellular
gastric
colon
anticarcinogenic properties
breast
DOES NOT
what in obsesity pts increases risk of CAD
high TAG and low LDL
what can obesity be a carcinogix
insulin resistance => hyperinsulinma (d/t high IGF-1)=>
increase cell proliferation and inhibit apoptosis
THIS IS WHY OBESITY CAN BE CARCINOGENIC
low iron causes
hypochromic microcytic anemia
low ionine causes
goiter
hypothryoidism
low copper causes
muscle weaknes
neurodefects
abnormal collagen cross-linking
low fluoride causes
dental carries
low selenium causes
<3 problems
myopathy
cardiomyopathy (keshan disease)
