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MOD I Exam II > Chapter 9 > Flashcards

Chapter 9 Flashcards

1
Q

What is GBD?

A

global burden disease is the burden caused by environmental diseases has on us , like communicable and nutrional diseases

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2
Q

What is DALY

A

disability adjusted life year

the sum of years of life lost d/t premature mortality and disease

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3
Q

What global health trend do we see with AIDS from 1990-2010

A

increase in the mortalitiy d/t AIDS and HIV.

maybe because people do not see them as a disease killing illness

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4
Q

what is health loss

what is the single leading cause of health loss

A

health loss => morbidity and premature death

undernutrition

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5
Q

What are the leading causes of death in developed countries?

A

Ischemic heart disease and cerebrovascular disease

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6
Q

Postnatally, what are the 3 conditions that are preventable that cause deaths in children under 5 y/o?

A

1) Pneumonia
2) Diarrheal diseases
3) Malaria

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7
Q

In developing nations, 5/10 leading causes of death are due to what?

What are they?

A

infectious diseases

  1. Respiratory diseases
  2. HIV/AIDS
  3. Diearrheal disease
  4. Tb
  5. Maleria
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8
Q

We are seeing a increase in lifes lost due to what dieases

A

Cardiovascular

HIV/AIDS/TB

Cancer

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9
Q

We are seeing a decrease in lifes lost due to what dieases

A

Neonatal conditions

Diarrheal, lower respiratory infections and other common infectious diseases

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10
Q

What emerging infectious diseases are coming up?

A
  1. New strains and organisms (multi-drug resistant TB)
  2. Diseases that previously affected other species but now affect humans (HIV)
  3. Diseases caused by an increase in pathogens (dengue fever related to climate change)
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11
Q

what is poised to be the global leading cause of environmental disease?

why

A

climate change

it is increasing diseases

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12
Q

what diseases are being worsened by heat and air pollution?

A
  1. Cardiovascular
  2. cerebrovascular
  3. respiratory diseases
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13
Q

what disease are being worsened by rising sea levels that are increasing flood and contaminating our waters

A

GI problems: gastroentertitis, cholera, food/waterborn infectious diseases

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14
Q

What diseases are being caused by increased temperature, crop failures and extreme weather variation?

give 2 examples

A

vector-born illnesses (maleria and dengue fever)

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15
Q

What is being caused by changed in local climate that disrupt crop production?

A

malnutrition

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16
Q

What is toxicology

A

distribution, effects and MOA of toxins

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17
Q

poisons

A

all substances are poisons; dose dependent

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18
Q

what are xenobiotics?

A

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

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19
Q

how does xenobiotics make ROS

A

by both detoxing and metabolizing them into reactive metobolites

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20
Q

What are the phases of detoxification of xenobiotics

A
  1. 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

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21
Q

Xenobiotics are metabolized by what?

Cause what?

A
  • CYP-450 system in ER of liver

- Either detoxification or conversion into active compounds that cause cell injury –> ROS

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22
Q

What are the inducers of CYP? (mnemonic)

A

SHADE

Smoking

Hormones

Alcohol

Drugs

Enviornmental chemicals

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23
Q

What decreases CYP activity?

A

Fasting and/or starvation

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24
Q

detoxification involves metabolism that forms what?

A

inactive water-soluble substances

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25
Q

how do most drugs and solvents enter cells

A

lipophilic and carried in blood by lipoproteins

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26
Q

Pollutants in the air, water an d soil are absorbed how?

Where do they act

A

lungs, GI tract and skin

They can act at the site of absorption or the organs they are stored and metabolized to

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27
Q

EPA puts limits on what? (6)

A 
sulfure dioxide
ozone
CO
particulate matter
nitrogen dioxide
AND LEAD
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28
Q

name imp outdoor air pollutants

A
  1. ozone (O3)
  2. sulfur dioxide
  3. CO
  4. particulate matter
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29
Q

what is ozone made and where does it accumulate

A

UV + O2 in the stratosphere and accumulates in ozone layer

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30
Q

prupose of ozone

in the last 35 years, what has happaned

A

protect us from harmful UVC

last 35 yrs, stratosphere has been shrinking d/t chlorforocarbons

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31
Q

what is ground level ozone toxicity?

A

ozone makes free radicals => damage epithelial cells in respiratory tract and type 1 alveolar => decreased lung function and chest discomfort

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32
Q

Exposure to ozone is more dangerous to ppl with

A
  1. asthma

2. emphysema`

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33
Q

Population at risk (PAR): ozone

healthy adults and children =>

athletes, outdoor workers, asthmatics=>

A

healthy adults and children => decreased lung function, increased
airway reactivity, lung inflammation

• athletes, outdoor workers, asthmatics=> decreased exercise capacity, increase
hospitalization

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34
Q

What makes sulfur dioxide

A

power plants that burn fossil fules, copper melting and paper mills

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35
Q

what creates witches brew

A

sulfur dioxide
ozone
particulate matter

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36
Q

sulfur dioxide (sulfuric acid and sulfur trioxide)

PAR: heathy adults =>

Individuals with chronic lung dz =>

Asthmatics =>

A

heathy adults => increased respiratory problems

  • Individuals with chronic lung dz => increased mortality
  • Asthmatics => decreased lung function and increased hospitilation
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37
Q

Particulate matter (soot) causes what?

What makes soot?

A

pulmonary inflammation and secondary cardiovascular effects

coal and oil-fired pwer plants

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38
Q

Which size particles are the most harmful?

What happens when inhaled?

A
  • Fine or ultrafine particles less than 10 μm in diameter

- Readily inhaled into alveoli where they are phagocytosed => inflammatory mediators

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39
Q

what are features of CO and when are they made

A

Carbon monoxide is a nonirritating, odorless, tasteless, and colorless gas

made when there is
incomplete oxidation of hydrocarbons

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40
Q

acute CO toxicity

A

usually quickly converted to CO2, but in small confined areas we make enough to cause coma or death in 5 min

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41
Q

Chronic CO poisoning occurs when working where

A

underground tunnels, parking gararages or highway booths

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42
Q

CO binds to Hb with ____ more affinity

____ saturation causes hypoxia

_____ saturation xauses unconscious or coma

A

200x

20-30

60-70

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43
Q

how does CO kill

what areas does it affect most

A

depress CNS and ischemia

basal ganglia and lenticular nuclei

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44
Q

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

A

perm mem loss
vision/hearing loss
speech loss

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45
Q

Acute poisoning by CO is marked by which characteristic morphology?

A

Cherry-red color of the skin and mucous membranes

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46
Q

if death occurs rapidly with CO, will morpholopical changes be seen?

What will they be

A

no, must last a while

edema
puntuate hemorrhages
hypoxia induced neuronal changes

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47
Q
  1. List pollutants associated with indoor air pollution
A
  1. Wood smoke (polycyclic hydrocarbons)
  2. Bioaerosols
  3. Radon: radioactive gas from uranium
  4. Formaldehyde from building materials
  5. Sick building syndrome many indoor pollutants d/t poor ventilation
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48
Q

Lead is a readily absorbed metal that binds to what?

Interferes with?

Leads to what kind of toxicities?

A

binds to sulfhydral groups and interferes with Ca2+ metabolism

  • Leads to: hematologic, skeletal, neurologic, GI, and renal toxicities
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49
Q

Most absorbed lead is incorporated into?

Competes with?

A
  • Bones and teeth

- Competes with calcium

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50
Q

High levels of lead cause CNS disturbances in both adult and children, but what condition is predominant in adults?

A

Peripheral neuropathies (foot drop and wrist drop)

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51
Q

Lead inhibits the activity of what 2 enzymes involved in heme synthesis?

Causes what type of anemia?

A
  • δ-aminolevulinic acid dehydratase and Ferrochelatase

- Microcytic hypochromic anemia (& mild hemolysis)

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52
Q

What morphological blood and bone marrow changes are present in lead poisoning?

Histological findings?

A

Ring sideroblasts —> RBCprecursors w/ iron-laden mitochondria that are detected with Prussian blue stain

  • Punctate basophilic stippling of the red cells
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53
Q

low levels of lead in kids cause

A

IQ defects
hyperactivity
poor organization skulls
brain damage

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54
Q

high levels of lead in others

A

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

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55
Q

lead poisoning occurs mostly in

A

kids

adults absorb less than 15%

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56
Q

what causes nerotoxic effects of lead

A

inhibiting NT that Ca2+ dysreg causes

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57
Q

lead lines occur where

A

epiphyses of bone (radiodense)

gums (hyperpigmented)

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58
Q

how does lead affect healing of fractures

abdomdomen

kidneys

A

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

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59
Q

Mercury mostly affects what organs?

A

CNS (developing brain)

Kidney

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60
Q

3 kinds of mercury?

Which one is the brain most susceptible to and why?

A
  1. Metallic mercury
  2. methyl mercury (organic)
  3. mercuric chloride (inorganic)

developing brain is most susceptible to methyl mercury

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61
Q

Which type of mercury causes tremors, gingivitis, and bizzare behavior when inhaled from dental amalgams?

MAD HATTER

A

metallic mercy

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62
Q

What type of mercury infected fish in the Minamata and Agano river?

A

merthyl mercury

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63
Q

What is minimata disease?

A

Mercury poisining that leads to:

  1. cerebral palsy
  2. deafness/blindness
  3. MR
  4. CNS defecfts in fetuses
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64
Q

What is the main protective mechanism from mercury induced damage to the CNS?

A

intracellular glutathoine, a sulfhydral donor

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65
Q

Arsenic affects what organs most commonly?

A

GI tract

Nervous System

Skin

Heart

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66
Q

Arsenic trioxide

is a frontline treatment for?

A

Acute promyelocytic leukemia

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67
Q

neurological effects caused by arensic poisoning are usually what?

A

sensorimotor neuropath: paresthesia, numbness and pain

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68
Q

chronic exposure to arsenic increases the risk for cancers of the lungs, bladder, and skin.

what will the skin cancer look like

A

(multiple

tumors on palms and soles of feet)

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69
Q

Cadmium is toxic to what systems?

Due to increased production of?

A
  • Kidneys and Lungs

- Increased production of ROS, thus, not directly toxic

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70
Q

The principal toxic effects of excess cadmium take the form of what diseases?

Due to?

A
  • Obstructive lung disease caused by necrosis of alveolar epithelial cells
  • Renal tubular damage that may progress to end-stage renal disease
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71
Q

what is the most important source of cadmium?

A

food

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72
Q

what is itai itai (ouch-ouch) disease)

A

when post-menopausal Japanese women drink cadmium-containing water, causes

osteoporosis + osteomalacia assx with RENAL disease

73
Q

What are examples of organic solvents

A
  1. chloroform
  2. carbon tetrachloride
  3. benzene
  4. 1,3 butadiene in rubber workser
74
Q

chloroform and carbon tetrachloride cause what

at acute and chronic levels

A

acute: dizziness and confusion => CNS
depression, coma

chronic: lower levels toxic to liver and kidneys

75
Q

benzene and 1,3-
butadiene in rubber
workers=>

A

stop differentiation of HPC in
BM => marrow aplasia and increase risk of
acute myeloid leukemia (AML)

76
Q

What are the most potent carcinogenes and how are they made

what do they cause?

A

polycylic hydrocarbons

fossil fuels

lung and bladder cancer

77
Q

what are Organochlorines

examples

A

synthetic lipophillic products that do not degrade

pestacides (DDT) and nonpestacides (PCB and dioxin)

78
Q

how do most organochlorines work?

A

disrupt hormonal balance d.t antiestrogenic and antiandrogenic activity

79
Q

Dioxins and PCBs can cause what skin disorder?

Affect CYPs how?

A
  • 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
80
Q

mineral dusts include what

A

coal dust
silica
asbestos
berrylium

81
Q

what do mineral dusts cause?

A

pneumoconiosis, a chronic,

nonneoplastic lung disease

82
Q

asbestors causes what

when is risk increased

when asbestos fibers become covered with iron and Ca2+, what are they callled

A

mesothelioma

when you smoke

ferrougous bodies

83
Q

** vinyl chloride can cause what UNCOMMON TUMOR

A

hepatic angiosarcoma

84
Q

BPA, used in food and water containers, does what

what population is more prone to ir

A

disrupts endocrine system, most often in babies bc they drink out of bottles

85
Q

Organophosphates can cause parylsis of DIAPRAGM and death. how?

A

inhibit ACh-ase=> increase ACh levels in body

86
Q

• _____ is the leading exogenous cause of human cancers, yet the most preventable COD

A

tobacco

87
Q

In US, smoking is responsible for ______ deaths

____ of all deaths in ppl who smoke are d/t lung cancer

A

> 400,000

1/3

88
Q

_____ of lung cancers are due to tobacco smoke

A

90%

89
Q

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.

A

5 years

21%

5 years

30 years

90
Q

_____% of nonsmokers are alive at age 70, but only _____% of smokers are.

o Difference in survival between smokers and non-smokers is ____years.

A

75%

50%

7.5 years

91
Q

Tobacco decreases overall survival through _______ effect?

How is this expressed?

A

dose-dependent effect

packs-years: average packs a day * years of smoking

92
Q

Which components of cigarette smoke are potent carcinogens and are directly involved in the development of lung cancer?

A

Polycyclic hydrocarbons

Nitrosamines

Other: tar, benzo[a]pyrene

93
Q

what component of tobacco smoke causes ganglionic stimulation and depression

and promotes tumor formation?

A

nicotene

94
Q

what components of tobacco

promote tumor production causes mucosal irritation?

A

phenol
formaldehyde

NO

95
Q

what causes tobacco smoke to impair O2 transport and utilization?

A

CO

96
Q

Tobacco and alcohol have a multiplicative interaction and can cause increase risk of what cancers?

A

laryngeal and oral cancers

97
Q

Agents in smoke irritate the tracheobronchial mucosa => cause inflammation and increased mucus
production (bronchitis) => metaplasia, which can then cause

A

squamous cell cancer

98
Q

____ workers and ____ miners who smoke have a 10-fold higher chance of lung carcinomas

A

asbestos

uranium

99
Q

what cancers are assx with smoking?

A 
eso
pancrease  
bladder 
kidney 
cervix 
BM
100
Q

how is cig smoking correlated with MI

A

athersclerosis => MI

smoking + HTN + hyper cholesoltema => multiplicative effect of MI

101
Q

Maternal smoking can cause what?

A

spontaneous abortion
preterm births
low birth weight

102
Q

is nicotene a carcinogene

A

no

103
Q

is passive smoking bad?

A

yes: assx with 30-60k cardiac deaths

1. 3x risk of lung cancer if living in a smokers home

104
Q

Worldwide, alcohol kills _______ people a year (___% of all deaths)

A
  1. 8 million
  2. 2 of all deaths

more widespread than other substances and cuases more deaths

105
Q

how does alcohol goes to all tissues and fluids in the body

in direct proportion to the blood level.

A

it is absorbed UNALTERED in stomach and small Intestine

106
Q

EtOH is metabolized into acetylaldehyde in 3 ways

where? and using what enzyme ?

star the most imporatnt

A
  1. in the cytsol of the liver cell via alcohol dehydrogenase**
  2. ER (microsome) of the liver cell via CYPS (CYP2E1)
  3. In the peroxisome (via catalse)
107
Q

After we convert alcohol => acetylaldehyde, what does it become?

A

go to mT and converted to acetate/acetic acid via (ALDH: acetyladehyde DH), which can be used in mT resp chain

108
Q

What is the direct, and toxic, product of alcohol oxidation?

A

Acetaldehyde

109
Q

Oxidation of ethanol by ADH (alcohol dehydrogenase) takes place in the?

A

cytosol

110
Q

The cytochrome P-450 system and its CYP2E1 isoform are located?

A

In the ER (microsome)

111
Q

What is the main cause of accumulation of fat in liver of alcoholics and lactic acidosis?

A

low NAD

in the mT,

NAD=> NADH, which decreases levels of NAD and increases lactic acid levels and steastosis

112
Q

_____ is the main agent associated with alcohol induced laryngeal and esophageal cancer

A

acetylaldehydr

113
Q

Those with one ______ allele (in 50% of azns)=>

higher risk of developing ESO cancer.

A

one ALDH2*2

114
Q

affects of acute alcoholism

A

CNS (Depressant)
hepatic steatosis
acute gastritis and ulceration

115
Q

what is the main site of chronic alcoholism?

what does it cause

these are assx with increased risk of what

A

liver

alocholic hepatitis and cirrhosis,

which are assx with portal HTN and increased risk of hepatocellular

116
Q

How does chronic alcoholism affect CNS

what does it cause

A

thiamine (vit B1) deficiency

peripheral neuropathy

wernicke-korsakoff syndrome

117
Q

chronic alocholism can lead to an ataxic gait, how?

A

atrophy the superior vermis of cerebellum

118
Q

how is alcochol good

A

20-30 (250mL) win a day=> protect against CAD by increasing HDL, which inhibits platelet aggregation and lower finbrinogen levels

119
Q

alcohol can cause hypothermia.

whaaaat and how?!

A

dilates superficial blood vessels

120
Q

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?

A

increase risk of breast cancer and thromboembolism => stroke

thus, good for a little, not for a long time

121
Q

Does menopausal hormonal therapy protect women older or younger than 60?

and of what

A

women younger than 60 from MI and CAD

no protections for grandmas

122
Q

oral contraceptives and cancers

breast cancer?

endometrial and ovarian cancers?

cervical cancer?

A

no increase risk for BC

protect against endometrial and ovarian

increase risk in cervical, especially in those who have HPV

123
Q

oral contraceptives and thrombembolism

A

3-6x increase risk for venous thrombosis pulmonary embolism, especially in smokers

124
Q

oral contraceptive and CVD risk in those younger than 30YO

A

no increase risk, unless pt is a smoker

125
Q

older patients who have been taking prolonged oral contraceptives have an increased risk for what tumor

A

a rare benign tumor- hepatic adenoma

126
Q

do anabolic steroids increase risk for MI

A

yes

127
Q

how is acetominophin detoxified

A

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

128
Q

Toxicity can occur in lower doses in alcoholics because alcohol induces ____ in the ____

A

CYP2E in the liver

129
Q

how do we tx acetominophin overdose

A

can be treated in the first 12 hours by giving N-acetylcysteine to increase glutathoine levels

130
Q

acetominophin causes Causes ___% of unintentional OD and ___% of acute liver failure

A

50%

50%

131
Q

In serious overdoses of acetaminophen, how does liver failure occur?

A

Beginning with centrilobular necrosis that may extend to entire lobules

*Liver transplantation will be the only hope for survival

132
Q

Acute salicylate (aspirin) overdose causes what acid-base shift, due to?

Followed by?

A
  • 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
133
Q

johnny took 3g of aspirin (acetylsalicyclic acid) a day for long periods of time. what does he have?

what sx will he show

A

chronic salicyclism

HA, dizziness, tinnitus, bleeding, coma, analgesic nephropahy

134
Q

______ occurs when you take aspirin + acetominophin together for many
years

A

analgesic nephropathy, Tubulointerstitial nephritis w/ renal papillary necrosis

135
Q

what causes bleeding when you have Chronic (salicylism

A

thromboxane A2 and cyclooxygenase is blocked => no platelets aggregate

136
Q

what factors of burn are of clinical significance?

A

depth,
% of body it covers,
internal injuries caused by inhaling fumes and heat,
efficacy of burn treatment

137
Q

how do we classify burns?

A

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

138
Q

what 2 things should people pay attention to when treating burns?

A

management of fluid and electrolytes

controlling the infection

139
Q

what do we want to monitor burn patients for, because they are the greatest threates to life?

in ones over 20%

A

sepsis
hypovolemic shock
respiratory insuffiency

140
Q

how do burn pts develop hypovolemix show

A

fluid shifts into interstial compartment at the burn site and systemically d/t [systemic inflammatory response syndrome] => hypovolemic show

can cause pulmonary edema

141
Q

what is malignant hyperthermia?

it pt sweating?

A

inherited mutation in RYR1 that causes a heat stroke like RAISE in core temperature when a anesthetic is given

pt is not sweating

142
Q

Total body irradiation will cause cells to look like CANCER cells. what are the feaures

A

form giant cells
nuclear/cytoplasmic swelling
form mitotic figures

143
Q

Major morphological consequences of total body irradiation

A
  1. interstitial fibrosis in lungs
  2. fibrosis of GI tract
  3. Atrophy and fibrosis of gonads
144
Q

An important pathophysiologic effect of burns is the development of what state?

A

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

–

145
Q

what cancers are assx with ioizing radiation

A
  1. leukemias
  2. THYROID tumors

AML is a 2nd cancer that can occur

146
Q

Which tissues are extremely vulnerable to radiation?

A

Tissue with high rate of cell division:

  • Gonads
  • Bone marrow
  • Lymphoid tissue
  • Mucosa of GI tract
147
Q

as we increase levels of total body radiation, what do we affect

A

acute radiation syndrome, which affects

hematopoetic (lymphocytes 1st, then bone marrow) => small bowel=> BRAIN

148
Q

0-1 Sv of total body radiation

A

NO EFECTS

149
Q

1-2 Sv=> affects _______ in 1 day- 1 week

o Signs and symptoms:

o lethal?

A

lymphocytes

granulocytopenia/ lymphopenia

not lethal

150
Q

2-10 Sv=> affects _______ in 2-6 weeks

o Signs and symptoms:

o lethal?

A

bone marrow

leukopenia, hair loss and vomitting, hemorrhave

variable: 0-80%

151
Q

10-20 Sv=> affects _______ in 5-14 days

o Signs and symptoms:

o lethal?

A

small bowel

D/V, fever amd electrolyte imbalance

100% yes

152
Q

> 50 Sv=> affects _______ in 1-4 hours

o Signs and symptoms:

o lethal?

A

brain

ataxia, coma, convulse, vomit

100%

153
Q

what is malnurition

A

Malnutrition (Protein energy malnutrition (PEM)) occurs when we do not eat enough protein/calories or when
we have a problem digesting/absorbing proteins

154
Q

Kwashiokor: ____ deprivation is more than ____ deprivation

A

protein deprivation is MORE

155
Q

Kwashiokor: protein deprivation is more than calorie deprivation

bb will have

A

protein loss in vsiceral comparment: hypoalbunemia => edema => look big

vit deficiency

fattty liver

immune def , with 2nd

156
Q

marasmis occurs when

A

weight of bb falls below 60% of normal height, sex and age

157
Q

marasmis will look

A

skinny
muscle loss
growth reatdation

158
Q

marismus bbs albumin levels will be what

A

normal bc they loose proteins from somatic compartment (skeletal mycsle)

thus, emaciated extremeties and anemia

159
Q

what is it called when when the diet is lacking one or all food sources (carbohydrates,
proteins, and/or lipids)

A

primary malnutrition

160
Q

what is it called when malabsorption, impaired utilization or storage, excess loss, or increased
need for nutrients

A

secobndary malnutrition

161
Q

What is the main site of injury from 1-2 Sv ionizing radiation?

2-10 Sv?

10-20 Sv?

> 50 Sv?

A

1-2 Sv = Lymphocytes

2-10 Sv = Bone marrow

10-20 Sv = Small bowel

> 50 Sv = Brain

162
Q

Which mediators secreted by tumors and during chronic inflammatory reactions contribute to development of Cachexia?

A
  • 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
163
Q

Proteolysis-inducing factor and proinflammatory cytokines cause skeletal muscle breakdown in cachexia through what path

A

NF-kB induced activation of the ubiquitin proteasome pathwa

164
Q

anorexia causes

A

amenorrhea**
decrease in thyroid hormone
decrease in bone densirty

165
Q

Bulimia: causes what

A
  1. hypokalemia: electrolyte imbalance => <3 problems, r

2. rupture of ESO and gastric bc we are throwin up

166
Q

what is a complication of both anorexia and bullimeia?

A

cardiac arrhythmia and sudden death d/t hypokalemia

167
Q

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.

  1. Leptin: ____
  2. Insulin: _____
  3. Ghrelin: ___
  4. PYY: ____
A

anabolic
catabolic

adipocytes

pancreatic B cells

stomach

intestines

168
Q

Pro-inflammatory state assx with obesity can be ______

A

carcinogenic

169
Q

what is the main driver of metabolic syndromes

A

obsesity

high IGF-1: hyperinsulinema, glucose intolerance

170
Q

what is pickwickian syndrome

A

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)

171
Q

obsity increases risk for what cancers

A 
eso
pancrease 
colon
rectum
breast
endometrium
kidney 
thyroid 
gb
172
Q

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?
A

hepatocellular

gastric

colon

anticarcinogenic properties

breast

DOES NOT

173
Q

what in obsesity pts increases risk of CAD

A

high TAG and low LDL

174
Q

what can obesity be a carcinogix

A

insulin resistance => hyperinsulinma (d/t high IGF-1)=>
increase cell proliferation and inhibit apoptosis

THIS IS WHY OBESITY CAN BE CARCINOGENIC

175
Q

low iron causes

A

hypochromic microcytic anemia

176
Q

low ionine causes

A

goiter

hypothryoidism

177
Q

low copper causes

A

muscle weaknes

neurodefects

abnormal collagen cross-linking

178
Q

low fluoride causes

A

dental carries

179
Q

low selenium causes

A

<3 problems

myopathy
cardiomyopathy (keshan disease)

MOD I Exam II (16 decks)

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