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Environment and Nutrition Flashcards

1
Q

Diseases predicted to increase due to Climate Change

A
  • Cardiovascular disease.
  • Cerebrovascular disease.
  • Respiratory disease.
  • Gastroenteritis.
  • Vector-borne infectious diseases.
  • Malnutrition.
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2
Q

How is climate change predicted to increase the incidence of cardiovascular, cerebrovascular and respiratory disease

A

Increased heat waves and air pollution –> increased exacerbations.

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3
Q

How is climate change predicted to increase the incidence of gastroenteritis / cholera / other foodborne and waterborne infections

A

Increase of flooding, heavy rain and other environmental disasters –> increased contamination of food / water and disruption of clean water supplies / sewage treatments.

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4
Q

How is climate change predicted to increase the incidence of Vector-borne infections

A

Increased temperatures, crop failures and extreme weather variation –> changes to vector numbers and geographic distributions.

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5
Q

How is climate change predicted to increase the incidence of malnutrition

A

Changes in local climate –> disruption of crop production.^

^Likely to be most severe in tropical climates.

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6
Q

Toxicity

A
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7
Q

Poison

A

Any substance given at a dosage which causes harmful effects.

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8
Q

Xenobiotics

A

Exogenous chemical in the environment that are absorbed into the body and stored in various organs or metabolised.

Metabolised either to:

  • Inactive water soluble compounds (which are excreted).^

OR

  • Toxic metabolites.

^Detoxification.

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9
Q

Xenobiotic Metabolism

A
  1. Phase 1 reaction = Hydrolysis, reduction or oxidation of Xenobiotic with help of Cytochrome P-450 enzyme catalyst.
  2. Primary metabolite.
  3. Phase 2 reaction = Glucuronidation, sulfation, mehtylation or conjugation with glutathione (GSH).
  4. Water soluble compounds OR toxic metabolites.
  5. Excretion OR cell damage.
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10
Q

Cytochrome P450 enzymes (CYPs)

A
  • Heme-containing enzymes.
  • Each has its own preferred substrate.
  • Primarily in endoplasmic reticulum of hepatocytes.
  • Catalyses xenobiotic reactions to either inactive water-soluble OR active toxic metabolites.
  • By-product of either reaction = ROS (reactive oxygen species).
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11
Q

Cytochrome P-450 enzyme (CYP) inducers

A
  • Environmental chemicals.
  • Drugs.
  • Smoking.
  • EtOH.
  • Hormones.

NB. Fasting or starvation decrease CYP activity

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12
Q

Effects of cytochrome P-450 enzyme (CYP) inducers

A
  1. Inducer binds specific nuclear receptors.
  2. Combine with retinoic X receptor (RXR).
  3. Complex formed binds 5’-flanking region promotor elements of CYP gene.
  4. Activates transcription of CYP.
  5. Increased CYP activity.
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13
Q

Receptors which bind inducers to activate cytochrome P-450 (CYP)

A
  • Aryl hydrocarbon receptor.
  • Peroxisome proliferator-activated receptors (PPARs).
  • Constitute androstane receptor (CAR).
  • Pregnane X receptor (PXR).
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14
Q

Most common Outdoor Air Pollutants

A
  • Ground-level ozone (gas formed by nitrogen oxide and volatile organic compound reactions in presence of sunlight)
  • Sulfur dioxide.
  • Acid aerosols.
  • Particles < 10 microm diameter (“soot”).
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15
Q

Health effects of Outdoor Air Pollutants:
-Ground-level Ozone

A

Healthy adults and children:

  • Decreased lung function.
  • Increased airway reactivity.
  • Lung inflammation.

Athletes / outdoor workers / asthmatics:

  • Decreased exercise capacity.
  • Increased hospitalisatons.
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16
Q

Health effects of Outdoor Air Pollutants:
-Nitrogen dioxide

A

Healthy adults:

  • Increased airway reactivity.

Asthmatics:

  • Decreased lung function.

Children:

  • Increased respiratory infections.
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17
Q

Health effects of Outdoor Air Pollutants:
-Sulfur dioxide

A

Healthy adults:

  • Increased respiratory symptoms.

Chronic lung disease patients:

  • Increased mortality.

Asthmatics:

  • Increased hospitalisation.
  • Decreased lung function.
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18
Q

Health effects of Outdoor Air Pollutants:
-Acid aerosols

A

Healthy adults:

  • Altered mucociliary clearance.

Children:

  • Increased respiratory infections.

Asthmatics:

  • Decreased lung function.
  • Increased hospitalisations.
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19
Q

Health effects of Outdoor Air Pollutants:
-Particulate matter (“soot”)

A

Children:

  • Increased respiratory infections.

Chronic lung or heart disease patients:

  • Decreased lung function.

Asthmatics:

  • Excess mortality.
  • Increased attacks.
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20
Q

Carbon monoxide

A
  • Non-irritating.
  • Colourless.
  • Odourless.
  • Tasteless.
  • Produced during incomplete oxidation of hydrocarbons (e.g. car engines, furnaces, cigarettes).
  • Bind Hb with high affinity (carboxyHb) –> CNS depression and systemic asphyxiation..
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21
Q

Chronic CO poisoning

A
  • Occurs when exposed to low-level persistent CO.
  • CarboxyHb is very stable once formed.
  • Persistnet carboxyHb –> slowly developing hypoxia –> widespread iscaemic changes in CNS.^
  • May have permanent memory / vision / hearing / speech loss despite cessation of CO exposure.
  • Dx by blood carboxyHb levels.

^Most commonly basal ganglia and lenticular nuclei.

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22
Q

Acute CO poisoning

A
  • Usually accidental or suicide attempt.
  • Chrctrsd by generalized cherry-red coloured skin and mucous membranes (in light-skinned people).
  • Rapid death = no morphologic changes.
  • Slower death = edematous brain, punctate haemorrhages, hypoxia-induced neuronal changes.
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23
Q

Common Indoor Air Pollutants

A
  • Smoke.
  • Bioaerosols.
  • Radon.
  • Formaldehyde.
  • CO.
  • NO2.
  • Asbestos.
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24
Q

Health effects of Indoor Air Pollutants:
-Smoke

From burning of organic materials (wood, dung, charcoal).

A
  • Lung infections.
  • Cancer.^

^May contain carcinogenic polycyclic hydrocarbons.

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25
Q

Indoor Air Pollutants:
Bioaerosols:
-Examples

A
  • Microbes (e.g. Legionnaires, viruses).
  • Allergens (e.g. pet dander, dust mites, fungi, moulds).
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26
Q

Indoor Air Pollutants:
-Radon

A
  • Radioactive gas.
  • Derived from uranium.
  • Present in soil and homes.
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27
Q

Health effects of Indoor Air Pollutants:
-Radon

A
  • Lung cancer.
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28
Q

Health effects of Indoor Air Pollutants:
-Formaldehyde

Carcinogen

A
  • Breathing difficulties.
  • Burning sensation in eyes and throat.
  • Trigger asthma attacks.

NB. In concentrations of >=0.1 ppm.

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29
Q

Sources of Lead:
-Occupational

A
  • Spray painting.
  • Foundry work.
  • Mining and extracting lead.
  • Battery manufacturing.
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30
Q

Sources of Lead:
-Non-occupational

A
  • Water supply.^
  • Paint dust and flakes^ in older housing.
  • Automotive exhaust.
  • Urban soil.

^Most common sources.

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31
Q

Lead Absorption in Children
from food

A

50% or greater.

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32
Q

Lead absorption in Adults
from food

33
Q

Effects of 10 microg / mL lead in children

Measured blood levels

A

Developmental toxicity:

  • Decreased IQ.
  • Decreased hearing.
  • Decreased growth.
  • Impaired peripheral nerve function.
  • Foetal effects (through tranplacental transfer)
34
Q

Effects of 10 - 20 microg / mL lead in children

Measured blood levels

A
  • Altered calcium homeostasis.
  • Altered vitamin D metabolism.
  • Increased level of erythrocyte protoporphyrin.
  • Decreased nerve conduction velocity.
35
Q

Effects of 40 microg / mL lead in children

Measured blood levels

A

Decreased Hb synthesis.

36
Q

Effects of 70 - 100 microg / mL lead in children

Measured blood levels

A
  • Colic.
  • Frank anaemia.
  • Nephropathy.
  • Encephalopathy.
37
Q

Effects of 150 microg / mL lead in children

Measured blood levels

38
Q

Organ where majority of lead is absorbed

80 - 85%

A

Developing teeth and bone.

39
Q

Effects of lead in developing teeth and bone

A
  • Competes with calcium.
  • Binds phosphate.
40
Q

Lead Half Life in teeth and bone

A

20 - 30 years.

41
Q

Morphology Features of Lead:
-Bone changes in children

i.e. developing bone.

Chrctrstc feature

A

Radiodense lead line deposits in epiphyses due to impaired remodelling of calcified cartilage.

42
Q

Morphology Features of Lead Poisoning:
-Bone marrow changes

NB. Changes occur rapidly and are most chrctrstc features.

A

Ring sideroblasts.

Ring sideroblasts = precursor red cells with** iron-laden** mitochondria. Detected with Prussian blue stain.

43
Q

Morphology Features of Lead:
-How ring sideroblasts formed

A
  • Lead binds ferrochelatase^ –> impaired heme synthesis –> cannot incorporate iron into heme –> excess iron in precursor cells.

^Ferrochelatase = enzyme involved in heme synthesis which has a sulfhydryl group. Lead has high affinity for sulfhydryl groups.

44
Q

Morphology Features of Lead:
-Peripheral blood changes

NB. Changes occur rapidly and are most chrctrstc features.

A
  • Microcytic, hypochromic anaemia.
  • Mild haemolysis.
  • Basophilic stippling of RBCs.
45
Q

Morphology Features of Lead:
-How peripheral blood changes occur

A
  1. Lead binds delta-aminolevulinic acid dehydratase and ferrochelatase –> impaired haemoglobin synthesis (no iron in heme) –> microcytosis, hypochromic anaemia.
  2. Lead inhibits Na+ and K+ dependent ATPases in cell membranes –> increased RBC fragility –> haemolysis.
46
Q

Pathological Features of Lead:
-Brain changes in child

A
  • Encephalopathy.
  • Mental deterioration.
  • Impaired brain development of fetus (pregnant women with lead toxicity).
47
Q

Morphology Features of Lead:
-Brain changes in child

A
  • Brain oedema.
  • Demyelination of cerebral and cerebellar white matter.
  • Necrosis of cortical neurons.
  • Diffuse astrocytic proliferation.

NB. seen with severe lead poisoning.

48
Q

Are peripheral and central nervous system lead abnormalties in children reversible or irreversible?

A

Irreversible.

49
Q

Pathological Features of Lead:
-Brain changes in adults

A
  • Headaches.
  • Memory loss.
50
Q

Morphology Features of Lead:
-Peripheral nervous system changes in adults

A
  • Demyelinating neuropathy.

NB. Typically motor nerves of commonly used muscles (e.g. extensor muscles of wrist and fingers –> wristdrop followed by peroneal muscles –> footdrop).

51
Q

Pathological Features of Lead:
-GI changes

A
  • Severe, poorly localised abdominal pain (lead colic).
52
Q

Pathological Features of Lead:
-Kidney changes

A
  • Chronic tubulointerstitial disease.
  • Renal failure.
53
Q

Morphology Features of Lead:
-Kidney changes

A
  • Proximal tubular damage with intranuclear inclusions of protein aggregates.
  • Chronic: Interstitial fibrosis.
54
Q

Pathological Features of Lead:
-Gum (gingiva) changes

A
  • Lead line.

Hyperpigmentation from excess lead.

55
Q

Pathological Features of Lead:
-Other

A

Gout^ from decreased uric acid excretion (due to renal failure)

^Saturnine gout.

56
Q

Mercury:
-Forms

A
  • Metallic mercury (elemental mercury).
  • Inorganic mercury compounds (mostly mercuric chloride).
  • Organic mercury (mostly methyl mercury).
57
Q

Mercury:
-Sources

A
  • Contaminated fish^ (methyl mercury).
  • Mercury vapors (metallic mercury in dental amalgams).

^Most common source.

58
Q

Mercury:
-Most common organs affected

A
  • Central nervous system.^
  • Kidney.

^Associated with accumulation of methyl mercury.

59
Q

Mercury:
-Minamata disease

A

In utero fetal mercury poisoning.

Manifestations:

  • Cerebral palsy.
  • Deafness.
  • Blindness.
  • Intellectual disability.
60
Q

Mercury:
-Mad Hatter disease

A

Inhaled mercury poisoning.

Symptoms:

  • Tremor.
  • Gingivitis.
  • Bizarre behaviours.
61
Q

Mercury:
-Bodies protective mechanism

A

Intracellular glutathione (GSH).

GSH has sulfhydryl group –> acts as sulfhydryl donor for mercury (i.e. binds mercury preventing mercury damage to CNS and kidneys).

NB. Mercury (like lead) has high affinity for sulfhydryl groups.

62
Q

Mercury:
-Kidney damage

A
  • Acute tubular necrosis.
  • Renal failure.
  • Nephrotic syndrome (chronic exposure).
63
Q

Mercury:
-GI manifestations

A
  • Ulcerations.
  • Bloody diarrhoea.
64
Q

Arsenic:
-Sources

A
  • Soil.
  • Water.
  • Wood preservatives.
  • Herbicides.
65
Q

Arsenic poisoning:
-Mechanism of action

A

Interferes with mitochondrial oxidative phosphorylation and function of variety of proteins.

66
Q

Arsenic poisoning:
-Main organs affected

A
  • GI tract.
  • CNS.
  • Cardiovascular system.
  • Skin.

NB. Large quantities are often fatal.

67
Q

Arsenic poisoning:
-CNS effects

A

Sensorimotor neuropathy.

NB. Occurs 2 - 8 weeks post exposure.

68
Q

Arsenic poisoning:
-Cardiovascular effects

A
  • Hypertension.
  • Prolonged QTc.
  • Ventricular arrhythmia.
69
Q

Arsenic poisoning:
-Skin effects

A
  • Hyperpigmentation.
  • Hyperkeratosis.

NB. Occurs with chronic exposure.

70
Q

Arsenic poisoning:
-Other effects of chronic exposure

A

Increased risk for development of lung, bladder and skin^ cancer.

^Usually on palms and soles and often in multiple numbers.

71
Q

Cadmium:
-Sources

A
  • Nickel-cadmium batteries.
  • Mining pollutant.
  • Electroplating pollutant.
  • Chemical fertilisers –> contamination of plants / food^ and soil.

^Most important source of exposure.

72
Q

Cadmium:
-Main organs affected

A
  • Kidneys.
  • Lungs.
73
Q

Effects of tobacco on human health

74
Q

Which respiratory infection are Vitamin D deficiency patients susceptible to due to decreased cathelicidin?

75
Q

What are the fat soluble vitamins?

A
  • A.
  • D.
  • E.
  • K.
76
Q

What vitamin deficiency is common in cystic fibrosis and why?

A

Vitamin D deficiency.

Why:
Impairment of fat soluble vitamins (ADEK)

77
Q

Niacin:
-Which vitamin is it and what can deficiency in this vitamin cause

A

Vitamin:

  • Vitamin B3.

Deficiency causes:
The 3 D’s:

  • Dementia.
  • Dermatitis.
  • Diarrhoea.
78
Q

What are the histology features of a duodenal biopsy in coealic disease

A
  • Villous atrophy (gives duodenal surface flat appearance as opposed to normal long finger-like projections of villi).
  • Crypt hyperplasia (crypts elongated in the lamina propria).
  • Intraepithelial lymphocytes.
79
Q

What are the symptoms of coeliac disease and what are some general lab findings

A

Symptoms:

  • Lethargy.
  • Fatigue.
  • Abdominal pain.
  • Diarrhoea.

General lab findings:

  • Anaemia.
  • Low iron.
  • Low Vitamin B.

Basic Pathology (14 decks)

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