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.
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.
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.
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.
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.
6
Q
Toxicity
A
7
Q
Poison
A
Any substance given at a dosage which causes harmful effects.
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.
9
Q
Xenobiotic Metabolism
A
- Phase 1 reaction = Hydrolysis, reduction or oxidation of Xenobiotic with help of Cytochrome P-450 enzyme catalyst.
- Primary metabolite.
- Phase 2 reaction = Glucuronidation, sulfation, mehtylation or conjugation with glutathione (GSH).
- Water soluble compounds OR toxic metabolites.
- Excretion OR cell damage.
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).
11
Q
Cytochrome P-450 enzyme (CYP) inducers
A
- Environmental chemicals.
- Drugs.
- Smoking.
- EtOH.
- Hormones.
NB. Fasting or starvation decrease CYP activity
12
Q
Effects of cytochrome P-450 enzyme (CYP) inducers
A
- Inducer binds specific nuclear receptors.
- Combine with retinoic X receptor (RXR).
- Complex formed binds 5’-flanking region promotor elements of CYP gene.
- Activates transcription of CYP.
- Increased CYP activity.
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).
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”).
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.
16
Q
Health effects of Outdoor Air Pollutants:
-Nitrogen dioxide
A
Healthy adults:
- Increased airway reactivity.
Asthmatics:
- Decreased lung function.
Children:
- Increased respiratory infections.
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.
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.
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.
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..
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.
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.
23
Q
Common Indoor Air Pollutants
A
- Smoke.
- Bioaerosols.
- Radon.
- Formaldehyde.
- CO.
- NO2.
- Asbestos.
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.
25
Indoor Air Pollutants:
Bioaerosols:
*-Examples*
* Microbes (e.g. Legionnaires, viruses).
* Allergens (e.g. pet dander, dust mites, fungi, moulds).
26
Indoor Air Pollutants:
*-Radon*
* Radioactive gas.
* Derived from uranium.
* Present in soil and homes.
27
Health effects of Indoor Air Pollutants:
*-Radon*
* Lung cancer.
28
Health effects of Indoor Air Pollutants:
*-Formaldehyde*
## Footnote
Carcinogen
* Breathing difficulties.
* Burning sensation in eyes and throat.
* Trigger asthma attacks.
## Footnote
**NB.** In concentrations of >=0.1 ppm.
29
Sources of Lead:
*-Occupational*
* Spray painting.
* Foundry work.
* Mining and extracting lead.
* Battery manufacturing.
30
Sources of Lead:
*-Non-occupational*
* **Water supply.**^
* **Paint dust and flakes**^ in older housing.
* Automotive exhaust.
* Urban soil.
## Footnote
^Most common sources.
31
Lead Absorption in Children
from food
50% or greater.
32
Lead absorption in Adults
from food
15%.
33
Effects of **10 microg / mL** lead in children
| Measured blood levels
Developmental toxicity:
* Decreased IQ.
* Decreased hearing.
* Decreased growth.
* Impaired peripheral nerve function.
* Foetal effects (through tranplacental transfer)
34
Effects of **10 - 20 microg / mL** lead in children
| Measured blood levels
* Altered calcium homeostasis.
* Altered vitamin D metabolism.
* Increased level of erythrocyte protoporphyrin.
* Decreased nerve conduction velocity.
35
Effects of **40 microg / mL** lead in children
| Measured blood levels
Decreased Hb synthesis.
36
Effects of **70 - 100 microg / mL** lead in children
| Measured blood levels
* Colic.
* Frank anaemia.
* Nephropathy.
* Encephalopathy.
37
Effects of **150 microg / mL** lead in children
| Measured blood levels
Death.
38
Organ where majority of lead is absorbed
## Footnote
80 - 85%
Developing teeth and bone.
39
Effects of lead in developing teeth and bone
* Competes with calcium.
* Binds phosphate.
40
Lead Half Life in teeth and bone
20 - 30 years.
41
Morphology Features of Lead:
*-Bone changes in children*
| i.e. developing bone.
## Footnote
**Chrctrstc feature**
**Radiodense lead line** deposits in epiphyses due to impaired remodelling of calcified cartilage.
42
Morphology Features of Lead Poisoning:
*-Bone marrow changes*
## Footnote
**NB.** Changes occur rapidly and are most **chrctrstc features**.
Ring sideroblasts.
## Footnote
Ring sideroblasts = **precursor red cells** with** iron-laden** mitochondria. Detected with **Prussian blue stain**.
43
Morphology Features of Lead:
*-How ring sideroblasts formed*
* Lead binds ferrochelatase^ --> impaired heme synthesis --> cannot incorporate iron into heme --> excess iron in precursor cells.
## Footnote
^Ferrochelatase = enzyme involved in heme synthesis which has a sulfhydryl group. Lead has high affinity for sulfhydryl groups.
44
Morphology Features of Lead:
*-Peripheral blood changes*
## Footnote
**NB.** Changes occur rapidly and are most **chrctrstc features**.
* Microcytic, hypochromic anaemia.
* Mild haemolysis.
* Basophilic stippling of RBCs.
45
Morphology Features of Lead:
*-How peripheral blood changes occur*
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
Pathological Features of Lead:
*-Brain changes in child*
* Encephalopathy.
* Mental deterioration.
* Impaired brain development of fetus (pregnant women with lead toxicity).
47
Morphology Features of Lead:
*-Brain changes in child*
* Brain oedema.
* Demyelination of cerebral and cerebellar white matter.
* Necrosis of cortical neurons.
* Diffuse astrocytic proliferation.
## Footnote
**NB.** seen with severe lead poisoning.
48
Are peripheral and central nervous system lead abnormalties in children reversible or irreversible?
Irreversible.
49
Pathological Features of Lead:
*-Brain changes in adults*
* Headaches.
* Memory loss.
50
Morphology Features of Lead:
*-Peripheral nervous system changes in adults*
* Demyelinating neuropathy.
## Footnote
**NB.** Typically motor nerves of commonly used muscles (e.g. extensor muscles of wrist and fingers --> **wristdrop** followed by peroneal muscles --> **footdrop**).
51
Pathological Features of Lead:
*-GI changes*
* Severe, poorly localised abdominal pain (lead colic).
52
Pathological Features of Lead:
*-Kidney changes*
* Chronic tubulointerstitial disease.
* Renal failure.
53
Morphology Features of Lead:
*-Kidney changes*
* Proximal tubular damage with intranuclear inclusions of protein aggregates.
* Chronic: Interstitial fibrosis.
54
Pathological Features of Lead:
*-Gum (gingiva) changes*
* Lead line.
## Footnote
Hyperpigmentation from excess lead.
55
Pathological Features of Lead:
*-Other*
**Gout**^ from decreased uric acid excretion (due to renal failure)
## Footnote
^Saturnine gout.
56
Mercury:
*-Forms*
* Metallic mercury (elemental mercury).
* Inorganic mercury compounds (mostly mercuric chloride).
* Organic mercury (mostly methyl mercury).
57
Mercury:
*-Sources*
* **Contaminated fish**^ (methyl mercury).
* Mercury vapors (metallic mercury in dental amalgams).
## Footnote
^Most common source.
58
Mercury:
*-Most common organs affected*
* Central nervous system.^
* Kidney.
## Footnote
^Associated with accumulation of methyl mercury.
59
Mercury:
*-Minamata disease*
In utero fetal mercury poisoning.
Manifestations:
* Cerebral palsy.
* Deafness.
* Blindness.
* Intellectual disability.
60
Mercury:
*-Mad Hatter disease*
Inhaled mercury poisoning.
Symptoms:
* Tremor.
* Gingivitis.
* Bizarre behaviours.
61
Mercury:
*-Bodies protective mechanism*
Intracellular glutathione (GSH).
GSH has sulfhydryl group --> acts as sulfhydryl donor for mercury (i.e. binds mercury preventing mercury damage to CNS and kidneys).
## Footnote
**NB.** Mercury (like lead) has high affinity for sulfhydryl groups.
62
Mercury:
*-Kidney damage*
* Acute tubular necrosis.
* Renal failure.
* Nephrotic syndrome (chronic exposure).
63
Mercury:
*-GI manifestations*
* Ulcerations.
* Bloody diarrhoea.
64
Arsenic:
*-Sources*
* Soil.
* Water.
* Wood preservatives.
* Herbicides.
65
Arsenic poisoning:
*-Mechanism of action*
Interferes with **mitochondrial oxidative phosphorylation** and function of variety of proteins.
66
Arsenic poisoning:
*-Main organs affected*
* GI tract.
* CNS.
* Cardiovascular system.
* Skin.
## Footnote
**NB.** Large quantities are often fatal.
67
Arsenic poisoning:
*-CNS effects*
Sensorimotor neuropathy.
## Footnote
**NB.** Occurs 2 - 8 weeks post exposure.
68
Arsenic poisoning:
*-Cardiovascular effects*
* Hypertension.
* Prolonged QTc.
* Ventricular arrhythmia.
69
Arsenic poisoning:
*-Skin effects*
* Hyperpigmentation.
* Hyperkeratosis.
## Footnote
**NB.** Occurs with chronic exposure.
70
Arsenic poisoning:
*-Other effects of chronic exposure*
Increased risk for development of lung, bladder and skin^ **cancer**.
## Footnote
^Usually on palms and soles and often in multiple numbers.
71
Cadmium:
*-Sources*
* Nickel-cadmium batteries.
* Mining pollutant.
* Electroplating pollutant.
* Chemical fertilisers --> contamination of plants / **food**^ and soil.
## Footnote
^Most important source of exposure.
72
Cadmium:
*-Main organs affected*
* Kidneys.
* Lungs.
73
Effects of tobacco on human health
74
Which respiratory infection are Vitamin D deficiency patients susceptible to due to decreased cathelicidin?
TB
75
What are the fat soluble vitamins?
* A.
* D.
* E.
* K.
76
What vitamin deficiency is common in cystic fibrosis and why?
Vitamin D deficiency.
**Why:**
Impairment of fat soluble vitamins (ADEK)
77
Niacin:
*-Which vitamin is it and what can deficiency in this vitamin cause*
Vitamin:
* Vitamin B3.
Deficiency causes:
The 3 D's:
* Dementia.
* Dermatitis.
* Diarrhoea.
78
What are the histology features of a duodenal biopsy in coealic disease
* 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
What are the symptoms of coeliac disease and what are some general lab findings
Symptoms:
* Lethargy.
* Fatigue.
* Abdominal pain.
* Diarrhoea.
General lab findings:
* Anaemia.
* Low iron.
* Low Vitamin B.
