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Nutrition > Recap 6 (nutri) > Flashcards

Recap 6 (nutri) Flashcards

1
Q

2 phases of xenobiotics products metabolism

A
  1. Chemical undergo hydrolysis, oxidation or reduction
    - catalyst = CP450 (+++ hepatocytes in ER) -> detoxify xenobiotics or convert into active compounds -> produce ROS
    - CYP inducer = chemicals, drugs, smoking, alcohol, hormones = bind to Sp receptors (PPAR, CAR, PXR) -> heterodimerize with retinoic X receptor (RXR) -> active promoter of CYP
    - CYP inhibitors = fasting, starvation
  2. Transforming into water-soluble compounds : glucuronidation, sulfation, methylation, conjugation with glutathione
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2
Q

Effects of O3 (ozone air polluant)

A

Produced by interaction of UV and O2 = ozone layer
Ground level ozone = formed by rx of nitrogen oxides and volatile organic compounds -> ROS injure respi epith cell and type 1 alveolar cells

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3
Q

Effects of CO

A

Systemic asphyxiant
Source =incomplete oxidation of hydrocarbons
Short lived in atmosphere because rapidly oxidized to CO2
SNC depression
++ischemic changes in basal ganglia and lenticular nuclei
Cherry-red color of skin
If prolonged = edema brain, H+, neuronal change not Sp = systemic hypoxia

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4
Q

Effects of radon

A

Radioactive gas derived from uranium in soils and homes
Lung cancer

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5
Q

Morphology of lead toxicity

A

Bind sulfhydryl (high affinity) groups = interfere with calcium metabolism -> hematopoietic, skeletal, neuro, GI, renal toxicity
Interferes in 2 enzymes in heme synthesis = delta aminolerulinic acid dehydratase and ferrochelatase = iron incorporation in heme in impaired
Inhibe Na et K dependent ATPase = RBC fragle = hemolysis
1. Blood and bone marrow =
inhibe ferrochelatase -> ring sideroblast (punctuate basophilic stipping), red cell precursors with iron laden mitochondria
microcytic hypochromic anemia with mild hemolysis
2. Children irreversible, adult reversible
3. DX = elevated blood lead and GR free protoporphyrin or zinc protoporphyrin
4. 80-85% absorb in developing teath and bone, 5-10% blood, rest = soft tissue

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6
Q

Mercury, effects, soruces, mechanism

A

Binds sulfhydryl groups in certain proteins with high affinity = CNS, kidney
Source = mercury vapor from dental amalgams, contaminated fish
Effects = lipid solubility facilitate accumulation in brain, gut (ulcers, bloody d+), renal failure
- IC GSH act as sulfhydryl donor = main protective mechanism against mercury

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7
Q

Arsenic toxicity

A

Interferes with mitochondrial oxidate phosphorylation
—> sensorimotor neuropathy, hyperT, skin changes, risk cancer
++ TGI, nervous system, skin, heart

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8
Q

Calcium toxicity

A

Requires uptake into cells by tramsporters = ZIP8
-> lungs and kidneys

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9
Q

Benzene, 1,3-butadiene toxicity

A

Increase risk of leukemia
Disrupt progenitor cell differentiation
Benzene is oxidized to an epoxide by CYP2E

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10
Q

Bisphenol (BPA) toxicity

A

Endocrine disruptor, heart disease

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11
Q

Carcinogens in lung cancers

A

Polycyclic hydrocarbon and nitrosamines

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12
Q

Metabolism of alcohol

A

Absorb in stomach/small intestines -> distribution -> metabolized to acetaldehyde in liver by 3 enzymes = deshydrogenase (cytosol), CP450, enzymes (RE) and catalase -> convertion to acetaldehyde dehydrogenase to acetate = used in mitochondria respiration chain or lipid synthesis

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13
Q

Effects of alcohol

A
  • alcohol oxidation causes reduction of NAD (need for fatty acid oxidation of lactate in pyruvate) -> accumule fat in liver
  • ROS generation by metabolism by CYPE1
  • release LPS of G- in flora -> production TNF by Kupffer -> hepatic injury
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14
Q

Acetaminophen metabolism

A

95% detox by phase II enzymes liver
5% metabolized by CYP2E to NAPQI (centrolobular necrosis)
NAPQI covalently bind hepatic proteins = damage to cellular membrane and mitochondria dysfunction

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15
Q

Lungs injury :
1. Water soluble gas
2. Lipid soluble gas

A
  1. Water = chlorine, sulfur oxides, ammonia = react with water to form acids/alkalis -> inflamm and swelling -> partial/complete obstruction
  2. Lipid = nitrous oxide = reach deeper airways producing pneumonitis
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16
Q

Mechanism of heat stroke

A

Sustained contraction of skeletal muscles, muscle necrosis by nitrosylation of RYR1 in the sarcoplasmic reticulum of skeletal muscle -> allows calcium to leak into cytoplasm -> stimule muscle contraction and heat production

17
Q

etiology of malignant hyperthermia

A

Mutations in gene like RYR1 that control calcium levels
Exposure to certain anesthetic triggers rapid rise in calcium -> muscle rigidity + increase heat production

18
Q

Ionizing radiation on lymphoid systems

A

High/large exposure = severe lymphopenia within hours, shrink lymph nodes and spleen (radiation kills lympho directly)
Brief rise in neutrophils followed by neutropenia within several days
Granulocytes return to normal within 2-3 months
Very high dose = kill hematopoietic stem cells = permanent aplasia

19
Q

Marasmus (severe lack of calory) mechanism

A

Low production of leptin -> stimule hypothalamic-pituitary-adrenal axis to produce cortisol that contribute to lipolysis
Marginal depletion of visceral proteins and somatic proteins

20
Q

Anorexia and bullumia pathognomonic change

A

Increase fat in bone marrow with mucinous matrix = pathognomonic

21
Q

What vitamines can be endogenously synthesized?

A

D = from precursors steroids
K, biotin = intestinal, microflora
Niacin = from tryptophan (amino acid)

22
Q

Vitamine A function, metabolism

A

Maintain normal vision = with 4 forms of vit A(rhodopsin, iodopsin)
Regulation cell growth/differenciation = activation of retinoic acid receptor (RAR)= release of corepressors and formation of heterodimers with another retinoid receptor (RXR)
-> all-trans retinoic acid highest affinity for RAR
Regulation of lipid metabolism = RXR activated by 9-cis retinoic acid
- B carotene converted to vitA
- absorption requires bile, pancreatic enzymes, antioxidant activity in food

23
Q

Vit A deficiency and toxicity

A

DEFICIENCY = vision loss, eptih metaplasia, dry eye, loss mucociliary epith respi, desquame keratin debris in urinary tract (stone), hyperplasia/keratin of epidermis (dermatosis), immune deficiency
TOXICITY
Aigue - headache, dizzy, v+, stupor, blurred vision
Chronic - retinoic acid stimulate osteoclast = bone resorption. Synthetic retinoids = teratogenic effects

24
Q

VitD sources

A

Endogenous synthesis from 7-dehydrocholesterol in a photochemical rx -> cholecalciferol (vitD3)
Diet = ergosterol (plants, grain, fish)

25
Q

VitD metabolism steps

A
  1. Photochemical synthesis of vitD from 7-dehycrocholesterol in the skin and absorb vitD from food in guts
  2. Binding of vitD to plasma a1-globulin (DBP) and transport to liver
  3. Conversion of vitD into 25-hydroxycholecalciferol (25-OH-D) in the liver by CYP27A1
  4. Conversion of 25-OH-D into 1,25 dihydroxyvitamine D in the kidney by enzyme a1-hydroxylase
    1,25 dihydroD binds nuclear vitamine D-R -> associates with RXR
    Also binds membrane-associated vitD-R (mVDR) activate protein kinase C = open calcium channels
    Immunomodulatory, antiproliferative effects
26
Q

VitD regulation in kidneys

A

HYPOCALCEMIA = stimule secretion of PTH -> hausse conversion of 25-OH-D to 1,25 dihydroxyvitamine D by upregulating 1a-hydroxylase
HYPOPHOSPHATEMIA = upregulate 1a-hydroxylase

27
Q

Effects of vitD on calcium and P

A
  • stimule intestinal Ca absorption (1,25dihydroD increase absorption by increase expression of TRPV6
  • stimule calcium reabsorption in kidney (expression of TRPV5 = Ca influx in distal tubule)
    TRPV5 also regulated by PTH
  • 1,25dihydro and PTH enhance expression of RANKL (R-activator or NFkB) on osteoclasts -> RANKL binds RANK on preosteoclasts induce maturation -> secretion of hypochloric acid and active proteases (cathepsin K) -> release Ca and P
  • mineralisation of bones = stimule osteoblasts to synthesize osteocalcin (calcium-binding protein involved in Ca deposition)
28
Q

VitD deficiency

A

Less vitD = hypocalcemia = elevated PTH :
- active renal 1a-hydroxylase = increase active vitD and calcium absorption
- increase resorption of calcium from bone
- decrease renal calcium excretion, increase renal phosphate excretion (normal calcium restored but hypophospho can persist = impaired bone mineralisation)

29
Q

Non skeletal effect of vitD

A

Synthesis of 1,25dihydroD by CYP27B in macrophages can be stimulated by TLR during infections

30
Q

Functions of vitC

A

Activates prolyl and lysyl hydroxylase from inactive precursors = hydroxylation of procollagen
Antioxidant
Modulate immune response

31
Q

Mechanism of obesity

A
  1. Nutrient intake -> POMC cleaved from POMC/CART neurons -> a-melanocyte-stimulating hormone (MSH) -> active MC3/4R-R in 2nd order neurons -> reduce food intake and increase energy expenditure by producing BDNF, TSH and CRH
  2. Fasting active NPY/AgRP neurons to release NPY = active Y1 et Y5-R in 2nd order neurons = increase food intake by producing MCH and orexin + reduce energy expenditure by downregulating sympathetic output
  3. NYP/AgRP neurons directly inhibit POMC/CART neurons
32
Q

Leptin (secreted by fat cells) pathology in obesity

A

Mutation in leptin gene or R = massive obesity
Mutation in melanocortin-R 4 gene (MC4R) more common
Anorexigenic response of leptin blunted in obesity = leptin resistance
Insulin exerts = anorexigenic response

33
Q

Pathogenesis of thermogenesis

A

Catabolic effect, controlled by hypothalamic signals that increase the release of norepinephrine from sympathetic nerve endings in adipose tissue

34
Q

Functions of adiponectin

A
  • stimulate fatty acid oxidation in skeletal muscle = reduce levels
  • decrease glucose production in liver
  • increase insulin sensitivity
  • antiinflamm, antiatherogenic, antiprolif and cardioprotective
    R = AdipoR1 et R2
    Binding of adiponectin = active cAMP-dependent kinase (prot kinase A) -> phospho et inactive acetyl coenzyme A carboxylase (needed for fatty acid synthesis)
35
Q

Production of cytokines by white adipose tissue

A

TNF, IL1, IL6, IL18
In obese = chronic proinflamm state with high levels of C-reactive protein (CRP)

36
Q

What does insulin resistance and hyperinsulinemia lead to?

A

Leads to retention of sodium, expansion of blood volume, prod of excess norepinephrine, smooth muscle proliferation = hallmarks of hypertension

37
Q

Possible mechanisms in cancer

A
  • Elevated insulin level (rise insulin-like growth factor 1 = mitogen, IGFR-1 activates RAS and PI3K/AKT)
  • effects on steroids hormones = cell growth in breast, uterus, other
  • adiponectin reduced and it normally suppress cell proliferation and promotes apoptosis by promoting p53 and p21
  • proinflammatory state
38
Q

What does mutation in codon 249 of TP53 gene indicate?

A

Signature of aflatoxine exposition

Nutrition (13 decks)

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