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MOD 2 > Chapter 9: Enviornmental and Nutritional Diseases > Flashcards

Chapter 9: Enviornmental and Nutritional Diseases Flashcards

1
Q

What are the leading causes of death in developed countries?

A

Ischemic heart disease and cerebrovascular disease

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2
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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3
Q

Activation of Xenobiotics to generate toxic compounds occurs in 2 phases, what are they?

A

Phase I: chemicals undergo hydrolysis, oxidation, or reduction (by CYP 450)

Phase II: often metabolized to water soluble compounds through glucuronidation, sulfation, methylation, and conjugation w/ glutathione

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4
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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5
Q

What are the inducers of CYP? (mnemonic)

A

SHADE

Smoking

Hormones

Alcohol

Drugs

Enviornmental chemicals

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6
Q

What decreases CYP activity?

A

Fasting and/or starvation

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7
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 by macrophages and neutrophils,respond by releasinginflammatory mediators
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8
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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9
Q

Lead is a readily absorbed metal that binds to what?

Interferes with?

Leads to what kind of toxicities?

A
  • Binds to sulfhydryl groups in proteins and interferes with CALCIUM metabolism
  • Leads to: hematologic, skeletal, neurologic, GI, and renal toxicities
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10
Q

Most absorbed lead is incorporated into?

Competes with?

A
  • Bones and teeth
  • Competes with calcium
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11
Q

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

A

Peripheral neuropathies

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12
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

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13
Q

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

Histological findings?

A

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

- Punctate basophilic stippling of the red cells

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14
Q

What kind of brain/CNS damage is associated with children in lead poisoning?

Adults?

A
  • In children = brain damage
  • In adults = peripheral demyelinating neuropathy (wrist drop and foot-drop)
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15
Q

Mercury mostly affects what organs?

A

CNS

Kidney

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16
Q

Arsenic affects what organs most commonly?

A

GI tract

Nervous System

Skin

Heart

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17
Q

Arsenic trioxide is a frontline treatment for?

A

Acute promyelocytic leukemia

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18
Q

Cadmium is toxic to what systems?

Due to increased production of?

A
  • Kidneys and Lungs
  • Increased production of ROS
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19
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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20
Q

BPAs have been known to be a potential ________ disruptor.

Elevated urine BPA linked to?

A
  • Endocrine disruptor
  • Elevated urine BPA linked to heart disease
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21
Q

What are among the most potent carcinogens and are released during the combustion of fossil fuels, particularly coal and gas at high temps?

Implicated in the development of what diseases?

A
  • Polycyclic Hydrocarbons
  • Lung and bladder cancer
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22
Q

Organochlorines (i.e., DDT, PCB, dioxins) disrupt what?

A

Hormonal balance due to antiestrogenic and antiandrogenic activity

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23
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
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24
Q

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

A

Polycyclic hydrocarbons

Nitrosamines

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25
Q

Carcinogens from cigarette smoke are processed by CYPs, but some of the intermediates produced are electrophilic and form what?

A

DNA adducts; persistence of these adducts can cause mutations in oncogenes and tumor suppressors

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26
Q

What are the causal mechanisms for the development of atherosclerosis in smokers?

A
  • Increased platelet aggregation
  • Decreased myocardial O2 supply
  • Increased O2 demand
  • Decreased threshold for ventricular fibrillation
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27
Q

Passive smoke inhalation (second-hand smoke) in non-smokers can be estimated by measuring the blood levels of?

A

Cotinine, a metabolite of nicotine

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28
Q

How does alcohol potentiate the depressant effects of narcotic, sedative, and other psychoactive drugs?

A
  • Alcohol induces CYPs
  • Competes with other CYPE21 substrates and delays drug catabolism
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29
Q

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

A

Acetaldehyde

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30
Q

About 50% of Asians have very low alcohol dehyrogenase activity, due to what?

What is the normal allele and the inactive variant?

What effect does the inactive variant have?

A
  • Substitution of lysine for glutamine at residue 487
  • Normal allele = ALDH2*1
  • Inactive variant = ALDH2*2 = dominant negative
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31
Q

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

A

Cytosol = most important route

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32
Q

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

A

In the ER (microsome)

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33
Q

Oxidation of alcohol by alcohol dehydrogenase causes the reduction of which molecule?

What is this molecule important for?

A
  • Reduction of NAD to NADH (decreased NAD and increased NADH)
  • NAD is required for fatty acid oxidation in the liver and for the conversion of lactate —> pyruvate
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34
Q

The main cause of accumulation of fat in the liver of alcoholics is deficiency of?

What else does this cause in alcoholics?

A
  • Deficiency of NAD, required for fatty acid oxidation in liver
  • Increased NADH/NAD ration also causes lactic acidosis
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35
Q

How does alcohol consumption lead to lipid peroxidation of hepatocyte cell membranes?

A

Metabolism of ethanol in the liver by CYP2E1 produces ROS, causes lipid peroxidation

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36
Q

What effect does alcohol have on gram negative bacteria in the intestinal flora?

Stimulates the production of?

A
  • Causes the release of endotoxin (lipopolysaccharide)
  • Stimulates production of TNF and other cytokines from macrophages and Kupffer cells, leading to hepatic injury
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37
Q

Menopausal hormone therapy (MHT) increases the risk for?

A
  • Breast cancer (after 5-6 yrs use), ovarian and endometrial cancers
  • Stroke and venous thromboembolism, including DVT and pulmonary embolism
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38
Q

What is the effect of oral contraceptives on development of breast carcinomas, endometrial cancer, and ovarian cancers?

A
  • Do not increase breast cancer risk
  • Have a protective effect against endometrial and ovarian cancers
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39
Q

What is the relationship between oral contraceptives and thromboembolism?

A
  • Associated with a threefold to sixfold INCREASED risk of svenous thrombosis and pulmonary thromboembolism
  • Due to hypercoagulable state induced by elevated hepatic synthesis of coagulation factors
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40
Q

There is a well-defined association between the devlopment of what type of tumor in older woman who have used OCs for prolonged periods?

A

Rare benign hepatic tumor (hepatic adenoma)

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41
Q

What is the cause of 50% of cases of acute liver failure, with 30% mortality, in the US?

A

Acetaminophen toxicity

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42
Q

At therapeutic doses, 95% of acetaminophen undergoes detoxification in the liver by what?

Excreted as?

A
  • Phase II enzymes
  • Excreted as glucuronate or sulfate conjugates
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43
Q

How is the other 5% of acetaminophen metabolized and what is the product of this metabolism?

How is this product usually dealt with?

Large doses of this toxic metabolite lead to?

A
  • Through CYP2E –> NAPQI (N-acetyl-p-benzoquinoneimine) = highly reactive metabolite
  • NAPQI is usually conjugated with glutathione (GSH)
  • In large doses, unconjugated NAPQI accumulates and causes hepatocellular injury, leading to centrilobular necrosis that may progress to liver failure
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44
Q

What are the 2 mechanisms in which the toxic metabolite of acetaminophin, NAPQI, produces injury within the liver?

A

1) Covalent binding to hepatic proteins which causes damage to cellular membranes and mitochondrial dysfunction
2) Depletion of GSH, making hepatocytes more susceptible to ROS induced injury

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45
Q

Why does acetaminophen toxicitiy occur in lower doses in chronic alcoholics?

A

Due to alcohol inducing CYP2E in liver

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46
Q

A patient presents to the ED with nausea, vomiting, diarrhea, and eventually shock after ingesting unknown pills from the medicine cabinet, a few days later they develop jaundice.

What do you suspect the culprit to be?

A

Acetaminophen toxicity

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47
Q

How can acetaminophen toxicity (ODs) be treated within 12 hours of ingestion?

A

Administration of N-acetylcysteine, which restores GSH levels

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48
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

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49
Q

Often Aspirin overdose results from accidental ingestion of a large number of tablets by children or attempted suicide by adults. What is a much less common cause?

A

Ointments containing oil of wintergreen (methyl salicylate)

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50
Q

Acute salicylate 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 and accumulation of pyruvate and lactate, due to uncoupling of OxPhos and inhibition of the Krebs cycle
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51
Q

A patient presents to the ED with a hx of headaches, dizziness, ringing in the ears (tinnitus), hearing impairment, mental confusion, drowsiness, nausea, vomiting, and diarrhea.

They tell you they take an OTC for chronic pain management, what do you suspect is the culprit of their symptoms?

A

Chronic aspirin toxicity (salicylism)

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52
Q

Chronic aspirin toxicity may lead to what GI issues?

A
  • Acute erosive gastritis, leading to:
  • Overt or covert GI bleeding and lead to gastric ulceration
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53
Q

Bleeding disorders can be caused by chronic aspirin ingestion, what are the signs of this?

A

Petechial hemorrhages may appear in skin and internal viscera, and bleeding from gastric ulcerations may be exaggerated.

*Remember that primary hemostasis disorders = defects in platelets = mucocutaneous bleeding = petechia, purpura, and ecchymosis

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54
Q

Proprietary analgesic mixtures of aspirin and phenacetin or its active metabolite, acetaminophen, when taken over several years, can cause?

A

Tubulointerstitial nephritis w/ renal papillary necrosis, referred to as analgesic nephropathy

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55
Q

Cocaine blocks the reupatake of?

Stimulates release of?

A
  • Dopamine in the CNS
  • Epi and NE at adrenergic nerve endings; while stimulating presynaptic release of NE
56
Q

What are the pulmonary complications that can arise as a result of Heroin use?

A
  • Moderate to severe edema
  • Septic embolism from endocarditis
  • Lung abscess
  • Opportunistic infections
  • Foreign-body granulomas (from talc and other adulterants)
57
Q

What are the 4 most common places of infection complications as a result of heroin use?

A

1) Skin and subcutaneous tissue
2) Heart valves
3) Liver
4) Lungs

58
Q

Endocarditis in heroin abusers often takes a distinctive form involving?

Most cases causes by what bacteria?

A
  • Right-sided heart valves, particularly tricuspid
  • Most cases, caused by S. aureus
59
Q

What is the most common infection among individuals addicted to heroin?

Acquired how?

A

Viral hepatitis acquired through sharing needles

60
Q

What 2 forms of kidney disease are most frequently encountered in heroin/opiate abusers?

A

1) Amyloidosis (secondary to skin infections)
2) Focal and segmental glomerulosclerosis

61
Q

What kind of burns involve injury to the dermis?

A

Partial thickness burns (2nd degree)

62
Q

What kind of burns extend to the subcutaneous tissue?

Those that involve damage to the muscle tissue?

A
  • Full-thickness (3rd degree)
  • Now called full-thickness, but damage to muscle beneath subcutaneous tissue were formerly called 4th degree burns
63
Q

Which type of burn is confined to the epidermis?

A

Superficial (1st degree)

64
Q

What are the greatest threats to life in burn patients?

A

Shock, sepsis, and respiratory insufficiency

65
Q

Shift of the body’s fluid into the interstitial compartment, both at the burn site and systemically, following a severe burn, is due to?

Leads to?

A
  • Due to the Systemic inflammatory response syndrome (SIRS)
  • Leads to shock
66
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

67
Q

Burn sites are ideal growth enviornments for microorganisms and virtually all burns become colonized with bacteria. Which is the most common offender?

Other strains?

A
  • Pseudomonas aeruginosa = most common
  • S. aureus (methicillin-resistant) = MRSA
  • Fungi, particularly Candida species
68
Q

What are the most common serious complications produced by direct bacteremic spread in burn victims?

A

- Pneumonia

- Septic shock w/ renal failure and/or acute respiratory distress syndrome

69
Q

Which gases are more likely to reach the deeper airways and produce pneumonitis?

A

Lipid-soluble gases, such as NO and products of burning plastics

70
Q

What type of scarring is a common complication of burn injury?

Marked by excessive?

A
  • Hypertrophic scarring
  • Marked by excessive deposition of collagen in the healing wound bed
71
Q

Morphologically how do full-thickness burns appear in comparison to partial-thickness burns?

A

Full-thickness = white or charred, dry, and painless (destruction of nerve endings)

Partial-thickness = pink or mottled with blisters and painful

72
Q

Histologically what is seen with devitalized tissue and the vital tissue surrounding burns?

Quicky accumulates what?

A

Coagulative necrosis, adjacent to vital tissue that quickly accumulates inflammatory cells and marked exudation

73
Q

In heat stroke, the hyperthermia is accompanied by?

A

Marked generalized vasodilation, with peripheral pooling of blood and decreased effective circulating blood volume

74
Q

Sustained contractions of skeletal muscle can exacerbate hyperthermia in someone suffering a heat stroke, leading to muscle necrosis known as?

Results from?

A
  • Rhabdomyolysis
  • Nitrosylation of ryanodine receptor 1 (RYR1), located in SR of skeletal muscle
  • Heat stroke deranges RYR1 function and allows calcium to leak into the cytoplasm, stimulating muscle contraction and heat production
75
Q

Inherited mutaitons in RYR1 occur in a condition called?

Characterized by?

A
  • Malignant hyperthermia
  • Characterized by a “heat-stroke-like” rise in core body temp and muscle contractures following exposure to common anesthetics
76
Q

High humidity, wet clothing, and dilation of superficial blood vessels resulting from ingestion of alcohol all contribute to?

A

Lowering of body temperature —> Hypothermia

77
Q

Hypothermia causes injury by 2 mechanisms, what are they?

A

Direct = physical disruption within cells by high salt concentrations caused by the crystallization of intra- and extracellular water

Indirect = result from circulatory changes; vary depending on rate and duration of the temperature drop

78
Q

Slow chilling (indirect mechanism) may have what physiologic effects?

A

May induce vasoconstriction and increase vascular permeability, leading to edema, and hypoxia

*Typical of “trench foot” seen in soldiers during WWI, frequently causing gangrene

79
Q

Sudden, persistent chilling (indirect mechanism) may have what physiologic effects?

What type of injury can occur?

A
  • Vasoconstriction and increased viscocity of the blood in the local area mau cause ischemic injury and degenerative changes in peripheral nerves
  • Vascular injury and edema become evident only after the temp begins to normalize
80
Q

Ionizing radiation such as that used in diagnostic imaging can produce what short- and long-term effects?

A

Fibrosis

Mutagenesis

Carcinogenesis

Teratogenesis (malformation in a developing fetus)

81
Q

Differentiate Curie (Ci) vs. Gray (Gy) vs. Sievert (Sv) units of radiation.

A

Curie (Ci) = amount of radiation emitted by a source

Gray (Gy) = energy absorbed by the target tissue per unit mass

Sievert (Sv) = depends on the biologic rather than the physical effects of radiation

82
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
83
Q

What is the major mechanism by which DNA is damaged by ionizing radiation?

A

Production of ROS from rxns with free radicals generated by radiolysis of water

84
Q

What are the acute effects of marrow irradiation on peripheral blood counts of granulocytes, neutrophils, and platelets (i.e., neutropenia, anemia, thrombocytopenia)?

A
  • Neutropenia appears within several days; often near zero by end of 2nd week
  • Recovery of normal granulocyte count may require 2-3 months
  • Thrombocytopenia appears by end of first week
  • Anemia appears after 2-3 weeks and may persist for months
85
Q

Very high doses of radiation kill marrow stem cells and induce?

A

Permanent aplasia (aplastic anemia) = failure of blood count recovery

86
Q

What is the “bystander effect” produced by damaged cells from radiation?

A
  • Abnormal cells are able to alter the behavior of nonirradiated surrounding cells through the production of GFs and cytokines
  • Referred to as non-target effects of radiation
87
Q

What are common sites of fibrosis following radiation therapy?

A
  • Lungs
  • Salivary glands
  • Colorectal
  • Pelvic areas
88
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

89
Q

What is the most common repair pathway for double-stranded breaks of DNA caused by ionizing radiation?

What common mutations result from this pathway?

A
  • Nonhomologous end joining (NHEJ)
  • Short deletions or duplications, or gross chromosomal aberrations such as translocations and inversions
90
Q

A BMI less than _____ kg/m2 is considered malnourished?

A child whose weight falls less than ______% of normal is considered malnourished?

A

A BMI less than 16 kg/m2 is considered malnourished

A child whose weight falls less than 80% of normal is considered malnourished

91
Q

Marasmus affects which protein compartment of the body?

Which hormone is low and what does this trigger?

What occurs to the extremities and head?

A
  • Catabolism and depletion of the somatic protein compartment
  • Production of leptin is low, may stimulate H-P-A axis to produce high levels of cortisol, which contributes to lipolysis
  • Extremities are emaciated, by comparison the head appears too large for the body
92
Q

Kwashiorkor occurs when?

Depletion of which protein compartment?

Levels of albumin?

A
  • Occurs when protein deprivation is relatively more severe than the deficit in total calories
  • Marked protein deprivation of the visceral compartment, with resultant hypoalbuminemia —> generalized or dependent edema
93
Q

Albumin levels in Marasmus and Kwashiorkor?

A
  • In Marasmus, the albumin levels are normal
  • In Kwashiorkor, there is hypoalbuminemia –> generalized or dependent edema
94
Q

What are the characteristics of the skin and hair in children with Kwashiorkor?

A
  • Skin lesions, with alternating zones of hyperpigmentation, areas of desquamation, and hypopigmentation, giving a “flaky paint” appearance
  • Hair changes include overall loss of color or alternating bands of pale and darker hair
95
Q

What is the liver like in Kwashiorkor?

A

Enlarged, fatty liver from reduced synthesis of the carrier protein component of lipoproteins

96
Q

What morphological changes occur to the small bowel of a child with Kwashiorkor?

Most often manifested as?

A
  • Decrease in the mitotic index in the crypts and glands, associated with mucosal atrophy and loss of villi and microvilli
  • Loss of small intestinal enzymes, most often manifested as disaccharide deficiency

*Infants w/ Kwashiorkor initially may not respond well to full-strength, milk-based diets

97
Q

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

A
  • Proteolysis-inducing factor: glycosylated polypeptide 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

98
Q

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

A

NF-kB induced activation of the ubiquitin proteasome pathway, promoting degradation of structural proteins such as myosin heavy chain by upregulating expression of several muscle-specific ubiquitin ligases

99
Q

What clinical finding is so common in Anorexia that its presence is considered a diagnostic feature?

A

Amenorrhea

100
Q

What are major complications that may result from Anorexia?

A

Cardiac arrhythmia and sudden death, resulting from hypokalemia

101
Q

What are the 3 major medical complications associate with Bulimia?

A

1) Electrolyte imbalance (hypokalemia), predisposing pt to cardiac arrhythmias
2) Pulmonary aspiration of gastric contents
3) Esophageal and gastric rupture

102
Q

Which vitamins can be synthesized endogenously?

A
  • Vit D from steroids
  • Vit K from biotin by intestinal microflora
  • Niacin from tryptophan
103
Q

What are the 3 major functions of Vitamin A?

A

1) Maintenance of vision
2) Regulation of cell growth and differentiation
3) Regulation of lipid metabolism

104
Q

Vitamin A supplmentation can reduce the morbidty and mortality from some forms of?

Also in preschool children with what disease?

A
  • Some forms of diarrhea
  • Improve clinical outcome of measles
105
Q

Vitamin A used in the treatment of what disorders?

A
  • Severe acne and some forms of psoriasis
  • Tx of acute promyelocytic leukemia
106
Q

What are the most devastating consquences of Vitamin A deficiency?

A
  • Xerophthalamia (dry eye) gives rise to epithelial metaplasia
  • Followed by buildup of keratin debris in small opaque plaques (Bitot spots)
  • Progresses to erosion of the roughened corneal surface, softening and destruction of the cornea (keratomalacia) and blindness
107
Q

Effect of Vitamin A deficiency on the immune system?

Leads to?

A

Immune deficiency, responsible for higher mortality rates from common infections such as measles, pneumonia, and infectious diarrhea

108
Q

Why should synthetic retinoids, such as those used to tx acne, be avoided in pregnant woman?

A

Well-established teratogenic effects of retinoids

109
Q

Deformation of the chest results from overgrowth of cartilage or osteoid tissue at the costochondral junction, producing what characteristc morphology in Rickets?

A

Rachitic rosary

110
Q

What skeletal deformities are commonly seen in Rickets?

A
  • Pectus carinatum (“pigeon” brest deformity)
  • Excessive Lumbar lordosis
  • Bowing of the legs
111
Q

Spinocerebellar degeneration is a deficiency syndrome of what vitamin?

A

Vitamin E

112
Q

Cheilosis, stomatitis, glossitis, dermatitis, and corneal vascularization are all associated with what vitamin deficiency?

A

Riboflavin (vitamin B2)

113
Q

Megaloblastic pernicious anemia and degeneration of posterolateral spinal cord tracts are a result of what vitamin deficiency?

A

Vitamin B12

114
Q

What is the deficiency syndrome of Niacin? (The 3 D’s)

A
  • Pellagra
  • Dementia
  • Dermatitis
  • Diarrhea
115
Q

Megaloblastic anemia and neural tube defects are a result of what vitamin defect?

A

Folate

116
Q

Cheilosis, glossitis, dermatitis, peripheral neuropathy, and dismaintenance of myelinization of spinal cord tracts is a result of what vitamin deficiency?

A

Vitamin B6 (pyridoxine)

117
Q

A rash around the eyes, mouth, nose, and anus called acrodermatitis enteropathica results from a deficiency in what vitamin?

A

Zinc

118
Q

Hypochromic microcytic anemia results from a deficiency in what vitamin?

A

Iron

119
Q

Muscle weakness, neurologic defects, and abnormal collagen crosslinking due to a deficiency in what vitamin?

A

Copper

120
Q

Myopathy and cardiomyopathy (Keshan disease) due to a deficiency in what vitamin?

A

Selenium

121
Q

Vitamin C deficiency has what consequences?

A
  • Impaired collagen formation leads to:
  • Impaired wound healing
  • Inadequate synthesis of osteoid
  • Mucosal bleeding (gums) and joints
122
Q

Which immune cell can synthesize 1,25-dihydroxyvitamin D?

How?

A
  • Macrophages, through the activity of CYP27B in the mitochondria
  • Pathogen-induced activation of TLR in macrophages causes increased expression of vitamin D receptor and CYP27B, leading to local synthesis and activation of vitamin-D-dependent gene expression
123
Q

POMC/CART producing α-MSH that activates MC3/4R in second order neurons regulate what component of hunger and food intake?

A

Anorexigenic effect

124
Q

NPY/AgRP activating Y1/5 receptors in second order neurons regulate what component of hunger and food intake?

A

Promote food intake (orexigenic effect)

125
Q

Haploinsufficiency of brain-derived neurotrophic factor (BDNF), an imoortant component of signaling downstream of MC4R in the hypothalamus is associated with obesity in patients with what syndrome?

A

WAGR syndrome (Wilms tumor, aniridia, genitourinary defects, mental retardation, and obesity) = very rare

126
Q

What are levels of PYY like in Prader-Willi syndrome?

A

Decreased

127
Q

What is 6 times more likely in obese people than lean people, especially women?

A

Cholelithiasis (gallstones)

128
Q

In very obese individuals the constellation of respiratory abnormalities encompassing Hypoventilation syndrome, is known as?

A

Pickwickian syndrome

129
Q

Obesity causes what kind of cancer in women?

Due to what?

A
  • Uterine and breast
  • Increased estrogen synthesis
130
Q

Aflatoxin is involved in the development of what cancer in parts of Asia and Africa?

A

Hepatocellular carcinomas

131
Q

What cancers are associated with nitrosamines and nitrosamides?

A

Gastric cancers

132
Q

What is the single leading global cause of health loss (defined as morbidity and premature death)?

A

Undernutrition

133
Q

Exposures of a fetus to high levels of mercury in utero may lead to what disease?

Characterized by?

A
  • Minamata disease
  • Cerebral palsy, deafness, blindness, and mental retardation
134
Q

Naphthylamines, 4-aminobiphenyl, benzidine, and rubber products have all be implicated in the development of what cancer?

A

Bladder cancer

135
Q

Silica, nickel, arsenic, chromium, mustard gas, and uranium have all be implicated in the devlopment of what cancer?

A

Lung cancer

136
Q

Effectivness of all-trans-retinoic acid in the Tx of acute promyelocytic leukemia lies in its ability to bind what?

A

The PML-RARα fusion protein

MOD 2 (9 decks)

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