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MOD II Exam I > Chapter 9 > Flashcards

Chapter 9 Flashcards

1
Q

Single leading global cause of health loss (morbidity and premature death)

A

Malnutrition

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2
Q

Exogenous chemicals in the environment in air, water, food, and soil that may be absorbed into the body through inhalation, ingestion, and skin contact

A

Xenobiotic

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3
Q

Mechanism of action of cytochrome p450 as it relates to xenobiotics

A

CYP450 is the most important catalyst in phase I reactions of xenobiotic metabolism

It catalyzes reactions that either detoxify the xenobiotic or (less commonly) convert them into active compounds that cause cell injury

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4
Q

Readily absorbed metal that binds sulfhydryl groups in proteins and interferes with calcium metabolism —> hematologic, skeletal, neurologic, GI, and renal toxicities

A

Lead

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5
Q

Symptoms of low vs. high level lead poisoning

A

Low level = subtle defects in intellectual capacity, hyperactivity, poor organizational skills

High level = CNS disturbances, peripheral neuropathy of extensor muscles of wrist and fingers, foot drop, radiodense “lead lines” on x-ray or at gumline, poor fracture healing, microcytic hypochromic anemia, kidney damage including intranuclear inclusions and eventual interstitial fibrosis + renal failure —possible saturnine gout d/t decreases in uric acid secretion

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6
Q

How is lead poisoning definitively diagnosed

A

Increased blood levels of lead and/or free (or zinc-bound) protoporphyrin

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7
Q

Lead exposure inhibits enzymes involved in heme synthesis. What 2 enzymes are affected?

A

Delta-aminolevulinic acid dehydratase

Ferrochelatase (catalyzes incorporation of iron into protoporphyrin)

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8
Q

____ binds sulfhydryl groups in certain proteins with high affinity, leading to damage in CNS and kidney; main sources of exposure include contaminated fish, metallic vapors in dental amalgams, and rivers/streams contaminated by gold mining

A

Mercury

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9
Q

Result of inhalation vs. ingestion of mercury

A

Inhalation —> tremor, gingivitis, bizarre behavior

Ingestion —> cerebral palsy, deafness, blindness, mental retardation, major CNS defects in fetus (methyl mercury)

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10
Q

Main cellular protective mechanism against mercury

A

Intracellular glutathione

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11
Q

_____ interferes with several aspects of cell metabolism by replacing phosphates in ATP, leading to toxicities that are most prominent in the GI tract, nervous system, skin, and heart

A

Arsenic

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12
Q

Arsenic is used as a frontline treatment for what type of cancer?

A

Promyelocytic leukemia

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13
Q

Effects of arsenic exposure

A

Acute GI, CV, and CNS toxicities that are often fatal; drinking contaminated water may cause non-malignant respiratory disease

Neurologic effects include sensorimotor neuropathy characterized by paresthesias, numbness, and pain

Skin changes include hyperpigmentation and hyperkeratosis

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14
Q

Most serious consequence of arsenic exposure

A

Carcinogenesis —> lungs, bladder, skin

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15
Q

What makes arsenic-caused skin cancers distinct from other etiologies?

A

Often appear in multiple locations and on the palms and soles

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16
Q

____ is preferentially toxic to the kidneys and lungs through uncertain mechansims that may involve increased production of ROS; most important mechanism of exposure is through contaminated food

A

Cadmium

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17
Q

Principal toxic effects of cadmium exposure

A

Obstructive lung disease d/t necrosis of alveolar epithelial cells
Renal tubular damage
Skeletal abnormalities d/t calcium loss
Postmenopausal osteoporosis, osteomalacia, and renal disease
Elevated risk of lung cancer

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18
Q

Examples of organic solvents and their potential risks to human health

A

Chloroform and carbon tetrachloride — dizziness, confusion, CNS depression, coma, kidney and liver toxicities

Benzene and 1,3-butadiene — increased risk of AML

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19
Q

Risks associated with exposure to organochlorines (and halogenated organic compounds in general) like DDT, lindane, aldrin, dieldrin, PCBs, dioxin, etc

A

Disruption of hormonal balance — antiestrogenic or antiandrogenic activity

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20
Q

Risks associated with polycyclic hydrocarbon exposure

A

Lung and bladder cancers

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21
Q

Health risks associated with dioxins and PCBs

A

Chloracne = folliculitis and dermatosis

Abnormalities of liver and CNS

Abnormalities of drug metabolism (these toxins induce CYPs)

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22
Q

Health risks associated with mineral dust inhalation such as coal dust, silica, asbestos, and beryllium

A

Chronic, nonneoplastic lung diseases = pneumoconiosis

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23
Q

Health risks associated with exposure to bisphenol A (BPA)

A

Potential endocrine disruptor

Heart disease

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24
Q

Effects of tobacco smoke constituents

A

Carcinogenesis (tar, polycyclic hydrocarbons, nitrosamine)

Ganglionic stimulation and depression; tumor promotion (nicotine)

Impaired O2 transport and utilization (CO)

Toxicity to cilia and mucosal irritation (formaldehyde, nitrogen oxides)

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25
Q

3 ways that smoking contributes to lung cancer

A

Direct irritant effect on tracheobronchial mucosa —> bronchitis

Recruitment of leukocytes to lungs —> increased elastase production —> emphysema

Carcinogenesis from hydrocarbons and nitrosamines whose solubility is increased by CYPs and phase II enzymes; some intermediates may mutate DNA directly

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26
Q

Most alcohol in the blood is oxidized to ______ by 3 enzyme systems. What are the 3 enzyme systems?

A

Acetaldehyde

Alcohol dehydrogenase (primary) - in cytoplasm of hepatocytes
Microsomal ethanol-oxidizing system (CYPs)
Catalase

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27
Q

Oxidation of ethanol produces toxic metabolites and disrupts certain metabolic pathways. What are some examples?

A

Acetaldehyde: responsible for some acute effects of alcohol and development of oral cancers

Increased NADH: NAD ratio —> lactic acidosis; NAD deficiency

ROS generation —> causes lipid peroxidation in hepatocyte cell membranes and release of endotoxin from gram-negative bacteria in intestinal flora

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28
Q

Vitamin defiency associated with chronic alcoholism; what are the consequences?

A

Thiamine (B1) deficiency —> peripheral neuropathy, wernicke-korsakoff syndrome, cerebral atrophy, cerebellar degeneration, optic neuropathy

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29
Q

Agents that tend to cause adverse drug reaction in bone marrow and blood cells

A

Antineoplastic agents, immunosuppressives, chloramphenicol —> granulocytopenia, aplastic anemia, pancytopenia

Penicillin, methyldopa, quinidine, heparin —> hemolytic anemia, thrombocytopenia

30
Q

Agents that tend to cause adverse drug reaction in skin

A

Antineoplastic agents, sulfonomides, hydantoins, some abx —> urticaria, papules, vesicles, petechiae, exfoliative dermatitis, fixed drug eruptions, abnormal pigmentation

31
Q

Agents that tend to cause adverse drug reaction in cardiac system

A

Theophylline, hydantoins, digoxin —> arrhythmias

Doxorubicin, daunorubicin -> cardiomyopathy

32
Q

Agents that tend to cause adverse drug reaction in renal system

A

Penicillamine -> glomerulonephritis

Aminoglycoside abx, cyclosporin, amphotericin B —> acute tubular necrosis

Phenacetin, salicylates —> tubulointerstitial diseases with papillary necrosis

33
Q

Agents that tend to cause adverse drug reaction in pulmonary system

A

Salicylates —> asthma

Nitrofurantoin —> acute pneumonitis

Busulfan, nitrofurantoin, bleomycin —> interstitial fibrosis

34
Q

Agents that tend to cause adverse drug reaction in hepatic system

A

Tetracycline —> fatty change

Halothane, isoniazid, acetaminophen —> diffuse hepatocellular change

Chlorpromazine, estrogen, contraceptives —> cholestasis

35
Q

Agents that tend to cause adverse drug reaction in CNS

A

Salicylates —> tinnitus, dizziness

Phenothiazine antipsychotics —> acute dystonic reactions and parkinsonian syndrome

Sedatives —> respiratory depression

36
Q

Risk:benefit ratio for menopausal hormone therapy in terms of breast cancer, atherosclerosis, coronary disease, stroke, and embolism

A

Increases risk of breast cancer after median time of 5-6 years (unless woman had hysterectomy)

May protect from atherosclerosis and coronary disease in women <60

Increases risk of stroke and thromboembolism including DVT and PE

37
Q

Oral contraceptives impact on cancer risk

A

Do not increase breast cancer risk; Protective against endometrial and ovarian cancers

May increase risk of cervical cancer in women infected with HPV; increased risk of hepatic adenoma in older women with prolonged OC use

38
Q

A male adolescent patient presents with the following:
Stunted growth, acne, gynecomastia, testicular atrophy, psychiatric disturbance, and hepatic cholestasis

What agent is likely to cause these adverse effects?

A

Anabolic steroids

39
Q

How does acetaminophen detoxification produce liver damage?

A

5% of it is metabolized via CYP2E to NAPQI, a highly reactive metabolite normally conjugated to glutathione. NAPQI accumulates and causes hepatocellular injury when drug is taken in large doses. Result is centrilobular necrosis and subsequent liver failure

[injury by NAPQI occurs by covalent binding to hepatic proteins and depletion of glutathione]

40
Q

Effects of acute aspirin overdose

A 
Respiratory alkalosis
Metabolic acidosis (causes eventual nausea and coma)
41
Q

Effects of chronic aspirin toxicity

A

Headaches, dizziness, tinnitus, hearing impairment, mental confusion, drowsiness, nausea, vomiting, diarrhea, convulsions, coma, acute erosive gastritis

42
Q

MOA and examples of opioid narcotics

A

Mu opioid receptor agonists

Heroin
Hydromorphone (dilaudid)
Oxycodone
Methadone
Meperidine (demerol)
43
Q

MOA and examples of sedative-hypnotics

A

GABA(a) receptor agonists

Barbiturates
Ethanol
Methaqualone
Glutethimide
Ethchlorvynol
44
Q

MOA and examples of psychomotor stimulants

A

Dopamine transporter antagonists

Cocaine
Amphetamines
MDMA
Ecstasy
Meth
45
Q

MOA and examples of phencyclidine-like drugs

A

NMDA glutamate receptor channel antagonists

PCP
Ketamine

46
Q

MOA and examples of hallucinogens

A

Serotonin 5-HT2 receptor agonists

LSD
Mescaline
Psilocybin

47
Q

Greatest threats to life in burn patients

A

Shock
Sepsis
Respiratory insufficiency

48
Q

Cause and clinical presentation of malignant hyperthermia

A

Caused by inherited mutation in RYR1

Sweating ceases and core body temp rises to more than 40 C leading to multiorgan dysfunction; marked vasodilation with peripheral pooling of blood and decreased effective circulating blood volume; hyperkalemia, tachycardia, arrhythmias, and other systemic effects, sustained contractions of skeletal muscles exacerbate hyperthermia and lead to muscle necrosis (rhabdomyelosis)

49
Q

Ionizing radation has what acute effect on hematopoietic and lymphoid systems?

A

Lymphopenia

50
Q

Clinical features of Kwarshiorkor

A 
Hypoalbuminemia —> edema
“Flaky paint” skin lesions
Loss of pigmentation in hair
Enlarged fatty liver
Apathy, listlessness, loss of appetite
Immune defects
51
Q

Clinical features of marasmus

A

Growth retardation and loss of muscle and subcutaneous fat d/t catabolism and depletion

Extremities are emaciated, anemia, vitamin deficiencies, immune deficiencies, low leptin production —> lipolysis

52
Q

Consequences of Vitamin A deficiency

A

Night blindness, xerophthalmia, bitot spots, corneal ulcers, keratomalacia, squamous metaplasia (long-term), renal stones, vulnerability to infections (measles)

53
Q

Consequences of vit A toxicity

A

Headache, dizziness, vomiting, stupor, blurred vision

Weight loss, anorexia, nausea, vomiting, bone and joint pain

54
Q

Consequences of vitamin D deficiency

A

Rickets in children — craniotabes, frontal bossing and square head, rachitic rosary (deformation of chest), pigeon chest deformity, lumbar lordosis, bowing of legs

Osteomalacia in adults

55
Q

Vitamin D toxicity

A

Metastatic calcifications of soft tissues (kidney) in children

Bone pain and hypercalcemia in adults

56
Q

Clinical features of vitamin E deficiency

A

Spinocerebellar degeneration

57
Q

Clinical features of vitamin K deficiency

A

Bleeding diathesis

58
Q

Clinical features of vitamin B1 (thiamine) deficiency

A

Dry and wet beriberi
Wernicke syndrome
Korsakoff syndrome

59
Q

Clinical features of vitamin B2 (riboflavin) deficiency

A 
Ariboflavinosis
Cheilosis
Stomatitis
Glossitis
Dermatitis
Corneal vascularization
60
Q

Clinical features of niacin deficiency

A

Pellagra (dementia, dermatitis, diarrhea)

61
Q

Clinical features of vitamin B6 deficiency

A

Cheilosis
Glossitis
Dermatitis
Peripheral neuropathy

62
Q

Clinical features of vitamin B12 deficiency

A

Megaloblastic pernicious anemia

Degeneration of posterolateral spinal cord tracts

63
Q

Clinical features of folate deficiency

A

Megaloblastic anemia

Neural tube defects

64
Q

Clinical features of zinc deficiency

A 
Rash around eyes, mouth, nose, and anus
Anorexia and diarrhea
Growth retardation in children
Depressed mental function
Depressed wound healing and immune response
Impaired night vision
Infertility
65
Q

Clinical features of iron deficiency

A

Hypochromic microcytic anemia (likely d/t GI tract pathology)

66
Q

Clinical features of iodine deficiency

A

Goiter

Hypothyroidism

67
Q

Clinical features of copper deficiency

A

Muscle weakness
Neurologic defects
Abnormal collagen cross-linking

68
Q

Clinical features of selenium deficiency

A

Myopathy

Cardiomyopathy (keshan disease)

69
Q

What causes obesity in WAGR syndrome?

A

Haploinsufficiency of BDNF (important component of signaling downstream of MC4R in hypothalamus)

70
Q

Mechanisms by which obesity may contribute to carcinogenesis

A

Elevated insulin levels — free IGF-1 is a mitogen that activates RAS and PI3/AKT pathways

Increased synthesis of steroid hormones (estrogen) through effect of adipose tissue aromatases

Proinflammatory state in which cytokines may cause carcinogenesis

MOD II Exam I (4 decks)

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