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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
3 ways that smoking contributes to lung cancer
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
26
Most alcohol in the blood is oxidized to ______ by 3 enzyme systems. What are the 3 enzyme systems?
Acetaldehyde Alcohol dehydrogenase (primary) - in cytoplasm of hepatocytes Microsomal ethanol-oxidizing system (CYPs) Catalase
27
Oxidation of ethanol produces toxic metabolites and disrupts certain metabolic pathways. What are some examples?
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
28
Vitamin defiency associated with chronic alcoholism; what are the consequences?
Thiamine (B1) deficiency —> peripheral neuropathy, wernicke-korsakoff syndrome, cerebral atrophy, cerebellar degeneration, optic neuropathy
29
Agents that tend to cause adverse drug reaction in bone marrow and blood cells
Antineoplastic agents, immunosuppressives, chloramphenicol —> granulocytopenia, aplastic anemia, pancytopenia Penicillin, methyldopa, quinidine, heparin —> hemolytic anemia, thrombocytopenia
30
Agents that tend to cause adverse drug reaction in skin
Antineoplastic agents, sulfonomides, hydantoins, some abx —> urticaria, papules, vesicles, petechiae, exfoliative dermatitis, fixed drug eruptions, abnormal pigmentation
31
Agents that tend to cause adverse drug reaction in cardiac system
Theophylline, hydantoins, digoxin —> arrhythmias Doxorubicin, daunorubicin -> cardiomyopathy
32
Agents that tend to cause adverse drug reaction in renal system
Penicillamine -> glomerulonephritis Aminoglycoside abx, cyclosporin, amphotericin B —> acute tubular necrosis Phenacetin, salicylates —> tubulointerstitial diseases with papillary necrosis
33
Agents that tend to cause adverse drug reaction in pulmonary system
Salicylates —> asthma Nitrofurantoin —> acute pneumonitis Busulfan, nitrofurantoin, bleomycin —> interstitial fibrosis
34
Agents that tend to cause adverse drug reaction in hepatic system
Tetracycline —> fatty change Halothane, isoniazid, acetaminophen —> diffuse hepatocellular change Chlorpromazine, estrogen, contraceptives —> cholestasis
35
Agents that tend to cause adverse drug reaction in CNS
Salicylates —> tinnitus, dizziness Phenothiazine antipsychotics —> acute dystonic reactions and parkinsonian syndrome Sedatives —> respiratory depression
36
Risk:benefit ratio for menopausal hormone therapy in terms of breast cancer, atherosclerosis, coronary disease, stroke, and embolism
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
Oral contraceptives impact on cancer risk
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
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?
Anabolic steroids
39
How does acetaminophen detoxification produce liver damage?
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
Effects of acute aspirin overdose
``` Respiratory alkalosis Metabolic acidosis (causes eventual nausea and coma) ```
41
Effects of chronic aspirin toxicity
Headaches, dizziness, tinnitus, hearing impairment, mental confusion, drowsiness, nausea, vomiting, diarrhea, convulsions, coma, acute erosive gastritis
42
MOA and examples of opioid narcotics
Mu opioid receptor agonists ``` Heroin Hydromorphone (dilaudid) Oxycodone Methadone Meperidine (demerol) ```
43
MOA and examples of sedative-hypnotics
GABA(a) receptor agonists ``` Barbiturates Ethanol Methaqualone Glutethimide Ethchlorvynol ```
44
MOA and examples of psychomotor stimulants
Dopamine transporter antagonists ``` Cocaine Amphetamines MDMA Ecstasy Meth ```
45
MOA and examples of phencyclidine-like drugs
NMDA glutamate receptor channel antagonists PCP Ketamine
46
MOA and examples of hallucinogens
Serotonin 5-HT2 receptor agonists LSD Mescaline Psilocybin
47
Greatest threats to life in burn patients
Shock Sepsis Respiratory insufficiency
48
Cause and clinical presentation of malignant hyperthermia
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
Ionizing radation has what acute effect on hematopoietic and lymphoid systems?
Lymphopenia
50
Clinical features of Kwarshiorkor
``` Hypoalbuminemia —> edema “Flaky paint” skin lesions Loss of pigmentation in hair Enlarged fatty liver Apathy, listlessness, loss of appetite Immune defects ```
51
Clinical features of marasmus
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
Consequences of Vitamin A deficiency
Night blindness, xerophthalmia, bitot spots, corneal ulcers, keratomalacia, squamous metaplasia (long-term), renal stones, vulnerability to infections (measles)
53
Consequences of vit A toxicity
Headache, dizziness, vomiting, stupor, blurred vision Weight loss, anorexia, nausea, vomiting, bone and joint pain
54
Consequences of vitamin D deficiency
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
Vitamin D toxicity
Metastatic calcifications of soft tissues (kidney) in children Bone pain and hypercalcemia in adults
56
Clinical features of vitamin E deficiency
Spinocerebellar degeneration
57
Clinical features of vitamin K deficiency
Bleeding diathesis
58
Clinical features of vitamin B1 (thiamine) deficiency
Dry and wet beriberi Wernicke syndrome Korsakoff syndrome
59
Clinical features of vitamin B2 (riboflavin) deficiency
``` Ariboflavinosis Cheilosis Stomatitis Glossitis Dermatitis Corneal vascularization ```
60
Clinical features of niacin deficiency
Pellagra (dementia, dermatitis, diarrhea)
61
Clinical features of vitamin B6 deficiency
Cheilosis Glossitis Dermatitis Peripheral neuropathy
62
Clinical features of vitamin B12 deficiency
Megaloblastic pernicious anemia | Degeneration of posterolateral spinal cord tracts
63
Clinical features of folate deficiency
Megaloblastic anemia | Neural tube defects
64
Clinical features of zinc deficiency
``` 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
Clinical features of iron deficiency
Hypochromic microcytic anemia (likely d/t GI tract pathology)
66
Clinical features of iodine deficiency
Goiter | Hypothyroidism
67
Clinical features of copper deficiency
Muscle weakness Neurologic defects Abnormal collagen cross-linking
68
Clinical features of selenium deficiency
Myopathy | Cardiomyopathy (keshan disease)
69
What causes obesity in WAGR syndrome?
Haploinsufficiency of BDNF (important component of signaling downstream of MC4R in hypothalamus)
70
Mechanisms by which obesity may contribute to carcinogenesis
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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