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Robbins first 10 chapters > Chapter 9 > Flashcards

Chapter 9 Flashcards

1
Q

Xenobiotics

A

-exogenous chemicals in the air, water, etc that are inhaled, ingested, etc

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2
Q

Phase I reactions

A
  • first step of either metabolizing xenobiotics to inactive metabolites or activating them into toxic compounds
  • involved hydrolysis, oxidation, or reduction reactions
  • most important catalyst is cytochrome p-450 enzymes
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3
Q

Phase II reactions

A
  • metabolism of phase I products into excretable water-soluble compounds
  • glucuronidation, sulfation, methylation or glutathione conjugation
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4
Q

Carbon monoxide

A
  • product of incomplete oxidation of carbonaceous materials
  • systemic asphyxiant that causes CNS depression
  • hemoglobin has 200x greater affinity for CO than for oxygen, and so does not carry oxygen resulting in hypoxia at low concentrations, and unconsciousness and death at high concentrations (in 5 min in a garage)
  • chronic CO poisoning: ischemic changes in CNS especially basal ganglia
  • acute CO poisoning: cherry-red skin and mucus membranes; may see cerebral edema, punctate hemorrhages and hypoxia induced neuronal changes (changes not specific for CO but seen in any hypoxic injury)
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5
Q

Mercury

A
  • main sources: contaminated fish, mercury vapours from dental amalgams
  • methyl mercury (organic compound) accumulates in CNS and can cause deafness, mental retardation etc (Minamata disease), cerebral palsy, and kidney damage
  • CDC recommends low mercury intake in pregnancy to protect against fetal brain damage
  • ?autism link
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6
Q

Arsenic

A
  • found in herbal supplements, wood preservers, herbicides
  • causes cardiovascular, CNS and gastrointestinal toxicity
  • arsenic keratoses and SCC
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7
Q

Cadmium

A
  • from batteries, soil contamination (most commonly ingested)
  • causes obstructive lung disease and renal tubular damage that can progress to end stage renal disease
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8
Q

Vinyl chloride risk and who is at risk

A
  • angiosarcoma of the liver

- risk to producers of polyvinyl resins

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9
Q

Main steps in alcohol metabolism

A
  • converted to acetaldehyde by alcohol dehydrogenase in hepatocytes
  • acetaldehyde converted to acetate by acetaldehyde dehydrogenase
  • acetate then utilized by mitochondrial respiratory transport chain
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10
Q

Effects of chronic alcoholism

A

Liver: steatosis, steatohepatitis, cirrhosis
GI tract: gastritis, ulcers and varices can cause life-threatening bleeding; pancreatitis
CNS/PNS: thiamine deficiency causing Wernicke-Korsakoff syndrome and peripheral neuropathy
CV system: dilated cardiomyopathy
FAS
Cancer: oral cavitiy, esophagus, liver
Malnutrition and nutritional deficiencies

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11
Q

Mechanism of injury in acetaminophen toxicity

A
  • accumulation of NAPQI which binds to hepatic proteins causing damage to membranes and mitochondria, and depletion of GSH (which normally conjugates NAPQI), making hepatocytes more susceptible to ROS-induced injury
  • because alcohol induces CYP2E1 which metabolizes some acetaminophen to NAPQI, toxicity occurs at lower doses in alcoholics
  • in the normal setting, 95% of acetaminophen is detoxified by phase II enzymes, but in larger doses, the NAPQI pathway gets activated more
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12
Q

Histologic features of acetaminophen overdose

A

-centrilobular necrosis that may extend to involve entire lobules

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13
Q

Acute ASA overdose

A
  • respiratory alkalosis due to stimulation of medullary respiratory centres
  • then, metabolic acidosis producing nausea, coma
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14
Q

Effects of cocaine

A

Generally: blocks reuptake of dopamine and norepinephrine and epinephrine
Cardiovascular effects: acts as a sympathomimetic causing tachycardia, hypertension and peripheral vasoconstriction; also induces myocardial ischemia via coronary artery vasoconstriction; also lethal arrhythmias from ion transport disruption
CNS: hyperpyrexia
Pregnancy: fetal hypoxia due to vasoconstriction in placenta

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15
Q

Effects of heroin

A

Opioid agonist (Mu receptor)

Sudden death due to respiratory depression, arrhythmia and cardiac arrest and severe pulmonary edema
Pulmonary edema
Infections including endocarditis due to injections
Renal disease

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16
Q

Features determining the significance of a burn injury

A
  • depth of burn
  • percentage body surface involved
  • internal injuries caused by inhalation of hot and toxic fumes
  • promptness and efficacy of therapy, especially fluid resuscitation
17
Q

Types of electrical injuries

A
  • burns
  • ventricular fibrillation
  • cardiac/respiratory centre failure
  • tetanic muscle spasm resulting in prolonged grabbing in alternating currents
18
Q

Damage to DNA caused by ionizing radiation

A
  • double strand breaks, single base damage, single strand breaks, DNA-protein cross links
  • double strand breaks are the most serious because repair often produces mutations, which, if not corrected, may initiate carcinogenesis
19
Q

Marasmus

A
  • growth retardation and loss of muscle but visceral protein compartment (liver) is only marginally depleted, therefore albumin levels near normal
  • subcutaneous fat is mobilized for fuel
  • emaciated extremities; large head for body
20
Q

Kwashiorkor

A
  • protein deprivation > calorie deprivation
  • severe loss of the visceral protein compartment, leading to hypoalbuminemia and generalized edema
  • relative sparing of subcutaneous fat and muscle mass
  • enlarged fatty liver
21
Q

Functions of vitamin A

A
  • maintaining vision (required to build pigments)
  • differentiation of mucus-secreting epithelium (becomes keratinized without vitamin A)
  • roles in fatty acid metabolism
  • involved in host resistance to infections
22
Q

Effects of vitamin A deficiency

A
  • night blindness
  • xerophthalmia (dry eye)
  • squamous metaplasia of respiratory tissues causing loss of mucociliary epithelium and infection
  • follicular plugging in skin
  • immune deficiency
23
Q

Vitamin D deficiency

A
  • Rickets in children
  • Osteomalacia in adults
  • both due to an excess of unmineralized matrix
24
Q

Rickets

A
  • due to lack of Vitamin D
  • overgrowth of cartilage due to inadequate calcification with deposition of osteoid on inadequately mineralized cartilage with subsequent fractures and skeletal deformation
  • flattened occipital bones, frontal bossing, rachitic rosary (overgrowth of cartilage at the costochondral junction)
25
Q

Osteomalacia

A
  • deranged normal bone remodelling due to lack of vitamin D
  • excess persistent inadequately mineralized osteoid
  • histology: thickened matrix around normal basophilic mineralized bone
  • susceptible to fractures
26
Q

Main function of vitamin C

A
  • production of prolyl and lysyl hydroxylases that result in hydroxylation of procollagen
  • antioxidant properties: free radical scavenging
27
Q

Features of vitamin C deficiency

A
  • poor vessel support: bleeding gums, joints, skin
  • inadequate synthesis of osteoid
  • impaired wound healing
28
Q

Leptin

A
  • synthesized by fat cells
  • stimulates POMC/CART neurons in the hypothalamus that produce anorexigenic neuropeptides (MSH)
  • inhibits NPY neurons thereby inhibiting feeding-inducing neuropeptides
  • leptin is dimished when there are inadequate stores of body fat
  • leptin resistance may be a cause for obesity
29
Q

Ghrelin

A
  • produced in stomach and arcuate nucleus

- only known gut hormone that increases food intake

30
Q

Malformation

A
  • primary error of morphogenesis with an intrinsically abnormal developmental process
  • usually multifactorial rather than related to a single chromosomal defect
  • e.g. anencephaly
31
Q

Deformation

A
  • extrinsic disturbance of development caused by localized or generalized compression of the fetus by abnormal biomechanical forces
  • e.g. uterine constraint (maternal factors such as 1st pregnancy, leiomyomas, or placental factors such as oligohydramniosis, or fetal factors such as twins)
  • e.g. clubfeet
32
Q

Syndrome

A
  • constellation of congenial anomalies believed to be pathologically related but that cannot be explained by a single initiating defect
  • e.g. viral or specific chromosomal abnormalities that affect multiple tissues
33
Q

Aplasia

A

-absence of an organ due to failure of development of the primordium

34
Q

What three enzyme systems are responsible for metabolizing alcohol?

A
  • alcohol dehydrogenase
  • the microsomal ethanol oxidizing system
  • catalase

-latter two come into play at high blood alcohol concentrations

35
Q

Differentiate heat cramps, heat exhaustion and heat stroke.

A

Cramps: loss of electrolytes via sweating with cramping (usually after exercise)
Exhaustion: Collapse because of failure of CV system to compensate for hypovolemia
Stroke: Failure of thermoregulatory mechanisms resulting in high body temperature, generalized vasodilation with peripheral pooling, tachycardia, arrhythmia, and muscle necrosis (rhabdomyolysis)

36
Q

What are cachectic agents produced by tumors?

A
  • PIF (proteolysis inducing factor): causes muscle breakdown via NF-KB
  • LMF (lipid-mobilizing factor)
37
Q

What is the possible mechanism whereby obesity contributes to carcinogenesis?

A

May be through hyperinsulinemia and insulin resistance; with increase in IGF1, which is mitogenic and antiapoptotic and is highly expressed in many cancers
May also have an effect on steroid hormones that regulate cell growth in certain organs (e.g. estrogen for breast or uterus)

38
Q

How might sirtuins (increased by calorie restriction) prolong life?

A

May lower IGF1 levels with resistance to carcinogenesis

-also less oxidative damage and less decline in immunologic function

Robbins first 10 chapters (11 decks)

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