Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
45 Cards in this Set
- Front
- Back
|
Which of the following drugs can provide a therapeutic as well as diagnostic effect in patients with acute opiate intoxication?
A. nalmefene B. naloxone C. methadone D. A & B E. A, B, C |
D. A & B.
Both nalmefene and naloxone are opiate antagonists. When given to cases of suspected opiate overdose, they can suddenly reverse the effects of opiates. Patients who do not respond to opiate antagonists can presumably be excluded from opiate intoxication. Methadone is an opiate agonist used in the treatment of opiate addiction. do not respond to opiate antagonists can presumably be excluded from opiate intoxication. Methadone is an opiate agonist used in the treatment of opiate addiction. QCCP2, Opiates |
|
|
What is the mechanism of barbiturate-mediated CNS depression?
A. opiate receptor agonist B. NMDA receptor agonist C. potentiation of NMDA-dependent activity D. potentiation of GABA-dependent activity E. potentiation of glutamate-dependent activity |
D. potentiation of GABA-dependent activity.
Gamma aminobutyric acid (GABA) is a CNS inhibitor with an unclear mechanism of action. It is known that barbiturates can work through the GABA receptor and stimulate its activity, but not through the same mechanism as benzodiazepines. QCCP2, Barbiturates |
|
|
Which of the following conditions is associated with the highest average hCG levels?
A. normal intrauterine pregnancy B. ectopic pregnancy C. partial mole D. complete mole E. choriocarcinoma |
D. complete mole.
On average, gestational trophoblastic disease presents with hCG levels higher than those of a normal pregnancy. Complete moles have a much higher risk that any other pre-existing condition to develop choriocarcinoma. QCCP2, hCG in gestational trophoblastic disease |
|
|
Which of the following is a potential risk of long-term amphetamine use?
A. Alzheimer-like syndrome B. Parkinsonian syndrome C. rhabdomyolysis D. cirrhosis E. all of the above |
B. Parkinsonian syndrome.
Amphetamines work by stimulating the release of dopamine and in doing so can cause the death of the dopamine-secreting cells in the CNS. Lack of dopamine can result in a Parkinsonian condition, often where patients experience a locked-in phenomenon. QCCP2, Amphetamines |
|
|
What is the mechanism of action of phencyclidine?
A. direct serotonergic activity B. inhibition of serotonin reuptake C. direct cholinergic activity D. inhibition of catecholamine reuptake E. a combination of several of the above mechanisms |
D. inhibition of catecholamine reuptake.
PCP functions as an inhibitor of catecholamine reuptake. Beyond the hallucinatory activities of PCP, patients with active intoxication exhibit symptoms of dopamine toxicity - bradycardia, hypotension, hypoglycemia, and hypopnea. QCCP2, PCP |
|
|
At what blood alcohol level (BAL) does one start worrying about coma and death from alcohol poisoning (in general)?
A. 0.05% B. 0.1% C. 0.3% D. 0.4% E. 0.8% |
D. 0.4%.
Of course, if somebody survived a BAL of 0.8%, one would worry about coma and death, but the question asked at what BAL does one start to worry, and 0.4% is the level at which there is first a very real risk of coma and death. QCCP2, T1.19, Clinical Effects of Blood Alcohol |
|
|
What is the first hepatic metabolite of ethanol?
A. cocaethylene B. acetic acid C. methanol D. ethylene glycol E. acetaldehyde |
E. acetylaldehyde.
Both gastric and hepatic alcohol dehydrogenase facilitate the oxidation of ethanol to acetylaldehyde. When the alcohol dehydrogenase system is overwhelmed by excess ethanol, the microsomal ethanol oxidizing system contributes to the oxidation of ethanol. Acetylaldehyde is then further oxidized to acetate in the liver by aldehyde dehydrogenase. Many of the unpleasant side effects of alcohol - flushing, nausea, etc - are due to a buildup of acetaldehyde. The drug disulfram inhibits aldehyde dehydrogenase, perpetuating the unpleasant effects and helping to promote teetotalling. QCCP2, Ethanol |
|
|
Which sample is preferred for quantitative alcohol testing in a living patient with a suspected overdose?
A. vitreous humor B. breath C. whole blood D. urine E. serum |
E. serum.
Vitreous, breath alcohol, and whole blood are more commonly used in the post-mortem investigation of blood alcohol levels (just try to collect vitreous humor from a living patient!). Either serum or plasma are preferred samples when evaluating alcohol levels in living patients. Urine can be used, but usually only for qualitative testing. QCCP2, Ethanol |
|
|
In the legal definition of alcohol level limits for operation of a motor vehicle, what sample is used for standards?
A. vitreous humor B. breath C. whole blood D. urine E. serum |
C. whole blood.
Even though the previous question stated that plasma or serum is the preferred sample, one must carefully read the question. For overdose, the preferred sample is plasma or serum, but to define what level is safe to operate a motor vehicle, whole blood is used. This is important because whole blood ethanol levels are usually lower than serum levels. The legal limits vary by state but are typically in the range of 0.8-1.0%. QCCP2, Ethanol |
|
|
Under normal circumstances which test is the most sensitive and specific for chronic alcohol consumption?
A. carbohydrate-deficient transferrin (CDT) B. serum alkaline phosphatase (AP) C. gamma-glutamyl transferase (GGT) D. alcohol dehydrogenase (ADH) E. alanine aminotransferase (ALT) |
A. carbohydrate-deficient transferrin.
For the most part, CDT is the most sensitive and specific of the choices, though all of them can be altered with chronic alcohol consumption. CDT levels rise faster than GGT in response to ethanol. There are a few caveats with CDT, however. Heavy female drinkers have lower average levels than their male counterparts and certain liver diseases can cause CDT elevations in the absence of alcohol consumption. QCCP2, Ethanol |
|
|
Which of the following toxidromes is most likely to be seen in a farm worker who has just been spraying pesticides?
A. altered mental status, hypopnea/apnea B. salivation, lacrimation, urination, diarrhea, GI cramps, and emesis C. hyperthermia, dry skin, altered mental status, psychosis D. hypertension, tachycardia, mydriasis, anxiety, hyperthermia E. hallucinations, anxiety, hyperthermia |
B. salivation, lacrimation, urination, diarrhea, GI cramps, and emesis.
Certain insecticides, such as malathion and parathion, are converted to organophosphates after ingestion. Organophosphates are cholinesterase inhibitors with potent cholinergic activity. The mnemonic “SLUDGES” is helpful in remembering the cardinal features of cholinergic toxicity - salivation, lacrimation, urination, diarrhea, GI cramps, emesis. Imagine a farm worker trudging through a field of SLUDGE. QCCP2, T1.20, Common toxidromes |
|
|
What is the calculated osmolarity for a sodium of 140 mEq/L, blood urea nitrogen of 10 mg/dL, and a glucose of 180 mg/dL?
A. 340 mOsm/L B. 330 mOsm/L C. 318 mOsm/L D. 312 mOsm/L E. 384 mOsm/L |
E. 384 mOsm/L.
Sodium is the major serum osmolyte, but BUN and glucose both provide a significant amount of osmolytes, too. To calculate the serum osmolarity, multiply the sodium concentration by two, add BUN/2.5 and glucose/18. In this case, a sodium of 140 multiplied by two is 280, added to 10/2.5 plus 180/1.8 is 384 mOsm/L. QCCP2, Calculation of osmolar gap |
|
|
Which ingestion would be most suspect in a patient with both and anion and osmolar gap?
A. whiskey B. rubbing alcohol C. windshield washer fluid D. nail polish remover E. aspirin |
C. windshield washer fluid.
Ethanol, isopropanol, and acetone (as in whiskey, rubbing alcohol, and nail polish remover, respectively) all can cause an osmolar gap, but usually without a concomitant anion gap. Conversely, salicylates can cause an anion gap but no osmolar gap. Windshield wiper fluid contains methanol, which like the ethylene glycol in antifreeze can cause both an anion and osmolar gap. QCCP2, Tables 1.21 1.22 |
|
|
Which of the following values is calculated in an arterial blood gas analyzer?
A. oxygen saturation of blood B. hemoglobin oxygen affinity C. oxygen tension of blood D. pH of blood E. all of the above are directly measured by an ABG analyzer |
A. oxygen saturation of blood.
ABG analyzers measure oxygen tension and pH. From those values and a standard hemoglobin oxygen affinity graph, the oxygen saturation is calculated. Because the calculation is based on a standard curve, anything that affects the ability of hemoglobin to bind oxygen can cause inaccurate oxygen saturation readings. QCCP2, Measurement of blood gases |
|
|
Which of the following forms of hemoglobin will a pulse oximeter measure?
A. oxyhemoglobin B. deoxyhemoglobin C. carboxyhemoglobin D. A & B E. A, B, C |
D. A & B.
Pulse oximetry uses transdermal illumination to measure the absorption of light by oxyhemoglobin and deoxyhemoglobin. Alternate forms of hemoglobin, such as methemoglobin and carboxyhemoglobin can interfere with these results. QCCP2, Measurement of blood gases |
|
|
Why has ethanol been historically used in the treatment of ethylene glycol or methanol poisoning?
A. ethanol prevents the development of an anion gap B. ethanol increases diuresis and elimination C. ethanol directly binds methanol and ethylene glycol, effectively neutralizing them D. ethanol competes with ethylene glycol and methanol for alcohol dehydrogenase E. ethanol makes the patient less anxious |
D. ethanol competes with ethylene glycol and methanol for alcohol dehydrogenase.
While ethylene glycol and methanol have little direct toxicity, the metabolites glycolic acid/oxalate and formaldehyde/formic acid are both extremely toxic. The enzyme alcohol dehydrogenase is responsible for the metabolism of ethanol, methanol, and ethylene glycol. Supplying the patient with excess ethanol allows for competitive inhibition of alcohol dehydrogenase and therefore decreased production of toxic metabolites. In doing so, ethanol delays the development of an anion gap in patients with methanol and ethylene glyngestion - it does not prevent it. QCCP2, Toxic alcohol poisoning |
|
|
Which two body sites are the primary storage sites for lead? (pick two)
A. vitreous humor B. hair C. bone D. erythrocytes E. gingiva |
C. bone.
D. erythrocytes. In addition to bone and erythrocytes, a significant portion of lead is stored in the kidneys. QCCP2, Lead poisoning |
|
|
What is the preferred screening test for lead toxicity?
A. blood lead levels B. free erythrocyte protoporphyrin (FEP) C. zinc protoporphyrin (ZPP) D. hair lead levels E. urine lead levels |
A. blood lead levels.
Previously, FEP and ZPP were used as screening tools. Lead inhibits delta-ALA-dehydratase, an enzyme involved in heme synthesis. As a result, a precursor, free erythrocyte protoporphyrin (EP) accumulates. Furthermore, FEP can bind zinc and produce zinc protoporphyrin (ZPP). The problem with using ZPP and FEP as screening tools is that they are both non-specific and insufficiently sensitive. QCCP2, Lead poisoning |
|
|
Above what level is considered an elevated lead concentration when screening children?
A. 5 microgram/dL B. 10 microgram/dL C. 35 microgram/dL D. 50 microgram/dL E. 100 microgram/dL |
B. 10 micrograms/dL.
The CDC recommendations stipulate blood levels should be less than 10 micrograms/dL. For this only, blood lead levels by atomic absorption spectrophotometry are sufficiently sensitive. FEP and ZPP are only detectable at lead levels greater than 35 micrograms/dL, which is not sensitive enough for screening. QCCP2, Lead poisoning |
|
|
Which of the following modalities is best for measuring blood carbon monoxide levels?
A. pulse oximeter B. co-oximeter C. blood gas analyzer D. hemoglobin levels E. V/Q scan |
B. co-oximeter.
Co-oximeter analysis from either arterial or venous blood directly measures carbon monoxide-bound hemoglobin. Pulse oximeters and blood gas analyzers don't measure variant hemoglobins, such as hemoglobin-CO, and may actually provide falsely normal readings. Hemoglobin levels give no indication of carbon monoxide levels and a V/Q scan is to look for oxygenation/perfusion mismatch. QCCP2, Carbon monoxide (CO) poisoning |
|
|
Which of the following ancillary tools is used to assess the risk of acetaminophen overdose?
A. Levey-Jennings chart B. Rumack-Matthew nomogram C. Henderson-Hasselbalch equation D. Friedewald equation E. Michaelis-Menten equation |
B. Rumack-Matthew nomogram.
The Rumack-Matthew nomogram is a plot of acetaminophen levels (in micrograms/mL or micromoles/L) on the y axis v. time after ingestion on the x axis. Two straight lines of equal linear regressive slope are drawn to delimit those below as low risk and those above as high risk. Importantly, the nomogram is used with the assumption that the patient has taken a single ingestion of acetaminophen at a defined time at least four hours prior. QCCP2, Acetaminophen poisoning |
|
|
Which of the following compounds is the toxic metabolite of acetaminophen primarily responsible for hepatotoxicity?
A. acetaminophen phosphate B. N-acetylcysteine C. N-acetyl-p-benzoquinoneimine D. glutathione E. acetaminophen sulfate |
C. N-acetyl-p-benzoquinoneimine.
The cytochrome P450 system converts acetaminophen to the toxic metabolite, N-acetyl-p-benzoquinoneimine (NAPQI), which is responsible for the majority of the hepatic toxicity. Glutathione-S-transferase then converts NAPQI to a less toxic metabolite. However, in the process glutathione is depleted and excess NAPQI can cause direct zone 3 hepatic toxicity. Treatment is by providing excess glutathione equivalents in the form of N-acetylcysteine. QCCP2, Acetaminophen poisoning |
|
|
Which of the following is most consistent with cyanide poisoning?
A. elevated serum lactate, anion gap metabolic acidosis B. elevated serum lactate, metabolic alkalosis C. decreased serum lactate, anion gap metabolic acidosis D. decreased serum lactate, metabolic alkalosis E. normal serum lactate, normal serum pH |
A. elevated serum lactate, anion gap metabolic acidosis.
The causes of anion gap metabolic acidosis can be divided into two categories - conditions that cause elevated serum lactate, such as cyanide, and those that are due to unmeasured organic anions. Lactate elevation in cyanide poisoning is fairly universal, so a normal serum lactate can eliminate cyanide as a cause of patient symptoms. QCCP2, Cyanide poisoning |
|
|
Which of the following is most consistent with salicylate intoxication?
A. respiratory alkalosis B. metabolic acidosis C. respiratory acidosis D. A & B E. A, B, C |
E. A, B, C.
It all depends on when you check. Initially, aspirin triggers a tachypnea resulting in respiratory alkalosis. Then it facilitates anaerobic metabolism, the production of lactate (just like cyanide) and the development of an anion gap metabolic acidosis. Remember, “MUDPILES”? This is the mnemonic to help recall the causes of anion gap metabolic acidosis - methanol, uremia, diabetic ketoacidosis, paraldehyde, isoniazid, lactate, ethanol, salicylates. Eventually, this can be followed by CNS depression and a respiratory acidosis. QCCP2, Salicylates |
|
|
Which of the following is the most reliable test for the diagnosis of acute arsenic ingestion?
A. fingernail arsenic quantitation B. quantitative 24-hour urinary arsenic levels C. blood arsenic levels D. serum arsenic levels E. hair arsenic quantitation |
B. quantitative 24-hour urinary arsenic levels.
Another “go-with-the-longest-answer-if-you-don't-know” question. Blood arsenic is unreliable due to rapid clearance and distribution. Fingernails and hair can be used but elevated levels are more consistent with chronic prolonged ingestion or exposure. QCCP2, Arsenic |
|
|
Which of the following tests can give likelihood information for seizure risk in tricyclic antidepressant overdose?
A. blood oxygen partial pressure B. EKG C. urine sediment analysis D. renal biopsy E. none of the above |
B. EKG.
Actually, a widened QRS, in addition to an increased risk of arrhythmia, is predictive of a likelihood of seizures, especially if the QRS is greater than 0.1. QCCP2, Tricyclic antidepressants |
|
|
Which of the following types of poisoning can result in either autonomic instability and a desquamative erythematous rash of the palms and feet OR personality
changes with irritability and fine motor disturbances? A. lead B. mercury C. carbamates D. organophosphates E. arsenic |
B. mercury.
The chronic exposure to mercury usually occurs through occupational inhalation or ingestion of contaminated FISH. The manifestations of mercury usually take the form of one of two syndromes. Feer syndrome (acrodynia) has autonomic signs - sweating and hemodynamic instability in addition to the characteristic desquamation of the palms and soles. Erethism is more central nervous system-centered, with personality changes and fine motor difficulties. QCCP2, Mercury |
|
|
Which of the following tests can give likelihood information for seizure risk in tricyclic antidepressant overdose?
A. blood oxygen partial pressure B. EKG C. urine sediment analysis D. renal biopsy E. none of the above |
B. EKG.
Actually, a widened QRS, in addition to an increased risk of arrhythmia, is predictive of a likelihood of seizures, especially if the QRS is greater than 0.1. QCCP2, Tricyclic antidepressants |
|
|
A hat maker is suspected to have mercury poisoning due to his increasingly erratic behavior. What is the preferred method to confirm the diagnosis?
A. 24-hour urine mercury levels B. hair mercury levels C. whole blood mercury levels D. liver dry mercury weight E. vitreous mercury levels |
A. 24-hour urine mercury levels.
Elemental mercury is typically inhaled during occupational exposure. It is readily excreted in the urine. Organic mercury, however, is absorbed through the GI tract in contaminated food and not excreted in the urine. Therefore, hair or blood levels are used for diagnosis. Just try to collect vitreous humor from a living patient. QCCP2, Mercury |
|
|
Which of the following types of poisoning can result in either autonomic instability and a desquamative erythematous rash of the palms and feet OR personality
changes with irritability and fine motor disturbances? A. lead B. mercury C. carbamates D. organophosphates E. arsenic |
B. mercury.
The chronic exposure to mercury usually occurs through occupational inhalation or ingestion of contaminated FISH. The manifestations of mercury usually take the form of one of two syndromes. Feer syndrome (acrodynia) has autonomic signs - sweating and hemodynamic instability in addition to the characteristic desquamation of the palms and soles. Erethism is more central nervous system-centered, with personality changes and fine motor difficulties. QCCP2, Mercury |
|
|
Which of the following drugs can substantially alter the risk of digoxin toxicity?
A. fluoroquinolone B. alprazolam C. lithium D. quinidine E. aspirin |
D. quinidine.
Quinidine has multiple roles in enhancing the function of digoxin. It has a direct role in increasing the drug's effects on the heart, but also inhibits the elimination of digoxin by competing for the common P-glycoprotein binding site. As a result, both quinidine and digoxin toxicity is increased when simultaneously administered. QCCP2, Digoxin |
|
|
A hat maker is suspected to have mercury poisoning due to his increasingly erratic behavior. What is the preferred method to confirm the diagnosis?
A. 24-hour urine mercury levels B. hair mercury levels C. whole blood mercury levels D. liver dry mercury weight E. vitreous mercury levels |
A. 24-hour urine mercury levels.
Elemental mercury is typically inhaled during occupational exposure. It is readily excreted in the urine. Organic mercury, however, is absorbed through the GI tract in contaminated food and not excreted in the urine. Therefore, hair or blood levels are used for diagnosis. Just try to collect vitreous humor from a living patient. QCCP2, Mercury |
|
|
Which of the following means are used to metabolize procainamide?
A. hepatic B. renal C. respiratory D. A & B E. A, B, C |
D. A & B.
Procainamide is acetylated in the liver to an active metabolite, N-acetyl procainamide, which in turn is renally excreted. Therefore, both renal and liver dysfunction can affect procainamide levels. QCCP2, Procainamide |
|
|
Which of the following drugs can substantially alter the risk of digoxin toxicity?
A. fluoroquinolone B. alprazolam C. lithium D. quinidine E. aspirin |
D. quinidine.
Quinidine has multiple roles in enhancing the function of digoxin. It has a direct role in increasing the drug's effects on the heart, but also inhibits the elimination of digoxin by competing for the common P-glycoprotein binding site. As a result, both quinidine and digoxin toxicity is increased when simultaneously administered. QCCP2, Digoxin |
|
|
What's the most reliable means of predicting quinidine toxicity?
A. serum quinidine levels B. whole blood quinidine levels C. 24-hour urinary quinidine levels D. liver function tests E. EKG |
E. EKG.
Levels - serum, urinary, or otherwise - are unreliable. The only reliable means of assessing quinidine toxicity is by EKG. As the drug blocks ion channels, toxicity usually manifests with cardiac symptoms, such as a prolonged QT, widened QRS, and arrhythmias. QCCP2, Quinidine |
|
|
Which of the following means are used to metabolize procainamide?
A. hepatic B. renal C. respiratory D. A & B E. A, B, C |
D. A & B.
Procainamide is acetylated in the liver to an active metabolite, N-acetyl procainamide, which in turn is renally excreted. Therefore, both renal and liver dysfunction can affect procainamide levels. QCCP2, Procainamide |
|
|
Which of the following agents causes fetal hydantoin syndrome?
A. procainamide B. lithium C. quinidine D. amiodarone E. none of the above |
E. none of the above.
The causative agent of fetal hydantoin syndrome is in utero exposure of a fetus to phenytoin. The typical manifestations include characteristic facial anomalies, as well as growth and mental retardation. QCCP2, phenytoin |
|
|
What's the most reliable means of predicting quinidine toxicity?
A. serum quinidine levels B. whole blood quinidine levels C. 24-hour urinary quinidine levels D. liver function tests E. EKG |
E. EKG.
Levels - serum, urinary, or otherwise - are unreliable. The only reliable means of assessing quinidine toxicity is by EKG. As the drug blocks ion channels, toxicity usually manifests with cardiac symptoms, such as a prolonged QT, widened QRS, and arrhythmias. QCCP2, Quinidine |
|
|
What is the recommended monitoring interval for lithium levels in patients stable on therapy?
A. 1-3 days B. 1-3 weeks C. 1-3 months D. 6-12 months E. every other year |
C. 1-3 months.
Because of the very narrow therapeutic range and the proximity of therapeutic and toxic levels, it is of paramount importance to monitor levels for initial dosing. The half-life of lithium ranges from 8-40 hours, so steady levels will be achieved after 5 half-lives or 1.5 days to 1 week. Initially, it is recommended to check levels after the initial interval. Samples should be collected 12 hours after last dose. QCCP2, Lithium |
|
|
Which of the following agents causes fetal hydantoin syndrome?
A. procainamide B. lithium C. quinidine D. amiodarone E. none of the above |
E. none of the above.
The causative agent of fetal hydantoin syndrome is in utero exposure of a fetus to phenytoin. The typical manifestations include characteristic facial anomalies, as well as growth and mental retardation. QCCP2, phenytoin |
|
|
All of the following organs potentially have a significant risk of amiodarone toxicity, except:
A. thyroid B. kidney C. liver D. peripheral nerves E. lungs |
B. kidney.
The thyroid and lungs have the highest incidence of toxic reactions to amiodarone. It is also important to remember that amiodarone effects on the liver can affect warfarin and digoxin levels. QCCP2, Amiodarone |
|
|
What is the recommended monitoring interval for lithium levels in patients stable on therapy?
A. 1-3 days B. 1-3 weeks C. 1-3 months D. 6-12 months E. every other year |
C. 1-3 months.
Because of the very narrow therapeutic range and the proximity of therapeutic and toxic levels, it is of paramount importance to monitor levels for initial dosing. The half-life of lithium ranges from 8-40 hours, so steady levels will be achieved after 5 half-lives or 1.5 days to 1 week. Initially, it is recommended to check levels after the initial interval. Samples should be collected 12 hours after last dose. QCCP2, Lithium |
|
|
Which of the following fatty acids have several double bonds along their hydrocarbon chains?
A. saturated fatty acids B. monosaturated fatty acids C. monounsaturated fatty acids D. polysaturated fatty acids E. polyunsaturated fatty acids |
E. polyunsaturated fatty acids.
Whether a fatty acid is fully saturated with hydrogen groups (saturated) or has a single double bond (monounsaturated) with less hydrogen or even less hydrogen with multiple double bonds (polyunsaturated) affects its chemical properties. Saturated fatty acids are less fluid in the cell membrane due to their rigid structure. Unsaturated fatty acids have bends in their chains due to the double bonds and therefore pack less tightly into a membrane which leads to greater membrane fluidity. QCCP2, Lipids |
|
|
All of the following organs potentially have a significant risk of amiodarone toxicity, except:
A. thyroid B. kidney C. liver D. peripheral nerves E. lungs |
B. kidney.
The thyroid and lungs have the highest incidence of toxic reactions to amiodarone. It is also important to remember that amiodarone effects on the liver can affect warfarin and digoxin levels. QCCP2, Amiodarone |
|
|
Which of the following fatty acids have several double bonds along their hydrocarbon chains?
A. saturated fatty acids B. monosaturated fatty acids C. monounsaturated fatty acids D. polysaturated fatty acids E. polyunsaturated fatty acids |
E. polyunsaturated fatty acids.
Whether a fatty acid is fully saturated with hydrogen groups (saturated) or has a single double bond (monounsaturated) with less hydrogen or even less hydrogen with multiple double bonds (polyunsaturated) affects its chemical properties. Saturated fatty acids are less fluid in the cell membrane due to their rigid structure. Unsaturated fatty acids have bends in their chains due to the double bonds and therefore pack less tightly into a membrane which leads to greater membrane fluidity. QCCP2, Lipids |
