1
Q
What cellular process does chloramphenicol inhibit?
A
Protein synthesis.
2
Q
How does chloramphenicol inhibit protein synthesis?
A
It stops peptide bond formation.
3
Q
What important property of chloramphenicol allows it to treat serious infections like meningitis?
A
It crosses the blood–brain barrier (BBB).
4
Q
What serious adverse effects are associated with chloramphenicol?
A
Aplastic anemia
Gray baby syndrome
5
Q
What ribosomal subunit does erythromycin target?
A
50S ribosomal subunit.
6
Q
Why is erythromycin considered a convenient antibiotic for patients?
A
It comes in syrup form.
7
Q
What mild adverse effect occurs in about 3% of patients taking erythromycin?
A
Mild gastrointestinal discomfort.
8
Q
What type of infections is erythromycin particularly useful for?
A
Skin infections.
9
Q
What ribosomal subunit does streptomycin affect?
A
30S ribosomal subunit.
10
Q
What effect does streptomycin have on the ribosome?
A
It changes the shape of the 30S subunit, causing misreading of mRNA.
11
Q
What does misreading of mRNA mean during protein synthesis?
A
The ribosome reads the wrong code and produces incorrect proteins.
12
Q
What serious adverse effects are associated with aminoglycosides like streptomycin?
A
Kidney failure
Deafness
13
Q
What disease was streptomycin historically used to treat?
A
Tuberculosis (TB) (not used anymore)
14
Q
Why is streptomycin rarely used today for TB?
A
Because newer drugs are available.
15
Q
What ribosomal subunit do tetracyclines inhibit?
A
30S ribosomal subunit.
16
Q
What type of antimicrobial spectrum do tetracyclines have?
A
Broad spectrum against gram-positive and gram-negative bacteria.
17
Q
What infections are tetracyclines commonly used to treat?
A
Sexually transmitted diseases (STDs).
18
Q
What major gastrointestinal adverse effect can occur with tetracycline therapy?
A
Destruction of normal gut microbiota leading to severe diarrhea.
19
Q
What secondary infection can occur after tetracycline destroys normal gut flora?
A
Fungal infections.
20
Q
Why does tetracycline cause brown tooth discoloration?
A
Because tetracycline binds to calcium.
21
Q
Why is tetracycline dangerous during pregnancy?
A
It can cause skull deformities in the developing baby.
22
Q
What serious organ complications can tetracycline cause during pregnancy?
A
Liver failure and kidney failure.
23
Q
Why might tetracycline exposure occur through food?
A
Because it is sometimes used in animals and may be present in meat.
24
Q
What infection is rifampin commonly used to treat?
A
Tuberculosis.
25
What serious adverse effect can occur with high doses of rifampin?
Liver failure.
26
What cellular process do quinolones and fluoroquinolones inhibit?
DNA replication.
27
What infection can fluoroquinolones be used to treat?
Anthrax.
28
Why are fluoroquinolones limited in children and elderly patients?
Because they affect cartilage development.
29
Why should fluoroquinolones be avoided during pregnancy?
Because they can damage cartilage in the developing fetus.
30
How does polymyxin B kill bacteria?
It forms pores in the plasma membrane.
31
What organism is polymyxin B commonly used against?
Pseudomonas.
32
Why is polymyxin B usually used only topically?
Because it can damage the kidneys.
33
What enzyme pathway do sulfa drugs block?
PABA pathway in folic acid synthesis.
34
What does trimethoprim inhibit?
Folic acid synthesis.
35
What cellular processes are blocked when folic acid synthesis is inhibited?
DNA and RNA production.
36
What infection are sulfa drugs commonly used to treat?
Urinary tract infections (UTIs).
37
Why should sulfa drugs not be used during the third trimester of pregnancy?
They can cause neurological damage and jaundice in the baby.
38
What additional adverse effects can occur with sulfa drugs?
Anemia
Allergic reactions
39
What does the S stand for in the SAFE MOTHERS acronym?
Sulfa drugs.
40
What does the A stand for in SAFE MOTHERS?
Aminoglycosides.
41
What does the F represent in SAFE MOTHERS?
Fluoroquinolones.
42
What does the E represent in SAFE MOTHERS?
Erythromycin.
43
What three components make up a nucleotide?
Pentose sugar (ribose)
Phosphate group
Nitrogenous base
44
What antiviral drug is used for Herpes simplex virus types 2 and 3?
Acyclovir.
45
What antiviral drug is used for Herpes virus type 5?
Ganciclovir.
46
What antiviral drug is used for HIV?
Zidovudine
47
What antiviral drug is used for HIV and Hepatitis B?
Lamivudine
48
What antiviral drug is used for influenza and RSV?
Ribavirin.
49
What is Mechanism #1 in the “five ways to destroy organisms” framework?
Destroy or injure the cell wall.
50
Why does destroying the cell wall kill bacteria?
Because the cell wall maintains structural integrity; when it is destroyed the cell bursts and dies.
51
What is the mechanism of action of penicillins?
They destroy peptide linkages in peptidoglycan (PG) of the cell wall.
52
What specific structure in peptidoglycan does penicillin destroy?
The peptide cross-bridges (P of PG).
53
What happens to the bacterial cell after penicillin destroys the peptide linkages?
The cell wall disintegrates and the cell dies by osmotic lysis.
54
Why is it important to understand Chapter 4 when studying penicillin?
Because penicillin destroys the peptide linkages of peptidoglycan.
55
Is penicillin a single molecule?
No. Penicillins are a group of about 50 related molecules.
56
What structure is shared by all penicillins?
The beta-lactam ring (common nucleus).
57
What part of penicillin molecules varies between different penicillins?
The side chain (R group).
58
Why do penicillin molecules differ from each other?
Because small changes in the side chain produce different penicillin drugs.
59
What is the prototype natural penicillin mentioned in lecture?
Penicillin G.
60
Why must penicillin G usually be given by injection?
Because stomach acid destroys it, so it cannot be taken orally.
61
What advantage does the oral penicillin form have over penicillin G?
It can be taken orally because stomach acid does not destroy it.
62
What enzymes can destroy penicillin?
Penicillinases (beta-lactamases).
63
What do beta-lactamase enzymes do to penicillin?
They break open the beta-lactam ring.
64
What inactive compound forms when the beta-lactam ring is destroyed?
Penicilloid acid.
65
What happens clinically when bacteria produce beta-lactamases?
Penicillin treatment fails even if large doses are given.
66
How were semisynthetic penicillins developed?
By keeping the common nucleus and modifying the side chain.
67
What was one semisynthetic penicillin example mentioned in lecture?
Methicillin, worked for awhule until Staphococcus aureus become resistant.
68
What resistant organism evolved against methicillin?
MRSA – Methicillin-resistant Staphylococcus aureus.
69
What does the term spectrum mean in antibiotic therapy?
How many types of organisms a drug can attack.
70
What is the difference between narrow spectrum and broad spectrum antibiotics?
Narrow spectrum: attacks limited organisms
Broad spectrum: attacks many organisms.
71
What penicillin example was given that mainly targets gram-positive organisms?
Oxacillin - only gram positive but resitsant to penicillnases.
72
What penicillins were mentioned as extended spectrum drugs?
Ampicillin
Amoxicillin.
73
What advantage do ampicillin and amoxicillin have over earlier penicillins?
They can attack some gram-negative organisms as well.
74
What is the biggest contraindication for penicillin use?
Allergy.
75
What happens if a patient has a penicillin allergy?
Penicillin should never be used again.
76
What is the mechanism of action of cephalosporins?
They attack peptide cross-bridges in peptidoglycan (same mechanism as penicillin).
77
What advantage do cephalosporins have over penicillins?
They are resistant to penicillinases (beta-lactamases).
78
Do cephalosporins also contain a beta-lactam ring?
Yes.
79
Why are cephalosporins often more expensive than penicillins?
Because their molecular structure is larger and more complex.
80
What serious infection did the professor mention as being treated with cephalosporins?
Meningococcal meningitis.
81
Which generation of cephalosporins is considered the drug of choice for meningitis?
Third-generation cephalosporins.
82
How are semisynthetic cephalosporins classified?
By generations (1st, 2nd, 3rd, 4th, etc.).
83
What is generally true about later generations of cephalosporins?
They are more effective but more expensive.
84
What mild adverse effects are associated with cephalosporins?
Mild gastrointestinal disturbance
Nausea
Vomiting
Diarrhea
85
What other antibiotics attack the cell wall besides penicillins and cephalosporins?
Vancomycin
Bacitracin
86
How do beta-lactam antibiotics such as penicillins and cephalosporins kill bacteria?
They destroy peptide cross-bridges in peptidoglycan → cell wall breaks down → osmotic lysis → bacterial death.
87
What is Mechanism #2 in the “five ways to destroy organisms” framework?
Attack protein synthesis.
88
Why does stopping protein synthesis kill bacteria?
Because the cell cannot produce proteins needed for survival and function.
89
According to the professor, what three components are required for protein synthesis?
Ribosome (the factory)
mRNA being read
tRNA bringing amino acids
90
What ribosomal subunit does chloramphenicol bind to?
50S subunit.
91
What is the mechanism of action of chloramphenicol?
Inhibits peptide bond formation during translation.
92
What happens to protein synthesis when chloramphenicol blocks peptide bonds?
Amino acids cannot join together to form proteins.
93
What structural feature does chloramphenicol NOT contain compared with penicillin?
It does not contain a beta-lactam ring.
94
Why is chloramphenicol inexpensive to produce?
Because it is simple enough to be synthesized in a laboratory.
95
What rare but serious adverse effect limits the use of chloramphenicol?
Aplastic anemia (bone marrow suppression).
96
What condition in infants is associated with chloramphenicol toxicity?
Gray baby syndrome.
97
Why must chloramphenicol not be given during pregnancy?
Because it can cause gray baby syndrome in newborns.
98
Why is chloramphenicol still used cautiously for meningitis?
Because it crosses the blood–brain barrier.
99
What summary mechanism did the professor emphasize for chloramphenicol?
50S binding → blocks peptide bond formation → proteins cannot form.
100
What ribosomal subunit does erythromycin bind to?
50S subunit.
101
What mechanism does erythromycin use to inhibit protein synthesis?
Blocks ribosome movement along mRNA (blocks translocation).
102
What antibiotic family does erythromycin belong to?
Macrolides.
103
What other antibiotics belong to the macrolide group?
Azithromycin
Clarithromycin
104
When is erythromycin the drug of choice?
When a patient is allergic to penicillin.
105
Why is erythromycin commonly used for children?
Because it can be prepared as flavored syrup.
106
What infections did the professor mention as examples treated with erythromycin?
Throat infections (streptococcal infections)
Skin infections
Eye infections
107
What preventive treatment is given to newborn eyes to prevent infection from the birth canal?
Dilute erythromycin eye drops/ointment.
108
What adverse effect occurs in about 3% of patients taking erythromycin?
Mild gastrointestinal discomfort or nausea.
109
What ribosomal subunit do aminoglycosides bind to?
30S subunit.
110
What is the mechanism of action of aminoglycosides?
They change the shape of the 30S ribosomal subunit, causing misreading of mRNA.
111
What happens when mRNA is misread during translation?
Incomplete or incorrect proteins are produced.
112
What two types of translation errors did the professor describe from aminoglycoside action?
Ribosome stops reading early
Ribosome skips part of the mRNA
113
What is the end result of aminoglycoside-induced misreading of mRNA?
Incomplete proteins that cannot function.
114
What common examples of aminoglycosides were listed?
Streptomycin
Neomycin
Gentamicin
115
What serious adverse effect of aminoglycosides affects the kidneys?
Nephrotoxicity (kidney failure).
116
What serious adverse effect of aminoglycosides affects hearing?
Damage to the auditory/cochlear nerve leading to deafness.
117
What disease was streptomycin historically used to treat?
Tuberculosis (TB).
118
Why is streptomycin no longer used alone for tuberculosis?
Because of serious adverse effects and resistance concerns.
119
What ribosomal subunit does tetracycline act on?
30S subunit.
120
What is the mechanism of action of tetracycline?
Blocks the tRNA docking site on the ribosome.
121
What happens when tetracycline blocks the tRNA docking site?
tRNA cannot attach and protein synthesis stops.
122
What examples of semi-synthetic tetracyclines were mentioned?
Doxycycline
Minocycline
123
What advantage do semi-synthetic tetracyclines have?
They last longer in the body and may have improved spectrum.
124
Why is tetracycline considered one of the broadest spectrum antibiotics?
Because it acts against many gram-positive and gram-negative bacteria.
125
What infections are tetracycline drugs of choice for?
Chlamydia
Mycoplasma
126
What effect does tetracycline have on normal gut microbiota?
Destroys normal bacteria leading to severe diarrhea.
127
What secondary infection may occur after tetracycline disrupts gut microbiota?
Fungal infections.
128
Why does tetracycline cause tooth discoloration in children?
Because tetracycline binds to calcium in teeth.
129
What color change occurs in teeth from tetracycline exposure?
Brown discoloration.
130
Why is tetracycline especially dangerous during pregnancy?
It binds calcium and can cause severe fetal skull malformations.
131
What additional organ damage may occur with tetracycline during pregnancy?
Liver failure and kidney failure.
132
Why did the professor say tetracycline has more adverse effects than other drugs discussed?
Because it affects gut microbiota, teeth, bone development, and pregnancy outcomes.
133
Why did the professor mention tetracycline use in agriculture?
Farmers give it to animals to keep them healthy and increase weight.
134
What problem can result from tetracycline use in food production?
Antibiotic resistance.
135
What clinical problem can arise when patients previously exposed to tetracycline receive treatment?
The antibiotic may no longer work due to resistance.
136
How do the four protein synthesis antibiotics differ in their mechanisms?
Chloramphenicol
50S
Blocks peptide bond formation
Erythromycin
50S
Blocks ribosome movement (translocation)
Streptomycin
30S
Cause misreading of mRNA
Tetracycline
30S
Blocks tRNA docking site
137
What antibiotics attack the cell wall?
Penicillins
Cephalosporins
138
Which antibiotics attack the 50S ribosomal subunit during protein synthesis?
Chloramphenicol
Erythromycin
139
Which antibiotics attack the 30S ribosomal subunit during protein synthesis?
Tetracycline
Streptomycin
140
What is the third major mechanism used to destroy bacteria?
Inhibition of nucleic acid synthesis.
141
Which two major processes in nucleic acid synthesis can antibiotics inhibit?
Transcription
Replication
142
According to the professor, how many drugs/groups are emphasized for nucleic acid inhibition in this course?
Two groups.
143
What two names may be used interchangeably for this drug group in the lecture?
Rifampin and Rifamycin.
144
What step of nucleic acid synthesis does rifampin inhibit?
Transcription (DNA → RNA). Blocks RNA transcription
145
What enzyme does rifampin bind to?
RNA polymerase.
146
What happens to transcription when rifampin binds RNA polymerase?
DNA cannot be copied into RNA. It prevents copying DNA into mRNA/RNA
147
What major infections are treated with rifampin?
Tuberculosis (TB)
Leprosy
148
Why is rifampin particularly useful against mycobacterial infections?
Because it blocks transcription required for bacterial survival.
149
What is the main adverse effect of rifampin?
Liver damage or liver failure, especially in high doses.
150
Why are the liver and kidneys common targets for drug toxicity?
Because they are the body’s major detoxification organs.
151
Why should rifampin not be used during pregnancy?
Because of potential toxicity and liver damage risks.
152
What is the key summary for rifampin?
Inhibits transcription
Binds RNA polymerase
Used for TB and leprosy
Major risk: liver damage
153
What is the difference between quinolones and fluoroquinolones?
Fluoroquinolones are improved versions created by adding a fluorine atom.
154
What major improvement did fluoroquinolones provide compared to older quinolones?
Better tissue penetration and greater effectiveness.
155
What enzyme do quinolones and fluoroquinolones inhibit?
DNA gyrase.
156
What cellular process is blocked when DNA gyrase is inhibited?
DNA replication.
157
What part of the Chapter 8 diagram did the professor associate with quinolone action?
The replication step (blue part).
158
How did the professor abbreviate these drug groups in lecture?
Qs = Quinolones
FQs = Fluoroquinolones
159
What famous fluoroquinolone drug did the professor mention?
Ciprofloxacin (Cipro).
160
What type of infections are fluoroquinolones used to treat?
Anthrax
Legionellosis
Hard-to-treat infections
161
Why was ciprofloxacin especially highlighted in the lecture?
Because it is one of the most famous fluoroquinolones used for anthrax.
162
What major adverse effect is associated with fluoroquinolones?
Damage to cartilage development.
163
Why must fluoroquinolones be used carefully during pregnancy?
Because they can interfere with cartilage development in the fetus.
164
Which patient groups require caution when prescribing fluoroquinolones?
Pregnant patients
Young children
Elderly patients
165
Why can cartilage damage from fluoroquinolones increase risk in elderly patients?
Because it can contribute to falls, joint pain, and joint problems.
166
What are the two main antibiotic mechanisms that inhibit nucleic acid synthesis and how do they differ?
Rifampin
RNA polymerase
Transcription
Quinolones / Fluoroquinolones
DNA gyrase
DNA replication
167
What are the earlier drug targets that were quickly reviewed before nucleic acid synthesis drugs?
Cell wall and protein synthesis.
168
Which drugs were listed under cell wall inhibitors in the quick recap?
Penicillins and cephalosporins.
169
Which drugs were listed under protein synthesis inhibitors that act on the 50S larger subunit?
Chloramphenicol and erythromycin.
170
Which drugs were listed under protein synthesis inhibitors that act on the 30S smaller subunit?
Tetracycline and streptomycin.
171
What is the 3rd way to attack bacteria?
Inhibition of nucleic acid synthesis.
172
What two processes can be inhibited under nucleic acid synthesis?
Transcription and replication.
173
What are the two names the professor said may both be used for the first nucleic acid synthesis drug?
Rifampin or Rifamycin.
174
What does Rifampin or Rifamycin attack?
This drug attacks nucleic acid synthesis.
175
What specific part of nucleic acid synthesis does Rifampin attack?
It specifically attacks the transcription part.
176
What step of transcription does Rifampin block?
The step going from DNA → RNA.
177
What is the mechanism of Rifampin?
It blocks RNA transcription.
178
What enzyme does Rifampin bind to?
It binds to RNA polymerase.
179
What does Rifampin prevent when it binds RNA polymerase?
It prevents copying DNA into mRNA / RNA.
180
What major use did the professor emphasize for Rifampin?
Especially good as an anti-mycobacterial drug.
181
What diseases is Rifampin used for according to the notes?
Tuberculosis (TB) and leprosy.
182
What is the main adverse effect or limitation of Rifampin?
Main adverse effect: liver damage / liver failure, especially in high doses.
183
What did the professor remind students about the liver and kidneys in relation to drug toxicity?
Liver and kidneys are major cleansing organs, so it makes sense these are common sites of toxicity.
184
Is Rifampin used during pregnancy according to the notes?
No, not used during pregnancy.
185
What is the summary of Rifampin?
- attacks transcription
- binds RNA polymerase
- useful for TB/leprosy
- major risk = liver damage
186
How did the professor present quinolones and fluoroquinolones?
Quinolones = earlier form. Fluoroquinolones = newer, improved form.
187
What difference between quinolones and fluoroquinolones did the professor emphasize?
Fluoroquinolones were made by adding a fluoride atom.
188
What was kept the same when fluoroquinolones were developed from quinolones?
The same basic structure was kept.
189
What effect did adding a fluoride atom have on the drug?
This made the drug much more effective/superior.
190
What is the mechanism of quinolones and fluoroquinolones?
These drugs attack replication.
191
What enzyme do quinolones and fluoroquinolones specifically inhibit?
DNA gyrase.
192
What is the difference between Rifampin and quinolones/fluoroquinolones in terms of nucleic acid synthesis?
Rifampin = transcription
Quinolones/fluoroquinolones = replication
193
Why were fluoroquinolones developed according to the professor?
Original quinolones had reduced tissue penetration. Fluoroquinolones improved this.
194
What advantages do fluoroquinolones have over quinolones?
Better tissue penetration and better effect overall.
195
What very famous fluoroquinolone example did the professor give?
Ciprofloxacin.
196
What common registered trademark name did the professor mention for ciprofloxacin?
Cipro.
197
What naming pattern did the professor mention for other drugs in this group?
Other “-floxacin” drugs also belong here.
198
What time gap did the professor mention between quinolones and fluoroquinolones?
About a 20-year gap.
199
What uses were listed for quinolones and fluoroquinolones?
Anthrax, Legionellosis, and hard-to-treat infections.
200
What is one of the most famous examples for Cipro according to the professor?
Anthrax.
201
What major adverse effect or limitation comes with the strong tissue penetration of fluoroquinolones?
It affects cartilage development.
202
In which patient groups should fluoroquinolones be used very carefully?
Pregnancy, the very young, and the very elderly.
203
What did the professor say clinicians may ask before prescribing ciprofloxacin?
Clinicians may ask about the patient’s general health.
204
What can cartilage damage from fluoroquinolones contribute to?
Falls, joint pain, and joint problems.
205
Summary of Quinolones / Fluoroquinolones
Quinolones/fluoroquinolones: inhibit DNA gyrase, block replication, FQs are superior because they penetrate tissues better, example = ciprofloxacin, major concern = cartilage development.
206
What is the 4th way to attack bacteria?
Injury to the plasma membrane.
207
What is the target in the way to attack bacteria?
Plasma membrane.
208
What did the professor say about the mechanism of amphotericin and polymyxin?
The professor says the mechanism is the same idea whether using amphotericin or polymyxin.
209
What happens to the plasma membrane when these drugs act on it?
The drug destroys the phospholipid bilayer.
210
What structural damage do these drugs create in the plasma membrane?
Forms pores / openings in the plasma membrane.
211
What happens to the cell when pores form in the plasma membrane?
Cellular contents leak out.
212
What is the final result when cellular contents leak out of the cell?
Causes cell death.
213
What two drugs were mentioned in the lecture as plasma membrane–damaging drugs?
Polymyxin B and Amphotericin.
214
What is the mechanism shared by polymyxin and amphotericin in this lecture?
They form pores in the membrane.
215
What is the mechanism of action of these plasma membrane drugs?
Create openings in the plasma membrane.
216
What happens to the cell when these openings form in the plasma membrane?
Cellular contents leak out.
217
What is the final outcome when the cell loses its contents through these pores?
The cell dies.
218
What example drug was emphasized for plasma membrane injury?
Polymyxin B.
219
What type of infections is polymyxin B good for?
Bacterial infections, especially Pseudomonas.
220
What specific infection example did the professor emphasize for polymyxin B?
Pseudomonas burn wound infections.
221
What is the major limitation of polymyxin B use?
It can only be used as an ointment topically.
222
How should polymyxin B not be used?
Never systemic, never inject, never oral.
223
Why cannot polymyxin B be used systemically?
Because of kidney toxicity.
224
What happens if polymyxin B is given systemically?
It starts affecting kidneys quickly.
225
What is the summary of plasma membrane drugs?
Plasma membrane drugs form pores, leak cell contents, example = polymyxin B, useful for Pseudomonas, topical only because of kidney toxicity.
226
What is the 5th way to attack bacteria?
Inhibition of enzyme action.
227
What do the drugs in this category act on?
Enzymes.
228
What examples of drugs were given for inhibition of enzyme action?
Sulfa drugs and Trimethoprim. (sometimes these are combined)
229
What is the big idea behind how these drugs work?
These drugs act as competitive inhibitors.
230
What does it mean that these drugs act as competitive inhibitors?
They compete for the active site.
231
What substance do these drugs block in bacteria?
They block PABA.
232
What important metabolic process is blocked when PABA is blocked?
Folic acid synthesis.
233
What happens if folic acid synthesis is blocked in bacteria?
Nucleotides cannot be made.
234
What happens if nucleotides cannot be made?
DNA and RNA cannot be formed.
235
What happens to the organism if DNA and RNA cannot be formed?
The organism dies.
236
What are examples of sulfa drugs listed by the professor?
Sulfanilamide, Sulfadiazine, Sulfamethoxazole, and any similar sulfa drug.
237
What is the mechanism of sulfa drugs?
Inhibits the first enzyme in the PABA pathway.
238
How do sulfa drugs directly affect the metabolic pathway?
They directly block PABA.
239
What does blocking PABA prevent in bacteria?
Prevents folic acid synthesis.
240
What is Trimethoprim often combined with?
A sulfa drug.
241
Why is trimethoprim used together with sulfa drugs?
If the first step somehow escapes sulfa inhibition, trimethoprim blocks the second enzymatic step.
242
What concept describes using sulfa drugs and trimethoprim together?
A synergistic model.
243
What does a synergistic model mean in this context?
Two drugs attack the same overall pathway at two different points.
244
What are the advantages of using two drugs in this synergistic model?
It can reduce dosage and improve effectiveness.
245
What common infection are sulfa drugs and trimethoprim often used to treat?
UTIs (urinary tract infections).
246
According to the professor, how do the adverse effects of sulfa drugs compare with trimethoprim?
Sulfa drugs have more adverse effects than trimethoprim.
247
What is the first major adverse effect concern with sulfa drugs related to pregnancy?
Never give in pregnancy.
248
When during pregnancy are sulfa drugs especially dangerous?
Especially dangerous in the third trimester.
249
What severe effect can sulfa drugs cause in pregnancy?
Causes severe neurological damage.
250
Why is the third trimester especially dangerous when taking sulfa drugs?
Rapid fetal development is happening.
251
How did the professor describe giving sulfa drugs during late pregnancy?
An absolute no-no.
252
What liver-related condition can sulfa drugs cause?
Jaundice.
253
Why did the professor emphasize jaundice as an adverse effect concern?
Because the liver and kidneys are organs you do not want to damage.
254
What blood-related adverse effect can sulfa drugs cause?
Anemia.
255
What immune-related adverse effect is a major concern with sulfa drugs?
Allergies.
256
How did the professor describe trimethoprim compared with sulfa drugs in terms of severity of adverse effects?
Trimethoprim is a milder drug than sulfa.
257
What are the main adverse effects of trimethoprim?
Allergy and jaundice.
258
Why is trimethoprim considered milder than sulfa drugs?
It blocks lower down in the enzymatic pathway.
259
What memory aid did the professor bring back during this section?
Safe Moms Take Really Good Care.
260
What is the purpose of the memory aid “Safe Moms Take Really Good Care”?
Helps remember important drugs/adverse-effect groups.
261
What example did the professor explicitly link to the letter S in the acronym?
Sulfa drugs.
262
What example did the professor explicitly link to the letter F in the acronym?
Fluoroquinolones.
263
What are the five bacterial drug categories listed by the professor?
Cell wall, protein synthesis, nucleic acid synthesis, plasma membrane, enzyme action.
264
What three things should students understand about antimicrobial drugs according to the professor?
Basic treatments, why they work, and when they should not be used.
265
What cellular framework do antiviral drugs act within?
The genetics / nucleic acid framework.
266
According to the professor, how are antiviral drugs produced?
They are all made in the lab.
267
Do antiviral drugs come from nature according to the professor?
None come from nature.
268
Why are antiviral drugs often expensive?
They must be manufactured synthetically.
269
What disease did the professor use as an example where all drugs are manufactured synthetically?
HIV treatment.
270
What are the three parts of a nucleotide?
A base, a pentose sugar (ribose/deoxyribose), and a phosphate.
271
Which component of the nucleotide did the professor call the “troublemaker”?
The phosphate.
272
Because of this “troublemaker,” how are antiviral drugs designed?
As nucleosides, not full nucleotides.
273
What is a nucleoside?
Base + sugar minus phosphate.
274
How do nucleoside antiviral drugs work inside the cell?
They act as false nucleotides, they get incorporated into nucleic acid pathways.
275
What is the result of blocking these nucleic acid pathways?
Viral replication/load is reduced.
276
Do antiviral drugs usually remove the virus completely?
No.
277
What example did the professor give to explain that antivirals do not remove the virus completely?
HIV.
278
What happens to the virus in HIV even when antiviral drugs are used?
The virus remains inside.
279
What can antiviral drugs do even if they do not remove the virus completely?
Reduce viral load and slow progression of disease.
280
What is the base analog used in acyclovir?
G = guanine - a purine base.
281
What type of base is guanine?
A purine base.
282
What viruses does acyclovir treat according to the notes?
Herpes virus #2 and herpes virus #3.
283
What disease associated with herpes virus #3 can acyclovir treat?
Shingles.
284
What key association should you remember for acyclovir?
Guanine analog used for herpes / shingles treatment.
285
What base analog is used in ganciclovir?
G = guanine.
286
What virus is ganciclovir used to treat?
Herpes virus #5.
287
What infection commonly seen in HIV patients is treated with ganciclovir?
CMV infections.
288
Why is ganciclovir important for CMV infections in HIV patients?
CMV can cause eye infections and lead to blindness.
289
What benefit does ganciclovir provide in CMV infections?
It can reduce how quickly blindness develops.
290
What other names are used for zidovudine?
AZT or Azidothymidine.
291
What does the “T” in AZT indicate?
Thymine.
292
What infection is treated with zidovudine?
HIV infection.
293
What other name is used for lamivudine?
3TC.
294
What base analog is used in lamivudine?
C analog = cytosine.
295
What diseases does lamivudine treat?
HIV and Hepatitis B.
296
What infections is ribavirin often used to treat?
Influenza and RSV. (RSV in children low doses)
297
In which patient group is ribavirin often used at low doses?
Children.
298
What base analog did the professor say ribavirin commonly uses?
G analog (guanine).
299
What did the professor say about side effects of antiviral drugs in general?
All antivirals have side effects.
300
According to the professor, are there any antivirals without side effects?
No.
301
How do antibiotics differ from antivirals according to the professor?
Antibiotics often come from nature and are purified or modified.
302
How are antiviral drugs different from antibiotics in their origin?
Antivirals are made synthetically in the lab.
303
What are antivirals based on chemically?
Nucleoside analogs.
304
Why are antiviral drugs often more expensive than antibiotics?
They must be manufactured synthetically.
305
What is the typical effect of antivirals on viruses?
They reduce viral load rather than fully eliminate the virus.
306
What major problem did the professor say we are facing with antibiotics?
AMR = antimicrobial resistance.
307
What does AMR stand for?
Antimicrobial resistance.
308
What did the professor say industry will eventually need to do regarding antibiotics?
Find new ways to make or use these drugs.
309
What slow-growing diseases did the professor mention where treatment should not be stopped early?
• Tuberculosis (TB) • Leprosy • HIV (long-term antiviral therapy)
310
Why must treatment continue fully for slow-growing pathogens?
Because they have long generation times and can reappear if treatment stops early.
311
What can happen if treatment is stopped early for slow-growing infections?
• Infection may return • Patient’s weakened immune system may not control the infection
312
What is the key takeaway regarding antibiotic treatment duration?
Treatment length may vary depending on disease and clinician, but slow-growing serious infections require full treatment.
313
What acronym did the professor review to remember important drug risks?
“Safe Moms Take Really Good Care.”
314
What is the purpose of the acronym Safe Moms Take Really Good Care?
To remember drug groups that are important to consider in pregnancy or have significant adverse effects.
315
What drug class does S represent in the acronym “Safe Moms Take Really Good Care”?
Sulfa drugs.
316
What drug class does A represent in the acronym?
Aminoglycosides.
317
What drug class does F represent in the acronym?
Fluoroquinolones.
318
What drug is represented by E in the acronym?
Erythromycin (to some extent).
319
What drug is represented by M in the acronym?
Metronidazole.
320
What drug class does T represent in the acronym?
Tetracyclines.
321
What drug is represented by R in the acronym?
Ribavirin.
322
What drug group does A represent later in the acronym?
Antifungals.
323
What drug does C represent in the acronym?
Chloramphenicol.
324
What important adverse effect did the professor mention for metronidazole?
It can cause severe mutagenesis (gene mutations).
325
What developmental effects are associated with tetracyclines?
• Inhibition of bone growth • Effects on skull development
326
What virus infections may be treated with ribavirin?
• Influenza • RSV (respiratory syncytial virus)
327
What condition is caused by chloramphenicol in infants?
Gray baby syndrome.
328
What antibiotic did the professor briefly mention as being acceptable in pregnancy?
Rifampin.
329
What enzyme does rifampin target?
RNA polymerase.
330
What metabolic system does rifampin stimulate?
Microsomal cytochrome P450 enzymes.
331
What unusual effect does rifampin cause in body fluids?
Red/orange discoloration of body fluids.
332
Why should rifampin not be used alone?
Because rapid resistance develops if it is used as a single drug.
Microbiology
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