exam 2 (~20cards/ lecture; somewhat simplified) Flashcards
1
Q
What is inflammation?
A
A protective response of vascularized tissue to eliminate harmful agents and damaged tissue.
2
Q
What is the goal of inflammation?
A
To destroy, dilute, or sequester harmful agents to allow healing.
3
Q
What are the main components of inflammation?
A
Blood vessels, blood cells, plasma, mast cells, macrophages, fibroblasts.
4
Q
How do infections cause inflammation?
A
Bacteria, viruses, fungi trigger neutrophils via Toll-like receptors (TLRs).
5
Q
How does tissue necrosis lead to inflammation?
A
Necrotic cells release ATP, DNA, and uric acid, signaling inflammation.
6
Q
What is the role of hypoxia in inflammation?
A
Hypoxia leads to the release of HIF-1α, promoting inflammation.
7
Q
How do foreign bodies cause inflammation?
A
Splinters, sutures, dirt introduce microbes and cause tissue damage.
8
Q
What is the role of hypersensitivity reactions in inflammation?
A
Involves antibody-based or complement activation leading to excessive immune response.
9
Q
What are pattern recognition receptors (PRRs)?
A
Receptors that detect pathogen-associated (PAMPs) or damage-associated (DAMPs) molecular patterns.
10
Q
What are Toll-like receptors (TLRs) and their function?
A
They recognize bacterial DNA, endotoxins, viral RNA, and activate inflammatory mediators.
11
Q
What are the classical signs of inflammation?
A
Heat (Calor), Pain (Dolor), Redness (Rubor), Swelling (Tumor), Loss of Function.
12
Q
What occurs during the vascular stage of inflammation?
A
Transient vasoconstriction, followed by vasodilation and increased permeability leading to edema.
13
Q
What happens during the cellular stage of inflammation?
A
Neutrophils undergo margination, adhesion, emigration, chemotaxis, and phagocytosis.
14
Q
What is the role of neutrophils in inflammation?
A
First responders that produce reactive oxygen species (ROS) for pathogen destruction.
15
Q
What is the role of monocytes/macrophages in inflammation?
A
Arrive later to engulf dead tissue and help with resolution and repair.
16
Q
What are the roles of lymphocytes and eosinophils?
A
Lymphocytes are involved in chronic inflammation; eosinophils are present in parasitic infections/allergies.
17
Q
What are vasoactive amines in inflammation?
A
Histamine (vasodilation, permeability) and Serotonin (vasoconstriction).
18
Q
What are key arachidonic acid metabolites in inflammation?
A
Prostaglandins (fever, pain), Leukotrienes (bronchoconstriction, chemotaxis), Lipoxins (anti-inflammatory).
19
Q
What are the roles of cytokines (TNF, IL-1, IL-6) in inflammation?
A
Activate endothelium, induce fever, and stimulate acute-phase protein production.
20
Q
How do ROS and Nitric Oxide (NO) function in inflammation?
A
Kill microbes, but excessive ROS causes tissue damage.
21
Q
What are the functions of the complement system in inflammation?
A
C3a, C5a → Increase permeability, chemotaxis. C3b → Opsonization. C5-9 → Membrane Attack Complex.
22
Q
What is the best possible outcome of acute inflammation?
A
Complete resolution with full tissue restoration.
23
Q
What happens if tissue damage is severe?
A
Healing by fibrosis (scarring).
24
Q
What happens if inflammation persists?
A
Chronic inflammation with prolonged immune activation.
25
What is granulomatous inflammation, and what causes it?
A subtype of chronic inflammation with activated macrophage aggregates (epithelioid cells); seen in TB, leprosy, and sarcoidosis.
26
27
What did Rudolph Virchow say about disease?
“Disease cannot be understood unless it is realized that the ultimate abnormality must lie in the cell.”
28
What factors determine cellular homeostasis?
Type of affected cell, type and degree of injury, whether the injury is reversible or irreversible.
29
What is depurination?
Loss of purine bases (adenine, guanine) from DNA.
30
What is depyrimidination?
Loss of pyrimidine bases (cytosine, thymine) from DNA.
31
What is deamination and why is it harmful?
Converts cytosine to uracil, adenine to hypoxanthine, and 5-methyl-cytosine to thymine, leading to mutations.
32
What is the main cause of free radical DNA damage?
External factors like X-rays, gamma rays, and radiation generate hydroxyl radicals (OH•).
33
What does OH• radical do to DNA?
Causes base modifications (e.g., 8-hydroxyguanine), single-strand breaks, and double-strand breaks.
34
What is the role of DNA methylation in cellular injury?
S-adenosyl-methionine donates methyl groups, forming O-6-methylguanine, which can lead to mutations.
35
What are the consequences of DNA mutations?
Can be lethal or carcinogenic.
36
What enzyme is involved in DNA repair, and what happens when it’s overwhelmed?
Poly(ADP-ribose)polymerase (PARP) uses NAD for repair; excessive DNA damage depletes NAD, leading to cell death.
37
What is excitotoxicity?
Excess glutamate in neurons generates free radicals, leading to cell damage.
38
What is ischemia/reperfusion injury?
Restoring blood flow after ischemia increases reactive oxygen species (ROS), worsening damage.
39
What is RAGE activation and its consequence?
Receptor Against Glycosylated End Products (RAGE) is activated by β-amyloid, contributing to neurodegeneration.
40
How does drug metabolism contribute to cellular injury?
Some drugs produce reactive oxygen species as byproducts, leading to oxidative damage.
41
How does carbon tetrachloride (CCl₄) cause injury?
Metabolized by the liver’s P-450 system into toxic free radicals.
42
What are the effects of free radicals on biomolecules?
1. DNA – Base damage, strand breaks.
2. Proteins – Cross-linking, structural changes.
3. Membranes – Lipid peroxidation → Ca²⁺ influx → Cell death.
43
What are the three stages of lipid peroxidation?
1. Initiation – Free radicals steal electrons from lipids.
2. Propagation – Damage spreads.
3. Termination – Antioxidants stop the reaction.
44
What physical agents cause cellular injury?
Trauma, radiation, extreme temperatures, electric shock.
45
What chemical agents cause cellular injury?
Heavy metals (lead, mercury), poisons.
46
What biological agents cause cellular injury?
Viruses, bacteria, fungi, protozoa, prions.
47
How does aging contribute to cellular injury?
Loss of telomeres, accumulation of DNA damage, replication errors.
48
What are common cell injury markers and their significance?
• Troponins & CK-MB – Myocardial infarction.
• Amylase & Lipase – Acute pancreatitis.
49
What is reperfusion injury?
Restoring blood flow generates free radicals, exacerbating damage.
50
What is the difference between hypoxia and ischemia?
• Hypoxia – Lack of oxygen supply.
• Ischemia – Reduced blood flow due to a blocked vessel.
51
What are the key features of irreversible cell injury?
ATP depletion, Ca²⁺ influx, membrane damage, mitochondrial dysfunction, lysosomal enzyme leakage.
52
What is cellular adaptation?
The ability of cells to adjust to stress by altering their structure and function to maintain homeostasis.
53
What are the four main types of cellular adaptation?
1. Changes in size (hypertrophy, atrophy).
2. Changes in number (hyperplasia, hypoplasia).
3. Changes in cell type (metaplasia).
4. Cellular proliferation (neoplasia).
54
What is hypertrophy?
An increase in cell size due to increased functional demand or hormonal stimulation.
55
Give two examples of hypertrophy.
1. Cardiac hypertrophy from hypertension.
2. Muscle hypertrophy from exercise or increased workload.
56
What is hyperplasia?
An increase in cell number due to increased demand, hormones, or compensatory mechanisms.
57
Provide two examples of hyperplasia.
1. Parathyroid hyperplasia in response to hypocalcemia.
2. Liver regeneration after partial hepatectomy.
58
What is atrophy?
A reduction in cell size due to decreased workload, lack of nutrients, or aging.
59
Give two examples of atrophy.
1. Muscle atrophy from disuse (e.g., bed rest).
2. Brain atrophy in neurodegenerative diseases.
60
What is hypoplasia?
A reduction in cell number below normal levels, often congenital.
61
What is involution?
A decrease in cell number due to programmed cell death (apoptosis).
62
Provide two examples of involution.
1. Thymic involution in adulthood.
2. Endometrial involution after menstruation.
63
What is metaplasia?
A reversible replacement of one differentiated cell type with another due to chronic irritation.
64
Provide two examples of metaplasia.
1. Squamous metaplasia in the respiratory tract due to smoking.
2. Barrett’s esophagus: Squamous cells replaced by columnar cells due to acid reflux.
65
What is neoplasia?
The transformation of cells into an abnormal and uncontrolled proliferative state, potentially leading to cancer.
66
What factors influence cellular adaptation?
• Type of stress (e.g., mechanical, hormonal).
• Duration and severity of stress.
• Type of affected cell.
67
What are subcellular adaptations?
Changes in organelles to help cells cope with stress, such as increased mitochondria in hypertrophic cells.
68
What is a common cause of cardiac hypertrophy?
Hypertension, leading to increased workload on the heart.
69
What type of cellular adaptation occurs in prostatic hyperplasia?
Benign prostatic hyperplasia (BPH) involves hyperplasia of prostate gland cells.
70
What is the difference between physiological and pathological hyperplasia?
• Physiological: Normal response (e.g., breast tissue growth during pregnancy).
• Pathological: Abnormal overgrowth (e.g., endometrial hyperplasia).
71
How can metaplasia lead to cancer?
Chronic irritation or inflammation can cause metaplasia, which may progress to dysplasia and eventually cancer.
72
What is the consequence of prolonged atrophy?
It may lead to irreversible cell loss and tissue dysfunction.
73
What is the impact of hyperplasia on organ function?
Can be adaptive (e.g., liver regeneration) or pathological (e.g., thyroid enlargement in Graves’ disease).
74
How does chronic smoking affect the bronchial epithelium?
Causes squamous metaplasia, replacing normal ciliated columnar epithelium with squamous cells.
75
What is the key difference between hypertrophy and hyperplasia?
• Hypertrophy → Increased cell size.
• Hyperplasia → Increased cell number.
76
What is the difference between dystrophic and metastatic calcification?
• Dystrophic: Occurs in damaged/dead tissues despite normal blood calcium.
• Metastatic: Due to hypercalcemia, affecting normal tissues.
77
78
What is the primary method for classifying bacteria based on evolutionary relationships?
16S rRNA sequencing, as it is highly conserved but has variable regions for differentiation.
79
What are the three domains of life?
1. Bacteria – Includes microbiota and pathogens.
2. Archaea – Found in extreme environments, part of gut microbiota.
3. Eukarya – Includes humans, fungi, protozoa.
80
What is the difference between Gram-positive and Gram-negative bacteria?
• Gram-positive: Thick peptidoglycan layer, single membrane, stains purple.
• Gram-negative: Thin peptidoglycan, inner and outer membranes, stains pink.
81
What are examples of Gram-positive and Gram-negative bacteria?
• Gram-positive: Staphylococcus aureus
• Gram-negative: Escherichia coli.
82
What is the main structural component of bacterial cell walls?
Peptidoglycan, composed of N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM).
83
How does Gram staining differentiate bacteria?
• Gram-positive bacteria retain crystal violet due to thick peptidoglycan.
• Gram-negative bacteria lose crystal violet and take up safranin.
84
Name bacteria that do not stain well with Gram staining.
Mycoplasma (lacks a cell wall), Vibrio spp., Fusobacterium spp.
85
What are the steps of peptidoglycan synthesis?
1. NAM is synthesized from NAG.
2. Pentapeptide chain (D-Ala-D-Ala) is added.
3. Undecaprenyl carrier transports subunits to the membrane.
4. Penicillin-binding proteins (PBPs) crosslink peptidoglycan.
86
What antibiotics target peptidoglycan synthesis?
• Fosfomycin – Blocks NAM synthesis.
• D-Cycloserine – Inhibits D-Ala-D-Ala formation.
• Vancomycin – Binds D-Ala-D-Ala, blocking crosslinking.
• β-Lactams – Inhibit PBPs, preventing crosslinking.
87
What are the key differences between Gram-positive and Gram-negative membranes?
• Gram-positive: Contains lipoteichoic acids, contributing to charge and immune response.
• Gram-negative: Contains LPS (lipopolysaccharide), an endotoxin.
88
What is the structure of LPS in Gram-negative bacteria?
1. Lipid A – Causes endotoxic shock.
2. Core polysaccharide.
3. O-antigen – Recognized by the immune system.
89
What is a bacterial capsule and its function?
A protective layer that mediates adherence and protects against phagocytosis.
90
What is the function of bacterial pili and fimbriae?
• Fimbriae: Aid in adhesion to host cells.
• Pili: Mediate conjugation (DNA exchange) and some motility.
91
What is the function of bacterial flagella?
• Composed of flagellin, powered by the proton motive force, allowing motility.
92
What are the key components of bacterial chromosomes?
• Single circular chromosome.
• Supercoiled DNA using gyrase & topoisomerase IV.
93
What antibiotics target bacterial DNA replication?
• Fluoroquinolones – Inhibit DNA gyrase & topoisomerase IV.
94
What is a bacterial plasmid?
Small extrachromosomal DNA elements that carry genes for antibiotic resistance and virulence factors.
95
What is a biofilm?
A structured bacterial community embedded in a self-produced matrix, enhancing resistance.
96
How do biofilms resist antibiotics?
1. Physical protection – Matrix blocks penetration.
2. Metabolic changes – Reduced bacterial activity.
3. Efflux pumps – Expel antibiotics.
4. Dormant persister cells – Survive treatment.
97
What is the clinical significance of Gram-negative LPS?
LPS can trigger septic shock via Lipid A activation of the immune system.
98
What is the role of porins in Gram-negative bacteria?
Porins allow nutrient and antibiotic transport across the outer membrane.
99
What are endospores, and which bacteria form them?
Dormant, highly resistant structures formed by Bacillus and Clostridium.
100
What bacterial component is the target of penicillin?
Penicillin-binding proteins (PBPs), which crosslink peptidoglycan.
101
How does Mycoplasma differ from other bacteria?
Lacks a cell wall, making it resistant to β-lactams.
102
What is quorum sensing?
A communication system where bacteria regulate behavior using small diffusible signals.
103
What is bacterial metabolism?
The sum of biochemical processes that bacteria use to obtain energy, cycle nutrients, and interact with the host.
104
What is the significance of bacterial metabolism in microbiota ecology?
It supports nutrient cycling, affects the human host, and contributes to biofilm formation.
105
What glycolytic pathway do bacteria use?
The Embden-Meyerhof-Parnas (EMP) pathway, which converts glucose to pyruvate.
106
How much ATP is consumed and produced in bacterial glycolysis?
• 2 ATP consumed
• 4 ATP produced
• Net gain: 2 ATP.
107
What are the two ways bacteria oxidize NADH+H⁺?
1. Fermentation – Reducing pyruvate.
2. Respiration – Using the electron transport system.
108
How do bacteria metabolize complex sugars?
They use enzymes to break polysaccharides (starch, inulin, cellulose, etc.) into metabolizable sugars.
109
At what step do alternative sugars enter glycolysis?
At the Fructose-1,6-diphosphate stage.
110
Why do bacteria use fermentation?
To recycle NADH+H⁺ by reducing pyruvate.
111
What are common end products of bacterial fermentation?
• Acids (acetate, propionate, butyrate).
• Alcohols.
• Diols.
• Gases (CO₂, H₂).
112
How do short-chain fatty acids (SCFAs) affect the human body?
They influence gut health, metabolism, and the immune system.
113
How does Streptococcus mutans cause dental caries?
It ferments dietary sugars into lactic acid, which lowers pH and demineralizes enamel.
114
How does S. mutans store excess sugars?
It forms intracellular polysaccharides (IPS) and metabolizes them when dietary sugars are unavailable.
115
What is the role of sucrose in biofilm formation?
S. mutans uses sucrose to make biofilm matrix material.
116
How does xylitol prevent S. mutans growth?
• Xylitol is transported into cells via the phosphotransferase system (PTS).
• Xylitol-P accumulates and is toxic, leading to cell death.
117
How does xylitol gum enhance caries prevention?
It mechanically disrupts biofilm while reducing S. mutans growth.
118
How does S. mutans survive acidic conditions?
• F1-F0 ATPase pumps protons out.
• Membrane modifications enhance acid resistance.
• Protein & DNA repair mechanisms increase survival.
119
How do respiring bacteria generate energy?
They convert pyruvate → acetyl-CoA → CO₂, producing more ATP than fermentation.
120
What are the final electron acceptors in bacterial respiration?
• Aerobic respiration: Uses O₂.
• Anaerobic respiration: Uses nitrate, sulfate, or other compounds.
121
What are bacterial electron carriers?
1. Cytochromes.
2. Quinones.
3. Flavoproteins (Fe-S proteins).
122
How do bacteria generate ATP from the proton motive force?
• F0F1 ATP Synthase converts the proton gradient into ATP.
123
What are other uses of proton motive force?
• Bacterial motility (swimming).
• Uptake of small molecules.
• Fermenting bacteria use reverse ATPase to pump out protons.
124
How do bacteria exhibit metabolic flexibility?
• Use organic or inorganic electron donors.
• Switch between aerobic and anaerobic respiration.
125
What is metabolic cooperativity in biofilms?
• Fermentation products (e.g., lactate) are used by other bacteria.
• Biofilms share metabolic intermediates for mutual benefit.
126
How do bacteria regulate metabolic pathways?
• Transcription & translation control.
• Substrate availability regulates pathway activation.
127
What is the role of iron metabolism in bacteria?
• Bacteria use siderophores to scavenge iron.
• Hemolysis on blood agar releases iron from RBCs.
128
What is bacterial genetics?
The study of genetic material in bacteria, including chromosomes, plasmids, and mechanisms of gene transfer.
129
What type of chromosomes do bacteria typically have?
Usually single, circular chromosomes (some have linear chromosomes). Bacteria are haploid, so mutations are expressed in the next generation.
130
What are single nucleotide polymorphisms (SNPs)?
Small mutations in bacterial DNA caused by uncorrected DNA polymerase errors.
131
What is the typical bacterial mutation rate?
About 1 in 10⁶ genes per generation, but mismatch repair reduces it to 1 in 10⁸.
132
What are error-prone polymerases, and when are they activated?
DNA polymerases that lack proofreading, allowing them to bypass DNA damage; activated during oxidative stress or starvation.
133
What is horizontal gene transfer (HGT)?
The movement of genetic material between bacteria, allowing for genetic diversity and antibiotic resistance.
134
What are the three main mechanisms of HGT?
1. Transformation – Uptake of naked DNA. 2. Conjugation – Direct transfer between bacteria. 3. Transduction – Phage-mediated DNA transfer.
135
What is transformation in bacteria?
The process where competent bacteria take up free DNA from the environment.
136
What are key features of transformation?
• DNase-sensitive (free DNA can be degraded). • DNA is taken up as single-stranded DNA (ssDNA). • Requires homologous recombination (RecA-dependent) for integration.
137
What is bacterial conjugation?
A process where DNA is transferred between bacteria via direct cell-to-cell contact using a pilus.
138
What is the difference between F+ and F- bacteria?
• F+ (donor): Contains the F plasmid and transfers it to F-. • F- (recipient): Lacks the F plasmid and receives it.
139
What is Hfr conjugation?
When the F plasmid integrates into the bacterial chromosome, leading to transfer of chromosomal DNA.
140
What is transduction?
Gene transfer via bacteriophages (viruses that infect bacteria).
141
What are the two types of transduction?
1. Generalized transduction – Random bacterial DNA is packaged into a phage particle during the lytic cycle. 2. Specialized transduction – Phage integrates into the chromosome, excises with adjacent genes, and transfers them during the lysogenic cycle.
142
What are transposons?
"Jumping genes" – Mobile genetic elements that move within or between DNA molecules.
143
How do transposons contribute to bacterial evolution?
They carry antibiotic resistance genes and virulence factors, promoting adaptation.
144
What are conjugative transposons (ICE elements)?
Transposons that encode a Type IV secretion system and transfer between bacteria.
145
What are plasmids?
Small, circular extrachromosomal DNA molecules that replicate independently.
146
What do plasmids typically carry?
• Antibiotic resistance genes. • Virulence factors. • Metabolic adaptation genes.
147
What is the role of bacteriophages in bacterial genetics?
They can transfer genes, promote mutation, and contribute to bacterial evolution.
148
What is SCCmec, and why is it important in MRSA?
• Staphylococcal Chromosomal Cassette mec (SCCmec) carries methicillin resistance genes (mecA). • It integrates into Staphylococcus aureus, creating MRSA.
149
What is the CRISPR-Cas system?
A bacterial immune system that defends against foreign DNA (phages, plasmids).
150
How does the CRISPR-Cas system work?
1. CRISPR RNA (crRNA) detects foreign DNA. 2. Cas proteins cut and destroy invading DNA.
151
How does horizontal gene transfer contribute to bacterial evolution?
It allows rapid adaptation, acquisition of antibiotic resistance, and formation of pathogenic strains.
152
How do bacteria increase mutation rates under stress?
By using error-prone DNA polymerases to introduce mutations, increasing genetic diversity.
153
What are the four phases of bacterial growth?
1. Lag Phase – Bacteria adjust to new conditions.
2. Log (Exponential) Phase – Rapid cell division and growth.
3. Stationary Phase – Growth slows as nutrients deplete.
4. Death Phase – Cells die due to toxin buildup and starvation.
154
What is the primary method of bacterial replication?
Binary fission, where one cell divides into two identical daughter cells.
155
What are alternative bacterial replication methods?
• Fragmentation (e.g., filamentous bacteria).
• Budding (e.g., Gemmata obscuriglobus).
156
What are the different pH tolerances of bacteria?
• Neutrophiles: ~pH 7 (most pathogens).
• Acidophiles: Low pH (e.g., Lactobacillus).
• Alkaliphiles: High pH (e.g., Vibrio cholerae).
157
What temperature ranges do bacteria grow in?
• Psychrophiles: Cold environments.
• Mesophiles: 37°C (human pathogens).
• Thermophiles & Hyperthermophiles: High temperatures.
158
How does oxygen availability affect bacterial growth?
• Obligate Aerobes: Require O₂ (Mycobacterium tuberculosis).
• Obligate Anaerobes: Killed by O₂ (Clostridium spp.).
• Facultative Anaerobes: Grow with or without O₂ (E. coli).
• Microaerophiles: Prefer low O₂ (Helicobacter pylori).
• Aerotolerant Anaerobes: Do not use O₂ but tolerate it (Lactobacillus).
159
What is a bacterial biofilm?
A structured bacterial community embedded in a self-produced extracellular matrix.
160
Where are biofilms found?
• Natural surfaces (teeth, mucosa).
• Medical devices (catheters, implants).
• Environmental surfaces (pipes, rocks).
161
What are the stages of biofilm formation?
1. Attachment – Bacteria adhere to surfaces.
2. Microcolony Formation – Growth and secretion of matrix.
3. Maturation – Structured community develops.
4. Dispersal – Bacteria detach and spread.
162
What is the biofilm matrix made of?
• Polysaccharides.
• Proteins (e.g., amyloids).
• Extracellular DNA (eDNA).
163
What is quorum sensing?
A communication system using small signaling molecules to regulate bacterial behavior.
164
What are common quorum sensing signals?
• Gram-positive bacteria: Oligopeptides.
• Gram-negative bacteria: Homoserine lactones (HSL).
• Universal signal: Autoinducer-2 (AI-2).
165
Why are biofilms resistant to antibiotics?
1. Physical Protection – Matrix blocks penetration.
2. Metabolic Changes – Bacteria slow metabolism.
3. Efflux Pumps – Remove antibiotics.
4. Dormant Persister Cells – Survive antibiotics.
166
How do biofilms evade the immune system?
1. Poor antibody penetration.
2. Phagocytes cannot engulf biofilms.
3. Immune signaling is disrupted.
167
What is dental plaque?
A biofilm that forms on teeth, composed of bacteria, proteins, and salivary components.
168
How does Streptococcus mutans cause cavities?
• Ferments sugars → Lactic acid.
• Lowers pH → Enamel demineralization.
169
How does xylitol help prevent cavities?
• S. mutans takes up xylitol but cannot metabolize it, leading to toxic accumulation and cell death.
170
How do biofilms contribute to recurrent infections?
• Bacteria in biofilms shed planktonic cells, causing reinfection.
• Antibiotic treatment kills free-floating cells but leaves biofilm intact.
171
What are corncob and hedgehog structures in biofilms?
• Corncob structures: Corynebacterium filaments surrounded by Streptococci.
• Hedgehog structures: Small bacterial clusters between species pairs.
172
How does Fusobacterium nucleatum act as a bridge in dental biofilms?
It connects different bacterial species, enabling biofilm complexity.
173
174
What are antimicrobials?
Substances that target infectious agents, including bacteria, viruses, fungi, and parasites.
175
What are the four types of microbial infections?
1. Community-acquired infections – Contracted in daily life.
2. Nosocomial infections – Acquired in healthcare settings.
3. Opportunistic infections – Occur in immunocompromised patients.
4. Superinfections – Secondary infections due to antimicrobial therapy (e.g., C. difficile).
176
What is selective toxicity, and who introduced the concept?
Selective toxicity is the ability to kill microbes without harming the host, introduced by Paul Ehrlich.
177
What are the four types of antimicrobial therapy?
1. Prophylactic Therapy – Prevents infections (e.g., pre-surgical antibiotics).
2. Empirical Therapy – Based on most likely pathogen before lab results.
3. Definitive Therapy – Targeted treatment after lab confirmation.
4. Post-Treatment Suppressive Therapy – Prevents relapse in chronic infections.
178
How are antimicrobials classified by chemical structure?
• β-Lactams: Penicillins, Cephalosporins, Carbapenems, Monobactams.
• Aminoglycosides
• Macrolides
• Tetracyclines
• Fluoroquinolones
• Sulfonamides
• Lincosamides
• Glycopeptides (e.g., Vancomycin).
179
How are antimicrobials classified by mechanism of action?
1. Inhibit Cell Wall Synthesis – β-Lactams, Glycopeptides.
2. Disrupt Cell Membrane – Polymyxins, Daptomycin.
3. Inhibit Nucleic Acid Synthesis – Fluoroquinolones, Rifampin, Metronidazole.
4. Inhibit Protein Synthesis – Aminoglycosides (30S), Macrolides (50S).
5. Inhibit Metabolic Pathways – Sulfonamides, Trimethoprim.
180
What is the difference between broad-spectrum and narrow-spectrum antibiotics?
• Broad-spectrum: Effective against Gram-positive & Gram-negative bacteria, but increases resistance risk (e.g., Tetracyclines, Fluoroquinolones).
• Narrow-spectrum: Targets specific bacterial groups, less impact on normal microbiota (e.g., Penicillin G, Vancomycin).
181
What is the difference between bacteriostatic and bactericidal antibiotics?
• Bacteriostatic: Inhibits bacterial growth (e.g., Tetracyclines, Macrolides).
• Bactericidal: Kills bacteria (e.g., β-Lactams, Aminoglycosides).
182
What are MIC and MBC in antibiotic therapy?
• Minimum Inhibitory Concentration (MIC): Lowest antibiotic concentration that prevents bacterial growth.
• Minimum Bactericidal Concentration (MBC): Lowest concentration that kills bacteria.
183
What is the post-antibiotic effect (PAE)?
A phenomenon where bacterial suppression continues after drug clearance, common in Aminoglycosides & Fluoroquinolones.
184
What are four mechanisms of antimicrobial resistance?
1. Enzymatic Inactivation – β-Lactamases degrade β-Lactams.
2. Modification of Drug Targets – PBP mutations reduce β-Lactam binding.
3. Efflux Pumps – Actively remove antibiotics from bacterial cells.
4. Metabolic Bypass – Alternative pathways compensate for blocked steps.
185
What are extended-spectrum β-lactamases (ESBLs)?
Enzymes that degrade penicillins, cephalosporins, and some carbapenems, found in multi-drug resistant Gram-negative bacteria.
186
What are key principles of antibiotic stewardship?
1. Correct Diagnosis – Identify pathogen before prescribing antibiotics.
2. Use Narrow-Spectrum Antibiotics whenever possible.
3. Limit Empirical Therapy – Shift to Definitive Therapy when lab results arrive.
4. Avoid Unnecessary Prophylaxis.
5. Educate Patients – Ensure adherence to full treatment.
187
What are time-dependent and concentration-dependent antibiotics?
• Time-dependent: Effectiveness depends on time above MIC (e.g., β-Lactams, Vancomycin).
• Concentration-dependent: Effectiveness depends on peak concentration (e.g., Aminoglycosides, Fluoroquinolones).
188
What is a superinfection?
A secondary infection caused by antimicrobial therapy, such as C. difficile colitis after broad-spectrum antibiotics.
189
What is the mechanism of action of β-lactam antibiotics?
β-lactams inhibit peptidoglycan crosslinking by binding penicillin-binding proteins (PBPs), disrupting bacterial cell wall synthesis.
190
What are the major classes of β-lactam antibiotics?
1. Penicillins
2. Cephalosporins
3. Carbapenems
4. Monobactams (Aztreonam)
191
What are the four main types of penicillins?
1. Natural Penicillins (Penicillin G, Penicillin V)
2. Aminopenicillins (Amoxicillin, Ampicillin)
3. Antistaphylococcal Penicillins (Nafcillin, Oxacillin)
4. Antipseudomonal Penicillins (Piperacillin, Ticarcillin)
192
Which penicillins are effective against Pseudomonas?
Piperacillin & Ticarcillin, often combined with β-lactamase inhibitors.
193
What are common side effects of penicillins?
Hypersensitivity reactions (rash, anaphylaxis), GI upset, and seizures at high doses.
194
How do cephalosporin generations differ?
• ↑ Gram-negative coverage with increasing generations.
• ↓ Gram-positive coverage (except 5th gen).
• 3rd+ generations cross the BBB.
195
Which cephalosporin is effective against MRSA?
Ceftaroline (5th generation).
196
What is ceftriaxone used for?
Treats meningitis, gonorrhea, Lyme disease (3rd gen, long half-life).
197
What are carbapenems used for?
Broad-spectrum treatment for multi-drug resistant Gram-negative & anaerobic infections.
198
What is a major side effect of imipenem?
Seizures, especially in patients with renal dysfunction.
199
What is unique about aztreonam (monobactam)?
Effective against Gram-negative aerobes only and safe for penicillin-allergic patients.
200
What are the classes of protein synthesis inhibitors?
1. 30S inhibitors: Aminoglycosides, Tetracyclines
2. 50S inhibitors: Macrolides, Lincosamides, Chloramphenicol, Oxazolidinones.
201
How do aminoglycosides work?
Bind the 30S ribosome, causing misreading of mRNA and bacterial death.
202
What are major side effects of aminoglycosides?
Nephrotoxicity, ototoxicity, neuromuscular blockade.
203
Why should tetracyclines be avoided in children and pregnancy?
Cause teeth discoloration and bone growth inhibition.
204
What is the mechanism of macrolides?
Bind the 50S ribosome, inhibiting protein elongation.
205
What are the main uses of azithromycin?
Atypical pneumonia (Legionella, Mycoplasma, Chlamydia), STIs, respiratory infections.
206
What are the major side effects of macrolides?
QT prolongation, GI distress, CYP3A4 inhibition.
207
What is clindamycin mainly used for?
Anaerobic infections, MRSA, and dental infections.
208
What is a serious side effect of clindamycin?
C. difficile colitis (pseudomembranous colitis).
209
How does vancomycin work?
Binds D-Ala-D-Ala, inhibiting cell wall synthesis.
210
What are major side effects of vancomycin?
Nephrotoxicity, ototoxicity, Red Man Syndrome.
211
What is the mechanism of polymyxins?
Disrupt bacterial membranes, used for multi-drug resistant Gram-negative bacteria.
212
What are major side effects of polymyxins?
Neurotoxicity and nephrotoxicity.
213
What is the treatment for C. difficile infection?
Oral vancomycin or fidaxomicin.
214
What are the major classes of antimicrobials that target nucleic acid synthesis?
1. Fluoroquinolones – Inhibit DNA gyrase & topoisomerase IV.
2. Rifamycins (Rifampin) – Inhibit RNA polymerase.
3. Metronidazole – Causes DNA strand breaks via free radicals.
215
How do fluoroquinolones work?
They inhibit DNA gyrase (Gram-negative) and topoisomerase IV (Gram-positive), preventing bacterial DNA replication.
216
What is the clinical use of fluoroquinolones?
• Ciprofloxacin: UTIs, Pseudomonas, anthrax.
• Levofloxacin & Moxifloxacin: Respiratory infections, atypical pneumonia.
217
What are major side effects of fluoroquinolones?
• Tendon rupture (avoid in elderly, children, steroid use).
• QT prolongation (Moxifloxacin).
• GI distress, CNS effects (dizziness, headache).
218
How does rifampin work?
Inhibits bacterial RNA polymerase, blocking mRNA synthesis.
219
What are the clinical uses of rifampin?
• Tuberculosis (part of RIPE therapy).
• Meningococcal prophylaxis.
• Staphylococcal biofilm infections.
220
What are side effects of rifampin?
• Hepatotoxicity.
• Red/orange bodily fluids.
• Strong CYP450 inducer (drug interactions!).
221
How does metronidazole work?
Forms free radicals that damage bacterial DNA, leading to cell death.
222
What are the clinical uses of metronidazole?
• Anaerobic infections (Bacteroides, Clostridium, Fusobacterium).
• C. difficile colitis.
• Protozoal infections (Giardia, Trichomonas).
223
What are major side effects of metronidazole?
• Metallic taste.
• Disulfiram-like reaction with alcohol.
• GI upset, headache.
224
How do sulfonamides work?
Inhibit dihydropteroate synthase, blocking folic acid synthesis.
225
How does trimethoprim work?
Inhibits dihydrofolate reductase, preventing folate recycling.
226
What is the clinical use of TMP-SMX (trimethoprim-sulfamethoxazole)?
• UTIs, traveler’s diarrhea.
• Pneumocystis jirovecii pneumonia (PCP) prophylaxis in HIV.
• MRSA skin infections.
227
What are the main side effects of sulfonamides?
• Hypersensitivity reactions (Stevens-Johnson Syndrome).
• Photosensitivity.
• Hemolytic anemia (in G6PD deficiency).
228
What are the side effects of trimethoprim?
• Hyperkalemia.
• Megaloblastic anemia (due to folate inhibition).
• Leukopenia, granulocytopenia.
229
What are the four main mechanisms of antimicrobial resistance?
1. Drug inactivation – β-lactamases, aminoglycoside-modifying enzymes.
2. Target modification – Altered PBPs, ribosomal mutations.
3. Efflux pumps – Actively pump drugs out.
4. Metabolic bypass – Alternative pathways compensate.
230
How do bacteria resist fluoroquinolones?
Efflux pumps & DNA gyrase/topoisomerase mutations.
231
How do bacteria resist rifampin?
Mutations in RNA polymerase reduce drug binding.
232
How do bacteria resist aminoglycosides?
Enzymatic modification (acetylation, phosphorylation, adenylation).
233
How do bacteria resist macrolides?
Methylation of the 23S rRNA (erm gene), preventing drug binding.
234
What is the Kirby-Bauer disk diffusion test?
A test to measure zone of inhibition around antibiotic disks to assess bacterial susceptibility.
235
What is MIC vs. MBC?
• MIC (Minimum Inhibitory Concentration): Lowest antibiotic concentration that inhibits growth.
• MBC (Minimum Bactericidal Concentration): Lowest concentration that kills bacteria.
236
What is an ESBL (Extended-Spectrum β-Lactamase)?
An enzyme that degrades β-lactams, making Gram-negative bacteria resistant to penicillins and cephalosporins.
237
What are the key strategies in antimicrobial stewardship?
• Use narrow-spectrum antibiotics when possible.
• Minimize empirical therapy.
• Complete full antibiotic courses.
• Limit prophylactic antibiotic use.
238
Why should fluoroquinolones be avoided for simple infections?
Overuse contributes to rapid resistance and severe side effects.
239
What are the three possible bacterial responses to antibiotics?
1. Resistant bacteria – Continue growing despite the antibiotic.
2. Bacteriostatic effect – Growth stops but resumes after antibiotic removal.
3. Bactericidal effect – Bacteria are killed outright.
240
What is the difference between MIC and MBC?
• MIC (Minimum Inhibitory Concentration): Lowest antibiotic concentration that inhibits bacterial growth.
• MBC (Minimum Bactericidal Concentration): Lowest antibiotic concentration that kills bacteria.
241
How does the Kirby-Bauer disk diffusion test determine resistance?
• An antibiotic disk creates a zone of inhibition.
• Large zone = Sensitive bacteria.
• Small/no zone = Resistant bacteria.
242
What are the four main mechanisms of antibiotic resistance?
1. Enzymatic inactivation – β-lactamases degrade β-lactam antibiotics.
2. Target modification – Altered PBPs, ribosomal mutations.
3. Efflux pumps – Actively remove antibiotics.
4. Metabolic bypass – Alternative pathways compensate.
243
What are β-lactamases?
Enzymes that degrade β-lactam antibiotics, making bacteria resistant to penicillins and cephalosporins.
244
How do bacteria resist fluoroquinolones?
Efflux pumps & DNA gyrase/topoisomerase mutations.
245
How do bacteria resist aminoglycosides?
Enzymatic modification (acetylation, phosphorylation, adenylation).
246
How do bacteria resist macrolides?
Methylation of the 23S rRNA (erm gene), preventing drug binding.
247
How does MRSA resist β-lactams?
It carries the mecA gene, which encodes PBP2a, a modified penicillin-binding protein resistant to β-lactams.
248
What is the mechanism of vancomycin resistance in VRE?
VanA, VanB, VanC operons modify D-Ala-D-Ala to D-Ala-D-Lac, preventing vancomycin binding.
249
What are the three main methods of horizontal gene transfer (HGT)?
1. Transformation – Uptake of free DNA.
2. Conjugation – Transfer via pili/plasmids.
3. Transduction – Bacteriophage-mediated transfer.
250
What are transposons, and how do they contribute to antibiotic resistance?
"Jumping genes" that carry resistance genes and move between DNA molecules.
251
What are integrons?
Genetic elements that capture and express antibiotic resistance genes.
252
How do biofilms contribute to antibiotic resistance?
1. Physical protection – Matrix blocks antibiotics.
2. Metabolic dormancy – Bacteria slow metabolism.
3. Efflux pumps – Remove antibiotics.
4. Persister cells – Survive antibiotic treatment.
253
How do biofilms evade the immune system?
1. Poor antibody penetration.
2. Phagocytes cannot engulf biofilms.
3. Disrupt immune signaling.
254
What are the three clinical resistance categories?
1. Sensitive (S) – Bacteria inhibited by low doses.
2. Intermediate (I) – Higher doses required for inhibition.
3. Resistant (R) – Bacteria not inhibited at clinical doses.
255
What is an ESBL (Extended-Spectrum β-Lactamase)?
A β-lactamase enzyme that degrades penicillins and cephalosporins, making Gram-negative bacteria highly resistant.
256
What is carbapenem resistance, and why is it concerning?
Carbapenem-resistant Enterobacteriaceae (CRE) produce carbapenemases, making infections difficult to treat.
257
What are the key principles of antibiotic stewardship?
1. Use narrow-spectrum antibiotics when possible.
2. Limit empirical therapy.
3. Complete full antibiotic courses.
4. Avoid unnecessary prophylactic antibiotics.
258
How does inappropriate antibiotic use contribute to resistance?
• Overuse of broad-spectrum antibiotics.
• Incomplete treatment courses.
• Unnecessary prescriptions for viral infections.
259
What is post-antibiotic effect (PAE), and which drugs exhibit it?
A period of continued bacterial suppression after drug clearance, common in aminoglycosides & fluoroquinolones.
260
What is the difference between time-dependent and concentration-dependent antibiotics?
• Time-dependent: Effectiveness depends on time above MIC (e.g., β-Lactams, Vancomycin).
• Concentration-dependent: Effectiveness depends on peak concentration (e.g., Aminoglycosides, Fluoroquinolones).
261
How do efflux pumps contribute to antibiotic resistance?
They actively remove antibiotics from bacterial cells, reducing drug effectiveness.
262
How do bacteria resist rifampin?
Mutations in RNA polymerase reduce drug binding.
263
How do bacteria resist sulfonamides?
Mutations in dihydropteroate synthase allow folate synthesis despite drug presence.
264
What is the purpose of bacterial spore formation?
Spores allow bacteria to survive harsh environmental conditions, including heat, radiation, and desiccation.
265
What are the two major genera of clinically relevant spore-forming bacteria?
1. Clostridium (Anaerobic, Gram-positive rods).
2. Bacillus (Aerobic, Gram-positive rods).
266
What diseases are caused by Clostridium species?
• C. perfringens → Gas gangrene, food poisoning.
• C. botulinum → Botulism.
• C. tetani → Tetanus.
• C. difficile → Pseudomembranous colitis.
267
What are key characteristics of Clostridium species?
• Anaerobic metabolism (oxygen is toxic).
• Motile (except C. perfringens).
• Produces powerful toxins.
• Lacks catalase, oxidase, and peroxidase.
268
What is the primary toxin produced by Clostridium perfringens?
Alpha-toxin (phospholipase C), which destroys cell membranes, leading to gas gangrene.
269
How does Clostridium botulinum cause botulism?
• Produces botulinum toxin, a neurotoxin that blocks acetylcholine release, leading to flaccid paralysis.
270
What are the different forms of botulism?
• Foodborne → Ingestion of preformed toxin.
• Infant botulism → Ingestion of spores (e.g., from honey).
• Wound botulism → Infection via deep wounds.
271
How does Clostridium tetani cause tetanus?
Produces tetanospasmin, which blocks inhibitory neurotransmitters (GABA & glycine), causing muscle spasms.
272
What are the key symptoms of tetanus?
• Lockjaw (trismus).
• Sardonic grin (risus sardonicus).
• Arched back (opisthotonus).
• Convulsions, respiratory failure.
273
What is the treatment for tetanus?
1. Surgical debridement of wound.
2. Tetanus immune globulin (HTIG).
3. Tetanus toxoid booster (every 10 years).
274
How does C. difficile cause disease?
• Overgrows in the gut after antibiotic use (clindamycin, fluoroquinolones).
• Produces Toxin A (enterotoxin) and Toxin B (cytotoxin), leading to pseudomembranous colitis.
275
What is the treatment for C. difficile infection?
1. Discontinue offending antibiotic.
2. Metronidazole or oral vancomycin.
3. Fecal microbiota transplantation (FMT) for recurrent infections.
276
What are key characteristics of Bacillus species?
• Aerobic metabolism.
• Forms highly resistant spores.
• Found in soil, water, and animal products.
277
What are the three forms of anthrax caused by Bacillus anthracis?
1. Cutaneous anthrax → Painless black eschar.
2. Pulmonary anthrax (Woolsorter’s Disease) → Respiratory distress, high mortality.
3. Gastrointestinal anthrax → Ingestion of spores, rare but deadly.
278
What are the virulence factors of Bacillus anthracis?
1. Polyglutamate capsule (prevents phagocytosis).
2. Lethal Factor (LF) + Protective Antigen (PA) → Kills macrophages.
3. Edema Factor (EF) + PA → Causes severe swelling.
279
What is the treatment for anthrax?
Ciprofloxacin or doxycycline; vaccination for high-risk individuals.
280
What are the two forms of Bacillus cereus food poisoning?
1. Diarrheal Syndrome → Enterotoxin causes watery diarrhea (10-hour incubation).
2. Emetic Syndrome → Heat-stable toxin causes vomiting (1-5 hour incubation, associated with reheated rice).
281
How is Bacillus cereus food poisoning treated?
Supportive care (fluids); no antibiotics needed.
282
What makes bacterial spores so resistant?
• Thick peptidoglycan coat.
• Calcium-dipicolinate content.
• Low water content.
• DNA-protecting proteins.
283
What conditions kill bacterial spores?
• Autoclaving (121°C, 15 min, 15 psi).
• Bleach (10% solution).
• Gas sterilization (ethylene oxide).
284
What are anaerobic bacteria?
Bacteria that do not require oxygen for energy production or growth.
285
What are the three main categories of anaerobic bacteria based on oxygen tolerance?
1. Obligate anaerobes – Cannot grow in oxygen.
2. Aerotolerant anaerobes – Can survive but do not use oxygen.
3. Facultative anaerobes – Can grow with or without oxygen.
286
How do anaerobic bacteria generate energy?
Through fermentation (using organic intermediates) or anaerobic respiration (using inorganic molecules as electron acceptors).
287
Why are obligate anaerobes sensitive to oxygen?
They lack catalase, superoxide dismutase, and peroxidase, making them unable to detoxify reactive oxygen species.
288
What is oxidation-reduction potential (Eh), and why is it important for anaerobes?
Anaerobes grow in low Eh environments (≤ -175 mV), such as necrotic tissue, colon (-300 mV), and dental plaque (-200 mV).
289
Name a common Gram-positive anaerobic cocci.
Peptostreptococcus.
290
Name a common Gram-negative anaerobic cocci.
Veillonella.
291
Give an example of a spore-forming and non-spore-forming Gram-positive anaerobe.
• Spore-forming: Clostridium spp.
• Non-spore-forming: Actinomyces spp.
292
Name two important Gram-negative anaerobic bacilli.
Bacteroides and Fusobacterium.
293
List three virulence factors of anaerobic bacteria.
1. Capsules (e.g., Bacteroides fragilis).
2. Toxins and enzymes (hyaluronidase, collagenase).
3. Adhesion factors (pili, fimbriae).
294
Which anaerobe is the most common in infections?
Bacteroides fragilis.
295
Why are anaerobic infections often polymicrobial?
They occur alongside facultative bacteria, which create a low-oxygen environment.
296
Name three predisposing factors for anaerobic infections.
1. Tissue necrosis (e.g., trauma, malignancy).
2. Sterile site exposure (e.g., ruptured appendix).
3. Immunosuppression (e.g., diabetes, alcohol use).
297
Which anaerobes are commonly found in aspiration pneumonia?
Prevotella, Porphyromonas, Bacteroides, Fusobacterium.
298
Name three anaerobes involved in periodontitis.
Tannerella forsythia, Prevotella intermedia, Fusobacterium spp.
299
What is pericoronitis, and which anaerobes cause it?
Inflammation around a partially erupted molar; caused by Prevotella intermedia, Parvimonas micra, Tannerella forsythia.
300
What type of infection involves anaerobic bacteria in the pulp and periapical region?
Endodontic infections (e.g., pulpitis, pulp necrosis).
301
Name two anaerobes involved in diabetic foot ulcers.
Bacteroides fragilis and Fusobacterium.
302
Which anaerobe is most common in intra-abdominal infections?
Bacteroides fragilis (oxygen-tolerant and antibiotic-resistant).
303
What are two key diagnostic clues for anaerobic infections?
1. Foul odor (due to volatile short-chain fatty acids).
2. Gas formation in tissues.
304
Why is diagnosing anaerobic infections difficult?
1. Oxygen exposure kills anaerobes during sampling.
2. Slow lab growth delays identification.
3. Presence in normal flora can lead to sample contamination.
305
What are the best methods for collecting anaerobic bacteria samples?
Saliva, paper points, curettes, aspiration into anaerobic transport media.
306
What is the primary antibiotic used for anaerobic infections?
Metronidazole (damages bacterial DNA).
307
Name three other antibiotics effective against anaerobes.
1. Carbapenems (imipenem) – inhibits cell wall synthesis.
2. Clindamycin – inhibits protein synthesis.
3. β-lactam + β-lactamase inhibitors (e.g., amoxicillin-clavulanate).
308
What are the two key components of treating anaerobic infections?
1. Debridement & drainage of infected tissue.
2. Appropriate antibiotic therapy.
309
What are the four main components of the periodontium?
Gingiva, periodontal ligament, cementum, alveolar bone
310
What are the key functions of the periodontium?
Supports teeth, absorbs occlusal forces, maintains tooth position, and provides defense against microbial invasion
311
What are the two types of cementum?
Acellular cementum (covers cervical root) and cellular cementum (apical third and furcations)
312
How does gingivitis differ from periodontitis?
Gingivitis is reversible inflammation with no attachment loss, while periodontitis involves irreversible bone and attachment loss
313
What is dental plaque biofilm, and why is it important in periodontal disease?
A structured microbial community that adheres to teeth; primary cause of periodontal disease
314
Name three systemic risk factors for periodontitis.
Diabetes, smoking, genetic predisposition
315
What is the purpose of periodontal probing?
Measures pocket depth and attachment loss to assess periodontal health
316
What are the clinical signs of periodontitis?
Pocket formation, attachment loss, bleeding on probing, tooth mobility
317
How does smoking impact periodontal health?
Reduces blood flow, impairs immune response, and increases disease severity
318
What are the non-surgical treatments for periodontitis?
Scaling and root planing, antimicrobial therapy, and patient education on oral hygiene
319
Name two types of surgical periodontal therapies.
Flap surgery and bone grafting
320
What systemic diseases are linked to periodontal disease?
Cardiovascular disease, diabetes, adverse pregnancy outcomes
321
How does the periodontal ligament function?
Provides tooth attachment, absorbs forces, and transmits occlusal load to alveolar bone
322
What is the significance of the junctional epithelium?
Forms a seal between the tooth and gingiva, protecting against bacterial invasion
323
Why is periodontal maintenance therapy important?
Prevents disease recurrence, maintains oral health, and reinforces good oral hygiene
324
What is the key difference between gingivitis and periodontitis?
Gingivitis is reversible inflammation of the gingiva without bone loss, while periodontitis is irreversible and involves destruction of supporting bone and connective tissues.
325
Name three primary periodontal pathogens.
Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Tannerella forsythia.
326
What is the role of neutrophils in periodontal disease?
Neutrophils are the first line of defense, releasing enzymes and reactive oxygen species to fight bacteria, but excessive activation can contribute to tissue destruction.
327
What is the significance of lipopolysaccharides (LPS) in periodontitis?
LPS, found in gram-negative bacteria, triggers the host immune response, leading to inflammation and tissue damage.
328
What are the four stages of periodontal disease progression?
1. Initial Lesion – Neutrophil infiltration.
2. Early Lesion – T-cell dominated, collagen breakdown.
3. Established Lesion – Plasma cell infiltration, chronic inflammation.
4. Advanced Lesion – Alveolar bone loss, periodontal pocket formation.
329
What is the primary function of the RANK/RANKL pathway in periodontitis?
It promotes osteoclast activation, leading to alveolar bone resorption.
330
How does diabetes impact periodontal disease progression?
Diabetes increases inflammation, impairs healing, and enhances collagen breakdown, leading to more severe periodontitis.
331
What are the key pro-inflammatory cytokines in periodontitis?
IL-1β, TNF-α, IL-6—they contribute to inflammation, bone loss, and tissue degradation.
332
How does smoking affect periodontal disease?
Smoking reduces blood flow, neutrophil function, and fibroblast activity, leading to delayed healing and increased tissue destruction.
333
What is the primary function of matrix metalloproteinases (MMPs) in periodontitis?
MMPs degrade collagen and extracellular matrix, contributing to connective tissue destruction.
334
What is a periodontal pocket, and how is it formed?
A pathological deepening of the gingival sulcus due to attachment loss and apical migration of the junctional epithelium.
335
Name two host-modulation therapies for periodontitis.
1. Doxycycline (MMP inhibitor).
2. NSAIDs (reduce prostaglandin-mediated bone resorption).
336
What are some clinical signs of periodontitis?
Bleeding on probing, increased pocket depth, tooth mobility, radiographic bone loss.
337
How does stress contribute to periodontal disease?
Stress increases cortisol levels, which suppresses immune function and promotes inflammation.
338
What is the role of Th17 cells in periodontitis?
Th17 cells promote inflammation and bone resorption by increasing IL-17 production.
339
How does the complement system contribute to periodontal disease?
It enhances bacterial opsonization and inflammation, but excessive activation can lead to tissue destruction.
340
What is the main goal of scaling and root planing (SRP)?
To remove subgingival plaque and calculus, reducing inflammation and promoting tissue healing.
341
What are the main functions of B cells in periodontal disease?
B cells produce antibodies and contribute to chronic inflammation in advanced periodontitis.
342
What is the significance of prostaglandin E2 (PGE2) in periodontitis?
PGE2 promotes bone resorption and inflammation, worsening periodontal destruction.
343
How does antimicrobial therapy help in periodontitis?
Systemic or local antimicrobials reduce bacterial load and prevent further tissue destruction.
344
What radiographic findings suggest periodontitis?
Loss of alveolar bone height, presence of vertical and horizontal bone defects.
345
Name a systemic disease that is linked to periodontitis.
Cardiovascular disease—periodontal inflammation is associated with increased systemic inflammation and atherosclerosis.
346
What is the difference between supra- and subgingival plaque?
Supragingival: Above the gumline, mainly gram-positive bacteria.
Subgingival: Below the gumline, gram-negative anaerobes, more pathogenic.
347
What is the primary role of osteoclasts in periodontitis?
Osteoclasts break down alveolar bone, leading to tooth attachment loss.
348
What are some regenerative treatment options for periodontitis?
Bone grafts
Guided tissue regeneration (GTR)
Enamel matrix derivatives (EMD)
349
What is the key difference between gingivitis and periodontitis?
Gingivitis is reversible inflammation of the gingiva without bone loss, while periodontitis is irreversible and involves destruction of supporting bone and connective tissues.
350
Name three primary periodontal pathogens.
Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Tannerella forsythia.
351
What is the role of neutrophils in periodontal disease?
Neutrophils are the first line of defense, releasing enzymes and reactive oxygen species to fight bacteria, but excessive activation can contribute to tissue destruction.
352
What is the significance of lipopolysaccharides (LPS) in periodontitis?
LPS, found in gram-negative bacteria, triggers the host immune response, leading to inflammation and tissue damage.
353
What are the four stages of periodontal disease progression?
1. Initial Lesion – Neutrophil infiltration.
2. Early Lesion – T-cell dominated, collagen breakdown.
3. Established Lesion – Plasma cell infiltration, chronic inflammation.
4. Advanced Lesion – Alveolar bone loss, periodontal pocket formation.
354
What is the primary function of the RANK/RANKL pathway in periodontitis?
It promotes osteoclast activation, leading to alveolar bone resorption.
355
How does diabetes impact periodontal disease progression?
Diabetes increases inflammation, impairs healing, and enhances collagen breakdown, leading to more severe periodontitis.
356
What are the key pro-inflammatory cytokines in periodontitis?
IL-1β, TNF-α, IL-6—they contribute to inflammation, bone loss, and tissue degradation.
357
How does smoking affect periodontal disease?
Smoking reduces blood flow, neutrophil function, and fibroblast activity, leading to delayed healing and increased tissue destruction.
358
What is the primary function of matrix metalloproteinases (MMPs) in periodontitis?
MMPs degrade collagen and extracellular matrix, contributing to connective tissue destruction.
359
What is a periodontal pocket, and how is it formed?
A pathological deepening of the gingival sulcus due to attachment loss and apical migration of the junctional epithelium.
360
Name two host-modulation therapies for periodontitis.
1. Doxycycline (MMP inhibitor).
2. NSAIDs (reduce prostaglandin-mediated bone resorption).
361
What are some clinical signs of periodontitis?
Bleeding on probing, increased pocket depth, tooth mobility, radiographic bone loss.
362
How does stress contribute to periodontal disease?
Stress increases cortisol levels, which suppresses immune function and promotes inflammation.
363
What is the role of Th17 cells in periodontitis?
Th17 cells promote inflammation and bone resorption by increasing IL-17 production.
364
How does the complement system contribute to periodontal disease?
It enhances bacterial opsonization and inflammation, but excessive activation can lead to tissue destruction.
365
What is the main goal of scaling and root planing (SRP)?
To remove subgingival plaque and calculus, reducing inflammation and promoting tissue healing.
366
What are the main functions of B cells in periodontal disease?
B cells produce antibodies and contribute to chronic inflammation in advanced periodontitis.
367
What is the significance of prostaglandin E2 (PGE2) in periodontitis?
PGE2 promotes bone resorption and inflammation, worsening periodontal destruction.
368
How does antimicrobial therapy help in periodontitis?
Systemic or local antimicrobials reduce bacterial load and prevent further tissue destruction.
369
What radiographic findings suggest periodontitis?
Loss of alveolar bone height, presence of vertical and horizontal bone defects.
370
Name a systemic disease that is linked to periodontitis.
Cardiovascular disease—periodontal inflammation is associated with increased systemic inflammation and atherosclerosis.
371
What is the difference between supra- and subgingival plaque?
Supragingival: Above the gumline, mainly gram-positive bacteria.
Subgingival: Below the gumline, gram-negative anaerobes, more pathogenic.
372
What is the primary role of osteoclasts in periodontitis?
Osteoclasts break down alveolar bone, leading to tooth attachment loss.
373
What are some regenerative treatment options for periodontitis?
Bone grafts
Guided tissue regeneration (GTR)
Enamel matrix derivatives (EMD)
