LS PII Flashcards

1
Q

Four distinct forms of primary oral candidiasis

A
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2
Q
A

Pseudomembranous candidiasis – “Thrush”
“White Plaques Hide Red Layers Silently”

W: Whitish-yellow plaques on mucosa and tongue.
P: Plaques detach easily, revealing red, slightly bleeding mucosa.
H: Hyphal invasion reaches the stratum spinosum; may extend deeper in immunocompromised patients.
R: Risk factors: Antibiotics, corticosteroids, immunosuppressants, diabetes, anemia, leukemia.
L: Low immunity common in infants (5%) and immunocompromised individuals.
S: Often silent (asymptomatic).

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3
Q
A

Pseudomembranous candidiasis – “Thrush”

“Pretty Awesome Criminals Hate Hygiene”

P: Pseudomembranous Candidiasis - Whitish-yellow plaques that scrape off, leaving red, bleeding tissue.
A: Acute Atrophic Candidiasis - Localized redness and burning, commonly on the tongue and palate; linked to antibiotics.
C: Chronic Erythematous Candidiasis - Red, inflamed mucosa under dentures due to poor hygiene or continuous wear.
H: Hyperplastic Candidiasis - Thick white plaques, resistant to scraping, with potential for malignant transformation.
H: Hygiene and Host Factors - Loves environments with poor hygiene, reduced saliva, or antibiotic/steroid use.
This mnemonic captures the main oral manifestations and the opportunistic nature of Candida albicans in a memorable way.

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4
Q
A

Mnemonic for Acute Atrophic (Erythematous) Candidiasis:
“Red Tongue Feels Painful After Antibiotics”

R: Red mucosa on tongue, palate, or buccal surfaces.
T: Tongue and palate are the most common sites.
F: Fewer bacteria due to broad-spectrum antibiotics or corticosteroids, allowing Candida to thrive.
P: Pain or burning may accompany the redness.
A: Antibiotic cessation resolves the condition by restoring bacterial balance.

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5
Q
A

Mnemonic for Acute Atrophic (Erythematous) Candidiasis:
“Red Tongue Feels Painful After Antibiotics”

R: Red mucosa on tongue, palate, or buccal surfaces.
T: Tongue and palate are the most common sites.
F: Fewer bacteria due to broad-spectrum antibiotics or corticosteroids, allowing Candida to thrive.
P: Pain or burning may accompany the redness.
A: Antibiotic cessation resolves the condition by restoring bacterial balance.
**“Pretty Awesome Criminals Hate Hygiene”
**
P: Pseudomembranous Candidiasis - Whitish-yellow plaques that scrape off, leaving red, bleeding tissue.
A: Acute Atrophic Candidiasis - Localized redness and burning, commonly on the tongue and palate; linked to antibiotics.
C: Chronic Erythematous Candidiasis - Red, inflamed mucosa under dentures due to poor hygiene or continuous wear.
H: Hyperplastic Candidiasis - Thick white plaques, resistant to scraping, with potential for malignant transformation.
H: Hygiene and Host Factors - Loves environments with poor hygiene, reduced saliva, or antibiotic/steroid use.
This mnemonic captures the main oral manifestations and the opportunistic nature of Candida albicans in a memorable way.

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6
Q
A

Chronic erythematous candidiasis (denture stomatitis)
Red Dentures Cause Messy Nightcare”

R: Red mucosa beneath denture fitting surface (mostly palatal).
D: Denture hygiene is key; Candida colonizes the denture, not the mucosa.
C: Continuous wear or poor fit worsens the condition.
M: Miconazole applied to the denture surface for treatment.
N: Nightcare: Remove dentures while sleeping;
Non-metal dentures: Soak in 0.1% hypochlorite overnight.
Metal dentures: Soak in chlorhexidine.

“Pretty Awesome Criminals Hate Hygiene”

P: Pseudomembranous Candidiasis - Whitish-yellow plaques that scrape off, leaving red, bleeding tissue.
A: Acute Atrophic Candidiasis - Localized redness and burning, commonly on the tongue and palate; linked to antibiotics.
C: Chronic Erythematous Candidiasis - Red, inflamed mucosa under dentures due to poor hygiene or continuous wear.
H: Hyperplastic Candidiasis - Thick white plaques, resistant to scraping, with potential for malignant transformation.
H: Hygiene and Host Factors - Loves environments with poor hygiene, reduced saliva, or antibiotic/steroid use.
This mnemonic captures the main oral manifestations and the opportunistic nature of Candida albicans in a memorable way.

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7
Q
A

“Pretty Awesome Criminals Hate Hygiene”

P: Pseudomembranous Candidiasis - Whitish-yellow plaques that scrape off, leaving red, bleeding tissue.
A: Acute Atrophic Candidiasis - Localized redness and burning, commonly on the tongue and palate; linked to antibiotics.
C: Chronic Erythematous Candidiasis - Red, inflamed mucosa under dentures due to poor hygiene or continuous wear.
H: Hyperplastic Candidiasis - Thick white plaques, resistant to scraping, with potential for malignant transformation.
H: Hygiene and Host Factors - Loves environments with poor hygiene, reduced saliva, or antibiotic/steroid use.
This mnemonic captures the main oral manifestations and the opportunistic nature of Candida albicans in a memorable way.

“Thick White Smoking Danger”

T: Thickened white plaques (commissural region, dorsum of tongue).
W: White patches don’t rub off (distinguishes from pseudomembranous candidiasis).
S: Smoking habit almost always present.
D: Danger of malignancy (higher dysplasia risk, biopsy essential).
Key Points:
Management: Fluconazole 50 mg daily for 7-14 days + stop smoking.
Message: Inform patients of malignancy risk.

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8
Q

Secondary forms of oral candidiasis

A

“Angry Rhomboid Chronicity”

A: Angular Cheilitis - Erythematous, fissured lesions at mouth angles; linked to dentures, reduced vertical dimension, or nutritional deficiencies.
R: Rhomboid Glossitis (Median) - Symmetrical midline lesion on the tongue’s dorsum; associated with smoking and steroid inhalers.
C: Chronic Mucocutaneous Candidiasis - Candida infections on mucosa, skin, and nails; caused by congenital impaired immunity against Candida.

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9
Q

Oral Candidiasis Treatment:

A

Mnemonic for Oral Candidiasis Treatment:
“Never Forget Friendly Miconazole Care”

N: Nystatin - Oral suspension (100,000–600,000 IU/ml) as a rinse; hold before swallowing. Effective for localized oral candidiasis.
F: Fluconazole - Tablets: 200 mg on day 1, followed by 100–200 mg daily for 7–14 days. Suspension available for oral rinses.
F: Flucytosine - Systemic candidiasis: 250 mg twice daily or 10 mg/ml rinse for oropharyngeal forms (7–14 days).
M: Miconazole (Daktarin Oral Gel) - Effective for oral and throat infections but contraindicated with Warfarin.
C: Care for Dentures:
Acrylic: Soak in 0.5% sodium hypochlorite (1:10 bleach to water) for 10 minutes.
Metal-based: Use 0.2% chlorhexidine or antifungal solutions (e.g., Nystatin).
This mnemonic summarizes the treatments, key medications, and special considerations for managing oral candidiasis effectively.

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10
Q

r Rare Fungal Infections:

A

“All Cool Histories Need Perfect Memories”

A: Aspergillosis
C: Cryptococcosis
H: Histoplasmosis
N: North American Blastomycosis
P: Paracoccidioidomycosis (South American Blastomycosis)
M: Mucormycosis (zygomycosis, phycomycosis)
This mnemonic organizes the rare fungal infections for easier recall.

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11
Q
A

Aspergillosis – “The Necrotic Nightmare”: A vascular invader that thrives in weakened defenses, leaving necrosis and destruction in its wake.
Cryptococcosis – “The Silent Invader”: Hides in pigeon droppings, infiltrates the lungs, and spreads stealthily to the brain.
Histoplasmosis – “The Granuloma Gangster”: A spore-breathing outlaw causing ulcers and nodules, especially in immunocompromised hosts.
North American Blastomycosis – “The Lung Bandit”: Targets the lungs and spreads its gritty lesions to the skin and bones.
Paracoccidioidomycosis – “The Latin Lurker”: A fungal rogue causing chronic ulcers and scarring, endemic to South America.
Mucormycosis – “The Flesh-Eating Fiend”: Rapidly devours tissue in diabetic and immunocompromised victims, leaving destruction in its path.

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12
Q
A

Aspergillosis – “The Necrotic Nightmare”: A vascular invader that thrives in weakened defenses, leaving necrosis and destruction in its wake.
Cryptococcosis – “The Silent Invader”: Hides in pigeon droppings, infiltrates the lungs, and spreads stealthily to the brain.
Histoplasmosis – “The Granuloma Gangster”: A spore-breathing outlaw causing ulcers and nodules, especially in immunocompromised hosts.
North American Blastomycosis – “The Lung Bandit”: Targets the lungs and spreads its gritty lesions to the skin and bones.
Paracoccidioidomycosis – “The Latin Lurker”: A fungal rogue causing chronic ulcers and scarring, endemic to South America.
Mucormycosis – “The Flesh-Eating Fiend”: Rapidly devours tissue in diabetic and immunocompromised victims, leaving destruction in its path.

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13
Q
A

Aspergillosis – “The Necrotic Nightmare”: A vascular invader that thrives in weakened defenses, leaving necrosis and destruction in its wake.
Cryptococcosis – “The Silent Invader”: Hides in pigeon droppings, infiltrates the lungs, and spreads stealthily to the brain.
Histoplasmosis – “The Granuloma Gangster”: A spore-breathing outlaw causing ulcers and nodules, especially in immunocompromised hosts.
North American Blastomycosis – “The Lung Bandit”: Targets the lungs and spreads its gritty lesions to the skin and bones.
Paracoccidioidomycosis – “The Latin Lurker”: A fungal rogue causing chronic ulcers and scarring, endemic to South America.
Mucormycosis – “The Flesh-Eating Fiend”: Rapidly devours tissue in diabetic and immunocompromised victims, leaving destruction in its path.

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14
Q
A

Mnemonic for Blastomycosis: “BLAST Lesions Often Need Treatment”
B: Blastomyces dermatitidis - Chronic fungal infection.
L: Lungs and Skin commonly affected; oral/nasal lesions in 25%.
A: Any organ can be affected if disseminated (bones, marrow, genitals).
S: Squamous cell carcinoma, TB, and syphilis mimic oral lesions (ddx)
T: Treatment with ketoconazole, fluconazole, itraconazole, or amphotericin B.

Aspergillosis – “The Necrotic Nightmare”: A vascular invader that thrives in weakened defenses, leaving necrosis and destruction in its wake.
Cryptococcosis – “The Silent Invader”: Hides in pigeon droppings, infiltrates the lungs, and spreads stealthily to the brain.
Histoplasmosis – “The Granuloma Gangster”: A spore-breathing outlaw causing ulcers and nodules, especially in immunocompromised hosts.
North American Blastomycosis – “The Lung Bandit”: Targets the lungs and spreads its gritty lesions to the skin and bones.
Paracoccidioidomycosis – “The Latin Lurker”: A fungal rogue causing chronic ulcers and scarring, endemic to South America.
Mucormycosis – “The Flesh-Eating Fiend”: Rapidly devours tissue in diabetic and immunocompromised victims, leaving destruction in its path.

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15
Q
A

Mnemonic for Paracoccidioidomycosis: “PARA Ulcers Leave Painful Marks”
P: Paracoccidioides brasiliensis - Chronic granulomatous disease.
U: Ulcers with irregular borders and granular surface in oral cavity.
L: Lungs, lymph nodes, and mucocutaneous areas commonly affected.
P: Palate perforation in severe cases; soft/hard palate, tongue, and gingiva involved.
M: Mimics malignancies (SCC, TB, syphilis, lymphoma, etc.).
T: Treatment with Amphotericin B, ketoconazole, or itraconazole.
This mnemonic summarizes the key features and management for easy recall.

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16
Q
A

Mnemonic for Mucormycosis: “MUCOR Eats Bones Quickly”
M: Mucormycosis - Rare, fatal, acute fungal infection in immunocompromised patients.
E: Eschar lesions - Sharply demarcated ulcers with black necrotic tissue and exposed bone.
B: Blood vessel destruction - Causes thrombosis, ischemia, and necrosis.
Q: Quick spread - Rhino-cerebral form most common; other forms include pulmonary, gastrointestinal, and disseminated.
T: Treatment with Amphotericin B + surgical debridement.

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17
Q
A

Microorganisms Responsible
The likely culprit for the inflammation under the denture is Candida albicans, a fungus that thrives in moist, warm environments like the area under dentures. This condition is called denture stomatitis, and Candida is the primary pathogen.

Answer in Mnemonic: “RED CANDIDA”
R: Remove dentures overnight to let gums rest.
E: Elderly risk—less saliva and health issues like diabetes increase Candida growth.
D: Disinfect dentures with bleach (acrylic) or chlorhexidine (metal).
C: Clean daily—food and moisture trapped under dentures feed fungi.
A: Antifungals like Nystatin or Miconazole to kill Candida.
N: No tight fit—check dentures for irritation.
D: Don’t ignore redness—it stops at the denture border.
I: Identify systemic issues like diabetes.
D: Dry areas help—removing dentures at night reduces fungal growth.
A: Apply antifungal gel on the denture for quick action.
Summary in Lay Terms: Candida loves dark, moist places under dentures. Clean them daily, disinfect, use antifungals, and let gums rest at night. That’s how to evict this fungal squatter!

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18
Q

Describe the clinical presentation of herpangina and its typical oral manifestations.

A

“Fevered Ulcers Sorely Taste Painful.”

Fevered = Sudden Fever
Ulcers = Small vesicles rupture to form shallow ulcers
Sorely = Sore throat
Taste = Affects soft palate, tonsils, and uvula
Painful = The ulcers are painful

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19
Q

Co-infection with which virus is known to exacerbate periodontal disease in HIV-positive patients?
A Influenza
B Herpes Simplex Virus HSV C Hepatitis C
D Epstein-Barr Virus EBV

A
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20
Q

What are non-odontogenic infections?

A

Answer Infections that come from other areas around the mouth, such as the skin, tonsils, or sinuses.
Explanation Sometimes, infections in the mouth donʼt start with the teeth. They can come from other places like your skin or sinuses and then affect your mouth.

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21
Q

What are the typical clinical features (signs) of an odontogenic infection?Answer Severe pain, tenderness when chewing, fever (pyrexia), and swollen lymph nodes (lymphadenopathy).
Explanation If you have an infection in your teeth, it can make your tooth hurt really badly, feel sore when you chew, give you a fever, or make your neck swell up.

A

How can odontogenic infections lead to more serious problems in the body?

Answer They can spread to other parts of the face, neck, or even into t

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22
Q

What are the three main pathways through which infections can spread in the body?

A

Answer Through connective tissue spaces (fascial spaces), the lymphatic system, and the bloodstream.
Explanation Infections can travel around the body by moving through soft tissues, lymph nodes, or the blood.

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23
Q

Infections can spread to certain spaces in the face. Name at least two spaces where infection may spread and mention the type of teeth that usually cause the infection.

A

Answer Buccal space (between the cheeks) and masseteric space (near the jaw), often caused by molar (back) teeth infections.
Explanation Infections from teeth, especially the back ones, can spread to areas in the cheeks or jaw.

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24
Q
A
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25
Q

Why is it dangerous if an infection spreads to the lateral pharyngeal space, and what serious complication can occur?

A

Why is it dangerous if an infection spreads to the lateral pharyngeal space, and what serious complication can occur?
Answer The infection can spread to the neck and cause a descending neck infection, which can affect breathing and even reach the chest (mediastinum).
Explanation If the infection moves to this area, it can cause neck swelling and trouble breathing, and it can spread down to the chest, making it really dangerous.

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26
Q

How do infections that spread through the retropharyngeal space connect with the mediastinum, and why is this dangerous?

A

Answer The retropharyngeal space connects the back of the throat with the chest (mediastinum), and infection here can spread to the chest area, which can be life-threatening.
Explanation If germs spread from the throat down to the chest, it can cause serious complications, including chest infections that are very hard to treat.

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27
Q

What is the buccal space, and what infection source commonly affects it?

A

Answer The buccal space is located between the cheek muscles and is commonly affected by infections from the molar (back) teeth.
Explanation The buccal space is in your cheek area, and infections from your back teeth can spread there, causing swelling.

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28
Q

Where is the masseteric space located, and which teeth infections usually cause issues in this space?

A

usually cause issues in this space?
Answer The masseteric space is between the jawbone (mandible) and the masseter muscle, and it’s usually affected by infections from lower molar teeth.
Explanation This space is near the jaw, and infections from lower back teeth can cause problems there, often leading to trouble opening your mouth.

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29
Q

What is the significance of the pterygomandibular space in dentistry?

A

What is the significance of the pterygomandibular space in dentistry?
Answer It contains important nerves, including the inferior alveolar nerve, and is important for giving local anesthesia (numbing shots) in dental procedures.
Explanation This space is important because dentists inject numbing medicine here to stop you from feeling pain during certain dental procedures.

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30
Q

Which important structures are found in the carotid sheath, and why are infections in this area a concern?

A

Which important structures are found in the carotid sheath, and why are infections in this area a concern?
Answer The carotid sheath contains the carotid artery, jugular vein, and vagus nerve. Infections here can affect blood flow and vital functions.
Explanation This area has important blood vessels and a nerve that controls your heart and lungs, so if germs spread here, it can be very dangerous.

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31
Q

What does it mean when the swelling is “fluctuant,” and why is this important?

A

What does it mean when the swelling is “fluctuant,” and why is this important?
Answer: “Fluctuant” means there is fluid, like pus, inside the swelling, which can be felt when pressing on it.
Explanation If the swollen area feels soft and squishy, it likely means thereʼs pus inside, which signals that the infection needs to be drained.

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32
Q

What supportive treatments may be necessary for severe orofacial infections?

A

Answer Hydration through IV fluids and keeping the airway open (sometimes through a tracheotomy).
Explanation In serious cases, you might need fluids through a drip to keep hydrated or surgery to help you breathe if the infection is blocking your airway

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33
Q

When would a drain be used, and why is it important in treating an infection?

A

When would a drain be used, and why is it important in treating an infection?
Answer A drain is used to keep the area open so that pus can continue to drain out after surgery.
Know LO
36
Explanation After draining the infection, doctors often leave a little tube in place to keep the area open so the pus doesnʼt build up again.

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34
Q

What is an abscess, and how does the body typically respond to it?

A

Answer An abscess is a collection of pus that forms due to infection. The body tries to wall it off to prevent the infection from spreading.
Explanation An abscess is like a little pocket of pus that your body creates to trap the infection and stop it from spreading.

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35
Q

fistula vs sinus

A

A fistula is like a tunnel that forms between an infection (like a dental abscess) and another part of the body, such as the mouth, allowing pus to drain. A sinus, on the other hand, is a one-way track from the infection to the skin or gums, acting as a drain for the abscess.

A fistula is like a secret tunnel that the body creates when an infection (like a dental abscess) needs a way to release pus. This tunnel connects the infected area to another part of the body, like inside your mouth or even another space, so the pus can drain out. It’s a way for your body to relieve pressure, but it means the infection has created a connection it shouldn’t have.

A sinus, on the other hand, is more like a pipe with one end. It starts at the infection and comes out through the skin or gums, letting the pus escape. Unlike a fistula, it doesn’t connect to another internal area—just the outside of the body or mouth.

Think of it this way:

A fistula is a “two-way tunnel” (between two spaces).
A sinus is a “one-way drain” (from inside to outside).

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36
Q

What are the three possible outcomes when the body tries to resolve an abscess?

A

Answer The abscess can heal and form a scar, form a fistula (a pathway that allows pus to drain), or the infection can spread further.
Explanation The body can either heal the abscess with a scar, create a path for the pus to escape, or the infection can get worse and spread.

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37
Q

What is a fistula, and how is it related to an abscess?

A

What is a fistula, and how is it related to an abscess?
Answer A fistula is an abnormal pathway that allows pus from the
abscess to drain out of the body.
Explanation A fistula is like a tunnel that the body makes to let the pus from the abscess drain out, which can help relieve pressure.

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38
Q

What is cellulitis, and how is it different from an abscess?

A

Answer Cellulitis is a diffuse infection that spreads through the skin and tissues, without forming a clear pocket of pus like an abscess.
Explanation Cellulitis is when an infection spreads over a larger area of the skin and tissues, making it swollen and red, but without a pus-filled pocket.

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39
Q

Which of the following is a primary cause of odontogenic infections?
A Viral infections
B Progressive dental caries C Allergic reactions
D Systemic diseases

A

Correct Answer: B Progressive dental caries

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40
Q

True or False: Odontogenic infections only arise from sources within the oral cavity.

A

False They can also arise from nonodontogenic sources, such as surrounding skin, tonsils, or sinuses.)

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41
Q

What are the typical clinical features of an odontogenic infection?

A

Suggested Answer: Typical clinical features include severe pain, tenderness on percussion, pyrexia (fever), and lymphadenopathy (swollen lymph nodes).

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42
Q

Which type of odontogenic infection is commonly associated with trismus and affects the mandibular molars?
A Pterygomandibular space infection B Buccal space infection
C Submental space infection
D Masseteric space infection

A

D Masseteric space infection

43
Q

Clinical Scenario:
Emma Clark, a 28-year-old female, presented to the dental clinic with a painful swelling under her jaw. She reported that the swelling started two days ago and has progressively worsened, accompanied by difficulty swallowing and a slight fever. On examination, you note redness and tenderness in the submandibular region. You suspect an infection and decide to conduct further investigations to confirm the source and spread.
During the drainage procedure, what anatomical landmarks
would you avoid to prevent damage to vital structures?
* Facial artery and marginal mandibular nerve
* Inferior alveolar nerve
* Mental nerve
* Lingual nerve

A

Answer: Facial artery and marginal mandibular nerve

44
Q

How do probiotics work in your body?

A

Mnemonic: “B.A.L.A.N.C.E”

Boost good bacteria: Probiotics add more helpful bacteria to your gut.
Arm the immune system: They help fight harmful germs.
Level pH: Probiotics keep the gut environment balanced.
Aid digestion: They break down food better.
Nix bad bacteria: Probiotics crowd out harmful bugs.
Create vitamins: Some probiotics produce essential nutrients like B vitamins.
Ease inflammation: They calm the gut, reducing irritation and discomfort.

45
Q

True/False Question:
True or False: Probiotics can be used to treat bad breath.

A

Probiotics can help treat bad breath by balancing oral bacteria, reducing the growth of odor-causing microbes, and promoting a healthier mouth environment.

46
Q

Why might a dentist recommend probiotics to a patient?

A

Mnemonic: “P.R.O.B.I.O.T.I.C.S.”
Prevents gum disease (reduces inflammation and periodontal issues).
Reduces harmful bacteria (balances oral microbiota).
Overcomes bad breath (neutralizes odor-causing microbes).
Boosts healing (supports recovery after dental procedures).
Improves oral microbiome health.
Optimizes cavity prevention (inhibits harmful bacteria growth).
Targets oral infections (like candidiasis).
Influences overall health (gut-oral health connection).
Calms inflammation (reduces gum irritation).
Supports saliva production (promotes natural oral defenses).

47
Q

What are some of the limitations of using probiotics in dentistry?

A

Lay Term, Shortened:
Probiotics don’t stay in the mouth long, work differently for everyone, need regular use, can be pricey, and might not mix well with other treatments like mouthwash. Research is still catching up!

Mnemonic: “P.R.O.B.I.O.T.I.C.S.” (again, for consistency)
Poor colonization (short-term effects).
Research is evolving (limited studies).
Outcome varies (not one-size-fits-all).
Budget concerns (can be costly).
Interaction issues (with mouthwash/meds).
Optimal storage needed (sensitive to heat).
Tailored use (strain-specific).
Immunocompromised caution (not for everyone).
Convenience challenge (needs consistency).
Short-lived results (continuous use required)

48
Q

How might the oral microbiome be a source of probiotics in the future?

A

Modified strains: Tailored beneficial oral bacteria.
Innovative therapies: Use native microbes for treatment.
Control infections: Prevent bad bacteria overgrowth.
Restore balance: Promote healthy oral ecosystems.
Optimized solutions: Personalized probiotics for patients.
Lay Term, Shortened:
In the future, dentists could use good bacteria already in your mouth as custom probiotics to fight infections, restore balance, and keep your mouth healthy.

49
Q

Explain the role of mucins in saliva and their contribution to oral health.

A

Viscosity: Mucins make saliva thick and sticky.
Immune defense: Trap and clear harmful microbes.
Speech: Help with smooth talking.
Coating: Form a protective barrier on the mouth lining.
Oral lubrication: Make eating and swallowing easier.
Underpin swallowing: Facilitate movement of food.
Safety: Protect mucosa from damage.

50
Q

Describe how changes in saliva composition can affect the development of oral diseases.

A

Shield weakens: Reduced antimicrobial proteins mean less defense.
Acids linger: Low buffering capacity fails to neutralize acids.
Loss of protection: Pathogens grow unchecked.
Integrity declines: Oral tissues become more vulnerable.
Vulnerable to decay: Higher risk of dental caries and gum disease.
Attacks increase: Oral infections become more frequent.

51
Q

Explain the difference between primary and secondary secretion in the production of saliva.

A

xplain the difference between primary and secondary secretion in the production of saliva.
Suggested Answer: Primary secretion occurs in the acini and is similar to plasma, being isotonic. Secondary secretion occurs as the saliva passes through the ducts, where electrolytes are reabsorbed or secreted, leading to hypotonic saliva that is released into the oral cavity.
Think of saliva production like making a smoothie. The first step, primary secretion, happens in the acini, which are the tiny “kitchens” of your salivary glands. Here, the base ingredients are mixed, like water, proteins, and electrolytes, creating a solution thatʼs very similar to your blood plasma — itʼs packed with all the raw materials.
But this smoothie isnʼt ready yet! As it travels through the “smoothie machine” (which are the ducts in your salivary glands), the recipe gets adjusted. This is where the secondary secretion happens. The machine removes certain “ingredients” (like some sodium and chloride) and adds others (like potassium), making the final product more specialized.
By the time the saliva reaches your mouth, it’s different from the original mixture. Itʼs now hypotonic, meaning itʼs less salty than it started out, and perfectly designed to keep your mouth moist, comfortable, and clean! So, primary secretion is like making the base smoothie, while secondary secretion is like fine-tuning it on the way out.

52
Q

Explain how increased pulpal pressure during inflammation can lead to pulpal necrosis.

A

Pulpal pressure rises: Inflammation increases pressure in the pulp.
Restricted space: The confined pulp chamber limits expansion.
Edema forms: Vessels leak fluid, causing swelling.
Supply cut off: Collapsed venules block blood flow.
Starvation: Lack of blood causes pulp tissue to die (ischemic necrosis).

53
Q

```

~~~

Multiple Choice Question:
Why is chronic hyperplastic pulpitis (pulp polyp) more commonly seen in younger patients?
A Higher immune response
B Greater vascularity and ability to produce granulation tissue C Increased caries activity
D Frequent dental visits

A

Correct Answer: B Greater vascularity and ability to produce granulation tissue
Chronic hyperplastic pulpitis, also known as a pulp polyp, is something that happens when part of the inside of a tooth (called the pulp) gets inflamed and starts growing out of the tooth. It’s kind of like if you got a little boo-boo inside your tooth, and your body tried to heal it by putting a little bandage on it, but the bandage kept getting bigger.
Young people tend to see this more often because their bodies are really good at sending blood and healing stuff to places that need it. Their bodies can make a lot of what’s called granulation tissue, which is like the body’s way of forming a natural bandage. This helps in healing, but in the case of a tooth, it can overdo it and create a pulp polyp.
So, the reason you see this more in younger people is not because they eat more sweets or go to the dentist more, but because their bodies are just really good at trying to fix things inside their teeth, sometimes a little too good! Pulp polyps are usually
asymptomatic. Direct pressure during mastication may cause mild-to-moderate tenderness. Localized bleeding may occur when the soft tissue is manipulated or traumatized.

54
Q

True or False: Pulp polyps are typically asymptomatic because the pulp is exposed but remains vital.

A

True or False: Pulp polyps are typically asymptomatic because the pulp is exposed but remains vital.
Correct Answer: True
In the case of pulp polyps, there typically isn’t nerve pain. This is because the tissue, despite being exposed, remains vital and healthy. Essentially, the nerve within the pulp polyp is still alive and not irritated or inflamed to the point of causing pain. The process leading to a pulp polyp involves the development of granulation tissue, which is protective and can help insulate the nerve from stimuli that typically cause pain, such as heat, cold, or pressure.

So, generally, patients with pulp polyps do not experience the nerve pain that is often associated with other dental issues where the pulp is diseased or dying.

55
Q

Describe the typical clinical presentation of a pulp polyp.

A

Protruding mass: Red, fleshy tissue sticking out of the tooth.
Occurs in youth: Common in younger patients.
Large lesion: Associated with big cavities.
Yet painless: Usually asymptomatic due to healthy pulp.
Pulp vitality: Tissue remains alive and functional.

56
Q

Explain the difference between acute and chronic periapical periodontitis.

A

Mnemonic for Acute Periapical Periodontitis: “P.A.I.N.”
Percussion tenderness: Painful when tapped.
Acute inflammation: Rapid and intense.
Invisible on X-ray: No early radiographic changes.
Noticed pain: Patient feels significant discomfort.

Mnemonic for Chronic Periapical Periodontitis: “C.A.L.M.”
Cyst or granuloma: Periapical radiolucency seen on X-rays.
Asymptomatic: Often no pain.
Long-standing: Slow-developing condition.
Mineral loss: Bone breakdown around the apex.

57
Q

What is the primary difference between a periapical abscess and a periodontal abscess?

A
58
Q

True or False: A periapical abscess originates from the pulp and spreads to the periapical tissues.

A

Correct Answer: True

59
Q

Describe the clinical management of a patient presenting with a periapical abscess.

A

Mnemonic: “D.R.A.I.N.”
Drain the abscess: Via root canal or incision.
Remove infection: Root canal treatment or extraction clears the source.
Antibiotics: Use appropriate therapy to control the spread.
Infection control: Prevent further complications.
Necessary intervention: Definitive treatment ensures resolution.

60
Q

What is a pulp polyp, and in what type of teeth is it commonly found?

A

Answer A pulp polyp is an overgrowth of inflamed dental pulp tissue that protrudes from a large cavity in a tooth. It is commonly found in young patients with newly erupted molar teeth.

61
Q

What is the clinical appearance of a pulp polyp?

A

Answer A red, fleshy mass protruding from the cavity of the tooth,
usually painless unless it becomes infected.
Explanation It looks like a small red bump sticking out of the tooth with a big hole, and it usually doesnʼt hurt unless it gets infected.

62
Q

How is a pulp polyp treated?

A

Answer Treatment involves removing the polyp and either extracting the tooth or performing a root canal to remove the inflamed tissue. The dentist will either pull out the tooth or clean it up with a root canal to stop the polyp from coming back.

63
Q

What does necrotic pulp mean, and how does it affect the tooth?

A

Necrotic pulp means that the pulp inside the tooth is dead, which can lead to infection spreading to the surrounding bone.
Explanation The inside of the tooth dies and the infection can spread to the bone around the tooth, causing further problems.

64
Q

What are the clinical signs of chronic periapical periodontitis?

A

Mnemonic: “D.E.A.D.”
Dull response: Tooth doesn’t react to sensitivity tests.
Evident radiolucency: Dark area around the root on X-rays.
Abnormal swelling: Visible near the affected tooth.
Drainage tract: Sinus tract may be present.

Answer Signs include a tooth that doesnʼt respond to sensitivity tests, a radiolucent (dark) area around the tooth root on an X-ray, and swelling or a sinus tract near the tooth.
Explanation The tooth wonʼt feel anything when tested, and an X-ray will show a dark spot around the root, which means the infection is spreading. You might also see a bump near the tooth where pus is draining.

65
Q

What is the difference between acute and chronic periapical periodontitis?

A

Answer Acute periapical periodontitis involves sudden pain and inflammation with tenderness when biting, while chronic periapical periodontitis usually has no pain, but a persistent infection with bone loss.
Explanation In the acute type, it hurts a lot and feels sore when you bite, while the chronic type is less painful but causes long-term damage like bone loss.

66
Q

What are the symptoms of a dental abscess?

A

Mnemonic: “P.A.I.N.S.”
Pus drainage: Causes a bad taste in the mouth.
Ache: Severe toothache is the main symptom.
Increased sensitivity: Tooth reacts to hot and cold.
Noticeable swelling: On the face or gums.
Significant discomfort: Overall pain and irritation.

67
Q

A periapical abscess is always associated with severe pain and systemic symptoms.

A

r: False Periapical abscesses can sometimes be asymptomatic, especially in chronic cases.)
Periapical abscesses are not always associated with severe pain and systemic symptoms. While acute cases can cause intense pain and may lead to systemic effects like fever due to rapid inflammation and swelling, chronic periapical abscesses might not show noticeable symptoms. This is because chronic abscesses often develop a way to drain, reducing pressure and pain. Thus, itʼs false to say that these abscesses always cause severe symptoms; they can sometimes be asymptomatic, particularly in their chronic form.

68
Q

What are the potential outcomes if acute periapical periodontitis is left untreated?

A

Mnemonic: “N.E.S.T.S.”
Necrosis: Untreated leads to pulp death.
End abscess: Progression to a periapical abscess.
Spread: Infection can move to nearby tissues.
Transition: Develops into chronic periapical periodontitis.
Systemic risks: May result in cellulitis, osteomyelitis, or widespread infection.

69
Q
A
70
Q

Describe the management approach for a patient diagnosed with chronic osteomyelitis of the jaw.

A

Bone removal: Excise necrotic bone (sequestrae).
Oxygen therapy: Hyperbaric oxygen aids healing.
Necessary antibiotics: Long-term to fight infection.
Extraction: Remove affected teeth.
Surgical drainage: Manage associated abscesses.

71
Q

What triggers the initial onset of pulpal pain related to pressure changes, and how does it manifest clinically?

A

The onset of pulpal pain related to pressure changes is triggered by fluid movement up and down the dentinal tubules when dentine is exposed, altering pulp pressure and causing sharp pain, indicative of reversible pulpitis.
Tubule fluid: Movement triggers the pain.
Up and down: Fluid shifts along exposed dentinal tubules.
Balanced pressure lost: Altered pulp pressure causes discomfort.
Exposed dentin: Leads to sensitivity and sharp pain.
Signs reversible: Indicates reversible pulpitis.

72
Q

Differentiate between reversible and irreversible pulpitis in terms of symptoms and clinical testing responses.

A

Mnemonic for Reversible Pulpitis: “S.H.O.R.T.”
Stimuli: Triggered by hot, cold, sweet, or sour.
Healthy pulp: Pulp is inflamed but still salvageable.
Obvious pain: Immediate and sharp.
Responds quickly: Pain resolves when the stimulus is removed.
Tests positive: Reacts to electric pulp testing.
Mnemonic for Irreversible Pulpitis: “P.R.O.L.O.N.G.”
Persistent pain: Prolonged and delayed discomfort.
Response negative: Little to no reaction to sweet/sour stimuli.
Overwhelming damage: Pulp is beyond repair.
Lingering thermal pain: Reaction to hot/cold lasts longer.
Outcome poor: Requires root canal or extraction.
Negative testing: May have abnormal pulp test responses.
Greater severity: Indicates advanced inflammation.

73
Q

Describe the typical progression of infection from the pulp to the periapical tissues and the radiographic signs you might observe.

A

Mnemonic: “P.A.T.H.”
Pulpal infection: Bacteria and necrotic debris spread.
Apical foramen: Exit point for the infection to surrounding tissues.
Tenderness: Percussion sensitivity indicates inflammation.
Hole in bone: Widened ligament space visible on X-ray.

74
Q

What are the potential outcomes of acute periapical periodontitis due to trauma, and how can they be clinically identified?

A

Mnemonic: “R.E.S.O.R.T.”
Resolution: Healing without complications.
Entering necrosis: Pulp death, sometimes with hemorrhage.
Staining: Dark tooth discoloration due to necrotic pulp.
Observed pink tooth: Internal replacement resorption.
Resorption external: Can lead to ankylosis.

75
Q

How does chronic periapical periodontitis typically present, and what are its possible consequences if left untreated?

A

Mnemonic: “C.H.R.O.N.I.C.”
Clinically silent: May show no symptoms.
Health cycles: Abscess can flare up periodically.
Recrudescent abscess: Periodic episodes of infection.
Ongoing inflammation: Persists if untreated.
New granulation tissue: Bone replaced by inflammatory tissue.
Inflammatory bone loss: Destruction of surrounding bone.
Chronic state: Condition becomes long-lasting.

76
Q

What are the common initiating factors for reversible pulpitis and how can they lead to irreversible pulpitis?

A

Caries and trauma: Key initiating factors for pulp exposure.
Altered pressure: Fluid movement in tubules causes sharp pain.
Resolves: Reversible if inflammation is controlled.
Escalates: Can progress to irreversible pulpitis and necrosis if untreated.

77
Q

How does chronic periapical periodontitis develop and what are its potential consequences if left untreated?

A

Prolonged inflammation: Chronic response to pulpal infection.
Root tip changes: Granuloma or cyst formation occurs.
Ongoing infection: Persists without treatment.
Low-grade inflammation: Subtle but damaging over time.
Observable bone loss: Chronic inflammation erodes bone.
Neglect worsens: Leads to further complications like cysts.
Granuloma formation: A hallmark of chronic periapical periodontitis.

78
Q

What clinical conditions are associated with the initiation of pulpal and periapical infections according to the text?

A

Caries and trauma are primary initiators, leading to the exposure of the dental pulp to bacteria, which then causes inflammation and infection.

79
Q

How does a pulpal abscess form, and what are the subsequent risks mentioned in the text?

A

A pulpal abscess forms when bacteria invade the pulp chamber, leading to infection and pus formation. This can risk spreading the infection to periapical tissues, causing bone destruction and potential systemic effects.

80
Q

Describe the typical pathological changes in the pulp due to systemic influences mentioned in the pages.

A

Diabetes: Delays healing and increases infection risk.
Immunodeficiency: Weakens the body’s defense against infections.
Makes inflammation worse: Complicates the body’s response to injury.

81
Q

Periapical Periodontitis Progression

A

The infection from the tooth’s nerve can spread to the jawbone around the tip of the tooth root, causing swelling and pain, and if not treated, might damage the bone or spread infection further.

Mnemonic: “S.P.R.E.A.D.”
Spreads from nerve: Infection moves from the tooth’s pulp.
Pain and swelling: Signs of infection near the tooth root.
Root tip affected: Jawbone around the root becomes involved.
Erosion of bone: Infection can damage surrounding bone.
Advances further: Can spread beyond the tooth and jaw.
Demand treatment: Needs prompt care to prevent complications.

82
Q

What is osteomyelitis of the jaw and how might it develop from untreated pulpal and periapical infections?

A

Answer: Osteomyelitis is a severe bone infection that can occur when bacterial infection from periapical areas spreads deeply into the jawbone, causing extensive bone inflammation and necrosis.

83
Q

Describe the role of taste buds in the sensory function of the tongue.

A

Taste buds are specialized sensory organs located on the papillae of the tongue that detect the five basic taste modalities (sweet, sour, salty, bitter, umami) and transmit this information to the brain for processing.

84
Q

Which type of papillae on the tongue does not contain taste buds?

A

Filiform papillae

85
Q

True or False: Sour taste is detected by the activation of sodium channels in taste cells.

A

: False Sour taste is detected by the blockage of potassium channels due to cellular acidification.)

86
Q

Explain how the taste signal is transduced in the case of salty taste.

A

Mnemonic: “S.A.L.T.”
Sodium enters: Sodium ions flow into taste cells via ENaCs.
Activates cells: Sodium causes depolarization of the taste cell.
Leads to neurotransmitters: Release signals the presence of salt.
Transmits to brain: Brain identifies the salty taste.

Salty taste is transduced through epithelial sodium channels ENaCs) on taste cells, where sodium ions enter the cell, leading to depolarization and the release of neurotransmitters that signal the presence of salt to the brain.

87
Q

Describe the neural pathway for taste sensation from the tongue to the brain.

A

Front tastes Facial
Go Back to taste Gloss
Send to Nucleus for prep
Through Thalamus to Gusty Cortex

88
Q

What term describes a reduced ability to taste?

A

Correct Answer: B Hypogeusia True/False Question:

89
Q

rue/False Question:
True or False: Dysgeusia refers to a complete loss of taste.

A

Correct Answer: False Dysgeusia refers to a distortion or abnormal taste sensation.)
Hereʼs an easy way to remember that dysgeusia is not the complete loss of taste but rather an abnormal or distorted taste sensation:
Imagine youʼre tasting your favorite food, but suddenly, it tastes completely wrong—like chocolate that tastes salty or sweet things that taste bitter. Thatʼs dysgeusia: when your sense of taste gets “distorted” or “messed up,” but itʼs not gone.

90
Q

List three potential causes of taste or smell disturbances.

A

Possible causes include aging, head trauma, and upper respiratory infections.

91
Q

If Mia canʼt taste her ice cream as well as before, which nerve might not be working properly?
Facial nerve
Glossopharyngeal nerve
Trigeminal nerve
Both Facial and Glossopharyngeal nerves

A

: Both Facial and Glossopharyngeal nerves

92
Q

Odontogenic cysts are always lined by

A

epithelium derived from odontogenic tissues.

93
Q

Describe the process of cyst formation, focusing on the role of epithelial proliferation and degeneration.

A

Cell proliferation: Epithelial cells grow due to stimuli.
Yielding degeneration: Cells break down, forming a cystic lumen.
Stromal changes: Degeneration supports cyst development.
Tension increases: Fluid accumulation causes expansion.

94
Q

Differentiate between a dentigerous cyst and an eruption cyst.

A

Mnemonic for Dentigerous Cyst: “D.E.N.T.”
Develops in bone: Forms around unerupted tooth crowns.
Enclosed crown: Associated with reduced enamel epithelium.
No eruption: Tooth remains in the bone.
Traditional location: Found in hard tissue like the jawbone.
Mnemonic for Eruption Cyst: “S.O.F.T.”
Soft tissue: Found over erupting teeth in the gingiva.
Observable swelling: Appears bluish and bulging.
Forms during eruption: Tooth is breaking through the gum.
Temporary: Resolves as the tooth emerges.
These mnemonics differentiate between the two types of cysts based on location and characteristics!

95
Q

Which of the following is a histopathological feature of an odontogenic keratocyst?
A Thick, non-keratinized squamous epithelium
B Thin, parakeratinized stratified squamous epithelium C Presence of ameloblast-like cells
D Absence of a fibrous capsule

A

B Thin, parakeratinized stratified squamous epithelium

96
Q

Radicular cysts often show reactive hyperplasia of the epithelial lining with

A

cholesterol clefts and Rushton bodies.

97
Q

What is the clinical significance of finding Rushton bodies in a radicular cyst?

A

r: Rushton bodies are acellular, eosinophilic structures often found in the lining of radicular cysts. Their presence indicates longstanding chronic inflammation and may aid in the histopathological diagnosis of the cyst.

98
Q

Outline the management strategy for a patient diagnosed with a dentigerous cyst.

A

Mnemonic: “C.A.R.E.”
Cyst removal: Surgical enucleation is performed.
Associated tooth extracted: Unerupted tooth is removed.
Recurrence prevention: Entire cyst lining is carefully excised.
Evaluation: Follow-up radiographs ensure proper healing.

99
Q

What are the two main types of odontogenic cysts based on etiology?

A

Answer: The two main types are developmental and inflammatory odontogenic cysts.
Explanation: Developmental cysts form due to developmental abnormalities, while inflammatory cysts are caused by infections or inflammations in the teeth and surrounding tissues.

100
Q
  1. What is a dentigerous cyst, and where is it most commonly found?
A

tooth, most commonly around the mandibular third molars or maxillary canines.
Explanation: This cyst forms due to a separation of the reduced enamel epithelium from the crown of a tooth that hasnʼt yet erupted, often seen in wisdom teeth.

101
Q

What are the key histological features of a dentigerous cyst?

A

Answer: It has a thin lining of stratified squamous epithelium, an uninflamed fibrous capsule, and sometimes mucous cells or cholesterol crystals.
Explanation: The cyst lining is smooth and uninflamed, with occasional changes like goblet cells or cholesterol, which can help in diagnosis.

102
Q

How can you clinically recognize an eruption cyst?

A

Explanation: This type of cyst is often seen in children over new teeth coming through, and it may look bluish or purple due to blood mixing with the cyst fluid.

103
Q

What is an odontogenic keratocyst (OKC), and why is it clinically significant?

A

Answer: An OKC is a potentially aggressive cyst associated with the dental lamina, often found in the mandible and sometimes linked to Gorlin syndrome.
Explanation: OKCs grow quickly, can recur, and are sometimes linked to genetic conditions, so they require careful monitoring.

104
Q

. What are the key symptoms of Obstructive Sleep Apnoea OSA that you would look for in a patient?

A

Snoring loudly: Persistent, disruptive snoring during sleep.
Night gasping: Gasping or choking episodes.
Overwhelming sleepiness: Excessive daytime drowsiness.
Rising headaches: Morning headaches after waking.
Early dryness: Dry mouth or sore throat upon waking.