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Dentistry Year 2 Term 1 > Eshana Edris > Flashcards

Eshana Edris Flashcards

1
Q

What type of bacterias cause dento alveolar abscesses

What are the treatment options

A

Anaerobes such as fusobacteria, porphyromonas, beta haemolytic streptococci

Dranage through acess in root canal
Drainage through socket after extraction
Drainage through stab incision

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2
Q

What is cellulitis

What is lutwigs angina

A

Severe infection involving inflammation of the tissue spaces that carries a risk of developing into sepsis

Cellulitis involving SL and SM spaces

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3
Q

What is impetigo

What are its symptoms

What bacteria cause it

What is the treatment

A

Superficial bacterial infection of the skin affected by dermatitis or trauma

Fragile vesicles develop on skin which rupture to form crusted lesions

Streptococcus pyogenes, staph aureus

Improve hygeine and refer to GP for antibiotics

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4
Q

What is erysipelas

What re the symptoms

What bacteria cause it

What is the treatment

A

A superficial infection of the skin that spreads through lymphatic channels

Erythematous skin of face producing butterfly rash if bilateral

Beta haemolytic streptococci and staph aureus

Improve hygiene and refer to GP for antibiotics

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5
Q

What is scarlet fever

What are the symptoms

What bacteria cause it

A

A bacterial infection initially manifesting as pharyngo tonsillitis followed by fever development and rash due to toxin release from bacteria

White tongue for first 2 days, then red strawberry tongue from day 4

Beta haemolytic streptococci

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6
Q

What is syphilis

What bacteria cause it

A

An STD caused by chronic infection causing lesions on lips, oral cavity and genitals

Treponema pallidum

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7
Q

When does primary syphilis manifest

How long do lesions take to heal

What are the key symptoms
1

A

30-90 days after initial contact

3-8 weeks

Chancre- inflamed ulcerative lesion

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8
Q

When does secondary syphilis manifest

How long do lesions take to heal

What are the key symptoms
3

A

4-10 weeks after primary syphilis

3-12 weeks

Cutaneous rashes-dark patches on skin
Mucous patches- white or red patches that may have ulceration
Condylomata lata- papillary projections on tongue resembling viral warts

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9
Q

When does tertiary syphilis manifest

What are the key oral features
2

A

After a 1-30 year latency

Atrophic glossitis- atrophy of tongue with white discolouration of lingual mucosa which is pre malignant and carries risk of developing into squamous cell carcinoma
Gumma- causes perforation of hard palate due to destruction of tissue and bone

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10
Q

What are the oral manifestations of congenital syphilis

2

A

Hutchkinsons incisors

Mulberry molars

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11
Q

What bacteria cause tuberculosis

A

Mycobacterium tuberculosis

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12
Q

What is primary TB
What does it cause
What is the primary lesion called

What is secondary TB
Where does it effect

What is miliary TB

A

TB seen in previously unexposed patients causing chronic inflammation of the lungs
Ghons focus

TB occuring after latency period with reactivation caused by immunosuppression affecting pulmonary and extra pulmonary tissues

Diffuses disease involving several organ systems

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13
Q

What is actinomycosis

What bacteria cause it

A

Acute or chronic pattern of infection in cervico facial region usually after surgical insult or periodontitis characterised by extensive suppuration and fibrosis during abscess healing causing facial disfigurement

Actinomyces israelii, viscosus, naesludii, odontylyticus

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14
Q

What is noma/cancrum oris

What is the oral manifestation

What bacteria cause it

A

Gangrene of the oro facial tissues causing necrosis

Necrotising ulcerative mucositis

Anaerobes such as f. Necrophorum, f. Nucleatum, prevotella intermedia, borelia vincentii

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15
Q

What is sinusitis

How does it appear radiographically

A

Inflammation of the lining of the paranasal sinuses radiographicly appearing as hazy maxillary atrium

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16
Q

What is tonsillitis

What bacteria cause it

A

Inflammation of palatine tonsils

Beta haemolytic streptococci, staphylococci, H influenzae, F. Porphyromonas

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17
Q

What is gonorrhoea

A

Infection and inflammation of soft palate caused by oral sexual contact

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18
Q

What does pharmacokinetics mean

What does pharmacodynamics mean

A

Movement of drugs within the body ADME

The effect of drugs on the body

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19
Q

What does enteral mean

What does parenteral mean

What is bioavailibility

A

Drugs administered by oral route

Drugs administered by non gastrointestinal route

The proportion of drug reaching systemic circulation

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20
Q

What is the difference in lipid solubility of non polar vs polar molecules

What is the henderson hasselback equation

A

Non polar molecules (non ionised) are lipophilic so move freely across lipid bilayer

Polar molecules (ionised) are lipophobic so cannot move freely across lipid bilayer

BH+ ↔️ B + H+
When basic drug is in the presence of an acid equilibrium shifts towards left so in acidic enviroment of stomach bases more ionised so less likely to be absorbed- vice versa for acidic drugs

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21
Q

How does stability in acid effect drugs

What do enteric coatings do
3

A

Some acidic drugs such as penicillin G react with water in acidic conditions of stomach undergoing hydrolysis producing penicilloic acid which doesnt have the desired antibiotic activity

Prevents tablets from dissolving in acidic conditions of stomach but allows them to be more soluble at basic conditions of intestines
Prevents gastric distress and ulceration or nausea due to irritation
Provides delayed release

22
Q

What does it mean when a drug is affected by first pass metabolism

A

Once drug absorbed in GIT the hepatic portal system transports drugs to the liver - if drug is degraded by liver enzymes during first pass metabolism they will never enter bloodstream to exert therapeutic effects

23
Q

Why might the IV route be used

3

A

When rappid effect necessary
Large volume of drug required
Some drugs may cause tissue damage if administered other ways

24
Q

Benefits of SL and buccal routes

What properties must a drug have to use this route

A

Rapid absorption due to thin highly vascularised tissues
Drug passes directly into systemic circulation

Soluble in saliva
High lipid solubility

25
Q

What is the basic structure and nature of streptococcus

A

Gram negative cocci arranged in chains

26
Q

Where is streptococcus pyogenes found

How is it spread

What diseases does streptococcus pyogenes cause
4

What are the oral manifestations
2

A

Upper respiratory tract

Inhalation, direct contact, formites

Respiratory tract infections, skin infections, genital infections, non suppurative complications

Stomatitis scarlatina
Pyogenic granuloma

27
Q

Where are streptococcus viridans usually found

What form of streptococcus viridans cause dental caries

What form of streptococcus viridans cause endocarditis by entering bloodstream during tooth extraction
2

A

Normally present and non pathogenic in mouth and throat

S. Mutans

S. Sangius and s. Mitor

28
Q

What is the basic structure and nature of staphylococcus

A

Gram positive cocci arranged in grape like clusters

29
Q

Where is staphylococcus aureus usually present

How is it spread

What infections are caused by staphylococcus aureus
8

What is the oral manifestation of s aureus

A

Normally present in healthy individuals in nose , skin and hairs but can cause infection at sites with lowered host resistance

Direct contact, inhalation, ingestion, formites

Cutanous infections, deep infections, respiratory tract infections, septicemia, food poisoning, exfoliative skin diseases, TSS, nosocomial infections

Pyogenic granuloma on gingiva, lips, tongue, buccal mucosa

30
Q

What is the basic structure and nature of actinomyces

What infection is caused by actinomyces

What are the oral significance of actinomyces
2

A

Gram positive filamentous bacteria resembling fungi

Actinomycosis- chronic granulomatous disease characterised by swelling of connective tissue with supparation and discharge of sulphur granules from sinuses

Gingivitis and periodontitis
Root surface caries

31
Q

What is the basic structure and nature of clostridium

A

Gram positive spore forming anaerobic bacilli

32
Q

What does clostridium welchii/clostridium perfringes cause
2

What is its apperance

A

Gas gangrene
Food poisoning

Bacilli arranged singly in chains

33
Q

What is the characteristic apperance of clostridium tetani

What are the clinical features of tetanus
2

A

Drumstick apperance

Muscle stiffness and spasms initially at site of infection then spreading through somatic muscular system
Lockjaw

34
Q

What is the structure of M tuberculosis and what form of respiration

What is the test for tuberculosis
What is a positive test

A

Straight or slightly curved bacilli
Obligate aerobe

Tuberculin/mantoux test-PPD injected into forarm and observed for 72hrs for delayed hypersensitivity reaction
Erythema and induration of 10mm

35
Q

What is the symptoms of reversible pulpitis

A

Pulpal inflammation caused by bacteria toxins leaking into pulp characterised by mild sharp pain of short duration caused by stimulus that can usually be releaved with analgesics

36
Q

What is the symptoms of irreversible pulpitis

A

Sever pulp inflammation with bacterial invasion, neutrophil and macraphage infiltration with areas of necrosis, may be symptomless but usually characterised by spontaneous severe pain for prolonged periods often dull pain worse at night which can be aggravated by hot or cold

37
Q

What is the characteristics of acute apical periodontitis

A

Extreeme pain, swelling, necrotic pulp, TTP and mobility with minimal radiographic changes

38
Q

What is the characteristics of chronic apical periodontitis

A

Accumulation of granulation tissue containing fibroblasts, endothelial cells and inflammatory cells at apex of non vital tooth with bone and PDL destruction. Characterised by cholestrol clefting, periapical radiolucency, TTP, not always painful, tooth may be non responsive.

39
Q

What is agammaglobulinaenia

What diseases cause it and what percentage do these account for

A

Most common primary antibody deficiency characterised by lack of IgG

Brutons disease- 85%
Autosomal recessive disease- 15%

40
Q

What is hyper IgM syndrome

A

B cells fail to switch from IgM production to other forms so only IgM present

41
Q

What are antibodies IgA, IgD, IgE, IgG, IgM

What is there secreted form

What are their functions

A

IgA- monomer or dimer- found at mucosal surfaces to help protect mucosal barriers from pathogens, it dominates saliva
IgD- none- acts as antigen receptor for B cells during maturation
IgE- monomer- mast cell activation, type 1 hypersensitivity, protection against parasites and helminths
IgG- monomer- opsonisation, compliment activation, type 2 hypersensitivity, feedback inhibition of B cells
IgM- B cell antigen receptor, compliment activation, agglutination

42
Q

What is di george syndrome

What is SCID

A

Thymic aplasia results in T cell immunodefficiency often associated with parathyroid underdevelopment or absence

Mutation in gamma chain of interleukin receptors affects downstream signalling of interleukins
Requires bone marrow transplant

43
Q

What are compliment deficiencies caused by

What is the difference between early and late stage causes

A

Mutations in genes that code for compliment components

Mutations in genes for early proteins tend to be linked with autoimmune diseases

Mutations in genes for late stage proteins tend to be linked with increased susceptibility to bacterial infection

44
Q

What is the normal range of neutrophils
What is moderate neutropenia
What is severe nutropenia

A
  1. 5-7.5 x 10^9 cells/L
  2. 5-1.0 x 10^9 cells/L

Below 0.5 x 10^9 cells/L

45
Q

What does human immunoficiency virus cause

What is its mechanism of action

A

Loss of CD4 T cell function

HIV binds to CD4 receptors on T cells and macrophages and diffuses into cells to replicate, immune system recognises and destroys virally infected cells thus destroying its own immune cells

46
Q

What are the key oral manifestations of immunodeficiency

3

A

Erythematous candidiasis

Hairy leukoplakia

Herpes simplex ulceration dorsum of tongue

47
Q

How do tumours create immunosuppression

A

Cells of tumour release cytokines and growth factors that are immunosuppressive and interfere with normal immune response causing immune cells to be reprogrammed into immunosuppressive cells
Immunosuppressive treatments are also used to treat tumours

48
Q

What type of drug is methotrexate

What are these types of drugs used to treat

How do they work

What is the key oral side effect

A

Cytotoxic drug

Antineoplastics used to treat rheumatoid arthritis and crohns disease

Inhibit synthesis of nucleotide bases from folate resevoirs within cells so cell cant cells cant make new proteins or replicate and die, howeever this means they destroy any cells with high turnover such as immune cells or epithelial cells

Mucositis

49
Q

How does fingolimod work

What is it used to treat

A

Prevents T cells attacking neurones by trapping them in lymph nodes, fingolimod blocks S1P receptors on T cells so S1P cannot recruit them from lymph node

Multiple sclerosis

50
Q

What are some examples of corticosteroid drugs
2

What are they used to treat
2

How do they work

A

Prednisone, prednisolone

Asthma, COPD

Prevent inflammation by targeting monocytes and macrophages - decrease cytokine release, decrease nitric oxides, decrease prostaglandins and leukotrienes, decrease adhesion molecules, increase endonucleases to induce apoptosis

51
Q

What is rapamycin used for

How does it work

A

Used to inhibit transplant rejection

Anti proliferative drug that targets mTor pathway so immune cells less likely to survive (mTor pathway responsible for immune cell metabolism, growth, cell cycle, synthesis of new macromolecules)

52
Q

What is cyclosporin used for

How does it work

What is an oral side effect

A

Preventing transplant rejection

Inhibits T cell activation by blocking receptors in Tcell cytosol to inhibit calcineurin NFAT pathway

Drug induced gingival overgrowth appearing clinically as gingival swelling

Dentistry Year 2 Term 1 (6 decks)

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