Jenna Judd Flashcards

1
Q

During what weeks in embryology does the basic face develop

Fusion of What 5 processes are involved

A

4-10 weeks in utero

Frontonasal prominence
Maxillary process x2
Mandibular process x2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What embryological features form the primary palate

When does the primary palate form

What does the primary palate extend posteriorly to

A

Fusion of the two medial nasal prominences

Forms towards end of week 5 in utero

Incisive foramen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the process of development of primary palate

4 steps

A
  1. Week 4- frontonasal, maxillary and mandibular processes form
  2. End of week 4 endothelial thickenings form on frontonasal process making the nasal placodes
  3. Week 6- epithelium of nasal placode invaginates to form nasal pits dividing frontonasal prominence into medial and lateral frontonasal processes
  4. End of week 6 medial nasal processes merge with each other and maxillary process to form upper lip and primary palate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What weeks does the secondary palate develop

A

Weeks 6-10 in utero

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What happens during stage 1 of secondary palate formation

When does this happen

A

Week 6

Paired palatal shelves form from maxillary process and are orientated vertically separated by developing tongue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What happens during stage 2 of secondary palate formation

When does this happen

A

Week 7
Palatal shelves elevate to horizontal position above tongue
Palatal shelves contact each other but are separated by epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens during stage 3 of secondary palate formation

When does this happen

A

Week 10
Medial edge epithelium of palatal shelves fuse to form midline palatal seam which degenerates to allow palate to be composed of a continuum of mesynchyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the occurance rate of CLP

What side is CLP most common

What gender is cleft lip with or without cleft palate more common in

What gender is cleft palate on its own most common in

A

1 in 700 births

Left

Male

Female

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What causes cleft lip

What are the following types of cleft lip caused by

Oblique facial cleft
Median cleft lip
Bilateral cleft lip
Mandibular cleft

A

Failure of fusion of medial nasal prominence and maxillary process

Oblique facial cleft- lack of fusion between maxillary and lateral nasal prominence
Median CL- lack of fusion between two medial nasal processes
Bilateral CL- lack of fusion between maxillary and two medial nasal processes
Mandibular cleft- lack of fusion of first brachial arches or malformation of the symphysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What causes cleft palate

What can cleft palate result from
5

A

Cleft palate occurs when palatal shelves fail to fuse in the midline

  1. Cleft lip distorts development and stops palatal shelves fusing
  2. Failure of shelves to contact due to lack of growth or elevation
  3. Failure of epithelial breakdown following shelve contact
  4. Rupture after fusion of shelves
  5. Defective merging and consolidation of mesenchyme of the shelves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where does closure of secondary palate initiate

What is indicative of interference at the start of palate closure
What is indicative of interference part way through palate closure

A

Closure of palate initiates anteriorly then moves posteriorly

Full clefting
Partial clefting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the oral manifestations of CLP

5

A
Hypodontia
Microdontia
Abnormal tooth shape
Delayed eruption
Enamel defects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the human genome

When was the two initial drafts published

When was the final sequence published

A

The human genome is the complete set of nucleic acid sequences for humans encoded as DNA within the 23 chromosome pairs in cell nuclei and mitochondria

2001
2003

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is monogenic inheritance

Autosomal dominant
Autosomal recessive
X linked

What are some examples of monogenic conditions
3

A

Inheritance of a trait through one gene

Autosomal dominant- always expressed if present
Autosomal recessive- only expressed if two copies of the allele present
X linked- carried on x chromosome so carried by females and manifested in males

Cystic fibrosis
Sickle cell
Duchenne muscular dystrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is cystic fibrosis

How many carry the gene

What is its inheritance pattern

What is the genetic cause of CF

A

CF is an autosomal recessive disorder that causes severe lung damage due to abnormalities in mucus secretion causing thick sticky mucus, is is progressive , required daily care and reduces life expectancy

1 in 25

Often present as single isolated case in absence of family history

Delta F 508 mutation in the CFTR gene - deletion of 3 bases
CFTR is a chloride ion transporter that helps make mucus which cannot fold properly with missing F so misfolded CFTR held in ER and degraded

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the treatments of CF

Mucolytics
Antibiotics
Bronchodilators
New drug therapy (2)

A

Mucolytics - dornase alpha

Antibiotics- antibiotics for chest infections

Bronchodilators - beta 2 agonists (salbutamol), anticholinergics, theophylline

New drugs
Lumacraftor- corrects misprocessing of CFTR so more gets to cell surface
Ivacraftor- increases CFTR channel opening to increase chloride transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is sickle cell disease

What are the genetic causes

A

Sickle cell is an autosomal recessive disorder causing pain attacks, anaemia and organ damage as RBC misformed so become trapped

Caused by missence non conservative substitution mutation in which one base is changed in beta globulin gene
Glutamate (hydrophilic) replaced with valine (hydrophobic)
This change in AA sequence causes haemoglobin molecules to crystallise at low blood oxygen levels so RBCs sickle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Duchenne muscular dystrophy

What is the genetics

What is the inheritance pattern

A

Duchenne muscular dystrophy is a recessive x linked disorder causing progressive weakness and loss of muscle mass shortening life expectancy to mid 20s

X linked mutation in dystrophin gene making it non functional
Dystrophin connects cytoskeleton of muscle fibre to ECM for integrity

Carried by females and effects boys in a family

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is mitochondrial disease

What new therapy can be used to prevent mitochondrial disease

A

Mitochondrial disease is a multifactorial inherited disease carried by mother in the mitochondrial DNA causing compromised energy production so muscles don’t work properly

Donor egg cell combined with mothers nucleus and fathers sperm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the relationship between HER2 gene and breast cancer

What is a treatment for HER2 positive tumours and MOA

A

HER2 gene is involved in cell division, is some breast cancers HER2 is over expressed leading to uncontrolled cell division

Trastuzamab (Herceptin) : binds to HER2 causing cell cycle arrest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the MOA of penicillin

ADME

What are common side effects of all penicillins
6

A

Penicillins are a beta lactam bactericidal and act by interfering with bacterial cell wall synthesis by inhibiting cross linking of cell wall leading to lysis

They diffuse well into body tissues and fluids but penetration into cerebrospinal fluid is poor except when meninges are inflamed, they are excreted in urine in therapeutic concentrations

Diarrhoea, hypersensitivity, nausea, vomiting, skin reactions, thrombocytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Benzylpenicillin
MOA

ADME

Common side effects
2

A

Narrow spectrum bactericidal against gram + bacteria
Ineffective against many infections as most staph aureus bacteria now produce beta lactamase

A: IV or IM due to poor oral absorption as broken down by low stomach pH
M: 16-30% IM dose metabolised to penicilloic acid and small amounts to 6 aminopenicillanic

Fever, jerisch herxheimer reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Phenoxymethylpenicillin (Penicillin V)

MOA

ADME

Oral indications

A

Narrow spectrum bactericidal against gram + bacteria
Ineffective against many infections as most staph aureus bacteria now produce beta lactamase

A: usually administered orally as acid stable
M: 35-70% oral dose metabolised to penicilloic acid which is an inactive metabolite with small amounts metabolised to 6 aminopenicillanic acid

Dental abscesses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Flucloxacillin

MOA

A

A beta lactamase resistant bactericidal drug against gram + bacteria
Altered structure prevents inactivation by resistant bacteria producing beta lactamase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Amoxicillin
MOA

ADME

Dental implications (2)

A

Amoxicillin is a broad spectrum bactericidal drug against gram + and some gram -ve bacteria
It is inactivated by beta lactamase producing gram positive bacteria

A: oral route
M: metabolised to 7 metabolites in liver
E: kidneys

Dental abscess, pericoronitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is co amoxiclav

MOA

A

Co amoxiclav is a combination of amoxicillin, a beta lactam antibiotic and potassium clavulanate which is a beta lactamase inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is MOA of aminoglycosides

What are they used to treat

CI (2)

A

Aminoglycosides are broad spectrum protein synthesis inhibitors which prevent elongation at 30s ribosomal subunit leading to inaccurate mRNA translation

Used to treat gram -ve infections

Can be nephrotoxic and ototoxic

28
Q

What is the MOA of tetracyclines

What impacts its oral absorption

When is tetracycline CI

What tetracycline can we prescribe for sinusitis

A

Tetracyclines are broad spectrum bacteriostatic antibiotics that bind reversibly to 30s ribosome subunit blocking aminoacyl tRNA to prevent translation, they also inhibit MMPs

Absorption impaired when taken with calcium, magnesium or aluminium salts

Under 12, pregnancy

Doxycycline

29
Q

What is the MOA of macrolides

What is it effective against

What negative side effect can they cause

What are the CIs (2)

What macrolide can be prescribed for dental abscess

A

Macrolides are broad spectrum bacteriostatic antibiotics that bind to ribosomal 50s subunit to prevent translocation

Gram +ve and limited gram -ve infections

Electrolyte disturbances

Statins, pregnant or breastfeeding

Clarithromycin

30
Q

What is the MOA of lincosamides

What are they effective against

Which lincosamide can we prescribed for dental abscess

A

Lincosamides inhibit bind to 50s subunit of bacterial ribosome and prevent translocation thus inhibiting protein synthesis

Gram +ve aerobes

Clindamycin

31
Q

Metronidazole
MOA

ADME

Dental indications

Contraindication (1)

A

Metronidazole inhibits nucleic acid synthesis by interacting with DNA causing loss of helical structure
It is reduced to its active intermediate only in presence of anaerobic bacteria and acts against gram - anaerobes and protozoa

A: oral or enteral route- well absorbed and widely distributed including to saliva
M: hepatic hydroxylation, oxidation and glucaronidation to 2-hydroxymetronidazole
E: 60-80% kidney, 6-15% feces

Dental abscess, pericoronitis

Alcohol- disulfriram like reaction

32
Q

What are the symptoms of disulfiram like reaction

3

A

Nausea, vomiting, tachycardia

33
Q

What are the three theories of antibiotic resistance

A
  1. Bacteria acquires genes encoding enzymes like beta lactamase which hydrolyses beta lactam ring of antibiotic
  2. Bacteria acquires efflux pumps that eject antibiotic from cell
  3. Bacteria acquire genes that alter their cell wall so no antibiotic binding site
34
Q

What percentage of patients have penicillin allergy

What percentage of patients have severe immediate hypersensitivity reaction

What are the most common hypersensitivity reactions to penicillin

A

1-10%

0.5%

Type 1: immediate (anaphylaxis)
Type 3: immune complex mediated

35
Q

What is the MOA of polyenes

What are the two polyenes used in dentistry

A

Fungicidal by cell membrane disruption
Interfere with biosynthesis of ergosterol causing generation of pores in membrane, cytoplasmic leakage and cell death

Nystatin
Amphotericin B

36
Q

What are the MOA of azoles

What are the 2 azoles relevant to dentistry

What are their CIs (2)

A

Fungistatic by inhibition of ergosterol synthesis
Prevents fungi growth by inhibiting biosynthesis of ergosterol by interfering with enzyme lanosterol demethylase

Fluconazole
Miconazole

Warfarin, statins

37
Q

What is the MOA of aciclovir

ADME

Dental implications (3)

A

Aciclovir is a nucleoside analog that inhibits the action of viral DNA polymerase and DNA replication in herpes virus

A: usually given orally - low bioavailability 10-20%
M: metabolised by alchohol dehydrogenase and aldehyde dehydrogenase
E: 90-92% excreted unchanged in urine

Shingles, cold sores, primary herpetic gingivostomatitis

38
Q

What is the MOA of chlorhexidine

What is chlorhexidine effective against (4)

Absorption

Dental indication

A

OTC broad spectrum antimicrobial used as topical antiseptic for inflammatory conditions in dentistry
Disrupts microbial cell membranes as positive chlorohexadine molecules react with negatively charged phosphate groups on microbial cell wall - bacteriostatic at low conc, bactericidal at high conc

Gram +, gram -, yeast, viruses

30% active ingredient remains in mouth after rinsing which is released into oral fluids

Primary herpetic gingivostomatitis

39
Q

Candida albicans
Is it gram -ve or +ve
How many people have c albicans as an oral commensal
What percentage of oral yeasts does it account for

What are the 4 main forms and function of each

What is its mechanism of pathology

A

Gram +ve
35-55%
80%

Budding yeast like cells- easily spread to new sites
Pseudohyphae
Germ tubes
True hyphae- epithelium invasion

Opportunistic pathogen

40
Q

What are the innate immune systems response to candida infection (2)

What is the adaptive immune systems response to candida infection (1)

A

Antimicrobial peptides- found in saliva or produced by epithelial cells
Micro abscesses- collections of neutrophils form in epithelia due to candida infection

Cell mediated response

41
Q

What are the symptoms of acute pseudomembranous candidosis (thrush)

What are plaques composed of

Aetiology

Treatment 3

A

Creamy lightly adhered plaques over an erythematous oral mucosa usually on cheek palate or oropharynx which can be scraped off leaving a raw erythematous base. Usually cause discomfort, burning, bad taste

Plaques composed of desquamated epithelial cells and candida hyphae

Affects 5% newborns and 10% elderly debilitated individuals

Fluconazole, miconazole, nystatin

42
Q

What are the symptoms of acute erythematous stomatitis (antibiotic stomatitis)

Cause

Treatments
2 categories

A

Red shiny atrophic appearance sometimes with coexisting thrush, painful and exacerbated by spicy food

Opportunistic infection following use of broad spectrum antibiotics, inhaled steroids, HIV and xeristomia

Elimination of cause: spacer, rinse mouth after inhaler use
Antifungals: fluconazole, miconazole, nystatin

43
Q

What are the symptoms of chronic hyperplastic candidosis (candidal leukoplakia)

Aetiology

Why is eradication difficult

Treatment 3

A

White patch on buccal mucosa bilaterally or on dorsum of tongue that cannot be removed by scraping. It is associated with increase risk of malignant change. Usually asymptomatic

Usually seen in middle age male smokers, also associated with iron, folate, B12 deficiency

Candida hyphae present in superficial layers of epidermis

Smoking cessation, fluconazole, surgical excision

44
Q

What are the symptoms of chronic erythematous stomatitis (denture stomatitis)

Aetiology

Causes 6

Fungi prevalence% (3)

Treatment
3 categories

A

Redness of palate under denture bearing area with petechial whitish areas, usually symptomless

30-60% denture wearers, females:males 4:1

Causes: poor denture hygiene, over use of dentures, iron and vitamin deficiency, steroids, xerostomia, high sugar diet

C albicans 90%
Other candida spp 9%
Other 1%

Denture care- ease wear, hygiene, new dentures
Diet- reduce sugar intake
Antifungals- miconazole gel

45
Q

What are the symptoms of chronic muco cutaneous candidosis

Cause

Treatment

A

Oral candida lesions alongside cutaneous and nail lesions

An immune defect syndrome in which T lymphocytes fail to produce cytokines required for immunity against c albicans

Fluconazole

46
Q

What are the symptoms of angular cheilitis

What are some precipitating factors 4

What are the fungal causes % (3)

Treatment 2

A

Red cracked macerated skin at angles of mouth with gold crust

Trauma, inadequate vertical dimension of denture, iron deficiency, B12 deficiency

Candida albicans 20%
C albicans and staph aureus 60%
Staph aureus 20%

Miconazole cream, FBC and haematinics

47
Q

What are the symptoms of median rhomboid glossitis

Aetiology

Treatment

A

Form of denture stomatitis affecting dorsum of tongue creating well demarcated symmetrical red patch in posterior midline of ant 2/3 of tongue which may be raised or smooth, usually asymptomatic and accompanied by loss of filiform papilla

Seen in patients using steroid inhalers and smokers

Antifungals if symptomatic but cant improve appearance

48
Q

Lymphocyte
Appearance
Function

A

Spherical with large nucleus occupying most of vol

Adaptive immunity: T cells attack other cells, B cells release antibody, NK cells attack cells and bacteria

49
Q

Neutrophil
Appearance
Function

A

Multi lobed nucleus

First responders, phagocytosis, release cytotoxic chemicals via granules

50
Q

Mast cell
Appearance
Function

A

Contain histamine and heparin granules

Dilate blood vessels, induces inflammation, recruits macrophages and neutrophils, type 1 hypersensitivity reaction

51
Q

Basophil
Appearance
Function

A

2 lobed nucleus with dense granules

Releases histamine granules to promote inflammation, parasite defense

52
Q

Eosinophil
Appearance
Function

A

2 lobed nucleus with granules

Phagocytic particularly on antigen antibody complexes, antihistamine release, toxin release

53
Q

Monocyte
Appearance
Function

A

Large cell with horse shoe nucleus

Phagocytosis, antigen presentation

54
Q

Macrophage
Appearance
Function

A

Large cell with single round nucleus

Phagocytic, stimulates other immune cells

55
Q

Dendritic cells
Appearance
Function

A

Cells with dendritic processes

Present antigen on surface to trigger adaptive immunity, located in epithelia then migrate to LN when activated

56
Q

Statins (atorvastatin, simvastatin)
What key condition are they prescribed to treat

MOA

Dental relevance

A

Management of CV disease

Competitively inhibit HMG CoA reductase involved in cholesterol synthesis

Statins cant be taken with fluconazole, miconazole, clarithromycin

57
Q

Calcium channel blockers (amlodipine)

What key condition are they prescribed to treat

MOA

A

CV disease

Calcium channel blockers interfere with inward movement of calcium ions through slow channels of cell membrane, this increases relaxation of muscles to reduce vascular tone

58
Q

ACE inhibitors (rampril)

What key condition are they prescribed to treat

MOA

A

CV disease

ACE inhibitors interfere with RAA system by inhibiting ACE preventing the conversion of angiotensin 1 to angiotensin 2 leading to decreased blood pressure by decreased water retention and vasodilation

59
Q

Adrenergic blockers / beta blockers (bisoprolol)

What key condition are they prescribed to treat

MOA

Dental relavance

A

CV disease

Block affects of adrenaline so heart beats slower and vasodilation occurs

Avoid using lidocaine with bisoprolol

60
Q

Anti platelets (aspirin)

What key condition are they prescribed to treat

MOA

Dental relevance

A

CV disease

Irreversible COX inhibitor, this inhibits platelet aggregation by preventing formation of thromboxane A2

Cannot prescribe diclofenac or aspirin to patients on low dose aspirin

61
Q

What is levothyroxine prescribed to treat

MOA

A

Thyroid disease

Synthetic form of thyroxine acting as replacement

62
Q

What is omeprazole prescribed to treat

MOA

dental relevance

A

Acid reflux

Omeprazole is a proton pump inhibitor which inhibit gastric acid secretion by blocking proton pumps of gastric parietal cells

Proton pump inhibitors such as lansoprazole or omeprazole should be prescribes with NSAIDs in patients with peptic ulcer disease

63
Q

What Metformin prescribed to treat

MOA

A

Diabetes (type 2)

Metformin decreases gluconeogenesis and increases peripheral glucose use but only acts in presence of naturally produced insulin so patient must have some functioning pancreatic islet cells remaining

64
Q

What are tricyclic anti depressants used to treat (amitriptyline)

MOA

Dental relevance

A

Depression

Block reuptake of serotonin and noradrenaline in presynaptic terminals so higher conc in synaptic cleft

Should not use LA containing adrenaline on patients on TCAs

65
Q

What are selective serotonin reuptake inhibitors used to treat (sertraline, citalopram)

MOA

A

Depression

SSRIs block reabsorption of serotonin into neurones

66
Q

What is the key reliever used in management of respiratory disorders

What colour is the inhaler

MOA

A

Salbutamol - bronchodilator

Blue

Salbutamol activates beta 2 adrenergic receptors leading to activation of adenyl cyclase causing increased cAPM which lowers calcium conc resulting in bronchodilation

67
Q

What is the key preventer used in management of respiratory disorders

What colour is the inhaler

MOA

Dental relevance

A

Beclometasone - corticosteroid

Red/brown

Beclometasone mediates anti inflammatory actions by increasing transcription of genes coding for anti inflammatory proteins and suppressing inflammatory gene expression

Diclofenac CI in patients on beclometasone