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GDAN Flashcards

1
Q

If damaged, how do labile cells react

A

Labile = continuously dividing. React by hyperplasia.

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2
Q

If damaged, how do permanent cells react

A

Permanent cells = can’t divide anymore so react by hypertrophy e.g. cardiac cells.

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3
Q

If damaged, how do stable cells react

A

Stable means they can rejoin the cell cycle if they need to.

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4
Q

Types of excessive cell division

A

Developmental hamartoma or

Reactive/adaptive

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5
Q

Development excessive cell division

A

Excessive cell division during patient’s growth period and then stops. Normal tissues just extra e.g. moles, odontomas

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6
Q

Reactive/adaptive excessive cell division

A

Hyperplasia

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7
Q

Hyperplasia and examples

A

Increase in cell numbers, stops when stimulus is removed.
E.g. lack of iodine = not enough thyroid hormone so body makes more thyroid cells.
E.g. hyperplasia of gums.
Can be normal e.g. during pregnancy, growth and puberty.

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8
Q

Hypertrophy

A

Increase in cell size, happens w hyperplasia or on its own in muscles e.g. in skeletal muscle during exercise or smooth muscle in pregnancy.

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9
Q

Neoplasia

A

Uncontrolled cell growth that doesn’t stop when stimulus is removed

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10
Q

Types of developmental too little cell division

A 
Agenesis = doesn't develop at all.
Aplasia = doesn't develop normal structure.
Hypoplasia = less tissue formed e.g. in amelogenesis imperfecta or a class 2 mandible.
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11
Q

Agenesis

A

Cells don’t develop at all

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12
Q

Aplasia

A

Doesn’t develop normal structure

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13
Q

Hypoplasia

A

Less tissue formed

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14
Q

Atrophy

A

Decrease in cell size and number after growth due to imbalance of cell loss vs production. Apoptosis not necrosis.

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15
Q

Generalized atrophy examples

A

Due to hormones, age (e.g. mandible), starvation, bones (osteoporosis due to loss of mineral)

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16
Q

Localised atrophy

A

Ischemic (lack of blood and oxygen), lack of use e.g. a broken leg, denervation/neuropathic.

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17
Q

Metaplasia

A

Tissue differentiates within that germ layer e.g. connective tissue can’t be epithelial tissue. During the change, there’s an increased risk of cancer. Can be useful e.g. smokers respiratory epithelium in bronchi changes to SSE bc better protection.

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18
Q

Dysplasia

A

abnormal growth and differentiation

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19
Q

Ectopia

A

Normal tissue in abnormal place

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20
Q

Normal tissue adaptations

A

Hyperplasia, hypertrophy, atrophy

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21
Q

Invasion of cancer

A

Local spread into surrounding CT

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22
Q

Cytology

A

Features of the individual cells

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23
Q

Classifying cancers

A

By clinical behavior e.g. malignant or benign, or by tissue of origin/histogenesis.

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24
Q

Benign tumour pathology

A

Encapsulated, well defined borders, cells are the same as the tissue of origin e.g. not differentiated, exophytic growth, not metastasized.

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25
Q

Benign tumour effects

A

Pressure on blood vessels or organs. Obstruction. Carries out same function as tissue of origin e.g. secretes hormones.

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26
Q

Pathology of malignant tumours

A

Invade surrounding structures. Angiogenesis/get their own blood supply. No clear border/shape. Different stages of differentiated cells. Metastasises.

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27
Q

Benign tumour in glandular tissue

A

Adenoma

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28
Q

Benign tumour in epithelial lining

A

Papilloma

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29
Q

Benign tumour in fatty tissue

A

Lipoma

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30
Q

Melanoma

A

Malignant tumour of melancoytes

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31
Q

Leukaemia

A

Pre-malignant bone marrow cancer

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32
Q

Malignant tumour in germ cells

A

Teratoma

Can mimic any tissue (stem cells)

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33
Q

Cause of malignant tumours

A

Inherited factors e.g. DNA mutations and environmental factors (physical, chemical or viral)

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34
Q

Stages of cancer formation

A

Initiation = permanent DNA damage.
Promotion where the damaged cell is pushed towards becoming cancerous and proliferating.
Latent period = time between promotion and cancer/proliferation.

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35
Q

Pro-carcinogen

A

Not a carcinogen outside the body but becomes a carcinogen after body processes it.

36
Q

Co-carcinogen

A

Not a carcinogen inside or outside of body but when combined with a carcinogen inside the body it makes its effects much worse.

37
Q

Examples of chemical carcinogens

A

Smoking, diet e.g. burnt hydrocarbons

38
Q

Physical carcinogens examples

A

Ionising radiation (affects sensitive/replicating cells more).
UV
Damage DNA and cause mutations.

39
Q

Viral carcinogens examples

A

HPV, Hep B/C, Epstein-Barr virus.
Act by inserting genes into the DNA that affect the cell’s control mechanism e.g. oncogenes or inactivating tumour suppressor genes (HPV)

40
Q

Other influences that can cause cancer

A

Diet, alcohol, drugs, hormones, inflammation

41
Q

How does cancer screening works

A

It detects dysplasia/disorganisation of cells in the body which is pre-malignant.

42
Q

Modes of spread of cancer

A

Local invasion
Metastatic - lymphatic, haemotagenous (veins have thinner walls) and trans-coelomic spread (spread into serous cavities e.g. pleura)

43
Q

How can haemotagenous metastatic spread occur.

A

By embolism (bit of tumour breaks off into vessel) or by permeation.

44
Q

The effects of metastatic spread on the body

A

Infection, anaemia, metabolic shutdown (starvation), pressure, obstruction, destruction.
Effects of biochemicals released by the tumour cells e.g. fever, weight loss, endocrine problems.

45
Q

Grading and staging of cancer, TNM

A

Grading is to determine tumour’s aggression by looking at the cells and level of differentiation.
Staging is time related and to see the extent of the cancer.
T = size of tumour
N = nodes infected
M = metastasised

46
Q

How to diagnose cancer

A

Biopsy, CT/MRI, molecular analysis, fine needle aspirate of the cells.

47
Q

What does a mutation of PAX9 lead to

A

Oligodontia/missing teeth due to lack of bmp4.

48
Q

Amelogenin and what a lack of it can cause

A

Most abundant protein in enamel matrix and a mutation that means it’s not made can lead to amelogenesis imperfecta.

49
Q

Genetic fingerprinting

A

Relies on VNTRs. Get cut at specific regions and then detected using gel electrophoresis. Loci and number unique to each person.

50
Q

PCR

A

cDNA made by reverse transcription of RNA.
cDNA strands separated by heating to 94 degrees.
Cool to 54 degrees, add Taq bacteria (and Mg, has polymerase that works at these temps), primers and bases.
Heat to 72 degrees so bases bind.

51
Q

Problems with PCR

A

Poor precision, resolution and sensitivity, not automated and not quantitative.

52
Q

Phases of growth in children and their determinants

A

Infancy - nutrition
Childhood - growth hormone
Puberty - growth hormone, sex steroids

53
Q

3 basic ways to measure growth

A

BMI - <18.5 is underweight, >25 overweight, >30-40 is obese and morbidly obese.
Bones in the wrist - stage of epiphyseal maturation. Age at which it is in 50th centile is the bone age.
Height/weight chart

54
Q

Causes of short stature/failure to thrive

A

Genes, systemic/chronic illness, vasculature, metabolic, inter-uterinary growth retardation drugs e.g. alcohol, radiation, malnutrition.

55
Q

Types of defects that can affect growth and development

A

Environmental
Single system defect or multi-system defect (e.g. sequences, association, disorders)
Single gene or polygene defect
Chromosomal defect

56
Q

Dentinogenesis imperfecta

A

DI alone = non-collagenous defects e.g. mutation of dentine protein.
Dentine dysplasia
DI and OI = collagenous (type 1) protein defect.
Causes discolouration, bulbous crown and thin short roots, rapid TSL,

57
Q

Oesteogenesis imperfecta

A

Weak bones, bisphosphonates to treat can cause osteonecrosis, progressiv hearing loss, dentine changes.

58
Q

Cleidocranial dysostosis

A

IMO problems - mn clavicle, missing or supernumerary teeth, hypoplastic maxilla.

59
Q

Craniofacial malformation definition and types

A

Developmental problems of the head that affect physical and mental well being. Can be embryological (present at birth) e.g. clefts or arch 1 anomalies, or developmental (worsens or shown during growth) e.g. craniosynostosis.

60
Q

Cleft lip or palate effects

A

V common. Can cause speech problems, hearing problems (affected drainage of the middle ear), oro-nasal fistula, poor dentition. or jaw relationship.

61
Q

Midface clefts aetiology

A

Failure of the brain to divide into left and right hemispheres, affecting midline features.

62
Q

First arch anomalies

A

E.g. blood supply constricted or mutation in proteins that provide ectomesenchyme to the first arch = hypoplastic maxilla, airway problems, hearing problems.

63
Q

Craniosynostosis

A

Developmental - Early fusion of fibrous fissures, can cause intracranial pressure build up, hearing and speech problems, class 3 jaw.

64
Q

Achondroplasia

A

Developmental - Shortened lower limps and forearms, crowding bs smaller jaws bc cartilage not made into bone

65
Q

The pharyngeal arches structure

A

Separated externally and internally by pouches or clefts. Lined externally by ectoderm and internally by endoderm and mesoderm inside. Contain ectomesenchyme, nerve supply, vein and artery, muscle and associated with a skeletal component.

66
Q

Arch 1

A

Trigeminal nerve
The muscle of mastication, tensor veli palatini
Meckel’s cartilages and middle ear bones incus and malleus.

67
Q

Arch 2

A

Facial nerve
The muscle of facial expression
Stapes and styloid ligament/cartilage

68
Q

Arch 3

A

Glossopharyngeal nerve
Stylopharyngeal muscle
Hyoid bone

69
Q

Arch 4

A

Vagus nerve
Soft palate, pharyngeal constrictors and laryngeal muscles
Thyroid cartilage

70
Q

Arch 5

A

Cricoid cartilage

71
Q

Development of the tongue e.g. arches GRT what

A 
Mesoderm separating arch 1 and 2 GRT anterior 2/3 of the tongue.
Arch 2,3,4 GRT posterior 1/3 of tongue
Arch 2 = taste buds
Arch 4 = epiglottis
Endoderm GRT epithelium and glands
72
Q

Development of the maxillary process

A

Evident at 4-6 weeks when each structure starts to subdivide. First pharyngeal arch divides into superior and inferior processes (the maxillary processes are superior)

73
Q

Development of the nasal placode and primary palate at 5/6 weeks

A

Nasal placode develops from the frontonasal process. Begins to invaginate the frontonasal process and the frontonasal process grows forwards around it. Olfactory epithelium develops from nasal placode. The frontonasal process starts to thicken medially and laterally (medial and lateral nasal processes), medial thickening makes the primary palate.

74
Q

What does the maxillary process develop into and how

A

Maxillary process forms lateral borders of the mouth. It thickens medially and forms 2 processes - superiorly is the tecto-septal process (makes septal cartilage) and inferiorly is the palatine process.

75
Q

What does the growth of the palatal process depend on

A

Growth factors released by the ectomesenchyme and receptors in the ectoderm.

76
Q

What does the primary palate separate

A

The palatal processes and nose from the mouth anteriorly.

77
Q

Palatal elevation

A

At 8 weeks - embryo has a cervical fixture so lifts head of cardiac bulge. Mandible grows and widens so enough room for the tongue to drop so then palatal processes can move up and lay horizontally = secondary palate.

78
Q

What happens to the fetus at 10 weeks

A

Merging of the processes to form the palate. BMP from the ectomesenchyme causes apoptosis of the ectoderm/epithelial covering so that the processes can merge.
Fusion is complete at 12 weeks,

79
Q

What processes fuse to create the palate and what controls this

A

Palatal processes, primary palate and septum.

80
Q

What happens to the fetus’ palate at 15/16 weeks

A

Infiltration of bone into the anterior 2/3 and muscle into the posterior 1/3 of the palate.

81
Q

How do the rests of Malassez form and potential complications

A

Ectoderm/epithelial cells that weren’t removed. Can cause cysts or a small cleft bw the palate and septum.

82
Q

Final developments of the nose and mouth (face)

A

Medial nasal processes fuse and compress and elongate to form nose shape. Epithelium of maxilla and mandible fuse to form the mouth.

83
Q

Role of the osteocytes

A

A role in calcium homeostasis.
Detect pressure or fractures and release factors that cause bone resorption process to start.
Mediating compression and tension forces.

84
Q

Reversal lines and what excessive reversal lines indicate

A

Where bone as been remodelled e.g. due to orthodontics or tooth exfoliating/erupting, Excessive if excessive Oc activity or uncontrolled bone turnover e.g. Paget’s disease.

85
Q

Reasons for local bone remodelling

A

To change the shape of the bone, or due to changes in pressure or for calcium homeostasis.

86
Q

How do the epithelial cells lining the palate change from in embryo -> mature

A

Simple cuboidal -> multilayered flattened -> KSSE

GDAN (3 decks)

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