GDAN Flashcards
If damaged, how do labile cells react
Labile = continuously dividing. React by hyperplasia.
If damaged, how do permanent cells react
Permanent cells = can’t divide anymore so react by hypertrophy e.g. cardiac cells.
If damaged, how do stable cells react
Stable means they can rejoin the cell cycle if they need to.
Types of excessive cell division
Developmental hamartoma or
Reactive/adaptive
Development excessive cell division
Excessive cell division during patient’s growth period and then stops. Normal tissues just extra e.g. moles, odontomas
Reactive/adaptive excessive cell division
Hyperplasia
Hyperplasia and examples
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.
Hypertrophy
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.
Neoplasia
Uncontrolled cell growth that doesn’t stop when stimulus is removed
Types of developmental too little cell division
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.
Agenesis
Cells don’t develop at all
Aplasia
Doesn’t develop normal structure
Hypoplasia
Less tissue formed
Atrophy
Decrease in cell size and number after growth due to imbalance of cell loss vs production. Apoptosis not necrosis.
Generalized atrophy examples
Due to hormones, age (e.g. mandible), starvation, bones (osteoporosis due to loss of mineral)
Localised atrophy
Ischemic (lack of blood and oxygen), lack of use e.g. a broken leg, denervation/neuropathic.
Metaplasia
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.
Dysplasia
abnormal growth and differentiation
Ectopia
Normal tissue in abnormal place
Normal tissue adaptations
Hyperplasia, hypertrophy, atrophy
Invasion of cancer
Local spread into surrounding CT
Cytology
Features of the individual cells
Classifying cancers
By clinical behavior e.g. malignant or benign, or by tissue of origin/histogenesis.
Benign tumour pathology
Encapsulated, well defined borders, cells are the same as the tissue of origin e.g. not differentiated, exophytic growth, not metastasized.
Benign tumour effects
Pressure on blood vessels or organs. Obstruction. Carries out same function as tissue of origin e.g. secretes hormones.
Pathology of malignant tumours
Invade surrounding structures. Angiogenesis/get their own blood supply. No clear border/shape. Different stages of differentiated cells. Metastasises.
Benign tumour in glandular tissue
Adenoma
Benign tumour in epithelial lining
Papilloma
Benign tumour in fatty tissue
Lipoma
Melanoma
Malignant tumour of melancoytes
Leukaemia
Pre-malignant bone marrow cancer
Malignant tumour in germ cells
Teratoma
Can mimic any tissue (stem cells)
Cause of malignant tumours
Inherited factors e.g. DNA mutations and environmental factors (physical, chemical or viral)
Stages of cancer formation
Initiation = permanent DNA damage.
Promotion where the damaged cell is pushed towards becoming cancerous and proliferating.
Latent period = time between promotion and cancer/proliferation.
Pro-carcinogen
Not a carcinogen outside the body but becomes a carcinogen after body processes it.
Co-carcinogen
Not a carcinogen inside or outside of body but when combined with a carcinogen inside the body it makes its effects much worse.
Examples of chemical carcinogens
Smoking, diet e.g. burnt hydrocarbons
Physical carcinogens examples
Ionising radiation (affects sensitive/replicating cells more).
UV
Damage DNA and cause mutations.
Viral carcinogens examples
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)
Other influences that can cause cancer
Diet, alcohol, drugs, hormones, inflammation
How does cancer screening works
It detects dysplasia/disorganisation of cells in the body which is pre-malignant.
Modes of spread of cancer
Local invasion
Metastatic - lymphatic, haemotagenous (veins have thinner walls) and trans-coelomic spread (spread into serous cavities e.g. pleura)
How can haemotagenous metastatic spread occur.
By embolism (bit of tumour breaks off into vessel) or by permeation.
The effects of metastatic spread on the body
Infection, anaemia, metabolic shutdown (starvation), pressure, obstruction, destruction.
Effects of biochemicals released by the tumour cells e.g. fever, weight loss, endocrine problems.
Grading and staging of cancer, TNM
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
How to diagnose cancer
Biopsy, CT/MRI, molecular analysis, fine needle aspirate of the cells.
What does a mutation of PAX9 lead to
Oligodontia/missing teeth due to lack of bmp4.
Amelogenin and what a lack of it can cause
Most abundant protein in enamel matrix and a mutation that means it’s not made can lead to amelogenesis imperfecta.
Genetic fingerprinting
Relies on VNTRs. Get cut at specific regions and then detected using gel electrophoresis. Loci and number unique to each person.
PCR
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.
Problems with PCR
Poor precision, resolution and sensitivity, not automated and not quantitative.
Phases of growth in children and their determinants
Infancy - nutrition
Childhood - growth hormone
Puberty - growth hormone, sex steroids
3 basic ways to measure growth
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
Causes of short stature/failure to thrive
Genes, systemic/chronic illness, vasculature, metabolic, inter-uterinary growth retardation drugs e.g. alcohol, radiation, malnutrition.
Types of defects that can affect growth and development
Environmental
Single system defect or multi-system defect (e.g. sequences, association, disorders)
Single gene or polygene defect
Chromosomal defect
Dentinogenesis imperfecta
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,
Oesteogenesis imperfecta
Weak bones, bisphosphonates to treat can cause osteonecrosis, progressiv hearing loss, dentine changes.
Cleidocranial dysostosis
IMO problems - mn clavicle, missing or supernumerary teeth, hypoplastic maxilla.
Craniofacial malformation definition and types
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.
Cleft lip or palate effects
V common. Can cause speech problems, hearing problems (affected drainage of the middle ear), oro-nasal fistula, poor dentition. or jaw relationship.
Midface clefts aetiology
Failure of the brain to divide into left and right hemispheres, affecting midline features.
First arch anomalies
E.g. blood supply constricted or mutation in proteins that provide ectomesenchyme to the first arch = hypoplastic maxilla, airway problems, hearing problems.
Craniosynostosis
Developmental - Early fusion of fibrous fissures, can cause intracranial pressure build up, hearing and speech problems, class 3 jaw.
Achondroplasia
Developmental - Shortened lower limps and forearms, crowding bs smaller jaws bc cartilage not made into bone
The pharyngeal arches structure
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.
Arch 1
Trigeminal nerve
The muscle of mastication, tensor veli palatini
Meckel’s cartilages and middle ear bones incus and malleus.
Arch 2
Facial nerve
The muscle of facial expression
Stapes and styloid ligament/cartilage
Arch 3
Glossopharyngeal nerve
Stylopharyngeal muscle
Hyoid bone
Arch 4
Vagus nerve
Soft palate, pharyngeal constrictors and laryngeal muscles
Thyroid cartilage
Arch 5
Cricoid cartilage
Development of the tongue e.g. arches GRT what
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
Development of the maxillary process
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)
Development of the nasal placode and primary palate at 5/6 weeks
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.
What does the maxillary process develop into and how
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.
What does the growth of the palatal process depend on
Growth factors released by the ectomesenchyme and receptors in the ectoderm.
What does the primary palate separate
The palatal processes and nose from the mouth anteriorly.
Palatal elevation
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.
What happens to the fetus at 10 weeks
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,
What processes fuse to create the palate and what controls this
Palatal processes, primary palate and septum.
What happens to the fetus’ palate at 15/16 weeks
Infiltration of bone into the anterior 2/3 and muscle into the posterior 1/3 of the palate.
How do the rests of Malassez form and potential complications
Ectoderm/epithelial cells that weren’t removed. Can cause cysts or a small cleft bw the palate and septum.
Final developments of the nose and mouth (face)
Medial nasal processes fuse and compress and elongate to form nose shape. Epithelium of maxilla and mandible fuse to form the mouth.
Role of the osteocytes
A role in calcium homeostasis.
Detect pressure or fractures and release factors that cause bone resorption process to start.
Mediating compression and tension forces.
Reversal lines and what excessive reversal lines indicate
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.
Reasons for local bone remodelling
To change the shape of the bone, or due to changes in pressure or for calcium homeostasis.
How do the epithelial cells lining the palate change from in embryo -> mature
Simple cuboidal -> multilayered flattened -> KSSE
