Callum Cafferty Flashcards
What is primary, secondary, tertiary, quaternary protein structure
What type of bonds
Primary: sequence of amino acids in polypeptide chain with N terminus at start and C terminus at end- Peptide bonds
Secondary: local folding of polypeptide chain into alpha helix or beta pleated sheet- H bonds
Tertiary: 3d folding of protein to generate functional domains due to interactions between R groups- ionic bonds, disulphide bridges, hydrophilic/hydrophobic interactions, H bonds
Quaternary: association of multiple subunits - same bonds as tertiary structure
What is splicing
The selection of of different sections of DNA to be translated- Exons code for protein, Introns are non coding sections, selection of different combinations of exons created different proteins during alternate splicing
What is glycosylation
What are lipid anchors
What is phosphorylation
Attachment of sugar groups to form glycoproteins which facilitate protein interactions such as ligand binding and binding of proteins in ECM
Chemical groups that help proteins attach or associate with a membrane
Reversible addition of phosphate group
What causes amelogenesis imperfecta
3
Mutations in genes (AMELX and ENAM) that encode ECM proteins of enamel
Mutations in genes that encode proteases that remove organic matter from enamel as it matures
Mutations in SLC24A4 which codes for calcium transporter required to deliver calcium to teeth as they develop
What apperance on a childs growth chart warrants investigation
Plateauing of weight or height during childhood
What age does lymphoid tissue reach 100% of its size
7 years
At what age does neural tissue reach 90% of its size
At what age does neural tissue reach 96% of its size
7 years
10 years
What is the post natal growth spurs
What is the pre pubertal growth spurt
Rapid growth observed during first year of life followed by progressive decrease in growth rate till puberty
Rapid growth at onset of puberty occurring at 11 in girls and 13 in boys
Growth hormone/somatotrophin
What is its gland of origin What is its function What happens in excess What happens during deficiency How is its release regulated
Anterior pituitary gland
Stimulated chondocyte proliferation, production of insulin like growth factor 1, bone mineralisation , increases skeletal mass, promotes lipolysis and protein synthesis, antagonises insulin, stimulates immune function
Acromegaly in adults, pituatary gigantism in children
Impaired growth
Relase stimulated by GHRH from hypothalamus and inhibited by somatostatin (from hypothalamus), negative feedback, dietary carbohydrate, glucocorticoids
Thyroid hormones (T3 and T4)
What is its gland of origin What is its function What happens in excess What happens during deficiency How is its release regulated
Thyroid gland
Causes growth of nervous tissue and bone , increases glycogenolysis, increases basal metabolic rate
Hyperthyroidism causes increased bone turnover, accelerated growth, accelerated bone maturing so can lead to short stature
Hypothyroidism leads to cognitive and neurologic abnormalities, short stature and growth retardation, delayed bone maturation
Release stimulated by TSH from anterior pituitary, inhibited by negative feedback
Oestrogen
What is its gland of origin What is its function What happens in excess What happens during deficiency How is its release regulated
Ovaries
Controls puberty in females, strengthens bones, causes pubertal growth spurt
Excess can cause acne, breast cancer, fibroids
Deficiency can cause poor bone growth and menopausal symptoms such as osteoporosis
Release stimulated by FSH from anterior pituitary, inhibited by negative feedback
Androgens - testosterone and androstenedione
What is its gland of origin What is its function What happens in excess What happens during deficiency How is its release regulated
Testes, ovaries, adrenal glands
Testes formation, male pubertal development, inhibits fat deposition, promotes muscle mass
Hyperandrogenism - in females causes hirsutism, alopecia, hidradenitis suppurativa, acne, obesity
Hypoandrogenism- in men causes loss of libido, infertility, genital shrinkage, low muscle mass, osteoporosis
Release stimulated by FSH and LH from anterior pituitary, inhibited by negative feedback
What is endochondral ossification
What is the process 3
The formation of bone from a preceeding cartilagenous matrix which becomes replaced by bone and marrow
- periosteal bud invade cartilage model and allows mesenchymal cells to enter cartilage
- Invading mesenchymal cells mature into osteoblasts
- Osteoblasts deposit bone using the framework of calcified cartilage
What is intermembranous ossification
What is the process 3
Mineralisation of tissue with differentiation of mesenchymal cells to osteoblasts occuring within a membranous plate of mesenchymal cells
- At ossification centre mesenchymal cells differentiate into osteoblasts
- Osteoblasts deposit osteoid
- Thin sheet of woven bone called periosteal collar is deposited around shaft of cartilage model
What type of ossification happens in the cranial vault
Intramembranous ossification
What type of ossification occurs in cranial base growth
Endochondral ossification