Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

CYSTIC FIBROSIS & DEYED PUBER TY Define the processes of transcription and translation in protein synthesis Describe the changes in the nucleotide sequence of DNA and histone modifications that can result in disease Recall how changes in the nucleotide sequence and post-transcriptional modification can affect protein function Interpret Mendelian patterns of inheritance and define the associated risks in families Define carrier frequencies in the general population and calculate the associated risks Outline the mechanisms by which Na+ K+ and Cl- ions are transported across the cell membrane Draw and label the basic components and the accessory organs of the GI system Describe the structure and function of the exocrine pancreas Draw and label the basic components of the respiratory system Differentiate between the upper and lower respiratory tract and describe the microscopic changes that occur with progression through the conducting and respiratory zones Relate changes in CFTR function to alteration in gastrointestinal and respiratory function including malabsorption and problems with the muco-respiratory escalator Review the basic components of a healthy diet CYSTIC FIBROSIS Describe how nutrition from birth to puberty is managed in a CF patient Define the normal patterns of growth in infancy, childhood, and pubertal development ILOS Describe the tests used in the diagnosis of cystic fibrosis Classify the microorganisms of direct relevance to cystic fibrosis and define the effect of infection on the pulmonary system Define the barrier functions of the innate immune system Define the role of the innate immune system in detecting and resolving an acute infection for example cell types, cytokines, pyrokines Outline the multidisciplinary management of a cystic fibrosis patient Describe the essential cellular processes that are inhibited by the antibiotics used to treat bacterial infections arising in cystic fibrosis Outline the strategy for prescribing antibiotics focusing on the concept of ‘antibiotic custodianship’ and personalised prescription Explain the role of genetic counselling as an example of a specialist health care service Outline how genomic data have impacted on treatment regimens and life expectancy of affected individuals focusing on cystic fibrosis (revisit in week 7) Relate the experience of diagnosis and management of long-term conditions to family and other social circumstances Outline the stages of cognitive and psychosocial development Relate the experience of diagnosis and management of long-term conditions to family and other social circumstances Describe the different types of study used in clinical researchPROTEIN SYNTHESIS Location:Nucleus Initiation: RNA polymerase binds to the promoter region of DNA with the assistance of transcription factors DNA double helix unwinds Elongation: RNA polymerase moves along the template strand of DNA,synthesising a single strand of mRNA PROTEIN by adding complementary RNA nucleotides Termination: SYNTHESIS- Transcription continues until RNA polymerase reaches a termination signal in the DNA sequence, which signals the end of the gene (stop codon) TRANSCRIPTION The RNA polymerase detaches from the DNA, pre-mRNA is released Post-Transcriptional Modifications The mRNA undergoes several modifications before leaving the nucleus: Capping:A 5’ cap (a modified guanine nucleotide) is added to the start of the mRNA, protecting it from degradation & helping with ribosome binding Polyadenylation:A poly-A tail (a series of adenine nucleotides) is added to the 3’ end, enhancing mRNA stability & export from the nucleus Splicing:Introns are removed, & exons are joined together,resulting in mature mRNA Location:Cytoplasm (on ribosomes) Initiation: The small subunit of the ribosome binds to the 5’ cap of the mRNA & scans for the start codon (AUG) Once the start codon is located, a tRNA molecule carrying the amino acid methionine binds to the start codon The large ribosomal subunit then joins the small subunit, forming a functional ribosome Elongation: The ribosome moves along the mRNA, reading the sequence in codons (3 nucleotides) Each codon corresponds to a specific amino acid,which is brought to the ribosome by tRNA molecules The ribosome has three sites: PROTEIN A site (aminoacyl site):Accepts incoming tRNA carrying an amino acid P site (peptidyl site):Holds the tRNA carrying the growing polypeptide chain SYNTHESIS- E site (exit site):Where empty tRNA exits the ribosome As the ribosome moves along the mRNA, peptide bonds form between adjacent amino acids, creating a growing TRANSLATION polypeptide chain Termination: Translation continues until a stop codon (UAA, UAG, or UGA) is encountered Release factors bind to the stop codon,prompting the ribosome to release the newly synthesised polypeptide The ribosomal subunits dissociate,& the mRNA is released Post-Translational Modifications: After translation, the new protein may undergo various modifications,including: Folding:Proteins often fold into specific 3D shapes to become functional,chaperone proteins assist protein’s function,activity, & stabilitytion,glycosylation,acetylation,& ubiquitination,which can affect the Transport:Proteins are often transported to specific locations within or outside the cell,depending on their function  Na+ & K+ :  Passive transport across apical membrane- through Na+ channels from high to low concentration- what is this process called?  Active transport- Na+/K+ ATPase-ATP is hydrolysed to release energy which moves Na+ out of the cell & K+ into the cell against their concentration gradients (3:2) Cl- :  The CFTR (cystic fibrosis transmembrane regulator) protein is encoded by the CFTR gene  It is a member of the ATP-binding cassette family (ABC proteins) & has 1480 amino acid residues  It allows Cl- to cross the epithelial cell membrane when a concentration gradient exists IONTRANSPORT  It is found in epithelial cell membranes (usually on the apical side,facing the lumen)  ABC proteins have a modular structure with 4 conserved domains:there are 2 transmembrane domains and 2ATP binding domains;there is an additional domain called the Regulatory domain which regulates the activity of the protein  When the regulatory domain is phosphorylated,the channel can open; but this has to be accompanied by the binding ofATP at theATP binding domains for the opening of the channel to occur  The regulatory domain is phosphorylated by protein kinaseA that uses cyclic A and B  Cl- ions are more concentrated in the cell than outside,forming a concentration gradient therefore the Cl- ions will leave the cell via the CFTR protein channel  Na+ ions will also leave the cell via another separate channel in order to maintain electrical neutrality  To maintain osmotic potential,water will also diffuse out of the cell;this water will then hydrate the mucus and therefore lowers its viscosity so that it can move and leave the lungs as the cilia wafts it out EXOCRINE PANCREAS  Exocrine component (99% of the pancreas) is made up of glandular epithelial cells called acini  Secretes pancreatic juice which is delivered through the main & accessory pancreatic ducts into the duodenum  Juices are lipase,peptidases and amylase; pancreatic juice is rich in bicarbonate and digestive enzymes  Main pancreatic duct extends from the head to the tail of the pancreas which unites with the bile duct and opens into the duodenum at the major duodenal papilla-Ampulla of Vater  Genetic disease caused by a mutation of the CFTR gene in chromosome 7, affecting 1:2500 births  Autosomal recessive  Carrier rate is 1:25  Explain how unaffected parents can have a child with CF  What is the probability of 2 carriers having a child with CF?  What is the probability of any couple of having a child with CF? Pathophysiology:  CFTR (cystic fibrosis transmembrane conductance regulator) is an ABC protein, found in the cell membrane- is CFTR a transporter?  CFTR channel controls movement of Cl- out of cells down the concentration gradient WHAT IS CF?  When mutated, Cl- can not leave the cell therefore Na+ does not leave down the electrochemical gradient and H2O does not follow as there is not osmotic gradient created so the mucus is less hydrated, and becomes sticky and thick infections not waft the mucus that traps the pathogens, so the mucus stays stuck and the pathogens trapped now cause  What phenomenon is this referring to? It causes increased viscosity of secretions  What organs are affected?  What is the result of this? The following organisms can colonise patients with CF:  Staphylococcus aureus  Pseudomonas aeruginosa  Burkholderia cepacia  AspergillusGENETICS  2000 mutations are potential contributors to CF  100 mutations have been proven to directly cause CF The most common mutation is the F508del  Can you work out what this means? Mutation Effects:  CFTR synthesis- by introducing a stop codon,forms a shorter protein that is no longer functional;any protein that does not fold properly is degraded  Stability- deletion of amino acids alters the hydrogen bonds,Van derWaals forces & salt bridges,reducing the structural function  Ion channel function- reduces ability of the channel opening & closing  Abundance at the cell membrane- less are trafficked to the CSM even though the right number of protein is madeExam tip: Diamond- unknown sex (pregnant) Autosomal recessive? PEDIGREEANAL YSIS Coloured- affected Autosomal dominant? Square- male X-linked recessive? Circle- female Double horizontal line- consanguinity Oldest on the left,youngest on the right Dot in the shape- carrierAnswer: Autosomal dominant Vertical pattern of transmission Male & female affected equally If it wasAR- horizontal pattern of transmission If it was x-linked-‘T’ pattern What is the probability that the unborn child has the condition? Neonates- meconium ileus Recurrent chest infections Wheeze Widening of airways- what is this condition called?Why does it occur? FEATURES OF CF Malabsorption- steatorrhoea Liver disease Gallstones Osteoporosis Diabetes DIAGNOSIS  GuthrieTest- heel prick test at birth to screen for genetic conditions including CF Dried blood spot for IRT IRT- immunoreactive trypsinogen Found in blood,produced by pancreas If pancreatic duct is blocked,IRT leaks into the blood  SweatTest:  Patients with CF have high Cl-  2 electrodes & pilocarpine administered to the arm induce sweating  Cl- >60 mEq/l - CF  Normal range- <40 mEq/l CFTR genetic testing can be done after positive sweat test to confirm mutation CF MANAGEMENT Regular chest physiotherapy & postural drainage  High caloric diet with high fat intake- what are your thoughts on this?  Minimise contact with other patient with CF to avoid cross infection with Burkholderia cepacia & pseudomonas aeriuginosa  Vitamin supplements  Pancreatic enzyme supplements with meals  Lung transplant  Contraindicated in patents with BC  Lumacaftor/Ivacaftor for patients who are homogenous for the F508del mutation  Lumacaftor increases the number of CFTR proteins that are transported to the cell surface  Ivacaftor is a potentiator of CFTR already at the cell surface, increasing the probability that the defective channel will be open to allow Cl- to pass through the channel pore Triple combination therapy 2 corrector drugs + 1 potentiator drug Corrector drugs stabilise the mutated version & avoid degradation Elaxacaftor &Tezacaftor- correctors Ivacaftor- potentiator Why are fatty meals taken with them? Staphylococcus aureus- - Flucloxacillin (prophylaxis) - LT ABX to suppress MSSA respiratory infection in people with stable pulmonary disease - For people who have MSSA and become clinically unwell, consider PO or IV broad-spectrum ABX including an anti-SA agent - MRSA- seek microbiological advice on treatment MSSA- - Nafcillin: penicillin ABX effective against MSSA  Cefazolin MRSA- - Vancomycin: Often used for serious MRSA infections ABX FOR - Linezolid: An alternative for MRSA, especially in skin & soft tissue infections Pseudomonas aeruginosa- INFECTIVE PO, IV & inhaled ABX EXACERBATIONS Inhaled ABX: - Tobramycin: Often given as an inhaled solution - Aztreonam Systemic ABX: - Ceftazidime: broad-spectrum cephalosporin - Piperacillin-tazobactam: combination penicillin - Meropenem: carbapenem ABX - Ciprofloxacin: fluoroquinolone that may be used in certain cases Burkholderia cepacia- IV ABX Haemophilus influenzae- PO ABX NICE guidelines: https://www.nice.org.uk/guidance/ng78/chapter/recommendationsMCQSWhat is the most common mutation that causes cystic fibrosis? A) F506del B) F508del C) R117H D) G551D E) N1303K What is the test to detect Cl- concentration? A) Guthrie test B) CFTR genetic testing C) Sweat test D)Waterlow test E) Electrolyte testingWhat is the probability of a person to be a carrier of a mutation that can cause cystic fibrosis? A) 1:20 B) 1:5 C) 1:625 D) 1:25 E) 1:4 PatientA has been admitted to the hospital due to an infected exacerbation of cystic fibrosis.Which organism is unlikely to be the cause of this? A) Staphylococcus aureus B) Moraxella catarrhalis C) Pseudomonas aeruginosa D) Burkholderia cepacia E)AspergillusYou are called to see a 2 day-old neonate who was born 1 week premature following a premature rupture of membranes.He has failed to pass meconium in the first 24 hours and has begun vomiting.Y ou witness one episode of vomiting during the examination which is stained green,which you suspect is bile.On examination he is irritable with an obvious distension of the abdomen but is apyrexial with normal oxygen saturations.Palpation of the abdomen causes further irritation but you are unable to feel any discrete mass. What is the most likely underlying condition? A) Respiratory distress B)Appendicitis C)Acute pancreatitis D) Pyloric stenosis E) Cystic fibrosis Can you explain why the other conditions are not the answer?DELAYED PUBETY Contrast the mechanism of action between steroid and peptide hormones. Building on knowledge of steroid hormone action,describe the sequence of events that allow testosterone to perform its function, including:the trigger for its release;the cellular events that result from its binding to its cognate receptor;and its effects on specific body tissues. Explain the role of oestrogen and testosterone in the maturation of the male reproductive system. Outline the series of events that initiate and maintain spermatogenesis Define the three phases of linear growth and describe its hormonal regulation (GnRH, growth hormone,thyroid hormone and IGFs). Describe the physical and physiological changes that occur in the male and female during puberty DELAYED Draw and label the structure of a long bone and identify the cellular components Delineate the cellular mechanisms underpinning growth PUBERTY ILOS Calculate predicted adult height, identify the target centile range,and explain the differences in the growth and growth potential between males and females Identify the potential causes of short stature,the treatments,and the ethical issues associated with such treatment Describe how the biopsychosocial model explains the interactions between the psychosocial development of adolescents (including the role of body image) and health and wellbeing Describe the continuum of shared decision-making compare the potential benefits and costs of different ways patients and healthcare professionals make decisions about care Interpret the continuum of decision-making outlined in the GMC document‘0-18 years: guidance for all doctors’ in the circumstance of caring for a 15-year-old Explain‘Gillick competence’ and its assessment. Outline the clinical care for a young person who is transitioning including the ethical and legal considerations MECHANISM OF ACTION OF STEROID HORMONES Lipid solubility:lipophilic (fat-soluble) & can easily pass through the CSM of target cells Receptor binding:once inside the cell,they bind to specific intracellular receptors (cytoplasmic or nuclear receptors); binding often results in a conformational change in the receptor Translocation:hormone-receptor complex typically translocates to the nucleus if it is not already there DNA interaction:in the nucleus,the hormone-receptor complex binds to specific sequences of DNA known as hormone response elements (HREs) in the promoter region of target genes Gene regulation:binding can lead to the activation or repression of gene transcription, resulting in changes in mRNA levels;the increase or decrease in mRNA levels subsequently affects protein synthesis Physiological effects:newly synthesised proteins carry out various functions,leading to the physiological effects associated with the specific steroid hormone, such as metabolism regulation, immune response modulation,or changes in growth & development Overall,steroid hormones act primarily at the genomic level by modulating gene expression,which leads to long-term effects on cell function & behaviour MECHANISM OFACTION OF PEPTIDE HORMONES Peptide hormones have a different mechanism of action compared to steroid hormones, primarily because they are hydrophilic (water-soluble thus can’t easily cross the CSM Receptor binding:bind to specific receptors on the surface of target cells;typically G protein-coupled receptors (GPCRs) or receptor tyrosine kinases Signal transduction:binding activates intracellular signalling pathways;often involves the activation of G proteins or the autophosphorylation of the receptor itself Second messengers: activating pathways frequently leads to the production of second messengers,such as cAMP, inositol triphosphate (IP3), or diacylglycerol (DAG);these second messengers amplify the signal within the cell Cellular response:second messengers initiate a cascade of events that leads to various cellular responses,including changes in enzyme activity, ion channel conductance,& alterations in gene expression.The specific effects depend on the type of hormone and the target tissue Physiological effects:overall result of these processes leads to the physiological effects associated with the peptide hormone,such as changes in metabolism,growth, or immune function This mechanism allows peptide hormones to produce rapid and versatile effects,as they can act on multiple pathways & have immediate impacts on cellular function Spermatogenesis:helps in the maturation of sperm by promoting the development & function of Sertoli cells,which support & nourish developing sperm cells T estosterone regulation:influences testosterone levels in males;it is produced in small amounts in males through the aromatisation of androgens ROLE OF Development of male secondary sexual characteristics:helps growth of bone & muscle masse reproductive tract & influences the OESTROGEN ON THE Bone health:important for maintaining bone density in males. skeletal integrity levels help prevent osteoporosis & maintain MATURATION OF among individualsfunction:although its effects can vary widely THE MRS CV health:protective effects on CV health,which can indirectly benefit reproductive health by maintaining overall well-being Overall,while testosterone is the primary male sex hormone, reproductive system,influencing a variety of physiological processese  Development of male reproductive organs:during foetal development, testosterone is essential for the formation of male reproductive structures,including the testes, prostate, & seminal vesicles  Puberty & secondary sexual characteristics: testosterone levels surge during puberty,leading to the development of secondary sexual characteristics such as: Increased muscle mass and strength Growth of body and facial hair ROLE OF Deepening of the voice Increased bone density TESTOSTERONE  Spermatogenesis: works in conjunction with FSH to stimulate Sertoli cells, which support & nourish developing sperm cells ONTHE erectile function;it influences sexual behaviour & arousaldrive) & is crucial for normal MATURATION OF reproductive tissues,including the testes & prostate gland;also influences the production THE MRS of seminal fluid osteoporosis & support overall physical healthity & muscle mass, helping to prevent may relate to reproductive strategiesviour,including aggression & competitiveness, which  Overall,testosterone is fundamental for the development, maintenance,and proper functioning of the male reproductive system, influencing both physical characteristics and reproductive capabilitiesTESTOSTERONE Cholesterol- precursor molecule from which sex steroid hormones are produced  Oestrogen  Androgens- testosterone  Progestins- progesterone Mechanism:  Adipose tissue produces leptin  Leptin reaches the hypothalamus  Kisspeptin is formed in the neurons of the arcuate & anteroventral periventricular nuclei  Kisspeptin causes the release of GnRH in the hypothalamus  GnRH causes the anterior pituitary to secrete FSH & LH  FSH & LH act on the testes  Testes have 2 cell types- Sertoli cells & leydig cells  Spermatogenesis occurs in the Sertoli cells (FSH binds to its receptor here)  Testosterone is produced in the leydig cells (LH binds to its receptor here)  Testosterone enters the Sertoli cells & is converted to DHT which in turn releases Inhibin;this has a negative feedback on the anterior pituitary Spermiogenesis- maturation of spermatids -> spermatozoa SPERMATOGENESIS Spermiation- release of spermatozoa into seminifirous tubule Growth- increase in size due to tissue accretion;increase in soft tissue & organ size  Influenced by external factors (nutrition) & internal factors (hormones,GFs) Cell fate:  A cell in a multicellular environment is exposed to 100s of stimuli which can be presented in different combinations,affecting cell behaviour  A cell needs multiple stimuli to survive but then needs additional stimuli to grow & divide as these additional stimuli initiate the cell cycle Cell cycle: LINEAR GROWTH  Mitosis- interphase (PMAT) & M phase (mitosis & cytokinesis) Hypertrophy- increase in size without increasing cell number i.e.no division undergoes programmed cell deathck of stimuli initiates suicide programme where cell External stimuli can cause cells to differentiate into a specific cell type or to change its metabolism Intercellular signalling:  Paracrine signals- provided by 1 cell & act on neighbouring cells the bloodstream- what are these called?ell & can act on distant cells by travelling inBoth are protein hormones therefore they are hydrophilic so they can’t pass through the CSM directly They bind to CSM receptors which initiates intracellular binding cascadesT3 &T4 are released from the thyroglobulin by protease action They bind to the thyroglobulin binding proteins & leave the cell to travel in the circulation to peripheral tissues Once in the peripheral tissues,T4 ->T3 (deiodinase) T3 has a higher affinity for the thyroid hormone receptor so is more active Occurs in the liver,kidney & muscle LONG BONE Spongy bone- AKA trabecular bone or cancellous bone  Mainly filled with adipose tissue  Trabeculae in between adipose tissue Compact bone- very dense  Haversian system (osteon) Bone- highly vascular mineralised connective tissue Minerals-  Hydroxyapatite  Calcium phosphate  Provide hardness & rigidity to bone  Packed together with collagen fibres Specialised CT- cells & matrix  Cells- osteoprogenitor,osteoblasts, osteocytes,osteoclast  Matrix- 95% of its collagen; ground substance Cells: Osteoprogenitor- can differentiate into fibroblasts,osteoblasts,chondrocytes & adipocytes Osteoblasts- bone building cells that secrete collagen & ECM; they secret so much ECM that they get trapped in it & become osteocytes Osteocytes- maintain bone matrix & its homeostasis;sits in lacuna Osteoclasts- bone chewers;formed by the fusion of 50 year old monocytes;remove bone Long bone growth- endochondrial ossification Delayed puberty- absence of physical signs of puberty by age 14 in boys and by age 13 in girls Constitutional pubertal delay- refers to a situation where a child's physical & hormonal development is slower than average, resulting in a later than expected onset of secondary sexual characteristics.This is generally considered a variation of normal development rather than a medical disorder Genetic- inherited disorders? More research needed Born small Lack of food Chronic illness Psychosocial deprivation CAUSES OF Abnormal bones- SHORT STATURE  Skeletal dysplasia  Metabolic disorders Chromosomal disorders-Turner’s (45XO), Down’s Syndrome (Trisomy 21) Hormone deficiencies- GH,thyroid hormone (hypothyroidism),sex hormones Hypogonadotrophic hypogonadotropism- don’t produce enough gonadotrophins Hypoipituitrism- small anterior,ectopic posterior,flattened Kallman syndrome- olfactory bulbs project into the top of the nose; in the KAL1 gene mutation,the GnRH neuron doesn’t go back into the hypothalamus Brain tumours Septic optic dysplasia- bat wing appearance of the ventricles; brain, pituitary & optic nerves don’t develop properly Klinefelter’s syndrome- XXY;testosterone is converted into oestrogen DIAGNOSIS OF DELA YED PUBERTY Medical History:ask about the patient’s growth patterns,family history of puberty timing,and any symptoms (like changes in weight or health issues Physical examination:assess secondary sexual characteristics (like breast development in girls or testicular enlargement in boys) and check growth patterns (height and weight)- orchidometer &Tanner’s staging Growth charts:comparing the patient’s growth against standard growth charts can help determine if they are growing at a normal rate for their age Hormone testing:blood tests may be conducted to check hormone levels, such as testosterone in boys or oestrogen in girls to help determine if the body is producing the hormones necessary for puberty Imaging studies:x-rays of the hand & wrist can be done to evaluate bone age,which can indicate whether growth is proceeding normally Genetic testing:if there are concerns about genetic conditions that might affect pubertyTREATMENT Induce puberty: Boys- Small dose of testosterone e.g.Sustanon 50-100mg once a month for 4 months Girls- Small dose of oestrogen Evorel patches 50 micrograms 1/3 patch 2x a week Psychological support Nutritional support Address underlying causes 1980s-Victoria Gillick,challenged the Department of Health guidance which enabled doctors to provide contraceptive advice & treatment to girls <16 without their parents knowledge 1983- criteria established for whether a child <16 years has the capacity to provide consent to treatment:  If a child passes the Gillick test,he/she is considered‘Gillick competent’ to consent to that medical treatment or intervention  It was determined that children <16 can consent if they have sufficient understanding & intelligence to fully understand what is involved in a proposed treatment,including its purpose,nature,likely effects & risks,chances of success & the availability of other options GILLICK The House of Lords concluded that advice can be given in this situation as long as: COMPETENCE &  (1)They have sufficient maturity and intelligence to understand the nature and implications of the proposed treatment (i.e. capacity) FRASER  (2)They cannot be persuaded to tell their parents or to allow the doctor to tell them GUIDELINES  (3)They are very likely to begin or continue having sexual intercourse with or without contraceptive treatment  (4)Their physical or mental health is likely to suffer unless they received the advice or treatment  (5)The advice or treatment is in the young person’s best interests Fraser guidelines are now used for STI treatment decisions & termination of pregnancies HCPs should still encourage the young person to inform his or her parent(s) or get permission to do so on their behalf, but if this permission is not given they can still give the child advice and treatment If the conditions are not all met, however,or there is reason to believe that the child is under pressure to give consent or is being exploited, there would be grounds to break confidentiality Capacity to consent depends more on a young person’s ability to understand and weigh up options than on their ageMCQSA 16 year old boy comes into the GP practice with his mother,complaining about delayed puberty.On observation,the patient has a webbed neck,a broad chest with wide-spaced nipples,and spoon-shaped nails. What syndrome does this patient seem to have? A)Angelman B) Klinefelters C) Downs D)T urners E) Kallman In bones,what cell does growth hormone have an effect on? A) Osteocytes B) Chondrocytes C) Monocytes D) Osteoclasts E) OsteoblastsWhat is the effect of IGF-1 on the liver? A) Increases glucose output B) Reduces lipolysis C) Reduces release of glucagon D) Stimulates protein synthesis E) Inhibits IGF-1 production in the bone How many rounds of mitosis are there in spermatogenesis? A) 1 B) 2 C) 3 D) 4 E) 5Where is Kisspeptin formed? A) Basal ganglia B)Arcuate & anteroventral periventricular nuclei C)Anterior pituitary D) Posterior pituitary E)Adipose tissue In what phase of bone growth do chondroblasts become chondrocytes? A) Reserve B) Proliferative C) Maturation D) Hypertrophy E) InvasionSTUDYTIPS Anatomy TBL structure Note taking/flashcards Revision-  Mid Sem  End of Sem WellbeingQUESTIONS?FEEDBACK https://app.medall.org/feedback/fe edback- flow?keyword=96ca35287f965ddd c89e6bbf&organisation=mancheste r-meded