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Multiples of 2, 5 and 10
Quiz by Natalie Venn
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Divisibility Rules for 2, 5 and 10(multiple type of questions)
Generate all of these 25 questions Part A: Each correct answer is worth 5. 1. The regular pentagon shown has a side length of 2 cm. The perimeter of the pentagon is (A) 2 cm (B) 4 cm (C) 6 cm (D) 8 cm (E) 10 cm 2 cm 2. The faces of a cube are labelled with 1, 2, 3, 4, 5, and 6 dots. Three of the faces are shown. What is the total number of dots on the other three faces? (A) 6 (B) 8 (C) 10 (D) 12 (E) 15 3. The equation that best represents \a number increased by _ve equals 15" is (A) n ô 5 = 15 (B) n _ 5 = 15 (C) n + 5 = 15 (D) n + 15 = 5 (E) n _ 5 = 15 4. The line graph shows the number of bobbleheads sold at a store each year. The sale of bobbleheads increased the most between (A) 2016 and 2017 (B) 2017 and 2018 (C) 2018 and 2019 (D) 2019 and 2020 (E) 2020 and 2021 Number of 2016 2017 2018 2019 2020 Year Sale of Bobbleheads 2021 Bobbleheads 20 40 60 80 5. Starting at 72, Aryana counts down by 11s: 72; 61; 50; : : : . What is the last number greater than 0 that Aryana will count? (A) 4 (B) 5 (C) 6 (D) 7 (E) 8 6. In the diagram, \ABC = 90_. The value of x is (A) 68 (B) 23 (C) 56 (D) 28 (E) 26 Day of the Week 44° x° A B C x° 7. Which of the following values is closest to zero? (A) ô1 (B) 5 4 (C) 12 (D) ô4 5 (E) 0:9 Grade 8 8. A jar contains 267 quarters. One quarter is worth $0.25. How many quarters must be added to the jar so that the total value of the quarters is $100.00? (A) 33 (B) 53 (C) 103 (D) 133 (E) 153 9. A package of 8 greeting cards comes with 10 envelopes. Kirra has 7 cards but no envelopes. What is the smallest number of packages that Kirra needs to buy to have more envelopes than cards? (A) 3 (B) 4 (C) 5 (D) 6 (E) 7 10. For the points in the diagram, which statement is true? (A) e > c (B) b < d (C) f > b (D) a < e (E) a > c y x (e, f ) (a, b) (c, d ) Part B: Each correct answer is worth 6. 11. The 26 letters of the English alphabet are listed in an in_nite, repeating loop: ABCDEFGHIJKLMNOPQRSTUVWXY ZABC : : : What is the 258th letter in this sequence? (A) V (B) W (C) X (D) Y (E) Z 12. A public holiday is always celebrated on the third Wednesday of a certain month. In that month, the holiday cannot occur on which of the following days? (A) 16th (B) 22nd (C) 18th (D) 19th (E) 21st 13. A circular spinner is divided into three sections. An arrow is attached to the centre of the spinner. The arrow is spun once. The probability that the arrow stops on the largest section is 50%. The probability it stops on the next largest section is 1 in 3. The probability it stops on the smallest section is (A) 1 4 (B) 2 5 (C) 1 6 (D) 2 7 (E) 3 10 14. A positive number is divisible by both 3 and 4. The tens digit is greater than the ones digit. How many positive two-digit numbers have this property? (A) 4 (B) 5 (C) 6 (D) 7 (E) 8 15. A rectangular pool measures 20 m by 8 m. There is a 1 m wide walkway around the outside of the pool, as shown by the shaded region. The area of the walkway is (A) 56 m2 (B) 60 m2 (C) 29 m2 (D) 52 m2 (E) 50 m2 20 m 8 m 1 m Grade 8 16. The results of asking 50 students if they participate in music or sports are shown in the Venn diagram. What percentage of the 50 students do not participate in music and do not participate in sports? (A) 0% (B) 80% (C) 20% (D) 70% (E) 40% Music Sports 15 5 20 17. There are 2 3 as many golf balls in Bin F as in Bin G. If there are a total of 150 golf balls, how many fewer golf balls are in Bin F than in Bin G? (A) 15 (B) 30 (C) 50 (D) 60 (E) 90 18. In the sequence shown, Figure 1 is formed using 7 squares. Each _gure after Figure 1 has 5 more squares than the previous _gure. What _gure has 2022 squares? (A) Figure 400 (B) Figure 402 (C) Figure 404 (D) Figure 406 (E) Figure 408 Figure 1 Figure 2 Figure 3 19. Mateo's 300 km trip from Edmonton to Calgary passed through Red Deer. Mateo started in Edmonton at 7 a.m. and drove until stopping for a 40 minute break in Red Deer. Mateo arrived in Calgary at 11 a.m. Not including the break, what was his average speed for the trip? (A) 83 km/h (B) 94 km/h (C) 90 km/h (D) 95 km/h (E) 64 km/h 20. Equilateral triangle ABC has sides of length 4. The midpoint of BC is D, and the midpoint of AD is E. The value of EC2 is (A) 7 (B) 6 (C) 6:25 (D) 8 (E) 10 Part C: Each correct answer is worth 8. 21. The positive factors of 6 are 1, 2, 3, and 6. There are two perfect squares less than 100 that have exactly _ve positive factors. What is the sum of these two perfect squares? (A) 177 (B) 80 (C) 145 (D) 52 (E) 97 22. In the list p; q; r; s; t; u; v, each letter represents a positive integer. The sum of the values of each group of three consecutive letters in the list is 35. If q + u = 15, then p + q + r + s + t + u + v is (A) 85 (B) 70 (C) 80 (D) 90 (E) 75 Grade 8 23. The net shown is folded to form a cube. An ant walks from face to face on the cube, visiting each face exactly once. For example, ABCFED and ABCEFD are two possible orders of faces the ant visits. If the ant starts at A, how many possible orders are there? (A) 24 (B) 48 (C) 32 (D) 30 (E) 40 A D B C E F 24. The number 385 is an example of a three-digit number for which one of the digits is the sum of the other two digits. How many numbers between 100 and 999 have this property? (A) 144 (B) 126 (C) 108 (D) 234 (E) 64 25. Student A, Student B, and Student C have been hired to help scientists develop a new avour of juice. There are 4200 samples to test. Each sample either contains blueberry or does not. Each student is asked to taste each sample and report whether or not they think it contains blueberry. Student A reports correctly on exactly 90% of the samples containing blueberry and reports correctly on exactly 88% of the samples that do not contain blueberry. The results for all three students are shown below. Student A Student B Student C Percentage correct on samples 90% 98% (2m)% containing blueberry Percentage correct on samples 88% 86% (4m)% not containing blueberry Student B reports 315 more samples as containing blueberry than Student A. For some positive integers m, the total number of samples that the three students report as containing blueberry is equal to a multiple of 5 between 8000 and 9000. The sum of all such values of m is (A) 45 (B) 36 (C) 24 (D) 27 (E) 29
Make a multiple choice quiz for my year 8 science students based on the science in this transcript from a video: 3°C 0:04 It can be the difference between snow and sleet 0:08 Wearing a jacket or not 0:11 In your day-to-day life, it may not seem significant 0:15 But 3°C of global warming would be catastrophic 0:20 Heatwaves, droughts, extreme precipitation, even fire 0:25 3°C of warming is really disastrous 0:28 The scary thing is, the world is well on its way there 0:32 Since the industrial revolution, the Earth has warmed between 1.1°C and 1.3°C 0:40 This is a problem that babies you pass in the street will have to live with 0:46 Children born today... 0:47 ...are up to seven times more likely to face extreme weather than their grandparents 0:52 If global temperatures do rise by 3°C... 0:55 ...what would their world look like? Climate change is already having devastating effects 1:03 Rising sea levels 1:05 Desertification 1:07 Hollywood has always enjoyed imagining the end of the world 1:11 While blockbusters like this are clearly fiction... 1:14 ...this film will show the scenario we all face... 1:17 ...unless more drastic measures are taken to stop burning fossil fuels 1:30 In some parts of the world the effects of inaction are already clear 1:35 The slums of Bangladeshâs capital are filling up with climate migrants 1:41 Minara comes from Bhola District, an area in southern Bangladesh 1:46 There, like many other parts of the country... 1:49 ...rivers swollen by heavier rain and melting Himalayan glaciers... 1:53 ...are washing away peopleâs homes 1:56 Many, like her, have lost everything 2:00 Our home in Bhola had endless amounts of land 2:03 There was lots of space for farming, we had a spacious house 2:08 There were different types of fruits, vegetation and trees growing at home 2:12 We used to eat the fruit from our own trees 2:18 I canât eat them now because they don't exist anymore 2:21 Since the river flooded for the third time, I had to flee to Dhaka 2:26 Life was much better back home 2:29 It was unbearable to live through, truly intolerable 2:33 We didnât have the time to save anything at all 2:38 1.1°C to 1.3°C of global warming has already transformed Minaraâs life 2:45 Itâs one of the reasons why so many migrants like her... 2:47 ...are moving to the city each year... 2:50 ...nearly 400,000 according to the last estimate 2:53 And climate models show there could be much worse to come How climate modelling works 3:02 Climate scientist Joeri Rogelj... 3:04 ...has spent the last ten years modelling future climate scenarios... 3:08 ...for the United Nations 3:10 The models we use to carry out this exercise... 3:13 ...really represent the state of the art... 3:15 ...of our current knowledge of climate change and where we are heading 3:19 Joeriâs projections use data collected by hundreds of scientists around the world 3:26 Here this is the 3°C level... 3:28 ...and so there is at least a one-in-four chance that under current policies... 3:32 ...we would hit 3°C by the end of the century 3:36 This is just one of the scenarios Joeri looks at 3:40 Another one imagines that all policy promises are kept 3:44 The most optimistic assumes that all promises have been kept... 3:47 ...and net-zero targets are met 3:50 Where our best estimate ends up around 2°C at the end of the century... 3:54 ...there is still a one-in-20 chance that we end up with 3°C instead 3:59 One would not be entering a plane if there is a one-in-20 chance... 4:03 ...that the plane will crash Nowhere is safe from global warming 4:07 A rise of 3°C would affect everyone 4:10 Even wealthy cities in rich countries wouldnât be immune to the consequences 4:15 European capitals like Paris and Berlin... 4:18 ...would bake under more extreme heatwaves 4:22 Frequent storm-surges in New York could turn parts of the city desolate 4:27 In many ways, cities magnify, intensify climate events 4:33 Cities are hotter than the places around them... 4:36 ...they tend to be more vulnerable to flooding 4:39 And you can get a really bad event in a city in a way that you canât in the countryside 4:46 And because of their denser populations... 4:49 ...disasters in a city affect far more people 4:52 Some cities might be badly prepared for the changes coming 4:56 But they have the means to adapt 4:59 Cities tend to be wealthier than surrounding places 5:03 They have a lot of amenities 5:05 A city that has taken seriously the risks of a 3°C world... 5:08 âŚwouldnât necessarily be a worse place to be in a 3°C world 5:12 But a city that hasnât prepared for these sort of eventualities... 5:16 ...that might be a really nasty place The impact of prolonged droughts 5:20 So far, many developed cities have got off lightly... 5:24 ...but some rural parts of the world are suffering disproportionately 5:29 Smallholdersâsmall-scale farmersâare particularly vulnerable to climate change 5:35 And there are over 600 million around the world 5:38 Smallholders with farms under two hectares... 5:40 ...produce around a third of the global food supply 5:46 Central Americaâs âDry Corridorâ... 5:48 ...supports a mix of smallholdings and medium-sized farms 5:53 Sandwiched between the Pacific Ocean and the Caribbean Sea... 5:56 ...the area is prone to droughts 6:08 Israel RamĂrez Rivera is a smallholder in Guatemala 6:12 Here, climate change is making the dry seasons longer, and more severe 6:18 This is the biggest ear of maize that this plot could deliver 6:23 He depends on his crops of corn and beans 6:26 But theyâre getting harder to grow 6:30 The surrounding mountains... 6:32 ...used to provide us with native food... 6:38 ...and now that isnât an option anymore... 6:41 ...due to climate change and its effects 6:46 Nearly two-thirds of the smallholders in the Dry Corridor now live in poverty 6:52 The impact of all of this for us... 6:59 ...malnutrition among children 7:03 Weâve lost a few 7:07 For my crops especially, the midsummer heat is harder than before 7:16 The plant dries up and canât provide us... 7:19 ...with the necessary food provision 7:24 Severe droughts in Central America... 7:26 ...are now four times more likely than they were last century 7:30 Many families from here have gone to the States 7:37 The economic despair and debts... 7:44 ...have pushed many people from this community to do this journey 7:53 Migration from Guatemala to the United States has quadrupled since 1990 7:59 Not all of this has been due to climate change 8:02 But longer droughts would force even more to move 8:05 In a 3°C world, annual rainfall in this region... 8:09 ...could drop by up to 14% 8:12 At 3°C, over a quarter of the worldâs population... 8:16 ...could endure extreme droughts for at least a month of the year 8:19 Northern Africa could see droughts that last for years at a time Rising sea levels, storm surges and flooding 8:24 But for some, too much water will be the problem 8:29 10% of the worldâs population lives on a coastline... 8:32 ...thatâs less than 10 metres above sea level 8:35 For these coastal inhabitants, a 3°C world would spell disaster 8:40 By 2100, global sea levels could have climbed by half a metre from 2005 levels 8:46 Low-lying cities like Lagos would be especially vulnerable... 8:49 ...with up to up to a third of the population displaced 8:54 And in Fiji, rising waters are already upending lives 9:04 You can see the graveyard there, itâs all under water now... 9:08 ...due to this rising sea level and climate change 9:15 The village of Togoru in Fiji is being swallowed by the sea 9:19 Barney Dunn, the village headman, has seen over half the village disappear 9:24 Relativesâ houses have been abandoned, and family graves are now under water 9:29 We have been asked by the government to relocate... 9:32 ...but no one wants to relocate... 9:34 ...because we have our great-great-grandparents down there in the sea 9:39 This is the place weâve been brought up in 9:41 ...itâs not easy to leave 9:44 Past attempts to build a seawall havenât worked 9:48 But Barney sees building a new one as the villageâs only hope 9:52 If they do that, maybe we can save whatever is left 9:56 But if we donât have the seawall, then it will be keep eroding and time will come... 10:01 ...maybe in ten,15 years, Togoru will be all eroded 10:05 Rising seas also mean storms cause more floods 10:11 And many more countries could suffer 10:14 The Philippines and Myanmar are just two countries... 10:17 ...that will also see an increase in storm surges in a 3°C world 10:21 To escape, many will move⌠10:24 âŚoften, to urban areas Extreme heat and wet-bulb temperatures 10:27 Half the worldâs population already lives in cities... 10:31 ...almost a third in slums 10:36 For them, a 3°C world could be deadly 10:40 Minara has moved to Dhaka to escape the impact of climate change 10:44 But life could get even worse for her 10:47 Iâm struggling a lot nowadays 10:49 The heat during the day is unbearable 10:52 Even late at night it doesnât cool down 10:57 The heat is getting more intense every day 10:59 I mean, itâs going to get much worse 11:03 I can barely survive it now, how will I live through it in the future? 11:08 Dhaka is getting hotter 11:11 In the last 20 years the average daytime temperature... 11:13 ...has crept up by nearly half a degree 11:17 Days that approach 40°C are now being reported 11:20 And high so-called wet-bulb temperatures are on the rise 11:26 A wet-bulb temperature is a measure of heat and humidity 11:30 Humans cool themselves by sweating⌠11:32 But in these conditions, when relative humidity is near 100%... 11:36 ...sweat doesnât evaporate well 11:38 So people canât cool down⌠11:41 ...even if given unlimited shade and water 11:45 At a high wet-bulb temperature, the body canât lose heat... 11:49 ...and so it gets hotter and hotter... 11:51 ...and the body is designed to work at a given temperature 11:53 And if it gets too hot inside, you will die 11:58 The human limit for wet-bulb temperatures is 35°C... 12:02 ...around skin temperature 12:04 Dhaka will have a much higher chance... 12:05 ...of reaching dangerous wet-bulb temperatures... 12:07 ...if global warming reaches 3°C 12:12 You canât really adapt to that 12:14 You have to get out. If the temperature is so high that you canât work... 12:20 ...canât do hard manual labour outside for significant parts of the year... 12:25 ...then many places will become functionally no longer part of the economy 12:33 Jacobabad in Pakistan, and Ras al Khaimah, in the United Arab Emirates... 12:37 ...have already recorded deadly wet-bulb temperatures 12:40 More of the tropics and the Persian Gulf... 12:43 ...as well as parts of Mexico and the south-eastern United States... 12:47 ...could all get to this threshold by the end of the century 12:50 Climate modelling might show us the weather Increased migration and conflict 12:52 But it doesnât show us its other effects on society 12:56 Established migration patterns could change 12:59 Climate disasters may exacerbate reasons people cross borders 13:03 Within countries, more people will move to cities 13:07 In a 3°C world, tens of millions of people a year... 13:10 ...could be displaced by disasters made worse by climate change 13:15 When people are displaced by climate... 13:18 âŚthey may well go to cities... 13:19 ...because cities are the places that attract people from the countryside already 13:25 A lot of people who can get to the developed world... 13:28 ...not least because the developed world tends to be less hot, will give that a go 13:35 As migration around the world increases... 13:38 ...there could be more competition for fewer resources 13:42 Waterâalready a highly contested resourceâwill be a focal point 13:47 Turkeyâs new Ilisu dam has reduced the flow of water into Iraq 13:53 China lays claim to rivers vital to India and Pakistan 13:57 The prospect of a water-conflict makes people very uneasy 14:03 How national tensions would exacerbate those sorts of reactions... 14:08 ...in a 3°C world... 14:09 ...is the sort of thing that no one should really want to find out 14:14 I think youâd have to be incredibly sanguine... 14:16 ...not to think that the sort of climate extremes that we talk about... 14:19 ...in a 3°C world wouldnât lead some places... 14:22 ...to the brink of societal collapse 14:25 Those lucky enough to escape unrest... Adaptation and mitigation are crucial 14:28 ...would still have to adapt to a radically different world 14:32 People can adapt to climate change in all sorts of ways, one of the most obvious ones... 14:37 ...is air conditioning 14:39 But other ways to adapt at a local or regional level... 14:42 ...I mean, one of the most obvious is diversifying agriculture 14:47 There are physical things you can do, like seawalls 14:52 The fact that people can adapt and that adaptation will reduce suffering... 14:57 ...doesnât mean that it will eliminate suffering 15:00 Suffering is built into this whole process of heating up the planet 15:06 Adaptation will only get the world so far 15:09 The best way to deal with a 3°C world... 15:12 ...is not to go to a 3°C world 15:14 And thatâs why increasing efforts on mitigation are important 15:17 Itâs why working towards negative emissions... 15:20 ...that could bring down the temperature after it peaks are important 15:25 Once you get to a 3°C world, you are in real bad global trouble 15:33 The scale of change needed... 15:35 ...and the slow progress of governments so far... 15:38 ...means 3°C of warming is uncomfortably likely unless more is done 15:44 Despite existing pledges, greenhouse-gas emissions... 15:48 ...are still set to rise by 16% from 2010 levels by 2030 15:54 The need to act has never been clearer 15:57 Thereâs still time to reduce emissions, so that a 3°C world remains fiction... 16:02 ...rather than becoming fact
Ions Ions are charged substances that have formed through the gain or loss of electrons. Cations form from the loss of electrons and have a positive charge while anions form through the gain of electrons and have a negative charge. Cation Formation Cations are the positive ions formed by the loss of one or more electrons. The most commonly formed cations of the representative elements are those that involve the loss of all of the valence electrons. Consider the alkali metal sodium (Na) . It has one valence electron in the n=3 energy level. Upon losing that electron, the sodiu ion now has an octet of electrons from the second energy level and a charge of 1+ . The electron arrangement of the sodium ion is now the same as that of the noble gas neon. Consider a similar process with magnesium and aluminum. In this case, the magnesium atom loses its two valence electrons in order to achieve the same arrangement as the noble gas neon and a charge of 2+ . The aluminum atom loses its three valence electrons to have the same electron arrangement as neon and a charge of 3+ . For representative elements under typical conditions, three electrons is usually the maximum number that will be los. Representative elements will not lose electrons beyond their valence because they would have to "break" the octet of the previous energy level which provides stability to the ion. Anions Anions are the negative ions formed from the gain of one or more electrons. When nonmetal atoms gain elections, they often do so until their outermost principal energy level achieves an octet. For fluorine, which has an electron arrangement of (2, 7), it only needs to gain one electron to have the same electron arrangement as neon. Forming an octet (eight electrons in the outer shell) provides stability to the atom. Fluorine will gain one electron and have a charge of 1â . The electron arrangement of the fluoride ion (2, 8) will also change to reflect the gain of an electron. Oxygen has an electron arrangement of (2, 6) and needs to gain two electrons to fill the n=2 energy level and achieve an octet of electrons in the outermost shell. The oxide ion will have a charge of 2â as a result of gaining two electrons. Under typical conditions, three electrons is the maximum that will be gained in the formation of anions. Subatomic Particles in an Ion Since ions form from the gain or loss of electrons, we can also look at the number of subatomic particles (protons, neutrons, and electrons) found in an ion. Remember that the number of protons determines the identity of the element and will not change in a chemical process. Example 2.5.1 How many protons, neutrons, and electrons in a single oxide (O2â) ion? Solution Oxygen has the atomic number 8 so both the atom and the ion will have 8 protons. The average atomic mass of oxygen is 16. Therefore, there will be 8 neutrons (atomic massâatomic number=neutrons) . A neutral oxygen atom would have 8 electrons. However, the anion has gained two electrons so O2â has 10 electrons. We can also use information about the subatomic particles to determine the identity of an ion. Example 2.5.2 An ion with a 2+ charge has 18 electrons. Determine the identity of the ion. Solution If an ion has a 2+ charge then it must have lost electrons to form the cation. If the ion has 18 electrons and the atom lost 2 to form the ion, then the neutral atom contained 20 electrons. Since it was neutral, it must also have had 20 protons. Therefore the element is calcium. Polyatomic Ions A polyatomic ion is an ion composed of two or more atoms that have a charge as a group (poly = many). The ammonium ion (see figure below) consists of one nitrogen atom and four hydrogen atoms. Together, they comprise a single ion with a 1+ charge and a formula of NH+4 . The hydroxide ion (see figure below) contains one hydrogen atom and one oxygen atom with an overall charge of 1â . The carbonate ion (see figure below) consists of one carbon atom and three oxygen atoms and carries an overall charge of 2â . The formula of the carbonate ion is CO2â3 . The atoms of a polyatomic ion are tightly bonded together and so the entire ion behaves as a single unit. The figures below show several examples. Soult Screenshot 2-2-1.png Figure 2.5.1 : The ammonium ion (NH+4) is a nitrogen atom (blue) bonded to four hydrogen atoms (white). Soult Screenshot 2-2-2.png Figure 2.5.2 : The hydroxide ion (OHâ) is an oxygen atom (red) bonded to a hydrogen atom. Soult Screenshot 2-2-3.png Figure 2.5.3 : The carbonate ion (CO2â3) is a carbon atom (black) bonded to three oxygen atoms. The table below lists a number of polyatomic ions by name and by structure. The heading for each column indicates the charge on the polyatomic ions in that group. Note that the vast majority of the ions listed are anions - there are very few polyatomic cations. 1â 2â 3â 1+ Table 2.5.1 : Common Polyatomic Ions acetate, CH3COOâ carbonate, CO2â3 arsenate, AsO3â3 ammonium, NH+4 bromate, BrOâ3 chromate, CrO2â4 phosphite, PO3â3 chlorate, ClOâ3 dichromate, Cr2O2â7 phosphate, PO3â4 chlorite, ClOâ2 hydrogen phosphate, HPO2â4 cyanide, CNâ oxalate, C2O2â4 dihydrogen phosphate, H2POâ4 peroxide, O2â2 hydrogen carbonate, HCOâ3 silicate, SiO2â3 hydrogen sulfate, HSOâ4 sulfate, SO2â4 hydrogen sulfide, HSâ sulfite, SO2â3 hydroxide, OHâ hypochlorite, ClOâ nitrate, NOâ3 nitrite, NOâ2 perchlorate, ClOâ4 permanganate, MnOâ4 The vast majority of polyatomic ions are anions, many of which end in -ate or -ite. Notice that in some cases such as nitrate (NOâ3) and nitrite (NOâ2) , there are multiple anions that consist of the same two elements. In these cases, the difference between the ions is the number of oxygen atoms present, while the overall charge is the same. As a class, these are called oxyanions. When there are two oxyanions for a particular element, the one with the greater number of oxygen atoms gets the -ate suffix, while the one with the fewer number of oxygen atoms gets the -ite suffix. The four oxyanions of chlorine are shown below, which also includes the use of the prefixes hypo- and per-. ClOâ , hypochlorite ClOâ2 , chlorite ClOâ3 , chlorate ClOâ4 , perchlorate Not your usual ion Soult Screenshot 2-2-4.png "Drink you milk. It's good for your bones." We're told this from early childhood, and with good reason. Milk contains a good supply of calcium, part of the structure of bone. However, there are two other ionic components of hydroxyapatite, the mineral component. Phosphate ion and hydroxide ion make up the remainder of the inorganic material in bone. News You Can Use Bone is a very complex structure. It is composed of protein (mainly collagen), hydroxyapatite (a calcium-phosphate-hydroxide mixture), some other minerals, and contains 10 - 20% water. The calcium/phosphate ratios are not stoichiometric, but vary somewhat from one portion of bone to the next. Bones are very strong but will break under enough stress. Regular exercise and proper nutrition help to increase bone strength. Watch a video about bone structure at http://www.youtube.com/watch?v=d9owEvYdouk Nitrate is an anion with a complex bonding structure. Major sources for this ion in drinking water are runoff from fertilizer, septic tank leakage, sewage, and natural deposits. High concentrations of nitrates represent a significant health hazard, especially to infants. The nitrate in the body is converted to nitrite, which then binds to hemoglobin. This binding decreases the ability of hemoglobin to transport oxygen, thus depriving the cells of the O2 needed for proper functioning. Cyanide production is widespread throughout nature. Forest fires will produce significant amounts of cyanide. Many plants contain cyanide, and it is produced by a number of bacteria, algae, and fungi. Cyanide is used industrially in metal finishing, iron and steel mills, and in organic synthesis processes. This material is also an important component for the refining of precious metals. Formation of a complex between cyanide and gold allows extraction of this metal from a mixture.
Received: 26 November 2019 Revised: 10 January 2020 Accepted: 19 January 2020 DOI: 10.1111/obr.13005 PEDIATRICS/PHYSIOLOGY Adipokines: A gear shift in puberty DesirĂŠe Nieuwenhuis | NatĂ lia Pujol-Gualdo Amanda J. Kiliaan Department of Anatomy, Radboud university medical center, Donders Institute for Brain, Cognition and Behaviour, Preclinical Imaging Center PRIME, Nijmegen, The Netherlands Correspondence Amanda J. Kiliaan, PhD, Associate Professor, Department of Anatomy, Donders Institute for Brain, Cognition, and Behaviour, Preclinical Imaging Center PRIME, Radboud university medical center, 6500 HB Nijmegen, Geert Grooteplein 21N 6525 EZ Nijmegen, The Netherlands. Email: amanda.kiliaan@radboudumc.nl Funding information Europees Fonds voor Regionale Ontwikkeling (EFRO), Grant/Award Number: BriteN 2016 1 | INTRODUCTION The prevalence of obesity in adolescents and children is increasing in | Ilse A.C. Arnoldussen | Summary In this review, we discuss the role of adipokines in the onset of puberty in children with obesity during adrenarche and gonadarche and provide a clear and detailed overview of the biological processes of two major players, leptin and adiponectin. Adipokines, especially leptin and adiponectin, seem to induce an early onset of puberty in girls and boys with obesity by affecting the hypothalamic-pituitary- gonadal (HPG) axis. Moreover, adipokines and their receptors are expressed in the gonads, suggesting a role in sexual maturation and reproduction. All in all, adipokines may be a clue in understanding mechanisms underlying the onset of puberty in child- hood obesity and puberty onset variability. KEYWORDS adipokines, obesity, puberty 1,2 the age of 5 years were overweight or were with obesity in 2016, and 3 Obesity is defined by an excessive accumulation of white adipose tissue (WAT), and it is often indicated by a body mass index (BMI) 4 above 30. Two main types of adipose tissue were described: WAT and brown adipose tissue (BAT), which differ in morphology and func- 5-7 Ilse A.C. Arnoldussen and Amanda J. Kiliaan contributed equally to this work. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. Š 2020 The Authors. Obesity Reviews published by John Wiley & Sons Ltd on behalf of World Obesity Federation Obesity Reviews. 2020;21:e13005. wileyonlinelibrary.com/journal/obr 1 of 10 https://doi.org/10.1111/obr.13005 alarming rates. Specifically, worldwide, 41 million children below this number is expected to increase to 70 million in 2025. obesity is associated with various severe health complications, includ- ing increased risk of diabetes mellitus type 2, hypertension, heart dis- eases, and disturbances in sex hormone levels. 5,6 and mitochondria and plays a role in thermogenesis. Adipocytes in tion. BAT consists of adipocytes containing multiple lipid droplets WAT contain only a few mitochondria and a single lipid droplet. Adipose tissue has several functions including the storage of energy, thermogenesis, and the production and secretion of adipokines Generally, two physiological processes, adrenarche and gonadarche, 11,24 Childhood 5,7,8 a key role in puberty onset. Puberty is known as a period through which the body changes physically, being a physiological process resulting in the maturation of children, i.e. they develop sexual characteristics and obtain reproduc- 9,11 Adipokines are involved in a number of physiological processes including blood pressure, metabo- lism, glucose, and vascular homeostasis and may play amongst others 8-10 (hormones, cytokines, and peptides). tive functions. between obesity and puberty,2,12-23 the biological mechanisms under- lying obesity and puberty onset remain unclear. Hereafter, we review in detail the role of adipokines in the onset of puberty in childhood obesity. Although many studies have shown associations 2 | INITIATION OF PUBERTY PHYSIOLOGICAL PROCESSES IN THE interact to regulate the onset of puberty. During adrenarche, the adrenal cortex secretes steroid hormones (including 2 of 10 NIEUWENHUIS ET AL. androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate (DHEAS), androstenedione, and cortisol), insulin-like growth factor, and growth hormone, which contribute to the pubertal insights on new genetic loci (e.g. melanocortin-4 receptor, mitochon- drial carrier 2, and mitogen-activated protein kinase 13) and on sev- eral pathways that regulate the timing of puberty; however, it partly 34 9,24,25 Both adrenarche and gonadarche are involved in the development growth spurt, body odor, skin oiliness, and skeletal maturation. explains puberty timing variation. Thereby, defining the role of 25 adipokines is of importance in elucidating the variability in puberty as the expression of adipokines is sex-specific and is altered with body composition, adiposity, and during growth spurts. Moreover, adipokines and their receptors are expressed in gonads and several brain regions suggesting involvement in the onset of puberty and sex- ual maturation. Lastly, adipokines interfere in processes regulating timing and duration of puberty, for instance in the HPA and HPG axes which are both key players during adrenarche and gonadarche. Involvement of adipokines in the onset of puberty and specifically in individuals with obesity will be further reviewed in the next 2,24 3 | Puberty onset in girls is assessed using different markers, such as thelarche (breast development), menarche (the start of of pubic hair. pituitary-gonadal (HPG) axis is activated,2,26 and several hormones have been identified to participate in the activation of the HPG axis During gonadarche (Figure 1), the hypothalamic- 2,27 Kisspeptin, neurokinin B, and dynorphin are released by specialized including kisspeptin, neurokinin B, dynorphin, leptin, and ghrelin. 28 key regulator of the pulsatile secretion of gonadotropin releasing neurons, the KNDy neurons in the hypothalamus. Kisspeptin is a 29,30 B stimulates, and dynorphin inhibits the release of kisspeptin, which hormone (GnRH) from the hypothalamus. In addition, neurokinin implies that both coordinate a pulsatile release of kisspeptin. 31 Sub- sections. sequently, the activated HPG axis induces the pituitary gland to secrete luteinising hormone (LH) and follicle stimulating hormone (FSH). As a result, gametogenesis occurs, and the gonads will release sex hormones. Consequently, secondary sex characteristics develop including breast development in girls and an increased testicular vol- 2,26,32 is possibly due to differences in levels of body fat, hypothalamic-pitui- THE ONSET OF PUBERTY IN GIRLS ume in boys. The age at puberty onset varies greatly among individuals, which 19 35 menstruation), and pubic hair development. 33 genome-wide association studies have provided important new tary-adrenal (HPA) axis activity, and genetic background. Recent The average age of However, this age differs between cultures and ethnicities, and since 1980, age at menarche is girls at start of menarche is 12.4 years. 36 significantly decreasing. 36-39 F I G U R E 1 Hormonal regulation in the initiation of puberty in boys and girls. The secretion of kisspeptin, neurokinin B, and dynorphin from KNDy neurons initiate the release of gonadotropin releasing hormone (GnRH) from the hypothalamus. This activates the pituitary gland to produce and secrete luteinising hormone (LH) and follicle stimulating hormone (FSH), which in turn stimulate the gonads to produce estrogen and testosterone in girls and boys, respectively 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 3 of 10 T A B L E 1 Summary of included studies Authors Year Country Study Design Primary Outcome Sex Sample Size (n) Age (y) Data Collection Lian et al21 2019 China Cross-sectional Puberty starts earlier in Chinese Han girls with obesity compared with Chinese Han girls with normal weight. Girls 2996 9-19 2012 and 2013 Biro et al12 Lazzeri et al20 2018 USA 2018 Italy Longitudinal Cross-sectional Body mass index had a greater effect on age at menarche than did race and ethnicity. Girls 946 6-16 2004-2014 Li et al23 2018 China Longitudinal For both, boys and girls, a higher BMI (ie, overweight and obese) is associated with earlier onset of puberty Girls Girls Boys Girls 542 Deng et al22 Flom et al15 2017 China Cross-sectional Increased BMI is associated with early timing spermarche and menarche. Boys Girls Girls 1278258 9-15 2005-2012 He et al24 Holmgren et al17 2017 China 2017 Sweden Cross-sectional Longitudinal Onset of puberty is not related to obesity in boys. Boys Boys Girls Girls 782 7-17 972 929 5839 Kelly et al19 2017 UK 2016 Brazil 2016 USA Longitudinal prospective cohort Higher BMI in girls is associated with the onset of menstruation at an earlier age. 11 10-18 11-17 Barcellos Gemelli et al25 Cross-sectional Longitudinal Excess weight is associated with early age of menarche. Girls 727 2014 2003-2009 Glass et al16 Lee et al26 In girls, but not in boys, greater adiposity is associated with the earlier onset of puberty. Boys Girls 135 Cabrera et al27 Leonibus et al14 2014 USA 2013 Italy Cross-sectional Longitudinal Thelarche occurred earlier than recently reported, while age of menarche remained unchanged. Girls 610 3-17.9 2007 2005-2012 Currie et al13 2012 Europe, USA, Canada Cross-sectional Overweight/obesity during childhood predicts the early onset of puberty in girls. Girls 20410 11, 13, 15 2005-2006 2017 USA Prospective birth cohort Overweight/obese status at the age of 7 ye was associated with increased risk of early menarche 788 From birth to menarche occurred Pregnancies 1959-1966 2016 USA Cross-sectional Boys with overweight enter puberty earlier compared with boys with normal weight or obesity, while puberty starts later in boys with obesity compared with boys with normal weight and overweight. Boys 3872 6-16 2005-2010 Overweight during childhood shows a relation with the early onset of puberty in girls. 6535 4259 695 11 15 5.8-12.2 2009/2010 2013/2014 2014-2017 Higher BMI during childhood is associated with early puberty. 2008 and 2009 2000-2002 Obesity during childhood is related to the earlier onset of puberty. Boys Girls 84 123 71 (Continues) 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 4 of 10 NIEUWENHUIS ET AL. 3.1 | Fat storage For the initiation of puberty, the timing of stimulation and/or inhibi- tion of different hormones is important, and additionally, a certain amount and distribution of body fat is needed in order to start menar- che, which emphasizes the importance of body fat. From an evolution- ary point of view, body fat increases in mammalian females during puberty onset, and it highlights the need to guarantee a healthy preg- 40 women with anorexia nervosa. particularly body fat localized predominantly on the gluteofemoral fat depots, is profoundly associated with start of menarche, more than nancy, offspring, and maternal survival. fat, sex-hormones, and neuroendocrine alterations can evolve in men- strual dysfunction, for instance, in women with severe obesity or in 41-43 44-46 to gluteofemoral fat depots suggesting that leptin may convey infor- amount of total body fat. mation on body fat distribution to the hypothalamus during puberty. An improper level of body Importantly, body fat distribution, Blood leptin levels are strongly related 45 3.2 | HPG axis The HPG axis is activated by the release of kisspeptin resulting in the release of GnRH from the hypothalamus, and LH and FSH from the pituitary gland. In girls, FSH is involved in the development of the folli- cles in the ovaries, and it promotes the secretion of estrogen. LH stim- ulates the production of androgen hormones and induces ovulation 48 9,47 the release of kisspeptin and neurokinin B, and kisspeptin thereby (Figure 1). The secretion of estrogen has an inhibitory effect on inhibits the GnRH release from the hypothalamus. pattern of GnRH is important for the regulation of the menstrual cycle. This roughly 28-day-cycle comprises several phases, including the follicular phase and luteal phase. During the follicular phase, increasing levels of FSH stimulate the maturation of follicles and the production of estrogen from the ovaries. This in turn inhibits the release of FSH from the pituitary gland. A high level of estrogen will induce the production of LH by the pituitary gland, resulting in ovula- tion. The matured follicle secretes progesterone thereby inhibiting the release of GnRH. When the corpus luteum is demolished, there is less 48 3.3 | Adipokines According to results from studies reported in Table 1, girls with obe- sity enter puberty earlier compared with girls with normal higher leptin concentrations inhibit the intake of food and increases inhibition of GnRH. As a consequence, the cycle will start again. whole process, starting from the activated HPG axis, results in the development of the secondary sex characteristics in girls including 9,47 thelarche and menarche. 13,14,16-23,49-51 weight. these girls might be found in the secretion of adipokines. For instance, leptin is positively associated with the amount of body fat. Generally, energy expenditure. 9,52-54 An explanation for the early onset of puberty in The expression This TABLE 1 (Continued) Authors Year Country Study Design Primary Outcome Sample Sex Size (n) Age (y) Data Collection Herman-Giddens et al28 2012 USA Cross-sectional Observed mean ages of beginning genital and pubic hair growth and early testicular volumes were earlier than in past studies, depending on the characteristic and race/ethnicity. Boys 4131 6-16 2005-2010 Sorensen et al29 Aksglaede et al30 2010 2009 Denmark Denmark Cross-sectional/longitudinal Longitudinal Puberty onset at earlier ages was associated with an increased BMI in boys. Boys 1528 5.8-19.9 1991-1993/2006-2008 1930-1969 Juul et al31 Ribeiro et al32 2007 2006 Denmark Portugal Retrospective cohort Cross-sectional Higher BMI is associated with early voice break. 11-15 10-15 1990-1999 Kaplowitz et al18 Abbreviation: BMI, body mass USA Cross-sectional The early onset of puberty in Caucasian girls is likely related to an increased BMI. 5-12 1992-1993 2001 index. The higher BMI in boys and girls at 7 y of age, the earlier they enter puberty. Boys 21 612 Girls 135 223 Boys 463 Boys 382 Girls 437 Girls 10 750 Early sexual maturation in boys and girls is associated with overweight. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 5 of 10 Leptin may possibly play a role in adrenarche as its plasma level increases with higher levels of body fat and as it can modulate both girls. 33 ing adrenarche. In coherence, in children with obesity, the androgen These findings suggested that lower reproductive status was associated with higher total adiponectin concentrations and that a higher reproductive status was related to higher HMW adiponectin the HPA and HPG axes. These axes are functionally integrated dur- DHEAS was positively associated with leptin levels. Nevertheless, concentrations in girls. In addition, individuals with obesity often another study showed that enhanced adrenal androgen secretion in girls with premature adrenarche was not explained by leptin or BMI 55 ated with androgen levels in girls ; however, it was not related to levels. and IL-6. TNF-Îą alters, and IL-6 inhibits the expression of 56 8 In addition, the adipokine adiponectin was negatively associ- 57 differences of adiponectin seem to develop during the progression of 56 adiponectin (Figure 2). Thereby, a low level of total adiponectin and/or high levels of inflammatory cytokines in individuals with obe- sity can promote the onset of puberty. Many more adipokines are secreted by WAT including omentin, 52,65-67 9,36,62,68 adrenarche in girls with Prader-Willi syndrome. Interestingly, sex puberty. adrenarche; however, both are not required factors. Thus, leptin and adiponectin might be able to influence In gonadarche, leptin can stimulate the secretion of kisspeptin, and subsequently activation of the HPG axis, which eventually increases the expression of estrogen and androstenedione in the ova- 58 2,60 65-67 The expression of these ries (Figure 2). Ob gene in WAT, resulting in the synthesis and secretion of leptin. Thus, high levels of leptin promote onset of puberty in girls via secre- tion of kisspeptin, and estrogen stimulates leptin secretion addition- ally. Moreover, adiponectin can affect the HPG axis due to the expression of adiponectin receptors in the hypothalamus, pituitary In return, estrogen stimulates the expression of the 59 gland, and gonads. onset as it inhibits the secretion of kisspeptin and GnRH in the hypo- thalamus and the release of GH and LH in the pituitary gland, and 2,60-62 52,60 63 girls with central precocious puberty (CPP). Moreover, total adiponectin had negative correlations with progression of puberty in girls (defined by Tanner stages), whereas HMW adiponectin had FIGURE 2 Adipokinesaffectingthe initiation of puberty in girls. Leptin stimulates the release of kisspeptin in KNDy neurons, which activates the hypothalamus to produce gonadotropin releasing hormone (GnRH). In response to the release of GnRH, the pituitary gland secretes follicle stimulating hormone (FSH) and luteinising hormone (LH), which stimulates the ovaries to release estrogen resulting in the formation of secondary sex characteristics in girls. Estrogen stimulates the production of leptin. Adiponectin inhibits GnRH release resulting in reduced levels of GnRH and thereby a delayed onset of puberty. TNF- Îą and IL-6 inhibit the production of adiponectin and therefore stimulate the onset of puberty In detail, adiponectin is a regulator of puberty thereby inhibiting the onset of puberty (Figure 2). with obesity often have low levels of adiponectin. et al. showed that total adiponectin was significantly lower, whereas high molecular weight (HMW) adiponectin was significantly higher in ment. 55 63 develop a chronic low-grade inflammatory state, which can be indi- cated by a high level of circulating inflammatory cytokines like TNF-Îą 64 Individuals Sitticharoon positive associations with LH levels and the progression of puberty in 63 visfatin, resistin, and chemerin. and visfatin are expressed in the ovaries. adipokines in the ovaries suggests a role within the reproductive sys- tem; however, the exact biological processes have to be examined. Thus, specifically leptin, adiponectin, and inflammatory cytokines pro- duced by WAT could be permissive key players during an early onset of puberty in girls with obesity. As an exception, HMW adiponectin seems to have a stimulatory effect on peripheral repro- ductive function as HMW is not able to cross the blood brain 63 barrier. 4 | Markers that are used to assess puberty onset in boys are THE ONSET OF PUBERTY IN BOYS spermarche, voice break, testicular volume, and pubic hair develop- 35 spermarche develop in the early stages of puberty onset, voice In women, omentin, chemerin, While pubic hair development, larger testicular volume, and 69 testicular volume increases, which occurs at an average age of break usually appears in later stages of puberty. Generally, first 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 6 of 10 NIEUWENHUIS ET AL. 11.9 years, followed by the development of pubic hair at 12.2 years of average, and lastly, boys experience spermarche around an aver- 55 related with leptin levels. Thereby, leptin plausibly has a minor impact in adrenarche in boys. Since leptin receptors are found in the hypothalamus, pituitary gland, and testes, they might be involved in the onset of puberty by affecting the HPG axis during gonadarche. Leptin stimulates the release of kisspeptin and GnRH, and as a consequence, it accelerates the onset of puberty (Table 1, Figure 3). In contrast, adiponectin inhibits the secretion of GnRH, GH, LH, and FSH therewith delaying the onset of puberty. However, adiponectin levels are generally lower in men compared with women and even lower in men with obe- age age of 13.4 years. 70 4.1 | Fat storage Many aspects of the reproductive physiology are energetically demanding,71 and therefore, an adequate energy level is necessary. In boys, a dynamic change in body composition occurs around the age of 10 to 13 years, in which they gain approximately 40% of sity. culating inflammatory cytokines. levels can stimulate the HPG axis and therewith an early onset of puberty in boys. Nevertheless, leptin can inhibit the production of tes- 72 mostly consisting of lean mass, which causes exhaustion of most of fat. Subsequently, a growth spurt follows in which they gain tissue 72 in boys, an adequate amount of body fat is important in the onset of their body fat. These alterations in amount of body fat indicate that 4.2 | Puberty in boys is initiated by the release of kisspeptin. As mentioned before, this activates the HPG axis, resulting in the release of GnRH from the hypothalamus, and consequently the release of LH and FSH 9,74 puberty. tosterone from the testes, to estrogen (Figure 3). of the development of secondary sex characteristics in boys. Additionally, leptin can affect fertility in men as it can modulate the nutritional support of spermatogenesis, and moreover, dysfunction of spermatogenesis is associated with an increased leptin level and 73 58 2,60-62 HPG axis from the pituitary gland (Figure 1). and LH stimulates the secretion of testosterone from the testes, which inhibits the release of kisspeptin from the KNDy neurons and 9,48 in men, the release of kisspeptin is more consistent, causing a con- 29,48 subsequently GnRH from the hypothalamus. receptors expressed on KNDy neurons. In humans, KNDy neurons Contrarily to women, LH-induced testosterone levels lead to the stant release of LH. development of secondary sex characteristics in boys. differences between sexes in kisspeptin release are related to a sex- specific and sex steroid-dependent kisspeptin system as estrogen and progesterone modulate kisspeptin activity through the sex-steroid 48 in the infundibular nucleus are involved in negative and positive sex- 48 tal exposure to sex steroids and result in sex-specific differences in steroid feedbacks. kisspeptin release. These sexual dimorphisms are induced by perina- 75,76 4.3 | Adipokines The association between obesity and puberty onset in boys is rather controversial compared with findings in girls. Most studies reported an early onset of puberty in boys associated with increased ate adipose tissue from actual breast tissue. stages are more difficult to assess than female stages as boys lack a more determined marker such as menarche. Thirdly, puberty onset can be indicated by the activation of the HPG axis, and the presence of these secondary sex characteristics is the result of hormonal 2 14,17,22,23,50,51,77,78 BMI, 20,49 all while others reported no associations at Current markers used 79 16,80 or a delayed onset of puberty (Table 1). The presence of excessive adipose tissue can be involved in puberty onset in boys as the secretion of adipokines can modulate both adrenarche and gonadarche. Leptin can affect adrenarche by modulating both the HPG and HPA axes,33 and moreover, androgen levels were positively 55 nal androgen secretion in boys with premature adrenarche was not associated with plasma leptin levels. Nevertheless, enhanced adre- 9 In more detail, 61,62 adiponectin, and individuals with obesity often have high levels of cir- Moreover, inflammatory cytokines, TNF-Îą, and IL-6, inhibit expression of the leptin receptor in the testis. FSH induces spermatogenesis, too. function and role still have to be examined. 64 High leptin and low adiponectin and fat tissue can convert testosterone Both processes might result in the delay 29,61,79 81,82 In men, other adipokines like chemerin are found in the gonads 65 Thus, particularly high leptin and low adiponectin levels stimulate the HPG axis and thereby accelerate the onset of puberty in boys. Additionally, leptin can dysregulate the development of secondary sex characteristics and spermatogenesis by affecting testosterone levels and nutritional sup- port of spermatogenesis. 5 | LIMITATIONS AND FUTURE RESEARCH DIRECTIONS Even though multiple epidemiological studies have shown the link between puberty onset and obesity, there are some important limita- tions. Firstly, determining both the onset and stage of puberty is rather difficult. For instance, assessing the stage of breast develop- ment in girls with obesity is complicated as clinicians should differenti- 2 changes in response to the activated HPG axis. to determine the onset of puberty refer to secondary sex characteris- tics, such as testicular volume in boys and breast development in girls. A more accurate measurement of puberty onset would be to combine secondary sex characteristics with plasma or serum hormone level measurements such as LH, FSH, adipokines, e.g. leptin. Thereby, differences in puberty measurements could explain variations in the age of puberty onset between boys and girls within different Thereby, resistin is expressed in the testes of rats, but its exact 83 Secondly, male pubertal 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 7 of 10 FIGURE 3 Adipokines affecting the initiation of puberty in boys. Leptin activates kisspeptin secretion in KNDy neurons, this activates the production of gonadotropin releasing hormone (GnRH) from the hypothalamus. GnRH stimulates the pituitary gland to secrete follicle stimulating hormone (FSH) and luteinising hormone (LH), activating the production of testosterone from the testes allowing the development of secondary sex characteristics. Leptin also inhibits the production of testosterone, which may cause a delayed onset of puberty. Adiponectin inhibits GnRH release. Low levels of adiponectin, as a result of TNF-Îą and IL-6 expression, lead to a reduced inhibition of GnRH. In response to GnRH release, the pituitary gland will secrete FSH and LH, and the testes will produce testosterone resulting in the development of secondary sex characteristics in boys countries, and In addition, the inclusion of a of puberty. ferent time points is complicated, as subjects examined several decades ago presented pronounced differences concerning lifestyle patterns such as nutrition and exercise habits. Lastly, obesity or over- weight is often determined by BMI, a classification based on weight and height measurements. Additionally, it is important that all studies studies or across continents, ethnicities proper age range (8-16 years) is important when assessing the onset (Figure 4). 12-15,17,20-23,49,77-79,84,85 30,47 Furthermore, comparison between studies from dif- 86 Specifically in children, BMI is often dependent on age and growth use the same anthropometric standards and sex-specific cut-offs. 13,14,16-23,49-51,77-80 fat and would represent a more accurate measurement in its regard. Based on this review, several suggestions can be made for further research. Firstly, the roles of adipokines like resistin, chemerin, visfatin, and omentin in puberty onset, fertility, and sexual maturation should be examined in detail. Secondly, future research examining the onset of puberty should combine indicators of puberty onset (e.g. breast development or testicular volume) with plasma or serum hor- mone measurements such as LH, FSH, sex-steroids, adipokines (e.g. spurts. ment in case of growth spurts. distribution of body fat should be taken into account in determining puberty and obesity in children. For instance, the body adiposity index (BAI), which was introduced in 2011 by Bergman et al.,87 uses hip cir- cumference and height in order to estimate the percentage of body 87 Thereby, BMI is a less accurate measure- F I G U R E 4 87,88 Therefore, both percentage and Average age of puberty onset in Europe, China, and the United States according to several studies from Table 1. Age of puberty onset ranges from 8.47 to 13.33 years in girls and from 8.63 leptin), and body fat distribution (e.g. BAI,87 waist-hip ratio's and/or dual-energy X-ray absorptiometry (DXA)2). Additionally, defining con- sistent and general measurements of puberty in both boys and girls, combined with a proper age range (8-16 years), would facilitate the comparisons between different studies and their results. 12-15, 17, 20-23, 25-29, 31 to 13.7 years in boys. included if average age of markers used to assess puberty was not reported. Pink: girls. Blue: boys Studies (Table 1) were not 39, 56 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 8 of 10 NIEUWENHUIS ET AL. 6 | CONCLUSION In conclusion, epidemiological data regarding obesity and puberty onset in girls show similar outcomes as adiposity results in the early onset of puberty in girls. 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BMC Womens Health. 2018;18(1):168-174. thereby an early onset of obesity. leptin can inhibit the production of testosterone in boys and subse- quently inhibit the development of secondary sex characteristics affecting spermatogenesis. for other adipokines, like resistin and omentin, are present in the testes and ovaries suggesting a role in puberty or reproduction; 58, 71 however, their plausible function is still unknown. that adipokines may be key regulators in an early onset of puberty in both girls and boys with obesity, specifically by affecting the HPG axis during gonadarche. Future research should focus on assessing puberty onset by measuring consistent puberty markers and determine the percentage of body fat and its distribution and adipokines and hormone serum levels particularly involved in the HPG axis. CONFLICTS OF INTEREST The authors declare no conflict of interest. FUNDING INFORMATION This research was funded by Europees Fonds voor Regionale Ontwikkeling (EFRO), project BriteN 2016. ORCID Ilse A.C. Arnoldussen Amanda J. Kiliaan https://orcid.org/0000-0002-7395-5284 https://orcid.org/0000-0002-2158-6210 13, 14, 16-26, 29-32 Furthermore, several receptors Nevertheless, We conclude Search strategy We searched PubMed for articles published before Novem- ber 15th, 2019 using relevant keywords, including âonset of puberty and adiposity/obesityâ, âonset of pubertyâ, âchildren with obesityâ, âadipose tissueâ, âchildhood obesityâ, âadiposityâ, âobesityâ, âadipokine(s)â, âHPG axisâ, âadipokines ovary/ova- riesâ, or âadipokines testesâ, either alone or in combination. Selection criteria used were English language, longitudinal or cross-sectional studies assessing the onset of puberty, including menarche, thelarche, spermarche, or voice break, combined with high BMI or obesity/adiposity, and articles assessing or reviewing adipokines and its effects on the reproductive system. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 9 of 10 21. Lian Q, Mao Y, Luo S, et al. Puberty timing associated with obesity and central obesity in Chinese Han girls. BMC Pediatr. 2019; 19(1):1-7. 22. Deng Y, Liang J, Zong Y, et al. Timing of spermarche and menarche among urban students in Guangzhou, China: trends from 2005 to 2012 and association with Obesity. Sci Rep. 2018;8(1):263-270. 23. Li W, Liu Q. Association of prepubertal obesity with pubertal devel- opment in Chinese girls and boys: a longitudinal study. 2018;30: e23195. 24. Mendle J, Beltz AM, Carter R, Dorn LD. Understanding puberty and its measurement: ideas for research in a new generation. Journal of research on adolescence: the official journal of the Society for Research on Adolescence. 2019;29(1):82-95. 25. Pagani S, Meazza C, Gertosio C, Bozzola E, Bozzola M. Growth hor- mone receptor gene expression in puberty. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 2015;47:581-584. 26. Abreu AP, Kaiser UB. Pubertal development and regulation. Lancet Diabetes Endocrinol. 2016;4(3):254-264. 27. Aguirre RS, Eugster EA. Central precocious puberty: from genetics to treatment. Best Pract Res Clin Endocrinol Metab. 2018;32(4): 343-354. 28. Sultan C, Gaspari L, Maimoun L, Kalfa N, Paris F. Disorders of puberty. Best Pract Res Clin Obstet Gynaecol. 2018;48:62-89. 29. Skorupskaite K, George JT, Anderson RA. The kisspeptin-GnRH path- way in human reproductive health and disease. Hum Reprod Update. 2014;20(4):485-500. 30. Dahl SK, Amstalden M, Coolen L, Fitzgerald M, Lehman M. Dynorphin immunoreactive fibers contact GnRH neurons in the human hypothal- amus. Reprod Sci. 2009;16(8):781-787. 31. Navarro VM, Gottsch ML, Chavkin C, Okamura H, Clifton DK, Steiner RA. Regulation of gonadotropin-releasing hormone secretion by kisspeptin/dynorphin/neurokinin B neurons in the arcuate nucleus of the mouse. J Neurosci. 2009;29(38):11859-11866. 32. Zhai L, Liu J, Zhao J, et al. Association of obesity with onset of puberty and sex hormones in chinese girls: a 4-year longitudinal study. PLoS ONE. 2015;10(8):1-12, e0134656. 33. Cizza G, Dorn LD, Lotsikas A, Sereika S, Rotenstein D, Chrousos GP. Circulating plasma leptin and IGF-1 levels in girls with premature adrenarche: potential implications of a preliminary study. Horm Metab Res. 2001;33(3):138-143. 34. Cousminer DL, WidĂŠn E, Palmert MR. The genetics of pubertal timing in the general population: recent advances and evidence for sex-spec- ificity. Curr Opin Endocrinol Diabetes Obes. 2016;23(1):57-65. 35. Marshall WA, Tanner JM. Variations in pattern of pubertal changes in girls. Arch Dis Child. 1969;44(235):291-303. 36. Lacroix AE, Whitten R. Physiology. Treasure Island (FL): Menarche. StatPearls. StatPearls Publishing; 2018. 37. McDowell MA, Brody DJ, Hughes JP. Has Age at Menarche Chan- ged? Results from the National Health and Nutrition Examination Sur- vey (NHANES) 1999â2004. J Adolesc Health. 2007;40(3):227-231. 38. de Muinich Keizer SM, Mul D. Trends in pubertal development in Europe. Hum Reprod Update. 2001;7(3):287-291. 39. Talma H, SchĂśnbeck Y, van Dommelen P, Bakker B, van Buuren S, Hirasing RA. Trends in menarcheal age between 1955 and 2009 in the Netherlands. PLoS ONE. 2013;8:e60056-e60056. 40. Kaplan HS, Lancaster JB. An evolutionary and ecological analysis of human fertility, mating patterns, and parental investment. Off- spring: Human fertility behavior in biodemographic perspective. 2003;1: 170-223. 41. Mitan LA. Menstrual dysfunction in anorexia nervosa. J Pediatr Adolesc Gynecol. 2004;17(2):81-85. 42. Xu H, Li P-H, Barrow TM, et al. Obesity as an effect modifier of the association between menstrual abnormalities and hypertension in young adult women: Results from Project ELEFANT. PLoS ONE. 2018; 13(11):e0207929-e0207929. 43. Tauqeer Z, Gomez G, Stanford FC. Obesity in women: insights for the clinician. J Womens Health (Larchmt). 2018;27(4):444-457. 44. de Ridder CM, Thijssen JH, Bruning PF, Van den Brande JL, Zonderland ML, Erich WB. Body fat mass, body fat distribution, and pubertal development: a longitudinal study of physical and hormonal sexual maturation of girls. J Clin Endocrinol Metab. 1992;75(2): 442-446. 45. Lassek W, Gaulin S. Brief communication: menarche is related to fat distribution. Am J Phys Anthropol. 2007;133(4):1147-1151. 46. Loomba-Albrecht LA, Styne DM. Effect of puberty on body composi- tion. Curr Opin Endocrinol Diabetes Obes. 2009;16:10-15. 47. Simonneaux V, Bahougne T. A multi-oscillatory circadian system times female reproduction. Front Endocrinol. 2015;6:1-15. 48. Marques P, Skorupskaite K, George JT, Anderson RA. Physiology of GNRH and gonadotropin secretion. In: Feingold KR, Anawalt B, Boyce A, et al., eds. Endotext. Endotext.org: South Dartmouth (MA); 2000. 49. Barcellos Gemelli IF, Farias EDS, Souza OF. Age at menarche and its association with excess weight and body fat percentage in girls in the Southwestern Region of the Brazilian Amazon. J Pediatr Adolesc Gynecol. 2016;29(5):482-488. 50. Aksglaede L, Juul A, Olsen LW, Sorensen TI. Age at puberty and the emerging obesity epidemic. PLoS ONE. 2009;4:1-6, e8450. 51. Ribeiro J, Santos P, Duarte J, Mota J. Association between over- weight and early sexual maturation in Portuguese boys and girls. Ann Hum Biol. 2006;33(1):55-63. 52. Budak E, Fernandez Sanchez M, Bellver J, Cervero A, Simon C, Pellicer A. Interactions of the hormones leptin, ghrelin, adiponectin, resistin, and PYY3-36 with the reproductive system. Fertil Steril. 2006;85(6):1563-1581. 53. Castellano JM, Tena-Sempere M. Metabolic control of female puberty: potential therapeutic targets. Expert Opin Ther Targets. 2016; 20(10):1181-1193. 54. Venancio JC, Margatho LO, Rorato R, et al. Short-term high-fat diet increases leptin activation of CART neurons and advances puberty in female mice. Endocrinology. 2017;158(11):3929-3942. 55. l'Allemand D, Schmidt S, Rousson V, Brabant G, Gasser T, Gruters A. Associations between body mass, leptin, IGF-I and circulating adrenal androgens in children with obesity and premature adrenarche. Eur J Endocrinol. 2002;146(4):537-543. 56. BĂśttner A, Jr K, MĂźller G, et al. Gender Differences of adiponectin levels develop during the progression of puberty and are related to serum androgen levels. J Clin Endocrinol Metabol. 2004;89(8):4053- 4061. 57. Unanue N, Bazaes R, IĂąiguez G, Cortes F, Avila A, Mericq V. Adre- narche in Prader-Willi syndrome appears not related to insulin sensi- tivity and serum adiponectin. Horm Res. 2007;67(3):152-158. 58. Michalakis K, Mintziori G, Kaprara A, Tarlatzis BC, Goulis DG. The complex interaction between obesity, metabolic syndrome and repro- ductive axis: a narrative review. Metabolism: clinical and experimental. 2013;62(4):457-478. 59. Machinal-Quelin F, Dieudonne MN, Pecquery R, Leneveu MC, Giudicelli Y. Direct in vitro effects of androgens and estrogens on ob gene expression and leptin secretion in human adipose tissue. Endo- crine. 2002;18(2):179-184. 60. Dobrzyn K, Smolinska N, Kiezun M. Adiponectin: A new regulator of female reproductive system. Int J Endocrinol. 2018;2018:1-12, 7965071. 61. Martin LJ. Implications of adiponectin in linking metabolism to testic- ular function. Endocrine. 2014;46(1):16-28. 62. Mathew H, Castracane VD, Mantzoros C. Adipose tissue and repro- ductive health. Metabolism: clinical and experimental. 2018;86:18-32. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 10 of 10 NIEUWENHUIS ET AL. 63. Sitticharoon C, Sukharomana M, Likitmaskul S, Churintaraphan M, Maikaew P. 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The usefulness of circulating levels of leptin, kisspeptin, and neurokinin B in obese girls with precocious puberty. 2018;34:627-630. 69. Lee J, Song J, Hootman JM, et al. Obesity and other modifiable fac- tors for physical inactivity measured by accelerometer in adults with knee osteoarthritis: data from the osteoarthritis initiative (OAI). Arthritis Care Res (Hoboken). 2012;53-61. 70. Bramswig J, Dubbers A. Disorders of pubertal development. Deutsches Arzteblatt international. 2009;106:295-303. quiz 04 71. Elias CF, Purohit D. Leptin signaling and circuits in puberty and fertil- ity. Cell Mol Life Sci. 2013;70(5):841-862. 72. Riumallo J, Durnin JV. Changes in body composition in adolescent boys. Eur J Clin Nutr. 1988;42(2):107-112. 73. Siervogel RM, Demerath EW, Schubert C, et al. Puberty and body composition. Horm Res. 2003;60(Suppl 1):36-45. 74. Zhang J. Gong M. Andrologia: Review of the role of leptin in the regu- lation of male reproductive function; 2018. 75. Kauffman AS, Gottsch ML, Roa J, et al. Sexual differentiation of Kiss1 gene expression in the brain of the rat. Endocrinology. 2007;148(4): 1774-1783. 76. Zeydabadi Nejad S, Ramezani Tehrani F, Zadeh-Vakili A. The role of kisspeptin in female reproduction. Int J Endocrinol Metab. 2017;15:1- 11, e44337. 77. Sorensen K, Aksglaede L, Petersen JH, Juul A. Recent changes in pubertal timing in healthy Danish boys: associations with body mass index. J Clin Endocrinol Metab. 2010;95(1):263-270. 78. Juul A, Magnusdottir S, Scheike T, Prytz S, Skakkebaek NE. Age at voice break in Danish boys: effects of pre-pubertal body mass index and secular trend. Int J Androl. 2007;30(6):537-542. 79. Lee JM, Wasserman R, Kaciroti N, et al. Timing of puberty in overweight versus obese boys. Pediatrics. 2016;137(2):137-146, e20150164. 80. He F, Guan P, Liu Q, Crabtree D, Peng L, Wang H. The relationship between obesity and body compositions with respect to the timing of puberty in Chongqing adolescents: a cross-sectional study. BMC Pub- lic Health. 2017;17:664-673. 81. Ishikawa T, Fujioka H, Ishimura T, Takenaka A, Fujisawa M. Expres- sion of leptin and leptin receptor in the testis of fertile and infertile patients. Andrologia. 2007;39(1):22-27. 82. Martins AD, Moreira AC, Sa R, et al. Leptin modulates human Sertoli cells acetate production and glycolytic profile: a novel mechanism of obesity-induced male infertility? Biochim Biophys Acta. 1852;2015: 1824-1832. 83. Morash BA, Willkinson D, Ur E, Wilkinson M. Resistin expression and regulation in mouse pituitary. FEBS Lett. 2002;526(1-3):26-30. 84. Cabrera SM, Bright GM, Frane JW, Blethen SL, Lee PA. Age of thelarche and menarche in contemporary US females: a cross- sectional analysis. Journal of pediatric endocrinology & metabolism: JPEM. 2014;27(1-2):47-51. 85. Herman-Giddens ME, Steffes J, Harris D, et al. 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Obesity Reviews. 2020;21:e13005. https://doi.org/ 10.1111/obr.13005 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are gover
Chapter 22 Antihypertensive Drugs Hypertension Defined (JNC-8) Pharmacology Overview 7 main categories of drugs to treat HTN Adrenergic drugs (old friend) Angiotensin-converting enzyme (ACE) inhibitors Angiotensin II receptor blockers (ARBs) Calcium channel blockers (CCBs) Diuretics Vasodilators Direct renin inhibitors A. Adrenergic Drugs: 5 Subcategories and where they act A1. Adrenergic neuron blockers (central and peripheral)- we wonât talk about this A2. Alpha1 receptor blockers (peripheral) A3. Alpha2 receptor agonists (central) A4. Beta receptor blockers (peripheral) A5. Combined Îą and β receptor blockers (peripheral) A2. Peripherally Acting Adrenergic DrugAlpha1 Blockers (weâve met these) Doxazosin, prazosin, alfuzosin Block alpha1-receptors which causes BP to decrease Reduces peripheral vascular resistance and BP by dilating both arterial and venous blood vessels Main Use: benign prostatic hyperplasia (BPH) Alpha1 Blockers REMEMBER Tamsulosin (Flomax)* is an Îą1 blocker BUT *Tamsulosin is not used to control BP, just for BPH. A3. Centrally Acting Adrenergic DrugsAlpha 2 agonist Clonidine and methyldopa 1- Stimulate alpha2-adrenergic receptors. in the brain Decreases sympathetic outflow from the CNS which decreases NE production 2. Stimulate alpha2-adrenergic receptors in kidneys remember alpha 2 opposes alpha 1 Dilates peripheral blood vessels â lowers peripheral resistance â Results in decreased BP So âŚ.Clonidine (Catapres) Used primarily for its ability to decrease blood pressure in an urgent setting Also use in opioid withdrawal as previously discussed Oral (multiple times a day), and topical patch formulations Do not stop abruptly as it may lead to rebound hypertension In reality, Clonidine and methyldopa Not prescribed as first-line home antiHTN drugs High incidence of unwanted adverse effects: orthostatic hypotension, fatigue, and dizziness MIGHT be uses as adjunct drugs after other drugs have failed, in conjunction with other antiHTN such as diuretics A4. Adrenergic Drugs Selective Beta 1 Blockers Metoprolol, Atenolol Reduction of HR through β1 receptor blockade (remember adrenergic blocking of this receptor???) HR results in BP Cause reduced secretion of renin = BP A4. Adrenergic Drugs Selective Beta1 Blockers Nebivolol (Bystolic) Uses: hypertension and HF Action: blocks β1 receptors and produces vasodilatation, which results in a decrease in SVR High doses loses selectivity and blocks both β1 and β2 Less sexual dysfunction All BB- Do not stop abruptly; must be tapered over 1 to 2 weeks A4. Adrenergic Drugs NONSelective Beta Blockers Propranolol Acts equally on β1 and β2 Other uses include situational anxiety associated with public speaking, test taking As mentioned on previous slide, nebivolol at high doses becomes beta nonselective A5. Dual-Action Adrenergic Drugs Îą1 and β Receptor Blockers Dual antihypertensive effects of reduction in heart rate (beta1 receptor blockade) and vasodilation (alpha1 receptor blockade) Examples are carvedilol (common) and labetalol (not as common) A5. Dual-Action Adrenergic Drugs Îą1 and β Receptor Blockers Carvedilol (Coreg) Widely used drug that is well tolerated Uses: HTN, mild to moderate HF in conjunction with digoxin, diuretics, and ACE inhibitors Contraindications: severe bradycardia or unstable HF, bronchospastic conditions such as asthma, and various cardiac conduction problems Adrenergic Drugs Indications - HTN But also for Glaucoma (topical) BPH: doxazosin, prazosin, and terazosin (2 for 1) Management of severe HF when used with cardiac glycosides and diuretics Contraindications Acute HF- have to stabilize first MOAIs- yeah doesnât everything interact with MAOIs? Peptic ulcers Severe liver/kidney disease Asthma (with beta blockers) Adrenergic Drugs: Adverse Effects Orthostatic hypotension 1st-dose syncope Rebound hypertension with abrupt discontinuation Most common: Dry mouth, drowsiness, constipation, sedation Interactions- always check for specific drug interactions Can cause additive CNS depression with alcohol, benzodiazepines, opioids Question #1 When administering an alpha-adrenergic drug for hypertension, it is most important for the nurse to assess the patient for the development of what response? Hypotension Hyperkalemia Oliguria Respiratory distress Answer A Hypotension This is a key point in patient education These drugs have strong vasodilating properties and may cause severe hypotension, especially at the beginning of therapy. B. Angiotensin-Converting Enzyme Inhibitorsaka ACE Inhibitors or ACEi Large group of safe and effective drugs Currently are 10 ACEi Often used as first-line drugs for HF and hypertension May be combined with a thiazide diuretic, loop diuretic, or Calcium Channel Blocker (CCB) You need to understand the basics ACE Inhibitors: Review RAAS ACE converts angiotensin I, formed through the action of renin, to angiotensin II Angiotensin 2 is a potent vasoconstrictor and also induces aldosterone secretion by the adrenal glands Aldosterone stimulates sodium resorption (H20 follows Na Both act to raise BP which causes kidneys to reduce renin production ACEi= Great drug to treat HTN BUT contraindicated in pregnancy (2nd,3rd trimester due to fetal renal damage) and breastfeeding first few weeks after birth B. ACE Inhibitors - PRIL Lisinopril (Prinivil) super common, often the 1st drug Enalapril (Vasotec) also common Captopril (Capoten) great if liver disease present Benazepril (Lotensin) Fosinopril (Monopril) Perindopril (Aceon) Quinapril (Accupril) Ramipril (Altace) Trandolapril (Mavik) Primary Effects of the ACE Inhibitors Prevent Na (and H2O) resorption by inhibiting aldosterone secretion (volume reduction) (GO BACK TO RAAS DIAGRAM) blood volume decreases work of the heart preload, or the left ventricular end-diastolic volume which is important in HF ACE SUMMARY OF ACTIVITY 1) Prevent vasoconstriction caused by angiotensin 2 (2) Prevent aldosterone secretion ď¨ less sodium and water resorption Cardioprotective Effects of ACEi They slow progression of left ventricular hypertrophy (ventricular remodeling) after MI so considered cardioprotective ACE inhibitors have been shown to decrease morbidity and mortality in patients with HF Renal Protective Effects of ACEi ACE inhibitors: reduce glomerular filtration pressure by volume reduction Cardiovascular drug of choice for patients with diabetes since it helps protect kidneys by reducing pressure. Sometimes used low dose for kidney protection with DM without HTN B. ACEi Enalapril (Vasotec) Only ACEi available in both oral and IV Enalapril IV does not require cardiac monitoring Oral enalapril: prodrug (metabolized in liver) Improves patientâs chances of survival after an MI Reduces the incidence of HF B. ACEi Captopril (Capoten) Uses: prevention of ventricular remodeling after MI; reduce the risk of HF after MI Shortest half-lifeď¨ Must be administered multiple times throughout the day so this limits its use Not a prodrug so good for patient with liver disease Question #2 A patient with diabetes has a new prescription for the ACE inhibitor lisinopril. She questions this order because her provider has never told her that she has hypertension. What is the best explanation for this order? The doctor knows best The patient is confused This medication has cardioprotective properties This medication has a protective effect on the kidneys for patients with diabetes Answer D ACE inhibitors have been shown to have a protective effect on the kidneys because they reduce glomerular filtration pressure. This property makes them the cardiovascular drug of choice for patients with diabetes. Question #3 A patient with a history of pancreatitis and cirrhosis is also being treated for hypertension. Which drug will most likely be ordered for this patient? Clonidine Prazosin Diltiazem Captopril Answer D Captopril Captopril is not a prodrug; therefore, it does not need to be metabolized by the liver to be effective. This is an advantage in patients with liver disease. ACE Inhibitors: Adverse Effects *Dry, nonproductive cough, which reverses when therapy is stopped. This is a class effect Dizziness- Note: First-dose hypotensive effect may occur Headache & Fatigue Possible hyperkalemia ** Angioedema: rare but potentially fatal Not safe in pregnancy-are contraindicated during the second and third trimesters of pregnancy because of increased risk of fetal renal damage C. Angiotensin II Receptor Blockers(ARB) Considered an alternative to ACEi Less likely to cause a dry cough and hyper K+ that is common with ACE inhibitors Angiotensin II Receptor Blockers: Mechanism of Action Go back to RAAS diagram! ARBs affect primarily 2 places 1. Vascular smooth muscle - blocks vasoconstriction 2. Adrenal gland -Selectively blocks the binding of Ang 2 to certain Ang 2 receptors inhibiting secretion of aldosterone Lowers volume retention and BP Angiotensin II Receptor Blockers -ARTAN Losartan (Cozaar)- very common Eprosartan (Teveten) Valsartan (Diovan) Irbesartan (Avapro) Candesartan (Atacand) Olmesartan (Benicar) Telmisartan (Micardis) Azilsartan (Edarbi) C. ARB Losartan (Cozaar) Beneficial in patients with HTN and HF Used with caution in patients with kidney or liver dysfunction and in patients with renal artery stenosis ***Not safe for breastfeeding women and should not be used in pregnancy (Cat C 1st trimester, Cat D 2nd-3rd trimester), potential fetal toxicity Appear to be equally effective for the treatment of hypertension and well tolerated ARBs less likely to cause cough and hyperK+ but can still happen Evidence that ARBs are associated with lower mortality after MI than ACE inhibitors Never take ACEi and ARBs at the same time* 5. Calcium Channel Blockers (CCB) Primary use: HTN, angina, some dysrhythmias Cause smooth muscle relaxation by blocking the binding of calcium to its receptors, preventing muscle contraction Results in: Relaxed blood vessels to the heart Decreased peripheral smooth muscle tone Decreased SVResistance Decreased BP E. Diuretics First-line antiHTN in JNC 8 guidelines Decreases fluid volume The results from diuresis: preload, Peripheral resistance Overall effect ď Decreased workload of the heart and decreased BP Thiazide diuretics are the most commonly used diuretics for HTN Ie hydrochlorothiazide (HCTZ), chlorthalidone We will discuss diuretics further in the chapter on diuretics F. Vasodilators Directly relax arterial or venous smooth muscle (or both) Results in: Decreased SVR Decreased afterload Peripheral vasodilation Indicated for treatment of HTN May be used in combination with other drugs F. Vasodilators Hydralazine (Apresoline) Orally: routine cases of essential hypertension Injectable: hypertensive emergencies BiDil: specifically indicated as an adjunct for treatment of HF in African-American patients F. Vasodilators Sodium Nitroprusside (Nitropress) *Sodium nitroprusside and IV diazoxide are reserved for the management of hypertensive emergencies. Contraindications: severe HF, known inadequate cerebral perfusion (especially during neurosurgical procedures) F. Vasodilators Adverse Effects Hydralazine: dizziness, headache, tachycardia, edema, dyspnea, N/V/D, vitamin B6 deficiency, rash Sodium nitroprusside: hypotension, bradycardia, decreased platelet aggregation, rash G. Direct Renin Inhibitors Aliskirin (Tekturna) Blocks the RAS pathway at the point of activation. Inhibiting renin production prevents the downstream production of Ang II (potent vasoconstrictor) Adverse effects: N/V, severe hypotension, hyponatremia, hyperkalemia⌠Contraindicated in patients with DM taking ACEi or ARB Miscellaneous Antihypertensives Eplerenone (Inspra) Newer class of drugs called selective aldosterone blockers (remember RAAS?) Reduces BP by blocking the actions of aldosterone at its corresponding receptors in the kidney, heart, blood vessels, and brain Indications: routine treatment of hypertension and for post-MI HF Contraindicated if serum potassium levels are high (above 5.6 mEq/L) A Special Form of HTNTreatment of Pulmonary Hypertension Sildenafil and Tadalafil Commonly used for erectile dysfunction Used for pulmonary hypertension but with different trade names Sildenafil: Revatio* (Viagra for ED) Tadalafil: Adcirca* (Cialis for ED)
1. Multiple Choice** 1. When do children in England and Wales usually go to nursery school? a) At age 2 b) At age 3 or 4 c) At age 5 d) At age 7 **Answer:** b) At age 3 or 4 2. How many years do children stay in primary school? a) 4 years b) 5 years c) 6 years d) 7 years **Answer:** c) 6 years 3. At what age do students start secondary school? a) 5 b) 9 c) 11 d) 13 **Answer:** c) 11 4. When can students leave school if they donât want to continue? a) At 14 b) At 15 c) At 16 d) At 18 **Answer:** c) At 16 5. What is a mixed school? a) A school for boys only b) A school for girls only c) A school for both boys and girls d) A school for older students only **Answer:** c) A school for both boys and girls --- **2. True or False** 6. Students usually have to study between the ages of 5 and 18. **Answer:** True 7. University usually lasts one year. **Answer:** False (it usually lasts 3 or 4 years) 8. Some parents pay for private schools, but most children go to state schools. **Answer:** True 9. At age 16, students take A-level exams. **Answer:** False (they take GCSE exams at 16, A-levels later) --- **3. Short Answer** 10. What three main subjects do all students study until Year Eleven? **Answer:** English, Maths, and Science 11. What exams do students take at age 16? **Answer:** GCSE exams 12. What do students have to do a lot before exams? **Answer:** Revise (study) 13. What can students do if they fail an exam? **Answer:** Retake the exam 14. What is another word for a âstate schoolâ in Britain? **Answer:** Public school ---
ILLINOIS PROFESSIONAL TEACHING STANDARDS (2013) Standard 1 - Teaching Diverse Students â The competent teacher understands the diverse characteristics and abilities of each student and how individuals develop and learn within the context of their social, economic, cultural, linguistic, and academic experiences. The teacher uses these experiences to create instructional opportunities that maximize student learning. Knowledge Indicators â The competent teacher: 1A) understands the spectrum of student diversity (e.g., race and ethnicity, socioeconomic status, special education, gifted, English language learners (ELL), sexual orientation, gender, gender identity) and the assets that each student brings to learning across the curriculum; 1B) understands how each student constructs knowledge, acquires skills, and develops effective and efficient critical thinking and problem-solving capabilities; 1C) understands how teaching and student learning are influenced by development (physical, social and emotional, cognitive, linguistic), past experiences, talents, prior knowledge, economic circumstances and diversity within the community; 1D) understands the impact of cognitive, emotional, physical, and sensory disabilities on learning and communication pursuant to the Individuals with Disabilities Education Improvement Act (also referred to as âIDEAâ) (20 USC 1400 et seq.), its implementing regulations (34 CFR 300; 2006), Article 14 of the School Code [105 ILCS 5/Art.14] and 23 Ill. Adm. Code 226 (Special Education); 1E) understands the impact of linguistic and cultural diversity on learning and communication; 1F) understands his or her personal perspectives and biases and their effects on oneâs teaching; and 1G) understands how to identify individual needs and how to locate and access technology, services, and resources to address those needs. Performance Indicators â The competent teacher: 1H) analyzes and uses student information to design instruction that meets the diverse needs of students and leads to ongoing growth and achievement; 1I) stimulates prior knowledge and links new ideas to already familiar ideas and experiences; 1J) differentiates strategies, materials, pace, levels of complexity, and language to introduce concepts and principles so that they are meaningful to students at varying levels of development and to students with diverse learning needs; 1K) facilitates a learning community in which individual differences are respected; and 1L) uses information about studentsâ individual experiences, families, cultures, and communities to create meaningful learning opportunities and enrich instruction for all students. Standard 2 - Content Area and Pedagogical Knowledge â The competent teacher has in-depth understanding of content area knowledge that includes central concepts, methods of inquiry, structures of the disciplines, and content area literacy. The teacher creates meaningful learning experiences for each student based upon interactions among content area and pedagogical knowledge, and evidence-based practice. Knowledge Indicators â The competent teacher: 2A) understands theories and philosophies of learning and human development as they relate to the range of students in the classroom; 2B) understands major concepts, assumptions, debates, and principles; processes of inquiry; and theories that are central to the disciplines; 2C) understands the cognitive processes associated with various kinds of learning (e.g., critical and creative thinking, problem-structuring and problem-solving, invention, memorization, and recall) 2 and ensures attention to these learning processes so that students can master content standards; 2D) understands the relationship of knowledge within the disciplines to other content areas and to life applications; 2E) understands how diverse student characteristics and abilities affect processes of inquiry and influence patterns of learning; 2F) knows how to access the tools and knowledge related to latest findings (e.g., research, practice, methodologies) and technologies in the disciplines; 2G) understands the theory behind and the process for providing support to promote learning when concepts and skills are first being introduced; and 2H) understands the relationship among language acquisition (first and second), literacy development, and acquisition of academic content and skills. Performance Indicators â The competent teacher: 2I) evaluates teaching resources and materials for appropriateness as related to curricular content and each studentâs needs; 2J) uses differing viewpoints, theories, and methods of inquiry in teaching subject matter concepts; 2K) engages students in the processes of critical thinking and inquiry and addresses standards of evidence of the disciplines; 2L) demonstrates fluency in technology systems, uses technology to support instruction and enhance student learning, and designs learning experiences to develop student skills in the application of technology appropriate to the disciplines; 2M) uses a variety of explanations and multiple representations of concepts that capture key ideas to help each student develop conceptual understanding and address common misunderstandings; 2N) facilitates learning experiences that make connections to other content areas and to life experiences; 2O) designs learning experiences and utilizes assistive technology and digital tools to provide access to general curricular content to individuals with disabilities; 2P) adjusts practice to meet the needs of each student in the content areas; and 2Q) applies and adapts an array of content area literacy strategies to make all subject matter accessible to each student. Standard 3 - Planning for Differentiated Instruction â The competent teacher plans and designs instruction based on content area knowledge, diverse student characteristics, student performance data, curriculum goals, and the community context. The teacher plans for ongoing student growth and achievement. Knowledge Indicators â The competent teacher: 3A) understands the Illinois Learning Standards (23 Ill. Adm. Code 1.Appendix D), curriculum development process, content, learning theory, assessment, and student development and knows how to incorporate this knowledge in planning differentiated instruction; 3B) understands how to develop short- and long-range plans, including transition plans, consistent with curriculum goals, student diversity, and learning theory; 3C) understands cultural, linguistic, cognitive, physical, and social and emotional differences, and considers the needs of each student when planning instruction; 3D) understands when and how to adjust plans based on outcome data, as well as student needs, goals, and responses; 3E) understands the appropriate role of technology, including assistive technology, to address student needs, as well as how to incorporate contemporary tools and resources to maximize student learning; 3 3F) understands how to co-plan with other classroom teachers, parents or guardians, paraprofessionals, school specialists, and community representatives to design learning experiences; and 3G) understands how research and data guide instructional planning, delivery, and adaptation. Performance Indicators â The competent teacher: 3H) establishes high expectations for each studentâs learning and behavior; 3I) creates short-term and long-term plans to achieve the expectations for student learning; 3J) uses data to plan for differentiated instruction to allow for variations in individual learning needs; 3K) incorporates experiences into instructional practices that relate to a studentâs current life experiences and to future life experiences; 3L) creates approaches to learning that are interdisciplinary and that integrate multiple content areas; 3M) develops plans based on student responses and provides for different pathways based on student needs; 3N) accesses and uses a wide range of information and instructional technologies to enhance a studentâs ongoing growth and achievement; 3O) when planning instruction, addresses goals and objectives contained in plans developed under Section 504 of the Rehabilitation Act of 1973 (29 USC 794), individualized education programs (IEP) (see 23 Ill. Adm. Code 226 (Special Education)) or individual family service plans (IFSP) (see 23 Ill. Adm. Code 226 and 34 CFR 300.24; 2006); 3P) works with others to adapt and modify instruction to meet individual student needs; and 3Q) develops or selects relevant instructional content, materials, resources, and strategies (e.g., project-based learning) for differentiating instruction. Standard 4 - Learning Environment â The competent teacher structures a safe and healthy learning environment that facilitates cultural and linguistic responsiveness, emotional well-being, self-efficacy, positive social interaction, mutual respect, active engagement, academic risk-taking, self-motivation, and personal goal-setting. Knowledge Indicators â The competent teacher: 4A) understands principles of and strategies for effective classroom and behavior management; 4B) understands how individuals influence groups and how groups function in society; 4C) understands how to help students work cooperatively and productively in groups; 4D) understands factors (e.g., self-efficacy, positive social interaction) that influence motivation and engagement; 4E) knows how to assess the instructional environment to determine how best to meet a studentâs individual needs; 4F) understands laws, rules, and ethical considerations regarding behavior intervention planning and behavior management (e.g., bullying, crisis intervention, physical restraint); 4G) knows strategies to implement behavior management and behavior intervention planning to ensure a safe and productive learning environment; and 4H) understands the use of student data (formative and summative) to design and implement behavior management strategies. Performance Indicators â The competent teacher: 4I) creates a safe and healthy environment that maximizes student learning; 4J) creates clear expectations and procedures for communication and behavior and a physical setting conducive to achieving classroom goals; 4K) uses strategies to create a smoothly functioning learning community in which students assume responsibility for themselves and one another, participate in decision-making, work collaboratively and independently, use appropriate technology, and engage in purposeful learning activities; 4 4L) analyzes the classroom environment and makes decisions to enhance cultural and linguistic responsiveness, mutual respect, positive social relationships, student motivation, and classroom engagement; 4M) organizes, allocates, and manages time, materials, technology, and physical space to provide active and equitable engagement of students in productive learning activities; 4N) engages students in and monitors individual and group-learning activities that help them develop the motivation to learn; 4O) uses a variety of effective behavioral management techniques appropriate to the needs of all students that include positive behavior interventions and supports; 4P) modifies the learning environment (including the schedule and physical arrangement) to facilitate appropriate behaviors and learning for students with diverse learning characteristics; and 4Q) analyzes student behavior data to develop and support positive behavior. Standard 5 - Instructional Delivery â The competent teacher differentiates instruction by using a variety of strategies that support critical and creative thinking, problem-solving, and continuous growth and learning. This teacher understands that the classroom is a dynamic environment requiring ongoing modification of instruction to enhance learning for each student. Knowledge Indicators â The competent teacher: 5A) understands the cognitive processes associated with various kinds of learning; 5B) understands principles and techniques, along with advantages and limitations, associated with a wide range of evidence-based instructional practices; 5C) knows how to implement effective differentiated instruction through the use of a wide variety of materials, technologies, and resources; 5D) understands disciplinary and interdisciplinary instructional approaches and how they relate to life and career experiences; 5E) knows techniques for modifying instructional methods, materials, and the environment to facilitate learning for students with diverse learning characteristics; 5F) knows strategies to maximize student attentiveness and engagement; 5G) knows how to evaluate and use student performance data to adjust instruction while teaching; and 5H) understands when and how to adapt or modify instruction based on outcome data, as well as student needs, goals, and responses. Performance Indicators â The competent teacher: 5I) uses multiple teaching strategies, including adjusted pacing and flexible grouping, to engage students in active learning opportunities that promote the development of critical and creative thinking, problem-solving, and performance capabilities; 5J) monitors and adjusts strategies in response to feedback from the student; 5K) varies his or her role in the instructional process as instructor, facilitator, coach, or audience in relation to the content and purposes of instruction and the needs of students; 5L) develops a variety of clear, accurate presentations and representations of concepts, using alternative explanations to assist studentsâ understanding and presenting diverse perspectives to encourage critical and creative thinking; 5M) uses strategies and techniques for facilitating meaningful inclusion of individuals with a range of abilities and experiences; 5N) uses technology to accomplish differentiated instructional objectives that enhance learning for each student; 5O) models and facilitates effective use of current and emerging digital tools to locate, analyze, evaluate, and use information resources to support research and learning; 5P) uses student data to adapt the curriculum and implement instructional strategies and materials according to the characteristics of each student; 5 5Q) uses effective co-planning and co-teaching techniques to deliver instruction to all students; 5R) maximizes instructional time (e.g., minimizes transitional time); and 5S) implements appropriate evidence-based instructional strategies. Standard 6 - Reading, Writing, and Oral Communication â The competent teacher has foundational knowledge of reading, writing, and oral communication within the content area and recognizes and addresses student reading, writing, and oral communication needs to facilitate the acquisition of content knowledge. Knowledge Indicators â The competent teacher: 6A) understands appropriate and varied instructional approaches used before, during, and after reading, including those that develop word knowledge, vocabulary, comprehension, fluency, and strategy use in the content areas; 6B) understands that the reading process involves the construction of meaning through the interactions of the reader's background knowledge and experiences, the information in the text, and the purpose of the reading situation; 6C) understands communication theory, language development, and the role of language in learning; 6D) understands writing processes and their importance to content learning; 6E) knows and models standard conventions of written and oral communications; 6F) recognizes the relationships among reading, writing, and oral communication and understands how to integrate these components to increase content learning; 6G) understands how to design, select, modify, and evaluate a wide range of materials for the content areas and the reading needs of the student; 6H) understands how to use a variety of formal and informal assessments to recognize and address the reading, writing, and oral communication needs of each student; and 6I) knows appropriate and varied instructional approaches, including those that develop word knowledge, vocabulary, comprehension, fluency, and strategy use in the content areas. Performance Indicators â The competent teacher: 6J) selects, modifies, and uses a wide range of printed, visual, or auditory materials, and online resources appropriate to the content areas and the reading needs and levels of each student (including ELLs, and struggling and advanced readers); 6K) uses assessment data, student work samples, and observations from continuous monitoring of student progress to plan and evaluate effective content area reading, writing, and oral communication instruction; 6L) facilitates the use of appropriate word identification and vocabulary strategies to develop each studentâs understanding of content; 6M) teaches fluency strategies to facilitate comprehension of content; 6N) uses modeling, explanation, practice, and feedback to teach students to monitor and apply comprehension strategies independently, appropriate to the content learning; 6O) teaches students to analyze, evaluate, synthesize, and summarize information in single texts and across multiple texts, including electronic resources; 6P) teaches students to develop written text appropriate to the content areas that utilizes organization (e.g., compare/contrast, problem/solution), focus, elaboration, word choice, and standard conventions (e.g., punctuation, grammar); 6Q) integrates reading, writing, and oral communication to engage students in content learning; 6R) works with other teachers and support personnel to design, adjust, and modify instruction to meet studentsâ reading, writing, and oral communication needs; and 6S) stimulates discussion in the content areas for varied instructional and conversational purposes. Standard 7 - Assessment â The competent teacher understands and uses appropriate formative and summative assessments for determining student needs, monitoring student progress, measuring student 6 growth, and evaluating student outcomes. The teacher makes decisions driven by data about curricular and instructional effectiveness and adjusts practices to meet the needs of each student. Knowledge Indicators â The competent teacher: 7A) understands the purposes, characteristics, and limitations of different types of assessments, including standardized assessments, universal screening, curriculum-based assessment, and progress monitoring tools; 7B) understands that assessment is a means of evaluating how students learn and what they know and are able to do in order to meet the Illinois Learning Standards; 7C) understands measurement theory and assessment-related issues, such as validity, reliability, bias, and appropriate and accurate scoring; 7D) understands current terminology and procedures necessary for the appropriate analysis and interpretation of assessment data; 7E) understands how to select, construct, and use assessment strategies and instruments for diagnosis and evaluation of learning and instruction; 7F) knows research-based assessment strategies appropriate for each student; 7G) understands how to make data-driven decisions using assessment results to adjust practices to meet the needs of each student; 7H) knows legal provisions, rules, and guidelines regarding assessment and assessment accommodations for all student populations; and 7I) knows assessment and progress monitoring techniques to assess the effectiveness of instruction for each student. Performance Indicators â The competent teacher: 7J) uses assessment results to determine student performance levels, identify learning targets, select appropriate research-based instructional strategies, and implement instruction to enhance learning outcomes; 7K) appropriately uses a variety of formal and informal assessments to evaluate the understanding, progress, and performance of an individual student and the class as a whole; 7L) involves students in self-assessment activities to help them become aware of their strengths and needs and encourages them to establish goals for learning; 7M) maintains useful and accurate records of student work and performance; 7N) accurately interprets and clearly communicates aggregate student performance data to students, parents or guardians, colleagues, and the community in a manner that complies with the requirements of the Illinois School Student Records Act [105 ILCS 10], 23 Ill. Adm. Code 375 (Student Records), the Family Educational Rights and Privacy Act (FERPA) (20 USC 1232g) and its implementing regulations (34 CFR 99; December 9, 2008); 7O) effectively uses appropriate technologies to conduct assessments, monitor performance, and assess student progress; 7P) collaborates with families and other professionals involved in the assessment of each student; 7Q) uses various types of assessment procedures appropriately, including making accommodations for individual students in specific contexts; and 7R) uses assessment strategies and devices that are nondiscriminatory, and take into consideration the impact of disabilities, methods of communication, cultural background, and primary language on measuring knowledge and performance of students. Standard 8 - Collaborative Relationships â The competent teacher builds and maintains collaborative relationships to foster cognitive, linguistic, physical, and social and emotional development. This teacher works as a team member with professional colleagues, students, parents or guardians, and community members. Knowledge Indicators â The competent teacher: 8A) understands schools as organizations within the larger community context; 7 8B) understands the collaborative process and the skills necessary to initiate and carry out that process; 8C) collaborates with others in the use of data to design and implement effective school interventions that benefit all students; 8D) understands the benefits, barriers, and techniques involved in parent and family collaborations; 8E) understands school- and work-based learning environments and the need for collaboration with all organizations (e.g., businesses, community agencies, nonprofit organizations) to enhance student learning; 8F) understands the importance of participating on collaborative and problem-solving teams to create effective academic and behavioral interventions for all students; 8G) understands the various models of co-teaching and the procedures for implementing them across the curriculum; 8H) understands concerns of families of students with disabilities and knows appropriate strategies to collaborate with students and their families in addressing these concerns; and 8I) understands the roles and the importance of including students with disabilities, as appropriate, and all team members in planning individualized education programs (i.e, IEP, IFSP, Section 504 plan) for students with disabilities. Performance Indicators â The competent teacher: 8J) works with all school personnel (e.g., support staff, teachers, paraprofessionals) to develop learning climates for the school that encourage unity, support a sense of shared purpose, show trust in one another, and value individuals; 8K) participates in collaborative decision-making and problem-solving with colleagues and other professionals to achieve success for all students; 8L) initiates collaboration with others to create opportunities that enhance student learning; 8M) uses digital tools and resources to promote collaborative interactions; 8N) uses effective co-planning and co-teaching techniques to deliver instruction to each student; 8O) collaborates with school personnel in the implementation of appropriate assessment and instruction for designated students; 8P) develops professional relationships with parents and guardians that result in fair and equitable treatment of each student to support growth and learning; 8Q) establishes respectful and productive relationships with parents or guardians and seeks to develop cooperative partnerships to promote student learning and well-being; 8R) uses conflict resolution skills to enhance the effectiveness of collaboration and teamwork; 8S) participates in the design and implementation of individualized instruction for students with special needs (i.e., IEPs, IFSP, transition plans, Section 504 plans), ELLs, and students who are gifted; and 8T) identifies and utilizes community resources to enhance student learning and to provide opportunities for students to explore career opportunities. Standard 9 - Professionalism, Leadership, and Advocacy â The competent teacher is an ethical and reflective practitioner who exhibits professionalism; provides leadership in the learning community; and advocates for students, parents or guardians, and the profession. Knowledge Indicators â The competent teacher: 9A) evaluates best practices and research-based materials against benchmarks within the disciplines; 9B) knows laws and rules (e.g., mandatory reporting, sexual misconduct, corporal punishment) as a foundation for the fair and just treatment of all students and their families in the classroom and school; 9C) understands emergency response procedures as required under the School Safety Drill Act [105 ILCS 128/1], including school safety and crisis intervention protocol, initial response 8 actions (e.g., whether to stay in or evacuate a building), and first response to medical emergencies (e.g., first aid and life-saving techniques); 9D) identifies paths for continuous professional growth and improvement, including the design of a professional growth plan; 9E) is cognizant of his or her emerging and developed leadership skills and the applicability of those skills within a variety of learning communities; 9F) understands the roles of an advocate, the process of advocacy, and its place in combating or promoting certain school district practices affecting students; 9G) understands local and global societal issues and responsibilities in an evolving digital culture; and 9H) understands the importance of modeling appropriate dispositions in the classroom. Performance Indicators â The competent teacher: 9I) models professional behavior that reflects honesty, integrity, personal responsibility, confidentiality, altruism and respect; 9J) maintains accurate records, manages data effectively, and protects the confidentiality of information pertaining to each student and family; 9K) reflects on professional practice and resulting outcomes; engages in self-assessment; and adjusts practices to improve student performance, school goals, and professional growth; 9L) communicates with families, responds to concerns, and contributes to enhanced family participation in student education; 9M) communicates relevant information and ideas effectively to students, parents or guardians, and peers, using a variety of technology and digital-age media and formats; 9N) collaborates with other teachers, students, parents or guardians, specialists, administrators, and community partners to enhance studentsâ learning and school improvement; 9O) participates in professional development, professional organizations, and learning communities, and engages in peer coaching and mentoring activities to enhance personal growth and development; 9P) uses leadership skills that contribute to individual and collegial growth and development, school improvement, and the advancement of knowledge in the teaching profession; 9Q) proactively serves all students and their families with equity and honor and advocates on their behalf, ensuring the learning and well-being of each child in the classroom; 9R) is aware of and complies with the mandatory reporter provisions of Section 4 of the Abused and Neglected Child Reporting Act [325 ILCS 5/4]; 9S) models digital etiquette and responsible social actions in the use of digital technology; and 9T) models and teaches safe, legal, and ethical use of digital information and technology, including respect for copyright, intellectual property, and the appropriate documentation of sources.