She told the dog to _ _ _ _ still.

Alpha to Omega ai/ay

Essential Fatty Acids (EFA’s) • Fatty acids that must be ingested due to inability to synthesize them. • Required for many biological processes (cell walls, energy/ fuel for cellular functions, hormones, vitamin metabolism) • Alpha-linolenic acid (Omega 3) polyunsaturated fatty acid • Anti-inflammatory through production of anti-inflammatory eicosanoids (signaling molecules) series-3 prostaglandins, series -5 leukotrienes, and series-3 thromboxanes and inhibition of pro-inflammatory eicosanoids (prostaglandin E, leukotriene B4, inflammatory cytokines, Tumor necrosis factor-a, interleukin B1. • Source: Flax seed oil, Evening Primrose Oil (EPO) • Dose: 2-4 g QD

Grade 5 alpha -Introduction to decimals

Create a fun and engaging quiz centered on what makes todays K-12 students so unique the questions and answers for a Kahoot style Game introducing a group of school leaders in an urban district to Generations Alpha and Z. The objective of the game is provide education leaders with a foundational understanding of student assets in today's generation; and understanding of what they value in both relationships with adults and in the ways they learn

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 won’t talk about this A2. Alpha1 receptor blockers (peripheral) A3. Alpha2 receptor agonists (central) A4. Beta receptor blockers (peripheral) A5. Combined α and β receptor blockers (peripheral) A2. Peripherally Acting Adrenergic DrugAlpha1 Blockers (we’ve 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 α1 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 → lowers peripheral resistance → Results in decreased BP So ….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 α1 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 α1 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 doesn’t 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  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 patient’s 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-life 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  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)

Origin recognition ORC,MCM proteins helicase activity, ssDNA RPA, Primer synthesis polymers alpha/primase,Sliding clamp PCNA, primer removal RNase H, FEN1.Pol α/Primase synthesizes an RNA chain of 10 nucleotides followed by another 20 nucleotides of initiator DNA (iDNA). Because Pol α/Primase has no proofreading ability, this whole section of RNA/iDNA is removed. The exonucleases RNase H removes the RNA and Fen1 removed the iDNA. The gap is filled in by Pol δ and DNA ligase joins the 2 ends.Eukaryotic DNA Replication All have 5’ to 3’ Polymerase activity.

What do an ancient Greek philosopher and a 19th century Quaker have in common with Nobel Prize-winning scientists? Although they are separated over 2,400 years of history, each of them contributed to answering the eternal question: what is stuff made of? It was around 440 BCE that Democritus first proposed that everything in the world was made up of tiny particles surrounded by empty space. And he even speculated that they vary in size and shape depending on the substance they compose. He called these particles "atomos," Greek for indivisible. His ideas were opposed by the more popular philosophers of his day. Aristotle, for instance, disagreed completely, stating instead that matter was made of four elements: earth, wind, water and fire, and most later scientists followed suit. Atoms would remain all but forgotten until 1808, when a Quaker teacher named John Dalton sought to challenge Aristotelian theory. Whereas Democritus's atomism had been purely theoretical, Dalton showed that common substances always broke down into the same elements in the same proportions. He concluded that the various compounds were combinations of atoms of different elements, each of a particular size and mass that could neither be created nor destroyed. Though he received many honors for his work, as a Quaker, Dalton lived modestly until the end of his days. Atomic theory was now accepted by the scientific community, but the next major advancement would not come until nearly a century later with the physicist J.J. Thompson's 1897 discovery of the electron. In what we might call the chocolate chip cookie model of the atom, he showed atoms as uniformly packed spheres of positive matter filled with negatively charged electrons. Thompson won a Nobel Prize in 1906 for his electron discovery, but his model of the atom didn't stick around long. This was because he happened to have some pretty smart students, including a certain Ernest Rutherford, who would become known as the father of the nuclear age. While studying the effects of X-rays on gases, Rutherford decided to investigate atoms more closely by shooting small, positively charged alpha particles at a sheet of gold foil. Under Thompson's model, the atom's thinly dispersed positive charge would not be enough to deflect the particles in any one place. The effect would have been like a bunch of tennis balls punching through a thin paper screen. But while most of the particles did pass through, some bounced right back, suggesting that the foil was more like a thick net with a very large mesh. Rutherford concluded that atoms consisted largely of empty space with just a few electrons, while most of the mass was concentrated in the center, which he termed the nucleus. The alpha particles passed through the gaps but bounced back from the dense, positively charged nucleus. But the atomic theory wasn't complete just yet. In 1913, another of Thompson's students by the name of Niels Bohr expanded on Rutherford's nuclear model. Drawing on earlier work by Max Planck and Albert Einstein he stipulated that electrons orbit the nucleus at fixed energies and distances, able to jump from one level to another, but not to exist in the space between. Bohr's planetary model took center stage, but soon, it too encountered some complications. Experiments had shown that rather than simply being discrete particles, electrons simultaneously behaved like waves, not being confined to a particular point in space. And in formulating his famous uncertainty principle, Werner Heisenberg showed it was impossible to determine both the exact position and speed of electrons as they moved around an atom. The idea that electrons cannot be pinpointed but exist within a range of possible locations gave rise to the current quantum model of the atom, a fascinating theory with a whole new set of complexities whose implications have yet to be fully grasped. Even though our understanding of atoms keeps changing, the basic fact of atoms remains, so let's celebrate the triumph of atomic theory with some fireworks. As electrons circling an atom shift between energy levels, they absorb or release energy in the form of specific wavelengths of light, resulting in all the marvelous colors we see. And we can imagine Democritus watching from somewhere, satisfied that over two millennia later, he turned out to have been right all along.

Of the 7 billion people on Earth roughly 0:02 6 billion own a cell phone which is 0:05 pretty shocking given that only 4 and2 0:07 billion have access to a working toilet 0:09 so how are these popular gadgets 0:11 changing your body and brain If you're 0:13 looking down at your phone right now 0:15 your spine angle is equivalent to that 0:17 of an 8-year-old child sitting on your 0:19 neck which is fairly significant 0:21 considering people spend an average of 0:23 4.7 hours a day looking at their phone 0:26 this combined with the length of time 0:28 spent in front of computers has led to 0:30 an increase in the prevalence of myopia 0:32 or nearsightedness in North America in 0:34 the 1970s about one quar of the 0:36 population had myopia where today nearly 0:39 half do and in some parts of Asia 80 to 0:41 90% of the population is now nearsighted 0:44 and it can be hard to put your phone 0:46 down take for example the game Candy 0:48 Crush as you play the game you achieve 0:50 small goals causing your brain to be 0:52 rewarded with little bursts of dopamine 0:54 and eventually you're rewarded in the 0:56 game with new content this novelty also 0:58 gives little bursts of dopamine and 1:00 together create what is known as a 1:01 compulsion Loop which just happens to be 1:04 the same Loop responsible for the 1:05 behaviors associated with nicotine or 1:07 cocaine our brains are hardwired to make 1:10 us novelty seeking and this is why apps 1:12 on our phones are designed to constantly 1:14 provide us with new content making them 1:16 hard to put down as a result 93% of 1:19 young people aged 18 to 29 report using 1:21 their smartphone as a tool to avoid 1:23 boredom as opposed to other activities 1:26 like reading a book or engaging with 1:27 people around them this has created a 1:29 new term nomophobia the fear or anxiety 1:32 of being without your phone we also see 1:35 a change in brain patterns Alpha rhythms 1:37 are commonly associated with wakeful 1:39 relaxation like when your mind wanders 1:41 off whereas gamma waves are associated 1:44 with conscious attentiveness and 1:46 experiments have shown that when a cell 1:47 phone is transmitting say during a phone 1:49 call the power of these Alpha Waves is 1:52 significantly boosted meaning phone 1:54 Transmissions can literally change the 1:56 way your brain functions your smartphone 1:58 can also disrupt your sleep the screen 2:00 emits a blue light which has been shown 2:02 to alter our circadian rhythms 2:03 diminishing the time spent in deep Sleep 2:06 which is linked to the development of 2:07 diabetes cancer and obesity Studies have 2:10 shown that people who read on their 2:11 smartphone at night have a harder time 2:13 falling asleep and produce less 2:15 melatonin a hormone responsible for the 2:17 regulation of sleep wake Cycles Harvard 2:20 medical school advises the last 2 to 3 2:22 hours before bed be technology free so 2:24 pick up a book before bed instead of 2:26 course smartphones also completely 2:28 change our ability to access information 2:30 most notably in poor and minority 2:32 populations 7% of Americans are entirely 2:35 dependent on smartphones for their 2:37 access to the internet a 2014 study 2:40 found that the majority of smartphone 2:41 owners use their phone for online 2:43 banking to look up medical information 2:45 and searching for jobs so while phones 2:47 are in no way exclusively bad and have 2:50 been part of a positive change in the 2:51 world there's no denying that they are 2:53 changing us but many successful people 2:56 have now decided to take smartphone 2:58 vacations in order to increase 3:00 productivity in our new ASAP thought 3:01 video we break down the top six reasons 3:04 you should take a smartphone vacation 3:06 and how it could benefit your life right 3:08 now and subscribe for more weekly 3:09 science videos

I want to be a frontliner

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