What are muscles and what do they do?, Muscle Types, Muscle Contraction, Neuromuscular junction and transmission.

Some substances, such as macromolecules and nutrients, are too large to pass through the cell membrane by the transport processes you have studied so far. Cells employ two other transport mecha- nisms—endocytosis and exocytosis—to move such substances into or out of cells. Endocytosis and exocytosis are also used to transport large quantities of small molecules into or out of cells at a single time. Both endocytosis and exocytosis require cells to expend energy. Therefore, they are types of active transport. Endocytosis Endocytosis (EN-doh-sie-TOH-sis) is the process by which cells ingest external fluid, macromolecules, and large particles, including other cells. As you can see in Figure 5-7, these external materials are enclosed by a portion of the cell’s membrane, which folds into itself and forms a pouch. The pouch then pinches off from the cell membrane and becomes a membrane-bound organelle called a vesicle. Some of the vesicles fuse with lysosomes, and their con- tents are digested by lysosomal enzymes. Other vesicles that form during endocytosis fuse with other membrane-bound organelles. Two main types of endocytosis are based on the kind of material that is taken into the cell: pinocytosis (PIEN-oh-sie-TOH-sis) involves the transport of solutes or fluids, and phagocytosis (FAG-oh-sie-TOH-sis) is the movement of large particles or whole cells. Many unicellular organisms feed by phagocytosis. In addition, certain cells in animals use phagocytosis to ingest bacteria and viruses that invade the body. These cells, known as phagocytes, allow lysosomes to fuse with the vesicles that contain the ingested bacteria and viruses. Lysosomal enzymes then destroy the bacteria and viruses before they can harm the animal. CYTOSOL EXTERNAL ENVIRONMENT During endocytosis, the cell membrane folds around food or liquid and forms a small pouch. The pouch then pinches off from the cell membrane to become a vesicle. FIGURE 5-7 vesicle from the Latin vesicula, meaning “bladder” or “sac” Word Roots and Origins www.scilinks.org Topic: Endocytosis Keyword: HM60505 mb06se_homs02.qxd 5/18/07 11:03 AM Page 105 106 CHAPTER 5 1. Explain the difference between passive trans- port and active transport. 2. What functions do carrier proteins perform in active transport? 3. What provides the energy that drives the sodium-potassium pump? 4. Explain the difference between pinocytosis and phagocytosis. 5. Describe the steps involved in exocytosis. 6. How do endocytosis and exocytosis differ? How can that difference be seen? CRITICAL THINKING 7. Analyzing Information During intense exercise, potassium tends to accumulate in the fluid surrounding muscle cells. What membrane protein helps muscle cells counteract this tendency? Explain your answer. 8. Evaluating Differences How does the sodium- potassium pump differ from facilitated diffusion? 9. Relating Concepts The vesicles formed during pinocytosis are much smaller than those formed during phagocytosis. Explain. SECTION 2 REVIEW Vesicle Cell membrane EXTERNAL ENVIRONMENT CYTOSOL During exocytosis, a vesicle moves to the cell membrane, fuses with it, and then releases its contents to the outside of the cell. FIGURE 5-8 INSIDE OF CELL Vesicle OUTSIDE OF CELL Exocytosis Exocytosis (EK-soh-sie-TOH-sis) is the process by which a substance is released from the cell through a vesicle that transports the sub- stance to the cell surface and then fuses with the membrane to let the substance out of the cell. This process, illustrated in Figure 5-8, is basically the reverse of endocytosis. During exocytosis, vesi- cles release their contents into the cell’s external environment. Figure 5-8 also shows a photo of a vesicle during exocytosis. Cells may use exocytosis to release large molecules such as pro- teins, waste products, or toxins that would damage the cell if they were released within the cytosol. Recall that proteins are made on ribosomes and packaged into vesicles by the Golgi apparatus. The vesicles then move to the cell membrane and fuse with it, deliver- ing the proteins outside the cell. Cells in the nervous and endocrine systems also use exocytosis to release small molecules that control the activities of other cells.

Name: Marco Ramirez - “I Am Not Batman” TW: language It’s the middle of the night. And the sky is glowing like mad radioactive red. And if you squint, you could maybe see the moon through a thick layer of cigarette smoke and airplane exhaust that covers the entire city like mosquito net that won’t let the angels in. And if you look up high enough you could see me-standing on the edge of a eighty seven story building. And up there-a place for gargoyles and broken clock towers that have stayed still and dead for maybe like a hundred years-up there is me. And I’m freakin Batman. And I gots Bat-mobiles and Bat-a-rangs and freakin Bat-caves like for real, and all it takes is a broom closet or a back room or a fire escape and Danny’s hand-me-down jeans are gone. And my navy blue polo shirt? – The one that looks kinda good on me but has a hole on it near the butt from when it got snagged on the chain linked fence behind Arturo’s but it isn’t even a big deal cause I tuck that part in and its like all good? –that blue polo shirt? – It’s gone too. And I get like, like transformational. And nobody pulls out a belt and whips Batman for talking back –-Or for not talking back –And nobody calls Batman simple –- Or stupid –- Or skinny –- And nobody fires Batman’s brother from the Eastern Taxi Company ‘cause they was making cutbacks, neither, ‘cause they got nothing but respect, and not like afraid-respect. Just like respect-respect. ‘Cause nobody’s afraid of you. Cause Batman doesn’t mean nobody harm. Ever. Cause all Batman really wants to do is save people and maybe pay Abuela’s bills one day and die happy and maybe get like mad famous. For real.…And kill the Joker. Tonight, like most nights, I’m all alone. And I’m watching…And I’m waiting… Like a eagle. Or like a –no, yea, like a eagle. And my cape is flappin’ in the wind (‘cause it’s freakin’ long), and my pointy ears are on, and that mask that covers like half my face is on too, and I got like bulletproof stuff all in my chest so no one could hurt me and nobody – nobody – is gonna come between Batman, And Justice. From where I am I could hear everything. Somewhere in the city there’s a old lady picking Styrofoam leftovers up outta a trash can and she’s putting a piece of sesame chicken someone spit out into her own mouth. And somewhere there’s a doctor with a whack haircut in a black lab coat trying to find a cure for the diseases that are gonna make us all extinct for real one day. And somewhere there’s a man, a man in a janitor’s uniform, stumbling home drunk and dizzy after spending half his paycheck on forty-ounce bottles of twist-off beer and the other half on a four hour visit to some lady’s house on a street where the lights have all been shot out by people who’d rather do what they do, in this city, in the dark. And half a block away from JanitorMan there’s a group of good-for-nothings who don’t know no better waiting to beat JanitorMan with rusted bicycle chains and imitation Lousiville Sluggers, and if they don’t find a cent on him – which they won’t – they’ll just pound at him till the muscles in their arms start burning, till there’s no more teeth to crack out. But they don’t count on me. They don’t count on no dark night (with a stomach full of grocery store brand macaroni-and-cheese and cut up Vienna sausages), Cause they’d rather believe I don’t exist, And from eighty-seven stories up I could hear one of the good-for-nothings say “Gimmethecash” real fast (like that) just “Gimmethefuckingcash” and I see JAnitorMan mumble something in drunk language and turn pale and from eighty-seven stories up I could hear his stomach trying to hurl its way out of his Dickies. So I swoop down like and fast and I’m like darkness. I’m like SWOOSH –- And I throw a Bat-a-rang at the one naked lightbulb –- And they’re all like “whoa-motherfucker-who-just-turned-out-the-lights?” –“What’s that over there?” –-“What?” –- “Gimme whatchou got old man” –- “Did anybody hear that?!” –- “No, really” –- “There ain’t. No. Bat.” – But then –- One out of three good-for-nothings gets it to the head! And number Two swings blindly into the dark cape before him but before his fist hits anything I grab a trash can lid and –-- Right into the gut, and number One comes back with a jump-kick but I know judo-karate too so I’m like –-- Twice –-- but before I can do any more damage suddenly we all hear a CLIC – CLIC –And suddenly everything gets quiet And the one good-for-nothing left standing grips a handgun and aims straight up, like he’s holding Jesus hostage, like he’s threatening maybe to blow a hole in the moon. And the good-for-nothing who got it to the head who tried to jump-kick me and the other good-for-nothing who got it in the gut is both scrambling back away from the dark figure before him. And the drunk man the JanitorMan is huddled in a corner, praying to Saint Anthony ‘cause that’s the only one he could remember. And there’s me, Eyes glowing white, cape blowing softly in the wind. Bulletporoof chest heaving. My heart beating right through it in a Morse code for “fuck with me, just once, come on, just try.” And the one good-for-nothing left standing, the one with the handgun, he laughs he lowers his arm, and he points it at me and gives the moon a break, and he aims it right between my pointy ears, like goalposts and he’s special teams. And JanitorMan is still calling Saint Anthony but he ain’t pickin’ up, And for a second it seems like…maybe I’m gonna lose. Naw. SHOO – SHOO! FUACATA! --“Don’t kill me man!” –“SNAP! – Wrist CRACK – Neck – SLASH! – Skin – meets – acid – “AHH!!” –And he’s on the floor. And I’m standing over him. And I got the gun in MY hands now. And I hate guns, I hate holding ‘em cause I’m Batman, and –Batman don’t like guns ‘cause his parents got iced by guns a long time ago – but for just a second, my eyes glow white, and I hold this thing, for I could speak to the good-for-nothing in a language he maybe understands…CLIC – CLIC…And the good-for-nothings become good-for-disappearing into whatever toxic-waste-chemical-sludge-shit-hole they crawled out of. And it’s just me and JanitorMan. And I pick him up. And I wipe sweat and cheap perfume off his forehead. And he begs me not to hurt him and I grab him tight by his JanitorMan shirt collar and I pull him to my face, and he’s taller than me, but the cape helps so he listens when I look him straight in the eyes and I say two words to him: “Go home.” And he does, checking behind his shoulder every ten feet. And I SWOOSH from building to building on his way there, ‘cause I know where he lives. And I watch his hands where he lives. And I watch his hands tremble as he pulls out his keychain and opens the door to his building. And I’m back in bed before he even walks in through the front door. And I hear him turn on the faucet and pour himself a glass of warm tap water And he puts the glass back in the sink. And I hear his footsteps, And they get slower as they get to my room. And he creaks my door open like mad slow. And he takes a step in, which he never does. And he’s staring off into nowhere, his face the color of sidewalks in summer, and I act like I’m just waking up, and I say, “What’s up, Pop?” And JanitorMan says nothing to me. But I see, in the dark, I see his arms go limp and his head turns back, like towards me, and he lifts it for I could see his face, For I could see his eyes, And his cheeks is dripping but not with sweat. And he just stands there, breathing, like he remembers my eyes glowing white. Like he remembers my bulletproof chest. Like he remembers he’s my pop. And for a long time I don’t say nothing. And he turns around, hand on the doorknob, and he ain’t looking up my way but I hear him mumble two words to me. “I’m sorry.” And I lean over and open my window just a crack.… If you look up high enough you could see me. And from where I am? I could hear everything.

Wiggly Worms Small Animals, Big Changes. Do you know about earthworms? These small animals change the soil in big ways. Earthworm Bodies. An earthworm's body is shaped like one tube inside another. On the outside is a tube of muscle. On the inside is a tube that breaks down food. The body of an earthworm is made up of many parts. Each part is shaped like a ring and can bend and stretch. Earthworms move by stretching out their bodies and pulling themselves forward. Short, tough hairs on their bellies help them hold onto the ground. Slimy Worms! Earthworms are slimy. The slime helps keep earthworms cool and wet. It also helps earthworms slide through soil. After worms mate, a ball of slime forms. The slime dries into a cocoon. Baby worms come out of the cocoon. Earthworm Behavior. Earthworms build long tunnels underground. The tunnels protect worms from heat and sunlight. They also help earthworms hide from hungry animals. Earthworms are sometimes called night crawlers because they come out at night to feed. They use their mouths to pull dead leaves and plants into their tunnels. Earthworms Are Good for the Soil. Farmers love earthworms! When earthworms dig tunnels, they make space in the soil. The space helps plants get what they need to grow. Some people raise earthworms on worm farms. The earthworms eat food scraps, turning them into rich soil. Earthworm waste helps plants grow big and strong. Wanted: Earthworms! Farmers aren't the only ones who love earthworms. Moles, rats, and toads love juicy night crawlers. They love to eat them! Worms make good fishing bait because fish think earthworms are tasty, too. Earthworms are important food for these and other animals. Earthworms may be small, but they have a big job. Earthworms help plants grow!

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)

Nutrition Notes Nutrition- study of how your body uses food Process by which body uses nutrients How you look and feel Resist diseases and illness How you perform physically and mentally Nutrients: substances in food your body needs to grow, repair and supply energy to your body cells 6 Classes of Nutrients 1.Carbohydrates: 1 gram= 4 calories 2. Protein: 1 gram- 4 calories 3. Fats: 1 gram= 9 calories 4.Water 5. Vitamins 6. Minerals Calorie: measurement of energy in food Metabolism: Rate at which body burns energy(calories) Hunger: physical drive to eat Appetite: pshycological desire for food What influences your food choices: Foods you like Health Reasons Family and Culture Time & Money Advertising Emotions Friends Social Media: Modeling Nutrients Carbohydrates: your body’s main source of energy sugars/starches in food 45%-65% of diet #1 source of energy Simple: sugars converted to glucose= energy (fruits, dairy, honey, some manufactured foods) Complex: sugars linked together (starches) (grains, bread, pasta, beans, vegetables) Fiber: tough, indigestible carbohydrates Cleans our digestive system Prevents some types of cancer Prevents heart disease (fruits, vegetables, whole grains,nuts) 2. Protein: growth and repair of body tissues Made up of chemicals called “amino acids” Basic building material of all body cells (muscles, bones, skin, internal organs) Secondary source of energy protein(hemoglobin) attaches to oxygen in blood Functions as hormones regulating body functions 10-15% of diet *Body uses 20 Amino Acids found in food ( body produces 11 and 9 must come from diet) Essential amino acids: 9 amino acids body doesn't produce Complete Amino Acids: foods that contain all 9 essential amino acids ( animal products) Incomplete Amino Acids: food products that do not contain all 9 essential amino acids. Fats 15-25% of diet Secondary source of energy Blood clotting Controlling inflammation Maintains healthy skin/hair absorb /transport fat soluble vitamins Regulates body temperature Types of Fat Unsaturated: “good” fat Liquid at room temperature Can help fight heart disease (veg oil, nuts) Saturated: “bad” fat Solid at room temp Clogs arteries Causes strokes, heart attack, diabetes (animal products, meat, dairy) Cholesterol: waxy like fat substance found in meat products HDL: good type of cholesterol Body creates(liver) Creates cell wall, hormones, and vit D LDL: bad cholesterol- found in foods (clogs arteries) 4. Trans Fat: “one of the worst type of fats” Formed by a process called “hydrogenation”: adding Hydrogen molecules to unsaturated fats to make it more solid and resistant to chemical change. Vitamins A vitamin is a chemical compound that is needed in small amounts for the human body to work correctly. Vitamins are classified as either fat soluble (vitamins A, D, E and K) or water soluble (vitamins B and C). This difference between the two groups is very important. It determines how each vitamin acts within the body. The fat soluble vitamins are soluble in lipids (fats). Fat soluble vitamins can be stored in our body Water soluble vitamins must be taken every day Human body produces some amounts of Vitamin D & K

CELLULAR RESPIRATION CELLULAR RESPIRATION What is it? Cellular respiration is the process by which cells break down glucose (a simple sugar) and other organic molecules to release energy in the form of ATP (adenosine triphosphate), which powers cell activities. Overall equation: C6H12O6 + 6O2 ⟶ 6CO2 + 6H2O + ATP (energy) Stages of Cellular Respiration 1. Glycolysis (in the cytoplasm) • Where it happens: Cytoplasm (outside mitochondria) • What happens: o One molecule of glucose (6 carbons) is split into two molecules of pyruvate (3 carbons each). o 2 ATP are used to start the process. o 4 ATP are produced (net gain = 2 ATP). o 2 NADH (electron carriers) are also produced. Summary of glycolysis products per glucose: • 2 ATP (net gain) • 2 NADH • 2 Pyruvate 2. Krebs Cycle (Citric Acid Cycle) (in the mitochondrial matrix) • Where it happens: Mitochondrial matrix • What happens: o Each pyruvate (3C) is converted to acetyl-CoA (2C) before entering the cycle. o Acetyl-CoA combines with oxaloacetate (4C) to form citric acid (6C). o Through a series of enzyme-controlled reactions, citric acid is broken down, releasing CO₂, ATP, NADH, and FADH₂. Summary of Krebs Cycle products (per 2 pyruvates): • 2 ATP • 6 NADH • 2 FADH₂ • 4 CO₂ (exhaled as waste) 3. Electron Transport Chain (ETC) & Oxidative Phosphorylation (in the inner mitochondrial membrane) • Where it happens: Inner mitochondrial membrane (cristae) • What happens: o NADH and FADH₂ donate high-energy electrons to proteins in the ETC. o As electrons move through the chain, protons (H⁺) are pumped across the membrane, creating a proton gradient. o This gradient powers ATP synthase, which makes lots of ATP (like a turbine powered by flowing water). o Oxygen acts as the final electron acceptor, combining with electrons and hydrogen to form water (H₂O). Summary of ETC products: • About 34 ATP • H₂O Total Energy Yield from One Glucose (Aerobic Respiration) • Glycolysis → 2 ATP • Krebs Cycle → 2 ATP • ETC → ~34 ATP Total: ~38 ATP (usually 36 in eukaryotes due to energy costs) Anaerobic Respiration (When Oxygen is Absent) If oxygen is not available, cells switch to fermentation: • Alcoholic Fermentation (yeast & some bacteria): pyruvate → ethanol + CO₂ • Lactic Acid Fermentation (muscles & some bacteria): pyruvate → lactic acid These processes only make 2 ATP per glucose, much less efficient than aerobic respiration. Key Takeaway: Cellular respiration is like the cell’s power plant: glycolysis breaks glucose into smaller pieces, the Krebs cycle extracts more high-energy electrons, and the ETC uses those electrons to generate the bulk of ATP. Oxygen is essential for the final step, which is why we need to breathe to stay alive.

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