HUMAN PHYS REVIEW: RESPIRATION Basic Vocabulary: Pulmonary: Relating to the lungs Hypoxia: Lack of O2 Hypercapnia: Too much

uch CO2 *Breathing involves both water and heat loss Respiration involves: Gases moving by bulk flow down pressure gradients Pressure Gradients are created by muscular contraction Intercostal Muscles and Diaphragm Resistance by the diameter of conducting tubes Cellular Respiration VS External Respiration: Cellular: Intracellular reactions utilize oxygen and glucose to make carbon dioxide, water, and ATP External: exchange of gases between the environment and cells. Ventilation (Step 1): Air exchange between lungs and external air Functional unit of lungs = Alveoli Passage of air: Mouth -> Pharynx -> Larynx -> Trachea -> Bronchi (Branches that Trachea splits into) -> Bronchioles (Even smaller Branches) -> Alveoli (Location of Gas Exchange) Alveolus structure: individual air sacs that are netted by capillaries Surface area directly related to rate of diffusion Bronchioles preceding alveoli are wrapped in smooth muscle for resistance control Two Types of cells in Alveoli: Type I: Make up the sac, creates the architecture of alveoli Type II: Produce the liquid surfactant Bigger than type I cells only 1 or 2 per alveolus Surfactant lowers surface tension of the alveolar type I cells to each other by decreasing hydrogen bonding Allows lungs to inflate/deflate Type II cells = one of the last cells to develop in utero, therefore premature babies can often experience respiratory issues. *Some notes on Surface Tension: Surface tension refers to the tension that holds molecules together During exhalation, type I cells get closer closer and can adhere by surface tension Surfactant is necessary to allow for separation during inhalation.

 Exchange surface of gases = 3 layers thick Endolethium of capillary Shared Basement membrane Alveolus type I cell Inflation of Lungs: Intercostal muscles contract to expand thorax pulling lungs with them by fluid tension Diaphragm pulls lungs down. Mechanism for inflation: Lungs are located in a double layered fluid filled cavity called a pleura Inner layer = Visceral pleura are stuck to lungs Outer layer (Parietal) are stuck to ribs Intercostal muscles pull on parietal layer, which pulls on the intrapleural fluid by surface tension, which pulls on the visceral pleura ----> Lungs EXPANNDDDD Therefore, inflation of lungs involves the movement of soft tissue by surface tension Thorax size is used to create pressure gradient that drives the movement of air Gas Laws: Boyles Law: P = 1/V Increase in Volume = decrease in pressure Appliance: Difference in pressure between thorax and atmospheric pressure is what creates the pressure gradient needed for ventilation Ventilatory Issues: Altitude: High altitude = lower atmospheric air pressure Volume of thorax must be even greater to create an adequate pressure gradient --> difficulty breathing Pneumothorax: Disease state characterized by air getting between pleural layers of pleural in thorax The air decreases surface tension between pleural --> no adhesion Expanding chest wall will have no pull on soft tissues of the lungs Common among stabbing victims and tall people (Perforations in chest) Asthma: Disease state characterized by inflammation + Bronchoconstriction Causation: misregulated inflammatory response to an inflammatory stimulus such as dust, allergies, etc. Increases mucus production and resistance Less oxygen to alveoli, build up of CO2 in alveoli Other Important shit: Reserve Volumes: not used in normal breathing but can be voluntarily accessed

 Residual volume: Inaccessible volume of air in lungs Exists because it is impossible to collapse the chest cavity due to intrapleural fluid. No way to reduce lung volume all the way. Exchange of O2/CO2 between alveoli and capillary (step 2): Gases move along diffusion and pressure gradients Oxygen and Carbon Dioxide are both non-polar molecules that can diffuse freely across a lipid bilayer, no need for active transport MOAR GAS LAWS: Ficks Law: Diffusion Rate = (SA * Concentration Grad. * Permeability) / (Thickness) Membrane thickness is something that can only be altered in respiration due to the influence of mucus. Components of Atmospheric Air: (760 mmHg) 79% Nitrogen, 21% Oxygen, 0.033% Carbon Dioxide and Others Daltons Law: PT = P1 + P2 + P3.... (Total pressure = sum of partial pressures) Breathing is regulated in the body by levels of oxygen and carbon dioxide, therefore in response to partial pressures Regulated by chemoreceptors in blood that are sensitive to hypoxia and hypercapnia Henrys Law: Partial pressure of a liquid will equilibrate to that of a gas Appliance: important when considering pressure of blood and alveoli PO2 in air will equilibrate to PO2 in Alveoli which equilibrates to PO2 in blood Partial Pressure Change: Supplementing oxygen via nose tubes to change partial pressures Total pressure of air changes with increasing altitude change in total pressure also changes partial pressures More disgusting diseases to learn: Emphysema = decreased alveolar surface area less diffusion Type I cells start to die, holes start appearing in lungs Treatment = increase PO2 by oxygen tanks FOREVERRRR Pulmonary Edema: Cause = Increased blood pressure leading to an increased pressure in capillaries of lungs that causes fluid to get in between capillaries and alveoli Increase in diffusion distance! Shortness of breath In severe cases, fluids build up and alveoli start to swell Gas Transport in Blood (Step 3)/ Gas transfer between blood and tissues (Step 4) Highly dependent on Henrys law

 Alveoli partial pressures = Arterial partial pressures Tissue partial pressures (that is, the partial pressure in extracellular fluid, not inside the cells) = venous partial pressures Oxygen Transportation: 97% transported on hemoglobin (RBCs) 3% dissolved in plasma, this is the only portion that can be detected By Henrys law, lower alveolar PO2 leads to a decreased movement of O2 in blood brought upon by altitude of illness Heme groups in hemoglobin are what bind O2 Saturation of hemoglobin = dependant upon number of Heme groups that are bound to oxygen *****Saturation of hemoglobin and PO2 (of alveoli) follow a non-linear relationship From 60 to 100 mmHg PO2, heme groups have a strong affinity for binding oxygen Below 60 PO2, affinity starts to drop dramatically At 50 mmHg, you die forever! Significance: The lower the PO2, the easier hemoglobin can release oxygen When hemoglobin reaches oxygen deficient tissues where PO2 is low, heme groups show lesser affinity and release O2, allowing for transfer. More specifically PO2 of cells at rest = 40 mmHg, which corresponds to 75% hemoglobin saturation PO2 of cells can drop to 20 mmHg during exercise, allowing heme groups to transfer more oxygen Factors of Hemoglobin Affinity: Higher temperatures = lower affinity Higher PCO2 in blood = lower affinity for oxygen Excess CO2 = decrease in pH Hemoglobin recruited to carry CO2 Lower pH corresponds to lower hemoglobin affinity for oxygen Hemoglobin can also be recruited to carry H+ ions Fetal hemoglobin has a higher affinity than adult/maternal hemoglobin: Therefore, maternal uterine capillaries that travel through placenta lose oxygen to fetal placental capillaries due to differences in affinity Carbon Dioxide Transportation: 23% on red blood cells 7% dissolves in plasma, higher than that of oxygen because it is more soluble 70% carried in plasma as Bicarbonate H2O + CO2 <---> H2CO3 <---> H+ + HCO3 Products of cellular respiration <-> Carbonic acid <-> Bicarbonate and Hydrogen ions

 Higher concentrations of CO2 push the reaction towards the right, resulting in more acidic plasma Problematic as acidic conditions can denature proteins Exercise increases cellular respiration: body increases breath rate to decrease CO2 levels An increase in breath rate can also be due to high acidic levels in the body for any other reason Hypercapnia leads to acidosis (lower pH in blood) Acidosis is very dangerous and suppresses the CNS leading to coma and DEATTTTH Last step of respiration (5)- cellular utilization of oxygen and production of carbon dioxide Control of Respiration: Voluntary but also involuntary Involuntary cyclic innate breathing is directed by the respiratory center in the MEDULLA OBLONGATAAAAAA!!!! Breathing regulation is based on two inputs: PO2 and H+ levels Involves chemoreceptors Peripheral Chemoreceptors: located in aortic and carotid bodies detect oxygen and ph changes in blood Lie very close to baroreceptors that detect changes in blood pressure Central Chemoreceptors: Monitors pH changes in cerebrospinal fluid, what crosses over to the brain. Oxygen actually plays a lower role in regulation At 60 mmHg when hemoglobin affinity changes, PO2 will trigger an increase in ventilation Hemoglobin will always carry oxygen, difference b/t oxygen rich and oxygen deficient blood is actually very small the body can operate with lower rates of oxygen ****the real impetus to holding in breath = acid build up by carbon dioxide! At the end of holding in a breath, people typically will exhale PCO2 = real determinant that factors in breathing body detects hydrogen ion concentrations increases in hydrogen ion concentrations in plasma --> increased ventilation Chronic Obstructive Pulmonary disorder (COPD) Disease state characterized by the narrowing and muscus build up in the bronchioles reduces the lumen of respiratory passage ways Leads to chronic hypoxia and hypercapnia Chemoreceptors adapt so that the stimulus for chemoreceptors is longer based on PCO2 but rather O2

Renal Physiology (PISSSS) Urinary System Functions (6) Regulation of extracellular fluid volume and blood pressure regulates osmolarity --> drives bodily functions like thirst maintenance of ion balance Removes metabolic wastes and foreign substances Production of hormones: Erythropoietin (RBC Production) Urinary Mechanism Filter blood in the nephron --> remove most of the plasma from blood to the nephron Reabsorption: move useful substances in plasma back into the blood Secretion: involves the direct movement of foreign substances from blood to urine that the body inherently knows to be unwanted Excretion: peeing Urinary System Anatomy: Passage goes from: Kidney --> Ureter --> Bladder -->Uretha --> outside world Functional unit of urinary system = nephron Nephrons bridge between the cortex and medulla of the kidney, medullas drain into the ureters Nephrons are found within the cortex Nephron anatomy: Corpuscle: Capsule that surrounds a capillary nest, where filtration occurs Two layers, analogous to pleura of lungs Outer layer is attached to the wall of the capsule Inner layer is attached to the glomerulus and is composed of podocyte cells Lumen or capsular space is filled with intrapleural fluid Tubules: Long pipes were secretion/reabsorption occurs, the fine tuning of piss Glomerulus = bundle of capillaries that lie within the corpuscle these capillaries are fenestrated, MEANING THAT THEY HOLES IN THEIR WALLS! Allowing plasma to leak faster Fenestrations are not large enough to allow for the leaking of red blood cells or plasma proteins Podocytes: Cell structure involves branching feet called pedicles that wrap and intertwine around the capillaries of the glomerulus The space between pedicles, called filtration slits, line up with the fenestrations of the glomerulus Filtration membrane (3 layers thick) Endothelium of capillaries Basal membrane

 Layer of podocytes Renal Tubules: Long set of toobs Proximal Convoluted Tubule: mostly reabsorption, first section of tubule as it leaves from the glomerular capsule Loop of Henle: functions to concentrate/dilute urine by adding or removing water Distal Convoluted Tubule: mostly secretion, name of part of tubule as it nears the collecting duct Kidney Vasculature: Blood enters the glomerulus via the afferent arteriole and exits through the efferent arteriole Efferent arteriole --> peritubular capillaries, reabsorbs materials back into the blood Filtration is directly related to hydrostatic and osmotic pressure The concentration of solutes are generally higher in blood, leading to osmotic pressure that favors the movement of water from the tubules into the blood. plasma proteins are the main regulator of osmotic pressure Net flow between capillary and corpuscle is dependent upon relative strengths of hydrostatic and osmotic pressure. Osmotic pressure cannot be changed as plasma proteins are too big to be transported through fenestrations Filtration rate can only be influenced by relative strength of hydrostatic pressures! Arterioles can be dilated, allowing for the regulation of Blood pressure Blood solute concentration The Afferent arteriole has a greater diameter than the efferent arteriole increases the hydrostatic pressure within the glomerulus has a higher density of sympathetic and hormonal receptors, therefore its diameter changes more in response to physiological cues Filtration Non-specific process based solely on size filtered materials = water and only dissolved solutes, about 20% of plasma Glomerular filtrate = filtrate that goes into tubule filtration membrane = 1000x more permeable than a regular capillary GFR = glomerular filtration rate, average = 125 ml/min When considering GFR, a third factor must be considered which is the hydrostatic pressure of the corpuscle Fluid pressure in here can drive fluid back into the capillary Entire plasma volume of the body is filtered 60 times a day or 2.5 times an hour GFR is highly influenced by blood pressure Mean arterial pressures from 80-120 mmHg has no impact because there is compensation by changes in arteriole diameter Myogenic control of GFR:

 all arterioles have stretch receptors in their walls when stretch receptors are activated in the arteriole due to an increase in blood pressure, smooth muscles cells constrict to decrease flow into the glomerulus The myogenic reflex works to maintain steady flow during increased BP so that the glomerulus doesnt sustain any damage Juxtaglomerular Apparatus: Located where the afferent arteriole and DCT are adjacent to each other, near the glomerulus JGA cells = smooth muscle cells of the afferent arteriole serve to sense changes in blood pressure Macula Densa cells = enlarged epithelial cells on the DCT that act as osmo, chemo, and mechanoreceptors to detect changes in solute concentration in the tubular lumen The two populations of cells communicate by paracrine signaling When solute concentration is higher in the DCT, macula densa cells send a paracrine message to the juxtaglomerular cells to constrict and thus decrease GFR JGA cells also secrete renin which increases solute reabsorption Hormonal Regulation of GFR: Vasoconstrictors (epinephrine and angiotensin II) --> decrease GFR Vasodilators: Increase GFR Reabsorption: Can happen through either active or passive transport or both Reabsorption does not move by bulk flow Proteins are not reabsorbed as they travel by exo/endocytosis Tubule Anatomy: Tubular lumen surrounded by tubular epitheleal cells Reabsorption of nutrients must go from the tubular lumen --> interstitial fluid --> Blood plasma Crosses luminal membrane than basolateral membrane Transcellular transport influenced through movement of Na+ Counter Transport: Na+ travels down concentration gradient from tubular lumen to tubule epitheleal cells H+ moves in the opposite direction against its concentration gradient by active transport due to counter transport mechanism Cotransport: Na+ travels down concentration gradient from tubular lumen to tubule epitheleal cells bring glucose molecules with it, thereby increasing rate of glucose transfer Now in epitheleal cells:

 Na+ must be moved into blood so concentration gradient can exist between tubular lumen and proximal tubule cells Done by K+/Na+ pump Potassium can be moved into the cell and out back into blood or into tubular lumen both reabsorbed and secreted level of K+ is finite for bodily function K+ in = Na+ out Movement of sodium creates an osmotic gradient that allows for the movement of water water moves towards blood Diabetes involves a slow transport rate due to quick saturation, not enough glucose reabsorbed. Transport from interstitial space into peritubular capillaries: moves by bulk flow, following the movement of water pressure in peritubular capillaries = very very low Glycosuria: excretion of glucose into urine Amount excreted = amt filtered - amt reabsorbed Excreted = increases with blood concentration - remains constant due to number of receptors Secretion: active transfer of molecules from peritubular capillaries to tubular lumen mediated transport enhances filtration above and beyond GFR Involves transporter proteins, which can be controlled by signaling pathways, hormones, etc. Renal Clearance Clearance = (Urine concentration x volume)/plasma concentration 100% clearance means all is excreted, 0% means all is reabsorbed Diabetes Mellitus and the Kidneys: increased plasma concentration of glucose leads to an increase in blood pressure as the body always tries to reabsorb glucose, reabsorption is thereby working at 100% saturation Leads to an increase in GFR More glucose rich filtrate produced Due to the higher concentration of solute in the filtrate more water remains in the nephron tubule as osmotic pressure is reduced More urine production (with glucose) + more water --> dehydration Hormones: Vasopressin (ADH: Antidiuretic hormone): Opens aquaporins in the tubule that allows for a faster movement of water out of the tubule and into the blood. Hypothalamus and posterior pituitary

 inhibited by alcohol consumption Less vasopressin means less water resorption, so you pee a lot more Aldosterone: Controls sodium reabsorption Since water and sodium movement are related, so are vasopressin and aldosterone Also controls potassium to a degree as the movement of Na+ involves Na+/K+ pumps Mechanism for production of aldosterone: Blood pressure decreases Juxtaglomerular cells secrete renin into blood (renin is an enzyme) Angiotensinogen (precursor in blood) + renin --> angiotensin I Angiotensin I + ACE (angioconverting enzyme) --> Angiotensin II Reaches adrenal medulla, triggering the release of aldosterone Angiotensin II increases blood pressure by increasing vasopressin secretion increasing thirst vasoconstriction increasing the symphathetic innervation of the heart ACE inhibitors = BP drugs Atrial natriuretic hormone: secreted by right atrium of the heart myocardial cells of the right atrium respond to stretch decreases water reabsorption, only known hormone to do so increases GFR and decreases Na+ reabsorption only mechanism for decreasing blood pressure pH Homeostasis: H+ denatures proteins by fucking with hydrogen bonds PCT can secrete H+ and reabsorb HCO3 kidneys filter 1 lb of bicarbonate a day must be reabsorbed

Nutrient Usage and Storage Basics: Energy within the glucose molecule is used to convert ADP to ATP for cellular respiration Glucose homeostasis is vital to the human body Carbs are broken down into monosaccharides, extra is stored as glycogen Proteins are mostly used for anabolic (building) purposes Lipids can be stored or used for cellular respiration Proteins/carbs are absorbed into the hepatic portal system but lipids are absorbed into the lymph system Events in Metabolism and Storage Absorptive state: ingested nutrients are entering the blood stream from the GI tract during this phase Lasts for about 4 hours after each meal Most of time awake is spent in the absorptive state Carbohydrates absorption: Blood glucose levels rise Excess is stored as glycogen in the skeletal muscles and liver If glycogen storage is full, the liver can convert glucose into lipids, stored as adipose tissue Lipids absorption: enter lymph system from the GI tract, then into the blood plasma Can be utilized immediately or stored into adipose tissue Some stuff on Cholesterol: type of lipid absolutely necessary for human function No real metabolic value, as it cannot be used for cellular respiration. More structural purposes Too much cholesterol can lead to atherosclerosis Can be synthesized from lipids if needed Liver = regulator of cholesterol levels as it can remove/add cholesterol to/from blood removed cholesterol is packaged into bile Level of saturated fat in diet influences the set point of cholesterol that the liver tolerates in the blood. Cholesterol (hydrophobic) cannot travel through hydrophillic blood Therefore cholesterol must attach to hydrophillic lipoproteins HDL (high density lipoprotein) LDL (Low density lipoprotein) VLDL (Very low density lipoprotein) HDL removes cholesterol from the blood and deliver it to the liver or endocrine glands for storage Good cholesterol

 LDLs and VLDLs supply cholesterol for membranes but are more likely to cause clogging Proteins Absorption: Absorbed as amino acids can be converted to metabolic precursors in liver if no other source of energy is present This involves removing amino groups from the amino acids removed amine group becomes urea, which requires water to be converted into urine Using only proteins involves lots of water excretion Post absorptive state: GI tract is empty of nutrients and stored nutrients must be used for metabolism (generally takes place during sleep) Sources of glucose include: glycogen in the liver Adipose tissue by lipolysis products include: Glycerol --> converted to glucose in the liver Triglycerides: can be used directly by most cells Slow process that requires lots oxygen --> feeling of fatigue Glycogen in muscles: products include pyruvate and lactate Lactate can be converted to glucose Protein breakdown and conversion to glucose Done by muscle break down all over the body (non-discriminant) gluconeogenesis: process of making glucose from fat or protein sources very slow and can only provide up to 720 calories a day In starvation, organs go into glucose sparing mode so that the majority of glucose goes to the brain Control of Nutrient Use: Pancreases is also an endocrine organ that produces insulin and glucagon Epinepherine and cortisol also have an impact on nutrient use Sympathetic innervation to liver and adipose allows for break down of fat storage during emergencies Insulin: hormone that is regulated by blood glucose levels made by beta cells in the pancreas Insulin controls cell-expression of glucose receptors, allowing for cells to take in glucose Brain does not require insulin but skeletal and cardiac muscle and adipose cells do Promotes glycogen production Inhibits glucose secretion by the liver Glucose can be used and stored in the presence of insulin Nothing from storage is used Insulin is regulated by:

blood glucose levels incretins: enteroendocrine cells that release insulin hormones by inhibiting insulin, the brain can take up more glucose

Diabetes Mellitus: Type I - Autoimmune disease immune cells attach beta cells in pancreas --> inability to produce insulin Type II - caused by genetic and lifestyle factors cells become insulin resistant and no longer respond Later beta cells start slowing down insulin production Gestational diabetes: diabetes brought upon by pregnancy, unknown cause baby is not diabetic and takes in free floating glucose, --->BIGASS BABY Glucagon: produced by alpha cells of the pancreas increases glycogen breakdown and gluconeogenesis in the liver Symphathetic innervations stimulates glucagon secretions Leptin: suppresses appetite and stimulates metabolism made by adipocytes amount released is proportional to the amount of fat in adipose tissue Ghrelin made by stomach lining cells in response to a lack of stretch (ie empty stomach) stimulates appetite Satiety Signals Insulin release stretch receptors in the GI tract Leptin Increase in body temp Thrifty gene: genes that promote storage Thrifty phenotype hypothesis: availability of food in utero can influence expression of thrifty genes later in life.

Blood Functions of Blood include: Transport of oxygen, nutrients, hormones, water, CO2, and waste Protection: white blood cells travel in blood = form of protection Temperature: how close blood flows to surface of skin Composition of blood: liquid = plasma Plasma = mostly water thicker/more viscous than water salty, 0.9% NaCl solids: formed elements cells or fragments red blood cells white blood cells (leukocytes) platelets (thrombocytes) --> for blood clotting, prevents blood loss Components of blood can be isolated via centrifugation: clotting factors = low density, found in plasma RBC = most dense and accounts for 47% of volume White blood cells = 1%, plasma = 58% Plasma with clotting factors removed is known as serum Plasma proteins from liver account for 8% of plasma volume: Albumin: most abundant osmotic regulator increases viscosity Gamma Globulin - antibodies, protect from pathogens Fibrinogen - part of clotting mechanism precipitate out during bleeding to form a fibrous network Various protein carriers that carry hydrophobic molecules that dont dissolve in blood Remaining 2% of plasma volume include charged ions dissolved gases glucose + amino acids Formed elements (solids) in blood = fully matured incapable of mitosis stem cells in red bone marrow give rise to all blood cells children have red marrow in most bones, adults only a few

Life span of blood cells: RBC = 120 days WBC = highly varied, 6 hrs - 80 years Platelets: 10 days RBC breakdown/recycling: Iron is released into plasma and bound to transferrin iron brought to either bone marrow for new RBC production or to liver for storage on ferritin Iron recycling is not a perfect process, so iron must be in the diet Folic Acid: dietary precursor to the nucleic acid thymine lack in folic acid = no cell division only works in conjunction with vitamin B12 B12 found only in animal products lack of B12 (ex veganism) --> pernicious anemia Cell division/maturation of RBC is triggered by erythropoietin hormone hormone released by kidnets decrease in oxygen levels to kidneys leads to an increase in erythropoietin Erythropoietin production can also be triggered by testosterone RBC development: Nucleus gets pushed out organelles shrink and disappear cytoplasm shrinks Mature RBC cells have the following features: biconcave disc shape, allowing for greater surface area and diffusion flexibility so that they can get through tight spaces Contents (RBC) No mitochondria, ATP production by glycolysis only no ER = no protein production = inability to repair self Lots of hemoglobin --> iron containing protein that carries O2 Hemoglobin: binds also to CO2 (actually has a higher affinity for CO2) Binds to H+ and can thus act as a buffer Hematocrit = measuring the %RBC of total blood volume If < normal value --> Anemia Anemia:

 Naming based on size and hemoglobin content size (cytic), ex. microcytic or macrocytic Content: (chromic), hypo- or hyper Other types include Pernicious (lack of B12) Iron deficiency sickle cell Causes include: losing blood (menstruation, hemorrhoids, etc.) Iron deficiency due to pathogen evasion ie infection Myeloproliferative blood cell disorders: Too many WBC = leukemia Too much RBC = polycythemia vera erythrocytosis: increased blood viscosity from too much RBC Blood doping using erythropoetin --> thrombi (blood clot in vessels) --> tissue damage Blood types/groups: A, B, AB, or O + or Each RBC expresses proteins on its surface called surface antigens Two types of proteins are A and B Rh factor is also antigen which the RBC can be positive or negative for Blood compatibility: Your body makes antibodies against antigens that you do not express antibodies bind to their correlated antigen causing cells to clump (agglutination) danger!!! Rh factor = exception. To be truly Rh negative, you must be exposed to Rh factor first to start producing an antibody against it. Erythroblastosis Fetalis: Dad is Rh+ and mom is Rh Baby is Rh+ (dominant) Baby is born, mom is exposed to blood and dvelops anti Rh antibodies 2nd pregnancy: baby is Rh+, moms anti-Rh antibodies cross the placenta and start destroying the babys RBCs rhogam shot is given Leukocytes (WBC): Low WBC count = immunocomprised Hgih WBC count = actively fighting infection

Thrombocytes (platelets) small cell fragments for clotting are broken off edges of cytoplasm of megakaryocyte in bone marrow Have ER w/o nucleus so can make chemicals involved in clotting Platelet activation and hemostasis: Hemostasis: stoppage of blood loss Platelets + fibrinogen gather to stop blood loss Vessel damage exposes connective tissue: collagen in CT binds platelets Platelets - collagen --> activates platelets and release of platelet secretory vesicles autocrine and paracrine signalling make platelets stick to each other this makes platelets contract and compress Plug that was just created now must be turned into a clot protein prothrombin cleaved into thrombin Fibrinogen + thrombin ---> Fibrin monomers that polymerize into a fibrous net. Hemostatic control: nearby endothelial cells secrete prostacyclin and nitric oxide which inhibit platelet activation

Cardiovascular System The Cardiovascular system serves to transport oxygen, nutrients, waste products, etc. Core concepts of cardio: Liquids + gases move down pressure gradients a pressure gradient must exist in order for the cardiovascular system to function Blood moves by bulk flow Systemic Circulation (blood to body) Left side of heart pumps oxygenated blood (97 O2) to body Pulmonary Circulation (Blood to lungs) Right side of heart pumps deoxygenated blood (70% O2) to lungs The Heart is a muscle yo: Two sided pump that creates the driving pressure for blood Top two chambers = atria and they receive blood from vessels Bottom 2 chambers are called ventricles, pump blood out Heart pumps in parallel, atria pump together and ventricles pump together Ventricular muscle cell depolarization must be: rapid: Influx of Na+ Have a long absolute refractory period: Ca++ channels that stay open for longer open later than Na+ channels Have a short relative refractory period to be ready for next impulse: K+ exits cells At rest, sodium channels and calcium channels are closed Nodal Cell depolarization must: spontaneously depolarize (pacemaker potential): Open Na+ and Ca++ channels even when the voltage is negative More Ca++ open at threshold -->rapid depolarization be rapid have a long absolute refractory period open Ca++ channels Have a short relative refractory period to be ready for next impulse K+ exits Does not depolarize all the way to +30, stops at 0 Autonomic Innervation of the Heart Parasympathetic NS (slow down heart rate) increase K+ permeability decrease Ca++ permeability Sympathetic NS (increase heart rate) increases Ca++ and Na+ permeability

Portal Systems: two capillary beds in a series, link one organ to another without returning blood to heart Hepatic portal vein: delivers nutrients to liver from intestines, low O2 content Hypothalamus-pituitary portal system Kidneys DIGESTION Entero = pertaining to the GI tract Digestion involves breaking polymers into monomers by hydrolysis Mechanical digestion Chemical digestion Regulated by neural and hormonal inputs Involves 3 phases of control: Cephalic phase: in your head: sight, smell, emotional state trigger activity in GI tract Gastric phase: takes place in stomach Intestinal phase: takes place in intestine Properties of saliva amylase - begin digestion slightly basic to neutralize acidic waste from bacteria and stomach acid in esophagus antibodies lubrication Muscles move food through the GI tract Peristalsis: involuntary waves of contraction and relaxation of smooths muscles in the organ walls (fast) Segmentation: contractions in the small intestine that chop and mix the ingested food slow Stomach Anatomy and Function folded interior allows for expansion lined with deep pits called gastric pits, gastric glands located at the bottom Gastric products include: pepsinogen HCl Intrinsic factor --> binds vitamin B12, allowing it to be absorbed in the small intestine Gastrin -> hormone that stimulates acid secretion and gastric/intestinal motility mucus for protection Small intestine: Motility by segmentation Chyme that has been moved to small intestine is hypertonic due to solutes in food secretes mineral ions to coat lining and protect cells water follows by osmosis

 Stretch/detection of biomolecules in the first portion of the small intestine provide neural feedback to slow the rate of stomach emptying Fat has the greatest impact Villus anatomy highly vascularized to absorb nutrients innervated by artery with oxygenated blood has a vein which drains to the hepatic portal Lacteal: specialized lymphatic vessel that absorbs fats Small intestines secretions: bile from the liver/gall bladder: emulsify fats and contain waste products for inclusion in the feces Pancreatic juice --< digestive enzymes HCO3 BUFFER Large Intestine: functions to absorb water and vitamins from the remaining material COMPACTS POOP colonized by bacteria important in breakdown of starch produce vitamin K produces gas through cellular respiration Motility is slow The Appendix: haven for bacteria, repopulates the large intestine after diarrheal disease has some lymph tissue in wall Colon function: transport of Na+ Accessory organs and their functions in Digestion: The liver filters out nutrients and oxygen from blood Hepatocytes = cells of the liver lots of rough ER to make plasma protein Lots of smooth ER to breakdown fats, detoxify blood, and produce bile salts Peroxisomes: breakdown of some poisons including alcohol storage of sugar, vitamins, minerals breakdown of RBCs Gall bladder stores bile Bile contains: bile salts Products of RBC breakdown (green color) cholesterol More Disgusting diseases: Cholera: bacteria that prevents the small intestine from absorbing water

 DEATH BY DIARRHEA Gall stones: condensation of cholesterol in bile Gall stones can block ducts leading to PAIN Pancreatic Enzymes: Trypsin: breaks peptide bonds Lipase: breaks down triglycerides Amylase: splits polysaccharides Ribo and dexoyribonuclease: breaks down DNA and RNA Hormones of Digestion: Gastrin (stomach): stimulates acid secretion and sm + lg intestine motility CCK (sm intestine): stimulates bile release and inhibits gastric emptying Secretin (sm intestine): inhibits acid and motility in stomach, stimulates HCO3 release into sm intestine GIP (sm intestine): presence of carb or fat triggers release of pancreatic enzymes

Sensory Physiology Vocabularies: Stimulus: change in internal/external environment that triggers a response Receptors = transducers, that is they convert stimulus energy into electrical action potentials. They exist in the following two forms: specialized ends of neurons (ex. touch sensations) specialized cells that communicate with neurons (involves neurotransmitters) Exteroreceptors: surface of body Interoreceptors: innervate internal organs Sensation vs Perception: Perception = interpretation of stimuli by brain receptors can be susceptible to multiple forms of stimuli, although perception may remain the same Sensation: conscious awareness of sensory information Stimulus to AP: In sensory neurons: stimulus opens ion channels --> graded potential voltage-gated channels are further away in some sensory neurons Graded potentials must summate to a great amount for action potential to occur Prevents sensational overload In sensory receptor cells: stimulus alters release of NT either increases or decreases NT production, does not stop and go. NT is always being produced Magnitude of graded potentials influence AP frequency intensity of sensation is perceived by # of APs, not strength or magnitude of a single AP Adaption: a decrease in receptor sensitivity despite constant strength of stimulus Sensory unit: a single sensory neuron with its receptor endings or a sensory neuron + its receptor cell area encompassed by sensory unit = receptive field Magnitude of stimulus impacts # of neuron/receptor cell endings that receive stimulus more nerve endings that are impacted = higher frequency of APs = higher degree of perception Even if multiple nerve endings are involved, the same sensory unit = a single sensation Receptive fields and sensation: Small receptive field = precise location + very sensitive Large receptive fields = unexact location, not very sensitive Acuity: the degree of accurate perception Lateral inhibition: the capacity of an excited neuron to reduce the activity of its neighbors

allows for precision neuron with strongest stimulus wins involves excitatory/inhibitory synapses involves neurotransmitter GABA

Afferent sensory pathways are specific (only mechanical info, only taste info, etc.) location in brain for processing is specific as well information is integrated here Majority of each sensory network resides in the CNS, therefore peripheral sensation can get mixed up phantom limbs: intact portion of the sensory pathway continues to send signals to the CNS Referred pain: pain impulses from viscera are perceived as originating from the skin Factors that affect perception: emotion, personality, stress, social background difference from existing condition drugs brain control over conscious perception: sensations can be cancelled within a brain much sensory system is devoted to detecting changes that we are unaware of changes in blood pressure/blood chemistry Reflexes: neural circuits that operate without conscious control (involuntary) work to maintain homeostasis Types of reflexes include: monosynaptic: simple reflex where the afferent neuron synapses directly onto the efferent neuron polysynaptic: more than one synapse --> slower Ipsalateral: reflex on lateral side same side reflex Contralateral: opposite side reflex Stretch reflex: a muscle contraction in response to stretching within the muscle (ex. knee jerk) generally monosynaptic Postural reflex: maintenance of balance when center of gravity shifts inputs come from vision, equilibrium, proprioception, etc. All reflexes have synapses within the spinal cord, some have ascending tracts to the brain spinal cord injury - reflexes below point of injury are maintained General vs special senses: somatic senses: pain, temp, touch, stretch, pressure, etc. Special senses: gustation, olfaction, vision, equilibrium, and hearing (TOUCH AINT SPECIAL) limited to the head

Receptor classification: distribution: somatic vs visceral stimulus origin: extero-intero and proprioceptors: detect changes in limb position, located in muscles, tendons, and joints. General Senses: proprioception: mechanoreceptors that detect stretch of muscles/ligaments to determine body position Tactile sensation: touch, heat cold, pressure, etc. specialized structures for different functions small receptive fields Pain reception: nocireceptors, respond to tissue damage Primary motor cortex and primary somatosensory cortex are adjacent: somatosensory cortex = posterior to primary motor cortex receives sensory info from efferent sensory neurons primary motor cortex = controls voluntary movement Temperature: sensed by dentritic endings of unmyelinated sensory neurons contains ion channels that open at specific temperatures Pain: stimuli: mechanical deformation of tissue, extremes of temps, chemicals chemicals include harmful acids + bases cell damage triggers release of histamines cytokines Neurons have ligand gated channels (nocireceptors) unmyelinated mostly use substance P Gustation (Aka contact chemoreception): taste cells housed in taste buds on tongue mouth and throat taste buds housed in papillae in tongue taste buds are comprised of gustatory cells + basal cells basal cells replace gustatory cells every 7 to 10 days 5 tastes: salty, sweet, sour, bitter, and umami possible 6th taste = sensation geared towards fats Capsaicin = spice found in hot spicy foods signals through oral TRPV1 receptors --> similar sensation to heat pain number of taste buds is determined by genetics high number of taste buds = super taster spicy tolerance = fewer taste buds

Olfaction: chemoreceptors 80% of food flavor comes from smell olfactory receptor neurons are replaced by stem cells every 2 months 1 o 2 types of known neurogenesis female sex hormones increase neurogenesis --> heightened sense of smell during pregnancy Olfactory organs: epithelium in nasal cavity = location of cell bodies and dendrites of olfactory receptor cells axons extend through base of skull and into olfactory bulb synapses with neurons of olfactory nerve Vision: photoreceptors in the eyes