Exam 3: GI and Cardiovascular Flashcards

Question

Composition, release, and breakdown of bile

Answer 1

Bile made from liver for fat digestion in response to CCK and secretin Bile = water + HCO3- + bile salts + bile pigments (bilirubin) + others CCK stimulates bile salt making from hepatocytes Secretin stimulates secretion of HCO3- by biliary ductal cells and HCO3- neutralizes acidic chyme from stomach Bile pigment is from hemolysis - gives greenish color - conjugated bilirubin is excreted by kidneys - elevated bilirubin leads to jaundice Other (electrolytes, cholesterol, phospholipids) --------------------------------------------------------- Secretion and storage: 1. CCK -> bile salts by hepatocytes 2. Secretin stimulates HCO3- by ductal cells 3. Bile collected in bile ducts and stored in gall bladder - stores concentrated bile by reabsorbing water - concentrated bile is needed for fat digestion 1. CCK -> contraction of gallbladder 2. CCK -> relaxation of sphincter of Oddi -> bile flow into duodenum assisting in fat emulsification 3. Once used, 95% bile salt is reabsorbed into enterohepatic vein of ilium and recycled

Answer 2

Gallstones: **crystals** formed due to too much cholesterol or bilirubin & **block passage of bile** - **Intrahepatic bile duct stones** (hepatolithiasis) - **gallbladder stones** (cholecystolithiasis) - **extrahepatic** bile duct stones They cause abdominal pain, jaundice, bloating, **deficient fat digestion**, inflammation (cholecystitis) or infection

Answer 3

Pancreatic exocrine glands secrete pancreatic juice for digestion of carbohydrates, proteins, lipids, and nucleic acids * * pancreatic juice = water, HCO3-, enzymes * * pancreatic enzymes are either active or inactive * * active lipases and amylases don't need an activator * * inactive zymogens must be converted to active by an activator (usually trypsin) Endocrine glands of pancreas secrete pancreatic hormones such as insulin and glucagon to control blood glucose

Answer 4

The production of pancreatic juice (H2O, HCO3-, enzymes) is stimulated by CCK and secretin CCK stimulates production of pancreatic enzymes (active and inactive) Secretin stimulates HCO3- secretion They both go through the same duct into the duodenum in the small intestine

Answer 5

Sialorrhea: drooling/excess saliva - due to lack of swallowing (cerebral palsy, parkinsons) - or excess production of saliva - can be treated with anti-cholinergic medications to slow down parasympathetic portion) Xerostomia: dry mouth - medications, aging, radiation, Sjogren's syndrom -> less saliva -> problems with chewing/swallowing -> plaque, tooth decay, gum disease, mouth sore

Answer 6

Liver: - detoxifies metabolites, synthesizes proteins and produces biochemicals (bile); necessary for digestion and growth gallbladder: - Stores and concentrates bile

Answer 7

Inflamed or damaged pancreas Causes: gallstones, excessive alcohol intake, cystic fibrosis, elevated fat in plasma Symptoms: abdominal pain, bloating, flatulence, deficiency in digestion and absorption of food due to deficiency in pancreatic digestive juice and maybe cancer

Answer 8

Zymogens, which need to be converted to active through an activator

Answer 9

Triggered by sensory stimuli (sight, smell, taste, touch) and the 1st 30min of a meal Voluntary: 1. Mastication (chewing) - teeth, muscle, tongue, saliva - increases digestion speed - mixes food with saliva -> partial digestion of starch with amylase in mouth -> bolus leaving mouth to esophagus contains (carbs: partial digestion, protein: no digestion, fat: no digestion) 2. Initiation of deglutition (swallowing) - move bolus into the esophagus - voluntary oral phase - involuntary pharyngeal phase - involuntary esophageal phase Involuntary (mediated by parasympathetic NS, PNS of ANS): 1. salivary secretion 2. swallowing reflex - control center in medulla dictates movement of mouth, pharynx, larynx, & esophagus; once tactile receptors in pharynx are activated (pharyngeal phase), it can't be stopped 3. esophageal peristalsis 4. gastric secretion and motility

Answer 10

Upper esophageal sphincter (UES) (skeletal) Lower esophageal sphincter (LES) (smooth) UES relaxes so bolus can enter esophagus Peristalsis: - most prominent in GI tract - produces series of reflexes involving vagal nerves in response to distention of wall by bolus - muscle contracts on mouth side, relaxes on stomach side of bolus allowing propulsion of bolus Once bolus is pushed into stomach, LES relaxes and constricts Primary: controlled by brainstem and requires vagal efferent activity; 5 sec from pharynx to LES Secondary: slower, weaker, local reflex initiated by unsuccessful primary (if food does not move through esophagus)

Answer 11

Gastroesophageal reflex disease (GRD, GERD): esophagitis Burning sensation caused by reflux of acid from stomach into esophagus due to decreased LES pressure (Relaxed LES) Fat, ethanol, chocolate peppermint, caffeine and theophylline, smoking, barbiturates, **progesterone** (prego), and in large stomach volume and supine posture Can result in esophageal ulcers Barretts esophagus linked to GERD - new lining similar to stomach - linked to esophageal cancer

Answer 12

Triggered by arrival of bolus (gastric distention) -> vagal stimulation -> gastric secretion and gastric motility partially digested carbs, undigested proteins, undigested fats arriving to stomach 1. function of stomach - stores food - kills bacteria using HCl - enzyme digestion of proteins - regulates movement of chyme into duodenum through pyloric sphincter (stomach emptying) 2. gastric secretion for digestion - mucous cell: mucus - parietal cells: HCl & intrinsic factor (IF) - Chief cells: pepsinogen (zymogen), HCL leads to pepsin (active endopeptidase) -> partial digestion of proteins

Answer 13

- mucous cell: mucus - parietal cells: HCl & intrinsic factor (IF) - Chief cells: pepsinogen (zymogen), HCL leads to pepsin (active endopeptidase) -> partial digestion of proteins

Answer 14

Synthesized by parietal cell Cytosol: carbonic anhydrase - H2O + CO2 --> H2CO3 --> H+ + HCO3- At basolateral membrane: - HCO3- (bicarbonate)/Cl- --> blood/ICF Apical membrane: Cl-, K+ ions -> lumen by conductance channels H+ ion is pumped into lumen, in exchange for K+ through the action of the proton pump (H+/K+ ATPase); K+ recycled ------------------------------------------------------------- Gastric HCl: denatures ingested proteins (after tertiary proteins) so become more digestible activates pepsinogen (zymogen) from chief cells to pepsin -> partial digestion of proteins inactivate salivary amylase ------------------------------------------------------------- Factors stimulating gastric HCl secretion: ACh -> PNS activation (vagus nerve) Gastrin -> from G cells in response to Ach Histamine -> from ECL cells in response to Ach Histamine potentiates Ach and gastric effects -> best target to inhibit gastric acid secretion - histamine H2 receptor antagonist Prostaglandin - inhibits HCl secretion

Answer 15

partial digestion of proteins --> enzyme pepsin (15-25% normally) Inactivation of salivary amylase (no further digestion of starch) Absorption of alcohol: 20% Absorption of acidic drugs like aspirin: rapidly absorbed in stomach

Answer 16

Gastric mucosa is guarded by "barrier" that provides protection against attack factors (acid, pepsin, bacteria, bile salts, aspirin, alcohol) Mucosa calls rapidly turn over (epithelium replaced in 3 days) Tight junction prevent HCl from leaking past epithelial cell layer; parietal and chief cells impermeable to HCl Mucosa cells secrete alkaline mucus containing HCO3- to neutralize HCl High blood flow in mucosa (to dilute and wash out) In response to acid-insult, mucosa cells secrete prostaglandins that inhibit gastric secretion and increase blood flow

Answer 17

Erosion of the mucosa of the stomach (or duodenum) extending into the muscularis externa Produced by action of HCl, refluxed bile salts, pepsin, or ingested irritant substances Erosions of mucosa/submucosa are normal but ulcers are not ------------------------------------------------------------- Causes: - excessive secretion of HCl or exaggerated action of HCl - excessive gastric secretion: **zollinger-ellison syndrom** (caused by gastrinoma) - **helicobacter pylori bacterium** weakens protective mucosa coating, allowing acid to get to sensitive lining beneath - **acute gastritis**: histamine released by tissue damage and inflammation stimulate further acid secretion

Answer 18

AKA vomiting Activation of vomit center in medulla by: - activation of peripheral (intestinal) receptors -> vagal afferent - central chemoreceptor activation (psychogenic: pregnancy) - visual and vestibular mismatch Vomit center: - vagal efferent to the GI -> relaxes sphincters in esophagus, stomach, and duodenum - phrenic and spinal nerves to skeletal muscle for respiration -> skeletal muscles contracts to generate force

Answer 19

Bolus enters stomach from esophagus (fed state) -> Gastric distention -> vagus nerve stimulates gastric motility/muscle contraction and acid secretion -> peristaltic waves/propulsion of chyme toward the pyloric sphincter -> gastric pressure increases causing retropulsion -> acid chyme relaxes pylori sphincter -> gastric emptying Gastroparesis (delayed gastric emptying) may be caused by damage to the vagus nerve

Answer 20

**Migrating motor complex (MMC)** aka interdigestive myoelectric complex Burst of "housekeeping" contractions in response to **MOTILIN** (hormone from stomach and duodenum) MMC cleans leftover digestion and prevents bacterial growth Initiated at the stomach & moves to small intestine

Answer 21

Vagus nerve -> motility Hormones (CCK & Secretin) -> secretion of bile and pancreatic juice -> digestion of carbs, proteins, and fat -> absorption of nutrients, vitamins, minerals and water Acidic chyme and distention of duodenum - partially digested carbs - partially digested proteins - undigested fat

Answer 22

Small: - requires secretion of CCK and secretin - required bile salts, pancreatic enzymes, and brush boarder enzymes - leads to complete digestion of carbs, protein , and fat monomers - electrolytes absorb nutrients, vitamins, minerals and water - 90% of water and electrolytes are being absorbed here - segmentations and peristalsis Large: - fermentation of soluble fiber and resistant starch by bacteria - Colonocytes absorb vitamins, electrolytes and water produced by bacteria - 10% water and electrolytes absorbed here - defecation reflex (waste compaction and absorption) - Haustration and mass movement

Answer 23

3-5m 1. Duodenum (connected to duct to pancreatic and bile duct) - shortest 2. Jejunum 3. Ileum Villi and microvilli increase surface area and several types of mucosa cells Specialized cells in mucosa - goblet (mucus secreting) - intestinal crypt with stem cells - absorbs enterocytes and brush boarder enzymes Lymphatic Peyer's patches - aggregated lymphoid nodules for immune surveillance and immune reactions

Answer 24

Duodenal distention with acidic chyme -> secretion of hormones secretin and cholecystokinin (CCK) -> secretion of bile and pancreatic juice CCK from duodenum - released due to fat and protein content in chyme - increases production of pancreatic enzymes and bile salts - increases contraction of gall bladder and relaxation of sphincter of Oddi -> flow of bile and pancreatic juice in duodenum -> digestion Secretin from duodenum - released due to duodenal pH < 4.5 - increases HCO3- by pancreas - increases HCO3- by the liver (part of bile)

Answer 25

requires pancreatic amylase and brush boarder enzyme disaccharides to monosaccharides 1. oligosaccharides (product of digestion by salivary amylase) 2. Pancreatic amylase in lumen - oligosaccharides -> disaccharides (maltase, sucrose, lactose) 3. brush boarder enzymes - disaccharides -> monosaccharides -> enterocytes

Answer 26

No glucose secondary transporter: - driving force: Na+ concentration gradient across the apical membrane: maintained by the activity of Na-K pump in the basolateral membrane and secretory crypt cells Fructose by facilitated diffusion Monosaccharides into enterocytes -> capillaries -> enterohepatic portal vessel

Answer 27

Caused by decrease in lactase production by age, genetics, or temporary decline in lactase production due to inflammation in gut wall (celiac disease) Leads to a cause of osmotic diarrhea

Answer 28

1. oligopeptides (comes from digestion by gastric pepsin) 2. zymogens in pancreatic juice are activated - bush boarder enzyme enterokinase/enteropeptidase: trypsinogen -> trypsin - trypsin activates other zymogen peptidases (oligopeptides -> dipeptides)

Answer 29

1. fat globule - bile salts -> **fat emulsification** (fat globules -> fat emulsion droplets in micelle) 2. pancreatic lipase: emulsion droplets -> **free fatty acids + monoglycerides** 3. formation of mixed micelle (free fatty acids + monoglycerides + bile salts) -> **diffuse through enterocytes** -> resynthesized fat packaged into lipoprotein complex **chylomicron** in enterocytes -> exocytosis -> lacteal -> **lymphatic circulation** -> general circulation Chylomicrons deposit triglycerides into fat cells: - Chylomicrons/triglycerides reach the fat tissue; triglycerides are hydrolyzed by endothelial lipoprotein lipase into fatty acids and monoglycerides, which enter the adipocyte - they are resynthesized into triglycerides (in fat cells) - The chylomicron remnants are taken to the liver and repackaged into VLDL (very low density lipoprotein) which delivers triglycerides to the peripheral tissues including the fat tissue.

Answer 30

if bile secretion in sm intestine is blocked, fat digestion can be compromised can be due to pancreatitis and would compromise digestion of fats, proteins and carbs

Answer 31

Duodenum: iron: carrier-mediated absorption Duodenum & Jejunum: * monosaccharides: Na-dependent carrier-mediated absorption * amino acids: Na-dependent carrier-mediated absorption * fatty acids and monoglycerol: passive diffusion into enterocytes * 90% of electrolytes (Na, Cl, K, Ca++)- carrier-mediated absorption * Water - passive diffusion via the osmotic gradient Ileum: Bile salts, vitamin B12-IF complex: carrier-mediated absorption

Answer 32

Into **portal vein** They are absorbed predominantly in the small intestine by **specific carriermediated transport systems**, except: - Vitamin **B12**: due to size and charge, B12 must bind to **intrinsic factor** (secreted by stomach parietal cells)- the complex binds to receptors in the **terminal ileum** and absorbed by endocytosis: if intrinsic factor is lost, pernicious anemia occurs

Answer 33

(A, D, E & K) in mixed micelles with FFA into enterocytes by diffusion Within the enterocyte, they are incorporated into chylomicrons and exported via exocytosis into lacteal -> lymphatic circulation

Answer 34

Autoimmune deficiency of absorption immune reaction to eating gluten Gluten triggers an immune response in the small intestine The response to gluten damages the lining of small intestine and prevents it from being able to absorb some nutrients - can lead to diarrhea, fatigue, weight loss, bloating and anemia Can affect growth and development in children

Answer 35

1.5m Appendix, Cecum, Ascending Colon -> Transverse Colon -> Descending Colon, Sigmoid Colon, Rectum & Anal Canal - Outer surface bulges outward to form haustra (small pouches which give segmented appearance) - cecum connected to ileum absorbs about 10% of electrolytes and water (apical membrane and colonocytes) large intestinal cells have tons of bacteria with their own digestive enzymes - digestion and fermentation of resistant starch and soluble fiber to short chain fatty acids -> used by colonocytes to make energy or absorbed into cappilaries -> hepatic portal vein - synthesis of vitamin K, B complexes, and folic acid -> vit K absorbed by diffusion; water soluble vitamins by carrier-mediated transport

Answer 36

Slowed segmentation contractions in haustra (haustral churning) - causes chyme to be churned in the intestine exposing the gut contents to a larger surface area of epithelium maximizing absorption - occurs continuously Mass movement, a type of propulsion motility not seen elsewhere in the digestive tube - occurs once or twice per day; involves a sudden, uniform peristaltic contraction of smooth muscle of the gut which originates at the transverse colon and rapidly moves faces into the rectum, which is normally empty -> urge to defecate

Answer 37

Mass movement: - general contractions occurring in response to the arrival of chyme in the duodenum, propelling the chyme toward the rectum - Leads to urge to defecate. - The contraction may be stimulated by eating. When this occurs it is called the gastro-colic reflex Defecation: - voiding fecal material - controlled by PNS - can be modulated by higher CNS centers - external anal sphincter is under voluntary control Defecation reflex: 1. afferent sensory to local (myenteric plexus) & parasympathetic (spinal cord/sacral) neurons 2. efferent motor neurons to smooth muscle of the rectum: (1) strong peristalsis (2) relaxation of the internal anal sphincter - contraction of the external anal sphincter 3. signal to the cerebrum for an urge to defecate 4. motor neurons from the CNS to (1) external anal sphincter for relaxation (2) smooth muscles of the rectum for stronger peristalsis, and (3) abdominal muscle (contraction) 5. fecal material into the anal canal

Answer 38

Transportation: - respiratory (O2 and CO2) - nutritive (carry absorbed digestion products to liver and tissues) - excretory (carry metabolic wastes to kidneys to be excreted) Regulation: - hormonal (carry hormones to target tissues) - temperature (divert blood to cool or warm the body) Protection: - blood clotting (preventing blood loss) - immune (leukocytes protect against disease causing agents)

Answer 39

straw colored liquid consisting of H2O and dissolved solutes - ions, metabolites, hormones, antibodies - Na+ is the major solute in plasma Plasma proteins: - 7-9% of plasma - albumin (from liver) is about 60-80% of plasma proteins and provides colloid osmotic pressure needed to draw H2O from interstitial fluid capillaries (maintains blood pressure) - alpha and beta globulins (liver): transport lipids and fat soluble vitamins - gamma globulin (lymphocytes): antibodies that function in immunity - fibrinogen (clotting factor): converted into fibrin during clotting process

Answer 40

Hematocrit: % of blood that is RBCs -> normally 40-50%

Answer 41

ERYTHROCYTES (RBCs) - promote diffusion of gases - lack nuclei and mitochondria - replaced every 3-4 months - each RBC contains hemoglobin that contains iron - iron group of the heme helps transport O2 from lungs to tissues ------------------------------------------------------------- LEUKOCYTES (WBCs) - almost invisible - contain nuclei and mitochondria granular: detoxify foreign substances 1. neutrophils 2. eosinophils 3. basophils agranular: produces antibodies 1. lymphocytes 2, monocytes ------------------------------------------------------------- PLATELETS - fragments of megakaryocytes (smallest formed element) - lack nuclei - short lived (5-9 days) - maintain integrity of blood vessel wall Important in blood clotting - most of mass of the clot - release serotonin to vasoconstrict and reduce blood to the area

Answer 42

- Caused by damage to endothelium wall - Most clotting factors produced by liver and the conversion of fibrinogen to fibrin by thrombin is common to both pathways Intrinsic - Exposes subendothelial tissue (collagen) to the blood - Exposure to collagen (and other negatively charged surfaces activates plasma protein ‘factors’ to form fibrin) Extrinsic - Damaged tissue releases thromboplastin - Thromboplastin is not a part of the blood, so called “extrinsic” - Thromboplastin initiates a short cut to formation of fibrin Plasmin eventually dissolves clots

Answer 43

AP of myocardial cells stimulate opening of VG Ca++ channels in sarcolemma Ca++ diffuses down gradient into cell - stimulating opening of Ca++ release channels in sarcoplasmic reticulum (SR) by a Ca++ induced Ca++ release mechanism (different than skeletal) - Ca++ binds to troponin and stimulates contraction (similar to skeletal) During repolarization, cytosolic Ca++ is transported into the extracellular fluid via Na-Ca exchangers and into the SR via Ca++ ATPase ----------------------------------------------------------- -Cardiac depolarization begins in sinoatrial node in right atria - Spreads to other atria - Passes to the ventricle septum to the bottom of the heart and to walls of the ventricle - atria contract to push blood in ventricle - ventricles contract to push blood up and out large arteries

Answer 44

Pulmonary circulation: - path of blood from right ventricle -> lungs -> back to heart Systemic circulation: - oxygen-rich blood pumped to all organ systems to supply nutrients Rate of blood flow through systemic circulation = flow rate through pulmonary circulation

Answer 45

Refractory periods last almost as long as contraction VG Na+ must reset at repolarized potentials before they can open again Contractions lasts almost 300 msec This is NOT tetanus

Answer 46

Electrocardiogram: Measure of electrical activity of the heart per unit of time (NOT the flow of blood through the heart or APs) 3 major waves: P wave, QRS complex, T wave P wave - atrial depolarization QRS complex - ventricular depolarization - atrial repolarization T wave - ventricular repolarization

Answer 47

The valves prevent backward flow of blood; one way inlets and one way outlets (Everything in one direction) Produce heart sounds - closing of AV (atrioventricular) and semilunar valves - Lub (first sound) produced by AV valves during isovolumetric contraction - Dub (second sound) produced by closing of semilunar valves when pressure in the ventricles falls below pressure in the arteries

Answer 48

The repeating pattern of contraction and relaxation of the heart Systole: - Phase of contraction. Diastole: - Phase of relaxation End-diastolic volume (EDV) - total volume of blood in the ventricles at the end of diastole Stroke volume (SV) - amount of blood ejected from ventricles (EDV-ESV) during systole End-systolic volume (ESV) - amount of blood left in the ventricles at the end of systole ----------------------------------------------------------------- 1. Atrial Systole - phase of contraction - push 10-30% more blood into ventricle 2. Isovolumetric contraction (isometric) - Contraction of ventricle causes ventricular pressure to rise above atrial pressure - AV valves close - Ventricular pressure is less than aortic pressure - Semilunar valves are closed and volume of blood in ventricle is EDV 3. Ejection - contraction of the ventricle causes ventricular pressure to rise above aortic pressure (~80 mmHg) - semilunar valves open - ventricular pressure is greater than atrial pressure - AV valves are closed and volume of blood ejected is SV 4. Isovolumetric relaxation - Ventricular pressure drops below aortic pressure and back pressure causes semilunar valves to close - AV valves are still closed - blood volume in ventricle ESV 5. Rapid filling of ventricles - Ventricular pressure decreases velow atrial pressure - AV valves open - Rapid ventricular filling occurs

Answer 49

* Sarcomeres contain actin and myosin * Contract via sliding-filament mechanism * Activated by calcium transients * Myocardial cells bifurcated * Joined by gap junctions (electrical synapses) * APs occur spontaneously * Spread among cells via gap junctions * Cells behave as one unit (syncytium) Myocardial A.P. - depolarization from gap junction - Rapid upshoot from Na+ channels opening and inward diffusion of Na+ - plateau phase from Ca++ inward flow (stays depolarized) - rapid repolarization from rapid outward diffusion of K+ - then resting membrane potential

Answer 50

Arteries (take blood away from heart) (pressure) Elastic arteries - numerous layers of elastin fibers between smooth muscle - expand when pressure of blood rises - act as recoil system when ventricles relax Muscular arteries - less elastic and have thicker layer of smooth muscle - diameter changes slightly as BP rises and falls Arterioles - contain highest % smooth muscle - greatest pressure drop - greatest resistance to flow

Answer 51

Capillaries (exchange) Small blood vessels of 1 epithelial cell thick; provide direct access to cells and permits exchange of nutrients and wastes Continuous - adjacent endothelial cells tightly joined together - intracellular channels that permit passage of molecules (other than proteins) between capillary blood and tissue fluid - muscle, lungs, and adipose tissue Fenestrated - wide intercellular pores that provide greater permeability - kidneys, endocrine glands, and intestines Discontinuous (sinusoidal) - have large, leaky capillaries - liver, spleen, and bone marrow

Answer 52

Balance between tissue fluid and blood plasma - distribution of extracellular between plasma and interstitial compartments is in a state of dynamic equilibrium Capillary hydrostatic pressure - blood pressure exerted against the inner capillary wall - promotes movement of fluid into tissues (filtration) Colloid osmotic pressure - exerted by plasma proteins - promotes fluid reabsorption into circulatory system

Answer 53

Veins (volume) Arteries (pressure) Most of blood volume (2/3) is contained in venous system Venules - formed when capillaries unite Veins - contain little smooth muscle or elastin - capacitance vessels (blood reservoirs) - contain one way valves that ensure blood flow to the heart Skeletal muscle pump and contraction of diaphragm - aid in venous blood return to the heart

Answer 54

Most dynamic change in pressure -> left ventricle Average is the greatest -> Large arteries Biggest drop due to resistance -> Small arteries and arterioles

Answer 55

Mean Arteriole Pressure (MAP) Depends on how much blood is being pumped by the heart into the arteries (cardiac output) and diameter of the arterioles (small arteries) allow blood to leave arteries (and into capillaries) MAP = cardiac output * total peripheral resistance Garden hose analogy: - turn on hose all the way (water pressure) (cardiac output) - when trying to get more water pressure you halfway block the water to get a higher pressure (same as a high resistance)

Answer 56

Auscultation (art of listening) - indirect method of correlating blood pressure and arterial sounds Laminar flow - normal blood flow - blood in the central axial stream moves faster than blood flowing closer t o the artery wall - smooth and silent Turbulent flow - vibrations produced in the artery when cuff pressure is greater than diastolic pressure and lower than systolic pressure - blood hitting the walls of the artery, making noise - this is what is happening when taking blood pressure using a cuff _______________________________________________________________________ 1. Blood pressure cuff inflated above systolic pressure, occluding the artery 2. As cuff pressure is lowered, the blood will flow only when systolic pressure is above cuff pressure, producing the sounds of Korotkoff 3. Korotkoff sounds will be heard until cuff pressure equals diastolic pressure, causing the sounds to disappear Average arterial BP = 120/80 mmHg Average pulmonary BP = 22/8 mmHg

Answer 57

It is the expansion of the artery in response to the volume of blood ejected by the left ventricle Pulse pressure = systolic P - diastolic P Calculating MAP: - represents average arterial pressure during the cardiac cycle - closer to diastolic pressure as the period of diastole is longer than the period of systole MAP = diastolic pressure + 1/3 pulse pressure MAP = cardiac output * TPR (total peripheral resistance)

Answer 58

Cardiac output = Heart rate * Stroke volume Stroke volume = the volume of blood ejected from the heart's left ventricle with each beat, or stroke Volume of blood pumped each minute by the ventricles - pumping ability of the heart is a function of beats/min (HR) and volume of blood ejected per beat (SV) - total blood volume averages about 5.5 liters Each ventricle pumps the equivalent of the total blood volume each min (resting) -------------------------------------------------------------------------------------------------- Autonomic control of CO: Parasympathetic stimulation (lowering HR) - negative chronotropic effect (does not directly influence contraction strength: SV -> iontropy) Sympathetic stimulation (increasing HR & SV) - positive chronotropic effect on HR (timing) - positive iontropic effect on contractility (strength of contraction)

Answer 59

SA node initiates the action potentials in the heart APs in SA node: - Demonstrate automaticity (all on their own) which functions as the pacemaker - Spontaneous depolarization (pacemaker potential) -> I(f) channels (funny) open in response to repolarization (allow inward diffusion of Na+) Cells do not maintain a stable resting membrane potential, it is always changing Depolarization: - VG Ca++ channels open and Ca++ diffuses inward Repolarization: - VG K+ channels open and K+ diffuses outward SA node spreads APs to working myocardial cells via gap junctions --------------------------------------------------------------------------------------------------- Regulation of HR: Without neuronal influences, the heart beats 90 times per minute Autonomic control - symp and para nerves innervate the SA node - NE and Epi increase AP frequency (HR) (sympathetic NS) - ACh decreases AP frequency (HR) (parasympathetic NS) Cardiac control center (medulla oblongata) coordinates activity of autonomic innervation

Answer 60

Frank-starling Law: - relationship between EDV, contraction force and SV - intrinsic mechanism -> varying degree of stretching of myocardium by EDV -> as EDV increases, myocardium is increasingly stretched and contracts more forcefully -> as the ventricles fill, the myocardium stretched; so that the sarcomere myofilaments overlap increases to generate more crossbridges Contractility: - strength of contraction at any given fiber length - depends upon sympathoadrenal system: -> NE and Epi produce an increase in contractile strength - Also depends on iontropic effect (more Ca++ available to sarcomeres) - at a given EDV

Answer 61

EDV-length tension curve EDV (most blood in ventricle at this time) - volume of blood in the ventricles at end of diastole - frank-starling relationship (length-tension) curve Contractility - strength of ventricular contraction **at a given length** - Ca++ availability to attach to troponin Anything that increases cross bridges will increase contraction and increase SV

Answer 62

TPR: - impedance to the ejection of blood from ventricle - the pressure of arteries before the ventricle contracts is a function of TPR MAP = cardiac output * TPR

Answer 63

Physical laws describing blood flow: - the flow of blood through the vascular system is due to the difference in pressure at the two ends (ΔP) Flow = ΔP/R - R = TPR (sum of all vascular resistance within the systemic circulation) - blood flow directly proportioned to pressure differences - inversely proportional to resistance Major regulators of blood flow: - MAP - Vascular resistance to flow Resistance – Opposition to blood flow. – directly proportional to length of vessel and to the viscosity of the blood. – Inversely proportional to 4th power of the radius of the vessel R = Ln / (r^4) – L = length of the vessel – n = viscosity of blood – r = radius of the vessel (inversely related) Arterial blood flow is in parallel

Answer 64

Symapthoadrenal (NE and Epi): 1. increase CO (heart rate & SV) 2. Increase TPR - alpha-adrenergic stimulation (vasoconstriction of arterioles in skin and viscera - beta adrenergic stimulation (vasodilation of arterioles to skeletal muscles)

Answer 65

Stretch receptors located in the aortic arch and carotid sinuses An increase in pressure causes the walls of these regions to stretch, increasing frequency of APs Baroreceptors send APs to vasomotor control and cardiac control centers in the medulla Baroreceptor reflex activated with changes in BP More sensitive to decrease in pressure and sudden changes in pressure

Answer 66

Parasympathetic NS - innervation is limited and promotes vasodilation to the digestive tract, external genitalia, and salivary glands - less important than sympathetic NS in control of TPR Metabolic regulation - how metabolically active is that tissue? - sensory receptors sense chemical changes in environment - vasodilation: 1. decreased O2 2. Increased CO2 3. Decreased pH 4. Increased adenosine or K+ Autoregulation (important for the brain) - myogenic (originating in smooth muscle) control mechanism: - occurs because of the stretch of the vascular smooth muscle - a decrease in systemic arterial pressure causes cerebral vessels to dilate - high blood pressure causes cerebral vessels to constrict in order to maintain adequate flow Chemical ligand regulators: - endothelium in blood vessels produces several paracrine regulators - endothelium of arterioles contains eNOS (endothelial nitric oxide synthase) which produces nitric oxide (NO) - NO diffuses into smooth muscle (vasodilation) - bradykinin (sweat gland) -> vasodilation to skin capillaries Coronary -> autonomic and heart Skeletal -> autonomic and metabolic (primary during exercise) Cerebral -> metabolic and myogenic (vessels sensitive to stretch)

Answer 67

Vascular resistance decreases to skeletal muscles. – Blood flow to skeletal muscles increases – CO increase (HR and SV) * Blood flow to brain stays same – HR increases to maximum of 190 beats/min * Ejection fraction increases due to increased contractility (SV/EDV) (usually 60% at rest) Vascular resistance: – Decreases to skeletal muscle. – Increases to GI tract and skin. – TPR might not change much…except… exercising on a hot day (some blood going to different places)

Answer 68

Arrhythmias - abnormal heart rhythms Bradycardia - HR slower < 60 beats/min Tachycardia - HR > 100 beats/min Flutter - extreme rapid rates of excitation and contraction of atria or ventricles - atrial flutter degenerates into atrial fibrillation Fibrillation - contractions of different groups of myocardial cells at different times - coordination of pumping is impossible - ventricular fibrillation is life-threatening

Answer 69

What is it? - aka AFib - most common type of irregular heartbeat - the abnormal firing of electrical impulses causes the atria (top chamber of heart) to quiver (fibrillate) - there's no P waves - irregular R wave intervals - ventricles are steady though - types (proximal, persistent, permanent) What can it cause? - blood clots in atria, and can block blood vessels in the brain, causing stroke How is it treated? - electrical paddles and cardioversion, ablation (get rid of extra stimulating spots), **blood thinners**!!, anti-arrhythmic medications (b-blockers( How do blood thinners work? - these help prevent the risk of stroke - prevent blood from clotting Which pathway is targeted? - ???

Answer 70

Heart murmurs: Valves Abnormal heart sounds produced by abnormal patterns of blood flow in the heart (turbulence) Murmurs produced as blood regurgitates through valve flaps due to damaged or defective valves - valves become damaged by antibodies made in response to an infection, or congenital defects - Mitral (biscuspid) valve becomes thickened and calcified - Damage to papillary muscles - valves do not close properly/stenosis (not opening all the way) !!!! -------------------------------------------------------------------------------------------------- Heart murmurs: Holes Septal defects: - usually congenital - holes in septum between left and right sides of the heart - may occur in interatrial or interventricular septum - blood passes from left to right during contraction, can mix during diastole, depends on which pressure is higher Blood mixing between the two ventricles

Answer 71

Form of hardening of the arteries Causes: 1. Damage to the endothelial cell wall due to hypertension, smoking, high cholesterol, diabetes 2. Cytokines are secreted by endothelium; platelets; macrophages, and lymphocytes, leading to an immune response and attracting more monocytes and lymphocytes 3. Monocytes become macrophages and engulf lipids and transform into foam cells 4. Smooth muscle cells synthesize connective tissue proteins - smooth muscle cells migrate to tunica interna, and proliferate forming fibrous plaques Cholesterol and lipoproteins causing the plaque: 1. lipoproteins carry lipids in the blood 2. cholesterol is carried TO arteries by Low-density lipoproteins (LDL), which are produced in liver and are high in people who have a rich saturated fat diet 3. cholesterol is carried AWAY from arterial wall by high-density lipoproteins (HDLs) - HDL protect against atherosclerosis - HDL low in sedentary people and higher in people who exercise - Drugs that raise HDL are statins, fibrates, or high doses of niacin Steps: 1. LDL deposits cholesterol between layers in artery wall 2. Fatty streak between vessel walls 3. Immune response 4. Foam cells expand plaque 5. Plaque is unstable and can rupture and blood clot forms (thrombus) 6. Heart muscle can start to die --------------------------------------------------------------------------------------------------- Treatment: Cardiac cath: - insert catheter to blood stream, inject dye, measure profusion of heart muscle by visualizing the dye - Fix through use of angioplasty, a balloon that opens up the artery (temporary fix), then apply a mesh stint to keep it unblocked Bypass: - treats blocked heart arteries by creating new passages for blood flow to your heart - takes arteries or veins from other parts of your body (called grafts) and using them to reroute blood around the clogged artery

Answer 72

Ischemia: - oxygen supply to tissue is deficient - most common cause is atherosclerosis of coronary arteries - increased [lactic acid] produced by anaerobic metabolism - classic chest pain (substernal pain) Myocardial infarction (aka heart attack): - changes in ST segment of ECG - Can determine if someone had a heart attack through: increased blood levels of creatine phosphokinase (CPK), lactate dehydrogenase (LDH), and troponins (T and I) ---------------------------------------------------------------------------------------------------- Symptoms: Both genders have: chest discomfort, pain and discomfort in other areas, in one or both arms, the back, neck, jaw or stomach, shortness of breath, Other signs may include breaking out in a cold sweat, nausea, or lightheadedness More common in women: - back, neck, jaw pain - shortness of breath - nausea

Answer 73

Greater than 130/80 mmHg Primary hypertension: - know the person has it but not sure why Secondary hypertension: - know why it is occurring (i.e. person has kidney disease) Dangers: - people asymptomatic until substantial vascular damage occurs (atherosclerosis) - increases workflow of the heart - congestive heart failure - damage cerebral blood vessels -> stroke ---------------------------------------------------------------------------------------------------- Treatment: 1. Modification of lifestyle - stop smoking - moderate alcohol - weight reduce - exercise - reduce salt intake - high diet in potassium 2. Medications - Diuretics: increase urine volume (blood volume goes down) - B-blockers: decrease HR (decrease cardiac output) - Calcium antagonists: block Ca++ channels (vasodilator) (decrease TPR) - ACE inhibitors: inhibit conversion of angiotensin II - Angiotensin II-receptor antagonists: block receptors

Answer 74

Cardiac output is insufficient to maintain the blood flow required by the body (i.e. meet metabolic demand) - increased venous volume and pressure Caused by: - myocardial infarction (most common) - congenital defects - hypertension - aortic (semilunar) valve stenosis - disturbances in electrolyte concentrations (K+ and Ca++) Treated with vasodilators and diuretics 50% within 5 years will die when being diagnosed heart failure