Exam 3: GI and Cardiovascular Flashcards
Relationship between digestive system and others
Digestive system is like a disassembly line
Breaks down huge macromolecules in ingested food into smaller molecules that can be absorbed across the wall of the tube and into the circulatory system and excrete waste material
CardioVasc system distributes the nutrients and oxygen in all body cells and gets rid of waste and CO2 to disposal organs
Respiratory system takes the oxygen and eliminates CO2
Urinary system eliminates the nitrogenous waste and excess ions
Primary digestive organs and accessory organs
Primary (hollow tube, GI tract, alimentary canal which moves food along and involved in secretion, digestion, absorption and motility)
- mouth/oral cavity
- pharynx
- esophagus
- stomach
- small intestine
- large intestine
- rectum
- anus
Accessory (help with digestion but are not part of alimentary canal)
- teeth
- tongue
- salivary glands
- liver
- gallbladder
- pancreas
Major functions of the digestive tract
Main functions: secretion, digestion, absorption, and motility
Region specific motilities:
- esophagus -> rapid pass
- %50 of stomach contents emptied -> 2.5-3hrs
- %50 emptying of small intestine -> 3-4hrs
- transit through colon -> 30-40hrs
Highest secretion in the upper part of the small intestine (duodenum) leads to highest digestion -> absorption into hepatic portal vein (hydrophilic molecules) and into lymphatic vessels (hydrophobic molecules)
Secretion aids the digestion and absorption and helps with homeostatic fluid exchange (highest level occurs in intestine; small»_space; large)
Locations of skeletal and smooth muscles in the digestive tract
Skeletal:
- chewing or masticatory muscles
- tongue
- upper esophageal sphincter
- upper esophagus
- external anal sphincter
Rest of GI tract is SMOOTH muscle
- controlled by local reflex as well as autonomic nervous system
- totally under involuntary control
Characteristics of skeletal and GI smooth muscles
Smooth muscles:
- contraction is by phosphorylation of myosin (dephosphorylation causes relaxation)
- activator (Ach) -> A.P. induced membrane depolarization -> Voltage gated Ca++ channels open -> Ca++ influx -> activation of myosin light chain kinase (MLCK) -> p-myosin -> contraction
- inhibitor signal (NO) -> increase in cGMP -> activation of myosin light chain phosphate (MLCP) -> dephosphorylation of myosin -> relaxation
- makes up organs
Skeletal:
- A.P. arrives at neuromuscular junction
- Ach is released, binds to receptor, opens Na channels, leads to A.P. in sarcolemma
- A.P. travels down T-Tubules
- leads to cross-bridge cycling
- muscle shortens and contracts
Compare and contrast tonic, peristalsis and segmentation
Tonic:
- sustained contraction no movement of food
- occurs at the sphincters to separate one region from another
PHASIC (peristalsis and segmentation)
- in GI except sphincters
Peristalsis:
- Adjacent segments of the GI canal alternately contract and relax UNIDIRECTIONAL movement of food
- prominent in esophagus
- rhythmic, contraction-relaxation of smooth muscle for propulsion of a bolus of food/chyme
- contraction behind the food (mouth side)
- relaxation in front of the food (anal side)
Segmentation:
- non-adjacent segments of the GI canal contract and relax BIDIRECTIONAL movement of food
- prominent in the small intestine»_space; large intestine
- stationary contraction
- slows progression of chyme, which allows digestion and absorption via the epithelial cells
Structural layers of the GI walls
- Serosa (outer most)
- Muscular externa (longitudinal-circular)
- Submucosa
- Mucosa
- Lumen
Most common organization (mucosa - submucosa - muscularis externa - serosa) but regional differences for specific regions
Components of the enteric nervous system
The brain of the gut
Myenteric plexus + submucosal plexus
Local nervous system controlling GI activities and secretion and motility
- Sensory neurons receive info from sensory receptors in the mucosa & muscle and relay to interneurons
- Interneurons function as integrating center
- Motor neurons act on effector cells of smooth muscle, secretory cells and endocrine cells
Modulated by the innervation/activity of ANS (para and symp)
Million of neurons in the gut
Slow waves and what they do
With phasic contraction
AKA: basic electrical rhythm (BER) and are oscillating depolarizing membrane potential found in GI smooth muscle (repeating depolarizatin and repolarization)
“Myogenic” (myogenic electrical rhythm) slow waves are pacemaker cells - interstitial cells of Cajal (ICC) of the myenteric plexus
- pacemaker cells and smooth muscle are electrically coupled via gap junctions
Different frequency of slow waves:
- 10-20/min in the small intestine
- 3-8/min in the stomach and colon
typically no contraction (No A.P.)
How does the autonomic nervous system affect GI activity
ANS innervates GI wall modulating electrical activity of ENS and or smooth muscle
When there is stretch, neurotransmitter or hormones, membrane potential may become over he threshold potential and generate A.P. -> contraction
Explain gastroenteric reflexes
- Upstream afferent stimulates downstream effect
- downstream afferent inhibits upstream effect
Gastroileal:
- increased gastric activity
- increased motility of ileum and movement of chyme through ileocecal sphincter
Gastrocolic:
- increased gastric activity
- increased motility of large intestine
Ileogastric:
- distension of ileum
- decreased gastric motility
What is the alimentary canal?
Mouth to anus (30ft long)
Differences lead to differences in motility, digestion, and absorption
describe the muscosa
Most variable layer in structure and function!
Epithelial cells
1) Protective epithelia - most abundant in the esophagus
2) Secretory epithelia - through entire GI tract
- mucus secreting cells (goblet cells in small intestine)
- enteroendocrine cells secreting hormones (gastrin-secreting G cells in the stomach)
- enterochromaffin-like (ECL) cells secreting neurotransmitters (histamine)
3) Absorptive epithelia
- enterocytes: most abundant in the small intestine; some in the large intestine
Lamina propria: connective tissue (immune cells, lacteal & capillaries)
Muscularis mucosae: A smooth muscle layer responsible for the folds and villi which increase surface area
Describe the submucosa
Connective tissue layer with arteries, veins, and lymph vessels
Submucosal plexus (meissner’s plexus):
It senses the environment within the lumen, and regulates the blood flow, epithelial cell function, and secretion from exocrine glands
In regions where these functions are minimal (esophagus, the submucous plexus is sparse)
Describe the muscularis externa
Circular and longitudinal muscle in perpendicular orientation
Myenteric plexus (Auerbach’s plexus) between longitudinal and circular layers of muscle; primary controls motility of the digestive tract by controlling contraction and relaxation of circular and longitudinal muscles independently
Describe the serosa
Covers the organs in the body cavities; Adventitia attaches the organ to the surrounding tissues (found in the esophagus)
Explain short reflexes
Mediated by activities of the ENS
Sensory neurons in mucosa respond to changes (stretch), low pH, and high osmolarity
Interneurons within ENS
Motor neurons activate effectors (muscle, secretory epithelia, blood vessel) -> changes GI activity (motility, secretion and blood flow)
Explain long reflexes
Explain how neural and hormonal inputs work together to modulate GI function
What are accessory glands and name them
Glands that aid digestion but are not apart of the alimentary canal
Salivary: saliva formation and control
Liver: bile component; CCK and bile salts; secretin and HCO3-
Gallbladder: Bile concentration; CCK and bile secretion
Pancreas: Pancreatic juice components; CCK and pancreatic enzymes; secretin and HCO3-
The 2 GI strategies for efficient digestion and absorption
- structural modification with intestinal villi and microvilli to increase the surface area of absorption
- Chemicals of exocrine secretions for modulating motility, digestion and absorption
- secretion from exocrine glands into lumen through a duct include enzymes, organic/inorganic compounds, ions, and acids
- rate of content of exocrine secretions is modified by hormones from ductless endocrine glands of stomach and small intestines
Understand how saliva is made and what controls the rate of flow and composition
3 main salivary glands: parotid, submandibular, and sublingual make majority of saliva
- initial isotonic saliva becomes hypotonic final saliva in salivary duct
- initial saliva is secreted by terminal acini
- saliva is modified in the striated duct; impermeable to water; secretion of K+/HCO3- into lumen; reabsorption of Na+/Cl- into blood
- ends with hypotonic saliva into collecting ducts and oral cavity
Composition depends on the flow which dictates modification in the striated duct
ANS controls saliva secretion and flow
- (MAJOR) parasympathetic stimulation: increases production -> increases flow of saliva/less modification -> more watery saliva
- (less important) sympathetic stimulation: decreases production; increases protein secretion; decreases saliva flow/more modification -> thick saliva
Structural characteristics of the liver and the role of hepatic portal system
Liver:
- detoxifies metabolites, synthesizes proteins and produces biochemicals (bile); necessary for digestion and growth
Hepatic lobule(main structure)
- portal triads: hepatic artery, portal vein, bile duct
- central vein
- hepatic plates: 1-2 hepatocytes thick: separated by sinusoids and bile canaliculi networks
- kupffer phagocytic cells: lines the walls of sinusoids
Hepatic portal system:
- system of veins that connect the capillaries of spleen and gastrointestinal tract (lower esophagus, stomach, small & large intestine, upper anal canal) to the liver sinusoids
- carries hydrophilic substances that are absorbed from small intestine
- system is designed to get rid of toxic substances from the body
Liver diseases:
- Hepatitis from viruses
- fatty liver disease and cirrhosis from alcohol or poisons
- cancer
Understand recycling of bile salt
CCK stimulates bile salt production by hepatocytes
Bile salts are derivatives of cholesterol; have amphipathic property which helps fat emulsification
Recycled by enterohepatic circulation.
- CCK -> contraction of gallbladder
- CCK -> relaxation of sphincter of Oddi -> bile flow into duodenum assisting in fat emulsification
- Once used, 95% bile salt is reabsorbed into enterohepatic vein of ilium and recycled
Composition, release, and breakdown of bile
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:
- CCK -> bile salts by hepatocytes
- Secretin stimulates HCO3- by ductal cells
- Bile collected in bile ducts and stored in gall bladder
- stores concentrated bile by reabsorbing water
- concentrated bile is needed for fat digestion - CCK -> contraction of gallbladder
- CCK -> relaxation of sphincter of Oddi -> bile flow into duodenum assisting in fat emulsification
- Once used, 95% bile salt is reabsorbed into enterohepatic vein of ilium and recycled
What are gallstones and how do they affect GI activity
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
Structural and functional characteristics of pancreas
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
Relationship in the secretion of bile and pancreatic secretions
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
Diseases of saliva production
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
Functions of the liver and gallbladder
Liver:
- detoxifies metabolites, synthesizes proteins and produces biochemicals (bile); necessary for digestion and growth
gallbladder:
- Stores and concentrates bile
Explain pancreatitis, causes and symptoms
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
Explain inactive pancreatic enzymes and name them, the enzyme, and the activator
Zymogens, which need to be converted to active through an activator
Triggers and events of cephalic phase
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
Esophagus peristalsis (primary and secondary)
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)
Causes of heartburn
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
Triggers and events of gastric phase
Triggered by arrival of bolus (gastric distention) -> vagal stimulation -> gastric secretion and gastric motility
partially digested carbs, undigested proteins, undigested fats arriving to stomach
- function of stomach
- stores food
- kills bacteria using HCl
- enzyme digestion of proteins
- regulates movement of chyme into duodenum through pyloric sphincter (stomach emptying) - 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
Content of gastric juice
- mucous cell: mucus
- parietal cells: HCl & intrinsic factor (IF)
- Chief cells: pepsinogen (zymogen), HCL leads to pepsin (active endopeptidase) -> partial digestion of proteins
Secretion and function of gastric HCl
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
The organic compounds that are digested in the stomach and by what enzyme(s)
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
Protective mechanisms for gastric mucosa from HCl
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
What is an ulcer and what causes it
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
Mechanisms of emesis
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
Gastric motility and emptying during feeding
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
Gastric emptying between meals (fasting state)
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
Triggers for the intestinal phase
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
Explain digestion and absorption of small and large intestine
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
Structural characteristics of small intestine
3-5m
- Duodenum (connected to duct to pancreatic and bile duct) - shortest
- Jejunum
- 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
Explain digestion in small intestine in terms of bile and pancreatic juice
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)
Explain carb digestion in small intestine
requires pancreatic amylase and brush boarder enzyme disaccharides to monosaccharides
- oligosaccharides (product of digestion by salivary amylase)
- Pancreatic amylase in lumen
- oligosaccharides -> disaccharides (maltase, sucrose, lactose) - brush boarder enzymes
- disaccharides -> monosaccharides -> enterocytes
Explain absorption of monosaccharides into enterocytes
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
Explain lactose intolerance
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
Describe the path of ingested carbs through the GI tract
Explain protein digestion and absorption in small intestine
- oligopeptides (comes from digestion by gastric pepsin)
- zymogens in pancreatic juice are activated
- bush boarder enzyme enterokinase/enteropeptidase: trypsinogen -> trypsin
- trypsin activates other zymogen peptidases (oligopeptides -> dipeptides)
Describe the path of ingested proteins through the GI tract
Explain digestion and absorption of fat in small intestine
- fat globule
- bile salts -> fat emulsification (fat globules -> fat emulsion droplets in micelle) - pancreatic lipase: emulsion droplets -> free fatty acids + monoglycerides
- 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.
Describe the path of ingested fat through the GI tract
Explain a deficiency in pancreatic enzymes
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
Absorption of nutrients, minerals and water in small intestine
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
Absorption of water-soluble vitamins into portal vein and name them
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
Absorption of fat-soluable vitamins
(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
Describe celiac disease
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
Structure and characteristics of large intestine
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
Explain motility of the colon
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
Explain motility and defecation reflex
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
Explain constipation
Explain diarrhea
Explain inflammatory bowel diseases and their names
Explain inflammatory bowel syndrome
Functions of the circulatory system
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)
Explain the overall intestinal phase and the pathway
Components of the circulatory system
Identify major components of plasma
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
Know and calculate hematocrit
Hematocrit: % of blood that is RBCs -> normally 40-50%
Similarities and differences between the formed elements
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
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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
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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
Describe process of blood clotting
- 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
Excitation-Contraction coupling (Ca++ induced Ca++ release) and pumping
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
Sequential pathway of blood in the CV system; define the pulmonary and systemic circulation
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
Property of refractoriness
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
Path of electrical conduction through the heart and correlate cardiac electrical activity (depolarization and repolarization) with the waves on the ECG
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
Name and locate the different heart valves, what is their function
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
Steps of the cardiac cycle
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
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1. Atrial Systole
- phase of contraction
- push 10-30% more blood into ventricle
- 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
- AV valves close
- 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
- semilunar valves open
- 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 - Rapid filling of ventricles
- Ventricular pressure decreases velow atrial pressure
- AV valves open
- Rapid ventricular filling occurs
Draw the pressure volume relation for the left ventricle from memory. Include the ECG & heart sounds and label the steps of the cardiac cycle (include EDV and ESV)
Review of cardiac muscle cells and myocardial A.P.
- 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
Similarities and differences between elastic arteries, muscular arteries and arterioles
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
Distinguish between different types of capillaries and organs they perfuse
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
Define pressures involved in filtration and reabsorption in the capillaries
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
Recognize structural and functional differences between the arteries and veins (pressure vs. blood volume)
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
Pressure changes in systemic CV system (left to large veins), where it’s most dynamic, where avg is greatest, where the biggest drop is due to resistance
Most dynamic change in pressure -> left ventricle
Average is the greatest -> Large arteries
Biggest drop due to resistance -> Small arteries and arterioles
What is MAP (garden hose analogy)? What will increase MAP? How?
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)
Know how to measure blood pressure using a sphygmometer (laminar flow, turbulent flow)
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
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- Blood pressure cuff inflated above systolic pressure, occluding the artery
- As cuff pressure is lowered, the blood will flow only when systolic pressure is above cuff pressure, producing the sounds of Korotkoff
- 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
How to calculate the pulse pressure and MAP
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)
Define cardiac output and autonomic control of cardiac output
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)
How is heart rate regulated at the level of the SA node (chronotropy)?
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
Difference between the Frank-Starling law and contractility (inotropy)
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
How is stroke volume regulated?
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
Define total peripheral resistance
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
Identify the major physical regulators of blood flow
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
How does sympathoadrenal signaling regulate tone? Differential changes in blood flow to gut vs. muscle?
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)
The mechanisms that underline the Baroreceptor reflex
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
The major types of tissue-specific regulation of blood flow to the heart, blood, brain and skin
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)
The cardiovascular changes that occur with exercise
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)
Recognize the ECG characteristics of associated with types of
arrhythmia and which is the most dangerous
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
What is atrial fibrillation? What can this cause? How is it treated? How do blood thinners work? Which pathway is targeted?
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?
- ???
How do murmurs occurs? Valves vs. Holes
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
Steps that cause atherosclerosis and know how it is treated (cardiac cath vs. bypass)
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:
- lipoproteins carry lipids in the blood
- 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
- 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
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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
The gender-specific differences in the symptoms for myocardial ischemia or myocardial infarction
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
The cutoff for hypertension and extrapolate why certain drugs are used to treat hypertension (i.e. how do they help lower MAP)
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:
- Modification of lifestyle
- stop smoking
- moderate alcohol
- weight reduce
- exercise
- reduce salt intake
- high diet in potassium - 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
What is heart failure, the causes and medications
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
