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193 Cards in this Set
- Front
- Back
- 3rd side (hint)
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What happens to the hematocrit of a pregnant woman?
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it goes down by 2-3%, called "physiological anemia"
-but total red cell volume increases up to 30% (in proportion to blood volume increase and plasma volume increase the hematocrit actually goes down) |
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What happens to the blood viscosity of a pregnant woman?
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it goes down
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What happens to the resting CO of a pregnant woman?
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it is increased 30-50% (about 7L/min)
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What explains the increased CO seen in pregnant women?
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1)SV increases by 30% (from increased vascular volume)
2)heart rate increases 20% 3)increase in ventricular volumes promoting Frank-Starling mechanisms on performance 4)ejection fraction increased by 5% |
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Describe how systemic vascular resistance changes during pregnancy in the mother.
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it is decreased up to 50% b/c of:
-addition of low resistance uteroplacental circulation -increased blood levels of estrogen and local mediators (PGE1, 2) =decreases afterload, increases aortic compliance, improves SV |
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How does blood pressure change during pregnancy?
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it decreases until mid-pregnancy, then returns to the non-pregnant state
-decrease in MAP is due to drop in TPVR |
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Where does gas exchange occur in the fetus?
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the placenta, NOT THE LUNGS
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How does the heart of the fetus work?
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in parallel, not in series like the normal adult heart
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What carries oxygenated blood from the placenta to the fetus?
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the umbilical vein
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What carries deoxygenated blood and waste from the fetus back to the mother?
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the umbilical arteries
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What functions does the placenta perform for the fetus and how is this achieved?
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-GI-nutrition
-liver-nutrition and waste removal -kidneys-fluid and electrolyte balance, waste removal -large quantities of blood are pumped through the placenta and smaller amounts to the organs to meet the needs of the fetus, achieved by unique channels or shunts |
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What is the ductus venosus?
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arises from umbilical vein
-shunts blood from directly into the IVC and bypasses the liver (allows oxygenated blood from placenta to bypass liver) -carries 50% of blood from placenta |
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What is the foramen ovale?
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oval hole in the septum dividing the atria
-shunts blood from the right atrium into the left atrium |
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What is the ductus arteriosus?
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shunts blood from the pulmonary artery into the aorta
-represents a right to left shunt just like foramen ovale |
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What is the CCO (combined cardiac output) in the fetus referring to?
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the R and L sides of the fetal heart are in parallel and b/c the inputs and outputs of the 2 sides mix the sum of the outputs is the CCO
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What is the CCO from both ventricles?
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100%
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What is the CCO in the thoracic aorta?
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69%
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How much of the CCO do the lungs receive in the fetus?
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7%, b/c they are high resistance and compressed by liquid
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How much of the CCO does the placenta receive?
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50%, it's low resistance
-flow to the placenta shunts flow away from the viscera and kidneys |
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How much of the CCO enters the RA and where is it coming from?
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69% total
-50% comes from the ductus venosus emptying directly into IVC -19% (from GI and IVC) |
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Of the 69% of CCO that enter the RA, how much is shunted into the LA?
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27%
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Where does the remainder of the CCO go once the placenta is accounted for?
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21% goes to the brain
7% to the lungs 3% to the coronaries |
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What is the O2 saturation of fetal blood entering the placenta?
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60%
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What is the O2 saturation of blood that goes from the placenta to the IVC?
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85%
-saturation then decreases to 70% b/c of mixing with the venous blood from IVC |
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What is the O2 sat. in the RA of fetus?
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55% from mixing with cerebral venous return
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What is the O2 sat. in the LA of the fetus?
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70% b/c of shunt through the foramen ovale
-O2 sat. decreases to only 65% |
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What is the O2 sat. of blood in the aorta of the fetus?
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drops to 60% from the 65% that was in the LA b/c of mixing with deoxygenated blood from the RV through the ductus arteriosus
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What causes the establishment of the pulmonary circulation after birth?
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the first breath inflates lungs resulting in:
-relaxation of pulmonary precap. vessels by O2 -main change is decrease in pulmonary resistance and pressure -increases blood flow in pulm. circuit -pulmonary pressure falls below aortic pressure eventually and flow through the ductus arteriosus is reversed (now a left to right shunt) |
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What leads to closure of the foramen ovale in the fetus?
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blood flow to the LA increases b/c of increased use of the pulmonary circuit
-LA pressure exceeds RA pressure -closes the functional foramen ovale |
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Describe the physiological changes that occur as a result of cutting the umbilical cord.
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decreases venous return to the RA
-reduces atrial pressures -ductus venosus closes and resistance in systemic circuit increases -venous return to the heart decreases, decreasing RA and LA pressures |
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Describe the perinatal changes in circulation. (in the fetus)
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-loss of low resistance placental circulation
-decreased Pulm. vasc. resis. in response to rising arterial PO2 -Hgb sat. increases -rising TPR; transformation of heart from parallel to series -closure of shunts -increase CO of LV, while RV decreases, output of each becomes equal -decrease in thickness of RV, increase in LV b/c increase in TPR -BP gradually increases, HR decreases |
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Describe an atrial septal defect.
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it is failure of the foramen ovale to close
-produces a L to R shunt -sends oxygenated blood into the RA and provides more blood to the lungs -leads to dilation of RV, RA, and pulmonary vessels, and pulmonary hypertension -increases O2 sat. of right side of heart |
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Describe a ventricular septal defect.
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produces a L to R shunt
-sends oxygenated blood to the RV and provides more blood to lungs -pulmonary hypertension -increased blood return to LA -increases O2 sat. in RV and pulm. artery -also leads to L. heart remodeling |
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Describe a patent Ductus arteriosus.
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produces a L to R shunt (flow from aorta to pulm. artery)
-increases pulmonary and RV pressures -LA and LV overloaded b/c of increased blood volume -systemic blood is usually oxygenated -increases the pressure and O2 sat. of pulm. artery and pressure of RV |
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What are the 4 digestive processes that the digestive system performs?
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MADS
motility absorption digestion secretion |
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What does the steady low level of tone present in the sm. mm. in the GI tract do?
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maintains steady pressure on contents of the GI tract
-prevents permanent distension of GI tract walls |
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What are the 2 types of motility in the GI tract?
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1)propulsive-push contents forward at varying speeds
-rate depends on specific area of GI tract -esophagus=rapid, sm. intestine=slow 2)mixing-mix food with digestive juices (digestion) and exposes contents to surfaces of GI tract (absorption) |
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Motility at either end of the GI tract involves what type of muscle (chewing, swallowing, and defecation)?
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skeletal muscle under voluntary control
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In what form are most carbohydrates ingested as?
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polysaccharides-starch, glycogen, and cellulose
-less ingested as disaccharides (sucrose and lactose for example) |
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What form are most dietary fats in?
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triglycerides
TG=glycerol + 3 fatty acids -during digestion, 2 FA are split off by lipase enzyme leaving a monoglyceride |
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What are the 4 basic layers of the GI tract?
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FROM THE OUTSIDE IN
serosa muscularis externa(myenteric or auerbach's plexus)-outer longitudinal, inner circular layer submucosa (meissner's plexus) mucosa (mucous membrane, lamina propria, muscularis mucosa) |
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Describe what is contained in the mucus membrane portion of the mucosa of the GI tract.
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exocrine cells-enzymes
endocrine cells-hormones epithelial cells-absorption |
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What layer of the GI tract contains the lymphoid tissue?
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the lamina propria
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Describe the submucosa of the GI tract.
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layer of CT
-provides GI tract with distensibility/elasticity contains: larger blood and lymph vessels submucous plexus (meissner's plexus |
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What are the interstitial cells of Cajal?
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they are pacesetter cells located btwn. the outer long. and inner circ. layers of smooth muscle in the myenteric plexus in the muscularis externa layer
-they cause slow wave potentials -pacesetter cells determine the RATE of rhythmic contraction |
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What will neurons that release vasoactive intestinal peptide promote smooth muscle to do?
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relax (in GI tract intrinsic nerve plexuses, work on myenteric and auerbach's plexus)
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What is the purpose of chewing?
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-grind and mix food with saliva
-stimulate taste buds -reflexly increase salivary secretion, gastric, pancreatic and bile secretions to prepare GI tract for food |
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Describe the composition of saliva.
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99.5% water
0.5% electrolytes salivary proteins -amylase, mucus, and lysozyme |
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What does salivary amylase do?
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breaks polysaccharides into maltose (2 glucose molecules)
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What does salivary lysozyme do?
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it has antibacterial action that lyses bacteria
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What are the functions of saliva?
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1)solvent for molecules to stimulate taste buds
2)aids speech-facilitates lip and tongue movement 3)keeps teeth and mouth clean 4)contains HCO3- buffers-neutralize acids from food and from bacteria in mouth helps prevent tooth decay |
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Describe the tonicity of saliva.
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it is hypotonic b/c it is secreted into ducts (as isotonic) and the ductal cells then absorb Na and Cl and K and bicarbonate are pumped into the saliva and secreted
(the duct cells are H2O impermeable therefore saliva is mostly water |
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What stimulates salivary secretion?
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PNS and SNS
PNS-watery, enzyme rich (normally dominant) uses Ach, muscarinic, IP3 and increase Ca SNS-less volume, mucus rich (active with stress) uses NE, Beta, AC, increases cAMP |
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What is xerostomia and what causes it?
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decreased saliva production
causes: -diseases:salivary gland infections (staph) or stones, mumps -radiation and chemo -over 400 meds sx: dry mouth, difficulty chewing and swallowing, inarticulate speech, increased dental caries, facial pain tx: no alcohol/tobacco/caffeine, sip more water, extra care of teeth |
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Why is the gastroesophageal sphincter closed when there is no peristalsis?
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to prevent gastric reflux
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What is achalasia?
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The Lower esophageal sphincter fails to relax during swallowing and food does not enter stomach
tx:surgery, drugs to inhibit tone (botox, Ca channel blockers) |
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What are the 3 phases of the swallowing reflex?
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oral
pharyngeal esophageal |
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Describe the oral phase of the swallowing reflex.
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a bolus of food is forced to the rear of the mouth towards the pharynx
-stimulates tactile (somatosensory) receptors which sends afferent input to the medullary swallowing center via vagus and CN IX |
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Describe the pharyngeal phase of the swallowing reflex.
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the soft palate is pulled upwards which prevents reflux of food into the nasopharynx
-the epiglottis moves to cover larynx which then moves forward and upward against the epiglottis =prevents food entering trachea (<1s) -upper esophageal sphincter relaxes and allows food to pass from pharynx to esophagus -peristaltic wave begins in pharynx and propels food through open sphincter |
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Describe the esophageal phase of swallowing.
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lasts <10s
-controlled in part by swallowing center -swallowing is initiated voluntarily but once started cannot be stopped - |
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How is diagnosis of a swallowing disorder made?
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cineradiography (swallow barium prep, Xray and videotape movement)
upper endoscopy manometry (measure timing and strength of esophageal and valve contractions) -can be caused by degenerative neuro. disorders like ALS and Myasthenia gravis |
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What are the 3 main functions of the stomach?
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1)storage-allows emptying into small intestine at a rate appropriate for optimal digestion and absorption
2)secretes HCl-to start protein digestion 3)mixing-mixing movements pulverize food with gastric secretions, produce chyme |
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HOw much does the volume of the stomach change during eating?
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a 30 fold change in volume from empty to full
-little change in stomach wall tension and intragastric pressure |
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How does the stomach accommodate a large increase in volume?
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-the rugae flatten with intake of food
-this reflex relaxation=receptive relaxation -triggered by eating and mediated by the vagus nerve -eating more than 1.5 liters of food will over-distend the stomach and cause in increase in intragastric pressure |
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What controls the receptive relaxation in the stomach?
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a vagovagal reflex
-both afferent and efferent limbs of the reflex are carried in the vagus nerve -VIP-postgang. peptidergic vagal nerve fibers |
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Where are gastric contents stored?
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in the body of the stomach
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Describe the movement of gastric contents through the stomach.
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-pacesetter cells in the upper fundus generate slow wave potentials moving towards the pyloric sphincter
-the peristaltic waves spread to antrum and pyloric sphincter -waves are different for various stomach regions -there are thin muscle layers in the upper regions which creates weak waves -thicker muscle layer in the antrum which creates strong waves -the chyme hits the closed pyloric sphincter which propels it back into the stomach and mixes the contents |
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Describe factors that modify the rate of gastric emptying.
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1)amount of chyme in the stomach-the emptying rate is proportional to the amount of chyme
2)stomach distension-->increases gastric motility via direct effect of stretch on the sm. mm. and involvement of intrinsic plexuses (vagus n.) 3)chyme fluidity-increased fluidity=faster emptying and vice versa |
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What is of primary importance when it comes to factors that modify the rate of gastric emptying?
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duodenal factors
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WHat are the duodenal factors that modify the rate of gastric emptying?
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fat, acid, distension, and hypertonicity
-these 4 factors activate duodenal receptors and trigger a neural/hormonal response -decrease the excitability of gastric sm. mm. -decrease rate of gastric emptying Neural response: -mediated by intrinsic nerve plesxuses (short reflex) -autonomic nerves (long reflex) Hormonal response: -enterogastrones released from duodenal mucosa (secretin and CCK) |
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How does fat modify the rate of gastric emptying?
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fat in the duodenum inhibits emptying of gastric contents
-mediated by CCK secreted by I cells |
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How does acid in the duodenum affect the rate of gastric emptying?
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it inhibits emptying of gastric contents
-mediated by reflexes in the enteric NS -stomach secretes HCl which is emptied into the duodenum and neutralized by Sodium bicarb. (from pancreas) -unneutralized H+ in duodenum inhibits gastric emptying until complete neutralization occurs -unneutralized H+ in duodenum affects pancreatic enzymes (HOW?) |
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How does hypertonicity in the duodenum affect the gastric rate of emptying?
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if absorption rate of AA and glucose doesn't keep up with the rate of protein and carb. digestion
-these stay in chyme which will result in an increase in osmolarity of the duodenal contents so water will cross the duodenal wall and enter the lumen -to prevent this, gastric emptying is reflexively inhibited when there is an increase in the osmolarity of duodenal contents |
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How does the distension of the duodenum affect gastric emptying?
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chyme in the duodenum inhibits gastric emptying and allow duodenum time to catch up
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Describe vomiting.
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coordinated by the vomiting center in the medulla
-via ANS discharge vomiting is preceded by salivation, increased HR, sweating, nausea -wave of reverse peristalsis from mid SI towards duodenum, pyloric sphincter and stomach relax, deep forced inspiration followed by closure of the glottis, diaphragm contracts and pushes downward on the stomach, ab mm. contract and compress abdominal cavity which increases intra-abdominal pressure and forces viscera upwards, stomach contents pushed upwards and out |
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What are some causes of vomiting?
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1)touch on back of throat POTENT
2)stomach irritation/distension (or duodenum) 3)increased cranial pressure during head trauma 4)rotation of head (motion sickness) 5)chemicals-act on upper GI tract or stimulate chemoreceptors in the chemoreceptors trigger zone (next to vomiting center) 6)psychogenic factors -emotion, nauseating sights, anxiety |
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At what rate does the stomach secrete gastric juice?
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2L/day
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What secretes gastric juice in the stomach?
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the gastric mucosa which has 2 areas:
oxyntic mucosa (lines body and fundus) pyloric gland area (lines antrum) |
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What are the 3 types of exocrine secretory cells?
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mucous cells
chief cells parietal (oxyntic) cells |
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What do chief cells in the stomach secrete?
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pepsinogen
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What do parietal cells secrete?
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HCl and intrinsic factor
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What do the ECL cells in the stomach secrete?
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histamine (paracrine)
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Where does gastrin come from and what is its function?
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G cells
released in response to eating -it stimulates: H+ secretion from parietal cells growth of the gastric mucosa |
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What produces somatostatin and what is its function?
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D cells
it inhibits: HCl secretion, gastrin release, and histamine release |
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What does omeprazole do?
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it blocks the H/K exchanger on parietal cells to decrease HCl production in the stomach
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What are the 3 main antagonists of parietal cell function?
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somatostatin, prostaglandins, and EGF and TGF-alpha
-all 3 work through Gi proteins, adenylate cyclase and decrease cAMP |
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What are the 3 main agonists of parietal cell function?
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histamine-binds to H2 receptors and works through Gs protein using cAMP (increase)
2)Ach-on M3 receptors which open Ca channels 3)gastrin-binds to CCKb receptors and work through Ca |
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What are the 3 main functions of HCl?
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1)activates pepsinogen to pepsin
2)aids in the breakdown of CT and proteins 3)kills most microorganisms ingested with food along with salivary lysozyme |
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What is pepsinogen?
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the MAJOR constituent of gastric secretion
-synthesized and packaged by RER and golgi -released in inactive form by exocytosis -it is then activated by HCl into pepsin which acts on other pepsinogens to produce more pepsin (=autocatalytic) -initiates protein digestion |
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Where is B12 absorbed?
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in the ileum
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How is B12 absorbed?
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it binds with intrinsic factor which is secreted by parietal cells in the stomach, the complex then binds with receptors in the terminal ileum and receptor mediated endocytosis is stimulated
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What is B12 bound to in portal blood?
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transcobalamin II
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What happens when there is an absence of intrinsic factor?
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vitamin B12 isn't absorbed
-decreased RBCs and nerve function -tx: regular oral dose/I.M. injections of B12 sx:fatigue, SOB, tingling sensations, difficulty walking |
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What are the 3 phases of gastric secretion?
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cephalic, gastric, intestinal
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Describe the cephalic phase of gastric secretion.
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-increased secretion of HCl and pepsinogen due to stimuli acting in the head (smell, taste, etc)
-vagus directly stim. parietal cells to release HCl -vagus releases GRP which acts on G cells to produce gastrin which circulates back to the parietal cells and stimulates HCl production |
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Describe the gastric phase of gastric secretion.
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-occurs when food is in the stomach
-HCl secretion stimulated by vagus (direct or indirect on G cells), distension of antrum stim. G cells, or effect of AA and small peptides which stim. G cells to release gastrin-->stim. HCl secretion |
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Describe the intestinal phase of gastric secretion.
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it is INHIBITORY!
-mediated by breakdown products of protein digestion -flow of gastric juice is decreased as chyme enters the sm. intestine b/c don't need a lot of acid when food is no longer in stomach |
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What are 3 things that decrease gastric secretion?
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1)meal moves from stomach into the duodenum
2)foods leave stomach-gastric juices accumulate which decreases gastric pH and increases somatostatin release 3)fat, acid, duodenal distension all decrease gastric secretion -enterogastric reflex and enterogastrones suppress gastric secretory cells and decrease excitability of gastric SM cells |
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What does the mucus in the stomach do?
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1)protects against mechanical injury (lubrication)
2)protects stomach wall from self digestion (inhibits pepsin) 3)protects against acid injury-neutralizes HCl near gastric lining (the mucus is alkaline in nature) |
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What are peptic ulcers?
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they are caused by a broken mucosal barrier, reflux in the esophagus, or dumping of excessive acidic gastric contents into duodenum
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What is helicobacter pylori?
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a bacterium that causes >80% of peptic ulcers
-it causes a persistent inflammatory response by releasing cytotoxins into the gastric mucosal barrier -other factors that contribute are ethyl alchohol and NSAIDs |
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What type of ulcer is more common: duodenal or gastric?
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duodenal
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What is motilin?
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it is peptidergic and is secreted from the upper duodenum during fasting
-it increases GI motility-starts MMC's (90 mins) |
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What is segmentation in the sm. intestines?
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primary means of motility during digestion of a meal
-oscillating closely spaced contractions of circular sm. mm. layer along length of intestine -it mixes enzymes with the contents -initiated by SI pacesetter cells |
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What is segmentation in the duodenum due to?
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local distension when chyme enters (contractions occur about 12/minute)
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What is segmentation in the ileum due to?
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due to gastrin =gastroileal reflex
-secreted in response to chyme in stomach (contractions occur about 9/minute) |
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How long does it take contents to move through the sm. intestines?
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3-5 hours which gives plenty of time to fully digest and absorb nutrients
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What is the migrating motility complex in the small intestines?
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it is the peristaltic waves that occur when most of the meal is absorbed, segmentation ceases and MMC takes over
-at next meal: MMC stops and segmentation takes over again -it is an in-btwn meal motility that is caused by a repetitive/peristaltic wave (waves occur every 90 mins) |
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What contributes to relaxation of the ileocecal sphincter?
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-distension on the ileal side
-when food is in the stomach and gastrin is released |
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What is succus entericus?
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the aqueous salt and mucus solution secreted by the exocrine gland cells in the SI mucosa
-does not contain any digestive enzymes |
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Describe the digestion of starch starting with the mouth.
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alpha amylase starts to digest it in the mouth, alpha amylase is inactivated in the stomach
-then acted on by pancreatic amylase which creates disaccharides which can then be acted upon by other specific enzymes to create monosaccharides to be absorbed |
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Where are the enzymes that breakdown disaccharides into monosaccharides found in the small intestine?
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on the brush border membrane
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How are the monosaccharides transported into the enterocyte?
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by Na dependent active transport
-then are absorbed into blood by using facilitated diffusion (GLUT transporters) to pass through the basal membrane of enterocytes |
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How would you test for lactose intolerance using the breath test?
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drink a lactose solution,
monitor H+ in breath at timed intervals b/c bacteria in intestines produce H+ from undigested lactose |
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What is enterokinase (enteropeptidase) and where is it found?
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it activates pancreatic enzyme trypsinogen to produce trypsin
-found on the small intestine brush border membrane |
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What are some endopeptidases?
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trypsin, pepsin, chymotrypsin
-they hydrolyze interior protein bonds |
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Name an exopeptidase.
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carboxypeptidase A/B
-hydrolyze 1 AA at a time from C-end |
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How are AAs absorbed into the small intestines?
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through Na dependent active transport
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Is pepsin necessary for adequate protein digestion?
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no
-pancreatic and BBE alone can adequately digest protein |
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How are small peptide fragments broken up to be absorbed?
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by the aminopeptidases in the brush border membrane which yields AAs which can then be absorbed
-or di and tripeptides can also be absorbed on H+-dependent cotransporters |
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How is pancreatic lipase activated?
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it is initially inactive in bile salts
-procolipase is secreted with pancreatic juices and is cleaved to colipase by trypsin -colipase then binds with pancreatic lipase to activate it |
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What is the job of pancreatic lipase in fat digestion?
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hydrolyzes TG in emulsified fat to yield MG + 2 FFA
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Describe the digestion and absorption of fats.
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-dietary fat is emulsified by bile salts
-lipase then cleaves TG -->MG + 2FFAs -micelles formed from bile salts and products of lipase -as micelles approach enterocytes the MG and FFA leave the micelle and passively diffuse through the luminal PM -MG and FFA re-esterified to form TG in the cell which then aggregate and are coated with apoproteins -then form water soluble chylomicrons which are extruded through exocytosis through BM of enterocyte |
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Where does most iron absorption occur?
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in duodenum
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留学生
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りゅうがくせい (detain 留 work w blade 刀 & mu ム)
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foreign exchange student
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What are some causes of diarrhea?
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-excess intestinal motility (irritation of gut wall from bacterial/viral infection) or stress
-excess intestinal secretion due to cholera -leading cause of infant death in developing countries |
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How is secretory diarrhea caused?
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cholera or E.coli for example can stimulate alpha s receptors which activate Gs protein and AC which increases cAMP and increases activity of CFTR receptor which increases Cl- secretion-->water and Na follow which causes diarrhea
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What is absorbed into the blood at the jejunum?
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NaHCO3
by action of Na/K ATPase and HCO3- channel |
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What is absorbed into the blood at the ileum?
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NaCl
by action of Na/K ATPase and chloride channel |
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What are the 3 factors that play a role in how celiac disease appears?
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1)length of time one is breast fed (longer BF=later onset)
2)age one starts eating gluten-containing foods 3)amount of gluten-containing foods one eats |
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How is a diagnosis of Celiacs made?
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increased levels of anti-tissue transglutaminase Ab
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What is Crohn's disease?
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a chronic autoimmune disease, it is an inflammatory bowel disease
-occurs in many areas of GIT (mouth to anus, most commonly ileum) -intestinal wall becomes thick -ulcers frequent tx:steroids (anti-inflammatory) -edema, redness, granular appearance of intestine |
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What do the islets of Langerhans secrete?
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insulin-beta cells (65%)
glucagon-alpha cells (20%) somatostatin-delta cells (10%) |
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What branch of the ANS stimulates the pancreas?
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PNS through the vagus
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Where are exocrine pancreatic enzymes made and stored?
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they are synthesized in the RER and golgi of the acinar cells and stored in zymogen granules until release through exocytosis
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What 3 types of pancreatic enzymes do acinar cells secrete?
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1)pancreatic proteases-trypsinogen, chymotrypsinogen, and procarboxypeptidase (for protein digestion)
2)pancreatic alpha amylase-secreted active form-cleaves polysaccs into disaccs 3)pancreatic lipase-active hydrolyzes dietary TG into MG + 2FA |
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What activates the pancreatic proteolytic enzymes?
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trypsin (which is originally activated by enterokinase/enteropeptidase in the duodenum)
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What is the major source of lipase?
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the pancreas
-without the pancreas would lead to fat maldigestion -protein and carbs would be okay still |
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What is steatorrhea and what can cause it?
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excess undigested fat in the feces (60-70%)
-typical of cystic fibrosis |
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What are the 2 main reasons that the acidic chyme from the stomach must be neutralized quickly once it enters the duodenum?
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1)it protects acidic damage to duodenal wall
2)it allows optimal functioning of pancreatic enzymes |
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WHat is acid chyme neutralized by in the duodenum?
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NaHCO3 rich fluid secreted from pancreas (largest part of pancreatic secretion)
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At rest, what is the dominant place of secretion in pancreatic ducts?
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intercalated and interlobular ducts
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What does secretin do in the pancreas and where does it come from?
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it comes from S cells in the duodenum (in response to high H+)
-it stimulates the aqueous component of pancreatic secretions which increases flow rate and subsequent HCO3- secretion in the extralobular ductal system of the pancreas |
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What is the main source of regulation for pancreatic exocrine secretion?
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hormonal control
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What time period is the major stim. of pancreatic secretion happening?
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during the intestinal phase of digestion as chyme enters the SI
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What 2 major enterogastrones are released during the intestinal phase of digestion?
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CCK
secretin |
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What does secretin do to cAMP levels?
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it decreases them
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What does CCK do to Ca levels?
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decreases them along with IP3 stimulating enzyme release from the pancreas
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What is a causative factor for pancreatitis?
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alcohol
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What are risk factors for developing pancreatic cancer?
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smoking, and caloric intake
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What happens to bile salts after they are secreted into bile?
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they are reabsorbed into blood via active transport in the terminal ileum (after participating in fat dig. and abs)
-then returned to the liver via hepatic portal system which recycles them and resecretes them into bile |
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What does choleretic mean?
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any substance that increases bile secretion by the liver
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WHat does secretin do to bile secretion?
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is increases bile secretion by the liver ducts
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What effect does the vagus nerve have on bile secretion in the liver?
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very minor role during the cephalic phase of digestion
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What are the 3 ways that jaundice can occur?
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1)pre-hepatic/hemolytic-increased breakdown of RBCs, liver gets more bilirubin than can excrete
2)hepatic-liver diseased 3)post-hepatic-bile duct obstructed (gall stone) bilirubin not excreted |
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What are the 4 organic constituents of bile?
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cholesterol, lecithin, bilirubin, bile salts (it is an aqueous alkaline fluid)
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How much fecal matter is expelled/day?
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150 mL
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Are there villi in the large int?
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no, only in SI
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What is secreted by the large intestines?
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no enzymes!
mostly just mucus (alkaline to neutralize acids produced from local bacterial fermentation) to help lubricate and to protect from bacteria gases and acids, lot of goblet cells |
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What is the major motility method of the large int?
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haustral contractions, slow and non-propulsive
-initiated by autonomous rhythmicity of colonic SM -controlled locally by intrinsic plexuses -similar to SI segmentation but less frequent (about every 30 mins) |
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How often do mass movements occur in the LI?
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1-3/day
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What is the gastrocolic reflex?
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food in the stomach causes distension-->increased PNS activity and CCK and gastrin increase motility-->increases frequency of mass movements in LI
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Describe what conditions have to be met for defecation to occur?
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-external anal sphincter is relaxed
-voluntary contraction of ab muscles -valsalva maneuver increases intra-ab. pressure -rectum SM contracts to create pressure which forces contents out -as rectum fills with feces, the internal anal sphincter relaxes |
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What does Hirschsprung lead to?
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lack on enteric nervous system prevents the Internal anal sphincter from relaxing = megacolon
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What increases mucosal secretions in the LI?
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mechanical/chemical stimulation of colonic mucosa
-mediated by short reflexes and PNS |
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In what contractile states are the abdominal mm. and external anal sphincter during gas expulsion?
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contracted
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What is amebiasis?
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parasitic bowel infection common in the tropics
-sx:cramps, diarrhea, fatigue, increased gas, painful urge to defecate (tenesmus) tests: stool culture tx:IV rehydration and oral metronidazole |
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What is VO2 max?
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the maximum capacity for oxygen consumption during exercise
-reflects body's ability to transport and use O2 -best measure of exercise intensity |
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What is the Fick equation?
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VO2= CO X a-v O2 difference
-just states that exercise capacity is governed by the ability of the CV system to deliver blood and oxygen to the working muscles and the ability of the tissues to extract O2 from the blood |
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Does arterial oxygen content usually change with exercise?
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no, fairly constant
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How is the working muscles demand for oxygen met?
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increasing blood flow to the muscle
-increasing blood pumped to the heart -shunting and redistribution of blood -metabolic vasodilation in muscle -decrease in TPR |
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At higher intensities, what contributes more to the increase in CO??
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increased HR instead of SV as is the case at lower intensity exerciseq
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What is the increase in HR seen during exercise due to?
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withdraw of PNS and stim. of SNS
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At what filling times will diastolic filling decrease significantly ??
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less than 0.1 seconds (helps to maintain constant SV at incraesed HR
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Why does SV increase during exercise?
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increased venous return and filling increases EDV, frank-starling mechanism, also contractility increased due to SNS and increased HR, and increased catecholamines=also increases ejection fraction
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How does oxygen extraction during exercise increase?
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b/c there is an increased a-v O2 difference, venous oxygen content is decreased
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What causes vasodilation in exercising muscle leading to increased blood flow?
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local metabolites such as lactate, adenosine, K+, H+,
the vasodilation decreases TPR and increases blood flow to the muscles |
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What happens during dynamic exercise?
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systolic BP rises, diastolic may decrease b/c of decrease TPR
-little to moderate incerase in MAP MAP=CO X TPR |
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What happens during static exercise?
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mechanical compression of peripheral arterial system
-increased TPR, decreased muscle blood flow -both systolic and diastolic pressures rise -MAP increases b/c diastolic increase, CO increases which is HR induced, not SV -sustained static effor impedes venous return and therefore SV |
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What are some extracardiac sources of heart failure?
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high pressure overload (HTN)
volume overload (renal failure) -where work and demand exceed supply |
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What would left heart failure cause?
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increased LA pressure leads to pulmonary congestion and dyspnea
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What would R. heart failure cause?
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increase RA pressure leads to systemic congestion and lower extremity edema
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What happens to contractility during heart failure?
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it is decreased
initially SNS stimulation increases contractility but the heart eventually wears out and this fix is very short lived (decreased cardiac NE stores, decreased beta adren. density, and decreased catecholamine sensitivity) |
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What do the kidney's do during heart failure to compensate for the decrease in CO?
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they retain water to increase blood volume which increase EDV (leads to exercise intolerance b/c they have more volume but no sensitivity to SNS stimulation so they can't increase their CO)
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What is a forward failure of the heart?
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less than adequate SV
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What is a backward failure of the heart?
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blood backs up in the venous system=CHF
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What leads to eccentric hypertrophy?
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volume overload,
-ventricle becomes dilated, involves increase in mass such that wall thickness remains relatively normal (can hold more blood but can't necessarily pump it out) |
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What leads to concentric hypertrophy?
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pressure overload
-hypertrophy of actual walls due to stenoses or HTN, increases in wall thickness -not as much filling can occur |
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What is cardiogenic shock?
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depressed cyocardial function
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What is hypovolemic/hemorrhagic shock?
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low blood volume
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What is vasogenic shock?
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vessel produced
-massive vasodilations caused by sepsis or anaphylactic shock |
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What is neurogenic shock?
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loss of vascular tone due to inhibition of SNS constrictor nerves
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What is the function of CCK (4 of them)?
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delays gastric emptying
relaxes the sphincter of oddi stimulates the gall bladder to secrete bile increases enzyme release from pancreatic acinar cells |
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