Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
205 Cards in this Set
- Front
- Back
|
Transporters on the apical membrane of Salivary duct cells?
|
Na + /H + exchanger
Cl - / HCO 3- exchanger H + /K + ATPase |
|
|
Transporters on the apical membrane of parietal cells?
|
H + /K + ATPase
K + channels Cl - channels (ClC or CFTR) |
|
|
Transporters on the apical membrane of pancreatic duct cells?
|
Cl - / HCO 3
- exchanger CFTR Cl - channels |
|
|
Transporters on the apical membrane of small intesting crypt cells?
|
CFTR Cl - channels
|
|
|
Transporters on the apical membrane of jejunum epithelial cells?
|
Na-coupled sugar
transporter Na-coupled AA transporter Na + /H + exchanger |
|
|
Transporters on the apical membrane of ilium epithelial cells?
|
Na-coupled sugar
transporter Na-coupled AA transporter Na + /H + exchanger Cl - / HCO 3 - exchanger |
|
|
Transporters on the apical membrane of Colon cells?
|
Na + channels (ENaC)
K + channels Na + /H + exchanger Cl - / HCO 3 - exchanger |
|
|
Transporters on the basolateral membrane of salivary duct cells
|
Na + /K + ATPase
Cl - channels |
|
|
Transporters on the basolateral membrane of parietal cells?
|
Na + /K + ATPase
K + channels Cl - / HCO 3 - exchanger |
|
|
Transporters on the basolateral membrane of pancreatic duct cells?
|
Na + /K + ATPase
K + channels Na + /H + exchanger Na + /K + /2Cl cotransporter |
|
|
Transporters on the basolateral membrane of small intestine crypt cells?
|
Na + /K + ATPase
Na + /K + /2Cl cotransporter |
|
|
Transporters on the basolateral membrane of jejenum epithelial cells?
|
Na + /K + ATPase
sugar transporter (facilitated transporters) AA transporter HCO 3 - transporter |
|
|
Transporters on the basolateral membrane of ilium epithelial cells?
|
Na + /K + ATPase
sugar or AA transporters Cl - transporter |
|
|
Transporters on the basolateral membrane of colon cells?
|
Na + /K + ATPase
K + channels Cl - channels Na + /H + exchanger |
|
|
What is the net secretion and /or net
absorption of salivary duct cells? |
Secretion of K & HCO 3
- Absorption of Na & Cl |
|
|
What is the net secretion and /or net
absorption of parietal cells? |
Secretion of HCl
No absorption (or absorption of HCO 3 - ) |
|
|
What is the net secretion and /or net
absorption of pancreatic duct cells? |
Secretion of Cl - & HCO 3
- Absorption of H + |
|
|
What is the net secretion and /or net
absorption of small intestine crypt cells? |
Secretion of Cl - & H 2 0 & Na +
No absorption |
|
|
What is the net secretion and /or net
absorption of jejunum epithelial cells? |
Secretion of H +
Absorption Na + & HCO 3 - |
|
|
What is the net secretion and /or net
absorption of ilium epithelial cells? |
Secretion of H + & HCO 3
- Absorption Na + & Cl - |
|
|
What is the net secretion and /or net
absorption of colon cells? |
Secretion of K + & HCO 3
- Absorption of Na + |
|
|
What is the combined cardiac output in the ventricles of the fetus?
|
100%
|
|
|
What is the combined cardiac output in the thoracic aorta of the fetus?
|
69%
|
|
|
What is the combined cardiac output in the brain, lungs and coronaries of the fetus? How is it divided?
|
31% Total
Brain 21% Lungs 7% Coronaries 3% |
|
|
What is the oxygen saturation of blood as it returns to the placenta from the fetus?
|
60%
|
|
|
What is the fetal oxygen saturation of blood as it prepares to enter the IVC from the placenta?
|
85%
|
|
|
What is the oxygen saturation of blood from the placenta once it mixes with the deoxiginated blood returning to the IVC from fetal circulation?
|
Drops from 85-70%
|
|
|
What is the oxygen saturation of blood in the right ventricle?
|
55% due to further mixing of cerebral venous return
|
|
|
How does right ventricular O2 saturation compare with Left ventricular O2 saturation?
|
It is lower. LA O2 saturation is about 65% because 70% 02 from IVC goes into foramen ovale and mixes with pummonary return dropping it to 65% in LV.
|
|
|
What is the O2 in the descending aorta?
|
65% sauration from LV drops to 60% with mixing of blood from RV ductus arteriosis.
|
|
|
What are what haustral contractions?
how often do they occur? |
slow & nonpropulsive mixing contractions of the LI
every 30 minutes |
|
|
What is the gastrocolic reflex?
|
Food in stomach → increase in PNS →incresases motility → increase frequency of mass movements in the LI
distension → increase in CCK & Gastrin →incresases motility → increase frequency of mass movements in the LI |
|
|
What is the role of the large intestine?
|
Mainly drying and storage of undigested food.
|
|
|
What are the anitomical features of the large intestines?
|
No Vili
Deeper cripts and more goblet cells that secret mucus |
|
|
What is the major motility method of the LI? How are they controlled
|
haustral contractions
intrinsic prexuses |
|
|
How is deification reflex mediated?
|
When colon fills at least 25% internal anal sphincter opens and urge to defecate occurs.
External anal sphincter must relax, voluntary contraction of the abdominal muscles and valsalva.intrabdominal pressure increase and feces expelled. |
|
|
How can deification be delayed?
|
– external anal sphincter is contracted
– the distended rectal wall gradually relaxes & the urge subsides. |
|
|
What will happen if there is a problem with the external anal sphincter?
|
Defication would occur involuntaryily when rectum is full
|
|
|
What will happen if there is a problem with the enteric nervous system?
|
Hirschsprung – lack of enteric neurons – don’t relax Internal Anal Sphinctor - megacolon results
|
|
|
What are Mass Movements?
|
Occur in the Li 1-3 times a day where content is propelled from transverse colon to sigmoid colon
|
|
|
How is how intestinal gas is expelled?
|
Voluntarily against contracted abdominal muscles & external anal sphincter
|
|
|
What is amebiasis?
|
Parasitic Bowel infection –
Entamoeba histolytica. Common in tropics (with poor sanitation) sx: Symptoms: cramps, diarrhea, fatigue, ↑ gas, |
|
|
What is the medical term for a feeling of incomplete defecation ?
|
tenesmus
|
|
|
What does the large intestine secrete?
|
Alkaline mucous to lubricate and neutralize colonic bacreria fermentation
|
|
|
Increase flow rates in the LI have what effect?
|
↑ flow rates of intestinal secretion
Will ↑ K secretion → ↑ K loss Resulting in hypokalemia |
|
|
How much fecal matter enters the colon each day and how much is excreted?
|
500 ml/day→ 150ml eliminated/day.
|
|
|
What is Segmentation motility and where does it occur?
|
In the small intestines
contractions of circular smooth muscles mix contents with enzymes Little to no forward movement |
|
|
What is the Migrating Motility Complex?
|
peristaltic waves that occur inbetween meals or when most of a meal has been absorbed. Occurs every 90 minutes or so.
Contraction in front of bolus, relaxation behind |
|
|
What is the role of the role of the Ileocecal juncture?
|
it prevents bacteria from LI from entering small intestine and the sphinctor is mostly a constricted tone
|
|
|
What are the effects of the PNS on the small intestine?
|
via the Vagus nerve
Stim → ↑ contraction of intestinal Smooth Muscle Release Ach (cholinergic), and motilin (peptidergic) |
|
|
What are the effects of the SNS on the small intestine?
|
SNS – via fibers that originate in
celic and superior mesenteric ganglia. Stim ↓ contraction of intestinal Smooth Muscle |
|
|
What are Brush Border Enzymes?
|
Brush border enzymes are digestive enzymes located in the membrane of the brush border (microvilli) on intestinal epithelial cells.
Enterokinase & Aminopeptidase |
|
|
What is the patophysiology behind lactose intolerance?
|
inadequacy in lactase which makes lactose undigestible.
Lactose is osmotic active and pulls in water causing cramping and diaharrhea. Bacteria in LI attack lactose → produce ↑ CO 2 & methane gas. |
|
|
What are the functions of the small intestine?
|
Site where most absorption takes place....
Mix Absorb Propell |
|
|
What initiates segmentation motility?
How long are the segment contractions? |
Initiated by SI pacesetter cells
12 minutes in the diodenum 9 minutes in the ilium |
|
|
HOw long does it take contents to move through the SI?
|
3-5 hours
|
|
|
What is Enterokinase?
What else is it called? Where is it made/ What does it do? |
Its a BBE
Activates pancreatic enzyme trypsinogen to form trypsin AKA enteropeptidase Made in the crypts of the duodenum |
|
|
What are aminopeptidases?
What are their two classifications? |
Complete protein digestion by hydrolyzing small peptide fragments into AA
Enteropeptidases and Exopeptidases |
|
|
What do Endopeptidases do?
|
degrade proteins by hydrolizing interior protein bonds
(ex. Pepsin, trypsin, chymotrypsin) |
|
|
What do exopeptidases do?
|
hydrolyze 1 AA at a time from C-end Carboxypeptidase A/B
|
|
|
What is the action of acetylcholine in the enteric nervous system?
|
Contraction of smooth muscle in the wall
relaxation og sphinctors increase salivary secretion increase gastric secretion increase pancreatic secretion |
|
|
What is the action of norepinepherine in the enteric nervous system?
|
relaxation of smooth muscle in wall
contraction of sphincters increase salivary secretion |
|
|
What is the action of VIP (vasoactive intestinal peptide) in the enteric nervous system?
|
relaxation of smooth muscle
increase intestinal secretion increase pancreatic secretion |
|
|
What is the action of GRP ( Gastrin releasing Peptide) in the enteric nervous system?
|
increase gastric secretion
|
|
|
What is the action of enkephalins (opiates) in the enteric nervous system?
|
contraction og smooth muscle
decrease intestinal secretion |
|
|
What is the action of neuropeptide Y in the enteric nervous system?
|
relaxation of smooth muscle
decreased intestinal secretion |
|
|
What is the action of Substance P in the enteric nervous system?
|
contraction of smooth muscle
|
|
|
What 4 GI Peptides are considered hormones?
|
Gastrin
CCK secretin Gastric inhibitory peptide (aka glucose dependednt insulinotropic peptide) |
|
|
What major GI peptide is a known to have paracrine function
|
somatostatin - secreted in stomach (basally)
Released then activates parietal cells in the stomach |
|
|
What are the neurocrines in the GI?
|
Ach
NE VIP GRP Opiates/enkephalins Neuropeptide Y Substance P |
|
|
What is the site of secretion for gastrin?
|
G cells in the stomach
|
|
|
What is the site of secretion for CCK - Cholecystokinin?
|
I cells in the duodenumand jejumum
|
|
|
What is the site of secretion for Secretin?
|
s cells in the duodenum
|
|
|
What is the site of secretion for Glucose Dependent Insulinotropic Peptide?
|
K cells in the duodenum and jejunum
|
|
|
What are the factors that act as stimulus for secretion for gastrin (3)?
|
Small Peptides and AA
Distension of the stomach Vagal Stimulation with GRP |
|
|
What is the stimulus for secretion for CCK? 2
What is NOT a stimulus |
Small Peptides and AA
Fatty acids Monoglycerides NOT TAGS |
|
|
What is the stimulus for secretion for Secretin?
|
H+ in the duodenum
Fatty acids in the duodenum |
|
|
What is the stimulus for secretion for GIP (glucose dependent insulinotropic peptide)?
|
Only GI hormone secreted in response to all three types of nutrients:
AA Fatty Acids Oral Glucose |
|
|
What is the action of gastrin?
|
increase gastric H+ secretion
stimulate growth of gastric mucosa |
|
|
What is the action of CCK? (5)
|
Functions Generally to promote fat digestion and absorption
increase pancreatic enzyme secretions increase pancreatic HC03- stimulates contraction of gallbladder and relaxation of sphincter of oddi stimulates growth og exocrine pancreas and gallbladder inhibits gastric emptying |
|
|
What is the action of Secretin? (4)
|
increase pancreatic HCO3- secretion
increase biliary HCO3- secretion decrease gastric H+ secretion Inhibits trophic effect of gastrin on gastric mucosa |
|
|
What is the action of GIP?
|
increase insulin secretion in pancreatic B cells
decrease gastric H+ secretion |
|
|
What is motilin? Where is it secreted from?
|
Secreted from the upper duodenum during fasting states and is responsible for myoelectric complexes (90 min interval)
|
|
|
What is the role of pancreatic polypeptide?
|
secreted by pancrease in respionse to carbs, proteins or lipids
not considered an "officail" hormone inhibits pancreati secretio of HCO3- and enzymes |
|
|
What is the role if enteroglucagon?
|
It is released from inteston cells in response to low blood glucose levels and diirects liver to increase glycogenolysis and gluconeogenisis
|
|
|
Where is somatostatin released from?
|
D cells stomach
delta cells in the endocrine pancrease ( and hypothalimus?) |
|
|
What is the role of somatostatin?
|
it inhibits the secretion of other GI hormones and inhibits gastric H+
|
|
|
What role does histamine have in the GI tract?
|
ECL cells secrete histamine whic activates cAMP and triggers H+ secretion
Cimretidine blocks somatastatin inhibits |
|
|
Describe slow waves in the GI tract
|
they are oscillating depolarization and repolarization of the membrane porential of smooth muscle cells. They are NOT ACTION POTENTIALS
|
|
|
What is the rate of frequency of slow waves in the GI tract/
|
Varies
Stomach slowest at 3 slow waves/min Duodenum highest at 12 slow waves/min Ilium slows to 9 slow waves/min |
|
|
Where do slow waves originate from?
|
interstitial cells of Cajal which are int he myenteric plexus
they are considered the pacemaker cells for GI smoothe muscle |
|
|
What produces opening of the lower esophageal sphincter?
|
Vagus nerve releasing VIP neurotransmitter
|
|
|
What is the SNS/PNS innervation of the stomach
|
PNS via Vagus in the myenteric plexus
SNS via fibers from the celiac gangion |
|
|
What is receptive relaxation?
|
distention of the lower esophageal sphinctor and orad stomach. It reduces the perssure and increases the volume
|
|
|
What does "vagovagal" reflex mean?
|
Both afferent and efferent limbs of the reflex are carried on the vagus nerve
|
|
|
A vagotimy would have what effect on the stomach?
|
eliminate receptive relaxation
|
|
|
What does the orad region of the stomach include?
|
the fundus and upper body
|
|
|
Where are stomach contractions the strongest?
|
Pyloric region
|
|
|
What is retropulsion?
|
gastric contents that are propelled back into the stomach for further mixing and reduction particle size before being sent to the duodenum
|
|
|
What are the two major factors that inhibit gastric emptying?
|
Fat-Mediated by CCK
H+ mediated by the enteric nervous system |
|
|
The enteric nervous system has what control/responsibility in the small intestine?
|
coordinate segmentation contractions and peristaltic contractions
|
|
|
How is vomiting controlled?
|
via the vomiting center in the medulla brought by afferent fibers in the back of the throat, gi tract and chemoreceptors in the fourth ventricle
|
|
|
Describe the vomiting reflex? IN order
|
reverse paristalsis in SI
relaxation of stomach pyloris forced inspiration to increase abdominal pressure relaxation of lower esophageal sphinctor forceful expilsiong of stomach and duodenal contents |
|
|
What are the characteristics of saliva secretion?
|
High HC)3-
High K+ Hypotonic a-amylase and lingual lipase |
|
|
What factors increase saliva secretion?
|
Parasympatheuc (prominent)
Sympatheic stimulation |
|
|
What factors decrease saliva secretion? 3
|
sleep
dehydraion atropine |
|
|
What are the characteristc gastric secretions?
|
HCL
Pepsinogen Intrinsic Factor |
|
|
What factors increase gastric secretions?
|
gastrin, Ach, histamine (HCL)
Parasympatheics (pepsinogen and IF) |
|
|
What factos decrease gastric secretion of H+?
|
H+ in the stomach
chyme in the duodenum somatistatin atropine cimetidine omperazole |
|
|
What are the characteristics of pancreatic secretions
|
High HCo3-
Isotonic Pancreatic lipase, amalayse and protease |
|
|
What factors increase pancreatic secretions?
|
Secretin, CCk & parasympathetics (HCO3-)
CCK & parasympatheics (pancreatic lipases, amylases and proteases) |
|
|
What are the characteristic secretions of bile? What factors increase secretion?
|
bile salts
biliruben phosphlipids (CCK) cholesterol (PS) |
|
|
What factor decreases bile secretion?
|
Ileal resection
|
|
|
What are the three salivary glands and what do they produce?
|
Parotid glands; serous cells secrete water, ions and enzymes
Submaxillary and sublingual are serous and mucous secreting aqueous fluid and mucin glycoproteisn for lubrication |
|
|
Describe salivary formation
|
Acinar cells in acinus produce inital salive with water, ions enzymesand mucus
Secretion moves to a striated duct and are modified via ductal cells to become hypotonic |
|
|
how does saliva compare to plasma?
|
When secreted from the acinar cells the saliva is isotoniv
aftermidifcation by the dictal cells it becomes hypotonic (more nacl is absorbed the khco3 anf ductal cells are water impermiable) |
|
|
What is the effect of flow rate on the composition of salica/
|
the higher the flow rate the more closely saliva resebles plasma because it has less time to be modified.
the lesser the flow rate the more time for modifcation and the less like plasma it is |
|
|
What do the acinar cells secrete?
|
a-amylase
lingual lipase ,icing glycoporteins IgA kallikrein (vasodialator increase blood and salivary flow) |
|
|
Generally describe the PNS mechanism/innervation of salivary glands
|
PNS is carreid by facial ad glossopharyngeal
post-ganglionic release ach which acts on muscarinic receptors activating IP3 and increasing intracellular Ca2+ |
|
|
Generally describe the SNS mechanism/innervation of salivary glands
|
Sympathetic input from T1-T3 synapse on superior cervical ganglion
NE is released and interacts with B-adernergic receptors on acinar and ductal cells increasing cAMP |
|
|
What do parietal cells secrete?
|
HCl and IF
|
|
|
What do chief cells secrete?
|
pepsinogen
|
|
|
What do g-cells secrete?
|
gastrin into Circulation
|
|
|
what do mucus neck cells secrete?
|
mucus hco3- and pepsinogen
|
|
|
How does atropine work?
|
it block muscarinc receptors (and on parietal cells, subsequently the action of Ach
|
|
|
How does gastrin exert its effect?
|
secreted into circualtion from the stomach antrum
delivered back to the stomach via circulation where it binds to CCK on parietal cells stimulating H+ secretion |
|
|
What is the significance of drugs like cimetidine?
|
it blocks histamine to decreaes H+ secretion, but since histamine also potentiates the actions of Ach and gastrin, it has a greater than expected effect
|
|
|
What three factors induce H+ secretion in parietal cells/
|
Ach
histamine and gastrin |
|
|
What is xerostomia?
|
Xerostomia is the medical term for the subjective complaint of dry mouth due to a lack of saliva.
|
|
|
What is the function of lysozyme?
|
antibacterial action –
lyzes bacteria |
|
|
What is the function of amylase?
|
breaks
polysaccharides into maltose (2 glucose) |
|
|
What is Achalasia?
|
Achalasia is a disorder of the tube that carries food from the mouth to the stomach (esophagus), which affects the ability of the esophagus to move food toward the stomach. LES fails to relax during
swallowing – |
|
|
What neurological disorders can cause difficulty swallowing?
|
Amyotrophic lateral sclerosis (ALS)
Myasthenia gravis |
|
|
What is Schatzki’s ring?
|
A Schatzki ring or is a narrowing of the lower part of the esophagus that can cause difficulty swallowing. The narrowing is caused by a ring of mucosal tissue (which lines the esophagus) or muscular tissue.[1] Patients with Schatzki rings can develop intermittent dysphagia (difficulty swallowing), or, more seriously, a completely blocked esophagus.
|
|
|
The swallowing reflex has what phases?
|
oral pharyngeal esophageal
A sequentially programmed all or none reflex |
|
|
What are the three phases of gastric secretion and
|
Cephalic Phase
gastric Intestinal Phase |
|
|
what is happening in the cephalic phase?
|
HCL and Pepsinogen are increaseing
The cephalic phase of gastric secretion occurs even before food enters the stomach, especially while it is being eaten. It results from the sight, smell, thought, or taste of food, and the greater the appetite, the more intense is the stimulation |
|
|
what is happening in the gastric phase?
|
AA, small peptides & stomach
distension → stimulate HCl release from parietal cells occurs when food is in the stomach |
|
|
what is happening in the intestinal phase?
|
• Mediated by products of protein
digestion • This phase is inhibitory. • Flow of gastric juice ↓ as chyme enters the small intestine enters the small intestine. |
|
|
Which phase of gastric emptying has the most HCl secretion? The least?
|
Most gastric 60%
Least intestinal 10% |
|
|
What causes peptic ulcers?
|
-Broken gastric mucosal barrier.
-gastric/stomach wall injured by acidic/enzymatic contents. - Reflux in the esophagus. - Dumping of excessive acidic gastric contents into duodenum |
|
|
What is exocrine pancreas?
|
90%
the cells/components that drain to the main pancreatic duct, which drains directly into the duodenum. Acini form sacs → connect to ductal tree → empty in duodenum. Intercalated ducts - intralobular ducts – extralobular ducts – Main duct – enters duodenum |
|
|
What is endocrine pancreas?
|
The hormonal secreting cells in the pancrease (2%)
Ilests of langerans... • Insulin (65%) β cells • Glucagon (20%) α cells • Somatostatin (10%) δ cells |
|
|
What is steatorrhea and what causes it?
|
excess undigested fat excreted in feces (60 70%) – lack of pancreatic lipase enzymes
– typical of CF disease |
|
|
What environment is best for pancreatic enzymes?
|
slightly alkaline
|
|
|
What is the role of pancreatic lipase?
|
hydrolyzes dietary TG into MG +2FA
|
|
|
What is the role of pancreatic amylase?
|
cleaves polysaccs into disaccs
|
|
|
What are three pancreatic proteases?
|
Trypsinogen, chymotrypsinogen & procarboxypeptidase (inactive form)
|
|
|
How are Trypsinogen, chymotrypsinogen & procarboxypeptidase acitvated?
|
by enteropepridase by duodenal mucosa cells
|
|
|
How is pancreatic exocrine secretion mainly regulated?
|
Hormonally
|
|
|
When does most of the pancratic secretion occur?
|
80% during the intestinal phase of digestion
|
|
|
What is an enterogastrones?
|
any hormone secreted by the mucosa of the duodenum in the lower gastrointestinal tract in response to dietary lipids that inhibits the caudal (or "forward, analward") motion of the contents of chyme.
Examples include: * secretin[1] * cholecystokinin[2] * gastric inhibitory peptide[3] |
|
|
What is Pancreatitis?
|
Inflammation/infection of pancreas
Can be acute or chronic (gallstones ns islet death) |
|
|
What is the significance and symptoms of Pancreatic Cancer?
|
4-5 leading COD in the US
Sx: weight loss abdominal pain jaundice fatigue clay stools, back pain ½ of patients die within 6 weeks of diagnosis 10% live 1 year 1% live 5 years Increase risk over 50 yo |
|
|
What are bile salts?
|
Bile salts are:
1. derivatives of cholesterol 2. actively secreted into bile. 3. reabsorbed into blood via active transport mechanisms in the terminal ileum (after participating in fat dig & abs) 4. returned to liver via hepatic portal system. |
|
|
What is the role of bile salts in enterohepatic cirtulation?
|
bile salts are recycled between the SI and liver so that they don't need to be resynthesized
|
|
|
What are the componetns of bile?
|
• bile salts
• Cholesterol • Lecithin • bilirubin and aqueous alkaline fluid |
|
|
How much bile is secreted a day?
|
250 ml to 1 liter a day
|
|
|
What is the action of bile salts?
|
emulsifies fats to increase surface area for digestion
|
|
|
What is Bilirubin?
|
A componet of bile formed by the breakdown of RBC's from heme part of hemoglobin extracted from blood in hepatocyte and excreted into bile.
|
|
|
What is cholesystitis?
|
inflammation of the gallbladder
often caused by cholelithiasis which is gall stones |
|
|
What are Choleretics? name 3
|
any substance that increases bile synthesis by the liver
Chemical: Bile Salts Neural:Vagus Hormonal: Secretin |
|
|
What is Jaundice?
|
When billiruben production > excretion
Prehepatic: Problem before liver where excessive RBC breakdown or other factor gives liver more than it can excrete Hepatic jaundice: problem with the liver Posthepatic: problem after the liver like bile duct obstruction |
|
|
What is Cirrhosis?
|
– Prolonged hepatic inflammation – associated with alcohol
– Damaged hepatocytes are replaced by connective tissue. – ↓active liver tissue → chronic liver failure. Symptoms: jaundice weightloss emesis abdominal pain abdominal – Symptoms: jaundice, weightloss, emesis, abdominal pain, abdominal ascites – Treatment: Stop intake of alcohol, diuretics, antibiotics Fluid retention |
|
|
What is the Major stimulant of aqueous ductal secretion in the pancreas?
|
Secretin stimulates the extralobular ducts & ↑’s HCO 3
|
|
|
What are CCK's affect on acinar cells?
|
It ↑’s intracellular IP 3 & Ca 2+
|
|
|
What is Zollinger-Ellison syndrome?
|
A gastrinoma or a tumor in the pancreas or duodenum that secretes excess of gastrin leading to ulceration in the duodenum, stomach and the small intestine
|
|
|
Describe carbohydrate digestion and absorption generally.
|
Salivary and pancreatic amylases break sugars into disaccharides
BBE's break disaccharides into monosaccharides where they are transported and absorbed. |
|
|
By what mechanism is glucose absorbed into the SI?
|
Na+ Glucose Co-transport
SI epithelial cell then blood |
|
|
By what mechanism is galactose absorbed into the SI?
|
Na+ Galactose Co-transport - SI epithelial cell then blood
|
|
|
By what mechanism is fructose absorbed into the SI?
|
facilitated diffusion - straight into blood
|
|
|
What are the components of starch?
|
a-dextrins
maltose maltitriose |
|
|
What are the products of protein digestion and how are they absorbed?
|
Amino Acids-Na+/AA transporter
Dipeptides- H+dipeptide cotransport Tripeptides- H+tripeptide cotransport |
|
|
How are Fats Digested & Absorbed?
|
1 • Dietary fat is emulsified via detergent action of bile salts →
suspension of fat droplets • Lipase – hydrolyzes TG → MG and 2 Fatty Acids • These water-insoluble products – carried on inside of water-soluble micelles. – formed from bile salts. 4 • As micelles approach absorptive epithelial surface → MG & FFA leave micelles → passively diffuse through luminal plasma membrane. membrane. • MG & FFA → Re-esterified to form TG in the cell. • TG → aggregate → coated with Apoproteins, i.e. ApoB TG → aggregate → coated with chylomicrons → extruded through basal membrane of SI epithelial cell – via exocytosis. |
|
|
Oligopeptides require what before being absorbed?
|
to be broke down further by BBE
|
|
|
How is Fe absorbed?
|
Fe3+ is reduced to Fe2+ which can cross into entero cyte. Fe2+ bunds to apoferitin in the intestinal cell
binds to transferrin in blood |
|
|
What is diahrreha?
|
excess loss of intestinal contents which causes dehydration, etabolic acidosis (loss of HCO 3- ) and an increase in K + secretion in colon (hypokalemia)
|
|
|
What is celiac disease?
|
An inherited AI disease where one is allergic to gluten and intestinal villi flatten reducing absorption
|
|
|
What is Crohn’s Disease?
|
a form of inflammatory bowel disease (IBD). It usually affects the intestines, but may occur anywhere from the mouth to the end of the rectum (anus).
the intestinal wall becomes thick and ulcers |
|
|
How can you increase bloof flow to the working muscle? (4)
|
a. Increasing blood pumped by the heart.
b. Shunting and redistribution of blood. c. Metabolic vasodilation in working muscle. d. Decrease in total peripheral resistance. |
|
|
How is CO Increased with Exercise?
|
Initallally stroke volume plateaus so that HR affects co more than
SV at higher levels of exertion |
|
|
What is the equation for maximal heart rate?
|
220-age
|
|
|
How is HR is controlled by a
balance of parasympathetic and sympathetic activity? |
Initial increase in heart rate is due to VAGAL withdrawl, not Sympathertics. However as exercise continuities (around 100 bpm) sympathetic take over!
|
|
|
How does exercise effect ventricular filling time? How does this effect diastolic filling, and why?
|
Left ventricular filling time goes down but diastolic filling is maintained because sympatherics increase the rate of relaxation to compensate.
|
|
|
How does stroke volume compare in a trained vs untrained person during exercise?
|
Stroke volume increases proportionally with exercise intensity.
In non athletes resting SV is lower than in athletes and both can go up the same range during exercise making the exersie rate for nonatheletes also lower. They both cap out about 40-60% of maximal capacity after which it plateaus. |
|
|
Why does SV increase in exercise?
|
Preload increases: Increased venous return and filling increases EDV.
Contractility increases do to SNS innervation |
|
|
↑ contractility has what effect on ejection fraction, ESV and SV?
|
↑ ejection fraction = ↓ ESV = ↑ SV
|
|
|
What is Oxygen extraction?
|
the difference between the arterial and venous concentrations of oxygen (CaO2-CvO2).
Increases 3 fold during exercise because more 02 is consumed and less is brought back in venous system |
|
|
How does Redistribution of Blood of blood work during exercise?
|
Compliance = P/V
SNS constriction to unnecessary areas increases venous return by puttng more blood into a "smaller" system |
|
|
How is working muscle vasodialted?
|
Usually under SNS constriction at rest, but metabolically active substances like CO2, H+, adnosine and lactatae cause vasodialation
|
|
|
What are the exceptions to blood redistribution in exercise?
|
Skin: moderate lets vasodialate so it can cool, intense vasocnstricts to increase cartiac output
heart (may increase) and brain are maintained... |
|
|
What changes occur with detaining?
|
Rapid decrease in CO and VO 2max
HR max does not change!!!! |
|
|
What is heart failure?
|
Heart failure is caused by any condition which reduces the
efficiency of the myocardium through acute damage or overloading. |
|
|
What are the three basic adaptations that occur with heart failure?
|
• hypertrophy
• dilation • contractility |
|
|
What is the result of left heart failure?
|
Left atrial pressure leads to pulmonary congestion and dyspnea
|
|
|
What is the result of right heart failure?
|
Right atrial pressure leads to systemic congestion
lower extremity edema |
|
|
What happens to contractility with heart failure? How does the body try to compensate?
|
In a failing heart, contractility is reduced
SNS stimulation increases contractility temporarily Effects of SNS stimulation eventually depressed Kidney’s sense decrease in CO and retain water to increase blood volume. Leads to an increase in EDV (preload increase) to try to maintain stroke volume. Vasoconstriction increases afterload though |
|
|
What is Decompensated Failure?
|
decrease in contractility worsens
SV not maintained muscle fibers are stretched beyond there optimal length decreased effectiveness of increased EDV |
|
|
Forward failure:
|
less than adequate SV, soemthing wrong with the heart
|
|
|
Backward failure is?
|
blood backs up in the venous system
problem with something down the line (like kidemys holding too much fluid) causes CHF |
|
|
Wht is Eccentric Hypertrophy?
What is being added/ |
VOLUME overload causes increase in muscle mass that is
distributed such that wall thickness remains relatively normal Sarcomeres |
|
|
What is concentric hypertrophy?
|
PRESSURE overload that increases wall thickness from chronic SNS stimulation
• ratio of contractile proteins/ mitochondria increases |
|
|
What would cause eccentric hypertrophy? Concentric
|
E: regurgitation/increased diastolic pressure
C: stenoses, hypertension |
|
|
What factors become desensitized in heart failure from increased SNS stimulation?
|
↓ cardiac NE stores
↓ β-adrenoceptor density ↓ catecholamine sensitivity |
|
|
How does Right Ventricle Failure cause edema?
|
↑ venous pressure
↑ capillary pressure ↑ formation of tissue fluid edema (ascites) |
