Medical Physiology Block 6 Week 1 Flashcards Preview

Physiology & Pathology > Medical Physiology Block 6 Week 1 > Flashcards

Flashcards in Medical Physiology Block 6 Week 1 Deck (75):
1

Identify the different segments of the gastrointestinal tract, their locations, and the sphincters that regulate movement of chyme through it.

1. oropharynx (sphincter = upper esophageal; glands: parotid and salivary); 2. esophagus (lower esophageal sphincter); 3. stomach (pyloric sphincter); 4. Small intestine- duodenum, jejunum, and ileum (iliocecal; glands: pancreas); 5. Large intestine- ascending colon, transverse colon, descending colon, anus (internal anal sphincter and external anal sphincter

2

Digestion requires enzymes secreted from where in the body?

mouth (salivary glands), stomach, pancreas, and small intestine

3

What organs are derived from the foregut of the primitive gut tube? what artery supplies this division and what is the origination of parasympathetic innervation?

esophagus, stomach, parts of the duodenum, liver, pancreas, gall bladder, pharynges, lungs, thyroid, and spleen; celiac artery and vagus nerve

4

What organs are derived from the midgut? what artery supplies this division and what is the origination of parasympathetic innervation?

parts of the duodenum, jejunum, ileum, cecum, appendix, ascending colon, and parts of the transverse colon; superior mesenteric artery and vagus nerve

5

What organs are derived from the hindgut? what artery supplies this division and what is the origination of parasympathetic innervation?

parts of the transverse colon, descending colon, and rectum; inferior mesenteric artery and pelvic splanchnic nerves

6

Do the foregut rotate during development? midgut? hindgut?

Yes, 90 degree rotation to the right; yes, a further 180 degree rotation; No

7

Define a peritoneal organ; retroperitoneal organ

has a mesentery and is almost completely enclosed in peritoneum (is mobile); partially covered with peritoneum and is immobile (covered only anteriorly)

8

What is peritoneum comparable to in other parts of the body? what are mesenteries?

pleural cavity: visceral and parietal layers (parietal layer lines the abdominal cavity and visceral layer forms the serosa of abdominal organs); portions of the peritoneum that suspend the gut and its derivatives and provide path for blood vessels and nerves to viscera

9

The greater omentum is formed from? how many layers is it?

double layer of dorsal mesentery; four

10

What are the major peritoneal organs?

stomach, liver, spleen, jejunum, ileum, appendix, and transverse colon

11

What are the major retroperitoneal organs?

thoracic esophagus, kidneys, adrenals, ureter, aorta, inferior vena cava, anus

12

Which organs lost a mesentery during development (secondary retroperitoneal; dorsal mesentery joined with body wall)?

parts of duodenum, majority of pancreas, ascending colon, descending colon, and parts of rectum

13

When the stomach rotates 90 degrees clockwise, what happens to the right vagus nerve?

becomes posterior vagal trunk

14

What attaches to the greater curvature of the stomach?

dorsal mesentery; it is considered the greater curvature becomes the dorsal portion of the stomach proliferates faster than the ventral portion

15

What is the ventral mesentery attached to?

liver (from behind); develops into lesser omentum

16

The appendix is appended to which organ? what quadrant is it located in?

cecum; lower right

17

Describe the arterial, venous, and lymph flow of the GI tract

arteries along the muscular layer branch into arterioles at submucosa (form a plexus), which branch into capillaries in the mucosal villi; Venules emerging from the villi and mucosal and muscularis layers converge into veins (exit the intestinal wall, paralleling the arterial supply); lipophilic nutrients are taken up by lacteals, which merge with lymphatics and drain into thoracic duct

18

What does the majority of the blood flow to the liver come from? What are the consequence of portal hypertension?

portal vein which carries blood away from the other GI tract organs; ascities (liver cirhossis and collateral blood pools such as caput medusae, varices, and hemorrhoids)

19

Describe postprandial (after a meal) hyperemia.

CNS anticipatory increase in blood flow during cephalic phase; production of vasodilator metabolites; local increases in blood osmolarity; CCK and other hormones may increase intestinal blood flow (BLOOD FLOW INCREASES SEQUENTIALLY DOWN THE GI TRACT); contractions decrease blood flow

20

In regards to the enteric nervous system, what stimulates vasoconstriction of splanchnic vessel? vasodilation?

alpha adrenergic innervation; vagal nerve stimulation indirectly increases blood flow

21

What is the result of sustained splachnic vasoconstriction following a severe hemorrhage?

the ischemic mucosal epithelia slough off (susceptible due to countercurrent flow); endotoxic shock (bacteria and toxins escape from lumen; normally detoxified by liver)

22

Which sphincter has the highest resting pressure?

upper esophageal sphincter

23

What happens to the pressure in the esophagus after swallowing? What happens to the glottis and how is breathing affected? Can pressure be below zero, and if so why?

After a dry swallow (UES relaxes), the pressure wave of primary peristalsis (contraction/relaxation) moves sequentially down the esophagus; glottis is closed and breathing is inhibited; yes and this is reflective of thoracic pressure (and work of respiratory muscles)

24

What is a method for measuring pleural pressure?

inflating a balloon in the esophagus

25

Describe differences between upper esophagus and lower esophagus.

upper esophageal sphincter consists of striated muscle; lower esophageal sphincter is composed of specialized smooth muscle; relaxation of the lower esophageal sphincter only occurs after the UES has returned to resting pressure (triggered by distension of the esophagus or swallowing)

26

What is the primary type of motility in the esophagus?

caudad propulsion of bolus toward the stomach (peristalsis)

27

Describe the process of swallowing from initiation to entry into the stomach, including regulation by cranial nerves and the enteric nerve system.

Food is moved to the esophagus by the movement of the tongue (hypoglossal nerve) and the palatal and pharyngeal muscles (CNs IX and X); closure of the glottis and lifting of the larynx during swallowing inhibits breathing and prevents aspiration; relaxation of the UES allows food to enter the esophagus; relaxation of the LES is mediated by VIP; (SWALLOWING IS A REFLEX ACTION COORDINATED IN THE SWALLOWING CENTER OF THE MEDULLA; AFFERENTS ARE CARRIED BY THE GLOSSOPHARYNGEAL AND VAGUS NERVES); the only action in swallowing that is involuntary is closing the mouth on a bolus and propulsion of food toward the pharynx by the tongue

28

Describe the different movements that occur in the GI tract.

peristalsis: upstream contraction of circular muscle and relaxation of longitudinal muscle (downstream relaxation of circular muscle and contraction of longitudinal muscle); churning: segmental, nonpropulsive contractions (circular muscle; promotes absorption by decreasing unstirred water layer); migrating motor complexes are propulsive contractions initiated during fasting mediated by motilin (periods of inactivity followed by rapid bursts of contractions; downstream sphincter is relaxed to allow caudad propulsion of undigested material)

29

Describe the pressure and contraction changes in the muscles of the rectum and anal sphincters during defecation.

Movement of feces into rectum initiates defecation, relaxation of inner anal sphincter (reservoir function), contraction of external sphincter (unless voluntarily relaxed)

30

Describe the enteric nervous system.

submucosal plexus (Meissner plexus): a collection of ganglia and interneurons of the ENS, predominately responsible for regulating epithelial function and some circular smooth muscle function (secretion and blood flow); myenteric plexus (Auerbach plexus), predominately responsible for regulating longitudinal and some circular smooth muscle function (motility)

31

Is the ENS myelinated? Can the ENS function without control from the CNS?

Yes; yes

32

The enteric nervous system is similar to what other cell type in the body where information is processed by specialized cells within the organ and modulated by the CNS?

"similar concept to generation of a heartbeat" (where contractions are stimulated by pacemaker cells and heart rate is modulated by the vagus nerve)

33

Parasympathetic fibers reach the stomach and small intestine through which nerve? sympathethic innervation? terminal colon?

vagus; greater and lesser splanchnic nerves; pelvic splanchnic nerve;

34

The neurotransmitter/receptor pair of preganglionic sympathetic fibers is?

Acetylcholine/nicotinic receptor (sodium channel)

35

What kind of afferent signals from the GI tract are sensed by the CNS?

stretch (fullness) and chemosensation (toxicity)

36

How can the autonomic nervous system modulate the ENS?

Parasympathetic activity stimulates intestinal motility and glandular secretion which increases intestinal metabolism (cephalic phase); sympathetic fibers decrease splanchnic blood flow

37

How do sympathetic fibers reach the ENS?

post-ganglionic fibers originate in the celiac, superior mesenteric, and inferior mesenteric ganglia and travel along the arteries (may directly innervate parts of the GI tract)

38

Describe the major types of nerve cells in the ENS according to function (sensory, interneural, motor neurons) and the corresponding neurotransmitters and their functions

sensory neurons (some respond to stretch); excitatory motor neurons (release acetylcholine or substance P); inhibitory neuron (VIP or NO)

39

Describe interstitial cells of Cajal.

Modified smooth muscles cells connected to other smooth muscle cells by gap junctions (syncytium); generate slow waves (backbone of action potential generation) and thus act as pacemakers (cells found in the duodenum have the most frequent slow wave generation)

40

Compare and contrast the regulation of gut function by nerves, hormones, and paracrine regulators.

neurocrines (VIP, GRP, and enkephalins): released peptides act as neurotransmitters; paracrine (somatostatin and histamine): released from endocrine cells and act on neighboring cells; hormones (gastrin, CCK, secretion, GIP): are released from endocrine cells in the GI mucosa into the portal circulation, enter the
general circulation

41

Name seven GI hormones.

gastrin, CCK, secretin, GIP, leptin, grehlin, motilin

42

What is an incretin?

hormones that modify release of other hormones (principle of "feed forward" or "anticipation"); GIP (anticipatory release of insulin)

43

Describe major morphological and functional features of epithelial sensory cells

contain microvilli (brush border) and many granules; sense luminal pH, osmolarity, and nutrient content

44

Describe paracrine and neurocrine actions of serotonin (5-hydroxy-tryptamine). enkephalins?

faster motility and electrolyte secretion (paracrine stimulation of epithelial cells; released by ECL cells); enkephalins decrease motility and electrolyte secretion indirectly increasing absorption

45

Summarize the functions of the stomach

reservoir, churning and mixing of chyme, generating an acidic environment, secretion of mucin, and production of intrinsic factor

46

How is the composition of gastric luminal fluid affected by intake of a meal, as well as variable gastric secretions of acid, alkali, and attendant salts?

Ingesting food causes a marked fall in gastric [H +] because the food buffers the preexisting H +. However, as the food leaves the stomach and as the rate of H + secretion increases, [H +] slowly rises to its “interdigestive” level.

47

Identify the proteins secreted into the gastric lumen by chief cells, parietal cells, and mucous cells. Contrast the functions and regulation of these secretions.

both HCl, functions to activate pepsinogen, and intrinsic factor, necessary for vitamin B12 absorption, are produced by parietal cells (stimulated by gastrin, Ach, and His; inhibited by low pH, prostaglandins, and chyme in the duodenun); chief cells produce pepsinogen, which when activated to pepsin digests proteins (stimulated by Ach, gastrin, and HCl; inhibited by protons through somatostatin); gastrin is produced by G cells, which increases His, HCl, and pepsinogen secretion (stimulated by GRP, stomach distension, and small peptides; inhibited by protons via somatostatin); mucus, produced by mucous cells or Goblet cells, forms a gel protecting mucosa from HCl and pepsin and also traps bicarbonate (stimulated by Ach)

48

What region of the stomach are parietal cells found? chief cells? G cells? mucous cells? D cells?

body/fundus; body/fundus; antrum; entire stomach; body/fundus and antrum

49

What are the three divisions of the stomach?

cardia, body/fundus, antrum (+ pylorus)

50

Describe the role of HCl in the gastric digestion of carbohydrates and protein, and how pepsinogen is activated.

Low pH is required for both pepsinogen activation and pepsin activity; Besides being dependent on low pH, pepsinogen is also autoactivated (newly formed pepsin cleaves other pepsinogen molecules to pepsin)

51

Describe the luminal pH of the stomach in the basal fasted state versus the time course of changes in luminal pH after a mixed meal.

Considerable variability in basal acid secretion is seen among physiologically normal individuals, and the resting intragastric pH can range from 3 to 7; buffering power of food and other factors determine the pH in the interdigestive phase

52

Describe how parietal cells H-K-ATPase activity can be inhibited physiologically and pharmacologically.

omeprazole irreversibly inactivates the proton pump blocking proton secretion (inability to activate pepsinogen)

53

Describe the ion transport mechanisms and cellular enzymes needed to allow parietal cell homeostasis during gastric acid secretion.

ACh and gastrin each bind to specific receptors (M 3 and CCK B, respectively) that are coupled to the G protein Ga q. The result is activation of PLC, which ultimately leads to the activation of PKC and the release of Ca 2+. The histamine binds to an H 2 receptor, coupled through Ga s to adenylyl cyclase (AC). The result is production of cAMP and activation of PKA. Two inhibitors of acid secretion also act directly on the parietal cell. Somatostatin and prostaglandins bind to separate receptors that are linked to Ga

54

What secreted substances contribute to regulation of gastric acid secretion via paracrine, hormonal, and neuroendocrine pathways.

paracrine: His from ECl cells and somatostatin from D cells; hormonal: somatostatin and gastrin from antrum; neuroendocrine: Ach from ENS, which is innervated by vagus nerve

55

List the mechanisms contributing to gastric mucosal defense

unstirred water layer (poor diffusion), mucous gel, and trapped bicarbonate

56

How does hydrocholoric acid get across the gastric diffusion barrier?

Viscous fingering (movement of bulk fluid through gelatinous substance)

57

How can the gastric diffusion barrier be disturbed and what is the result?

If H+ penetrates into the gastric epithelium, it damages mast cells, which release histamine and other agents, thereby setting up an inflammatory response. If the insult is mild, the ensuing increase in blood flow can promote the production of both mucus and by the mucus cells. If the insult is more severe, the inflammatory response leads to a decrease in blood flow and thus to cell injury.

58

Describe the role of duodenal contents in regulating gastric secretion.

peptones stimulate duodenal G cells to secrete gastrin; absorbed amino acid increase gastric acid secretion; duodenal endocrine cells release an entero-oyxntin to increase gastric acid secretion

59

Describe local and central reflex mechanisms involved in receptive relaxation of the proximal stomach.

small increases in volume do not cause increases in intragastric pressure until a threshold is reached, after which intragastric pressure rises steeply (accommodation); Vagotomy abolishes a major portion of gastric accommodation (normally modulates)

60

Describe how the physical and chemical composition of a meal is sensed by the stomach and duodenum to affect the rate of gastric emptying.

gastric emptying is delayed by fat/protein in the duodenum (stimulating CCK release and gastric distension), protons in the duodenum (vagovagal), high content of calories, and stomach contents that are hypertonic or hypotonic; other mechanisms signal through secretin and GIP

61

Describe the function of gastric peristalsis, the pyloric sphincter, and in controlling gastric emptying rate.

contractions of the stomach propel chyme through the pylorus at a regulated rate. pyloric sphincter contraction at the time of antral contraction limits the movement of chyme into the duodenum and promotes mixing by forceful regurgitation of antral contents back to the fundus (retropulsion)

62

What are mechanisms that delay gastric emptying?

the coordinated function of fundic relaxation; inhibition of antral motor activity; stimulation of isolated, phasic contractions of the pyloric sphincter; and altered intestinal motor activity

63

Describe the volume and composition of salivary fluid coming from major salivary glands.

salivary glands produce approximately 1.5 L/day of saliva; presence of α-amylase, lingual lipase; hypotonic: high concentration of potassium bicarbonate

64

How does flow rate change the composition of salivary fluid?

At the lowest flow rates, saliva has the lowest osmolarity and lowest Na+, Cl–, and HCO3– concentrations, but has the highest K+ concentration; At the highest flow rates, the composition of saliva is closest to that of plasma.

65

Describe the stimuli and neural pathways involved in promoting salivary secretion

parasympathetic innervation is necessary for maintaining the normal mass of salivary glands. Clinically, some medications (particularly psychiatric drugs) have “anticholinergic” properties that are most commonly manifested as “dry mouth." ; sympathetic innervation also increases salivary secretions to a lesser extent

66

Describe the physiological function of the components of saliva.

prevent dehydration of oral mucosa and provide lubrication for mastication

67

Describe the ion transport mechanisms responsible for fluid secretion by salivary glands.

ion gradient is maintained by Na-K pump; Na/K/Cl cotransporter (driven by sodium gradient) drives 3 sodium, 3 potassium, and 6 chloride into the acinar cell; Intracellular accumulation of chloride establishes an electrochemical gradient that chloride secretion into the lumen through apical membrane chloride channels; transepithelial voltage becomes more lumen-negative and drives paracellular sodium transport into the lumen (water, through aquaporin channels, follows sodium)

68

List the major components secreted by the exocrine pancreas and the principal cell types involved in this secretion.

acinar cells secrete enzymes, NaCl, and water; duct cels secrete sodium bicarbonate

69

Describe the mechanisms by which chyme from the stomach is neutralized in the duodenum.

bicarbonate in the duodenum neutralizes HCl in chyme entering the stomach (and deactivates pepsin)

70

Describe the mechanism by which pancreatic zymogens are activated in the small intestine.

Trypsinogen is activated by enterokinase in the small intestine

71

List the stimuli that release secretin and CCK and explain the route by which these regulatory peptides stimulate the pancreas.

when protons enter the duodenum, S cells secrete secretin, which acts on pancreatic ductal cells to increase bicarbonate production; fatty acids and peptones stimulate CCK secretion, which subsequently increases pancreatic secretion

72

Describe the role of CFTR in pancreatic ductal secretion

activation of CFTR receptor causes a efflux of ATP, which then binds to an apical purinergic receptor that activates outwardly rectifying chloride channels in an autocrine/paracrine fashion increasing chloride recycling

73

Describe the role of the autonomic nerves and peptide hormones in the regulation of pancreatic secretion.

During the cephalic phase, the sight, taste, or smell of food stimulates pancreatic acinar cells, through the vagus nerve and muscarinic cholinergic receptors, to release digestive enzymes and, to a lesser extent, stimulates duct cells to secrete HCO 3− and fluid; The arrival of gastric acid in the duodenum stimulates S cells to release secretin, which stimulates duct cells to secrete HCO 3− and fluid. Protein and lipid breakdown products have two effects. First, they stimulate I cells to release CCK, which causes acinar cells to release digestive enzymes. Second, they stimulate afferent pathways that initiate a vagovagal reflex that primarily stimulates the acinar cells through M 3 cholinergic receptors.

74

Describe the mechanisms by which HCO3 is secreted by pancreatic ductal cells.

Secretin activates the cAMP signaling pathway and opens the CFTR Cl − channels through phosphorylation. Cl − movement out of the cell leads to basolateral membrane depolarization, thus generating the electrical gradient that favors NaHCO 3 cotransport.

75

Describe the process of digestive enzyme synthesis and packaging and how this process maintains the integrity of the pancreas.

Within the Golgi complex , secretory proteins are segregated away from lysosomal enzymes; secretory proteins exit the Golgi complex in condensing vacuoles (segregated from other vacuoles)