Physiology Ii - Gi

Front 1

SLOW WAVES:

- Are spontaneous rhythmical undulations of resting membrane potential around baseline of ______, generated by ___?

Back 1

* undulations of resting membrane potential around baseline of (-50-60 mV)
generated by specialized smooth muscle cells (Cajal).

Front 2

How are slow waves conducted along a GI section (between cells)?

Frequency with which waves are generated?

Back 2

B/o Gap Junctions, slow waves are conducted along a GI section.

- Slow waves occur with a frequency of 3–12 / min depending on the gut section.

Front 3

critical threshold potential ?


what happens next?

Back 3

slow wave peak reaches critical threshold potential at (-40/–35mV) !!!!

* causes V/G Ca+ channels to open -> rapid influx of Ca+ causes spike potentials & muscle contractions, spread along GI section

Front 4

amplitude of slow waves can be modulated by

Back 4

1. PRIMING FACTORS

2. Hyperpolarizing factors

Front 5

PRIMING FACTORS

Back 5

PRIMING FACTORS which depolarize smooth muscle membrane -> more slow waves reach threshold -> GI motility increases: e.g. gut wall stretching, PS stimulation, some GI hormones

Front 6

Hyperpolarizing factors

Back 6

Hyperpolarizing factors -> harder for slow waves to reach threshold potention -> GI motility decreases, e.g. sympathetic stimulation, some GI hormones

Front 7

GI motility involves two basic pattern:

Back 7

1. Segmentation / Mixing (above): Localized contraction of mostly circular muscles
2. Peristalsis / Propulsion
Circular contraction behind bolus; contraction travels toward anus over longer distance = strong local reflex called
ADAPTIVE RELAXATION

Front 8

What can cause TRP (traumatic reticuloperitonitis)?

What results from this?

Back 8

if cow injests nail or foreign object, and it perforates reticulum

allows leakage of ingesta and bacteria, which contaminates the peritoneal cavity.

inflammation can obstruct vagal innervation ->
Receptor damage or inhibition -> motlility in reticulum decreases -> ruminal stasis (vagal indigestion)

Front 9

cell to cell signaling


system responsible to sending hormones via blood stream

Back 9

Paracrine

endocrine

Front 10

Most important DUODENAL factors for reducing stomach emptying rate are:
(not looking what is secreted, but for the specific things they stimulate e.g. receptor)

Back 10

All following are part of enterogastric inhibition:
- incr. pressure in duodenal lumen
- low pH
- HIGH FAT CONTENT IN DUODENUM
- high peptide conc
- high osmoregularity

Front 11

What happens if pH in gut (duodenum) too low?

Back 11

: duodenal endocrine cells react to low pH values -> release Secretin into circulation -> stimulates pancreas and liver to release buffers into the gut

Front 12

main excitatory neutrotransmitter of GI?


inhibitory neutrotransmitter of GI?

Back 12

(for most part actions of neurotransmitters in gut are reversed)
* Acetylcholine (mostly excitatory)

* norepinephrine (mostly inhibitory)

Front 13

Myenteric plexus has what kind of receptors?
Efferent (motor) neuron are associated with what types of cells?
What is influenced here?

Back 13

Mechanoreceptors monitor degree of muscle stretching -> Efferent (motor) neurons to muscle cells -> influence GI motility

Hint: Myenteric MMM

Front 14

Submucosal plexus has what kind of receptors? Efferent (motor) neuron are associated with what types of cells?
What is influenced here?

Back 14

Chemoreceptors monitor chemicals (=nutrients, pH) -> Efferent (motor) neuron to secretory, endocrine and mucus cells -> influences GI secretions

Front 15

stimulation of the parasympathetic nerves

Back 15

mostly stimulates the GI’s functions, e.g.:
- increases motility
- increases secretion rates
- decreases sphincter tones

Front 16

Sympathetic fibers originate from ?

Back 16

sympath. fiber originate between segments T5 to L2, and pass to mesenteric ganglia

Front 17

stimulation of the sympathetic system causes what changes in GI function? sphincter tone? secretions?

Back 17

stimulation of the sympathetic system
mostly inhibits activity of GI functions,
e.g. - decreases motility
- decreases secretions
- increases sphincter tone

Front 18

Where are Crypts of
Lieberkuehn located?

Name Cell types found there? (five of them)

Back 18

small intestine and colon (both)

STEM CELLS, found w/i the
Crypts of Lieberkuehn differentiate into:
1. young enterocytes: secretory
2. mature enterocytes: absorptive; do not express BBM enzymes and transporters.
3. ENDOCRINE CELLS: produce
endocrines, e.g. CCK, secretin
4. MUCUS CELLS
5. PANETH CELLS

Front 19

local reflexes controlled by

central reflexes controlled by ?

Back 19

Enteric NS

Autonomic NS

- both use same receptors within the gastrointestinal wall , for most part

Front 20

Distension of the GI wall causes what chain of events ?

(looking for specifc factor)

Back 20

stimulation via mechanoreceptors -> release of priming factors -> opening of ligand-gated ion channels -> depolariz. of smooth muscles membranes -> passing slow waves will reach threshold -> spike potentials -> contractions

Front 21

inflammatory mediators of GI?

Back 21

prostaglandins
histamine
cytokines

Front 22

inflam. mediators act as _____crines, typically stimulating secretory and motility functions of GI, leading to ______

Back 22

inflam. mediators act as PARACRINES (cell to cell signaling) typically stimulating secretory and motility functions of GI, leading to PERISTALTIC RUSH (diarrhea)

Front 23

PERISTALTIC RUSH

Back 23

powerful and rapid peristaltic movements of sm. int. caused by intense mucosal inflammation = protective response to quickly push potentially harmful contents into Large Intestines

Front 24

How could Large Redworm (Strongylus vulgaris) have lead to an infarction within the large colon??
note: Large Redworms larvae live within a horse’s vascular system at the aorta / intestinal artery junction.

Back 24

Need to burrow through endothelium of artery to get to mucosa -> tissue damage & clot formation -> blockage of GI arteries -> lack of perfusion -) ischemia (lack of blood supply)

Front 25

How can hypoxia of tissues (affected by redworm) lead to necrosis?

Back 25

hypoxia=> anaerobic metabolism -> lack of ATP and increase in lactic acid -> inhibition of na/k pumps and other enzymes/proteins with intracellular accumulation of na -. Cellular swelling and death.

Front 26

Septicemia

Back 26

presence of pathogenic organisms in bloodstream, leading to sepsis

Front 27

How does saliva of animals differ from humans?
(give specific pH)

Which ions are secreted?

Back 27

Animal Saliva is slightly hypotonic, slightly alkaline
(pH 7.2-8.4), and K-rich

Acini secrete mucus & K+ and HCO3- , while Na+ & Cl-taking up

Front 28

diagnostic indicator of liver disease

Back 28

increased amount of bile acids in plasma
-> b/c damaged hepatocytes cannot extract bile acids from portal blood

Front 29

“warming up” phase (of digestive organs) innervated by what cranial nerve? ...duh

Back 29

CN X and initiate VAGAL REFLEXES
leading to mild stimulation of the stomach, small intestines, pancreas
and bile = “warming up” phase

Front 30

Why do ruminants produce continuously large volumes of alkaline saliva rich in bicarbonate & phosphate buffers?

Back 30

essential to neutralize
fermentation products in the rumen!
(i guess products cause low pH)

Front 31

Give 3 or 4 examples of what might cause megaesophagus ?

Back 31

e.g. caused by:
- Achalasia:
lower sphincter fails to relax due to genetic malfunction of myenteric
plexus
- or a Persistent Right Aortic Arch:
mechanical obstruction
- myasthenia gravis (acetylcholine receptor deficit or damage) neuromusclar disorder, means "grave muscle weakness", problem with vol.musc.
- idiopathic

Front 32

Which clinical signs would lead to suspicion of a PRAA?

Back 32

regurgitation after eating malnutrition (coughing, aspiration of food, pneumonia)

Front 33

At which age would PRAA disorder typically show up?

Back 33

at time of weaning.
(b/c of eating solid food)

Front 34

Describe a cross section of a typical gut wall

Back 34

Consists of an outer layer of longitudinal muscle, and inner layer of circular muscle and a lamina muscularis mucosa

Front 35

Lipids (triglycerides) broken down into

Back 35

Lipids (triglycerides) broken down into monoglycerides and fatty acids (2)

Front 36

-slow waves are ?

(how many / minutes?)

Back 36

-slow waves are spontaneous rhythmical undulations of the resting membrane potential, generated by specialized smooth muscles (3-12/min)

Front 37

-spike potential is reached and a contraction happens only when a ?

Back 37

when a slow wave peak reaches critical threshold potential (-40/-35mV), voltage gated calcium channels open -> rapid influx of calcium causes spike potentials and elicits muscle contractions

Front 38

Priming factors include:

* leads to ?

Back 38

Priming factors include: any stimulation (of mechano- or chemoreceptors) that bring the slow waves closer to threshold!

e.g. gut wall stretching, parasympathetic stimulation, some GI hormones

* leads to increased motility

Front 39

salivary amylase (omnivores only)

Back 39

salivary amylase (in omnivores only) start carbohydrate digestion!!

Front 40

purpose of esophageal sphincters?

Back 40

* Upper and lower esophageal sphincters are tightly closed when not in swallowing process
* avoid entry of air and esophageal reflux of gastric contents

Front 41

Name the digestive functions of the stomach

Back 41

1. Temporary storage of food
2. Mixing of food with gastric secretions and liquefaction of ingesta into chyme
3. Chemical and enzymatic digestion, particularly of proteins
4. Controlled release of liquefied chyme into the small intestines

Front 42

IS absorption a physiological gastric function?

Back 42

NO!

Front 43

3 functions of gastric motility

Back 43

1. Mixing (distal stomach) = food stim. enhancement of peristalsis originating in pacemaker area
2. Release of chyme: mixing slowly liquefies content
3. During fasting phases (empty stomach): occas. strong peristaltic waves occur btw. stomach and ileum while pylorus is relaxed= MMC

Front 44

Parietal cells secrete?

Back 44

HCl and Intrinsic factor

Front 45

Enterochromaffin-like cells secrete?

Back 45

Enterochromaffin-like cells: Histamine

Front 46

Chief cells secrete

Back 46

Chief cells: Pepsinogen or Prochymosin

Front 47

G (endocrine) cells secrete:

why? from where?

Back 47

G (endocrine) cells: Gastrin, pyloric region only

- released in resp. to high polypeptide content

Front 48

principle functions of Histamine

released in response to?

Back 48

released from enterchromaffin cells (strong stimulus), released in response to Gastrin

histamine is inflammatory mediator, act as paracrines, typically stimulating secretory (HCl!!!) and motility functions
of the GI, leading to :

Front 49

Principle functions of Gastrin:

What stimulates its release?
What is released is response to gastrin secretion?
What inhibits Gastrin release?

Back 49

Released from G cells into blood in response to peptides (mild direct stimulus). increases HCl secretion and gastric motility.

Histamine is released from EC cells in response to gastrin.

When pH < 2, Gastrin release becomes blocked and vagal and local reflexes become inhibited to prevent excessive acidification. (Self-limitation of stomach)

Front 50

3 control phases of gastric functions

Back 50

1. Cephalic phase: anticipation of food, etc.
2. Gastric phase
3. Intestinal phase=when chyme arrives in duodenum

Front 51

Describe functions of Gastric phase:

Back 51

arrival of food in stomach, stimulation of gastric mechano and chemoreceptors leading to strong stimulation of local (plexus) and central (vagal) reflexes.
Effects: relaxation of muscles (accommodation) in proximal parts
Vigorous muscle contractions (mixing/grinding) in distal parts
String stimulation of all gastric secretions with massive HCl release

Front 52

Describe enterogastric reflex:

What is transmitter?
Where is receptor located? Effector?

Back 52

Inhibitory stimulus from SI to stomach; transmitted by secretin and cholecystokinin (CCK) to reduce gastric secretions.

Front 53

Storage occurs mostly in proximal stomach,
facilitated by the ______.

Back 53

Accommodation reflex

reduction in muscle tone in proximal parts -> relaxation -> expansion of stomach w/o pressure increase

Front 54

Describe functions of Intestinal phase

Back 54

Intestinal phase=when chyme arrives in duodenum -> inhibition of gastric glands and motility due to activation of receptors in the small intestines=prevents overloading of small intestines (negative feedback)
Stimuli:
Distention of small intestines
High acidity
High nutrient content
Irritation of mucosa
=enterogastric reflex

Front 55

G (endocrine) cells?

Back 55

Gastrin

Gastrin released from G cells into blood in response to peptides (mild direct stimulus)

Gastrin increases HCl secretion and gastric motility

Front 56

Explain the functions of hydrochloric acid

Back 56

- To macerate ingesta into fluid
- To denature proteins (quatrenary and tertiary structure)
- To begin emulsification of fats
- To activate the proteolytic enzymes pepsinogen or prochymosin
- To be bacteriacidal

Front 57

principle functions of Intrinsic factor

Back 57

released from parietal cells, co-secreted with HCl, essential for absortption of vit B-12 -> necessary cofactor for erythropoiesis

Front 58

principle functions of prochymosin

Back 58

nursing animals secrete procymosin instead of pepsinogens (rennin in calves), specific for coagulation of casein

Front 59

ENTEROCHROMAFFIN-LIKE cells secrete? (In response to what?)
What are affects?

Back 59

Histamine

Histamine is released in response to Gastrin
(= strong stimulus); like gastrin promotes HCl secretion but in as paracrine (cell to cell)

"effect of gastrin is partly - or entirely - mediated by histamine"
- Fig.14.35, p.535

Front 60

SECRETION OF MUCUS is controlled by
(name cells and specific hormone promoting secr.)

Back 60

SECRETION OF MUCUS is controlled by local reflexes (enteric NS)
and central reflexes (Vagus): lead to synthesis of prostaglandin
(PGE2) in goblet cells -> increases mucus & bicarbonate release.

Front 61

goblet cells produce ?

Back 61

MUCUS

synthesis of prostaglandin (PGE2)

Front 62

Parietal cells secrete what into stomach lumen?

Back 62

HCl + Intrinsic factors

Front 63

How does the local and central reflexes control motility (increase it)?

Back 63

It leads to synthesis of PROSTAGLANDIN (PGE2) in goblet cells which increases mucus and HCO3- release

Front 64

Which drugs interfere with PG synthesis (and thus release of mucus and HCO3-)?

Back 64

NSAIDS

Front 65

principle functions of pepsinogens

Back 65

Pepsinogens: prescurors of pepsins
* activated in low pH
* are proteolytic enzymes -> initiate protein digestion (hydrolysis of collagen by splitting large ppt. into smaller ppt. and some oligopeptides

Front 66

which part of stomach is non-glandular?

Back 66

distal

Front 67

Semi-solid and solid foods require
grinding and mixing with gastric juices into
fluid ____ before it can pass the pylorus
(= strong, sieve-like sphincter)

Back 67

mixing with gastric juices into
fluid CHYME before it can pass the pylorus

Front 68

Migrating motor complexes

Back 68

Occasional strong peristaltic waves occur between stomach and ileum while pylorus is relaxed
> clear stomach and small intestine of undigested food particles

Front 69

interstitial Cajal cells

Back 69

PACEMAKER CELLS that lie between circular and longitudinal muscle layers in both stomach and intestines.

conduct repetitive and spontaneous oscillations in membrane potential transmitted thr. gap junctions.

Ca+ flowing into muscle during AP will induce CONTRACTION

Front 70

Name a few (of 35) regulatory peptides of GI:

Back 70

Gastrin, Somatostatin, Secretin,
Cholecystokinin, Gastric inhibitory peptide, Motilin, Enteroglucagon, Peptide YY etc

Front 71

Which have positive effect on HCL secretion?
A. histamine
B. Gastrin
C. NSAIDs
D. sympathetic innervation
E. acetylcholine

Back 71

histamine, gastrin, acetylcholine

- all req. for MAX secretion of HCl

Front 72

location of "vomiting center"

Back 72

brain stem

Front 73

CONSEQUENCES OF SEVERE VOMITING

Back 73

loss of fluid -> hypovolemia -> blood pressure down / circulatory shock
loss of K+ -> hypokalemia -> hyperpolarization of membranes -> reduced
excitability of nerve/muscle cells -> weakness + hyporeflexia
loss of H+ -> metabolic alkalosis -> hypoventilation

Front 74

COMPONENTS of Gastro-Intestinal barrier are:

Back 74

- Mucus and Bicarbonate –
- Prostaglandin E2: incr. blood flow, mucus and HCO3 secretions
- Epithelial cells w/tight junctions and stem cells = high regen. capacity
- Bactericidal peptides / immunoglobulins A

Front 75

causes of disruption to barrier

therapy?

Back 75

NSAIDs (inhibit PGE2 which promotes mucus/HC03), stress, ISCHEMIA, INFECTIONS

THERAPY: stress relief, histamine (H2) blockers (histamine, released b/c of irritation, promotes HCl secretion), proton pump blockers,
antibiotics (if infection is cause of probkem)

Front 76

Purpose of Co-operation between the PANCREAS, BILE and small intestinal MUCOSA?

Back 76

1. Neutralization of gastric acid (via buffers) to avoid mucosal damage
2. Hydrolysis of macromolecules into micromolecules for absorption

Front 77

pancreatic enzymes to function, which require pH of?

this is enabled by ?

Back 77

pH > 5

BICARBONATE Solution: secreted by the pancreatic duct system to
(neutralizes gastric acid)

Front 78

3 major groups of DIGESTIVE ENZYMES produced in the pancreatic Acini are ?

Back 78

The 3 major groups of DIGESTIVE ENZYMES are amylolytic, proteolytic and lipolytic

Front 79

a-Amylase digests ?

Where is secreted from?
pH requirement?

Back 79

* a-Amylase digests most soluble but not structural carbohydrates

* Amylase splits polysaccharides into oligosaccharides

* secreted from pancreatic duct system, req. pH >5

Front 80

name some PROTEOLYTIC ENZYMES

Back 80

Trypsinogen, Chymotrypsinogen, Pro-Elastase, Pro- Carboxypeptidases, etc

Front 81

Proteolytic enzymes are secreted in vesicles as inactive pro-enzymes for what reason?

Proteolytic enzymes produce mostly?

Back 81

to avoid autodigestion

Proteolytic enzymes produce mostly oligopeptides

Front 82

stimulation of the exocrine pancreas begins with ?

MAIN PHASE of
pancreatic stimulation ? via what 2 hormones?

Back 82

CEPHALIC PHASE (“warming up”).

INTESTINAL PHASE
= MAIN PHASE of
pancreatic stimulation via 2
hormones:
SECRETIN and CCK

Front 83

Direct digestive functions of the LIVER are:

Back 83

- to facilitate digestion and abs. of fats and lipophilic vitamins via SECRETION of BILE ACIDS
- to neutralize acidic chyme via bicarbonate secretion

Front 84

What cells secrete bile juice (including bile acids and other components)? What does bile juice consist of?

Not asking structure of bile acids...that's a seperate question.

Back 84

1. Hepatocytes secrete
- Bile acids (> 50% of solutes)
- Lipophilic waste products, e.g bile
pigments = bilirubin, cholesterol etc
2. Duct cells secrete
- Bicarbonate
- Electrolytes and water

Front 85

BILE ACIDS are derived from

Back 85

cholesterol

Front 86

cholesterol conjugated with A.A.to form

Back 86

BILE ACIDS!! -> DETERGENT = has hydrophilic and lipophilic end

Front 87

Bile acid RECYCLING:
bile acids are re-absorbed in
___, re-enter _____and are secreted
again and again (up to 20 times).

Back 87

95% of bile acids are re-absorbed in ILEUM, re-enter LIVER and are secreted again and again (up to 20 times).

Front 88

The re-uptake of bile acids into liver stimulates _____ to secrete more bile juice.

Back 88

The re-uptake of bile acids into liver stimulates HEPATOCYTES to secrete more bile juice = positive feedback

Front 89

salivation controlled by what cranial nerves?

Back 89

When chewing and/or salivating parasympathetic efferents via
CN VII & IX -> more salivation

Front 90

STEM CELLS differentiate into ?
(just names and type of cell)

Back 90

o Young enterocytes -> Secretory cells!
(line Crypts of Lieberkuehn)
o Mature enterocytes -> Absorptive cells -> BBM

Front 91

Stem cells also differentiate into:

Back 91

ENDOCRINE CELLS: produce endocrines, e.g. CCK, secretin
MUCUS CELLS
PANETH CELLS

Front 92

YOUNG ENTEROCYTES secrete ?

Back 92

* secrete large volumes of INTESTINAL FLUID to facilitate digestion & abs. through active Cl secretion into gut lumen -> creates electrical gradient -> pulls Na+ in -> H2O follows (ca. 2 liters/day/man) -> dilution of chyme!!
Note: some toxins, inflam. mediators and viruses
stimulate Cl- transport

Front 93

What are only enzymes that require very low pH (1-3)?

Back 93

pepsinogens

Front 94

What does cephalic phase entail?

Back 94

- chewing, swallowing
- mechan. and chem. (in some sp.) digest. begins
- "warming up" during which signals sent stomach, acc.glands, even S.I. to prepare for food!

Front 95

Why is myasthenia gravis a problem in pregastric digestion?
Breed most common in?

Back 95

AcH receptor deficit, so problem with motor end plate, also problem getting into stomach
- seen in sharpe' most

Front 96

What are secretions that also occur during cephalic phase?

Back 96

mucus, gastrin, histamine, HCl, pepsinogen

- secretions start (mildly) after stimulation of vagus nerve by mechano- and chemoreceptors
- although this secretions most likely intensify during gastric phase (when food how actually enter stomach)

Front 97

What is unusual about vagus nerve stimulation and accomodation reflex?

Back 97

- in digest., vagal innervation usually leads to smooth muscle constriction
- during acc.reflex, see red. in musc.tone (relax)
- likely uses different nt's e.g. nitric oxide or VIP

Front 98

1. Where does salivary amylase work?
2. What exactly does it break down? Bonds?

Back 98

up to proximal stomach during storage phase where pH not too low ~30% digested
(expand on this)

a-Amylase hydrolyses only a-1-4 linkages of polysaccherides; products are oligo- and some disaccharides (mostly maltose), which cannot be absorbed

Front 99

How does emulsification work?
Objective here?

Back 99

* Emuls. referes to process of mixing two or more immiscible (unblendable) liquids

* Bile acids attach to surfaces of fat globules -> vigorous mixing in aqueous chyme -> globules break up into smaller pieces -> increases S.A. for action of pancreatic lipases!
* after hydrolysis by lipases, form micelles and can be transported in aqueous layer with chyme

Front 100

MATURE ENTEROCYTES secrete? what is their purpose?

Back 100

- develop microvilli -> BBM
- containing digestive enzymes
and absorptive mechanisms.
- products of LUMINAL digestion hydrolyzed further, to be absorbed

Front 101

trypsinogen is secreted by?

activated by?
what stimulates it release?
what trypsin do?

Back 101

trypsinogen is secreted by pancrease in vesicle with inhibitory compound; activated into trypsin by enteropeptidase (from SI.).
- trypsin formed first stim. further release of trypsinogen and rest of proteolytic enz.

Front 102

what is luminal phase of digestion?

Back 102

Luminal phase = macromolecules e.g. polysaccherides into smaller but still not absorbable pieces; e.g. oligo- and some disaccharides.

Front 103

Brushborder phase of starch digestion ?
(what bonds broken here?)

Back 103

Oligo- and disaccharidases within the BBM (e.g. maltase) hydrolyse a-1-4
and a-1-6 linkages; endproducts are monosaccharides (Glc) = ABSORBABLE MONOMER

Front 104

Can dietary DISACCHARIDES (sucrose and lactose) be hydrolyzed by alpha-Amylase?

Back 104

NO, require disaccharidASE in BBM.

Front 105

Absorption of Glucose and Galactose into absorptive cells occurs
via ?

Back 105

secondary active Na-cotransport mechanism,

which depends on electrochemical SODIUM GRADIENT, created by the Na/K pump at the basolateral side.
~requires intact enterocytes

Front 106

Fructose is absorbed via ?

Back 106

facilitated diffusion.
~requires intact enterocytes

Front 107

Newborns of some species can absorb colostral immunoglobulins (by endocytosis). The digestion of these proteins is avoided by:

Back 107

- limited HCl secretion
- limited pro-chymosin secretion
- a trypsin inhibitor in the colostrum

Front 108

how can toxin affect absorption?

Back 108

Many of these transporters are inhibited by enterotoxins except for the
Na-Glc transporter !

Front 109

Process of Fat digest and absorption:

Back 109

1. Fat globules EMULSIFIED by HCl and conj. bile acids
2. Pancr.lipase / colipase attach to fat globule surface; HYDROLYSE triG into MONOGLYCERIDES & free FA
3. micelles
4. transport to BBM and diffuse in
5. Free conj. bile acids return to emulsify more fat globules or form new micelles

Front 110

after being absorbed into enterocytes:
Triglycerides, cholesterol, phospholipids, fat-soluble vitamins and newly formed
lipoproteins aggregate into ?

Back 110

Triglycerides, cholesterol, phospholipids, fat-soluble vitamins and newly formed
lipoproteins aggregate into CHYLOMICRONS

Front 111

How is water reabsorbed in sm.int.?

Back 111

secretions in proximal part greatly incr. osmoreg, so eventually electrocytes (mainly Na+) diffuse back into cells passively -> water follows

Front 112

By the time chyme leaves
the small intestines, ca
____% of its water content
have been reabsorbed!

Back 112

80-90% of water content
have been reabsorbed in sm. intestine!

Front 113

SECRETORY Diarrhea

Back 113

Direct stimulation/irritation of secretory/mucus cells by enterotoxins (from e.coli), inflammatory mediators, etc to secrete more fluid

Front 114

Why would SECRETORY Diarrhea cause metabolic acidosis?

what else happens?

Back 114

bicarbonate loss (leaves before can be reabsorbed) -> metabolic acidosis

fluid loss -> hypovolemia -> hypoxia/metab.acidosis/tissue damage + shock and circulatory collapse
also
K+ loss -> hypokalemia -> hyperpolarization of nerve/muscle membranes
-> weakness, hyporeflexia

Front 115

OSMOTIC (malabsorptive) Diarrhea

Causes?

Back 115

gut lumen contains large # of molecules which are poorly
absorbed -> high osmolality of chyme -> water is “sucked” into lumen
- accum. of partially digested ingesta due to e.g.pancreatic
deficiency (GI mucosa is intact)
- loss of absorptive cells due to mucosal damage (inflammations, infections/ some toxins) -> digestion cannot be completed and micromolecules cannot be absorbed

Front 116

GASTRO-ILEAL REFLEX

Back 116

At end of SI digestion, animal will take in next meal -> gastric distension -> SPHINCTER OPENS and ingesta is propelled into caecum

Front 117

serotonin, dopamine, CCK, ATP, somatostatin,bombesin, motilin, substance P, vasoactive intestinal peptide, etc are examples of ?

Back 117

neurotransmitters

Front 118

What is secreted by cells of LI to help motility and protect cells?

Back 118

Bicarbonate-rich fluid and mucus: buffering of
fermentation products (VFA's!!!!) to protect mucosa

Front 119

Vitamin produced by bacteria of LI

Back 119

Vit K

Front 120

Absorption in LI regulated by:

Back 120

Sodium via active Na-K pump, followed by chloride and water; pump is regulated by ALDERSTERONE

Aldersterone stimulates uptake of sodium; H2O follows Na+

Front 121

How can psychogenic tension produce diarrhea?

Back 121

parasympathetic stimulation -> increased HCO3 secretion

Front 122

2 reflexes involved in defecation?

which is more significant or supports other?

Back 122

1. Myenteric reflex:
pressure receptors in rectum -> stimulates myenteric plexus -> peristalsis & internal
sphincter relaxation -> defecation
(myenteric reflex is a weak reflex, needs to be fortified by parasympathetic reflex)

2. PS reflex (via pelvic nerves):
Rectum distention -> PS. fibers / pelvic nerves -> intensified peristalsis

Front 123

What origin of pelvic nerve?

Back 123

S1-S3

Front 124

Defecation reflex can be blocked by voluntary constriction of

Back 124

external sphincter and puborectal muscles (via pudendal nerve)

Front 125

Pelvic Nerve damage leads to?

Back 125

Pelvic Nerve damage -> paralyses defecation reflex -> constipation (this is more dangerous than incontinence, but the latter leads to more euthasia)

also affects bladder, urine dribbling, urinary incontinence

Front 126

Pudendal Nerve damage

Back 126

Pudendal Nerve damage -> abolishes control -> incontinence

~b/c this is nerve that innervates external sphincter

Front 127

Polydipsia

Back 127

thirst

Front 128

hepatitis

Back 128

inflammation of liver char. by presence of inflammatory cells in tissue of organ.
Can be self-limiting or progress to fibrosis (scarring) and cirrhosis.

Front 129

Cholangitis

Back 129

Cholangitis is an infection or inflammation of common bile duct

Front 130

Cholestasis

Back 130

cholestasis is condition where bile cannot flow from the liver to the duodenum.

2 types:
1. due to obstruction e.g. gallstone or malignancy
2. metabolic types: disturbances in bile formation b/c of genetic defects or acquired as side effect of many medications.

Front 131

Neoplasm

Back 131

abnormal growth e.g. tumor

Front 132

Polyphagia

Steatorrhea

Back 132

excessive hunger

excess fat in feces, often due to lack of bile acids due to any number of causes e.g. cholangitis, cirrhosis,

Front 133

What are 4 zones (of stratification) for ruminal ingesta?

Back 133

1. Gas cap: microorganisms produce gas during fermentation

2. Solid zone: dorsal rumen receives undigested plant matte
3. Liquid zone
4. Potential escape zone

Front 134

Potential escape zone:

What gets out?
Where does it go?

Back 134

only sufficiently fermented (=small) particles and fluid moves from here into the omasum

Front 135

In what breed is exocrine pancreas insufficiency common?

what condition is corollary of EPI?

Back 135

german shepards

diabetes mellitus (due to insulin loss)

Front 136

Fermentation products?

Back 136

VFA's, CO2, CH4

Front 137

VFA's are absorbed via ?

Back 137

simple diffision

Front 138

hindgut inflammation

can lead to?

Back 138

colitis e.g. caused by bacterial infections

diarrhea

Front 139

RUCTUS = ?

What does it refer to?

Back 139

belching? or removing of gas byproducts from fermentation

Secondary Contraction = B-cycle = Eructation contraction of the Reticulorumen and Ructus

Front 140

What happens during A-cycle of rumen contraction?

Back 140

1. contraction of reticulum, dilation of omasal orifice
2. light, plant material (on top) pours into dorsal sac; heavy stuff remains
3. cranio-caudal contraction: squeezes rest into ventral sac to ferment
4. contraction of ventral sac pushes toward reticulum where cycle starts again
5. fluid and finer material flows into omasal orifice

Front 141

Where is omasal orifice located in cow stomach?

What passes through here?

Back 141

in Reticulum/Reticulo-ruminal fold, near cranial sac

only sufficiently fermented (=small) particles and fluid move from here into the omasum

Front 142

How many A-cycles are completed before can proceed to B-cycle?

Back 142

2-3 A-cycles

Front 143

During B-cycle (eructation), what allows sphincter relaxation and escape of gas into esophagus?

Back 143

gas forward to the cardia
region -> activates cardia receptors -> sphincter relaxation -> gas enters
esophagus -> antiperistaltic wave moves gas orally

Front 144

Why is bad idea to keep cow in lateral recumbency during anesthesia?

What can happen?

Back 144

Inhibition of ructus -> obstruction of esophagus, ruminal stasis) -> accumulation of gas -> BLOAT
-> pressure on thoracic organs -> circulatory failure

Front 145

what reflex controls the reticulorumen motility?

Back 145

Vagal reflex


-controls the reticulorumen motility, involving
- receptors in the mouth, forestomach, stomach, s.I.
- vagal afferent (=sensory) fibers
- motility centre in the medulla oblongata
- vagal efferent (=motor) fibers

Front 146

pH range of reticulorumen?

what happens if outside this range?

Back 146

Chemo receptors: monitor pH (normal range 5.5-6.8);

depress motility when
pH falls < 5.0 to slow down fermentation

Front 147

Is reticulorumen motility spontaneous or does it react to stimuli?
What drives it?

Back 147

Motility centre shows no spontaneous activity = needs to be driven by excitatory signals from receptors

Front 148

what is strong local reflex
______ related to peristalsis?

Back 148

ADAPTIVE RELAXATION

relaxation caudal to bolus

Front 149

Clinical signs of vagal indigestion or traumatic reticuloperitonitis?

Back 149

Motlility in r/r decreases so:
§ But the omasum is controlled by intrinsic ns and keeps contracting and taking in material and if reticulum hasn’t contracted,plant mater will enter omasal orifice
§ As omasum opens and sucks in plant matter: passes to aboomasum,
□ Unfermented / udigested plant material in feces!!!

Front 150

max retention time of digesta in reticulorumen?

max retention time of digesta in omasum?

Back 150

72 hours, for really coarse fiber
(lush grass or concentrates)

Retention time ca. ½-3 hrs
of omasum

Front 151

Ruminal Bacteria types

Back 151

ca. 200 species; mostly anaerobic , grouped
according to function, e.g.: cellulolytic, amylolytic,
proteolytic, methanogenic, etc

Front 152

ADH causes what feeling ?
What else?

What reflex do these stimulate?

Back 152

thirst
also coppersalts and sodiumsalts

reticular groove reflex: groove blocks off rumen, so indigested material bypasses rumen and goes right to omasum (protects to oral drugs or milk in neonates)

Front 153

Maltose

Back 153

disaccharide formed from two units of glucose joined with an α(1→4)bond.

Front 154

lactose is ?

Back 154

disaccharides (formed from galactose and glucose)

Front 155

name 3 structural carbohydrates

Back 155

Cellulose
Hemicellulose
Pectin
(structural Ch, = containing B- linkages)

Front 156

name 3 main VFA's and their relative %

Back 156

BUTYRATE 10%
PROPRIONATE 20-30%
ACETATE 60-70%

Front 157

If feed cow lots of grains, propionate and Acetate can form from ?
What happens if feed too much starch and grains?

Back 157

lactate, b/c low pH favors lactic acid producing bacteria

fermentation also occurs rapidly, more VFA's form faster than can be absorbed and buffered, H+(out)/Na+(in) exchanger overloaded, so pH drops, RUMEN ACIDOSIS, Drop in pH inhibits Na+/ K+ pump, leading to further accumulation of H+ and of Na+ , Intracellular Na , edema, => necrosis (ruminitis)

Front 158

fermentation yields ATP via the main ____ pathway

Back 158

acetate

Front 159

partly utilize ATP to regenerate which reduced co-factors ??

Where do co-factors come from?
Why regenerate co-factors?

Back 159

(NADH2 -> NAD+)

via proprionate and butyrate

to keep pathways open

Front 160

Main purpose of omasum?

Where are microbes digested?

Back 160

absorption of VFA's, bicarb, H2O

abomasum, via HCl

Front 161

what do ruminal microrobes require?

Back 161

NH3 and VFA's (which they produce)

Front 162

NPNs (urea, nitrates) supply
is achieved via:

Back 162

1. Dietary Supplementation
2. the Rumino-Hepatic
Nitrogen re-cycling:

Front 163

If ruminal NH3 concentration is low ->

Back 163

If ruminal NH3 concentration is low -> urea is secreted directly or via saliva into the rumen for bacterial growth.

Front 164

If ruminal NH3 concentration is high ->

Back 164

If ruminal NH3 concentration is high -> urea is excreted via kidneys.

Front 165

Where do ruminants get protein?

Back 165

digest microbes in SI, abomasum, omasum

Front 166

enteric IMMUNE system release what inflammatory mediators?

Back 166

if challenged, releases inflammatory mediators, e.g. prostaglandins, histamine, cytokines, etc

Front 167

2 strong vasodilators of GI blood supply?

GI BLOOD FLOW is also stim. by?

Back 167

several endocrines, i.p. by bradykinin and kallidin

* decreased oxygen / increased CO2 conc. during activity phases
* pumping action of GI movements

Front 168

2 common tumors in dogs

Back 168

mast cell tumor and gastronoma

Front 169

What % of VFA's are absorbed in r/r?

in omasum?

Back 169

70-85%

8-18%

Front 170

in forestomach (r/r) which form of VFAs absorb better (ionized or undissociated)?

Back 170

undissociated

Front 171

Because pka value for VFA (4.6-4.8) far below normal rumen pH, the proportion of undissociated acid _____ when pH falls after feeding (esp. if a lot of grains).

What does this mean in terms of absorption?

Back 171

increases when pH falls, b/c acids happy at low pH

undissociated = readily absorbed

Front 172

at pH 6.8 high roughage diet yield higher proportion of which VFA?

Back 172

more acetate!!! (dissociated or ionized form of acetic acid)

- not abs. easily

Front 173

grass tetany

what is it?
caused by?

Back 173

Low concentration of Mg+ or low Mg/Ca ratio in ECF leads to influx of Ca+ into nerve ending and increase AcH release. Tetany char. by involuntary contraction of muscles,
Why? Mg abs. reduced if feed contains high K+ (e.g. fertilizer), or if cow feeding on alot of immature grass.

Front 174

how does acetyl choline affect secretions in stomach? how does it stimulate?

Back 174

AcH stimulates chief cells, parietal cells, and mucin-producing cells, AcH (like histamine) binds to receptors e.g. on parietal cells and evoke secretion.

Front 175

rennin does what?

Back 175

young ruminant produce rennin which in acidic environment cause precip. and coag. of milk protein casein. Coag. incr. retention in abomasum and allows for more complete digestion
(pepsin also coagulates milk but action is much slower)

Front 176

endocrine portion of pancrease produces?

exocrine portion produces?

Back 176

insulin and glucagon

pancreatic juice, which has important digestive functions

Front 177

where is bile made?

Back 177

liver, but stored in gall bladder

Although bile duct may join pancreatic duct (which secretes pancr.juice) in some species, don't confuse them. Bile does NOT come from pancreas.

Front 178

where is CCK secreted from?

ALL functions of CCK? ALL targets?

Back 178

Secreted by endocrine cells of proximal small intestine (found in Cr. of Lieberkuehn)
1. When chyme in duodenum, releases CCK, causes gallbladder to release conc. bile.
2. causes incr. release of pancreatic enzymes
3. reduces gastric motility

Front 179

When is secretin released?
From Where?
all functions of secretin? targets?

Back 179

WHEN PH LOW SECRETIN RELEASED FROM DUOD. in blood:
1. main target for secretin is pancreas, to secrete HCO3-rich fluid, which flows into prox. intestine thr.pancreatic duct. acts as buffer.
2. stimulates LIVER to release buffer
3. reduces gastric secretions

Front 180

trypsinogen comes from?
When is required to activate trypsinogen?

Back 180

trypsinogen from pancreas

requires enteropeptidase from intestine to make active trypsin

Front 181

Where are bile salts reabsorbed. (to be recycled)?

Why bile salts and not bile acid form?

Back 181

bile salts reabs. and returned to liver by portal vein

Bile salt is ionized form, not soluble in fat, so remain in small intestine (not reabsorbed) until reaches distal end