GI 3

where is lactate produced

large intestine (by bacteria)

another name for slow segmental contractions of large intestine

haustral rolling/churning

thickened bands of longitudinal muscle layer creates…

pouches called haustra

gastrocolic reflex stimulated by food in stomach and causes defacation reflex

mass peristalsis

which 2 reflexes are initiated by distention of rectum?

short reflex and long reflex

local peristaltic waves in large intestine

short reflex

relaxation of internal sphincter and contraction of external. made more forceful by parasympathetic input

long reflex

what disregulation mainly induces diarrhea

secretion

what alters normal gut flora

use of penicillin based antibiotics

why would someone be more prone to C. difficile infections

alterations of normal gut flora, which reduces the inhibitor bacteria of C. difficile

watery diarrhea, fever, nausea, abdominal pain

colitis

used for recurring C. difficile infections by putting good bacteria back into the colon

fecal transplant through colonoscopy

where is the vomiting centre

medulla

what triggers vomiting centre

• balance disturbance

• drugs, toxins, metabolites in blood

• sensory receptor input from stomach (by irritants)

1. retrograde contractions in small intestine and stomach

2. involuntary contraction of abdominal inspiratory muslces (diaphragm) and increases in gastric pressure

3. relaxation of esophageal sphincters

responses caused by vomiting centre

where are 80% of lymphocytes located?

GALT (gut associated lymphoid tissue)

cells that play a role in immune response by sampling lumen contents and receptor mediated endocytosis

M (microfold) cells

• transports antigens to machrophages, lymphocytes, and dendritic cells

• releases cytokines

M cells

what can cytokines do

attract more immune cells to site of invasion and trigger diarrhea to flush out pathogen

what regulates intake

behvioural mechanisms (brain)

prandial state

anabolism

post absorptive state

catabolism

hunger centre

lateral hypthalamus

satiety centre

ventromedial hypothalamus, but more areas involved

fat rat

ventromedial hypthalamic syndrome

skinny rat

lateral hypothalamic syndrome

ARC and PVN

areas important in satiety, but ARC is also involved in hunger

glucostatic and lipostatic theories

long term regulation of feeding behaviour

glucose metabolism in hypothalamus regulates food intake

glucostatic theory

why is glucostatic theory not good

we have limited ability to store glucose

signals from the body’s fat stores regulate food intake

lipostatic theory

why is lipostatic theory accepted

TAG storage reservoir is higher

gene causing lack of leptin production

ob/ob

protein released from adipocytes that regulates body mass by acting directly on hypothalamus nuerons that decrease appetite and increase energy expenditure

leptin

if people have normal leptin levels, why do they get fat?

brain is less responsive to leptin

what part of hypothalamus does leptin act on

ARC

inhibits lateral feeding centre and activation of PVN

high leptin

increased TSH and ACTH from pituitary (increases metabolic rate)

humoral response of PVN

increased sympathetic output (increases body temp)

visceromotor response of PVN

release of anorectic peptides

high leptin

1. reduced activation of a-MSH and CART neurons

2. activation of NPY and AgRP containing neurons

reduced leptin

orexigenic peptides

low leptin

• reduced activation of PVN (decreased TSH and ACTH)

• decreased metabolic rate

• activation of parasympathetic output

reduced activation of a-MSH and CART neurons

• stimulation of feeding centre

• further inhibition of PVN

activation of NPY and AgRP containing neurons

aMSH and CART neurons are activated by…

leptin

major controller of metabolic rate

PVN

2 orexigenic peptides

mch and orexin

mch

continuation of eating

orexin

initiation of meal

ghrelin, gastric distension, cck, insulin

primary regulators of short-term satiety and appetite

released by cells in stomach in response to emptying (less stretch)

ghrelin

orexogenic signal

ghrelin

stimulates NPY and AGRP neurons in arcuate to drive feeding

ghrelin

if you lack NPY and AgRP neurons will you respond to ghrelin

no

has connections of PVN and ARC

NTS in medulla

satiety

cck

lowered blood sugar (in response to high insulin in gastric and cephalic phase)

feedforward mechanism, activating NPY/AgRP neurons

increased insulin in intestinal phase

satiety signal through activating aMSH and CART neurons of arcuate nucleus which inhibits feeding behaviour

full or hungry: high leptin levels

full

full or hungry: aMSH/CART neurons

full

full or hungry: NPY/AgRP neurons

hungry

full or hungry: TSH/ACTH release

full

full or hungry: sympathetic output

full

full or hungry: parasympathetic output

hungry

why does marijuana make you hungry?

it indirectly activates NPY/AgRP neurons in ARC

why is bomb cal a slight overestimation?

we do not completely digest and absorb most foods

measures all heat release (aerobic and anaerobic) from a person through temperature changes

direct calorimetry

slight underestimation because it only measures changes in O2 and CO2 (not anaerobic)

indirect calorimetry

lowest metabolic rate, usually measured as RMR

BMR

does BMR take into account the thermogenic cost of food?

yes

releases insulin release by exocytosis

Calcium

insulin binds…

RTK

glucagon binds…

GPCR

does glucagon promote catabolism

yes

aMSH/CART neurons activate…

PVN

TSH and ACTH release is promoted by…

PVN