GIT tract 3 Flashcards

1
Q

net absorption

A

Take in a certain amount, excrete a certain volume alongside secretion and absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

aborption and secretion noral

A

volume moving from blood to gut lumen is less than lumen to blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

malabsroption

A
absent or defective digestive enzymes
-	defects in transported protein
-	diseases/infections of the small intestine
examples of malabsroption
1)	lactase deficiency
-	lactose intolerance
2)	coeliac disease
-	abnormal immune response to gluten
-	loss of mucosal epithelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

diarrhoea

A

Increase stool volume or increased frequency of defecation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

osmotic involvemtn in diarrhoea

A

increased solutes in lumen causes less water reasoprtion
- poorly absorbed substrate, high conc of substrate that cannot cross lumen so water moves into the lumen rather than increasing water levesl in gut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

secretory involvemetn in diarrohea

A

Increases secretion of water into the lumen (secretion exceeds absorption)
not due to osmotic effect
- cholera toxin (defect function of chloride channel opening up Cl- channel, too much chloride into gut, water follows increased secretion of water)
- laxatives, hormones, drugs (antidepressants), caffeine
- bile acid malabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

cholera caused by

A

bacterial toxins from cholerae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how does cholera work

A

toxin enters cells and is activated in the ER
binds a G protien
activates adenylate cyclase
production cyclic AMP
activates chloride channel
chrlodie moves out of channel into lumen of gut, followe by soidum and water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

inflammaiton involvemtn in diarrhoea

A

pathogens breach and damage the absorptive epithelium

  • clostridium difficile
  • invasive parasites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

degranged motility in diarrhoea

A

Altered transit time hence less time for water reabsorption

- irritable bowel syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

colon motility and what it allows

A

segmented contractions in segmented region
allows
- mixing contents
- retain material in the proximal colon (fermentaion, water absroption)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

gasto colic repsonce

A

mass movement of material into aboral end of colon - ready for defection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what allows defecation

A

regualting movemnt of material and opening of sphincters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

defecation

A

Faeces moved into rectum (via gasto colic response) – leads to dissension

  • activates stretch receptors
  • afferent signals to the spinal cord
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

when convinemtn to defecate and what is involved

A
  • voluntary motor nerves are inhibited allowing the external anal sphincter to relax
    Automimic informs need, voluntary decides whether it is convent

Symp and parasymp
- stimulate contraction of the rectum and relaxation of the internal anal sphincter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

voluntary and involuntary defacation

A

External is voluntary , internal is autonomic controlled

17
Q

incontinence and what it leads to

A

pelvic floor damage
pudendal nerev damaged
Alters ability to control and regulate
- can cause loss of control of emptying, defecation could occur involuntarily or problems being unable to defecate

18
Q

defecation failure causes

A

spinal injuries

outlet blockages

19
Q

storage vs empyting defacation muscles

A

storage
- contracted spincters and relazaiton of colon/rectum
emptying
- relaxation of spincters and contraction of colon/rectum

20
Q

emesis

A

protective mechanisms to prevent damafe to GI tract and ingestion of contaminated/toxic substances

21
Q

detectors of toxins
pre ingestion
pre absoption
post absroption

A
pre ingestion
- sight, smell ,tastes
pre absoption
- toxin dectection in lumen
- mechano/chemo receptors
- explusion
post absroption
- chemoreceptive trigger zone
induced nausea to prevent further ingestion
activates voimiting centters
22
Q

thngs that make us sick

A

1) food poisoning
2) bowel disease
3) motion/vestibular disease
4) pregnancy
5) head injury
6) radiation/chemotherapy
7) surgery/ anaesthesia
8) drugs
9) pain

23
Q

nausea symptoms

A
  • pallor
  • sweating
  • salivation
  • irregular breathing
  • increased HR
  • retching (several, increased force)
24
Q

GI motor control of nausea steps

A

1) contraction of small intestine
- retrograde giant
- contracts return intestinal contents to the stomach
2) stomach relaxes
- proximal stomach relates to accommodate returning intestinal contents
- antral motility inhibited to prevent gastric emptying
3) contraction of diapgragm and abdominal wall
- expulsion

25
Q

steps for vomiting

A

Deep inspiration allows closure of glottis, protects respiratory tract

  • air and saliva drawn into oesophagus
  • protection and decrease in oesophageal pressure
  • soft pallet elevated to prevent entry into the nasopharynx and nose
  • expiration against closed glottis and abdominal contraction
  • increase intra abdominal pressure
  • relaxation of lower oesophageal sphincter
  • passage of contents into oesophagus
  • relaxation of the UOS
  • violent expulsion force stomach and abdominal contraction
26
Q

during retching

A

upper oesophageal spincter remains closed (open for vomiting)

27
Q

where is the vomiting centre

A

4th ventricel in medulla oblongata

28
Q

vomiting centre

A

contains cheoreceptors sampling blood

sigals from higher centres

29
Q

what detects motion sickness

A

vestibular system

30
Q

emetic repsonce to anticancer therapry

A

acute recognise toxins
delayed responce due to damae to epithelium as the entero chromaffin cells damaged
- anticipatory senssros to

31
Q

anti emetics work by

A

blocking activation of vomiting centre
Chemoreceptor trigger zone – Ondanstron (5-HT antagonist)

Block receptors for the histamines