AS Lecture 1/2 - Burden of GI disease & Oesophagus and Stomach Flashcards Preview

LSS 2 - Abdomen, Alimentary and Urinary systems > AS Lecture 1/2 - Burden of GI disease & Oesophagus and Stomach > Flashcards

Flashcards in AS Lecture 1/2 - Burden of GI disease & Oesophagus and Stomach Deck (86):
1

What is digestion?

Process of breaking down macromolecules to allow absorption

2

What is absorption?

Process of moving nutrients and water across a membrane

3

How can digestion take place?

Mechanically: Chewing, gastric churning, peristalsis OR enzymatically

4

What happens after ingestion?

Either direct excretion/absorption OR digestion

5

What are the components of the GIS?

Parotid gland, sublingual gland, submandibular gland, oesophagus, liver, stomach, gall bladder, pancreas, duodenum, jejenum, ileum, appendix, ascending colon, descending colon, sigmoid colon, rectum, anus

6

What are some diseases specific to each part of the GI system?


Main: LIVER - hence hepatology


7

What is disease burden - the checklist?


Burden to the patient, economy, population, society


8

What are the different classes of symptoms that  can be caused by GIT diseases?


General, Upper GI, hepatobiliary, mid GI, lower GI


9

What are some general symptoms of GIT diseases?

Anorexia, weight loss, anaemia

10

What are some UGI symptoms?

Haematemesis, melaena, N and V, Dysphagia, odynophagia, heartburn, Acid regurgitation, belching, chest pain, epigastric pain

11

What are some hepatobiliary symptoms?

RUQ pain, Biliary colic, Jaundice, Dark urine, pale stool, abdominal distention

12

What are some mid GI symptoms?

Abdominal pain, steatorrhea, diarrhoea, abdominal distention

13

What are some lower GI symptoms?

Abdominal pain, bleeding, constipation, diarrhoea, incontinence

14

Why is incontinence important?

A patient won't want to share that they are incontinent - embarrassing

15

What are the 4 places that show signs due to GIS disease?

General, hands, abdomen, anus and rectum

16

What signs are generally visible?

Cachexia, obesity, lymphadenopathy, anaemia, jaundice

17

What are some signs on the hands?

Koilinychia, leuconychia, clubbing, dupytrens contracture, tachycardia, tremor

18

What are some signs of the abdomen?

Organ enlargement, mass, tenderness, distension

19

What are some signs of the anus and rectum?

Haemorrhoids, fistula, fissure, rectal masses or proctitis

20

What investigations can be used for the GI systems?

History, Basic physical examination, Haematology/biochem/microbio (blood test, tumour markers, urea, etc), procedures (x-ray, mri, colonoscopy)

21

What is the biggest specific killer of people in UK, wrt GID?

Liver cirrhosis

22

What is the biggest portion of systemic cancers in the UK?

Gastrointestinal

23

What position is GI most likely to cause problems and lead to death?

4th (don't need to know but to appreciate)

24

What is happening to the trend of alcoholic liver disease vs. liver cancer?

Alcoholic liver disease is high among younger populations, and decreases with age BUT liver cancer increases with age, affecting the older generations

25

In which sex, is alcoholic liver disease and liver cancer more common?

Males

26

Which GI cancers are common?

Colorectal (2nd), Prostate(3rd), Oesophagus, pancreas, stomach (6th), liver (13th) [oral cancer commonish]

27

What are some prevalent inflammatory conditions that are burden?

Ulcerative colitis (1/500)
Crohn's disease (1/1000)
Coeliac disease (1/87)
Gastro-oesophageal reflux disease

28

How is ulcerative colitis treated and what causes it?

Treated: colectomy, Cause: thought to be autoimmune

29

What causes coeliac disease?

Gluten sensitivity

30

What are some pancreatic conditions?

Acute/chronic pancreatitis

31

What is acute pancreatitis?

Blockage of the pancreatic duct causes back up of pancreatic enzymes, causing severe inflammation - mild->life-threatening

32

What is chronic pancreatitis?

Permanent damage to pancreas, alcohol excess is the main cause and can greatly impair quality of life

33

What kind of infections can occur in the GIS?

Bacterial - Helicobacter pylori (nausea, bloating, weight loss), E. coli (Nausea, diarrhoea, cramps)
Virus - Norovirus (N, V, D)

34

How does H. pylori affect people globally?

Infects around 60% of people - 85% have no problems, 14% peptic ulcers, 1% gastric adenocarcinoma/lymphoma

35

What are GI disease risks based on?

Mainly on environment - energy intake, staple foods

36

What are the different effects on the economy from GID?

Mortality and lost years, absence from work, morbidity, NHS prescription costs, QALY, DALY

37

What do QALY and DALY mean?

Quality and Disability adjusted life years

38

What kind of healthcare costs are there (GI burden)?

In-patients, out-patients, primary care, community health and social care

39

What kind of other costs are there (GI burden)?

NHS costs and non-working costs

40

What are the costs of dyspepsia?

Only 2% consult GPs and 40% of adults suffer from it - OTC drugs

41

What is a cost effective screening programme in the UK - to do with GID?

Bowel cancer screening

42

What are the 4 detrimental social aspects of GID?

Dietary limitation (intolerances), flatulence (sound and smell), treatment (smell/slight), incontinence (soiling)

43

Which GI cancer has the poorest survival rate?

Pancreatic

44

What is the most common cause of GI-related death in a 75 year old man?

Cancer

45

What is the layer plan of the gut wall?

Mucosa (epithelium, lamina propria, muscularis mucosae), Submucosa (connective tissue w/nerve plexus), Muscularis (smooth muscle w/nerve plexus), serosa/adventitia (connective tissue +/- epithelium)

46

What is the structure of the oesophagus?

Starts at C5, passes through the thorax into the abdomen, close to the heart, laryngeal nerves

47

What is the purpose of the oesophagus?

Conduit for food, drink and swallowed secretions from pharynx to stomach

48

What are some complications of the place where the oesophagus is placed?

Close to the pericardium, so a rupture could lead to acidic contents/bacteria entering into the thorax and causing infections; also close to the recurrent laryngeal nerves, which could be damaged during surgery

49

What is the structure/function relationship of the oesophagus' epithelium?

It is non-keratinising, stratified squamous - very robust, as needs to protect underlying structures and deal with wear and tear - secrete mucous to help with bolus lubrication

50

What is the structure/function relationship of the oesophageal sphincters?

Upper/lower oesophageal sphincters - tonically active (need swallowing to open)
LOS needed to stop negative pressure drawing up the acid from stomach and UOS needed to close so breathing can occur

51

What is the structure of the oesophagus muscles?

Skeletal, transition between skeletal/smooth and then smooth - there is NO VOLUNTARY CONTROL

52

What is the process of swallowing and how is it controlled?

The swallowing centre in the brain sends a signal to open both sphincters, and when the bolus passes the UOS, it closes. The LOS stays open until the bolus has entered the stomach

53

How does peristalsis occur?

Smooth muscle - particularly circular muscle - immediately above bolus is contracted, below bolus is relaxed - longitudinal helps, but mainly circular

54

What are secondary peristaltic waves?

If the bolus hasn't reached the stomach and it is detected by the oesophagus, another wave of contraction is sent down the oesophagus, so the bolus can reach the stomach

55

What is the gastro-oesophageal junction?

Joining of oesophagus with stomach - where the LOS is to prevent reflux (prevented by diaphragm)

56

What is the LOS?

It is the diaphragm, assisting circular muscle at lower end of oesophagus

57

How does the level of the GOJ help to prevent reflux?

Negative pressure in thorax vs positive pressure in stomach would lead to acid being drawn up the oesophagus

58

What is a histological feature that can be seen at the GOJ?

Epithelial transition from stratified squamous to simple columnar AND gastric folds (rugae) are present in the stomach

59

What is the purpose of the epithelial transition in the GOJ?

Change in function as in stomach it has to be more secretory rather than protective

60

Why are the gastric folds present in the stomach?

Allows for huge changes of surface area - to expand and contract as required

61

How does belching work?

The OS are both opened and the pressure in the oesophagus causes the air to be pushed out - not pushing out by the stomach

62

What is the function of the stomach?

Break down food into smaller particles; holds food and releases at steady rate into duodenum; kills parasites and certain bacteria

63

What are the types of cell in the stomach lining?

Simple columnar, which invaginate into mucosa - tubular glands

64

What are the regions in the stomach and what do they produce?


Cardia and Pyloric regions - Mucus



Body and fundus - Mucus, HCl, pepsinogen



Antrum - Gastrin


65

What are the different cell types in the stomach?

Mucus secreting cells - secrete mucus high in carbonates, acting as a protective barrier for the lining of the stomach from the acid
Chief cells - secrete pepsinogen
Parietal cell - secrete H+ into the stomach

66

How much acid does the stomach produce in a day? (+some other facts)

2L/day
150mM H+ - very acidic!!

67

How do the mucus secreting cells protect the stomach lining?

They secrete mucins (gel coating) and pump out HCO3- which gets trapped in the mucus gel - this means that it can act as a buffer, neutralising the stomach acid

68

What is the pH at the stomach lining compared to the centre?

Mucus lining/epithelial surface - 6-7
Lumen - 1-2

69

How are chief cells adapted for their function in the stomach?

Protein secreting epithelial cell, abundant RER, golgi packaging and modifying for transport, masses of apical secretion granules

70

How are parietal cells adapted for their function in the stomach?

Many mitochondria, cytoplasmic tubulovesicles (contain H+/K+ ATPase, merge with cannaliculi when cell activated), internal cannaliculi (reservoirs near the apical membrane)

71

How is the acid produced in the parietal cell?

Carbonic anhydrase catalyses CO2 + H2O into H+ and HCO3-, then Na+/K+ pumps, bring K+ in which then diffuses into the cannaliculi. The HCO3- are moved out of the cell via pump which brings Cl- in which diffuse into the cannaliculi. The K+/H+ ATPase causes H+ to enter cannaliculi and K+ into the cell

72

How would inhibition of carbonic anhydrase influence acid secretion in the stomach?

Decreases acid secretion

73

How does pepsinogen work?

Produced by chief cell - is an acidic precursor which needs the acidic pH of the stomach (HCl) to enzymatically cleave each other, to produce pepsin (which is needed to break down proteins)

74

What is gastrin?

Released in pyloric antrum - to stimulate acid secretion.

75

What is the mechanism of gastrin release?

Ingested proteins increase the pH of the stomach contents, removing inhibition of gastrin, which causes more acid production to decrease the pH.

76

What does gastrin act on?

Gastrin acts on parietal cells to increase acid secretions and can stimulate histamine release as well

77

What are the 3 phases of gastric secretion?

Cephalic phase, gastric phase, intestinal phase

78

What is the cephalic phase and where does it take place?

Occurs in brain - when thought/sight/smell of food occurs, brain activates vagus nerve to release ACh and react with parietal cells, or cause histamine release to increase acid production

79

What is the gastric phase and where does it take place?

Once food reaches stomach - stomach reacts to distension (stretch receptors), sends signal up to brain saying there is food present (reflex - to send signal to increase acid secretion)
Also chemoreceptors present to trigger gastrin secretion

80

What does the enteric nervous system do?

It reacts to the distension as well, and increased acid secretion

81

What is the intestinal phase and where does it take place?

Mainly inhibition phase - as stomach contents pass to intestine, sends signal to brain if pH is low, to switch off gastrin secretion OR low pH in chyme causes 3 hormones to be secreted, so they can be reabsorbed into stomach to reduce gastrin/acid/other stomach secretions

82

What are the 3 hormones (enterogastrones) secreted in response to low pH in the chyme (enterogastric reflex)?

Gastric inhibitory peptide, cholecystokinin, secretin

83

What is the counter intestinal cycle - the excitatory version?

If the protein concentration in the duodenum is too high, gastrin secretion is stimulated, and acid is increased

84

What part of acid secretion would you inhibit to reduce acid secretion?

Histamine receptor antagonist (Ranitidine)
K+/H+ ATPase inhibitor (Omeprazole)

85

Which of the following stimuli would be most likely to
decrease acid secretion in the stomach?
A. Chyme fatty acid content
B. Increased acetylcholine secretion
C. Increased gastrin secretion
D. Protein content of the meal
E. Stomach distension

Chyme fatty acid content

86

Which of the following structures within the
parietal cell contains the most H+/K+ ATPase?
A. Canaliculi
B. Carbonic anhydrase
C. Golgi body
D. Mitochondria
E. Tubulovesicles

Tubulovesicles