Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

sem 4 > GIT case 1-4 > Flashcards

GIT case 1-4 Flashcards

1
Q

What is the inverse care law?

A

the places/people that need the most help have the least ressources

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

What is virtue ethics?

A

how we ought to act: being rather than doing

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

maslow’s hierarchy of needs

A 
physiological needs
safety and security
love and belonging
self-esteem
self actualisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the limitations of Shared Decision Making?

A
  1. not enough info given by doctors to patients
  2. lack of involvement of patients in decision making to the level they wish
  3. underused techniques to enable patient recall and understanding
  4. commission of key info
  5. language patients do not understand
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

different types of bias in diagnosis?

A
  • anchoring (locking diagnosis too early: unable to adjust to ne info)
  • availability (similar recent condition)
  • confirmation (looking for info to prove theory, rather than disprove)
  • diagnosis momentum (acceptance of remade diagnosis without enough skepticism)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

difference between basic care and clinical care

A

basic: solids, drinks; spoons, straws, assistance
clinical: drips, NG tubes, PEGs, TPN

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

6 activities of processing food

A
  • ingest
  • propulsion (swallowing and peristalsis)
  • mechanical breakdown (chewing, mixing food with saliva, churning of stomach, segmentation)
  • digesting
  • absorption
  • defecation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

cells of oral mucosa

A

thick stratified squamous epithelium

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

what do defensins do

A

inhibit bacterial growth in oral tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

different types of teeth and what they do

A

incisors (2): slice and cut
canines (1): tear and rip
premolars (2): grind and crush
molars (3): grind (and crush)

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

composition of saliva

A
  • water (90%)
  • lingual lipases an alpha-amylase (slightly acidic(pH: 6.75-7): optimal condition for enzyme function)
  • mucoproteins as mucins (lubricant)
  • lysozyme
  • IgA
  • electrolytes
  • calcium and phosphate (dental repair)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

control of salivation:

A
  • salivatory nuclei in medulla and pons
  • mechano and chemoreceptors: produce saliva with high H2O content
  • food induce production of enzymes
  • higher brain centres
  • irritation of lower digestive tract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

enteric nervous system made up of?

what do they respond to, what do they produce

A
  • submucosal (Meissner’s) plexus found in submucosa: chemoreceptors: stimulate glands, dilate vessels, secrete hormones/ peptides
  • myenteric (Auerbach’s) plexus found in muscular external: mechanoreceptors: descending and ascending fibres that contract/relax circular and longitudinal muscles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

enteric nervous system pacemaker cells

A

interstitial cells of Cajal: set timing of contraction waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

muscle fibres of muscular layer of oesophagus

A
  • skeletal in first third (voluntary)
  • mixed smooth an skeletal in middle third
  • smooth in last third (involuntary)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

4 histological layers of oesophagus?

A

mucosa
submucosa
muscular layer
adventia (serosa beyond diaphragm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

where peristalsis in stomach?

A

lower part

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what control rate of emptying of stomach?

A

caloric value of contents of duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

histological parts of stomach that form rugae

A

mucosa and submucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

functions of stomach?

A 
storage and mixing
digestion (proteina dn nucleic acids)
enzyme activation 
bacteria killing
intrinsic factor synthesis (main true function)
absorption (alcohol, H2O, drugs, B12)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

cells present in different parts of stomach

A
  • cardia: mucous cells
  • body/fundus: all cell types
  • pylorus: mucous cells and enteroendocrine / G cells, D cells (antrum)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

gastric secretions

A
  • HCl
  • mucus
  • pepsinogen
  • intrinsic factor
  • gastrin
  • somatostatin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

effect of contraction of circular smooth muscle

A

squeezes gut content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

effect of contraction of longitudinal muscle

A

shortens that portion of gut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

histological lining of oesophagus?

A

stratified squamous epithelium (to resist abrasion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

role of HCl in stomach

A
  • produces pepsin from pepsinogen

- acidifies lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

role of gastrin

A

-stimulate acid production
-stimulate chief cells
-Increases antral muscle mobility and promotes stomach contractions.
Strengthens antral contractions against the pylorus, and relaxes the pyloric sphincter, which increases the rate of gastric emptying
-Plays a role in the relaxation of the ileocecal valve
-Induces pancreatic secretions and gallbladder emptying
-Gastrin contributes to the gastrocolic reflex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

role of somatostatin

A

inhibit release of gastrin, insulin, glucagon (an others: look them up)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

different cells of stomach and function

A
  • surface epithelium cells (HCO3- and mucus)
  • goblet cells (mucus)
  • mucous cells (mucus and pepsinogen)
  • parietal cells (gastric acid and intrinsic factor)
  • chief cells (pepsinogen and gastric lipase)
  • G cells (gastrin)
  • D cells (somatostatin)
  • ECL cells (histamine)
  • endocrine cells (ghrelin/leptin) (look this up)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

control of pepsinogen release

A

vagus nerve: acetylcholine

gastrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

control of HCl release

A

vagus (acetylcholine)
gastrin (G cells)
histamine (ECC)
other hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

gastric acid secretion inhibited by

A
  • somatostatin (via decrease in gastrin release)
  • secretin (via decrease in gastrin release)
  • gastric inhibitory peptides and other enterogastrones (directly on parietal cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

phases of gastric secretion

A
  • cephalic (vagus and acetylcholine stimulate G and parietal cells) 40% of secretion
  • gastric (distention and reflex activation of enteric neurones+ vagus + digested proteins stimulate G cells) 50% of secretion
  • intestinal phase: aa present in bloodstream stimulate parietal cells (10% secretions)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

gastric and duodenal mechanisms of gastric secretion inhibition

A

-proteins in stomach at as buffer to keep luminal pH>3, when stomach empties, luminal ph<3: D cells release somatostatin –> reduction in acid secretion

  • acidification of duodenal lumen releases secretin: inhibits gastrin secretion
  • acidification of duodenal lumen and presence of fatty acids and salt releases gastric inhibitory peptide: acts on parietal cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

gastrin: where is it produced and major actions

A

G cells (antrum-jejenum)

relax cardia, increase antral activity and gastric acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

motilin: where is it produced and major actions

A

duodenum-jejenum

increase gastric acid secretion and stomach activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Gastric inhibitory peptide (GIP): where is it produced and major actions

A

duodenum-jejenum

“incretin”: decrease gastric secretion, enhance insulin secretion, decreases glucagon secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

cholecystokinin (CCK): where is it produced and major actions

A

small intestine

relaxes stomach (slow stomach emptying), contracts gallbladder, increases pancreatic secretion, satiety, potentiates secretive action of liver, relax sphincter of Oddi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

secretin: where is it produced and major actions

A

small intestine

inhibition G cells
relaxes stomach, increases HCO3- secretion by pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

vasoactive intestinal peptide (VIP): where is it produced and major actions

A

glands and nerves

increases intestinal electrolyte secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

migrating motor complex

A 
done by ENS and ANS
in inter digestive state
release of motilin: stimulates strong sequential contractions by ANS
remove dead cells and sweep anything out
4 phases (3 phase is active one)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

when does inter digestive activity stop?

A

ingestion of food
gastrin (released by stomach)
CCK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what is absorbed in duodenum

A

iron
carbohydrates
proteins, lipids, sodium and water
(bile salts)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is absorbed in jejenum

A

carbohydrates
proteins, lipids, sodium and water
(bile salts)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is absorbed in ileum

A

bile salts
cobalamin (vit B12)
proteins, lipids, sodium and water, potassium
carbohydrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

MOA of Orlistat

A

reacts with serine residues at active site of gastric and pancreatic lipases: prevent breakdown of dietary fat into fatty acids and glycerol: decrease absorption of 30% of dietary fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

bariatric surgery

A 
BMI>40 kg/m2
Failure to maintain weight loss by non surgical means over period of months/years
-gastric banding
-gastric bypass
-biliopancreatic diversion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

difference in active and passive euthanasia (euthanasia by action or ommission)

A

passive: withholding consent to lifesaving/prolonging treatment
active: performing action that has lethal effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

difference voluntary/non voluntary/involuntary euthanasia

A
  • voluntary: person requested to be killed
  • non-voluntary: person made no request and gave no request to be killed
  • involuntary: person who is killed made an expressed wish to the contrary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

def assisted suicide

A

person provide info/means/guidance to take own life with intention

physician assisted suicide: when doctor involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

doctrine of double effect

A

when harm is a foreseen but intended consequence (i.e. with surgery, or pain medicine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what impermeable to phospholipid bilayer?

A
  • ions

- polar molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

membrane structure

A

phospholipid polar heads face interstitial fluid

sterols: struck integrity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

different types of membrane transport proteins

A
  • (simple diffusion ie gases)
  • channels (passive: driven by electrochemical gradients)
  • carriers (passive: driven by electrochemical gradients)
  • pumps (active: atpases)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

function of Na+,K+-ATPase (sodium pump)

A
  • Na+ in, K+ out
  • K+ gradient generates membrane potential (-60 mV)
  • Na+ gradient for secondary active transport
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

ion channels control

A
  • gated by intracellular or extracellular messengers

- voltage gated by membrane potential changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

uniport
symport
antiport

A
  • facilitated diffusion
  • cotransport
  • countertransport (exchange)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

facilitated diffusion

A

highly lecture carrier protein
passive transport
driven by concentration gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

where are glucose transporters found in the body?

A 
GLUT1: red cells, brain, kidney, placenta
GLUT2: liver, intestine
GLUT3: astrocytes, neurones
GLUT4: adipocytes, muscles
GLUT5: intestine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

def secondary active transport

A

using previously established gradient of ATPases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

protein family that determines tight junction permeability

A

claudin family proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

% salivary secretion in unstimulated and stimulated state (gland)?

A

unstimulated: 25% parotid, 60% submandibular, 7-8% sublingual and 7-8% minor glands
stimulated: 50% parotid, 35% submandibular, 7-8% sublingual and 7-8% minor glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

inorganic component of saliva

and changes with saliva flow

A 
from high to low concentration:
Na+ (increase)
HCO3- (increase)
Cl- (increases)
K+ (decreases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is secreted in the acinus and secreted and reabsorbed in duct

A

-secretion in acinus: Na+, Cl-, HCO3-, H20
(isotonic)

-reabsorption in the duct: Na+, Cl-
-secretion in duct: K+, HCO3-
(lower H20 permeability in duct)
(hypotonic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

generation of oesophageal peristalsis

A

swallowing: primary peristalsis
distention: secondary peristalsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

oropharyngeal dysphagia

A
  • abnormal bolus transfer to oesophagus
  • difficulty initiating swallow
  • a manifestation of primary disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

oesophageal dysphagia

A
  • abnormal bolus transport through oesophagus
  • food stops after initiation of swallow
  • oesophagus location of primary disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

most likely area of lesion in stroke patients with dysphagia

A

postcentral and pericentral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Chicago classification

A

achalasia or other obstruction

major motility disorder

minor motility disorder

normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what is achalasia?

A

failure of ring of muscle fibres (i.e. sphincters) of oesophagus to relax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

aetiology achalasia

A
  • associated with HLA-DQw1
  • may be autoimmune disorder (circulating ab to enteric neurons)
  • chronic infections: herpes zestr or measles virus?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

difference in presentation between achalasia and oesophageal cancer

A

oesophageal cancer: dysphagia for solids before liquids

achalasia: dysphagia for liquids and solids at the same time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

diagnosis of achalasia

A

clinical history
endoscopy (dilated oesophagus)
radiology + fluoroscopy (dilated + beak like narrowing, absence of peristalsis, spastic contractions (=vigorous achalasia with corkscrew appearance))
manometry (elevated resting LES pressure, incomplete LES relaxation, aperistalsis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

treatment for achalasia

A
  • botulinum toxin

- pneumatic dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

treatment for achalasia

A
  • botulinum toxin
  • pneumatic dilation
  • Hellers Myotomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

gastric motility in stomach

A

-fundus: relaxes on feeding: accommodate food without rise in pressure: vagal control (disorders of funds can cause early satiety)
l-antrum: pump s and churns (3 waves/min): emulsify contents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

when is CCK stimulated

A

presence of fatty kids, amino acids or HCl: stimulation of I cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

acinus and duct secretion pancreas

A

acinus: NaCl and H2O
duct: NaHCO3 and H2O

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

hormonal stimulation of pancreatic acinus (enzymes)

A

CCK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

hormonal stimulation of pancreatic duct (aqueous)

A

secretin (which also stimulates bile secretion by liver)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

role of stomach acid and iron

A

Fe3 –> Fe2 for absorption in duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

largest endocrine organ in body

A

gut epithelium (enteroendocrine cells): “taste” molecules to release appropriate molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

mechanism by which histamine increased release of H+

A
  • stimulate parietal cells

- increase cAMP: increase number of proton pumps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

what receptor does PPI act on

A

H+,K+ ATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

MOA of omeprazole

A
  • weak base, absorbed in SI and enters blood, enters and accumulates in acid spaces (canaliculi and tubulovesicles of parietal cells)
  • activated in acid by H+ to sulphenamide form –> cationic so trapped in canaliculi
  • irreversable S-S bond with H+-K+ATPase: blocks secretion of new pumps
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

difference between esomeprazole and omeprazole

A

omeprazole: mixture of optical (R & S) isomers
esomeprazole: S isomer (“more active” in humans)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

what are long term side effets of PPIs?

A

reduction in bone density

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

duodenal ulcers causes

A
  • bacterial infection H. Pylori
  • NSAIDs
  • Zollinger-Ellison syndrome (gastrin-secretin tumour)
  • risk factors: smoking, alcohol, caffeine etc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

def gastritis

A

inflammation of the stomach lining

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

secretion of secretin

A

HCl stimulation S cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

role of prostaglandin in stomach

A
  • maintains mucus barrier and stimulates HCO3 secretion

- decreases and production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

somatostatin secretion stimulation

A
  • increase blood glucose
  • increase aa
  • increase fatty acids
  • increased concentrations of several GI hormones from upper GIT in response to food intake (CCK, GIP, secretin, H+)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

H pylori virulence factors

A
  • flagella (bacterial motility and chemotaxis to colonise under mucosa)
  • urease: neutralise gastric acid + ammonium cytotoxic
  • CagA (cytokine associated gene A): affects cell signalling, reduces cell adhesion and changes cell phenotype from epithelial to mesenchymal cells (actin remodelling), IL-8 induction, apoptosis and host cell growth inhibition
  • exotoxin: VacA (vacuolating toxin A): induces vacuoles in host cells and pore like structures –> osmotic swelling + causes mitochondrial dysfunction, apoptosis, disrupts epithelial cell barrier and improves H. pylori ability to colonise gastric epithelium
  • babA (sialic-acid-binding adhesion): binds to Lewis b ABO blood group antigen on RBC and some epithelium cells —> DNA breaks in host cells and can lead to cancer-associated gene mutations
  • OipA (outer inflammatory protein adhesion): acts as an adhesion and associated with carcinogenesis
  • peptidoglycan lipopolysaccharide coating: causes inflam responses and adheres to host cell
  • secretory enzymes: mucinase, protease, lipase: gastric mucosal injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Mechanism of H. Pylori living in low pH

A
  • antrum: least acidic region
  • “burrow” through mucus + adheres to epithelium
  • metabolises urea (C02 + ammonia): increase local pH with NH3 and CO2 release –> control urea influx with H+gated urea channel
  • lives in cloud of ammonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

mechanism somatostatin decreases acid secretion

A

inhibitory:

  • G cells
  • ECL cells
  • (parietal cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

treatment H. pylori

A

quadruple therapy:

  • 2 antibiotics (claritheromycin, amoxicillin, metronidazole, tetracycline)
  • PPI
  • Bismuth compounds: improve antibiotic effectiveness

(Triple therapy; without bismuth)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

why do we have quadruple therapy

A

H. pylori divides at pH>5.5 + clarithromycin, amoxicillin and tetracycline all work best in dividing cells

–> PPI: raises pH

-bismuth: blocks H+ influx into H. pylori –> prolonges a less acidic environment as PPI effects wear off

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

NSAIDs and ulcers

A

-inhibit COX1: decreases PEG2 in mucosa of stomach and duodenum

  • PEG2: inhibits parietal cells and increase mucosal protection
  • -> inhibition of PEG2: increase H+ and decrease protection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

location find H. pylori

A
  • mucus layer gastric antrum (especially in gastric pits

- duodenal gastric metaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

gastric ulcers mechanism

A
  • H pylori, NSAIDS: decrease mucosal barrier
  • mucosa digested by H+ and pepsin
  • H+ secretory rates decrease (H+ leaks into mucosa)–> increase gastrin: increase H+ (due to lack of inhibition of H+ on G cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

duodenal ulcers mechanism

A
  • hyperacidity (+ H. Pylori)
  • increase H+: HCO3- buffer capacity overwhelmed
  • H+ and pepsin damaged to mucosa
  • H.Pylori indired actions (in one of two ways)
    1. damage to antrum inhibits somatostatin release: increase gastrin: increase H+
    2. spread of Pylori to duodenum: inhibits HCO3- secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

def odynophagia

A

pain on swallowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

def meleana

A

passage of dark tarry stools (containing decomposing stools), usually indication of bleeding in upper GIT (oesophagus, , stomach, duodenum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

def peritonitis

A

inflammation of peritoneum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

what is succossion splash

A

when percussing on abdomen, hear and see fluid splashing around due to gastric outlet obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Virchow’s node

Troisier’s sign

A

VN: left supraclavicular: first place cancer spreads for abdomen, thorax and thoracic duct

TS: clinical finding of a VN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

red flags for gastric and duodenal disorders

A

dysphagia, weight loss and older patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

investigations to do in gastric and duodenal disorders if no red flags

A
  • H.Pylori (stool antigen, urea breath test, gastric biopsy)
  • barium studies: abnormality in stomach wall: stretch with water and barium
  • OGD
  • pH (for acid reflux) and manometry (pressure)
  • BRAVO capsule (for acid)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

investigations for gastric and duodenal disorders in suspected malignant pathology

A
  • blood tests (FBC, UEs, LFTs, iron)
  • OGD (8 biopsies for cancer)
  • CT scan (staging: from neck to below pelvis: presence of cancer and staging)
  • PET-CT scan
  • laparoscopy: key hole surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

benign disease of stomach and duodenum

A
  • gastritis
  • peptic ulceration
  • GORD (gastroesophagel reflux disease)
  • achalasia
  • functional disorders (bloating, delayed gastric emptying)
  • Crohn’s disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

risk factors for peptic ulceration

A
  • H. Pylori
  • smoking
  • NSAIDS
  • caffeine
  • stress ulcers (Hb drop)
  • steroids, Crohn’s, drugs
112
Q

where bleeding and perforating ulcers

A

AUP PUB

posterior D1 bleed due to gasproduodenal artery haemorrhage

113
Q

hereditary diffuse gastric cancer mutation

A

CDH1

114
Q

mucus composition

A
  • water and ions (90%)
  • proteins (glycoproteins): 5-10%
  • mucins (mucus glycoproteins: 1-5%)
115
Q

liquid mucus, think mucus composition

A

liquid: low percentage of mins
thick: high percentage of mucins

116
Q

different types of mucins in mucus

A
  • free floating mucus: leaves molecules move through (i.e. O2, digested food), binds to other molecules (i.e. bacteria), interferes with delivery of drugs
  • membrane associated mucins: attaches mucus to epithelial cell, last line of defence, signal changes to cell
117
Q

mucus barrier layers

A
  • loose layer: beneficial bacteria here

- adherent layer: compact, very small pore size

118
Q

when are mucins released

A

mucins stored in packets (preformed molecules) in goblet cells and release when a protective barrier needs to be formed

119
Q

mucin composition

A

large glycoprotein polymer

  • protein at both ends
  • glycans (sugars) centrally: 80% of mass (sugar binds to things i.e. leptins on bacteria)
120
Q

different family members of gel forming mucins

A 
MUC2
MUC5AC
MUC5B
MUC6
MUC19
121
Q

role of mucins

A
  • space filling (gel formation)
  • protease resistance (host, viral, bacterial) by sugars
  • pathogen binding/evasion/killing
122
Q

how mucins form mucus

A

entanglement

cross links

123
Q

pathogen subversion to epithelial mucosal barrier

A
  • flaggelated
  • enzyme production that degrade mucins
  • toxins the kill epithelial cells or arrest intestinal cell division
  • injection of bacterial toxins into epithelial cells
  • disable tight junctions between adjacent epithelial cell
124
Q

glycocalyx in cell

A

another carbohydrate barrier to cell

125
Q

epithelial cell surface transmembrane (Tm) mucins structure

A

extracellular: carbohydrates + glycocalyx
transmembrane: lipid bilayer and receptors and adhesion molecules
cytoplasmic: cytoskeletal link/signal transduction proteins (+actin cytoskeleton)

126
Q

if pathogen binds to epithelial cll surface transmembrane mucin

A

extracellular part of mucin becomes detached signalling cytoskeletal link/Signal transduction proteins: replenish barrier

127
Q

where MUC5AC an MUC6 in GIT

A

corpus and antrum of stomach

128
Q

where MUC2 in GIT

A

duodenum to colon

129
Q

adhesins of H Pylori

A

BabA and SabA

130
Q

role of MUC5AC in defence against H Pylori

A

binding bacteria

131
Q

role of MUC6 in defence against H Pylori

A

growth inhibition: when glycans on MUC6 eaten by bacteria, causes cell wall synthesis

132
Q

role of MUC1 in defence against H Pylori

A

shed from cell surface when H Pylori binds (MUC5AC and MUC1 share some glycans)

133
Q 
NSAIDs :
use
MOA
SE
warnings
A

use: 1. mild to moderate pain 2. pain related to inflammation

MOA: inhibiting cyclooxyrgenase (synthesis of prostaglandins from arachidonic acid)

SE: COX1 inhibition effects: GIT toxicity, renal impairment, CV events

warnings: don’t use if: severe renal impairment, heart failure, liver failure, NSAID hypersensitivity

134
Q

COX 1

A

constitutive form: stimulates PG synthesis: preserve integrity of gastric mucosa, maintains renal perfusion (dilates afferent glomerular arterioles), inhibits thrombus formation in vascular endothelium

135
Q

COX2

A

inducible form: stimulates PG production that cause inflammation and pain

136
Q

how much pancreatic juice /day

A

1200-1500 ml

137
Q

enzymes for protein digestion secreted by pancreas

A

trypsin
chymotrypsin
carboxypolypetidase
elastase

138
Q

enzymes for fat digestion secreted by pancreas

A

pancreatic lipase
cholesterol esterase
phospholipase

139
Q

zygomens def

A

proenzyme: inactive form of enzyme

140
Q

pancreatic zygomens and activation

A

trypsinogen
chymotrypsinogen
procarboxypolypeptidase

activated by trypsin (trypsinogen activated by enterokinase which is secreted by intestinal mucosa when comes into contact with chyme)

141
Q

trypsin inhibitor secreted

A

secreted by granular cells in acini

142
Q

pancreatic secretion stimulation

A
  • Ach from vagus and other parasympathetic (mainly to acini)
  • CCK
  • secretin
143
Q

phases of pancreatic secretion

A
  • cephalic phase: 25% (done by vagus, vasoactive peptide, CCK, gastro releasing peptide)
  • gastric: distention of stomach, first absorption of nutriments + same hormones as cephalic
  • intestinal: 80%: CCK, secretin
144
Q

interaction of sodium bicarbonate from pancreatic secretions and HCl from stomach

A
  1. NaCl and carbonic acid
  2. dissociation of carbonic acid: CO2 + H20
    - -> CO2 absorbed into blood and respired by lungs
145
Q

neg feedback regulation of pancreatic secretion

A
  • pancreatic polypeptide (released from islets cells): inhib on acing enzyme secretion (local and central effect)
  • somatostatin: pancreatic acing inhibition and CNS inhibition
  • peptide YY (PYY): released by endocrine cells of distal SI in response to nutriments in ileum: acts on acing cells and via vagal nerve
146
Q

pancreatic lipase action

A

triglyceride hydrolysis:

triglyceride –> monoglyceride and 2 free fatty acids

147
Q

amylase action outcome

A

dissacharides (i.e. maltose) and trisaccharides (i.e. maltotriose)

148
Q

causes of acute pancreatitis

A 
Idiopathic (20%)
Gallstones (50%)
Ethanol (25%)
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom
Hyperkalaemia/hyperlipidaemia
ERCP (bile reflux from duodenum)
Drugs
149
Q

pathogenesis of acute pancreatitis

A

causes:
- pancreatic duct obstruction (gallstones, ampullarf obstruction, chronic alcoholism, ductal secretions) –> interstitial oedema –> impaired blog flow –> ischemia
- acinar cell injury (alcohol, drugs, trauma, ischemia, viruses): release of intracellular proenzymes and lysosomal hydrolyses –> activation of enzymes into and extracellular)
- defefective intracellular transport (metabolic injury, alcohol, duct obstruction): delivery of proenzymes to lysosomal compartment –> intracellular citations of enzymes

all of the above lead to acing cell injury and activated enzymes

lesions:

  • interstitial inflammation and oedema
  • proteolysis (proteases)
  • fat necrosis (lipase, phospholipase) + combines with Ca2+ to form insoluble salts
  • hemorrhage (elastase)
150
Q

acute pancreatitis signs and symptoms

A
  • abdo and back pain
  • nausea and vomiting
  • respiratory distress
  • fever
  • haemorrhage (proctalgia)
  • shock (hypotension, tachycardia and oliguria
  • elevated serum amylase (for 24 hours)
  • elevated serum lipase (72-96h)
  • gycosuria
  • hypocalcaemia (poor prognosis)
151
Q

def oliguria

A

low output of urine

152
Q

diagnosis of acute pancreatitis

A

severe abdo pain

  • blood test: amylase ad lipase enzymes in bloodstream
  • chest X ray: show calcification (exclude perforation)
  • CT: pancreatic necrosis, access or fluid collection
  • abdo ultrasound
153
Q

management of acute pancreatitis

A
  • ABC assessment
  • assess severity: Glasgow Imrie Score
  • Atlanta
  • support: replace fluids, NG secretion, analgesia, nutrition
154
Q

acute pancreatitis complications

A
  • acute fluid collection
  • pseudocysts
  • walled off pancreatic necrosis (WON)
155
Q

causes chronic pancreatitis

A
  • idiopathic (20-30%)
  • alcohol 60-70%
  • genetic (i.e. cystic fibrosis)
  • autoimmune (ie IgG4)
  • hyperlipidaemia, hypergyceriaemia
156
Q

pathogenesis of chronic pancreatitis

A
  • ductal obstruction by concretions (increased protein concentration in pancreatic juice creating ductal plugs, can calcify forming calciuli (calcium carbonate precipitates)
  • toxic metabolic: direct toxic effect on acinar cells: accumulation of lipids in cigar cells, acing cell loss and parenchymal fibrosis (change from acinar to ductal metaplasia)
  • oxidative stress: free radicals: membrane lipid oxidation and activation of transcription factors (attraction of mononuclear cells)–> promotion of fusion of zygomen granules and lysosomes, acid cell necrosis, inflammation, fibrosis
157
Q

sign/symptoms chronic pancreatitis

A
  • pain (epigastric to back and episodic)
  • malabsorption, weight loss, steatorrhoea
  • diabetes (type 3c)
  • jaudince (bile duct obstruction)
158
Q

diagnosis of chronic pancreatitis

A
  • faecal elastase
  • endoscopic ultrasound
  • CT/MRI
159
Q

management of chronic pancreatitis

A
  • lifestyle, smoking, alcohol
  • pain control (analgesia, management diabetes, endoscopic therapy, celiac nerve block, surgery for decompression)
  • treat malabsorption croon/pancreatin: combination of protease, lipase and amylase
160
Q

chronic pancreatitis complications

A

bleeding, obstruction, pancreatic cancer, survival (15-20 years from diagnosis)

161
Q

CHO absorption transporters

A
  • SGLT1: secondary active, Na+ dependent co transport (on apical surface: K+,Na+ ATPase) (for glucose)
  • GLUT5 (for fructose)
  • GLUT2 (for glucose, galactose)
162
Q

aa absorption transporters

A
  • PePT1 (cotransport with H+)
  • XAG- (for anionic aa: aspartate, glutamate: cotransport 2Na, , H+, K+)
  • B0: neutral aa: cotransport with Na+
  • b0+: cationic aa and cystine (aa)
  • PAT1: proline (aa)
163
Q

how do you know if you have with aa transporters

A

can find them in the urine (as proximal tubal has same transporters

164
Q

B0 transporter deficiency

A

hartnup disease

165
Q

b0+ transporter deficiency

A

kidney stones

166
Q

bile salts action on fat

A
  • emulsify large fat droplets: increase surface area for lipase action
  • mixed micelles formation: stabilise products of TG hydrolysis while they ar translocated from luminal to apical membrane
167
Q

emulsification process

A

core body temperature, peristalsis, salivary and pancreatic lipases

168
Q

mechanism of absorption of lipids

A
  • simple diffusion of FA: 50% in undissociated from so lipid soluble
  • FFA transporters: FAT and CD36 + SCFA transporters in colon
  • MG carrier mediated mechanisms for transport
169
Q

cholesterol absorption

A 
duodenum
NPC1L1 (Riemann-Pick C1 Like 1) protein: receptor medicated endocytosis
170
Q

drug that inhibits endocytosis of cholesterol

A

ezetimib

171
Q

SCFA

A

butyrate, propionate, acetate

  • poduced by bacteria fermentation in colon (finer component and incomplete digestion of CHO)
  • butyrate good, propionate and acetate bad
172
Q

absorption of SCFA

A

Secondary active transport:

SMCT1: SCFA and Na+ cotransport driven by Na+,K+ ATPase

173
Q

H20 absorption

A
  • moves down osmotic gradient
  • 8.4L/day, 6.5 in SI, 1.9 in colon
  • via junctional complexes between cells OR via SGLT1 and aa transporters (NOT aquaporins)
174
Q

which ions are excreted in faeces

A

K+ (paracellular absorption diffusion ileum and secretion in LI) and HCO3+ (due to neutralised)

175
Q

osmotic load def

A

unabsorbed water soluble solutes that increase fluid retention in bowel: lack of enzymes or transporters, damage to mucosal cells, secretion of ions by gut

176
Q

diarrhoea problem

A

increased osmotic load

177
Q

excretion rate of alcohol

A

1 unit/hour

178
Q

1 unit of alcohol in pure ethanol

A

10 ml or 8g

179
Q

alcohol liver disease stages

A
  • acute fatty change (aldehyde pathways instead of H20–> fat) REVERSIBLE
  • alcoholic hepatitis (Mallory’s hyaline) REVERSIBLE: inflame response causing:
  • hepatic fibrosis REVERSIBLE
  • cirrhosis IRREVERSIBLE (end stage liver disease, complete modularity, increase turnover of cells so increase risk of developing
  • Hepatocellular carcinoma
180
Q

mechanism of alcohol related disease

A
  • direct toxic effect
  • indirect metabolite effect
  • induction of enzyme systems esp cytochrome p450 (look at how this relates)
  • nutritional deficiency esp B group vit
  • liver function impairment
181
Q

non alcoholic steatohepatitis (NASH)

A
  • identical features to alcoholic hepatitis

- associated with obesity, DMT2, hyperlipideamia

182
Q

physical effects of alcohol

A

fetal alcohol syndrome

  • increase risk of head/neck/oral cancer
  • alcoholic cardiomyopathy
  • systemic hypertension
  • peripheral neuropathy
  • CNS problems: vit deficiency, Korsakoff’s psychosis, Wernicke’s encephalopathy
  • withdrawal syndromes
183
Q

GIT effects of alcohol

A
  • mouth/upper GIT:increase risk of cancers of upper GIT (esp tongue, ducal mucosa, pharynx, upper oesophagus) esp in spirit use and cig smoke
  • oesophagus: squamous carcinoma, varices (chronic liver disease)
  • stomach: acute gastritis, acute/chronic ulceration, portal gastropathy
184
Q

what are determinants of alcohol use

A

socioeconomic structures
political-legal structures
corporate market structures

185
Q

drivers of alcohol use

A

affordability
availability
acceptability

186
Q

moderators of alcohol use

A 
where
what
why
how
who

how much and how often

187
Q

consequences of alcohol use

A

alcohol related health, social and economic harm

188
Q

tools for screening for harmful drinking

A

CAGE

AUDIT (FAST and AUDIT-C)

189
Q

what is CAGE

A
  • have you ever attempted to CUT down on drinking
  • do you ever get ANNOYED when people complain about your drinking
  • do you ever feel GUILTY about things you have done while drinking
  • do you ever need a drink to get going in the morning (EYE OPENER)
190
Q

domains and content of AUDIT

A
  • hazardous alcohol use: frequency (of drinking and heavy drinking), quantity
  • dependence symptoms: impaired control, increase salience, morning drinking
  • harmful alcohol use: guilt, blackouts, alcohol related injuries, other concerns
191
Q

what is IRIS

A

improved health care response in prevent domestic violence and abuse

192
Q

what is HARKS

A

popped up on clinicians screen with patient file so clinician knows the patient suffers from domestic abuse and violence and remind them to ask about it:

humiliate
afraid
rape
kicks
safety
193
Q

2 week referral for oesophageal cancer if

A

-dysphagia or
-aged 55+ and with any of the following:
upper abdominal pain
reflux
dyspepsia

194
Q

Barrett’s oesophagus pathophysiology

A

-longstanding reflux: squamous epithelium –> columnar epithelium with intestinal metaplasia
(premalignant for adenocarcinoma)

195
Q

oesophageal cancer
types
risk factors

A

-upper 2/3: squamous cell carcinoma
lower 1/3: adenocarcinoma
-RF: (for SCC) smoking, alcohol, plummer-vinson syndrome, achalasia, corrosive strictures, coeliac disease, radiotherpatry treatment for breast cancer, (for adenocarcinoma):obesity, age, barrette’s oesophagus, longstanding heart burn, smoking, breast cancer treated with radiotherapy

196
Q

phases of swallowing

A

look it up

197
Q

absolute/relative poverty

A

absolute: standard of living fixed in world and if below you are in poverty
relative: beneath median 60% of country

198
Q

factors affecting poverty

A
  • 0 hour contracts
  • housing prices
  • universal credit: delayed benefits money + not enough
  • inflation
  • lack of education
199
Q

5 core dimensions of illness cognitions

A 
identity
perceived cause
time line
consequences
cure/control
200
Q

self regulatory model

A

stage 1: interpretation (symptom perception, social messages)

  • ->representation of health threat (illness cognitions)
  • ->emotional responses to health threat

stage 2: coping (approach coping, avoidance coping)

stage 3: appraisal (was coping strategy effective?)

201
Q

absorption in the colon

A
  • most in proximal colon
  • actively transport Na+ in: electrical potential for Cl- absorption and H20
  • antiport Cl-/HCO3-
  • K+ absorption: H+,K+ ATPase on basolateral side and K channels and K+,Cl- cotransporters (KCC1) on luminal side: necessary to drive Na+ (ENaC) transporter
202
Q

anxiety and physical health

A

anxiety can make physical health worse by:

  1. direct: acute/chronic physical effects of anxiety
  2. indirect: influence of behaviours (exercise, social support, diet, smoking)
203
Q

COM-B framework

A

behaviour affected by

  • capability
  • motivation (reflective i.e. weighing up and automatic i.e. habit)
  • opportunity (physical i.e. time and social i.e. peer pressure)
204
Q

PRIME theory

A

external environment affects internal environment (percepts, drivers, emotional states, arousal, ideas etc) which are affected by

  • Plans
  • Evaluation
  • Motives
  • Impulses
  • Responses
  • -> theory of decision making in a set moment
205
Q

Health Belief model

A

reflective motivation: explains intention

demographic variables affected by: susceptibility, severity, costs, benefit, cues to action, health motivation, perceived control
which all lead to likelihood of behaviour

206
Q

control of maximisation of nutrients absorption

A

-regulating motility
-controlling secretion of digestive juices
(-little control of absorption)

207
Q

receptors of the GIT and receptor activation effect

A
  • mechanoreceptors
  • osmoreceptors
  • chemoreceptors (acidity and digestive products)

activation causes:

  • hormones
  • nerves (short and long reflexes)
  • paracrine transmission (i.e. release of histamine)
208
Q

main sensory cell f GIT

A

enteroendocrine cell

209
Q

GLP-1: where is it produced, what does it do

A
  • duodenum-colon by enteroendocrine cells

- “incretin” (like GIP): enhances insult secretion, inhibits glucagon production

210
Q

gut hormones

A
  • short chain peptides

- secreted by enteroendocrine cells in mucosa

211
Q

excitatory and inhibitory neurotransmitters of the enteric nervous system

A

excitatory: acetylcholine, substance P, gastrin releasing peptide
inhibitory: nitric oxide, vasoactive intestinal peptide

212
Q

extrinsic nerves (ANS)

A
  • parasympathetic: preganglionic fibres synapse with ENS: release AChn SP, GRP (excitatory) and NO, VIP (inhibitory) –> vago-vagal reflex
  • sympathetic no major role in ‘day to day’ motility: noradrenaline, decrease motility, decrease blood flow
213
Q

def paracrine and endocrine

A

paracrine: released locally (binding nearby cell)
endocrine: secreting into systemic circulation

214
Q

enterochromaffin cells

A
  • mechano and chemo sensory cell
  • 90% of enteroendocrine cells are enterochromaffin cells
  • release serotonin
215
Q

problem with IBS and serotonin

A

in IBS have too much 5HT because SERT not working properly

216
Q

serotonin and motility

A
  • enterochromaffin cells release 5HT
  • 5HT picked up by intrinsic primary afferent neurons
  • short reflex: inhibitory motor neurone relax intestines in front of peristalsis mvnt and excitatory motor neurone that contracts intestines behind peristalsis mvnt
  • 5HT picked up by excitatory afferent signals to brain (long reflex)
217
Q

drug receptors for trials for IBS

A

5HT3 antagonists

5HT4 agonists

218
Q

control of vomiting

A

epithelium damaged: increase release of 5HT: stimulate 5HT3R which go to medulla oblongata: “vomiting centre”

(chemoreceptor trigger zone: for blood)

219
Q

def emesis

A

sudden expulsion of gut/gastric contents through oesophagus and mouth

220
Q

anti-emetics drug receptors

A

5HT3 antagonists

221
Q

opioid receptors expressed in GIT

A

mu, kappa, delta (mu is the important one)

222
Q

opioid receptors activation in GIT

A

G protein (G0):

  • activation K+ channels
  • Inhibits Ca2+ channels
  • -> decrease synaptic transmission:
  • main mechanism for analgesia + decrease motility (inhibitory motor neurones not stimulated): increase transit time in colon so more H2O absorbed –> constipation
223
Q

endogenous opioids in GIT

A
  • 4-8 aa
  • enkephalins and endomorphins
  • -> GPCR: Gi: decrease adenylate cyclase: decrease
224
Q

mechanism for increase intestinal secretion

A

PEG2 and secretin (secrataguoges): GPCR –> Gs: increase adenylate cyclase

225
Q

opioid antidiarrhoeal drugs

A
  • mu receptor agonists (Loperamide, Diphenoxylate + atropine)
  • enkephalinase inhibitors (enhance actions of endogenous enkephalins): Hidrasec
226
Q

primary and secondary peristalsis of oesophagi

A

primary: continuation of pharyngeal peristalsis
secondary: local reflexes (circular and longitudinal muscles)

227
Q

serosa and advertía: intra/extraperitoneal?

A

serosa: intra
advent: extra (linked to posterior abodo wall)

228
Q

effects of absence of gut bacteria

A 
behaviour
gut homeostasis
immune response under stress
body weight
brain development and gene expression
229
Q

use of faecal transplant therapy

A

Clostridium difficile (spore forming: hard to eliminate with antibiotics)

230
Q

Paneth cells:

  • location
  • secretions
  • stimulations
A
  • base of crypts in SI
  • alpha and beta defensives (antimicrobial peptides)
  • gut bacteria
231
Q

what secretes IgA

A

plasma cells

232
Q

how many stem cells does crypts have

A

6-8

233
Q

zone of cell renewal and differentiation in crypt

A

stem cell
proliferative zone
differentiation zone

234
Q

where do you find Peyer’s patches?

A

distal jejunum and ileum

235
Q

giardia Intestinalis

A
  • most common intestinal parasite found in the USA
  • 10-25 cysts can cause clinical disease
  • pathology: villous atrophy + crypt hyperplasia
  • enterocyte apoptosis
236
Q

where do you find gut associated lymphoid tissue

A

just below epithelial cells

237
Q

function of M cells

A

selective endocytosis of antigens, and transporting them to intraepithelial macrophages and lymphocytes, which then migrate to lymph nodes where an immune response can be initiated

238
Q

where are M cells found

A

Peyer’s patches
MALT
GALT

239
Q

lamina propria lymphocytes types

A

naive CD4+ T cells differentiate into:

  • Th1
  • Th2
  • Th17
  • Treg

Th1, Th2 and Th17 can cause pathology if they are out of control and Treg regulates this

240
Q

innate lymphoid cells

A
  • from common lymphoid progenitor
  • rely on IL2R singling
  • no T cell receptors
  • ILC1, 2 or 3
241
Q

ILC1

A
  • produce IFN gamma
  • NK cells are ILC1
  • express T-bet
242
Q

ILC2

A
  • also called nuocytes, NKC
  • IL5/IL13 producers
  • express RORalpha/GATA3
  • seen in allergy
  • respond to IL25/IL33
243
Q

ILC3

A
  • contributes to mucosal homeostasis
  • produce IL17A&F/IL22
  • express RORgammat
  • respond to IL23
  • important in fetal lymphoid organogenesis and GALT formation
244
Q

T cell activation

A

B7 (on APC) binding to CD28 (on T cell)

245
Q

T cell inactivation

A

B7 (on APC) binding to CTLA4 (on T cell)

246
Q

what is PD1/PDL1 interaction

A

PD1: immune suppressive molecule to avoid over-activation

247
Q

types of IBS and cause

A

ulcerative colitis
crohn’s disease

cause: dysregulation of host flora

248
Q

what is the cancer inflammation paradigm

A

balance between inflammation and cancer

249
Q

hallmarks of cancer

A
  • self-sufficient in growth signals
  • insensitivity to anti-growth signals
  • avoidance immune destruction
  • tumour promoting inflammation
  • tissue invasion and metastasis
  • limited replicative potential
  • sustained angiogenesis
  • genomic instability
  • deregulated metabolism
  • evading apoptosis
250
Q

2 oncogenes of colon cancer

A

beta-catenin and KRAS

251
Q

3 TSG in colon cancer

A

APC and p53 and Rb

252
Q

cell signalling pathway

A 
ligand
receptor
signalling cascade
transcription factors 
gene expression
253
Q

what is RAS

A

a GTPase (when bound to GTP it is on and activates downstream pathway)

254
Q

what does a mutation in RAS cause

A

locked into active form: conversion from GTP to GDP stops happening

255
Q

which pathway must be dysregulated in colon cancer

A

Wnt signalling

256
Q

what is Wnt?

A

growth factor

257
Q

which genes are involved in Wnt signalling

A

APC and beta catenin

258
Q

Wnt signalling pathway

A

unstimulated state: Wnt does not bind to receptor and beta-catenin is phosphorylated (and degraded) by Apc

stimulated state: Wnt binds to receptor: inactivation of GSK-3 beta complex: beta-catenin does not get phosphorylated by Apc: activates gene expression in the nucleus and drives cell proliferation

259
Q

how is Wnt signalling dysregulated

A
  • deletion of both copies of APC: beta catenin cannot be phosphorylated (80% of cases)
  • point mutation at phosphorylation site of beta catenin: can no longer be phosphorylated (20% of cases)
260
Q

which part of the cell cycle responds to mitogenic GFs and TGF-beta

A

G1 to the R point

G1 is only phase that responds to extracellular signals

261
Q

CDKs and cyclins of cell cycle

A
  • G1: CDK4/6, cyclin D
  • G1 (from R point) and beginning of S phase: CDK2 and cyclin E
  • beginning of S phase: CDK2 and cyclin A
  • end of S phase to end of G2: CDK1 and cyclin A
  • end of G2 and mitosis: CDK1 and cyclin B
262
Q

what are CDKs

A

cyclin dependent kinases: enzymes that phosphorylate substrates (bring changes to cell)

263
Q

P53 actions and P21 link

A

P53: cell cycle arrest (turns up P21 which inhibits CDKs/cyclins), DNA repair, block off angiogenesis and apoptosis (switches on proteins involved in cell death)

264
Q

what is genomic instability

A

high frequency of mutations within the genome

265
Q

genetic instability in colon cancer

A

HNPCC: mismatch repair
APC: chromosomal instability

266
Q

what are adenomatous polyps

A

polyps that carry high risk of cancer

267
Q

FAP

A

familial adenomatous polyposis (1%)

268
Q

APC

A
  • adenomatous polyposis coli
  • chromosome 5q21
  • mutated in 80-90% of sporadic colorectal cancers
269
Q

what happens to crypts if APC or beta catenin mutated

A

zones of proliferation will be higher up in the crypt: forms hyper proliferative zone which can turn into polyp

270
Q

HNPCC

A

hereditary non-polyposis colon cancer
2-3%
Lynch syndrome (ovary, SI, urinary tract, skin and brain)
-few polyps
-MHS2 and MLH1 mutated (promoter is methylated switching gene off): increases mutation rate

271
Q

what is micro satellite instability

A

genetic hypermutability

272
Q

mutated pathway of CRC with MSI

A

TGF-beta (inhibitory pathway): 90% of CRC with MSI: doesn’t cause cancer but increase mutations

273
Q

which mutations have highest mutation rate

A

mismatch repair (not chromosomal)

274
Q

when is immunotherapy used in colon cancer

A

for higher mutated phenotypes (MSI)

275
Q

metastatic cancer of right sided colon cancer

A

peritoneal and omental and liver

276
Q

which side of colon cancer has better outcome

A

left sided

277
Q

3 subtypes of colorectal cancer

A

pole hyper mutated (1%)
micro satellite instability (8-9%)
micro satellite stability (90%)

sem 4 (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions