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Pharm 2 > GI lecture > Flashcards

GI lecture Flashcards

1
Q

What are the 4 protective mechanisms to protect the GI tract?

A

-mucus
-bicarbonate
-prostaglandins
-mucosal blood flow

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2
Q

what are the 4 mechanisms of the GI tract that are aggressive and break things down?

A

-acid
-pepsin
-NSAIDS
-Helicobacter pylori

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3
Q

Review the food stimulus diagram. What is the pathway? (SR = short reflex, LR = long reflex)

A
  1. Food sensed -> signal to medulla oblongata –(LR)–> preganglionic parasympathetic neuron in vagus nerve –(LR)–> enteric plexus –(SR+LR)–>postganglionic parasympathetic and intrinsic enteric neurons –(SR+LR)–> effector cells –(SR+LR)–> secretion and motility
  2. food ingested -> hits gastric mucosa –(SR)–> sensory input –(SR)–> enteric plexus
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4
Q

What is the differences between long and short reflexes?

A

Long:
-integrated in CNS
-originate in or outside of GI tract

Short:
-integrated in enteric NS
-originate from internal change (pH, osmolarity, products etc.

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5
Q

What are cephalic reflexes?

A

-feedforward and emotional reflexes
-initiated and integrated outside GI

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6
Q

What is the pathway for the cephalic phase?

A

food stimulus -> cerebral cortex, hypothalamus, amygdala signal -> activate neurons in medulla -> sends ANS signal to
1. Salivary Glands via facial nerve, glossopharyngeal nerve, and symp innervation = inc. saliva, amylase, lysozymes, and lingual lipase (babies)
2. Enteric NS via vagal nerve = inc. gastric secretions and motility, accounts for 20% of gastric secretions while eating

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7
Q

What are the different cell types involved in the cephalic phase?

A

-Mucous neck cells
-parietal cells
-enterchromaffin-like cells
-chief cells
-D cells
-G cells

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8
Q

What is secreted by the mucous neck cells?

A

Mucus and bicarbonate

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9
Q

What stimuli release Mucus and bicarbonate from mucous neck cells?

A

-mucous = tonic secretion, irritated mucosa
-bicarbonate = secreted with mucus

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10
Q

what are the functions of mucous and bicarbonate?

A

-mucous keeps physical barrier between lumen and epithelium
-bicarbonate buffers gastric acid

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11
Q

What is secreted by parietal cells?

A

-gastric acid (HCl)
-Intrinsic factor

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12
Q

What is the stimulus needed to release HCl and intrinsic factor from parietal cells?

A

-Acetylcholine
-gastrin
-histamine

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13
Q

What is the function of Gastric acid and intrinsic factor?

A

-gastric acid = activates pepsin, kills bacteria
-intrinsic factor = complexes with vitamin B12 to permit abs.

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14
Q

What is secreted by enterochromaffin-like cells?

A

Histamine

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15
Q

What stimulus is required to release histamine from enterochromaffin-like cells?

A

-acetylcholine
-gastrin

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16
Q

what is the function of histamine?

A

-stimulates gastric acid secretion

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17
Q

what substances are secreted by Chief cells?

A

Pepsinogen and Gastric lipase

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18
Q

What is the stimulus required to release pepsinogen and gastric lipase from Chief cells?

A

-Acetylcholine
-acid
-secretin

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19
Q

What is the function of pepsinogen and gastric lipase?

A

-pepsinogen = digests proteins
-gastric lipase = digests fats

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20
Q

What is secreted by D cells?

A

Somatostatin

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21
Q

What is the stimulus required to release somatostatin from D cells?

A

acid in the stomach

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22
Q

What is the function of somatostatin?

A

inhibit gastric acid secretion

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23
Q

What is secreted by G cells?

A

gastrin

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24
Q

What stimulus is required to release gastrin from G cells?

A

-Acetylcholine
-peptides
-A.A.

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25
Q

what is the function of gastrin?

A

-stimulates gastric acid secretion

26
Q

What does gastrin target?

A

-ECL cell
-parietal cells

27
Q

What inhibits gastrin release?

A

somatostatin

28
Q

Where does Cholecystokinin come from and what stimulates its release?

A

-the intestine
-stimulated by fatty acids and AA

29
Q

What does cholecystokinin (CKK) target?

A

-gallbladder
-pancreas
-stomach

30
Q

What is the function of CCK?

A

-stimulate gallbladder contractions
-pancreatic enzyme secretion
-inhibit gastric emptying

31
Q

What feeling does CCK create?

A

satiety

32
Q

What two secretions are part of the gastrin family?

A

-gastrin
-cholecystokinin (CKK)

33
Q

What does motilin do?

A

-stimulates migrating motor complex
-helps keep things moving even when you’re not consuming food

34
Q

What stimulates the release of motilin?

A

-fasting
-released every 1.5-2h of fasting

35
Q

what is the target of motilin?

A

-gastric smooth muscle
-intestinal smooth muscle

36
Q

What secretion is in the peptide family?

A

motilin

37
Q

what secretions are part of the secretin family?

A

-secretin
-gastric inhibitory peptide (GIP)
-glucagon-like peptide 1 (GLP-1)

38
Q

What does secretin do?

A

-stimulates bicarbonate secretion
-inhibits gastric emptying and acid secretion

39
Q

What are the targets of secretin?

A

-pancreas
-stomach

40
Q

What stimulates the release of secretin?

A

acid in small intestine

41
Q

What does gastric inhibitory peptide do?

A

-stimulates insulin release
-inhibits gastric emptying and acid secretion

42
Q

What is the target for gastric inhibitory peptide?

A

-beta cells in pancreas

43
Q

what stimulates the release of gastric inhibitory peptide?

A

-glucose
-FA
-AA

44
Q

What does Glucagon-like peptide 1 do?

A

-stimulates insulin release
-inhibits glucagon release and gastric function

45
Q

What is the target for GLP-1?

A

endocrine pancreas

46
Q

What stimulates the release of GLP-1?

A

-mixed meal with fats and carbs entering the lumen

47
Q

What are the three main sections to the stomach lining?

A

-preepithelial
-epithelial
-subepithelial

48
Q

what is part of the epithelial layer of the stomach?

A

-cellular resistance
-growth factors
-prostaglandins
-cell proliferation

49
Q

Pathway for gastric HCl secretion

A

stimuli -> brain -> increased enteric neural discharge -> histamine secretion -> parietal cell secretes acid -> inceased HCl

-too much HCl inhibits gastrin secretion and no gastrin means no histamine and discharge simulation so HCl stops being produced

50
Q

Receptor Level of Gastric HCl secretion

A

-Acetylcholine input = neurocrine
-gastrin hormonal input = endocrine
-histamine input = paracrine
-Acetylcholine and gastrin receptors on ECL cell which secretes histamine
-histamine receptor on parietal cell -> transduction events -> H/K+ pumps secrete HCl

51
Q

Why do NSAIDS cause stomach issues?

A

-decreases prostaglandins = increase gastric acid, decrease sodium bicarbonate, decrease blood flow
-****

52
Q

What are some characteristics of the mucous layer?

A

-0.5mm thick
-has mucus gel that sodium bicarbonate is secreted into
-mucosa synth PGs, E2 and I2 = cytoprotective action

53
Q

What is triple therapy and quadruple therapy for eradicating H. Pylori?

A

-Triple therapy = 7day, PP inhibitor + amoxicillin/tetracycline + metronidazole/clarithromycin
-Quadruple therapy = 3 day, plus bismuth
-both are 80-85% effective

54
Q

What are the 2 ways H. Pylori causes ulcers?

A
  1. has urease activity -> increases pH -> causes G cell to produce more gastrin -> increases acid secretion
  2. has inflammatory mediators -> inhibit D cell -> no somatostatin -> no inhibition of gastrin release -> acid secretion not inhibited
55
Q

How does the urea breath test work?

A

-pt ingests urea with C13 -> if theres HP, it will produce urease and hydrolize the ingested urea into 13CO2 -> pt breath will be analyzed and if HP, then 13CO2 will be much higher than 12CO2

56
Q

What causes the dysregulated immune response for IBD?

A

-genetics
-environment

57
Q

List main Crohn’s symptoms

A

-chronic/nocturnal diarrea
-rectal bleeding
-abdominal pain
-weightloss
-fever
-fatigue
-extraintestinal = skin, eye, joint

58
Q

How is IBD treated and what are the treatment goals?

A

-symptomatically
-prevent complications
-improve QOF
-limit surgery
-suppress inflammation and reaction

59
Q

What are the two main types of IBD?

A

-Crohn’s Disease
-Ulcerative Colitis

60
Q

What are the risks with using anti-TNF drugs?

A

-5% get infusion reaction
-infection can lead to sepsis
-lymphoma
-drug induced lupus
-hepatotoxicity
-demyelinating disorder

61
Q

How does laxative abuse occur?

A
  1. using a laxative empties the colon so it will take longer to refill and eliminate waste than normal. This can be perceived as constipation
  2. constantly using a laxative = water is not absorbed from stool = body senses decrease in salt and water absorption = release of aldosterone = kidneys retain water and release potassium = potassium released from both stool and kidneys = hypokalemia = potassium required for peristalsis = low/no peristalsis = constipation

Pharm 2 (11 decks)

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