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Pathophys 2, Midterm > GI > Flashcards

GI Flashcards

1
Q

Where does the storage and further processing occur?

A

Liver

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2
Q

Peristaltis is contolled by what?

A

ANS

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3
Q

What are the 4 layers of GIT?

A

Mucosa (inner)
Submucosa
Muscularis
Serosa (advetia) continuous with mesentary

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4
Q

What is the name of the intrinsic nervous network of GI?

A

Enteric nervous system

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5
Q

What is the short (ENS reflex) loop?

A

Stimulus -> GIT receptors (mecano) -> ENS plexus -> smooth mucles and glands -> mucosal response

GIT receptors can -> brain and
Brain –> ens plexus (long reflex(vaso vagal reflex) )

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6
Q

What does tbe vagus nerve carry?

A

Parasympa and sympa fibers

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7
Q

What does the taste and food odours do on salivation?

A

Increase salivatipn and gastric juice secretion

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8
Q

What are the 3 glands for salivation?

A

Parotid
Submandibular
Sublingual

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9
Q

Saliva is:

A

Hypoosmotic
Neutral ph7.4

Regulated by ANS only
And para/sympa increase secretion

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10
Q

In saliva, what is ptyalin and mucus?

A

Ptyalin: carbohydrate digestion

Mucus : lubrication

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11
Q

What are the 3 mucles of esophagus?

A

Striated (at UES)
Mixed
Smooth (below LES)

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12
Q

The UES (upper esophagus sphincter) is ?

A

Relaxed

When contraction: prevent air into esophagus

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13
Q

The LES (lower esophagus sphincter) :

A 
Usually Contracted (precent gastric reflux) 
Relaxed : allows bolus to enter stomach
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14
Q

What is the oropharyngel phase of swallowing?

A

Voluntary
Regulated by trigeminal and brainstem

  1. Pressure to pharynx
  2. Reflex protecting airways
  3. Relax UES
  4. Contract pharyngeal constrictors
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15
Q

What is the esophageal phase of swallowing?

A
  1. Primary peristaltis in esophagus
  2. Relax LES
  3. Accomodate tgrough gastric relaxation

Vagal relax of LES

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16
Q

What is absorbed in stomach?

A

Alcohol and NSAIDs

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17
Q

Where does the vagus innervation occur?

A

Fundus (upper portion)

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18
Q

What is the proximal stomach?

A

Body of stomach, serosa to mucosa

Storage and receptive relaxation

Stops at pacemaker cells

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19
Q

What is the role of the pacemaker cells?

A

Basic electrical rhythm (BER)

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20
Q

What is the distal stomach?

A

Atrum, pylorus

Gastric peristalsis (max 3 min) 
Gastrin & parasympa  activity = increase 
Secretin & sympa activity = decrease
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21
Q

Gastrin ?

A

Increase peristalsis with parasympa

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22
Q

Secretin?

A

Decrease peristalsis with sympa

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23
Q

Gastric mixing

A

Antral systole -> increase velocity -> retropulsion

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24
Q

Gastric emptying:

A

Pyloric sphincter always open

Fluid: pressure
Solid: peristalsis

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25
Q

What does the enterogastric reflex do?

A

Decrease rate of emptying

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26
Q

What is enterogastric reflex?

A

Neural and hormonal
Short and long

Cholecystokinin (CCK) and secretin

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27
Q

What are the determinants of enterogastric reflex?

A
  1. Duodenal distension
  2. Chyme hyperosmolarity
  3. Very acidic chym pH
  4. High fat content
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28
Q

What is pepsinogene and pepsin

A

Pepsinogen : inactive form of pepsin
Pepsin : activated by gastric acid <2
digest proteins
Pepsin desactivated in intestine by alkaline pH

Ach increase secretion

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29
Q

Intrinsic factor

A

B12 abs

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30
Q

Gastroferritin

A

Increase iron absorption

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31
Q

Enterochromaffin-like cells (ELC) ?

A

Histamine -> increase HCl secretion

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32
Q

G-cells

A

Gastrin : increase HCl secretion

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33
Q

D-cells

A

Somatostatin -> decrease HCl

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34
Q

What are the fonctions of gastric glands?

A

Mucous neck cell : mucus secretion
Chief cell: pepsinogene
Parietal cell: HCl, intrinsic factor, gastroferritin
Endocrine cell: histamin, gastrin, somatostatin

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35
Q

What are the main functions of gastric acid?

A

HCl in stomach
HCo3 in urine

Dissolve food
Bactericidal agent
Pepsinogen-> pepsin

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36
Q

What is the 3x defense of gastric mucosal barrier?

A
  1. Mucus buffer layer (HCO3)
  2. Tight junctions
  3. Rapid mucius neck cell turnover
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37
Q

What is the role of prostaglandins in GMB?

A

Increase mucus & decrease acid secretion

NSAIDs (aas) inhib prostaglandin -> decrease GMB

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38
Q

H pylori

A

Kill mucuous cells + increase gastrin -> decrease GMB

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39
Q

What are the phases of gastric secretion?

A

Cephalic: thought, smell, taste of food
Gastric: stomach distension
Intestinal: histamine and digested proteins

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40
Q

What is secreted in cephalic phase?

A

Ach

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41
Q

What is secreted in gastric phase?

A

Gastrin

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42
Q

What is secreted in intestinal phase?

A

Histamine

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43
Q

What does CCK and secretin?

A

Decrease secretion
Enterogastric reflex

Digested proteins increase secretion of histamine

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44
Q

What is the main function of small intestin?

A

Complete digestion and absorption

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45
Q

Role of vili and microvili

A

Bush border -> increase surface area

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46
Q

Brush border

A

Increase surface area

Digestive enzymes & absorption

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47
Q

What is the ileocecal sphincter ?

A

Opening to colon

48
Q

Paneth cells

A

In crypts of lieberkuhm

Antibio secretions

49
Q

What are the cells in Crypts of Lieberhühn?

A

Paneth
Goblet
Enterocytes

50
Q

Goblet cells

A

Alkaline mucus secretion

51
Q

Enterocytes

A

Absorption

52
Q

What is ileogastric reflex ?

A

Ileum distension decrease gastric motility

53
Q

What is enterointestinal reflex?

A

Intestinal distension decrease -> decrease intestinal motility

54
Q

What is gastroileal reflex?

A

Gastric motility increase ileum motility and sphincter relax

55
Q

Ileocolic reflex?

A

Colon distension -> ileal sphincter constriction

56
Q

What does the stomach digest and absorbe?

A

Water and alcohol

57
Q

What in digested and absorbed in duodenum

A

Calcium, Sodium, Mg, iron
Fats, sugars, proteins
Water, vitamins

58
Q

Digested and absorbed in jejunun?

A

Sugar, proteins

59
Q

Digest/abs in ileum

A

Bile salts, B12, chloride

60
Q

Abs in colon

A

Water, electrolytes

61
Q

How are carbohydrates absorbed?

A

Via sodium-glocose co-transporter and GLUT

62
Q

Intestinal glucose abs is

A

Insulin independent

63
Q

Hiw are proteins absorbed?

A

Via sodium-dependent carriers

64
Q

How are fats abs?

A

Whit micelles

65
Q

What are mucelles?

A

Amphipathic

Bile salts -> absileum -> recycled at liver

66
Q

Gastrocolic reflex

A

Gastric secretion increase colon motility

67
Q

Macrophage (kupffer cell)

A

Infection prevention

68
Q

Hepatocyte

A

Detox blood & release nutrients

69
Q

Liver functions

A 
Lipid storage
Testos and estrogen metabo
Rbc destruction 
Bilirubin metabo
Bile and plasma prot synthesis
70
Q

What is bile secretion?

A

Liver -> hepatocyres synthesis cholesterol to form 1° bile acids -> galbladder -> duo/jejunun -> ileum -> actively transported across intestinal lumen into 2° bile acids -> diffuse passively across lumen

-> hepatic portal vein -> duo/jeju -> rectum

71
Q

Who abs and destroy old RBC?

A

Kupffer cells

Makes heme and globin

Heme -> iron and bilirubin

72
Q

What happens to iron and globin after RBC destruction?

A

Heme-> Iron -> iron pool

Globin -> amino acid pool

73
Q

Gallbladder contraction increase by

A

CCK

Vagus nerve

74
Q

2 types fluid by pancreas

A
  1. Enzyme rich: digestion
    Vagus and CCK increase secretion
  2. HCO3 : neutralization
    Secretin increase secretion
75
Q

What does anterokinase do?

A

In duodenal mucosa

Trypsinogen to trypsin

76
Q

What are the muscular events to vomiting

A
  1. Duodenal + gastric retrograde peristalsis
  2. LES relaxes + diaphragm & abdo contractions
  3. Increase thoracic pressure force open UES -> chyme expulsion

Parasympa control
Medulla

77
Q

What is CTZ?

A

Chemoreceptor trigger zone
Outside BBB
Drugs and toxins

78
Q

Osmotic diarrhea

A

Subs malabs -> osmose in colon -> large volume

79
Q

Secretory diarrhea

A

Bacterial or viral -> increase secretions, decrease absorption -> large volume

80
Q

Motility diarrhea

A

To fast, no abs -> small volume

81
Q

Types of dysphagia

A

mechanical : tumor, compression of esophagus

functional: neuromuscular disorders. impaired voluntary swallowing
achalasia: loss inhib neurons in lower esophagus –> no relax LES

82
Q

what is GERD? gastroeso reflux disease

A

abnormal LES relaxation/weak –> gastric reflux

83
Q

4 types of intestinal obstruction

A

volvulus, herniation, adhesion, intussusception

84
Q

intestinal obstruction pathophys

A

distension –>less fluid, E+ absorption –> alkalosis(high IO) or acidosis (LOW), ketosis, lactic acidosis

85
Q

Why high IO –> alkalosis

A

less chloride and more HCO3

86
Q

Why low or late IO makes acidosis ?

A

more H+ and less K

less bic and bile reabsorption

87
Q

What is chronic gastritis?

A

chronic inflammation + mucosal atrophy + increase risk of cancer

cause –> H+ pump and autoantibodies –> gastric mucosa atrophy and less secretions –> ulcers, pernicious anemia, bleeding, cancer

88
Q

what are peptic ulcers?

A

inflammation et autogestion

psycho stress ulcers

89
Q

what are duodenal ulcers ?

A

acid secretion or muscle spasm

relieved by antacids and meal

remission/exacerbation

90
Q

what is gastric ulcers?

A

more HCl secretion
defective mucosa barrier

no remission-exacerb
increase cancer

91
Q

stress ulcers

A

curling: burn injuries
Cushing : more vagal activity after brain trauma

coagulopathy

92
Q

What is the difference between Crohn and Ulcerative colitis?

A

Crohn: idiopathic inflammatory disorder of GI

Ulcerative: chronic inflammation of mucosal layer

93
Q

Hallmarks of UC?

A

colon and rectum, continuous lesions

autoimmune
exacerbation-remission

pancolitis: whole colon

94
Q

Hallmarks of CD?

A

cell mediated cytotoxicity –> skip lesions

transmural inflammation –> crypts destruction

95
Q

What is appetite regulation?

A

hypothalamus –> arcuate nucleus –>
anorexins –> catabolic –> less appetite and more metabolism

or orexins –> anabolic –> + appetite and less metabolism

96
Q

obesity and adipocytes

A

low grade inflammation and adipokine (leptin& adiponectin) pattern alterations –> T2DM & cardiovascular disease

97
Q

Leptin and obesity

A

eat ++ –> more leptin –> leptin resistance –> overeating –> weight gain –> hyperleptinemia –> more sympa activity –> HTN

98
Q

Adiponectin and obesity

A

adiponectin secreted to increase insulin sensitivity.

anti-inflammatoire & anti-arthrogenic

obesity –>less adiponectin –> insulin resistance –> T2DM

99
Q

What is Kwashiorkor?

A

protein insufficiency. normal fat

100
Q

What is portal hypertension?

A

increase of 3-10 mmhg

compli: varices, splenomegaly, respi dysfunction

101
Q

what happens when liver dysfunction? on encephalopathy

A

collateral vessels formation –> shunt blood around liver to systemic circulation –> toxins normally absorbed in liver are in blood –> ammonia in brain –> increase gaba –> less neurotransmission –> lethargy –> coma –> death

102
Q

What is the pathological Neonatal jaundice?

A

0-24h after birth

more bilirubine production –> less excretion –> less liver conjugation metabolism

  • unconjugated = lipid-soluble –> BBB
103
Q

What is kenictus?

A

chronic increase in unconjugated bilirubin in brain –> encephalopathy

tx: phototherapy

104
Q

what are the 4 clinical phases of hepatitis?

A
  1. incubation
  2. prodromal
  3. icteric
  4. recovery
105
Q

What is the incubation phase of hepatitis?

A

infection

106
Q

What is the prodromic phase of hepatitis?

A

about 2 weeks post-exposure
contagious ++
ends with jaundice

107
Q

what is the icteric phase ?

A

1-2 weeks post prodromal
lasts 2-6 weeks

hepatocellular necrosis + cholestasis
liver enlargement + painful

108
Q

What is the recovery phase of hepatitis?

A

6-8 weeks post exposure

jaundice resolution

109
Q

What are the transmission modes of Hepatitis A,B,D,C,E ?

A

A: sex, fecal-oral, parenteral
B,D: sex, parenteral,
C: parenteral
E: fecal-oral

110
Q

Which hepatitis are chronic?

A

B,C,D

111
Q

What does hep D require prior to infection?

A

infection by hep B

112
Q

What is Viral hepatitis B (HBV) ?

A

DNA virus

causes: cirrhose, chronic hepatitis, hepatocellular carcinoma

113
Q

What are the markers of HBV?

A

HBsAg: active HBV
HBeAg: HBV replication

114
Q

Are there vaccines for Hep C ?

A

no, only interferon antiviral therapy

115
Q

How does cirrhosis occur?

A

liver injury –> kupffer cell activation –> release inflammatory mediators –> fibrosis

chronic damage + fibrosis regeneration cycle –> cirrhosis

116
Q

what happens in alcoholic liver cirrhosis ?

A

alcohol –> increase acetaldehyde formation

+ inflammatory mediators –> necrosis

117
Q

What happens during acute pancreatitis ?

A

duct obstruction –> acing cell injury –> intracellular activation of enzymes –> auto digestion –> trypsin –> cell injury, proteolyses, edema, thrombosis, hemorrhage, necrosis

Pathophys 2, Midterm (4 decks)

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