Brainscape's Knowledge GenomeTM

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


See full index

GI/Endo/Repro > Assessment 1 > Flashcards

Assessment 1 Flashcards

1
Q

Parotid gland

A

Serous secretions

Salt, water, alpha amylase, lysozyme, lactoferrin

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

Submandibular gland

A

Mucins

More mucus, less water

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

Duodenum absorption

A

Water, iron, calcium

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

Jejunum absorption

A

Nutrients: sugars, AA, NaCl, Fe, Water

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

Ileum absorption

A

Bio salts

Bile salts

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

Colon absorption

A

NaCl, SCFA’s, Water

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

Mucins

A

Lubrication

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

Salivary alpha amylase

A

Digest starch/carbohydrates

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

Lingual lipase and salivary lipase

A

Digest fats

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

Lysozyme, secretory IgA, lactoferrin

A

Bacteria-static/cidal

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

Haptocorrin

A

Vit B12 chaperone

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

Exocrine pancreas

A

Alpha amylase
Trypsin, chymotrypsin, carboxypeptidase A/B and elastase
Lipase/Colipase
Nucleases

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

Splanchnic circulation

A

Portal vein from intestine directly to liver

Storage/metabolism/detoxification

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

Liver blood flow (2)

A

Portal vein: 80% input, nutrient rich, absorbed bile salts

Hepatic artery: 20% input, oxygen

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

GI smooth muscle

A

All smooht muscle except pharynx, 1st part of esophagus, external anal sphincter

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

3 layers of GI SM

A
  1. Outer longitudinal
  2. Inner circular
  3. Innermost oblique (stomach only)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

SM contraction pathway

A

Ca binds calmodulin –> MLCK –> myosin phosphorylated –> contraction

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

Submucosal Plexus

A

Meissner’s

Between mucosa and circular muscle layers

Senses environment in lumen. Regulates GI blood flow, epithelial cell function

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

Myenteric plexus

A

Between circular and longitudinal layers

Larger and more cell bodies
Control motility

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

Peristalsis and interneurons

A

Distention sensed by mucosa

Interneurons contract proximal SM and relax distal SM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Interstitial Cells of Cajal

A

Pacemakers of GI tract, spontaneous electrical rhythmicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

3 stages of deglutition

A

Oral (voluntary): tongue movs bolus back and swallowing occurs

Pharyngeal (reflex): Pharynx momentarily becomes pathway for swallowing

Esophageal: Peristalsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Esophageal phase

A

Bolus entering initiates primary peristalsis, LES/proximal stomach relaxes

Continued distention initiates secondary peristalsis

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

Lower esophageal sphincter relaxation (3)

A
  1. Swallowing
  2. Secondary peristalsis
  3. Transient LES relaxations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Ileal brake

A

Undigested food arrives in ileum –> gastric emptying/SI transit slowed

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

Duodenal phase

A

Endocrine: CCK
Paracrine: Serotonin via 5-HT4 receptor –> duodenal contraction

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

Migrating Motor Complex (MMC)

A

GI housekeeper

Sweep secretions and undigested food through SI

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

Large Bowel Contractions (2)

A

Non propagating/segmental: Mixes contents to absorb water - 95%

Propagating contractions (peristalsis): Propels contents forward, 5%, vary in speed/pressure

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

Slow propagating contractions

A

Less frequent, more powerful, ~6/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Fast propagating contractions

A

More frequent, low amplitude

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

Gastro-colic reflex

A

Following meal, colonic motility increases

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

Defecation reflex

A

Distention of rectum

Rate of filling = urgency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Xerostomia

A

Lack of salivary secretions

Leads to cavities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Salivary secretion regulation

A

Autonomic nervous control

Para/Symp action on acinar cells, increase secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Alpha amylase (action and location of secretion)

A

Digest complex carbohydrates

Parotid: minor
Pancreas: Excess

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

Carbohydrate digestion in SI

A

Luminal enzymes in SI

Reduce variety of molecules (Fructose, Glucose, Galactose)

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

Lactase deficiency

A

Lactose cannot be absorbed, creates osmotic gradient in lumen and osmotic diarrhea

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

Sugar absorption channels

A

SGLT1 - Na dependent Glu transport

GLUT5 - Fructose

GLUT2 - basolateral Glu/Fru transport

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

Zymogens

A

Enzymes that need to be activated

Pepsinogen + HCL –> Pepsin

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

Pancreatic zymogen activation

A

Enteropeptidase (intestinal epithelium) + Trypsinogen –> Trypsin

Trypsin activates pancreatic zymogens

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

Peptide/AA absorption

A

Protein digested in lumen or surface peptidases

AA absorbed all the way through

Dipeptides absorbed all the way or digested to AA by cytoplasmic peptidases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Protein absorption channels

A

PEPT1 - H/dipeptide cotransport

Na/AA co transport

AA transport

100% absorbed by end of jejunum

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

2 phases of fat absorption

A

Luminal

Mucosal

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

Steps of Luminal phase

A

Fat emulsification
Lipolysis
Solubilization by bile salts
Diffusion to mucosa

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

Fat emulsification

A

Breakdown of large fat droplets to smaller ones via motility

Stabilized by amphipathic fatty acids, dietary protein

Need pH > 6

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

Lipolysis

A

Breakdown of triglycerides/fatty acids

Pancreas is major source of lipases

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

Pancreatic lipase and bie salts

A

Bile salts block pancreatic lipase

Need colipase to prevent bile salt inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Bile salt secretion - CCK involvement

A

Dietary fats activate I cells which release CCK

CCK contracts gallbladder and relaxes sphincter of Oddi = Bile salt release into gut lumen

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

Micelle

A

Bile salts surround emulsified fats/vitamins/cholesterol etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Micelle benefits

A

Slower diffusion time

Much higher concentration of fatty acid diffused via micelle

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

Mucosal phase steps

A

Uptake into intestinal epithelial cells
Transport to ER
Resynthesis of TG
Formation of Chylomicron

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

Uptake into intestinal epithelial cells

A

FABP bind to FA and MG

FABP lowers FA concentration

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

Transport to ER

A

FABP transports FA /MG to smooth ER if C chain > 12

Straight to blood if C chain short

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

Smooth ER step

A

Triglycerides and phospholipds reformed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Chylomicron formation

A

Occurs in Golgi

Formed by TG, phospholipids, cholesterol, protein

Apoproteins guide to basolateral side

Enter lacteal and lymphatic system –> blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Achalasia

A

Failure to relax of smooth muscle in any region of GI

Loss of enteric inhibition = no relaxation

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

Inhibitory nitrergic neurons

A

Within myenteric plexus, mediate inhibition at LES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Esophageal Achalasia

A

Failure of LES relaxation - loss of nitrergic neuronal inhibition

Viral or inflammation–>autoimmune that results in myenteric plexus inflammation

Esophagogram: Birds beak appearance

Dysphagia, regurgitation (non bilious/acidic), weight loss, chest pain (rare)

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

Distal Esophageal spasm

A

DES

Uncommon disorder, impairment of neural function - corkscrew sign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

DES vs Achalasia

A

Achalasia has no LES relaxation

DES has relaxation but timing is off

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

Infantile hypertrophic pyloric stenosis

A

Non bilious vomiting in infants

Gastric outlet obstruction, pyloric antrum abnormalities

Olive like mass, RUQ

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

Hirschsprung disease

A

Lack of innervation of large bowel portions, cannot move stool

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

Internal anal sphincter Achalasia

A

Similar to Hirschsprung but ganglion cells present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Gastroparesis

A

Stomach cannot empty

Can be associated with diabetes

No mechanical obstruction

Bloating, nausea, vomiting

Test gastric emptying with radioactive marker

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

Dumping syndrome

A

Rapid gastric emptying

Large food particles delivered to SI and hard to digest

Osmotic gradient into lumen and osmotic diarrhea

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

Early vs late dumping

A

Early: Soon after eating
GI symptoms and vasomotor symptoms: flushing, perspiration, tachycardia, hypotension

Late: Delayed onset. Hypoglycemia, sweating, hunger, weakness, confusion, syncope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Intestinal Pseudo obstruction

A

Rare disorder

Repetitive/continuous symptoms of bowel obstruction

Dilated bowel in absence of lumen occlusion

Abdominal distention, bilious vomiting, Const/Diar

Absence of ICC’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Functional gastrointestinal disorders

A

Various disorders with combo of ab pain/discomfort and changes in bowel habits

Functional heartburn
IBS

Typical symptoms, normal PE, absence of alarm symptoms (GI bleed, fam history of colorectal cancer, weight loss)

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

IBS

A

Irritable Bowel Syndrome

Recurrent Ab pain or discomfort at least 3 days a month with: improvement with defecation, change in stool frequency, change in stool appearance

IBS-C
IBS-D
IBS-M

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

Functional Dyspepsia

A

No structural abnormality

Epigastric pain, epigastric burning, early satiation, bothersome postprandial fullness

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

COnstipation

A

Infrequent bowel movements, passage of hard stools

Motility abnormality: Decrease in HPAC

Drug induced abnormality: Increase mixing contractions, decrease propagating contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Metoclopramide

A

Prokinetic agent

Antireflux, gastroparesis, anti emetic

UGI dopaminergic stimulation

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

Cisapride

A

UGI - prokinetic

Gastroparesis

5-HT4 agonist - enhance ACh release

Not used in US because of arrhythmias

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

Bethanechol

A

Prokinetic

Gastroparesis

Cholinergic agonist

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

Dumping syndrome treatment

A

Dietary manipulation

Medications (usually not necessary): PPI - slow digestion
Anti-cholinergic/octreotide - slow transit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Intestinal pseudo obstruction meds

A

Prokinetic:

Neostigmine

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

Physiological control of emesis (4)

A

Chemoreceptor zone: 5HT4, D2, NK1

Vestibular: H1, Muscarinic

Cerebral cortex

GI: 5HT3, D2, NK1

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

CNS anti emetics

A

Phenzothiazines

Ethanolamines

Piperazines

Cannabinoids

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

ANS antiemetics

A

Anti-cholinergics

80
Q

CNS and ANS anti emetics

A

Metoclopramide

Ondansetron - selective hHT3 antagonist

81
Q

IBS drugs

A

Antismasmodics

Tricyclic antidepressants

SSRI’s

Bulk forming laxatives

Antimotility agents

5HT3 antagonists

5HT4 agonists - cisapride (not in US)

82
Q

Sympathetic Route 1

A

Preganglion fiber –> white ramus –> paravertegral ganglion –> synapse –> gray ramus –> postganglionic axon

83
Q

Sympathetic Route 2

A

Preganglion –> white ramus –> travel up/down paravertebral ganglion –> synapse –> gray ramus –> postganglionic axon

84
Q

Sympathetic route 3 (Thoracic)

A

Preganglion –> white ramus –> synapse –> splanchnic nerve to target

85
Q

Sympathetic route 4

A

Preganglion –> white ramus –> splanchnic nerve to target organ –> synapse on organ

86
Q

Aortic plexus

A

Pre/post ganglionic sympathetic fibers
Prasympathetic fibers
GVA’s

87
Q

Superior hypogastric plexus

A

Formed from aortic plexus that juts out at bifurcation

88
Q

Right and Left hypogastric nerves

A

Bifurcation of superior hypogastric plexus at sacral promontory

89
Q

Pelvic splanchnic nerves

A

S2-4 intermediolateral cell column

90
Q

Inferior hypogastric plexus

A

Pelvic splanchnic + Hypogastric nerves

91
Q

Sacral Splanchnic

A

From sacral sympathetic chain

GVE

92
Q

Greater splanchnic nerve

Level, ganglion location

A

T5-9
Celiac ganglion
Foregut

93
Q

Lesser splanchnic nerve

Level, ganglion

A

T10-11

Superior mesenteric ganglion

94
Q

Least splanchnic nerve

A

T12

Aorticorenal ganglion

95
Q

Salivary Acini HCO3 secretion (channels)

A

NKCC = solute entry
Cl + HCO3 co transport exit
Water goes through

96
Q

Salivary Duct HCO3 secretion

A

N/K ATP-ase

HCO3/Cl exchange
Bicarb out, Cl in

Na/K exchange on luminal side

Hypotonic KHCO3 fluid

97
Q

High flow - salivary secretion

A

Only Acinar

98
Q

Low flow - salivary secretion

A

Duct equilibrium

Hypotonic fluid

99
Q

Oxyntic gland

A

Mucus/HCO3

HCl/Intrinsic factor

Pepsinogen

100
Q

Pyloric Gland

A

Mucus/HCO3

Gastrin/Somatostatin

101
Q

Gastric bicarb secretion (channels)

A

Blood CO2 + H20 –> H + HCO3

HCO3/Cl luminal exchange

102
Q

Mucus secretion and protection

A

Mucins and bicarb secreted, cross links with secreted bicarb

Protect stomach lining

Buffers H and blocks pepsin

103
Q

Gastric gland components

A

Chief cell

Parietal cell

104
Q

Chief cell

A

Secretes pepsinogen

105
Q

Parietal cell secretions

A

HCl

Intrinsic factor

106
Q

Parietal cell HCl secretory pathway

A

Gastric H,K-ATPase

H out, K in, K recycled by K channel

107
Q

Intrinsic factor

A

B12 binding protein between duodenum and ileum

Receptor mediated endocytosis and degradation of IF in ileum

108
Q

Haptocorrin

A

Salivary gland B12 binding protein

Degraded by pancreatic proteases

109
Q

Parietal cell HCl regulation

A

H,K-ATPase stored in vesicles

Signal pushes vesicles to membrane, can take time

110
Q

Transcobalamin II

A

Intestinal B12 binding protein

Binds B12 in ileal epithelium, transcellular transit across epithelium

111
Q

PGE2 and stomach protection

A

Increases protective measures: Mucus/bicarb secretion

112
Q

NSAIDS/H pylori and stomach protection

A

Reduce Bicarb secretion

113
Q

Nicotine/gastrinomas/H pylori

A

Increase acid secretion

114
Q

Regulation of acid secretion: ECL/Gastrin/Somatostatin/Pasaymp control

A

ECL: Release histamine, acts on parietal cell to increase H,K-ATPase activity

Gastrin: Regulates ECL
More H,K-ATPase in parietal cells

Somatostatin: Inhibits Gastrin

Parasympathetic ACh: Stimulates Gastrin, Parietal cell
Inhibits Somatostatin

115
Q

Duodenal Bicarb secretion

A

Electrogenic or Electroneutral NaHCO3 secretion

HCO3/Cl exchange
HCO3 channel

116
Q

Cholera toxin mechanism

A

Via cAMP: Stimulates Cl secretion into lumen, inhibits Na/Cl uptake into epithelial cell

Diarrhea

117
Q

Enterotoxin vs Cytotoxin

A

Enterotoxin: Biochemical alteration only

Cytotoxin: Morphological alterations

118
Q

Inflammatory vs non inflammatory diarrhea

A

Non inflammatory: Watery, no blood, dehydration

Inflammatory: Mucoid and bloody, ab pain, small volume

119
Q

Exocrine pancreas secretions

A

Acinar: 80% Enzymes/NaCl

Duct cells: 5%
NaHCO3/water

120
Q

Pancrease secretion and flow

A

high flow = ductal

Low flow = acinar

121
Q

Pancreatic bicarb secretion channels

A

HCO3/Cl exchange with Cl recycling

Carbonic anhydrase

122
Q

Pancreatic regulation by duodenum

A

Fat –> I cells –> CCK –> act on acinar cells –> stimulate protein secretion

Acid secretion –> S cells –> Secretin acts on duct cells –> bicarb secretion

123
Q

Gut tube embryological origin

A

Endoderm

124
Q

Secondary retroperitoneal structures

A

Duodenum
Pancreas
Ascending and descending colon

125
Q

Foregut, midgut, hindgut blood supply

A

Foregut: Celiac artery
Midgut: Superior mesenteric artery
Hindgut: Inferior mesenteric artery

126
Q

Ventral mesentery associated with….

A

Foregut

127
Q

Esophageal atresia

A

Blind ending esophagus

128
Q

Esophageal stenosis

A

Esophageal narrowing

129
Q

Esophagotracheal fistula

A

Esophagus connected to trachea

130
Q

Polyhydraminos

A

Cannot swallow amniotic fluid –> Buildup of amniotic fluid

131
Q

Stomach development

Vagal nerve location

A

Dorsal end grows (greater curvature)

Rotates 90 degrees so greater curvature is on left

Left vagal nerve becomes anterior, right becomes posterior

132
Q

Pyloric stenosis

A

Thickening of muscle that happens several weeks after birth

Palpable olive in RUQ, projectile vomiting

133
Q

Spleen mesenchymal location

A

Within dorsal mesegastrium

134
Q

Spleen development after stomach rotation

A

Spleen rotates to left

Divides dorsal mesogastrium into gastrosplenic and splenorenal ligaments

135
Q

Duodenal atresia

A

Vomiting with bile

Due to recanalization of duodenum

Double bubble sign

136
Q

Liver development

A

Grows into ventral mesentary, touches diaphragm

Separates ventral mesentery into falcoform ligament and lesser omentum

137
Q

Lesser omentum containsL

A

Hepatogastric ligament

Hepatoduodenal ligament

138
Q

Pancreas development

A

Ventral bud swings around right of duodenum, fuses with dorsal bud

Ducts connect and form main pancreatic duct

139
Q

Annular pancreas

A

Ventral buds rotate in opposite direction and constrict bile opening

140
Q

Greater omentum formation

A

Expansion of gastrosplenic ligament

141
Q

Midgut development

A

Primary intestinal loop herniates into umbilical cord –> 90 degree rotation (SI on right, LI on left) –> rotates 180 degrees and pulls back in

142
Q

Intraperitoneal viscera

A

Stomach
Jejunum/Ileum
Transverse colon
Sigmoid colon

143
Q

Omphalocele

A

Abdominal contents protrude through umbilical ring - normal herniation that doesn’t return to ab cavity

Contents covered by amniotic cavity/parietal sac

144
Q

Gastroschisis

A

Ab contents protrude through ab wall

NOT covered by parietal sac/ amniotic cavity

145
Q

Umbilical hernia

A

Less severe omphalocele

Ab contents protrude through umbilical ring to lesser extent

Covered by skin

146
Q

Non rotation

A

Absence of second 180 degree rotation

Left sided colon

147
Q

Reversed rotation

A

180 degree rotation in wrong direction

148
Q

Mixed rotation

A

All other rotational disorders

149
Q

Volvulus

A

Twisting of intestines around itself = obstruction/ischemia

150
Q

Ileal (Meckel’s) diverticulum

A

Incomplete regression of vitelline duct

Diverticulum, cyst, fistula

151
Q

Cloaca development

A

Primitive urogenital sinus and rectum

152
Q

Cloacal membrane development

A

Urogenital membrane

Anal membrane

153
Q

Formation of anus

A

Anal membrane mesoderm thickens and sinks in = anal pit

Anal membrane breaks down

154
Q

Anal agenesis

A

Anal pit fails to form

Most difficult to fix

155
Q

Imperforate anal membrane

A

Failure of anal membrane to breakdown

156
Q

Anal stenosis

A

Incomplete breakdown of anal membrane

157
Q

Lesser sac formation

A

Liver swings to right and decreases space

Lesser sac behind stomach because of stomach rotation

158
Q

Interdigestive period

A

MMC’s every 90min

Motilin initiates MMC

159
Q

Motilin regulation

A

Duodenal acid
Vagus stimulation

Initiates MMC/increase gastric emptyin

160
Q

Digestive period phases

A

Cephalic phase
Gastric phase
Early Intestinal phase
Late Intestinal phase

161
Q

Cephalic phase

A

Neuronal stimuli (thinking about food)

Salivary secretion
Acid release via gastrin
Pancreatic enzyme/bile secretion via gastrin

162
Q

Gastric phase

A

Gastrin increases = Acid secretion into stomach

Lower salivary secretion

163
Q

G17 vs G34 Location & difference in food states

A

Antrum: G17
Duodenum: G34

Fasting: G34 > G17
Post prandial: G17 = G34

Food = G17 increase

164
Q

Gastrin regulation

A

Gastrin releasing peptide (Parasymp control)

Peptides/AA/Calcium

Somatostatin (-)

Low pH (-)

165
Q

Early intestinal phase

A

Low Gastrin and Motilin
More Secretin, CCK, Incretins

Fed motility pattern: Short peristaltic waves + segmentation to mix

166
Q

Secretin

A

Released from S cell in response to acidic environment

Act on Pancreas, release HCO3 from duct

167
Q

CCK

A

Need to be sulfonated and amidated to function

Gall bladder contraction/S o Oddi relaxation

Pacreatic release of enzymes from acinar cells

168
Q

Monitor peptide

A

Actively digested by proteases/lipases

No proteases/lipases = active monitor peptide = stimulation of I cell and CCK release

169
Q

Incretins

A

GLP-1
GIP

Luminal glucose releases into blood –> plasma glucose induces incretins to release insulin from pancreas

170
Q

Late intestinal phase

A

Food enters colon
Decrease CCK/Secretin
Bile salts recaptured
Motilin and MMC return

171
Q

Adenocarcinoma of esophagus

A

Distal esophagus

Associated with Barrett, dysplasia, reflux esophagitis

172
Q

Low grade dysplasia

A

Increased proliferation

Increased N:C ratio

173
Q

High grade dysplasia

A

Loss of nuclear polarity

Bizarre glandular architecture

174
Q

Squamous cell carcinoma

A

90-95% esophageal cancers

Alcohol, smoking, diet, HPV

175
Q

2 Histological types of gastric cancer

A

Intestinal: Differentiated, chronic gastritis, high risk areas

Diffuse: Less differentiated, de novo, Signer ring cells

176
Q

GIST

A

Gastrointestinal stromal tumor

Stomach>SI>other

ICC?

177
Q

PUD drug combinations

A

Clarithromycin+amoxicillin/metronidazole + PPI

Clarithromycin + tetracycline + PPI

178
Q

Antacid types

A

Aluminum
Magnesium
Calcium

179
Q

Aluminum antacid

A

Least potent
Constipation
Phosphate binder

180
Q

Magnesium antacid

A

Most potent, diarrhea, hypermagnesemia

181
Q

Calcium antacid

A

Rapid, constipation, hypercalcemia/alkalosis

Good Ca supp

182
Q

H2 antagonists

A

Cimetidine: P450 inhibitor - drug interactions

CNS side effects

183
Q

Misoprostil

A

Stimulates PGE2 receptors

Inhibits acid secretion, promotes bicarb/mucus secretion

Limited to active PUD

184
Q

Sucralfate

A

Combines with protein exudate to form barrier around ulcer base

Minimal side effects

185
Q

PPI

A

Omeprazole

186
Q

GERD drugs

A

Metaclopramide
Cisapride
Bethanechol

187
Q

Neonate bilious vomit –> Few dilated loops = ?

A

Proximal bowel obstruction - UGI

188
Q

Neonate bilious vomit –> Many dilated loops = ?

A

Distal bowel obstruction - Enema

189
Q

UGI –> Duodenal obstruction/corkscrew

A

Midgut volvulus

190
Q

Midgut volvulus scan characteristics

A

Doppler flow

SMA/SMV switched

191
Q

UGI –> double bubble

A

Duodenal atresia

192
Q

UGI –> multiple bubble

A

Jejunal atresia

193
Q

Enema –> small distal w/ size transition

A

Hirschsprung disease

194
Q

Enema –> small colon w/ abrupt end

A

Colonic atresia

Very dilated loops

195
Q

Enema –> micro-colon/pearls on a string/abdominal distention

A

Meconium ileus

Cystic fibrosis

196
Q

Enema –> micro colon/TI abruptly ends/failure to pass meconium

A

Ileal atresia

197
Q

Enema –> Colitis/micro colon/Looks like a fucking disaster

A

Total Hirschsprung disease

GI/Endo/Repro (8 decks)

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