Exam 1 Choudhury Review Flashcards
(163 cards)
1
Q
smooth muscle
A
one nucleus
unstriated
dense bodies present**
no troponin
has calmodulin
2
Q
mechanical connections
A
dense bodies
3
Q
electrical connections
A
gap junctions
4
Q
varicosities
A
axon swelling at each contact point
5
Q
smooth muscle innervation
A
both S and PS
lots of receptors for NT and hormones
6
Q
multi unit smooth m.
A
one nerve to each nerve cell
-finer motor control
7
Q
single unit smooth m.
A
one nerve to many muscle cells
-in visceral smooth m.
coordinated contraction
8
Q
graded slow wave
A
action potential possible
-not always cause AP
9
Q
interstitial cells of cajal
A
pacemaker of GI
-between long and circular muscles of muscularis externa layer
generate slow wave potentials
10
Q
slow wave potential
A
oscillation without contraction or reaching threshold
11
Q
depolarization of GI tract
A
slow Ca channels with slow inactivation
always ongoing cycle of contraction**
12
Q
action potential spike
A
Ca influx and K eflux
13
Q
3 major pathways to increase Ca
A
both extracellular and intracellular Ca
Ca rushes in from extracellular
binds to SR and releases intracellular Ca (CICR)
1 voltage gated
2 SR (voltage independent)
3 store-operated Ca channels (SOCs)
-also voltage independent
14
Q
pharmacomechanical coupling
A
hormones and neurotransmitters can initiate increased Ca via G-protein coupled receptors (voltage independent)
15
Q
Ca2+ excitation contraction coupling
A
phosphorylation of myosin in thick filament
- uses less ATP
- sustained contraction
16
Q
Ca2+ binding calmodulin
A
forms CaM - activates MLCK
MLCK phosphorylates myosin
increased ATPase activity
17
Q
latch state
A
maintain tension of smooth m. without fatigue
-low ATP consumption
18
Q
intrinsic nerves in GI?
A
submucosal and myenteric
S and PS innervation
19
Q
GI hormones
A
gastrin, secretin, CCK, GIP
-paracrines - somatostatin and histamine
20
Q
extrinsic neves in GI?
A
autonomic nerves
21
Q
Ach
A
parasympathetic
increased causes:
salvation, lacrimation, urination, contraction, GIT motility, defecation
decreased causes:
dry mouth, urine retention, constipation
22
Q
increased parasympathetic activity
A
promote digestive and absorptive processes
increases motility and secretions
23
Q
4 GI regulatory mechanisms
A
autonomic smooth m.
extrinsic nerves
intrinsic nerve plexuses
GI hormones
24
Q
sympathetic innervation of GI
A
promotes decreased motility and secretion, increased sphincter constriction
25
enteric nervous system
divisions of ANS
-PS and S to GI tract
intrinsic neural control
26
myenteric plexus
auerbachs - between long and circ muscle layers of muscularis externa
27
submucusal plexus
meissners - submucosa
28
auerbachs plexus
motility of GI smooth muscle
29
meissners plexus
secretion and blood flow
30
all GI hormones?
peptides
31
classification of GI hormones
endocrine
paracrine
neurocrine
32
5 GI peptide hormones
```
secretin
gastrin
CCK
GIP
motilin
```
33
candidate GI peptide hormones
pancreatic polypeptide
neurotensin
substance P
34
secretin
increased acid HCl is stimulus
increases pancreatic bicarbonate secretion
35
gastrin
increased by histamine
36
CCK
increased pancreatic enzyme secretion
37
GIP
inhibits gastrin secretion
| -increases insulin release
38
motilin
increases upper GI mobility (during fasting)
39
gastrin secretion
after a meal
- increase in gastric acid secretion
- antrum and duodenum
40
duodenum/jejunum secretions
secretin, CCK, GIP, motilin
41
histamine
paracrine
42
AcH
non-peptide neurocrine
43
natures antacid
secretin
44
secretin affects
released response to decreased pH
more pancreas and liver bicarbonate
decreased gastric emptying
increased pancreas growth
decreased gastrin release
45
gastrin affects
from G cells in gastric mucosa, duodenum and pancreas
-increased in response to high protein, Ca, decaf, wine
increases parietal cell HCl secretion directly and through histamine (from ECL cells)
increased gastric mobility
increased acid has negative feedback
increased GI mucosa growth
46
inhibitors of gastrin release
secretin and glucagon
47
CCK affects
```
released duodenum and jejunum
increased response to protein and fats
increased gallbladder contractions - increased bile
increases pancreatic bicarbonate
increases pancreatic growth
```
48
GIP affects
insulinotropic hormone
increased response to fat, protein, and GLUCOSE
decreases gastrin
increases insulin
49
motilin affects
every 90 seconds
in upper small intestine due to fasting or acid/fat
MMC
increased gastric and upper GI mobility
50
CCK vs. gastrin?
can activate eachothers receptors
51
enteroglucagon affects
increased with fat
pancreatic alpha cells
increase insulin and gastric secretion
delay gastric emptying
52
pancreatic polypeptide affects
increased with protein, fat, glucose
decreased pancreatic bicarb/enzymes
53
peptide YY
increased with fat
decrease gastric secretion and emptying
decrease intestine mobility
54
substance P
increase intestinal motlity and gallbladder contraction
neurocrine
55
neurotensin
increases glycogenolysis and decreased insulin and increase glucagon
neurocrine
56
VIP
relax intestine smooth m. and vascular smooth m.
vasodilates - NO
57
bomberin
vagal stimulation
| increases gastrin
58
enkephalin
increased opiate receptors and sphincter contractions
treat diarrhea***
59
somatostatin affects
decrease gastrin and decrease acid
60
histamine
ECL cells
increase with gastrin
increase parietal cell HCl secretion
61
H2 receptor blocker
antacid
| -blocks histamine receptors on parietal cells
62
zollinger ellison syndrome
non-beta cell tumor of pancreas or duodenum
increased gastrin
-ulcers, diarrhea, hypokalemia
aka gastrinoma
need high protein meal, IV Ca and secretin infusion
63
pancreatic cholera
increased VIP
-cancer of pancreatic islet cells
increase diarrhea
give fluids and electrolytes
64
saliva
hypotonic (active process)
65
alpha amylase
not essential
| -alpha 1-4 bonds of carbs
66
salivary regulation?
rate only affected by neuronal
hormonal affects composition
67
can you taste protein?
no
68
lysozyme
antibacterial
69
lactoferrin
chelates iron (antimicrobial)
70
lactoperoxidase
antibacterial
71
glycoprotein of IgA
against virus/bacteria
72
EGF/NGF
mucosal growth
73
kollikrein
activate bradykinin
increased blood flow to glands
74
bicarbonate
no tooth decay
neutralizes acid
75
salivon
functional unit secreting saliva
76
reabsorption in salivon?
reabsorb Na and Cl
| secrete K and HCO3
77
plasma
high Na Cl
| low K HCO3
78
low rate saliva
hypotonic and high K
79
high rate saliva
increased osmolality, increased HCO3-, alkaline, and increased Na
80
Na reabsorption
apical - Na enters ENaCs epithelial sodium channels
| basolateral - actively pumped out Na/K ATPase
81
Cl- reabsorption
apical - Cl enters Cl HCO3- exchanger
| basolateral - Cl- exits through Cl- channels
82
HCO3 secretion
Cl HCO3- exchanger
83
H2O in salivon
cannot be reabsorbed
| -tight junctions
84
K secretion
Na K ATPase
85
content of saliva in acini
H2O, Na, Cl, K, HCO3, amylase
86
hormonal control of saliva
ADH and aldosterone
| regulate composition
87
sympathetic saliva control
alpha beta receptors
88
parasympathetic saliva control
M3 receptors
89
increased activity saliva
smell, taste, sound, sight, spicy sour
90
decreased activity saliva
sleep, fear, ANTI-DEPRESSANT, dehydration, fatigue
91
drooling
increased nervous stimulation
treat with anticholinergics or remove sublingual gland
92
xerostomia
dry mouth with decreased saliva production
drugs, radiation, autoimmune
93
sjogrens syndrome
dry moth AND DRY EYES
- glandular atrophy
- also affects lacrimal glands
94
digoxin
increased Ca and K in saliva
95
addisions
increased Na in saliva
96
cushings
primary aldosteronism
decreased Na in saliva
NaCl is zero**
97
parkinsons
increased saliva
98
stomach secretions
proximal - HCl, pepsinogen, intrinsic factor, mucus, bicarb, water
distal - gastrin, somatostatin
99
intrinsic factor
for Vit B12 absorption in ileum
-aka cobalumine
needed to survive**
100
chief cells
pepsinogen and renin
101
ECL cells
histamine
102
G cells
gastrin
103
D cells
somatostatin
104
oxyntic gland
fundus and body of stomach
-parietal cells
-peptic (chief) cells
mucous cells
105
parietal cells
HCl and intrinsic factor
106
pyloric gland
antrum and pylorus
| -G cells and mucous cells
107
stomach mucosa
regenerated every 3 days
108
non parietal cell secretion
low rate
high Na and Cl
low H and K
109
parietal cell secretion
after a meal
high rate
high H and Cl
low Na and K
110
alkaline tide
venous blood leaving GI is alkaline
because bicarb dumped to blood and H+ goes to stomach (H/K ATPase)
111
direct affects on parietal cells
AcH from vagus to M3 receptors
histamine from ECL cells to H2 receptors
gastrin from G cells to CCK receptors
all increase acid secretion
112
indirect affects on parietal cells
AcH to M3 receptors on ECL causes histamine release
gastrin on CCK receptors on ECL causes histamine release
histamine then acts on parietal cells to increase acid secretion
113
cephalic phase
in head 30%
| via vagus
114
gastric phase
in stomach 50-60%
| food distending gastric mucosa
115
intestinal phase
in intestine 10%
| peptides in duodenum
116
acid release
AcH - neuronal
gastrin - hormonal
histamine - paracrine
117
somatostatin
inhibits G cells from producing gastrin
118
GIP
inhibits gastrin and acid secretion from parietal cells
119
secretin
decreases both gastrin and acid
nature antacid
120
3 duodenum hormones inhibiting acid secretion
secretin
GIP
CCK
121
secretin
too much acid food in duodenum
122
CCK
too much fat/protein
- increased pancreatic secretion
- increased gallbladder contraction
123
vagotomy
cut vagus nerve
inhibit gastric acid secretion
used to treat peptic ulcers
selective - cutting vagal nerves to parietal cells only
124
pepsinogen
secreted by chief cells
| stimulated by ACh, histamine, gastrin/CCK
125
intrinsic factor
from parietal cells
| necessary for absorption of vitamin B12
126
vitamin B12
needs intrinsic factor to bind to cubulin
127
mucus secretion
by surface cells
forms layer with bicarbonate
no acid damage to mucosa
128
if acid to gastric epithelium
destroys mast cells - histamine
| results in inflammation
129
agents damaging mucosal damage
alcohol
salicylates
h pylori
bile acids
130
ulcer formation
h pylori, NSAIDs (COX-1 inhibitor), stress
131
aspirin
weak acid - easily absorbed in low pH of stomach
breaks protective mucosal barrier
132
peptic ulcer disease
```
gastric ulcer
duodenal ulcer (much more)
```
133
h pylori infection
gastric ulcer disease
134
gastrinoma
cancer of stomach
- aka zollinger ellison syndrome
- increased gastrin secretion
results in gastric ulcer disease
135
gastrinoma
gastrin levels initially high
136
atrophic gastritis
lack parietal cells
| lower levels of gastrin initially
137
h pylori
gram negative bacteria
damages mucosal barrier layer
138
H2 receptor blockers
rantidine
cimentidine
decreases histamine activation of parietal cells
-increased gastric pH
139
proton pump inhibitor
omeparazole
makes it more alkaline (increases gastric pH)
140
antibiotics
clarithromycin
| cymoxicillin
141
side effects of PPIs
pneumonia
C difficle growth
osteoporosis
142
dicyclomine
AcH inhibitor
| -not very good
143
acinar cells of pancreas
pancreatic enzymes
144
ductal cells of pancreas
aqueous NaHCO3 solution
145
pancreas innervation?
inhibited by S
| stimulated by PS
146
stimulated ductal cells of pancreas
secretin - in response to too much acid
147
major protease in pancreatic juice
trypsinogen
148
stimulates acinar cells of pancreas
CCK, ACh, secretin, VIP
all increase Ca
-activation of protein kinases increases acinar cell secretion
CCK directly and indirectly (PNS cholinergic paths)
149
acinar fluid
isotonic
150
ACh and CCK
stimulate NaCl secretion
| phosphorylates ion channels
151
secretin mechanism
duct cells
| secretin generates electrical gradient favoring NaHCO3 cotransport
152
lipase
triglyceride digestion
necessary for survival
153
amylase
starch, glycogen digestion
154
trypsin
protein digestion
155
procolipase
move bile salts from fat particles
-makes way for lipase to come and break down the triglycerides
156
trypsin inhibitors
in acinar and ductal cells to protect mucosa
157
enterokinase
activates trypsinogen to trypsin
located in brush border of duodenal mucosal
158
CCK release
stored in I cells
releasing peptide and monitor peptide
-stimulate CCK release
GRP and ACh stimulate monitor peptide release
these signaling molecules are peptide - so they will get digested and stops CCK release
159
secretin release
from S cells in duodenal mucosa
acid stimulates ductal cells
160
achlorhydric
cannot secrete gastric acid
no stimulus for secretin release
-results in duodenal ulcer
161
potentiation on acinar cells
CCK and VIP result in even larger increase
162
steatorrhea
fat in stool
early sign of pancreatic dysfunction
-due to low pancreatic lipase release
163
pancreatitis
enzymes of pancreas eat itself
could be:
cancer
alcohol
gallstone obstruction
