Exam 5- GI Flashcards

(300 cards)

1
Q

Four processes of GI

A
  1. motility 2. secretion 3. digestion 4. absorption
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2
Q

motility types in GI

A

propulsive moments- moves contents forward mixing movement- for absorption

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3
Q

pathway through GI

A

mouth esophagus stomach sm. intestine -duodenum -jejunum -ileum colon

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4
Q

lengths of duodenum, jejunum, and ileum

A

duodenum = 10 in

jejunum = 8 ft

ileum = 12 ft

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5
Q

Layers of Gi

A

serosa

longitudinal muscle

myenteric plexus

circular muscle

submucosa

submucosal plexus

muscularis mucosa

lamina propria

epithelium

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6
Q

longitudinal muscle

A

smooth muscle runs along the length of the of GI with contraction= GI shortens and widens

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7
Q

circular muscle

A

wrapping around the GI tract with contraction= constriction/lumen decreases in diameter

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8
Q

muscularis mucosa

A

thin muscle layer moves mucosal lining

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9
Q

lamina propria

A

a CT layer

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10
Q

enteric nervous system controlled by___

A
  • generats patterns of activity directly in gut (w/out CNS) -hormones from CNS modulate it
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11
Q

Enteric NS subsections:

A
  • Myenteric plexus
  • Submucous plexus
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12
Q

myenteric plexus

A

in walls of GI innervates muscle layers

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13
Q

submucous plexus

A

connects with myenteric

sensory function -irritation, distension

motor function -controls secretion

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14
Q

reflex arcs of GI NSs

A

changes in pH shape etc are sensed by receptors (i.e. mechanoreceptors, Cosmo receptors)

—->send to enteric NS (local effects)

and

—-> CNS = (-) or (+) SNS/PSNS which affects enteric NS

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15
Q

gastrin

A

secreted by stomach in response to ingested protein (+) gastric motility

(+) gastric secretion

(+) secretion of HCL and enzymes

(+) ileal motility (move food so we have room for new food)

(+) gastroileal reflex

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16
Q

gastroileal reflex

A

food in stomach (+) motility of ileum (+) opens illeocecal sphincter

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17
Q

secretin

A

secreted by duodenum in response to acid

-neutralizes stomach acid

(-) gastric motility and secretion to slow food entering duodenum

(+) HCO3- from pancreas and liver to neutralize acid

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18
Q

cholecystokinin (CCK)

A

secreted to duodenum in response to fat or protein

(-) gastric motility and secretion

(+) secretion of pancreatic digestive enzymes

(+) bile release from gall bladder

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19
Q

glucose-dependent insulinotropic polypeptide (GIP)

A

secreted by duodenum in response to glucose

(-) gastric activity… motility and secretion for absorption

(+) insulin release

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20
Q

enterogastrones =

A

secretion CCK and GIP

decrease gastric motility and secretion increases sm. intestine motility and secretion

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21
Q

Interstitial Cells of Cajal (ICCs)

A
  • not neurons or sm. muscle but have sm. muscle qualities..
  • have gap junctions

=PACEMAKERS OF GI SYSTEM

  • spontaneously active, constantly generating signals
  • connected to myenteric plexus, smooth muscle and neural plexuses
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22
Q

slow waves

A

-take many seconds -different activity in different sections of GI

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23
Q

slow waves => contraction via___

A

hormones can make slow waves stronger resolution in an AP -endogenously generated (don’t need CNS)

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24
Q

GI Motor Neurons

A

makes sm. muscles more susceptibe to contract when it’s stimulated by a slow wave

-motor n. fires = some depolarization

∴ with slow wave = CONTRACTION

-can also drive secretions, (+) varicosities to release hormones

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25
Excitatory GI Motor Neurons
Excitatory Junctional Potential - Ach - Substance P
26
Inhibitory GI Motor Neurons
Inhibitory Junctional Potential - VIP= vasoactive intestinal peptide - NO when activated= physiological ileus (lack of contraction)
27
propulsive segment in peristalsis has ____ contracted
circular muscle
28
receiving segment of peristalsis has ____ contracted
longitudinal muscle
29
power propulsion
specialized rapid long distance movement -normal in large intestine, pathologic in sm. intestine
30
sm. intestine power propulsion
-used when there is an irritant we want to get out
31
power propulsion mechanism
32
segmentation (mixing) where does this happen??
in duodnum and colon - mixing in enzymes - food is not forward movemtn just moving back and forth
33
sphincters
=physiological valve - ring of smooth uscle - normally in a contractie state
34
upper esophageal sphincter
stops us from swallowing air =striated muscle
35
lower esophogeal sphincter
protects esoph. from H3O+ =smooth muscle
36
acinar gland secretions diagram
put diagram here pg 4 of gi secretiosn
37
myoepithelial cells
=contractie -\>more saliva into ducts
38
serous cells secrete? found where?
=\>amylase from zymogen granules -found in mouth and esophagus
39
ducts in mouth and esophagus secrete
HCO3- and K+
40
salivary amylase (ptyalin)
starts digestions of carbs
41
lingual lipase
metabolizes some fat | (in saliva)
42
mucins
in saliva lubrication for swallowing
43
saliva functions
digestion (minor) lubrication neutralize acid (HCO3-) solvent for taste aids in speech water balance (dry mouth (+) thirst)
44
rugae
longitudinal folds in stomach allow it to exapand
45
stomach functions
- reservoir for food - antral pump= mixes and propulses food
46
stomach anatomic regions vs functional regions
47
slow wave= AP where?
Stomach
48
diagram of stomach AP
49
gastric retropulsion
in stomach =backwards jet of contents towards the corpus -a few of these a minut during digestion breaks up food
50
chyme
semifluid substace that exits the stomach
51
cardiac glands of stomach
=mucous cells - near lower esoph. sphincter - protective
52
pyloric glands of stomach
=Gcells -secrete gastrin --(+)--\>stomach activity and secretion
53
oxyntic glands of stomach
mucous cells =\>mucus parietal cells =\> HCl and intrinsic factor chief cells =\> pepsinogen
54
HCl secreteion mechanism
55
alkaline tine
=secreting H+ to stomach HCO3- to blood
56
Regulation of HCl secretion
PSNS ---(+)----\> secretion ACh, gastrin, and histamine all (+) gastric secretions
57
cephalic phase of gastric secretion
thoughts, smell, taste, chewing, swallowing increase HCl and pepsinogen (preparing to eat, but no food in stomach)
58
gastric phase of gastric secretion
-food is in the stomach protien and stretching of stomach --(+)--\> increase in HCl, pepsinogen and gastric secretion
59
intestinal phase of gastric secretion
**decreased** HCL, pepsinogen **increased** secretion of enterogastrones (HCO3-, and enzymes)
60
pepsinogen activation
61
gastric juice functions
digestion-pepsinogen bacteriocidal- low pH supplies intrinsic factor
62
intrinsic factor
needed to absorb vit. B12 -without B12 pernicious anemia
63
hepatic portal circulation pathway
64
kupffer cells
in liver ~macrophages
65
siver sinusiods
highly permeable discontinuous capillaries
66
bile compostion
bile salts =detergents for fat digestion phospholipids bicarbonate cholesterol (an way to excrete extra) bilirubin (product of heme metabolism)
67
emuslification of fat
detergents keep fat in emulsion-surround droplet of fat -cholesterol nonpolar/polar... polar is outside, nonpolar faces lipases
68
pancreas function
mostly exocrine only 1-2% endocrine
69
sphincter of oddi
CCK ---(+)---\> relaxation of sphincter =release of pancreatic juice
70
coposition of pancreatic juice
bicarbonate - neutralizes stomach H3O+ proteases - protien metabolism pancreatic amylase - carbohydrate metabolism pancreatic lipase - fat metabolism
71
cephalic and gastric phases affect pancreatic secretion
small increase in secretion
72
intestinal phase and pancreatic secretion
large increases in secretions -contents are entering duodenum
73
Migrating motor complex (MMC)
=house keeping function - propagating wave of contraction that moves form antrum to ileum in ~90-120 min - clears out anything left in stomach/intestines - activity repeatively sweeps through sm intestine and continues to move to colon
74
small intestine secretions are from\_\_\_ which have these types of cells:
from the crypts of lieberkuhn =gastric glands contain: goblet cells epithelial stem cell paneth cells
75
goblet cells secrete what? where are they found?
mucus in the SMALL intestine
76
epithelial stem cells importance found where\_\_\_\_
found in SMALL intestine - high turnover of cells in GI, need to be replaced - also easily affected by radiation
77
paneth cells
in small intestine secrete anti-microbial peptides
78
ascending colon food duration
food only stays for a short amount of time
79
transverse colon food duration
food stays here for a while and dehydrates
80
descending colon food duration
short transit time
81
haustrations
mixing movements similar to sm. intestine but slower
82
power propulsion
can be pathological, but usually normal 3-4 times a day, associated with defication
83
gastrocolic reflex
increased activity in colon associated wiht eating
84
colon stores food\_\_
for 24-48 hrs trying to dehydrate it
85
defecation process
rectal disention triggers mechanoreceptors **defecation reflex:** contraction of rectum -\> relaxation of internal anal sphincter -\> peristalsis in sigmoid colon
86
Colon secretions
mucus bicarbonate (neutralize H+ from fermentation)
87
colon reabsorption
water and electrolytes (Na+ and Cl-)
88
colon gas
nitrogen from swallowed air bacterial fermation of undigested poly saccharides= CO2, CH4, H+, H2S,
89
esophagus mechanical obstruction causes
1. congential malformations - agenesis (absence) or atresia 2. stenosis (narrowing)
90
achalasia
-a form of functional obstruction =incmplete relaxation and increased tone in the lower esophageal sphincter and esophagel aperistalsis primary= congenital secondary= from something else like diabetes
91
esophageal varices
veins in the lower third of the esophagus drain into the hepatic portal vein - w/ hypertension = channels between the portal system and venous circulation - varices=swollen, associated with serosis can rupure -\>hematemesis (vomiting blood)
92
esophagitis caused by
**1. Mallory-Weiss tears** = esophagus is overly relaxed and then vomiting causes tears 2. chemicals (heavy alcohol/hot liquids) 3. infections
93
Gastroesophageal Reflux Disease
- esophageal sphincter doesnt work as it should- acid from stomach afects lower esophagus - middle aged people most commonly - causes esophageal ulceration, hematemesis, strictures, and barrett esophagus
94
barrett esophagus
premalignant condition associated with GERD - leads to adenocarcinoma - reddish patches or tongue-like projections of mucosa, above the gastroesophageal junctiona nd metaplastic gastric mucosa - start getting goblet cells
95
esophageal adenocarcinoma
usually in distal 1/3 of esophagus - flat lesions or large invasive masses - clinical features=pain difficulty swallowing, weight loss, vomiting - 5 year outlook is not good
96
esophageal squamous cell carcinoma
- affects more men than women - associated with hot beveridges, smoking and alcohol - half occur in the middle third of the esophagus - can become large masses that may obstruct the loumen or invade surround tissues (lungs aorta) clinical features=pain difficulty swallowing, obstruction, weight loss -5-year survival =10%... due to late detection
97
acute gastritis
inflamation of stomach - casues temporary pain, nausea, and hematemsis (vomiting blood) - melena= black, tar-like feces from blood - proctective mechanisms (HCO3- and mucus) have been overwhelmed, usually from drugs (NSAIDS)
98
acute peptic ulceration
- penetrating mucosal layer from long term NSAID use and stress - causes pain, nausea, and vomiting - pain releaved when eating
99
cushing ulcer
with a head injury = excessive vagal stimulation and too much gastric acid secretion =\> ulcer
100
chronic gastritic
ulcers usually caused from helicobacter pylori that colonize the stomach and cause excessive acid secretions - in stomach and duodenum - can find Ab to h. pylori in pts
101
autoimmune gastritis
Ab to parietal cells normally parietal cells =\> HCl and IF ∴ disease = low acid and pesinogen secretion
102
peptic ulcer disease
due to H. pylori, and NSAIDS - worsens with stress, smoking, and alcohol abuse - 4X more common i nduodenum - could cause hemmoraging - "coffee ground vommitting"- from blood and tissue being brokend down - perforration (from acid/pepsin) and scarring
103
gastric polyps
=nodlule that projects to surrounding tissue ## Footnote types: _1. inflammatory polyps_ _2. gastric adenomas_ -both related to gastritis (∴ in mid. aged ppl) _3. gastric adenocarcinomas_- chronic risk of chronic gastritis (delayed discovery = \<30% survival)
104
adhesions
scar tissue btw two loops of GI tubes causes them to not move as they should -usually after surgery
105
volvus
twisting of intestine cause a section to be cut off from the rest (loop)
106
intussusception
part of intestine "telescoped" in on itself
107
strangulation
-from herniation, adhesions, volvus or intussusception =loss of bloodflow =EMERGENCY... needs surgery
108
hirschsprung disease
="congenital aganglionic megacolon" - from improper development of enteric NS - starts in rectum and affects a variable amount of colon - MEGAcolon can't move well! =obstructive constipation
109
hemorrhoids
=dilated anal and perianal blood vessels - painful - often during pregnancy ~\> excessive straining or portal hypertensive = bright read blood (blood wasn't digested)
110
celiac disease
=gluten intolerance - immune reaction to gluten -with gluten = loss of villi= less absorption surface =diarrhea and weight loss
111
Diverticulitis
=ballooning pouches/diverticula form in colon - weaker tube btw tenia coli is stressed w/stool - occurs in \>60 yrs w/ low fiber diet - could rupture ...=papatenitus
112
inflammatory bowel disease
-from mucosal immune system reacting inapropriately (probably involves intestinal flora)
113
hygiene hypothesis
need to expose kids to pathogents to build immune system -aims to prevent inflammatory bowel disease
114
chron disease
a form of inflammatory bowel disease - can be found anywhere in GI - "skip lesions" and transmural lesions - causes diarrhea, fever, abd. pain, intermittent stress and diet can cause relapse
115
ulcerative colitis
a form of inflammatory bowel disease - limited to rectum and colon - always involves colon causes diarrhea, and pain -smoking can release symptoms
116
inflammatory polyps
= increased risk of cancer in colon
117
hyperplastic polyps
pts. \>50 yrs no malignant potential in colon
118
colonic adenomas
common above age 50 - can turn into adenocarcinoma ∴ we want to remove it - high fat diet contributes to this - can occur anywhere in the colon
119
colonic adenocarcinomas
most common GI tract malignancy #2 cancer killer (second to lung cancer) - happens anywhere in colon - causes anemia, bloody stool and cramping - if metastisized \<5% yr survival but, if lower stage could be 75% survival
120
carcinoid tumor in colon
a neuroendocrine tumor can release serotonin
121
coronoid syndrome
effects caused by carcinoid tumor in colon -causes flushing/sweating effects of NT
122
acute appendicitis
from an obstruction of the appendix -inflammation and pain in right lower quadrant with fever
123
most common tumor of the appendix
most common = carcinoid tumor
124
hepatic failure
=80-90% fxn lost chronic =most common
125
chronic hepatic failure
most common - jaundice, hypoalbuminemia, hyperammonemia, hypogonadism - fatal in weeks to months due to accumulation of toxins affecting multiple organ systems and impaired coagulation - nees a transplant
126
functions of bile
1. emulsification of afat 2. elimination of bilirubin, cholesterola nd highly lipid soluble foriegn substances (ie. drugs)
127
cholestasis
=impaired flow of bile
128
neonatal jauncice
-in newborns liver's ability to excrete biliruben hasn't been developed ∴ put babies uner ligts that breakdown biliruben in skin
129
hepatic encephalopathy
=CNS effects form liver failure due to high NH3 "amenemia" -mild brain dysfunction all the way to confusion, stupor, coma and death
130
cirrhosis
=fibrosis of the liver and abdominal changes in liver architecture =death of hepatocytes, deposition of ECM and vasculature changes =resistance to filtration = accuumulation in sinusoids =portal hypertension -initially may be asymptomatic, or cause weight loss, and weakness death is usually from liver failure, portal hypertension, or hepatocellulr carcinoma
131
portal hypertension
cirrosis is the most common cause increases resistance to filatration causes the hypertension
132
ascites (definition and pathogenesis)
=build-up of paritoneal fluid, jauncice, potbelly and esophogeal varicocities Pathogenesis 1. excess filtration through sinusiods due to sinusiodal hypertension and hypoalbuminia 2. increased hepatic lymph flow 3. Na+ and H2O retention by the kidneys due to high plasma aldosterone
133
splenomegaly
enlargement of spleen -culd rupture= hemorrhaging
134
hemochromatosis
=a build up of Fe in body \>1/3 accumulates in the liver common in men \>50 hemosiderin in organs triad: 1. abnormal brown color to skin 2. cirrosis 3. diabetes mellitus due to damaged beta cells
135
hemosiderin
a complex of iron and protiens
136
benign hepatic tumors
= caverous hemangioma (most common) =adenoma =hepatocellular carcinoma
137
cavernous hemangioma
=benign hepatic tumor -soft nodules full of blood
138
hepatic adenoma
benign hepatic tumor that may have malignant tumor
139
hepatocellular carcinoma
- benign hepatic tumor - associated with HBV or HCV infection, alcoholic cirrhosis, and exposure to aflatoxin - may be unifocal but usually massive tumor, multiocal tumor of diffuse infiltrating cancer - usually in pts with cirrhosis
140
cholelithiasis
=gallstones -may not have symptoms but pts have an "attack"= upper right quadrant pain types 1. cholesterol 2. pigmented
141
cholesterol stones
=most common -form with excessive secretion of cholestrol and bile
142
pigment stones
gall stones that contain billiruben form with excessive secretion of biliruben -dark color and radiopaque
143
cholecystis
=inflammation of gal bladder -needs to be rmoved
144
empyema
a form of acute cholecystitis gall bladder filled with puss
145
gangrenous cholecystis
a form of acute cholecystitis gall bladder is necrotic
146
acute calculous cholecystitis
=blockage of gall bladder duct leads to inflammation of gall bladder
147
symptoms of cholecystitis acute vs chronic
acute= pain in UR quadrant, cant digest fatty foods chronic= same as acute but less pronounced
148
carcinoma of the gallbladder pathogenesis?
-adenocarcinoma pathogenesis= gall stones (+) blockage (+) inflammation =predisposed to cancer dismal 5 yr outlook
149
acute pancreatitis
reversible inflammatory disorder - alcoholism or other inflammatory disorder causes this - morphology= microvascular leakage and edema, fat necrosis via lipases acute inflamation protelytic destrction and blood vessel damage... hemorrhage pathogenesis =activation of pancreatic enzymes causeing autodigestiion
150
chronic pancreatitis
most common cause = alcoholism morphology- fibrosis and acinar loss pathogenesis- unclear (maybe ductal obstruction from increased AA, toxic effects of alcohol acinar cells or oxidative stress) may be asymptomatic, or cause jaundice
151
pancreatic neoplasm types
serous cystadenoma mucinous cystic pancreatic adenocarcinoma
152
serous cystadenomas
pancreatic neoplasms fluid filled cysts most common after age 60 almos always benign abdominal pain
153
mucinous cystic neoplasms
pancreatic neoplasm mucous secreting cell adenoma 95% in women may lead to adenocarcinoma
154
pancreatic adenocarcinoma
pancreatic neoplasm 4th leading cancer killer 5 yr survival rate \<5% most pts over \>60 yrs usually silent until it impenge son another structure
155
GI has ___ to increase absorption \_\_\_
circular folds X 3 vili X 30 microvili X 600
156
starch
polysaccharide form plants most abundant carb in typical human diet
157
glycogen
polysaccharide from meat
158
cellulose
polysaccharide fromplant cell walls indigestible but provides fiber (keeps contents moving along)
159
sucrose
glucose-fructose
160
lactose
glucose-galactose milk sugar
161
maltose
glucose-glucose from malt
162
common monosacccharides in diet
glucose fructose galactose
163
mouth digestion
via salivary amylase -just starts digaestion
164
stomach digestion
fsalivary amylase is deactivated by low stomach pH so no digestion just mixing
165
small intestine digestion
does most of the carbohydrate digestion - pancreatic amylase =carb digestion - epithelial disaccharidases= break down disaccharrides in gut epithelium
166
sugar absorption
167
lipid types
triglycerides (90%) cholesterol phospholipids
168
lipid digestion mouth/stomach
via lingual lipase -just minor digestion
169
small intestine lipid digestion
via pancreatic lipase -emulsification then lipase has major role in metablolism
170
fat absorption
171
types of protien
protiens (\<100 AA) peptides amino acids
172
protien stomach digestion
VIA PEPSIN
173
small intestine protien digested via
**pancreatic enzymes** 1. trypsinogen 2. endopeptidases 3. exopeptidases **epithelial enzymes**
174
trypsinogen
activated by enteropeptidase to **trypsin** trypsin then activates other proenzymes
175
endopeptidases | (speicific types)
cleave **internal** peptide bonds =trypsin, chymotrypsin and elastase
176
exopeptidases
-cleaves **terminal** peptide bonds =procarboxypeptidases A & B
177
epithelial enzyes
in the wall of the duodenum cleave polypeptides to dipeptides, tripeptides, or amino acids
178
amino acid absorption
needs transpeptidases cant cross membrane
179
di- and tripeptide absorption
absorbed more efficiently thatn AA sometimes so these are "taken up" as well
180
protien absorption
usually don't want to absorb a straight protien it could cause an allergic rxn
181
fat soluble vitamins
A, D, E, and K
182
fat solluble vitamin absorption
easily cross cell membranes ∴ passively absorbed in the small intestine -can be toxic
183
water soluble vitamin absorption
passive and active processes in small intestine
184
vitamin B12 absorption
via intrinsic factor (secreted by parietal cells) -IF binds B12 an then is absorbed in ileum via transporter complex
185
intrinsic factor defficiency=
pernicious anemia =smooth shiny tongue
186
calcium absorption
1/3 is absorbed in the gut -transported by Ca2+ channels calbindin (Ca2+ binding protien) -stores Ca2+ and then is pumped out via ATPase
187
vitamin D and Ca2+ absorption
more of a hormone than a vitima -turns on gene expression of calbindin and Ca2+ ATPase
188
Fe absorption
important for heme - free Fe 3+ wil oxidize membranes - \>4,000 Fe 3+ stored in ferritin ∴ stays in epithelial cells - free Fe 3+ is transported out of enterocyte to blood by transport protien to transferin (binding protien in blood)
189
Ferratin
Fe binding protien in epithelial cells a way of excreting Fe bc enterocyts are often sloughed off =PRIMARY form of Fe regulation
190
Fe defficient affects gene expression
less ferritin (less excretion) more DMT (more absorption) (Bohr effect is DPG)
191
definition of gas exchange respiration
O2 from air and CO2 from cell sback out
192
trachea and bronchi have lots of\_\_\_\_\_\_\_
cartilage
193
conduction zone
no gas exchange =dead space -warms, humidifies, and removes junk from air trachea-\>bronchi-\>bronchiole
194
respiratory zone
-does gas exchange respiratory bronchiole-\>alveolus
195
Pleural pressure
=ALWAYS NEATIVE -chest wall wants to expand, and lungs want to shrink =keeps the lungs inflated
196
alveolar pressure if neg=\_\_ if pos=\_\_\_
negative = air fows in positive= air flows out
197
pneuothorax
hole in chest wall =air in pleural space Ppl goes to zero ∴ lungs collapsse and wall exapnds outward
198
with and increas in volume of the chest cavity = ___ of P in lungs
increase | (boyle's law)
199
normal inspiration mechanism=
contract diaphragm= it pulls down = increased volume of chest cavity = decreased P = air in
200
increased inspiration mechanism
contract external intercostal muscles adn accessory muscles in the neck =chest wall moves up and out =increased volum =decreased pressure
201
normal expiration mechanism
=passive diaphragm relaxation
202
increased expiration mechanism
= contract intercostals -\> pushes chest wall down and in = contract abdominals -\>pushes intestines up
203
during inspiration= pleural pressure\_\_\_ alveolar pressure \_\_\_ flow\_\_\_ total volume\_\_\_
pleural pressure= getting more negative alveolar pressure= negative flow= negative total volume= increases
204
during expiration pleural pressure\_\_\_ alveolar pressure \_\_\_ flow\_\_\_ tidal volume\_\_\_
pleural pressure= less negative alveolar pressure= positiv flow = positive (air out) tidal volume = decreasing
205
respiratory volumes and capacities
206
tidal volume=
normal breath 0.5 L
207
Inspiratory reserve volume
amount of air that can be inspire after normal inspiration
208
expiratory reserve volume
amount yo can breathe out after expiration
209
residual volume
= air you cant expire from lungs 1L
210
vital capacity
=total amount of air that can be moved = 5 L =TV+IRV+ERV
211
forced vital capacity
vital capacity as fast as possible normal =5L
212
obstructive disorder's effecton FVC and RV
FVC=3L RV= 3L (cant get air out) total =6L (ie emphysema - loss of alvoli and elastic recoil)
213
restrictive disorder's affect on FVC and RV
FVC= 3L RV= 1L total = 4L (cant get air in) -edema/fibrous tissue in lungs causes disorder
214
asthma
=episodes of reversible bronchial narrowig =primarily obstructive types 1. intrinsic (non-allergic/non-atopic)- due to stress/exercise 2. extrinsic (allergic/atopic)- due to inflammation, usually develops at a young age
215
extrinsic asthma mechanism
216
acute asthma
airway obstruction
217
chronic asthma
WBC accumulation =edema = increased mucus =hypersensitivity
218
COPD
=chronic obstructive pulmonary disease =5th leading cause of disease 1. chronic bronchitis 2. emphysema
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emphysema
="pink puffers" =normal O2 with increased breathing loss of alveoli adn elastic recoil =airways collapse (obstructive disorders) -proteases released
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proteases released during emphysema
1. elastase - destroys tissue 2. alpha 1 anti-trypsin- inhibits proteases (protects lungs)
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smoking's effect on lung proteases
(+) elastase (-) alpha1 anti-trypsin
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alpha1 anti-trypsin deficiency
a genitic disease ---\>pts develop emphysema
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chronic bronchitis
="blue bloaters" involves inflammation excess mucus-\> blocks airways = chronic cough
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draw cystic fibrosis issue
=mucus coating and airway blockage =bacterial infection!
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cystic fibrosis treatment
1. antibiotics and O2 for symptoms 2. gene therapy - hasn't been successfull - in 2012 therapy opens Cl- channel with a gating problem (4%)
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dead space | (name the two types)
inspired air not involved in gas exchange ## Footnote 1. anatomic= air in conducting space 2. alveolar= air in alveoli but no gas exchange
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total ventilation
amount of air moved/minute VT= (tidal volume)(frequency of breathing) (500)(12)= **6,000 mL/min**
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alveolar ventilation
amount of air moved that is involved in gas exchange/min Va=(tidal vol.-anatomic dead space)(freq. of breathing) =(500-150)(12) =**4200 mL/min**
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deep and slow breath vs shallow and fast?
deep and slow
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increase radius = ___ resistance
decrease (BIG TIME)
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greatest total resistance is in \_\_\_\_
large bronchi bc there are so few of them
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\_\_\_\_\_ are more important to airway resistance
bronchioles!
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PSNS and airway resistance controll
ACh (+) muscarinc R = AIRWAY CONSTRICTION at rest you dont need lots of O2
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SNS and Airway Resistance
Epi (+) **B**2 Receptor =AIRWAY DILATION
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Asthma treatment
=B2 agonist
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match airflow and bloodflow
with decreased CO2 = airway constriction
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increased compliance of lungs | (what diseases have this problem?)
=large change in V for a change in P =easy to inflate -emphysema- cant get air out
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decreased compliance
small change in volume for a change in pressure =hard to inflate - happens wiht restrictive disorders - work of lungs is increased
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surfactant
a lipoprotien decreases surface tension (-) alveoli from collapsing from type II alveolar cells made late in fetal development
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surface tension and radius
higher ST in smaller radii ∴ surfactant is more important and also works better in smaller radii lumens
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Total P of O2=
O2= PB x FO2 Barrometric P x Force of O2 =(760 mmHg)(0.21) =160 mmHg
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Partial pressure of inspired air=
PO2 = (PB-PH2O) x FO2 =(760-47) x (0.21) =150mmHg
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effects of high altitiude on partial P of ispired air
decreases it bc there's a decrease in total pressure PO2 = (380-47)(0.21) PO2 = 69.93
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the amount of gas dissolved in a liquid is proportional to \_\_\_
its partial pressure A LINEAR RELATIONSHIP
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things that will increase simple diffusion
1. increased surface area of membrane 2. increased diffusion coefficient - for gasses this is the amout dissolved 3. increasing the concentration gradient - for gasses this is the partial pressure difference 4. membrane thickness
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diffusion capacity
=the amount of gas the lungs can transfer to the blood
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two things that limit diffusion capacity (O2 transfer)
1. **perfustion limited**- diffusion capacity is limited by blood flow 2. **diffusion limited**- diffusion capacity is limited by the rate of diffusion ∴ to increase O2 in blood you need to increase bloodflow or increase the rate of diffusion
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in health getting O2 in blood is _____ limited
perfussion limited - becasue we reach equiliibrium always even if we increase the rate of diffussion so we should increase the rate of blood flow instead
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in circulatory system where is P high and low?
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pulmonary vascular resistance regulation
1. recruitment= open more capillaries 2. distension= increase radius of capillaries
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3 benefits of recruitment and distension
1. decreased resistance =no edema 2. decreased velocity of blood floow= more time for gass exchange 3. increased SA for gas exchange
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pulmonary vascular system is regulated by
hypoxia NOT autonomic NS
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when alveolus is blocked blood vessel\_\_\_
constricts
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at a higher altitude=
-decreased PO2 everywhere =general vasoconstriction =increased BP and work of heart
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atmosphere to lungs PO2 drops bc\_\_\_
1. H20 (humidifies) 2. its mixed with dead space air 3. its mixed with residual volume air PO2 160 to 105mmHg
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PO2 from alvolus to blood drops bc\_\_\_
shunting- some of the blood doesn't pass by alveoli, it passes other airways and it is at PO2 40 this mixed with PO2 105 yields PO2 100
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label the PO2 levels
160 105 100 100 \<40 40 40
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Dissolved O2 at PO2 of 100mmHg
0. 3ml O2/100ml of blood - this is a small amount
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at PO2 of 100mmHg there is ___ ml O2/100ml blood bound to Hb
20.1 =vast majority of O2 in blood is bound to Hb -doesnt contribute to PO2
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\_\_\_\_ is detected by chemoreceptors
dissolved O2, not bound to Hb
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- this is what is seen by the lungs - increasing PO2 doesn't saturate more Hb
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If PO2 drops to here... Hb is still nearly saturated
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PO2 =40
this is what's seen near normal tissue O2 IS COMMING OFF Hb Hb is at 75% saturation
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PO2 =25mmHg
what is seen near ACTIVE tissue =50% saturated Hb
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as O2 unbinds to Hb= \_\_\_\_ as O2 binds to Hb=\_\_\_\_
as O2 unbinds to Hb= Hb's affinity for O2 decreases as O2 binds to Hb= its easier to add O2
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Left shift happens when...
Left shift when P5O decreased (in an environment of high pH and low CO2 like lungs) =more O2 binds to Hg at a given PO2 ∴ we decrease DPG, CO2, temp and H+ (DPG is made by RBC during hypoxia/exercise)
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Right shift happens when...
P50 increases (in an environment of low pH and high CO2 like muscles) =more O2 comes off Hb at a give PO2 -we want this in active tissue ∴ increase PCO2, H+, temp, and DPG
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hypoxia=
insuficient O2 in the tissues
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diffusion impairment caused by
edema in the lungs
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diffusion impairment and decreased atmospheric PO2 cause\_\_\_ which is detected by ___ and causes \_\_\_\_
decreased O2 in arterial blood which is detected by chemoreceptors whic the (+) increased respriatory rate
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deficient RBC (anemia) causes =
less Hg ∴ less O2 -THIS IS NOT DETECTED BY CHEMORECEPTORS because amountof dissolved O2 is normal ∴ no stress is experienced
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CO poisioning
-causes less O2 to bind to Hb CHEMORECEPTORS WILL NOT DETECT THIS!! bc dissolved O2 levels are normal ∴ no stress is exprienced
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CO2 transported three ways:
1. 10% dissolved in plasma 2. 30% bound to carbamino protiens (Hb) 3. 60% bicarbonate ions CO2 + H2O \<=**CA**⇒ H2CO3 ⇔ H+ HCO3- (via carbonic anhydrase)
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Draw pathway of CO2 out of tissues with high CO2
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Haldane effect
when O2 binds to Hb ∴ less CO2 binds to Hb and is expired
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bohr effect
near active tissue there is high CO2 and H+ ∴more CO2 binds to Hb ∴ less O2 bound to Hb ∴ more O2 to muscles
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elements of the pulmonary system
**sensors:** detect changes - chemoreceptors - pulm. receptors in lungs **central controller:** region of brain that interprets sensory and directs resp. activity -in medulla (not well understood) **effectors:** -respiratory muscles (mostly the diapragm)
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\_\_\_ (+) inspiration
1. chemoreceptors detect high CO2, and H+ and low O2 2. pulmonary iritant receptors
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pulmonary stretch receptors
DO NOT inhibit normal inspiration (other brain centers do this) they ONLY protect against over inflation
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PO2 and PCO2 effects on respiraton
**PO2-** has to drop from 100 to 60 t stimulate breathing **PCO2-** any increase wil (+) breathing
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deep fast breathing =
decreases CO2 in blood ∴ you can hold your breath longer
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central chemoreceptors found \_\_\_ stimulated by\_\_\_ not stimulated by\_\_\_
in medla of brain ## Footnote **_stimulated by:_** 1. high CO2 in blood 2 high H+ in interstitial fluid **_NOT stimulated by:_** 1. high H+ in blood 2. low O2
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pathway of central chemoreceptor stimulation
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peripheral chemoreceptors
found in carotid and aortic bodies - measure arteiole blood - no BBB ∴ they detect blood's: high CO2 and H2O low O2
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slowly adapting pulmonary receptors
in lung bronchiole smooth muscle have the **Hering-Breuer reflex** =stops overinflation of lungs
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rapidly adapting pulmonary receptors
=irritant receptors respond to injury, inflammatin, touch, chemicals - complex effects (+) cough and some inspiration
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cheyne-stokes breathing=
deep-rapid breathing (over ventilation) then inhibits breathing ∴ (+) slower/stopped breathing ∴ (+) increased CO2 ∴ (+) deep rapid breathing again ="waxing and waning"
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cheyne-stokes breathing occurs in=
**1. 70% of people in heart failure** because: - not enough blood to chemoreceptors - (+) stimulation of pulmonary irritant receptors **2. people with brain damage** -respiratory centers damaged
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epiglottitis=
inflammation of the epiglottis -it swells and blocks to trachea =from injury or BACTERIAL infection tx: O2, antibiotics
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Laryngitis
= inflammation of the vocal cords =from overuse or VIRAL infection tx: rest, maybe corticosteroids to reduce inflammation
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larynx/tracheal tumors
1. "vocal cord nodules" or "singers nodules" - fibromas on vocal cords tx: surgery or rest 2. HPV oral lesions= benign mouth tumors - sugically removed BUT 30%of oral carcinomas have HPV
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\_\_\_ is associated with 30% of oral carcinomas
HPV= a cofactor for carcinoma
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95% of lung tumors are \_\_\_\_
carcinoma - 90% seem to involve smoking - poor survival bc it ofte metastisizes symptoms= coughing, short of breath , fatigue... less suicide than COPD tx: surgery, radiation, chemotherapy
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pneumonia=
inflammation of lungs -usually due to bact/viral infection but also can be autoimmune and fungal symptoms=difficulty breathing, fever and cough tx: vaccination for viral antibiotics for bacterial (or with viral to prevent onset of bacterial)
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pneumoconiosis
occupational lung diseases -inhalation of dust **coal workers** =black lung disease -\>inflammation -\>fibrosis and necrosis **asbestos** -\>inflammation -\> fibrosis and lots of MESOTHELIOMA (lung cancer)
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pulmonary embolism definition and causes
blood clot blocking an artery in the lungs -15% of unexpected deaths usually from DVT caused by: 1. immobility 2. hypercoagulative blood 3. blood vessel wall inflammation
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pulmonary embolism symptoms and tx
**symptoms**= chest pain, shortness of breath, caughing up blood may also be asymptomatic **treatment** = = O2 =antigoagulant \*prevention= compression stockings and mobilizing patients
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acute respiratory distress syndrome (ARDS)
distruption of alveolar capillary memb = pulmonary edema causes= sepsis, trauma, and pneumonia =releases inflammatory cytokines = increased PMNs =\> oxidative stress and proteases =\> CELL DAMAGE =40% death rate!
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