Exam 5- GI Flashcards
Four processes of GI
- motility 2. secretion 3. digestion 4. absorption
motility types in GI
propulsive moments- moves contents forward mixing movement- for absorption
pathway through GI
mouth esophagus stomach sm. intestine -duodenum -jejunum -ileum colon
lengths of duodenum, jejunum, and ileum
duodenum = 10 in
jejunum = 8 ft
ileum = 12 ft
Layers of Gi
serosa
longitudinal muscle
myenteric plexus
circular muscle
submucosa
submucosal plexus
muscularis mucosa
lamina propria
epithelium
longitudinal muscle
smooth muscle runs along the length of the of GI with contraction= GI shortens and widens
circular muscle
wrapping around the GI tract with contraction= constriction/lumen decreases in diameter
muscularis mucosa
thin muscle layer moves mucosal lining
lamina propria
a CT layer
enteric nervous system controlled by___
- generats patterns of activity directly in gut (w/out CNS) -hormones from CNS modulate it
Enteric NS subsections:
- Myenteric plexus
- Submucous plexus
myenteric plexus
in walls of GI innervates muscle layers
submucous plexus
connects with myenteric
sensory function -irritation, distension
motor function -controls secretion
reflex arcs of GI NSs
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
gastrin
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
gastroileal reflex
food in stomach (+) motility of ileum (+) opens illeocecal sphincter
secretin
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
cholecystokinin (CCK)
secreted to duodenum in response to fat or protein
(-) gastric motility and secretion
(+) secretion of pancreatic digestive enzymes
(+) bile release from gall bladder
glucose-dependent insulinotropic polypeptide (GIP)
secreted by duodenum in response to glucose
(-) gastric activity… motility and secretion for absorption
(+) insulin release
enterogastrones =
secretion CCK and GIP
decrease gastric motility and secretion increases sm. intestine motility and secretion
Interstitial Cells of Cajal (ICCs)
- 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
slow waves
-take many seconds -different activity in different sections of GI
slow waves => contraction via___
hormones can make slow waves stronger resolution in an AP -endogenously generated (don’t need CNS)
GI Motor Neurons
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
Excitatory GI Motor Neurons
Excitatory Junctional Potential
- Ach
- Substance P
Inhibitory GI Motor Neurons
Inhibitory Junctional Potential
- VIP= vasoactive intestinal peptide
- NO
when activated= physiological ileus (lack of contraction)
propulsive segment in peristalsis has ____ contracted
circular muscle
receiving segment of peristalsis has ____ contracted
longitudinal muscle
power propulsion
specialized rapid long distance movement -normal in large intestine, pathologic in sm. intestine
sm. intestine power propulsion
-used when there is an irritant we want to get out
power propulsion mechanism
segmentation (mixing)
where does this happen??
in duodnum and colon
- mixing in enzymes
- food is not forward movemtn just moving back and forth
sphincters
=physiological valve
- ring of smooth uscle
- normally in a contractie state
upper esophageal sphincter
stops us from swallowing air
=striated muscle
lower esophogeal sphincter
protects esoph. from H3O+
=smooth muscle
acinar gland secretions diagram
put diagram here pg 4 of gi secretiosn
myoepithelial cells
=contractie
->more saliva into ducts
serous cells
secrete? found where?
=>amylase from zymogen granules
-found in mouth and esophagus
ducts in mouth and esophagus secrete
HCO3- and K+
salivary amylase (ptyalin)
starts digestions of carbs
lingual lipase
metabolizes some fat
(in saliva)
mucins
in saliva
lubrication for swallowing
saliva functions
digestion (minor)
lubrication
neutralize acid (HCO3-)
solvent for taste
aids in speech
water balance (dry mouth (+) thirst)
rugae
longitudinal folds in stomach
allow it to exapand
stomach functions
- reservoir for food
- antral pump= mixes and propulses food
stomach anatomic regions vs functional regions
slow wave= AP where?
Stomach
diagram of stomach AP
gastric retropulsion
in stomach
=backwards jet of contents towards the corpus
-a few of these a minut during digestion
breaks up food
chyme
semifluid substace that exits the stomach
cardiac glands of stomach
=mucous cells
- near lower esoph. sphincter
- protective
pyloric glands of stomach
=Gcells
-secrete gastrin –(+)–>stomach activity and secretion
oxyntic glands of stomach
mucous cells =>mucus
parietal cells => HCl and intrinsic factor
chief cells => pepsinogen
HCl secreteion mechanism
alkaline tine
=secreting
H+ to stomach
HCO3- to blood
Regulation of HCl secretion
PSNS —(+)—-> secretion
ACh, gastrin, and histamine all (+) gastric secretions
cephalic phase of gastric secretion
thoughts, smell, taste, chewing, swallowing
increase HCl and pepsinogen
(preparing to eat, but no food in stomach)
gastric phase of gastric secretion
-food is in the stomach
protien and stretching of stomach –(+)–>
increase in HCl, pepsinogen and gastric secretion
intestinal phase of gastric secretion
decreased HCL, pepsinogen
increased secretion of enterogastrones (HCO3-, and enzymes)
pepsinogen activation
gastric juice functions
digestion-pepsinogen
bacteriocidal- low pH
supplies intrinsic factor
intrinsic factor
needed to absorb vit. B12
-without B12 pernicious anemia
hepatic portal circulation pathway
kupffer cells
in liver
~macrophages
siver sinusiods
highly permeable discontinuous capillaries
bile compostion
bile salts =detergents for fat digestion
phospholipids
bicarbonate
cholesterol (an way to excrete extra)
bilirubin (product of heme metabolism)
emuslification of fat
detergents keep fat in emulsion-surround droplet of fat
-cholesterol nonpolar/polar… polar is outside, nonpolar faces lipases
pancreas function
mostly exocrine
only 1-2% endocrine
sphincter of oddi
CCK —(+)—> relaxation of sphincter
=release of pancreatic juice
coposition of pancreatic juice
bicarbonate - neutralizes stomach H3O+
proteases - protien metabolism
pancreatic amylase - carbohydrate metabolism
pancreatic lipase - fat metabolism
cephalic and gastric phases affect pancreatic secretion
small increase in secretion
intestinal phase and pancreatic secretion
large increases in secretions
-contents are entering duodenum
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
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
goblet cells secrete what?
where are they found?
mucus
in the SMALL intestine
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
paneth cells
in small intestine
secrete anti-microbial peptides
ascending colon food duration
food only stays for a short amount of time
transverse colon food duration
food stays here for a while and dehydrates
descending colon food duration
short transit time
haustrations
mixing movements
similar to sm. intestine but slower
power propulsion
can be pathological, but usually normal
3-4 times a day, associated with defication
gastrocolic reflex
increased activity in colon associated wiht eating
colon stores food__
for 24-48 hrs trying to dehydrate it
defecation process
rectal disention triggers mechanoreceptors
defecation reflex: contraction of rectum -> relaxation of internal anal sphincter -> peristalsis in sigmoid colon
Colon secretions
mucus
bicarbonate (neutralize H+ from fermentation)
colon reabsorption
water and electrolytes (Na+ and Cl-)
colon gas
nitrogen from swallowed air
bacterial fermation of undigested poly saccharides=
CO2, CH4, H+, H2S,
esophagus mechanical obstruction causes
- congential malformations
- agenesis (absence) or atresia - stenosis (narrowing)
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
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)
esophagitis caused by
1. Mallory-Weiss tears = esophagus is overly relaxed and then vomiting causes tears
- chemicals (heavy alcohol/hot liquids)
- infections
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
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
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
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
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)
acute peptic ulceration
- penetrating mucosal layer from long term NSAID use and stress
- causes pain, nausea, and vomiting
- pain releaved when eating
cushing ulcer
with a head injury = excessive vagal stimulation
and too much gastric acid secretion => ulcer
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
autoimmune gastritis
Ab to parietal cells
normally parietal cells => HCl and IF
∴ disease = low acid and pesinogen secretion
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
gastric polyps
=nodlule that projects to surrounding tissue
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)
adhesions
scar tissue btw two loops of GI tubes causes them to not move as they should
-usually after surgery
volvus
twisting of intestine cause a section to be cut off from the rest (loop)
intussusception
part of intestine “telescoped” in on itself
strangulation
-from herniation, adhesions, volvus or intussusception
=loss of bloodflow
=EMERGENCY… needs surgery
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
hemorrhoids
=dilated anal and perianal blood vessels
- painful
- often during pregnancy ~> excessive straining
or portal hypertensive
= bright read blood (blood wasn’t digested)
celiac disease
=gluten intolerance - immune reaction to gluten
-with gluten = loss of villi= less absorption surface
=diarrhea and weight loss
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
inflammatory bowel disease
-from mucosal immune system reacting inapropriately
(probably involves intestinal flora)
hygiene hypothesis
need to expose kids to pathogents to build immune system
-aims to prevent inflammatory bowel disease
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
ulcerative colitis
a form of inflammatory bowel disease
- limited to rectum and colon
- always involves colon
causes diarrhea, and pain
-smoking can release symptoms
inflammatory polyps
= increased risk of cancer
in colon
hyperplastic polyps
pts. >50 yrs
no malignant potential
in colon
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
colonic adenocarcinomas
2 cancer killer (second to lung cancer)
most common GI tract malignancy
- happens anywhere in colon
- causes anemia, bloody stool and cramping
- if metastisized <5% yr survival but, if lower stage could be 75% survival
carcinoid tumor in colon
a neuroendocrine tumor
can release serotonin
coronoid syndrome
effects caused by carcinoid tumor in colon
-causes flushing/sweating effects of NT
acute appendicitis
from an obstruction of the appendix
-inflammation and pain in right lower quadrant with fever
most common tumor of the appendix
most common = carcinoid tumor
hepatic failure
=80-90% fxn lost
chronic =most common
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
functions of bile
- emulsification of afat
- elimination of bilirubin, cholesterola nd highly lipid soluble foriegn substances (ie. drugs)
cholestasis
=impaired flow of bile
neonatal jauncice
-in newborns liver’s ability to excrete biliruben hasn’t been developed
∴ put babies uner ligts that breakdown biliruben in skin
hepatic encephalopathy
=CNS effects form liver failure
due to high NH3 “amenemia”
-mild brain dysfunction all the way to confusion, stupor, coma and death
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
portal hypertension
cirrosis is the most common cause
increases resistance to filatration causes the hypertension
ascites (definition and pathogenesis)
=build-up of paritoneal fluid, jauncice, potbelly and esophogeal varicocities
Pathogenesis
- excess filtration through sinusiods due to sinusiodal hypertension and hypoalbuminia
- increased hepatic lymph flow
- Na+ and H2O retention by the kidneys due to high plasma aldosterone
splenomegaly
enlargement of spleen
-culd rupture= hemorrhaging
hemochromatosis
=a build up of Fe in body
>1/3 accumulates in the liver
common in men >50
hemosiderin in organs
triad:
- abnormal brown color to skin
- cirrosis
- diabetes mellitus due to damaged beta cells
hemosiderin
a complex of iron and protiens
benign hepatic tumors
= caverous hemangioma (most common)
=adenoma
=hepatocellular carcinoma
cavernous hemangioma
=benign hepatic tumor
-soft nodules full of blood
hepatic adenoma
benign hepatic tumor that may have malignant tumor
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
cholelithiasis
=gallstones
-may not have symptoms but pts have an “attack”= upper right quadrant pain
types
- cholesterol
- pigmented
cholesterol stones
=most common
-form with excessive secretion of cholestrol and bile
pigment stones
gall stones that contain billiruben
form with excessive secretion of biliruben
-dark color and radiopaque
cholecystis
=inflammation of gal bladder
-needs to be rmoved
empyema
a form of acute cholecystitis
gall bladder filled with puss
gangrenous cholecystis
a form of acute cholecystitis
gall bladder is necrotic
acute calculous cholecystitis
=blockage of gall bladder duct leads to inflammation of gall bladder
symptoms of cholecystitis acute vs chronic
acute= pain in UR quadrant, cant digest fatty foods
chronic= same as acute but less pronounced
carcinoma of the gallbladder
pathogenesis?
-adenocarcinoma
pathogenesis=
gall stones (+) blockage (+) inflammation
=predisposed to cancer
dismal 5 yr outlook
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
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
pancreatic neoplasm types
serous cystadenoma
mucinous cystic
pancreatic adenocarcinoma
serous cystadenomas
pancreatic neoplasms
fluid filled cysts most common after age 60
almos always benign
abdominal pain
mucinous cystic neoplasms
pancreatic neoplasm
mucous secreting cell adenoma
95% in women
may lead to adenocarcinoma
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
GI has ___ to increase absorption ___
circular folds X 3
vili X 30
microvili X 600
starch
polysaccharide
form plants
most abundant carb in typical human diet
glycogen
polysaccharide from meat
cellulose
polysaccharide
fromplant cell walls
indigestible but provides fiber (keeps contents moving along)
sucrose
glucose-fructose
lactose
glucose-galactose
milk sugar
maltose
glucose-glucose
from malt
common monosacccharides in diet
glucose
fructose
galactose
mouth digestion
via salivary amylase
-just starts digaestion
stomach digestion
fsalivary amylase is deactivated by low stomach pH
so no digestion just mixing
small intestine digestion
does most of the carbohydrate digestion
- pancreatic amylase =carb digestion
- epithelial disaccharidases= break down disaccharrides in gut epithelium
sugar absorption
lipid types
triglycerides (90%)
cholesterol
phospholipids
lipid digestion mouth/stomach
via lingual lipase
-just minor digestion
small intestine lipid digestion
via pancreatic lipase
-emulsification then lipase has major role in metablolism
fat absorption
types of protien
protiens (<100 AA)
peptides
amino acids
protien stomach digestion
VIA PEPSIN
small intestine protien digested via
pancreatic enzymes
- trypsinogen
- endopeptidases
- exopeptidases
epithelial enzymes
trypsinogen
activated by enteropeptidase to trypsin
trypsin then activates other proenzymes
endopeptidases
(speicific types)
cleave internal peptide bonds
=trypsin, chymotrypsin and elastase
exopeptidases
-cleaves terminal peptide bonds
=procarboxypeptidases A & B
epithelial enzyes
in the wall of the duodenum
cleave polypeptides to dipeptides, tripeptides, or amino acids
amino acid absorption
needs transpeptidases
cant cross membrane
di- and tripeptide absorption
absorbed more efficiently thatn AA sometimes so these are “taken up” as well
protien absorption
usually don’t want to absorb a straight protien
it could cause an allergic rxn
fat soluble vitamins
A, D, E, and K
fat solluble vitamin absorption
easily cross cell membranes ∴ passively absorbed in the small intestine
-can be toxic
water soluble vitamin absorption
passive and active processes in small intestine
vitamin B12 absorption
via intrinsic factor (secreted by parietal cells)
-IF binds B12 an then is absorbed in ileum via transporter complex
intrinsic factor defficiency=
pernicious anemia
=smooth shiny tongue
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
vitamin D and Ca2+ absorption
more of a hormone than a vitima
-turns on gene expression of calbindin and Ca2+ ATPase
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)
Ferratin
Fe binding protien in epithelial cells
a way of excreting Fe bc enterocyts are often sloughed off
=PRIMARY form of Fe regulation
Fe defficient affects gene expression
less ferritin (less excretion)
more DMT (more absorption)
(Bohr effect is DPG)
definition of gas exchange respiration
O2 from air and CO2 from cell sback out
trachea and bronchi have lots of_______
cartilage
conduction zone
no gas exchange
=dead space
-warms, humidifies, and removes junk from air
trachea->bronchi->bronchiole
respiratory zone
-does gas exchange
respiratory bronchiole->alveolus
Pleural pressure
=ALWAYS NEATIVE
-chest wall wants to expand, and lungs want to shrink
=keeps the lungs inflated
alveolar pressure
if neg=__
if pos=___
negative = air fows in
positive= air flows out
pneuothorax
hole in chest wall =air in pleural space
Ppl goes to zero ∴ lungs collapsse and wall exapnds outward
with and increas in volume of the chest cavity = ___ of P in lungs
increase
(boyle’s law)
normal inspiration mechanism=
contract diaphragm= it pulls down
= increased volume of chest cavity
= decreased P
= air in
increased inspiration mechanism
contract external intercostal muscles adn accessory muscles in the neck
=chest wall moves up and out
=increased volum
=decreased pressure
normal expiration mechanism
=passive diaphragm relaxation
increased expiration mechanism
= contract intercostals
-> pushes chest wall down and in
= contract abdominals
->pushes intestines up
during inspiration=
pleural pressure___
alveolar pressure ___
flow___
total volume___
pleural pressure= getting more negative
alveolar pressure= negative
flow= negative
total volume= increases
during expiration
pleural pressure___
alveolar pressure ___
flow___
tidal volume___
pleural pressure= less negative
alveolar pressure= positiv
flow = positive (air out)
tidal volume = decreasing
respiratory volumes and capacities
tidal volume=
normal breath
0.5 L
Inspiratory reserve volume
amount of air that can be inspire after normal inspiration
expiratory reserve volume
amount yo can breathe out after expiration
residual volume
= air you cant expire from lungs
1L
vital capacity
=total amount of air that can be moved
= 5 L
=TV+IRV+ERV
forced vital capacity
vital capacity as fast as possible
normal =5L
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)
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
asthma
=episodes of reversible bronchial narrowig
=primarily obstructive
types
- intrinsic (non-allergic/non-atopic)- due to stress/exercise
- extrinsic (allergic/atopic)- due to inflammation, usually develops at a young age
extrinsic asthma mechanism
acute asthma
airway obstruction
chronic asthma
WBC accumulation
=edema
= increased mucus
=hypersensitivity
COPD
=chronic obstructive pulmonary disease
=5th leading cause of disease
- chronic bronchitis
- emphysema
emphysema
=”pink puffers”
=normal O2 with increased breathing
loss of alveoli adn elastic recoil
=airways collapse (obstructive disorders)
-proteases released
proteases released during emphysema
- elastase - destroys tissue
- alpha 1 anti-trypsin- inhibits proteases (protects lungs)
smoking’s effect on lung proteases
(+) elastase
(-) alpha1 anti-trypsin
alpha1 anti-trypsin deficiency
a genitic disease
—>pts develop emphysema
chronic bronchitis
=”blue bloaters”
involves inflammation
excess mucus-> blocks airways = chronic cough
draw cystic fibrosis issue
=mucus coating and airway blockage
=bacterial infection!
cystic fibrosis treatment
- antibiotics and O2 for symptoms
- gene therapy - hasn’t been successfull
- in 2012 therapy opens Cl- channel with a gating problem (4%)
dead space
(name the two types)
inspired air not involved in gas exchange
- anatomic= air in conducting space
- alveolar= air in alveoli but no gas exchange
total ventilation
amount of air moved/minute
VT= (tidal volume)(frequency of breathing)
(500)(12)= 6,000 mL/min
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
deep and slow breath vs shallow and fast?
deep and slow
increase radius = ___ resistance
decrease (BIG TIME)
greatest total resistance is in ____
large bronchi
bc there are so few of them
_____ are more important to airway resistance
bronchioles!
PSNS and airway resistance controll
ACh (+) muscarinc R = AIRWAY CONSTRICTION
at rest you dont need lots of O2
SNS and Airway Resistance
Epi (+) B<strong>2</strong> Receptor
=AIRWAY DILATION
Asthma treatment
=B2 agonist
match airflow and bloodflow
with decreased CO2 = airway constriction
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
decreased compliance
small change in volume for a change in pressure
=hard to inflate
- happens wiht restrictive disorders
- work of lungs is increased
surfactant
a lipoprotien
decreases surface tension
(-) alveoli from collapsing
from type II alveolar cells
made late in fetal development
surface tension and radius
higher ST in smaller radii
∴ surfactant is more important and also works better in smaller radii lumens
Total P of O2=
O2= PB x FO2
Barrometric P x Force of O2
=(760 mmHg)(0.21)
=160 mmHg
Partial pressure of inspired air=
PO2 = (PB-PH2O) x FO2
=(760-47) x (0.21)
=150mmHg
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
the amount of gas dissolved in a liquid is proportional to ___
its partial pressure
A LINEAR RELATIONSHIP
things that will increase simple diffusion
- increased surface area of membrane
- increased diffusion coefficient - for gasses this is the amout dissolved
- increasing the concentration gradient - for gasses this is the partial pressure difference
- membrane thickness
diffusion capacity
=the amount of gas the lungs can transfer to the blood
two things that limit diffusion capacity (O2 transfer)
- perfustion limited- diffusion capacity is limited by blood flow
- 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
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
in circulatory system where is P high and low?
pulmonary vascular resistance regulation
- recruitment= open more capillaries
- distension= increase radius of capillaries
3 benefits of recruitment and distension
- decreased resistance =no edema
- decreased velocity of blood floow= more time for gass exchange
- increased SA for gas exchange
pulmonary vascular system is regulated by
hypoxia
NOT autonomic NS
when alveolus is blocked blood vessel___
constricts
at a higher altitude=
-decreased PO2 everywhere
=general vasoconstriction
=increased BP and work of heart
atmosphere to lungs PO2 drops bc___
- H20 (humidifies)
- its mixed with dead space air
- its mixed with residual volume air
PO2 160 to 105mmHg
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
label the PO2 levels
160
105
100
100
<40
40
40
Dissolved O2 at PO2 of 100mmHg
- 3ml O2/100ml of blood
- this is a small amount
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
____ is detected by chemoreceptors
dissolved O2, not bound to Hb
- this is what is seen by the lungs
- increasing PO2 doesn’t saturate more Hb
If PO2 drops to here… Hb is still nearly saturated
PO2 =40
this is what’s seen near normal tissue
O2 IS COMMING OFF Hb
Hb is at 75% saturation
PO2 =25mmHg
what is seen near ACTIVE tissue
=50% saturated Hb
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
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)
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
hypoxia=
insuficient O2 in the tissues
diffusion impairment caused by
edema in the lungs
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
deficient RBC (anemia) causes =
less Hg ∴ less O2
-THIS IS NOT DETECTED BY CHEMORECEPTORS because amountof dissolved O2 is normal
∴ no stress is experienced
CO poisioning
-causes less O2 to bind to Hb
CHEMORECEPTORS WILL NOT DETECT THIS!!
bc dissolved O2 levels are normal
∴ no stress is exprienced
CO2 transported three ways:
- 10% dissolved in plasma
- 30% bound to carbamino protiens (Hb)
- 60% bicarbonate ions
CO2 + H2O <=CA⇒ H2CO3 ⇔ H+ HCO3-
(via carbonic anhydrase)
Draw pathway of CO2 out of tissues with high CO2
Haldane effect
when O2 binds to Hb ∴ less CO2 binds to Hb and is expired
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
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)
___ (+) inspiration
- chemoreceptors
detect high CO2, and H+ and low O2
- pulmonary iritant receptors
pulmonary stretch receptors
DO NOT inhibit normal inspiration (other brain centers do this)
they ONLY protect against over inflation
PO2 and PCO2 effects on respiraton
PO2- has to drop from 100 to 60 t stimulate breathing
PCO2- any increase wil (+) breathing
deep fast breathing =
decreases CO2 in blood ∴ you can hold your breath longer
central chemoreceptors
found ___
stimulated by___
not stimulated by___
in medla of brain
stimulated by:
- high CO2 in blood
2 high H+ in interstitial fluid
NOT stimulated by:
- high H+ in blood
- low O2
pathway of central chemoreceptor stimulation
peripheral chemoreceptors
found in carotid and aortic bodies
- measure arteiole blood
- no BBB
∴ they detect blood’s:
high CO2 and H2O
low O2
slowly adapting pulmonary receptors
in lung bronchiole smooth muscle
have the Hering-Breuer reflex
=stops overinflation of lungs
rapidly adapting pulmonary receptors
=irritant receptors
respond to injury, inflammatin, touch, chemicals
- complex effects (+) cough and some inspiration
cheyne-stokes breathing=
deep-rapid breathing (over ventilation)
then inhibits breathing ∴ (+) slower/stopped breathing
∴ (+) increased CO2 ∴ (+) deep rapid breathing again
=”waxing and waning”
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
epiglottitis=
inflammation of the epiglottis
-it swells and blocks to trachea
=from injury or BACTERIAL infection
tx: O2, antibiotics
Laryngitis
= inflammation of the vocal cords
=from overuse or VIRAL infection
tx: rest, maybe corticosteroids to reduce inflammation
larynx/tracheal tumors
- “vocal cord nodules” or “singers nodules”
- fibromas on vocal cords
tx: surgery or rest - HPV oral lesions= benign mouth tumors
- sugically removed
BUT 30%of oral carcinomas have HPV
___ is associated with 30% of oral carcinomas
HPV= a cofactor for carcinoma
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
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)
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)
pulmonary embolism definition and causes
blood clot blocking an artery in the lungs
-15% of unexpected deaths
usually from DVT
caused by:
- immobility
- hypercoagulative blood
- blood vessel wall inflammation
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
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!
