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Pathophys > Exam 5- GI > Flashcards

Exam 5- GI Flashcards

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
Q

Excitatory GI Motor Neurons

A

Excitatory Junctional Potential

  • Ach
  • Substance P
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26
Q

Inhibitory GI Motor Neurons

A

Inhibitory Junctional Potential

  • VIP= vasoactive intestinal peptide
  • NO

when activated= physiological ileus (lack of contraction)

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27
Q

propulsive segment in peristalsis has ____ contracted

A

circular muscle

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28
Q

receiving segment of peristalsis has ____ contracted

A

longitudinal muscle

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29
Q

power propulsion

A

specialized rapid long distance movement -normal in large intestine, pathologic in sm. intestine

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30
Q

sm. intestine power propulsion

A

-used when there is an irritant we want to get out

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31
Q

power propulsion mechanism

A
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32
Q

segmentation (mixing)

where does this happen??

A

in duodnum and colon

  • mixing in enzymes
  • food is not forward movemtn just moving back and forth
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33
Q

sphincters

A

=physiological valve

  • ring of smooth uscle
  • normally in a contractie state
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34
Q

upper esophageal sphincter

A

stops us from swallowing air

=striated muscle

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35
Q

lower esophogeal sphincter

A

protects esoph. from H3O+

=smooth muscle

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36
Q

acinar gland secretions diagram

A

put diagram here pg 4 of gi secretiosn

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37
Q

myoepithelial cells

A

=contractie

->more saliva into ducts

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38
Q

serous cells

secrete? found where?

A

=>amylase from zymogen granules

-found in mouth and esophagus

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39
Q

ducts in mouth and esophagus secrete

A

HCO3- and K+

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40
Q

salivary amylase (ptyalin)

A

starts digestions of carbs

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41
Q

lingual lipase

A

metabolizes some fat

(in saliva)

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42
Q

mucins

A

in saliva

lubrication for swallowing

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43
Q

saliva functions

A

digestion (minor)

lubrication

neutralize acid (HCO3-)

solvent for taste

aids in speech

water balance (dry mouth (+) thirst)

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44
Q

rugae

A

longitudinal folds in stomach

allow it to exapand

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45
Q

stomach functions

A
  • reservoir for food
  • antral pump= mixes and propulses food
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46
Q

stomach anatomic regions vs functional regions

A
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47
Q

slow wave= AP where?

A

Stomach

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48
Q

diagram of stomach AP

A
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49
Q

gastric retropulsion

A

in stomach

=backwards jet of contents towards the corpus

-a few of these a minut during digestion

breaks up food

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50
Q

chyme

A

semifluid substace that exits the stomach

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51
Q

cardiac glands of stomach

A

=mucous cells

  • near lower esoph. sphincter
  • protective
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52
Q

pyloric glands of stomach

A

=Gcells

-secrete gastrin –(+)–>stomach activity and secretion

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53
Q

oxyntic glands of stomach

A

mucous cells =>mucus

parietal cells => HCl and intrinsic factor

chief cells => pepsinogen

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54
Q

HCl secreteion mechanism

A
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55
Q

alkaline tine

A

=secreting

H+ to stomach

HCO3- to blood

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56
Q

Regulation of HCl secretion

A

PSNS —(+)—-> secretion

ACh, gastrin, and histamine all (+) gastric secretions

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57
Q

cephalic phase of gastric secretion

A

thoughts, smell, taste, chewing, swallowing

increase HCl and pepsinogen

(preparing to eat, but no food in stomach)

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58
Q

gastric phase of gastric secretion

A

-food is in the stomach

protien and stretching of stomach –(+)–>

increase in HCl, pepsinogen and gastric secretion

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59
Q

intestinal phase of gastric secretion

A

decreased HCL, pepsinogen

increased secretion of enterogastrones (HCO3-, and enzymes)

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60
Q

pepsinogen activation

A
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61
Q

gastric juice functions

A

digestion-pepsinogen

bacteriocidal- low pH

supplies intrinsic factor

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62
Q

intrinsic factor

A

needed to absorb vit. B12

-without B12 pernicious anemia

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63
Q

hepatic portal circulation pathway

A
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64
Q

kupffer cells

A

in liver

~macrophages

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65
Q

siver sinusiods

A

highly permeable discontinuous capillaries

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66
Q

bile compostion

A

bile salts =detergents for fat digestion

phospholipids

bicarbonate

cholesterol (an way to excrete extra)

bilirubin (product of heme metabolism)

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67
Q

emuslification of fat

A

detergents keep fat in emulsion-surround droplet of fat

-cholesterol nonpolar/polar… polar is outside, nonpolar faces lipases

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68
Q

pancreas function

A

mostly exocrine

only 1-2% endocrine

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69
Q

sphincter of oddi

A

CCK —(+)—> relaxation of sphincter

=release of pancreatic juice

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70
Q

coposition of pancreatic juice

A

bicarbonate - neutralizes stomach H3O+

proteases - protien metabolism

pancreatic amylase - carbohydrate metabolism

pancreatic lipase - fat metabolism

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71
Q

cephalic and gastric phases affect pancreatic secretion

A

small increase in secretion

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72
Q

intestinal phase and pancreatic secretion

A

large increases in secretions

-contents are entering duodenum

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73
Q

Migrating motor complex (MMC)

A

=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
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74
Q

small intestine secretions are from___ which have these types of cells:

A

from the crypts of lieberkuhn

=gastric glands

contain:

goblet cells

epithelial stem cell

paneth cells

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75
Q

goblet cells secrete what?

where are they found?

A

mucus

in the SMALL intestine

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76
Q

epithelial stem cells importance

found where____

A

found in SMALL intestine

  • high turnover of cells in GI, need to be replaced
  • also easily affected by radiation
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77
Q

paneth cells

A

in small intestine

secrete anti-microbial peptides

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78
Q

ascending colon food duration

A

food only stays for a short amount of time

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79
Q

transverse colon food duration

A

food stays here for a while and dehydrates

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80
Q

descending colon food duration

A

short transit time

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81
Q

haustrations

A

mixing movements

similar to sm. intestine but slower

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82
Q

power propulsion

A

can be pathological, but usually normal

3-4 times a day, associated with defication

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83
Q

gastrocolic reflex

A

increased activity in colon associated wiht eating

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84
Q

colon stores food__

A

for 24-48 hrs trying to dehydrate it

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85
Q

defecation process

A

rectal disention triggers mechanoreceptors

defecation reflex: contraction of rectum -> relaxation of internal anal sphincter -> peristalsis in sigmoid colon

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86
Q

Colon secretions

A

mucus

bicarbonate (neutralize H+ from fermentation)

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87
Q

colon reabsorption

A

water and electrolytes (Na+ and Cl-)

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88
Q

colon gas

A

nitrogen from swallowed air

bacterial fermation of undigested poly saccharides=

CO2, CH4, H+, H2S,

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89
Q

esophagus mechanical obstruction causes

A
  1. congential malformations
    - agenesis (absence) or atresia
  2. stenosis (narrowing)
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90
Q

achalasia

A

-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

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91
Q

esophageal varices

A

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)

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92
Q

esophagitis caused by

A

1. Mallory-Weiss tears = esophagus is overly relaxed and then vomiting causes tears

  1. chemicals (heavy alcohol/hot liquids)
  2. infections
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93
Q

Gastroesophageal Reflux Disease

A
  • 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
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94
Q

barrett esophagus

A

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
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95
Q

esophageal adenocarcinoma

A

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
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96
Q

esophageal squamous cell carcinoma

A
  • 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

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97
Q

acute gastritis

A

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)
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98
Q

acute peptic ulceration

A
  • penetrating mucosal layer from long term NSAID use and stress
  • causes pain, nausea, and vomiting
  • pain releaved when eating
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99
Q

cushing ulcer

A

with a head injury = excessive vagal stimulation

and too much gastric acid secretion => ulcer

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100
Q

chronic gastritic

A

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
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101
Q

autoimmune gastritis

A

Ab to parietal cells

normally parietal cells => HCl and IF

∴ disease = low acid and pesinogen secretion

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102
Q

peptic ulcer disease

A

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
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103
Q

gastric polyps

A

=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)

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104
Q

adhesions

A

scar tissue btw two loops of GI tubes causes them to not move as they should

-usually after surgery

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105
Q

volvus

A

twisting of intestine cause a section to be cut off from the rest (loop)

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106
Q

intussusception

A

part of intestine “telescoped” in on itself

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107
Q

strangulation

A

-from herniation, adhesions, volvus or intussusception

=loss of bloodflow

=EMERGENCY… needs surgery

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108
Q

hirschsprung disease

A

=”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

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109
Q

hemorrhoids

A

=dilated anal and perianal blood vessels

  • painful
  • often during pregnancy ~> excessive straining

or portal hypertensive

= bright read blood (blood wasn’t digested)

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110
Q

celiac disease

A

=gluten intolerance - immune reaction to gluten

-with gluten = loss of villi= less absorption surface

=diarrhea and weight loss

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111
Q

Diverticulitis

A

=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
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112
Q

inflammatory bowel disease

A

-from mucosal immune system reacting inapropriately

(probably involves intestinal flora)

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113
Q

hygiene hypothesis

A

need to expose kids to pathogents to build immune system

-aims to prevent inflammatory bowel disease

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114
Q

chron disease

A

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
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115
Q

ulcerative colitis

A

a form of inflammatory bowel disease

  • limited to rectum and colon
  • always involves colon

causes diarrhea, and pain

-smoking can release symptoms

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116
Q

inflammatory polyps

A

= increased risk of cancer

in colon

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117
Q

hyperplastic polyps

A

pts. >50 yrs

no malignant potential

in colon

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118
Q

colonic adenomas

A

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
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119
Q

colonic adenocarcinomas

A

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
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120
Q

carcinoid tumor in colon

A

a neuroendocrine tumor

can release serotonin

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121
Q

coronoid syndrome

A

effects caused by carcinoid tumor in colon

-causes flushing/sweating effects of NT

122
Q

acute appendicitis

A

from an obstruction of the appendix

-inflammation and pain in right lower quadrant with fever

123
Q

most common tumor of the appendix

A

most common = carcinoid tumor

124
Q

hepatic failure

A

=80-90% fxn lost

chronic =most common

125
Q

chronic hepatic failure

A

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
Q

functions of bile

A
  1. emulsification of afat
  2. elimination of bilirubin, cholesterola nd highly lipid soluble foriegn substances (ie. drugs)
127
Q

cholestasis

A

=impaired flow of bile

128
Q

neonatal jauncice

A

-in newborns liver’s ability to excrete biliruben hasn’t been developed

∴ put babies uner ligts that breakdown biliruben in skin

129
Q

hepatic encephalopathy

A

=CNS effects form liver failure

due to high NH3 “amenemia”

-mild brain dysfunction all the way to confusion, stupor, coma and death

130
Q

cirrhosis

A

=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
Q

portal hypertension

A

cirrosis is the most common cause

increases resistance to filatration causes the hypertension

132
Q

ascites (definition and pathogenesis)

A

=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
Q

splenomegaly

A

enlargement of spleen

-culd rupture= hemorrhaging

134
Q

hemochromatosis

A

=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
Q

hemosiderin

A

a complex of iron and protiens

136
Q

benign hepatic tumors

A

= caverous hemangioma (most common)

=adenoma

=hepatocellular carcinoma

137
Q

cavernous hemangioma

A

=benign hepatic tumor

-soft nodules full of blood

138
Q

hepatic adenoma

A

benign hepatic tumor that may have malignant tumor

139
Q

hepatocellular carcinoma

A
  • 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
Q

cholelithiasis

A

=gallstones

-may not have symptoms but pts have an “attack”= upper right quadrant pain

types

  1. cholesterol
  2. pigmented
141
Q

cholesterol stones

A

=most common

-form with excessive secretion of cholestrol and bile

142
Q

pigment stones

A

gall stones that contain billiruben

form with excessive secretion of biliruben

-dark color and radiopaque

143
Q

cholecystis

A

=inflammation of gal bladder

-needs to be rmoved

144
Q

empyema

A

a form of acute cholecystitis

gall bladder filled with puss

145
Q

gangrenous cholecystis

A

a form of acute cholecystitis

gall bladder is necrotic

146
Q

acute calculous cholecystitis

A

=blockage of gall bladder duct leads to inflammation of gall bladder

147
Q

symptoms of cholecystitis acute vs chronic

A

acute= pain in UR quadrant, cant digest fatty foods

chronic= same as acute but less pronounced

148
Q

carcinoma of the gallbladder

pathogenesis?

A

-adenocarcinoma

pathogenesis=

gall stones (+) blockage (+) inflammation

=predisposed to cancer

dismal 5 yr outlook

149
Q

acute pancreatitis

A

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
Q

chronic pancreatitis

A

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
Q

pancreatic neoplasm types

A

serous cystadenoma

mucinous cystic

pancreatic adenocarcinoma

152
Q

serous cystadenomas

A

pancreatic neoplasms

fluid filled cysts most common after age 60

almos always benign

abdominal pain

153
Q

mucinous cystic neoplasms

A

pancreatic neoplasm

mucous secreting cell adenoma

95% in women

may lead to adenocarcinoma

154
Q

pancreatic adenocarcinoma

A

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
Q

GI has ___ to increase absorption ___

A

circular folds X 3

vili X 30

microvili X 600

156
Q

starch

A

polysaccharide

form plants

most abundant carb in typical human diet

157
Q

glycogen

A

polysaccharide from meat

158
Q

cellulose

A

polysaccharide

fromplant cell walls

indigestible but provides fiber (keeps contents moving along)

159
Q

sucrose

A

glucose-fructose

160
Q

lactose

A

glucose-galactose

milk sugar

161
Q

maltose

A

glucose-glucose

from malt

162
Q

common monosacccharides in diet

A

glucose

fructose

galactose

163
Q

mouth digestion

A

via salivary amylase

-just starts digaestion

164
Q

stomach digestion

A

fsalivary amylase is deactivated by low stomach pH

so no digestion just mixing

165
Q

small intestine digestion

A

does most of the carbohydrate digestion

  • pancreatic amylase =carb digestion
  • epithelial disaccharidases= break down disaccharrides in gut epithelium
166
Q

sugar absorption

A
167
Q

lipid types

A

triglycerides (90%)

cholesterol

phospholipids

168
Q

lipid digestion mouth/stomach

A

via lingual lipase

-just minor digestion

169
Q

small intestine lipid digestion

A

via pancreatic lipase

-emulsification then lipase has major role in metablolism

170
Q

fat absorption

A
171
Q

types of protien

A

protiens (<100 AA)

peptides

amino acids

172
Q

protien stomach digestion

A

VIA PEPSIN

173
Q

small intestine protien digested via

A

pancreatic enzymes

  1. trypsinogen
  2. endopeptidases
  3. exopeptidases

epithelial enzymes

174
Q

trypsinogen

A

activated by enteropeptidase to trypsin

trypsin then activates other proenzymes

175
Q

endopeptidases

(speicific types)

A

cleave internal peptide bonds

=trypsin, chymotrypsin and elastase

176
Q

exopeptidases

A

-cleaves terminal peptide bonds

=procarboxypeptidases A & B

177
Q

epithelial enzyes

A

in the wall of the duodenum

cleave polypeptides to dipeptides, tripeptides, or amino acids

178
Q

amino acid absorption

A

needs transpeptidases

cant cross membrane

179
Q

di- and tripeptide absorption

A

absorbed more efficiently thatn AA sometimes so these are “taken up” as well

180
Q

protien absorption

A

usually don’t want to absorb a straight protien

it could cause an allergic rxn

181
Q

fat soluble vitamins

A

A, D, E, and K

182
Q

fat solluble vitamin absorption

A

easily cross cell membranes ∴ passively absorbed in the small intestine

-can be toxic

183
Q

water soluble vitamin absorption

A

passive and active processes in small intestine

184
Q

vitamin B12 absorption

A

via intrinsic factor (secreted by parietal cells)

-IF binds B12 an then is absorbed in ileum via transporter complex

185
Q

intrinsic factor defficiency=

A

pernicious anemia

=smooth shiny tongue

186
Q

calcium absorption

A

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
Q

vitamin D and Ca2+ absorption

A

more of a hormone than a vitima

-turns on gene expression of calbindin and Ca2+ ATPase

188
Q

Fe absorption

A

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
Q

Ferratin

A

Fe binding protien in epithelial cells

a way of excreting Fe bc enterocyts are often sloughed off

=PRIMARY form of Fe regulation

190
Q

Fe defficient affects gene expression

A

less ferritin (less excretion)

more DMT (more absorption)

(Bohr effect is DPG)

191
Q

definition of gas exchange respiration

A

O2 from air and CO2 from cell sback out

192
Q

trachea and bronchi have lots of_______

A

cartilage

193
Q

conduction zone

A

no gas exchange

=dead space

-warms, humidifies, and removes junk from air

trachea->bronchi->bronchiole

194
Q

respiratory zone

A

-does gas exchange

respiratory bronchiole->alveolus

195
Q

Pleural pressure

A

=ALWAYS NEATIVE

-chest wall wants to expand, and lungs want to shrink

=keeps the lungs inflated

196
Q

alveolar pressure

if neg=__

if pos=___

A

negative = air fows in

positive= air flows out

197
Q

pneuothorax

A

hole in chest wall =air in pleural space

Ppl goes to zero ∴ lungs collapsse and wall exapnds outward

198
Q

with and increas in volume of the chest cavity = ___ of P in lungs

A

increase

(boyle’s law)

199
Q

normal inspiration mechanism=

A

contract diaphragm= it pulls down

= increased volume of chest cavity

= decreased P

= air in

200
Q

increased inspiration mechanism

A

contract external intercostal muscles adn accessory muscles in the neck

=chest wall moves up and out

=increased volum

=decreased pressure

201
Q

normal expiration mechanism

A

=passive diaphragm relaxation

202
Q

increased expiration mechanism

A

= contract intercostals

-> pushes chest wall down and in

= contract abdominals

->pushes intestines up

203
Q

during inspiration=

pleural pressure___

alveolar pressure ___

flow___

total volume___

A

pleural pressure= getting more negative

alveolar pressure= negative

flow= negative

total volume= increases

204
Q

during expiration

pleural pressure___

alveolar pressure ___

flow___

tidal volume___

A

pleural pressure= less negative

alveolar pressure= positiv

flow = positive (air out)

tidal volume = decreasing

205
Q

respiratory volumes and capacities

A
206
Q

tidal volume=

A

normal breath

0.5 L

207
Q

Inspiratory reserve volume

A

amount of air that can be inspire after normal inspiration

208
Q

expiratory reserve volume

A

amount yo can breathe out after expiration

209
Q

residual volume

A

= air you cant expire from lungs

1L

210
Q

vital capacity

A

=total amount of air that can be moved

= 5 L

=TV+IRV+ERV

211
Q

forced vital capacity

A

vital capacity as fast as possible

normal =5L

212
Q

obstructive disorder’s effecton FVC and RV

A

FVC=3L

RV= 3L (cant get air out)

total =6L

(ie emphysema - loss of alvoli and elastic recoil)

213
Q

restrictive disorder’s affect on FVC and RV

A

FVC= 3L

RV= 1L

total = 4L (cant get air in)

-edema/fibrous tissue in lungs causes disorder

214
Q

asthma

A

=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
Q

extrinsic asthma mechanism

A
216
Q

acute asthma

A

airway obstruction

217
Q

chronic asthma

A

WBC accumulation

=edema

= increased mucus

=hypersensitivity

218
Q

COPD

A

=chronic obstructive pulmonary disease

=5th leading cause of disease

  1. chronic bronchitis
  2. emphysema
219
Q

emphysema

A

=”pink puffers”

=normal O2 with increased breathing

loss of alveoli adn elastic recoil

=airways collapse (obstructive disorders)

-proteases released

220
Q

proteases released during emphysema

A
  1. elastase - destroys tissue
  2. alpha 1 anti-trypsin- inhibits proteases (protects lungs)
221
Q

smoking’s effect on lung proteases

A

(+) elastase

(-) alpha1 anti-trypsin

222
Q

alpha1 anti-trypsin deficiency

A

a genitic disease

—>pts develop emphysema

223
Q

chronic bronchitis

A

=”blue bloaters”

involves inflammation

excess mucus-> blocks airways = chronic cough

224
Q
A
225
Q

draw cystic fibrosis issue

A

=mucus coating and airway blockage

=bacterial infection!

226
Q

cystic fibrosis treatment

A
  1. antibiotics and O2 for symptoms
  2. gene therapy - hasn’t been successfull
    - in 2012 therapy opens Cl- channel with a gating problem (4%)
227
Q

dead space

(name the two types)

A

inspired air not involved in gas exchange

  1. anatomic= air in conducting space
  2. alveolar= air in alveoli but no gas exchange
228
Q

total ventilation

A

amount of air moved/minute

VT= (tidal volume)(frequency of breathing)

(500)(12)= 6,000 mL/min

229
Q

alveolar ventilation

A

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

230
Q

deep and slow breath vs shallow and fast?

A

deep and slow

231
Q

increase radius = ___ resistance

A

decrease (BIG TIME)

232
Q

greatest total resistance is in ____

A

large bronchi

bc there are so few of them

233
Q

_____ are more important to airway resistance

A

bronchioles!

234
Q

PSNS and airway resistance controll

A

ACh (+) muscarinc R = AIRWAY CONSTRICTION

at rest you dont need lots of O2

235
Q

SNS and Airway Resistance

A

Epi (+) B<strong>2</strong> Receptor

=AIRWAY DILATION

236
Q

Asthma treatment

A

=B2 agonist

237
Q

match airflow and bloodflow

A

with decreased CO2 = airway constriction

238
Q

increased compliance of lungs

(what diseases have this problem?)

A

=large change in V for a change in P

=easy to inflate

-emphysema- cant get air out

239
Q

decreased compliance

A

small change in volume for a change in pressure

=hard to inflate

  • happens wiht restrictive disorders
  • work of lungs is increased
240
Q

surfactant

A

a lipoprotien

decreases surface tension

(-) alveoli from collapsing

from type II alveolar cells

made late in fetal development

241
Q

surface tension and radius

A

higher ST in smaller radii

∴ surfactant is more important and also works better in smaller radii lumens

242
Q

Total P of O2=

A

O2= PB x FO2

Barrometric P x Force of O2

=(760 mmHg)(0.21)

=160 mmHg

243
Q

Partial pressure of inspired air=

A

PO2 = (PB-PH2O) x FO2

=(760-47) x (0.21)

=150mmHg

244
Q

effects of high altitiude on partial P of ispired air

A

decreases it bc there’s a decrease in total pressure

PO2 = (380-47)(0.21)

PO2 = 69.93

245
Q

the amount of gas dissolved in a liquid is proportional to ___

A

its partial pressure

A LINEAR RELATIONSHIP

246
Q

things that will increase simple diffusion

A
  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
247
Q

diffusion capacity

A

=the amount of gas the lungs can transfer to the blood

248
Q

two things that limit diffusion capacity (O2 transfer)

A
  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

249
Q

in health getting O2 in blood is _____ limited

A

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
250
Q

in circulatory system where is P high and low?

A
251
Q

pulmonary vascular resistance regulation

A
  1. recruitment= open more capillaries
  2. distension= increase radius of capillaries
252
Q

3 benefits of recruitment and distension

A
  1. decreased resistance =no edema
  2. decreased velocity of blood floow= more time for gass exchange
  3. increased SA for gas exchange
253
Q

pulmonary vascular system is regulated by

A

hypoxia

NOT autonomic NS

254
Q

when alveolus is blocked blood vessel___

A

constricts

255
Q

at a higher altitude=

A

-decreased PO2 everywhere

=general vasoconstriction

=increased BP and work of heart

256
Q

atmosphere to lungs PO2 drops bc___

A
  1. H20 (humidifies)
  2. its mixed with dead space air
  3. its mixed with residual volume air

PO2 160 to 105mmHg

257
Q

PO2 from alvolus to blood drops bc___

A

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

258
Q

label the PO2 levels

A

160

105

100

100

<40

40

40

259
Q

Dissolved O2 at PO2 of 100mmHg

A
  1. 3ml O2/100ml of blood
    - this is a small amount
260
Q

at PO2 of 100mmHg there is ___ ml O2/100ml blood bound to Hb

A

20.1

=vast majority of O2 in blood is bound to Hb

-doesnt contribute to PO2

261
Q

____ is detected by chemoreceptors

A

dissolved O2, not bound to Hb

262
Q
A
  • this is what is seen by the lungs
  • increasing PO2 doesn’t saturate more Hb
263
Q
A

If PO2 drops to here… Hb is still nearly saturated

264
Q

PO2 =40

A

this is what’s seen near normal tissue

O2 IS COMMING OFF Hb

Hb is at 75% saturation

265
Q

PO2 =25mmHg

A

what is seen near ACTIVE tissue

=50% saturated Hb

266
Q

as O2 unbinds to Hb= ____

as O2 binds to Hb=____

A

as O2 unbinds to Hb= Hb’s affinity for O2 decreases

as O2 binds to Hb= its easier to add O2

267
Q

Left shift happens when…

A

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)

268
Q

Right shift happens when…

A

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

269
Q

hypoxia=

A

insuficient O2 in the tissues

270
Q

diffusion impairment caused by

A

edema in the lungs

271
Q

diffusion impairment and decreased atmospheric PO2 cause___ which is detected by ___ and causes ____

A

decreased O2 in arterial blood

which is detected by chemoreceptors whic the (+) increased respriatory rate

272
Q

deficient RBC (anemia) causes =

A

less Hg ∴ less O2

-THIS IS NOT DETECTED BY CHEMORECEPTORS because amountof dissolved O2 is normal

∴ no stress is experienced

273
Q

CO poisioning

A

-causes less O2 to bind to Hb

CHEMORECEPTORS WILL NOT DETECT THIS!!

bc dissolved O2 levels are normal

∴ no stress is exprienced

274
Q

CO2 transported three ways:

A
  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)

275
Q

Draw pathway of CO2 out of tissues with high CO2

A
276
Q

Haldane effect

A

when O2 binds to Hb ∴ less CO2 binds to Hb and is expired

277
Q

bohr effect

A

near active tissue there is high CO2 and H+

∴more CO2 binds to Hb

∴ less O2 bound to Hb

∴ more O2 to muscles

278
Q

elements of the pulmonary system

A

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)

279
Q

___ (+) inspiration

A
  1. chemoreceptors

detect high CO2, and H+ and low O2

  1. pulmonary iritant receptors
280
Q

pulmonary stretch receptors

A

DO NOT inhibit normal inspiration (other brain centers do this)

they ONLY protect against over inflation

281
Q

PO2 and PCO2 effects on respiraton

A

PO2- has to drop from 100 to 60 t stimulate breathing

PCO2- any increase wil (+) breathing

282
Q

deep fast breathing =

A

decreases CO2 in blood ∴ you can hold your breath longer

283
Q

central chemoreceptors

found ___

stimulated by___

not stimulated by___

A

in medla of brain

stimulated by:

  1. high CO2 in blood

2 high H+ in interstitial fluid

NOT stimulated by:

  1. high H+ in blood
  2. low O2
284
Q

pathway of central chemoreceptor stimulation

A
285
Q

peripheral chemoreceptors

A

found in carotid and aortic bodies

  • measure arteiole blood
  • no BBB

∴ they detect blood’s:

high CO2 and H2O

low O2

286
Q

slowly adapting pulmonary receptors

A

in lung bronchiole smooth muscle

have the Hering-Breuer reflex

=stops overinflation of lungs

287
Q

rapidly adapting pulmonary receptors

A

=irritant receptors

respond to injury, inflammatin, touch, chemicals

  • complex effects (+) cough and some inspiration
288
Q

cheyne-stokes breathing=

A

deep-rapid breathing (over ventilation)

then inhibits breathing ∴ (+) slower/stopped breathing

∴ (+) increased CO2 ∴ (+) deep rapid breathing again

=”waxing and waning”

289
Q

cheyne-stokes breathing occurs in=

A

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

290
Q

epiglottitis=

A

inflammation of the epiglottis

-it swells and blocks to trachea

=from injury or BACTERIAL infection

tx: O2, antibiotics

291
Q

Laryngitis

A

= inflammation of the vocal cords

=from overuse or VIRAL infection

tx: rest, maybe corticosteroids to reduce inflammation

292
Q

larynx/tracheal tumors

A
  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

293
Q

___ is associated with 30% of oral carcinomas

A

HPV= a cofactor for carcinoma

294
Q

95% of lung tumors are ____

A

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

295
Q

pneumonia=

A

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)

296
Q

pneumoconiosis

A

occupational lung diseases

-inhalation of dust

coal workers =black lung disease

->inflammation ->fibrosis and necrosis

asbestos ->inflammation -> fibrosis and lots of MESOTHELIOMA (lung cancer)

297
Q

pulmonary embolism definition and causes

A

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
298
Q

pulmonary embolism symptoms and tx

A

symptoms=

chest pain, shortness of breath, caughing up blood

may also be asymptomatic

treatment =

= O2

=antigoagulant

*prevention= compression stockings and mobilizing patients

299
Q

acute respiratory distress syndrome (ARDS)

A

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!

300
Q
A

Pathophys (3 decks)

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