Anderson Digestive Flashcards
what innervates constrictor/swallowing muscles
CN 9 and 10 (mostly 10)
what innervates stylopharyngeus muscle?
CN9
what innervates and elevates palate?
CN 5 and CN 10
levator tensor palati
where is esophagus
what does it go through
innervated by
behind trachea
through esophageal hiatus in diaphragm
CN 10 (vagus)
what kind of muscle in esophagus?
upper is voluntary swallowing striated muscle
lower is involuntary peristalsis smooth muscle
most common pharyngeal cancer caused by smoking
SCC
spread to cervical LN etc
What needs to be ruled out with GERD?
hiatal hernia
sliding is most common
esophageal varices are often caused by
portal hypertension
- also alcoholic cirrhosis
metaplasia of distal esophagus is called ___
this causes what histological change____ and predisposes for _____
Barrett’s esophagus
squamous cell converts to columnar gastric cells
adenocarcinoma
layers of muscle in stomach
internal: oblique
middle: circular
external: longitudinal
attachments of stomach
main artery
lesser omentum (hepato duodenal, hepato gastric ligaments) greater omentum (peritoneal ligament): lots of fat and circulation off greater curvature of stomache.
- celiac arteri (L and R gastric)
acute gastitis caused by
chronic gastritis caused by
NSAIDS, ETOH, smoking, stress
- erosions
autoimmune, loss of parietal cells and IF, H pylori, B12 def
- no erosions
immune mediated destruction of parietal cells in stomach
hypochlorhydria
- also caused by chronic gastritis and hoshimotos thyroiditis, Addison’s
H. pylori predisposes ___
adenocarcinoma
compare gastric and duodenal ulcers
gastric: burning post-eating, better antacid, milk
duodenal: burning epigastric 1-3 hours after eating. Better eating, antacids
compare jejunum and ileum
ileum is longer, so has more blood flow, etc.
jejunum is shorter and less blood flow and lymphatic drainage, but there is more digestion going on.
where do mesenteries originate from
post abdominal wall
what could ileus or intususseption in adults be a sign of?
ischemic infarctive or metastatic cancer
involuntary smooth muscle
GI
resp
urinary
genital
what happens to muscle layers when you get to colon
lose layers of smooth muscle and have teniae coli: longitudinal bands that run length of colon to keep feces moving forward without peristalsis.
internal anal vs external anal sphincter
- internal is smooth muscle and responds to stretch, autonomic control
- external is striated muscle pudendal nerve and cognitive activity
iliocecal junction
end of ileum
cecum (appendix)
where is diverticulitis most common?
sigmoid colon
like appendicitis but on the left side
familial polyposis have increased risk for ___
colorectal cancer
Crohns vs UC
Crohns: skip lesions, more blood, more pain, fistulas
UC: more diarrhea, only rectum or continuous with whole colon
acute pancreatitis
abd pain, heavy alcohol use, autodigestion by proteases and lipase, elastases digest vessel walls, necrotic fat cells
lab: increase in amylase and lipase
acute liver failure
overwhelm liver with toxins
fulminant hep
go into kidney failure too
chronic liver failure
liver slowly dying
hypogonadism (phase 1 detox converts hormones and phase II…)
clotting problems (makes clotting proteins)
erythema
encephalopathy due to urea buildup because kidneys aren’t functioning
cholestasis
prehepatic causes:end up with unconjugated bilirubin because liver can’t convert
extrahepatic: conjugated bile, but it backs up because it can’t get out
blood supply to esophagus and stomach
to duodenum, small intestine, ascending colon, transverse colon
celiac
inf mesenteric
what are the three blood supplies to stomach and what do they branch from?
- splenic artery from celiac trunk gives short gastric and gastroepiploic arter that supply left side of stomach
- left gastric: back left side of stomach off celiac trunk
- right gastric from hepatic artery supplies right stomach
*all from celiac trunk
portal (venus) circulation
where does portal vein come from?
inf mesenteric vein drains through splenic veins
sup mesenteric meets splenic and they become portal vein
where do right and left gastric veins drain?
where does short gastric vein drain?
right and left gastric veins drain into portal
short gastric into gastroepiploic that drain into sup mesenteric vein
portal venus drainage fails with portal HTN because ____ and this leads to ____
what diseases cause this?
portal veins can’t drain which leads to ascites and engorgement form anastamotic areas.
any liver disease causes this and so does third trimester of pregnancy
when are varices and hemerroids common?
pregnancy and liver malfunction
what causes caput medusae
periumbilical veins which can’t drain in later pregnancy, portal HTN due to liver damage
mucosa of stomach
submucosal plexus is there for
myenteric plexus is there for
longitudinal muscle is outer decreases length
inner circular muscle: decreases diameter
submucosal/meissners plexus for gland secretion
myenteric/auerbach’s plexus for smooth muscle contractions/motility
histamine ____
G cells secrete ____
stimulates gastric H+
gastrin
what do somatostatin and histamine do? What are they?
somatostatin: inhibits GI hormone release and acid secretion
histamine: stimulates gastric acid H+ secretion
- both are paracrines
what secretes CCK and what does it do?
secreted from I cells in duodenum and jejunum
stimulates contraction of gallbladder and relaxation of sphincter of oddi
increases pancreatic enzymes and bicarb secretion
where is secretin secreted and what does it do?
secreted from S cells of duodenum
increases pancreatic and biliary bicarb secretion
decreases gastric acid secretion because stomach is empty
where is GIP secreted and what does it do?
duodenum and jejunum
increases insulin secretion and decreases H+ secretion
what stimulates the release of bile?
CCK from duodenum and jejunum
- what do chief cells secrete?
- parietal cells
- mucus cells
- G cells
- chief cells: pepsinogen
- parietal cells: HCl and intrinsic factor (IF)
- mucus cells: mucus
- G cells: gastrin
where are carbs digested? amino acids iron vit B12 bile salts fatty acids lipids proteins
carbs: duodenum and jejunum amino acids: duodenum and jejunum iron: duodenum vit B12: terminal ileum bile salts: terminal ileum fatty acids: mycelized though entire sm intestine lipids: sm intestine proteins: sm intestine
where is the common hepatic duct in relation to the common bile duct?
hepatic duct is above cystic duct and bile duct is below
one organ that can mix arterial and venus blood
this blood is presented to
liver
hepatocytes
kupfer cells
bile canaliculi
in liver - immune cells
produce bile
what is bile created from?
what does bile do?
most bile is
from cholesterol (primary: cholic acid and chenodeoxycholic acid)
secondary: deoxycholic and lithocholic acids are converted from primary bile acids by bacteria
bile micelles fat
most bile is reabsorbed
how do you hold on to bile?
why do you want to hold on to bile?
fiber
so that liver is forced to use more cholesterol to make more bile
how are bile acids conjugated to form bile salts?
glycine and taurine
urobilinogen and stercobilinogne
urobilinogen: reabsorbed and absorbed by kidneys and excreted as urobilin
stercobilinogen: stays in stool and gives it color
rate limiting step in bile acid synthesis
hydroxly group introduced at carbon 7 by 7-alpha-hydroxylase
inhibited by cholic acid
what type of hepatitis can lead to hepatic carcinoma?
which type is related to transfusions?
hep B
B and C
liver cancer
what is it associated with?
hepatocellular carcinoma
HBV/HCV, cirrhosis, viruses
4 F’s of cholelithiasis?
Female
Fat
Forty
Fertile
2 types of stones in gallbladder
cholesterol and pigment (unconjugated bilirubin)
where do medium and long chain fatty acids go?
to lymph, not blood stream as chylomicrons
where does right lymphatic drain?
left?
right subclavian
left subclavian via thoracic duct
where does lipid absorption start?
lingual lipase in mouth
stomach: heat liquifies lipids
- gastric lipase breaks down TG, short and med chain FAs which absorb directly into portal circulation
deficiencies: A,D,E,K
A: night blindness
D: rickets, osteomalacia
E: ataxia
K: factor 2,7,9,10 bleeding disorders
Vit B deficiencies
B1 (thiamin): beriberi
B2 (riboflavin): (FAD) cheilosis/glossitis (pellegra)
B3 (niacin): (NAD)
B5 (pantothenic acid): burning feet, HA, nausea
B (pyridoxine (PLP): microcytosis, neuropathy
B12 (cyanocobalamin): macrocytosis, pernicious anemia, neuropathy
How does B12 free folate?
B12 frees folate from its bound form to its coenzyme form (THF) by releasing a methyl group and creates methionine from homocysteine.
N-5-methyl- THF
in what type of reactions is vitamin c used
biotin?
hydroxylation reactions
cofactor in carboxylation reactions
what does vit K do besides clotting?
moves Ca in body
CT and bone function
vitamin A forms
storage form?
retinol (active)
retinol ester (non active)
cartotinoids (two retinols together): want to reduce to retinol
- thyroid needs retinol
***storage form: retinol palmate
parietal cells secrete
chief cells secrete
enteroedocrine
Hcl
pepsin
gastrin (from G-cells)
3 organs involved in vit D synthesis
skin: to cholecalciferol
liver: to 25-hydroxyl
kidney: 1-25-dihydro D3 (active)
- Ca out of bone (stim osteoclasts)
- Ca absorption in intestine
- increases serum Ca
what preserves glutathione?
what is needed to make glutathione?
vit C
cysteine and methionine and glycine make glutathione
