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38 Cards in this Set
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- Back
- 3rd side (hint)
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Gastrin
Source+ Action Regulated by |
G cells, antrum (end of stomach)
Gastrin (which stimulate Parietal cells-> HCl secretion), also increase gastric motility and mucosa growth! |
Pos stim: Vagal stim (GRP)
Neg stim: GIP? |
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CCK
Source+ Action Regulated by |
I cells, duodenum jejunum
contract GB, increase panc secretions, slow gastric emptying! |
Pos stim: FAs, amino acids, NOT CARBS -> fatty foods make cholelithiasis worse w/ fatty food, use small meals high in fat to regulate by pass "dumping syndrome" to slow stomach emptying and avoid huge sugar rush to the duodenum
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Secretin
Source+ Action Regulated by |
S cells, duodenum
increase bicarb and bile from pancreas, lower gastric acid secretion (natures antacid) |
Pos: acid and FAs in duodenum
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GIP
Source+ Action Regulated by |
K cells, duodenum, jejunum
increase insulin secretion, lower gastric H+ secretion |
Pos stim: Oral glucose, FAs, AAs (so all food)
Oral glucose>IV to get into body b/c of insulin secretion w/ oral glucose |
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VIP
Source+ Action Regulated by |
PSNS in sphincters, GB, small intestine
increase ion (Cl-) and H20 into gut lumen, relax SM and sphincters |
Pos stim: stretch, vagal stim, down by SNS input
VIPoma: watery diarhhea (non-alpha or beta cell islet cell tumor) |
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NO
Source+ Action Regulated by |
ECL cells
SM tone in LES |
loss of NO secretion -> achalasia
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Motilin
Source+ Action Regulated by |
Small intestine
MMCs in intestine |
Pos: empty GI tract, fasting state
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Intrinsic Factor
Source+ Action Regulated by |
Parietal cells (body of stomach)
Allow B12 absorption in terminal ileum |
Not really regulated, tied to parietal cell acid production
AI destruction of parietal cell from chronic gastritis: B12 deficiency |
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HCl
Source+ Action Regulated by |
Parietal cells (body stomach)
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Pos: histamine (ECL -> Histamine -> H2 receptor-> cAMP), ACh (Vagus-> M3 receptor->IP3/Ca), gastrin (GRP -> G cells-> gastrin->CCKB-R ->IP3/Ca)
Neg: somatostatin+PGE (Gi-> lower cAMP), secretin, atropine (block ACh on M3 receptors) |
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Pepsinogen
Source+ Action Regulated by |
Chief cells (body of stomach)
break down AAs |
Pos: acid, vagal stimulation
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Achalasia cause
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NO loss
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lower esophogeal sphincter tone down
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What causes stomach hyperplasia? When do you see high of that hormone?
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Gastrin
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Can go up in Zollinger-Ellison syndrome (also stimulate acid secretion)
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I cells
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CCK
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I cells: CCK
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S cells
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Secretin
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S cells: Secretin
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D cells
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Somatostatin
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D cells: Somatostatin
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K cells
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GIP
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K cells: GIP
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Brunner's glands
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in duodenum, stim by secretin
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secrete HCO3
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Peyer's patch
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ileum lymphoid tissue that make IgA
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macrophages, dendritic cells, B-lymphocytes, and T-lymphocytes
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Somatostatin
Function and location Regulation |
D cells (pancreas and GI mucosa)
lower HCl and pepsinogen secretion, lower pancreatic and intestine fluid secretion, lower GB contraction and lower insulin and glucagon release |
Pos: Acid, vagal stim
Inhib growth hormone -> analogue for VIPoma and carcinoid tumors |
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What converts trypsinogen to trypsin?
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enterokinase/enteropeptidase
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Trypsin activates other proenzymes and more trypsinogen (pos feedback look)
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What takes up monosaccharides
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glucose/galactose: SGLT1 (Na cotransport) (also seen in kidney 1+2)
Fructose: GLUT-5 faciliated diffusion |
Then passively transported on basal side by GLUT-2
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Where is Iron absorbed?
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Duodenum
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Low: anemia
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Where is B12 absorbed
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Distal Ilium along w/ bile acids
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Low: macrocytic megaloblastic anemia w/ parathesisias, other mental changes
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Where is Folate absorbed
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Jejunum
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low: macrocytic megaloblastic anemia, NTDs
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Indirect bilirubin=
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= unconjugated
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help
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Direct bilirubin=
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= conjucagted
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help
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Location of salivary gland tumors
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usualy benign, parotid gland
Adenoma: painless, movable mass Warthin's tumor: benign, salivary gland tissue trapped in lymph node |
mucoepidermoid carcinoma most common
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Location of oral cancer and presentation
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oral cancer is usually in base of mouth > tip of tongue
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leukoplakia
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Pneumonic for achalasia
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Cha = Chagas (heart, mexico) and CREST (scleroderma)
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Loss of myenteric plexus in LES, risk for esophogeal carcinoma up
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Borerhaave syndrome
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been-heavin' syndrome
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transmural esophogeal rupture
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Lye ingestion
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Esophogeal stricture
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dunno importance?
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Esophagitis related infections
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reflux, HSV-1, CMV, candida
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or chemical injestion
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Plummer-Vinson syndrome
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1) dysphagia (esophogeal webs)
2) iron-def anemia 3) Glossitis (burning tongue and mouth pain) |
Tx: iron supplementation
risk of SCC increased |
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Esophogeal webs: associations?
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bullous diseases (such as epidermolysis bullosa, pemphigus, and bullous pemphigoid), graft versus host disease involving the esophagus, and celiac disease
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pain and dysphagia
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RFs for Esophogeal Cancer
most common in US and abroad |
ABCDEF
Adeno = lower 1/3, SCC = upper and middle 3rds US: SCC = adeno (lots of acid reflux) Worldwide: SCC most common (HPV, smoking, etOH, chronic inflammation) |
alcohol, barretts, cigarrettes, diverticuli (Zenkers) esophageal webs (Pulmmer-vinson)/Esophagitis, Famililal
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Whipple's dz
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Tropheryma whippelii (gram +) infection
PAS-pos macrohages in instein |
arthralgias, cardiac and neurological signs, old men, malabsorbtion
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Pathophysiology of CF pancreatic insufficiency
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lack of Cl- transporter -> autodigestion of pancrease ->
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fat malabsorbtion and A,D,E,K malabsorbtion
can also be from obstructing cancer or chronic pancreatitis (EtOH) |
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Celiac sprue
histology related dz |
antigliadin antibodies, villious blunting, lymphocytic infiltrates, anti-transglutaminase antibodies
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Related to dermatitis herpetiformis (itchy chronic blister dz-> use dapsone)
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